12Paraphilic_Disorders_SexualDysfunctions_and_Gender_Dysphoria

12 Paraphilic Disorders, Sexual Dysfunctions, and Gender Dysphoria

Chapter Objectives

After reading this chapter, you should be able to do the following:

• Identify sexual behavior that is considered to be disordered.

• Name the various types of sexual dysfunctions.

• Explain how people with sexual dysfunctions can be helped.

• Explain how or if sexual dysfunctions can be prevented.

• Describe the etiology and treatment of gender dysphoria.

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Although sex is healthy, important, and worth discussing, it is not always a topic that is talked about openly. However, what to do, how to do it, and who to do it with are the central top- ics of movies, books, television shows, magazine articles, newspaper reports, popular music, Internet sites, and advertisements. Despite this avalanche of information, society’s attitudes toward sex remain conflicted and confused. Are some sex practices signs of mental illness? What is normal, anyway?

Because of people’s seemingly endless fascination with the topic, sex is the subject of a huge amount of professional literature. This chapter focuses on three aspects of this literature: paraphilic disor- ders, sexual dysfunctions, and gender dysphoria, as described in the DSM–5. The chapter is divided into three main sections. The first deals with the para- philias (unusual sexual desires or acts), the second examines sexual dysfunction (difficulties in per- forming sexual acts), and the third section discusses gender dysphoria (discomfort with one’s assigned sex role).

Although the focus of the chapter is on sexual behavior, it is wrong to think about these prob- lems as somehow separable from other aspects of a person’s life. As you will see, an individual’s sexual behavior is influenced by his or her genetic back- ground, medical condition, personal history, use of substances, psychological state (especially the pres- ence of anxiety or depression), and the prevailing cultural norms. To show how these factors come together to influence both normal and problematic sexual behavior, this chapter tells the story of four

people: Peter Hall, Anne Lawrence, and Anne’s two sons, Jared and Luke. Through a series of tragic circumstances, the lives of these four people intersected and were changed forever. We will begin with the case of Peter Hall.

Ray Fisher/Getty Hugh Hefner, the publisher of Playboy magazine (shown here in his earlier years), has been a recognizable symbol of sexual identity in Western culture.

The Case of Peter Hall: Part 1

Peter Hall was born with a silver spoon in his mouth. His successful stockbroker father sent him to elite private schools, and his mother made sure that he received the best music lessons. Each summer, he went on trips to the cultural capitals of Europe. Now in his late 40s, Peter speaks five languages, drives a Jaguar sports car, and owns a yacht and three homes. He is a familiar figure at art galleries and chairs the museum board. Charming and urbane, Peter is especially well known for his charity work with underprivileged boys. Not only does he sponsor sports teams and camps, but he has also looked after wayward youths. He has provided them with emotional and financial support; some have even lived in one of his homes. So, imagine the shock to the community when Peter was arrested and charged with child sexual assault. The following document displays a newspaper account of the case against Hall.

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Newspaper Story Describing the Arrest of Peter Hall Chair of Museum Board Arrested for Child Sexual Assault

by Ron Nicks

Businessman Peter Hall, aged 48, was arrested by Metro Police and charged with seven counts of child sexual assault. Hall had been under investigation since police were approached by Mrs. Anne Lawrence, a divorced schoolteacher from Ross River. She claimed that Hall had sexually abused her sons, Jared, now aged 13, and Luke, aged 10, and that the abuse had gone on for a year.

“At first, I thought Peter was the best thing that ever happened to my boys. Their father abandoned us, and I had to raise them alone. They needed a father figure, and I thought Peter was it.”

According to their mother, Jared and Luke met Hall last summer at the beach. They were admiring Hall’s classic antique surfboard when he struck up a conversation with the boys. Later that afternoon, he invited Anne and her sons to his beachfront apartment for refreshments. In the apartment, the boys played with Hall’s vast collection of video games and listened to his music CDs. They made plans to get together again the next day. After the summer, their relationship continued. On the weekends that Hall used the beachfront apartment, the boys were invited to join him. Often, their mother accompanied them.

“I went to his apartment many times,” says Anne. “I always found Peter pleasant and entertaining. He was so refined and cultured. I thought we were friends. Jared and Luke adored Peter, and he treated them like the sons he never had. He introduced them to opera and classical music. I thought he was the ideal father.”

Anne first began to suspect something was wrong when she found drugs (later identified as amphetamines) in Jared’s drawer. She went to Hall for help. He offered to pay for counseling and to enroll Jared in a special program for substance using teenagers. Because the program was located near his city home, Hall offered to have Jared live with him. What Hall neglected to tell Anne was that he was the source of Jared’s amphetamines. Jared moved in with Hall, and Anne visited him on many weekends. Instead of improving with treatment, however, Jared seemed to get worse. According to Anne, he often seemed “dazed and strung out.”

“One night I got a call from Peter telling me that Jared was ‘very sick.’ I hurried to Hall’s home. I knew something was seriously wrong when I saw the police car parked outside. I ran inside. There was Jared, just lying there, unconscious from what turned out to be an overdose of sleeping pills. We got him to the hospital and had his stomach pumped. When he awoke, he told me that he had tried to kill himself to get away from Peter, who not only used him for sex but also made him have sex with Peter’s friends.”

Anne soon learned that Jared was not Hall’s only victim; Luke had also been involved. The police investigation turned up five other boys who claimed that they, too, had been Hall’s victims. Police inspector Philip Langton, who led the investigation, searched Hall’s home after the arrest. “We found amphetamines and hundreds of photographs of naked boys, some as young as 5 years old. There were many computer games, toys, and videos—everything young boys might like. Hall’s home computer was full of photos of boys, as well as contacts and connections to pedophile sites around the world.”

Hall faces trial next March.

See appendix for full case study.

The Case of Peter Hall: Part 1 (continued)

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Section 12.1 Paraphilic Disorders (Paraphilias)

12.1 Paraphilic Disorders (Paraphilias) A breakthrough in research on sex occurred in the 1940s when Alfred Kinsey (1894–1956) and his col- leagues used surveys to paint a statistical portrait of the sexual behavior of 18,000 American men and women (Kinsey, Pomeroy, & Martin, 1948; Kinsey, Pomeroy, Martin, & Gebhard, 1953). Many of their findings were surprising, at least at the time. Prac- tices that were considered rare and harmful (mas- turbation, for instance) were actually found to be quite common. Since then, we have come to recog- nize that what constitutes acceptable sexual behav- ior is largely a function of cultural mores. Activities considered normal in one time and place may be prohibited in another (Giami, 2015). Nevertheless, independent of time and culture, we have been able to determine certain sexual behaviors that qualify as psychological disorders.

According to the DSM–5, the paraphilic disorders are characterized by intense sexual fantasies about, and urges to have (a) sex with nonhuman objects (bras or panties, for example), (b) sex that involves suffering on the part of oneself or one’s partner, or (c) sex with children. The person need not act out these fantasies to receive the diagnosis, although many do (American Psychiatric Association [APA], 2013). Although the DSM–5 describes only a small number of paraphilias, it contains an “unspecified” category that may include dozens, per- haps hundreds, more (Schewe, 1997). It seems that just about anything, from scuba diving suits to toilet seats, can become imbued with erotic significance. Despite their diverse range, all paraphilias share a central characteristic—in every case, sexual behavior has been discon- nected from a loving, consensual relationship with another adult. This category would be used, for example, in situations in which the clinician is confident that a paraphilia is present and causes distress or impairment (recall the maladaptive behavioral perspective discussed in Chapter 1), but there is insufficient diagnostic information present to determine the type of paraphilia (Krueger & Kaplan, 2015).

Almost all people with paraphilias are male (Handy & Meston, 2016; Konrad, Welke, & Opitz- Welke, 2015). Here is one possible explanation: Males may be more aware of their sexual arousal because they experience erections and have noticeable changes, whereas women may be aroused but may not report it because they experience sexuality differently and without obvious physical changes like an erection (Handy & Meston, 2016; Konrad, Welke, & Opitz-Welke, 2015). Another possible explanation is that women might not be attending to their genital responses and/or might be unable to accurately perceive their genital responses, thus lacking interoceptive aware- ness when genital arousal occurs (Handy & Meston, 2016). Regardless, some researchers believe that the reason(s) behind the significant gender split remain unknown (Konrad et al., 2015). It is unusual for a female to meet the diagnostic criteria for any of the paraphilias other than masoch- ism (for which they still represent the minority; APA, 2013).

Bettman/Getty The work of Alfred Kinsey during the 1940s challenged commonly held ideas about American sexual behavior.

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Diagnosis The main characteristics of the DSM–5 paraphilic disorders are summarized in this section. To qualify for one of these diagnoses, a person must have fantasies and urges that last at least six months. During this period, people need not restrict themselves solely to paraphilic fantasies or sex; they can engage in other types of sexual behavior as well. In most cases, however, paraphilias (more often, several paraphilias) become the person’s dominant form of sexual expression. Like compulsions, paraphilic disorders consume much of people’s lives (Guay, 2009). Individuals may engage in their paraphilia every day, sometimes several times each day. Some collect fetishistic objects (for example, shoes or bras) or photographs depict- ing their preferred paraphilic interest. Although some paraphiliacs are loners who keep their sexual behavior hidden, others are social enough to join interest groups of fellow paraphiliacs who meet either in person or on the Internet. They may share paraphilic objects or informa- tion, and, in some notorious cases of pedophilia, they may even share victims.

Exhibitionist Disorder The DSM–5 defines exhibitionist disorder as exposing one’s genitals to a stranger, sometimes accompanied by masturbation (APA, 2013). The desire to expose one’s genitals in public is often seen as a compulsive behavior. Affected individu- als (“flashers”) may be trying to shock the observer, and they often succeed. In some cases, exhibition- ism may involve the fantasy that the stranger will find the display sexually arousing. The disorder is usually found among teenage and young adult males who grew up in sexually repressive homes and have little experience with women.

Fetishistic Disorder The use of nonliving objects, such as shoes, bras, underpants, or leather clothing, in fantasy or directly to achieve sexual gratification, is called fetishistic disorder or, more commonly, fetishism. Some individuals have extensive fetish collections that they have purchased or, in some cases, stolen. They may masturbate while fondling the object, or they may ask their partners to don the object dur- ing sex. The fetishistic object is not just a stimulant

(many men are attracted by women in high heels and sheer stockings); it is detached from the female and sexually stimulating on its own. For people with fetishism, sex is impossible without the fetish. Using objects specifically designed for sexual stimulation (vibrators, for example) is not considered a sign of fetishism. Fetishism begins in puberty and tends to last a lifetime (APA, 2013).

Photodisc/Thinkstock Exhibitionism, or exposing one’s geni- tals to a stranger, is the most common sexual offense punishable by law.

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Section 12.1 Paraphilic Disorders (Paraphilias)

Frotteuristic Disorders Frottage is French for “rub,” and frotteuristic disorder involves touching or rubbing up against nonconsenting individuals, usually in crowded places. Typically, the individual gets behind a person in a crowd and rubs his or her genitals against the person’s buttocks or fondles the person with his or her hands. This behavior may be accompanied by fantasies of a sexual relationship with the individual. Most perpetrators run away as soon as the victim reacts. The behavior is most common in males aged 15–25 (APA, 2013).

Pedophilic Disorder (Pedophilia) Fantasizing about or engaging in sex with prepu- bescent children is termed pedophilic disorder or, more commonly, pedophilia. According to the DSM–5, pedophiles must be at least five years older than their victims (APA, 2013). Pedophiles, who seem to be exclusively male, generally focus on children younger than age 13. Most pedophiles pre- fer females, but some prefer males, and others are aroused by both (Hughes, 2007). Pedophiles may be sexually attracted only to children (exclusive type) or to both children and adults (nonexclusive type). Most are satisfied to fantasize about sex with chil- dren or to collect child pornography. Because this subgroup of pedophiles never acts out their fanta- sies, they typically do not get into trouble with the law (possession or distribution of child pornogra- phy is a crime, however). Among pedophiles who do engage in sex with children, some fondle them or masturbate in front of them. Others engage in sexual intercourse with children, sometimes using force to achieve their ends.

Pedophiles rationalize their behavior as “educat- ing” the child or giving the child sexual pleasure, or they allege that the child seduced them. Pedophiles may limit their activities to their own children (incest) or to others they know, or they may prey on strangers (Choi, Choo, Choi, & Woo, 2015). In gen- eral, pedophiles will usually prey on children they know, and within a short distance of where the pedophile lives. This may include extended family members who live nearby (Krueger & Kaplan, 2008). Some seek occupations (such as teaching) that bring them into contact with children. Pedophiles may physically threaten their victims to prevent disclosure, as well as provide gifts (toys, access to adult-themed video games like Call of Duty, and so on) to keep the child quiet, as well as to coerce the child to participate in the abusive situation. Pedophilic disorder usually begins in puberty and is highly resistant to punishment or treatment. (See Part 2 of Peter Hall’s case in the appendix.)

Alexander Koerner/Getty In 1977, French-Polish film director Roman Polanski was arrested and charged with unlawful sexual inter- course with a minor, then 13-year-old Samantha Geimer.

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Sexual Sadism Disorder

Fantasizing about inflicting or actually inflicting suf- fering or humiliation on another for sexual satisfac- tion is called sexual sadism disorder (APA, 2013). The term sadism is derived from the name of the Marquis de Sade (1740–1814), who wrote about his need to inflict humiliation and pain on others. Sadistic behaviors include whipping, torturing, cut- ting, beating, pinching, and spanking. Some people with sexual sadism find masochistic partners; oth- ers impose their desires on unwilling partners. Sex- ual sadism inflicted on nonconsenting partners is a criminal offense. The severity of sadistic acts tends to increase over time and, when associated with antisocial personality disorder, may lead to rape or even murder (Chan & Beauregard, 2016). Serial “lust murders,” in which men rape, often mutilate, and then deliberately kill their female victims, may be an extreme form of sexual sadism. Note, however, that neither rape nor murder is a paraphilia. Both seem motivated as much by hate and aggression as by lust, as the accompanying Highlight makes clear regarding rape.

Pantheon/Superstock The Marquis de Sade, namesake of the term sadism, had written extensively of his need to inflict pain and humiliation on others.

Highlight: Rape Is Not Sex

The previous definition of rape included only penile/vaginal penetration achieved against a person’s will by menace or force, or when the victim cannot give consent (because of intellectual disability, illness, intoxication, or being unconscious or comatose). Early in 2012 the Federal Bureau of Investigation (FBI) changed the definition to make the term more inclusive and more accurate. Most important, the phrase “carnal knowledge of a female forcibly and against her will” was removed. Now males and females can be victims or perpetrators. The new definition states, in part:

The penetration, no matter how slight, of the vagina or anus with any body part or object, or oral penetration by a sex organ of another person, without the consent of the victim . . . . The revised definition includes any gender of victim or perpetrator, and includes instances in which the victim is incapable of giving consent because of temporary or permanent mental or physical incapacity, including due to the influence of drugs or alcohol or because of age. The ability of the victim to give consent must be determined in accordance with state statute. Physical resistance from the victim is not required to demonstrate lack of consent. (FBI, 2012, p. 1)

Rape should be differentiated from sex with a minor, which is sometimes called statutory rape. Sex with a minor is always a crime, even when both parties consent to the sex.

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Section 12.1 Paraphilic Disorders (Paraphilias)

Sexual Masochism Disorder Sex involving real or imagined humiliation and suffering inflicted upon the self is described as sexual masochism disorder (APA, 2013). Females may fantasize about being held down and raped, for example. Males may stick themselves with pins or give themselves electric shocks while masturbating. When partners are involved, masochistic acts include whipping, bondage, and being urinated on. Some couples carry out elaborate sex rituals involving fetish- istic objects, such as leather-studded belts. Most of the time, physical damage is avoided, but, in some cases, masochists’ desire to feel pain can lead to serious injury or even death. For instance, some people may deprive themselves of oxygen by hanging from a noose or putting a plastic bag over their heads (hypoxyphilia or asphyxiophilia). The goal is to achieve enough oxygen depletion to enhance sexual arousal (Coluccia et al., 2016).

The accompanying Highlight addresses the question of whether sexual sadism and sexual masochism should be considered DSM–5 disorders.

Because many rapes are not reported, it is difficult to know how often rape occurs, but we do know that it is fairly common. In addition to any physical injury they suffer, rape victims may feel vulnerable, guilty, and depressed. The aftereffects of rape may include a negative attitude toward sex, an anxiety disorder, substance abuse, or all three. In addition, victims whose cases come to trial must endure humiliating questioning from defense lawyers, who attempt to demonstrate that the victim somehow provoked the attack (Campbell, 1998). Considerable psychological and community support is expended each year helping rape victims to reestablish their lives (Sacco, 2014).

Even though nonconsenting sex is a criterion for the paraphilic disorders (APA, 2013), rape is not considered a paraphilia because it is not primarily a sexual act. Although rape involves sexual penetration, rapists may not have erections or reach orgasm during their attack. They seem to be motivated not by sex but by the need to dominate, degrade, and subjugate their victims (Jamel, 2014). This is why rapes often include sadistic acts. Victims have had their breasts burned with cigarettes, their genitals mutilated, and, in extreme cases, they have been murdered.

According to one study, prevalence rates coming out of studies on university campuses range from 6% to 41% of college students being victims of attempted or completed rape (Jordan, 2014). When looking only at sexual assault, a more recent study found that prevalence rates of sexual assault were about 23% among first-year students (Conley et al., 2017). Regardless of the statistics, any percentage is too high.

What should you do if you or someone you know is a victim of rape? Most universities and colleges have a counseling center and/or a crisis hotline where you can report rape, either as a victim yourself or if a friend is a victim. In addition, you can visit http://rapecrisis.com/, a comprehensive website that also lists a 24-hour hotline: 210-349-7273. The website also has an online feature through which you can talk to counselors.

The Violence Against Women Act was reauthorized in 2013. It mandates services for all victims of domestic violence, sexual assault, dating violence and stalking, including but not limited to Native women, immigrants, LGBT victims, college students and youth, and public housing residents (Sacco, 2014). This is an important piece of legislation as it states that violence against any woman is considered a crime, no matter her race or ethnic background.

Highlight: Rape Is Not Sex (continued)

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Transvestic Disorder Cross-dressing for sexual pleasure by heterosexual males is called transvestic disorder (Balon, 2016). Most often, transvestic fetishists masturbate while wearing women’s clothes. Individuals may begin by wearing one article of women’s clothing, usually underwear, and stop there. Alternatively, they may progress to wearing an entire outfit and makeup. The behavior usually begins in childhood or adolescence and continues through adulthood and even through marriage. Cross-dressing by gay males (drag queens) to entertain an audience is not an example of transvestic fetishism. Some individuals find cross-dressing calming, even when no sex is involved. They may seek to live as women and may even have their sex surgi- cally reassigned. In general, however, cross-dressing by males who believe they are really females is not a form of fetishism but rather indicates gender dysphoria (discussed later in this chapter).

Voyeuristic Disorder Sexual fulfillment and excitement gained by watching unsuspecting people disrobe or engage in sex is called voyeuristic disorder. Watching people who know they are being observed is not considered a paraphilia (APA, 2013). Usually, men masturbate while “peeping” or later as they recall what they have seen. In severe cases, this is the person’s only form of sex. It begins

Highlight: Should Sexual Sadism and Sexual Masochism Disorder Be DSM–5 Diagnostic Categories?

We have spent the entire length of the book discussing mental disorders, and how to define abnormal behavior. There is one area that remains quite controversial: Are we as psychologists, and students, able to state with conviction that sexual sadism disorder and sexual masochism disorder are diagnosable? This question has led to much debate in the field, and outside of it. For example, Handy and Meston (2016) note that paraphilic fantasies are common in college-age students as well as in the general population. This is especially true for sadism and masochism or, to use as the authors’ term, BDSM (standing for “bondage & discipline/dominance & submission/sado-masochism”). Handy and Meston found that more than 60% of male college students fantasized about sadism and bondage, while more than 50% of female college students reported having had sexual fantasies in which they submitted to force or intrusive thoughts about being sexually victimized. It seems that what we are diagnosing appears to be occurring in the statistical majority of the population, which contradicts the statistical frequency definition of abnormal behavior.

An opposing viewpoint is posited by Konrad, Welke, and Opitz-Welke (2015), who note that in an empirical analysis conducted by Robertson and Knight (2015), it was discovered that sadism and psychopathy consistently predicted sexual and nonsexual violence. In addition, serial sex offenders were more likely to engage in sexual masochism (Konrad et al., 2015).

Not surprisingly, we are presenting to you opposing perspectives. Suppose a patient came to you asking for help to “get over” his love of being a sexual masochist. How would you handle this? Would you diagnose him with sexual masochism disorder? Are we discussing paraphilias, lifestyle choices, sexual preferences, or something else? These are just a few more questions for you to think about.

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in late adolescence; it cannot be diagnosed before age 18, since the DSM–5 states that there is “substantial difficulty in differentiating it from age-appropriate puberty-related sexual curi- osity and activity” (APA, 2013, p. 688). The course of the disorder varies based on the age of the individual (APA, 2013).

Unspecified Paraphilic Disorder The DSM–5 category of unspecified paraphilic disorder encompasses a mixed collection of sex- ual behaviors and interests including making obscene phone calls; having sex with corpses or animals; deriving sexual pleasure from enemas; and partialism, which is an intense sexual attraction to a specific body part, most often breasts or buttocks.

It is difficult to know how frequently paraphilias occur because people with paraphilic dis- orders rarely seek clinical assistance (Burgan, 2010). The limited data that are available as to prevalence come mainly from surveys of people who have been convicted of sex crimes— which is hardly a representative sample of the general population. Convicted sex criminals are not even a representative sample of people with paraphilias because most paraphilias are not illegal.

Another reason it is difficult to obtain accurate prevalence estimates is that paraphilic behav- ior may be masked by other diagnoses. For example, some people engage in paraphilic behav- ior only when intoxicated by alcohol or drugs, whereas others display paraphilic behavior only during psychotic episodes. These individuals will normally be diagnosed with substance intoxication or psychosis, respectively; their paraphilic behavior may never be officially recorded. Although it may be a difficult clinical judgment to make, people who deliberately use substances to help them act out their paraphilic fantasies should probably be diagnosed as having a paraphilic disorder because it is their primary disorder.

Etiology

Biological Causes Research on the biological causes of the paraphilias has concentrated on trying to find some physiological or anatomical difference between people with paraphilias and everyone else. Because sex drive is determined partly by hormone levels, and because paraphilias affect mainly men, researchers have tried to demonstrate that men with paraphilias have higher levels of male sex hormones than people without paraphilias. Similarly, because brain dam- age can lead to odd sexual behavior in animals, scientists have tried to find evidence that peo- ple with paraphilias have brain damage. Although both lines of investigation have produced some confirmatory evidence (Holoyda & Kellaher, 2016; Mohnke et al., 2014), the data are far from conclusive. One problem is that hormone levels are not tied directly to paraphilias. Most men with high hormone levels do not meet the diagnostic criteria for a paraphilia. A second problem is that hormone levels are affected by various substances. Because people with para- philic disorders, especially those convicted of sex crimes, may also use substances, it is not clear whether higher than normal hormone levels are the cause of paraphilias or the result of substance abuse (Langevin, 1992).

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Because paraphilias are largely a male phenomenon and some types seem to run in fam- ilies, researchers have suggested that they may be at least partly inherited. Keep in mind, though, that a trait does not have to be genetic to run in families. It is possible that members of each new generation are introduced to paraphilic behavior by their forebears. Pedophilia, for example, may be the result of one generation molesting the next (Zucker & Seto, 2015). In sum, it has not yet proved possible to identify a specific biological cause for any of the para- philias. Progress is likely to remain slow because research volunteers are rare, and, conse- quently, sample sizes are small. The same problems apply to research on the potential social and psychological etiologies of the paraphilias.

Social and Psychological Causes Because sexual behavior usually takes two people, it is a social process. You must first locate a potential partner, ascertain whether your desire is reciprocated, and then initiate the behav- iors that eventually lead to sex. In the paraphilic disorders, one or more of these preliminaries has somehow gone awry—those with a paraphilic disorder were thought to have a kind of “courtship disorder” (Freund & Seto, 1998). However, the “courtship theory” postulated by Freund and Seto (1998) is not supported by current data. Although the theory may sound rea- sonable, it does not offer etiological explanations for voyeuristic disorder, exhibitionist disor- der, frotteuristic disorder, and preferential rape (this means forcible sex agreed upon before- hand by both participants). That is, distortions of the normal courtship process in males is not a supported explanation for paraphilic disorders (Balon, 2013).

How do paraphilias evolve? The answer probably depends on the specific paraphilia and the specific person (Laws & O’Donohue, 1997). There appear to be common factors that apply to practically all paraphilias, however, and these are just what you might expect (Furnham & Haraldsen, 1998). Specifically, people with paraphilias seem to have had childhood and adolescent experiences that limited their ability to be aroused by consensual sexual activ- ity, increased their arousal by atypical stimuli, or restricted their ability to empathize with the victims of their paraphilic behavior. For example, some people with paraphilias were led to consider themselves unattractive, a feeling that produced severe social anxiety. Instead of dating and courtship, they turned to less socially threatening forms of sexual fulfillment, such as the paraphilias. Some people with paraphilias come from environments that fostered repressive, guilt-producing attitudes toward sex. There is also evidence that some people with paraphilias were sexually abused as children (Levenson & Grady, 2016; Thibaut et al., 2016). Their early experiences may have limited their ability to form intimate relationships later in life.

The psychological results of these early experiences—social anxiety, ignorance, guilt, fear (alone or in combination)—serve to misdirect sexual impulses away from intimate social rela- tionships and toward other sexual outlets. Once this happens, practically anything can take on sexual connotations (Love, 1993). Articles of women’s clothing, for example, can become fetishistic objects through classical conditioning. That is, they are conditioned stimuli whose presence during masturbation leads to their association with the conditioned response of orgasm (Sarver & Gros, 2014; Thibaut et al., 2016).

Paraphilic learning can also take place through operant conditioning. For example, when they were children, people with transvestic disorder may have been encouraged and rewarded for

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dressing as females. Modeling may also play a role in the development of paraphilias. Para- philic activity is common in pornography, and people without other sexual outlets may copy the behavior depicted in DVDs, online, and in magazines. Once tried, this behavior may be reinforced by masturbation and orgasm. However, some research suggests that conditioning is unlikely to play a significant role in the onset of paraphilic disorders (Zucker & Seto, 2015). What do you think?

In contrast to behavioral theories about the etiology of paraphilias, psychodynamic expla- nations focus on the apparent symbolism of these disorders. For example, men who don women’s clothing may be seeking a way out of their responsibilities (as fathers or providers). Similarly, people who seek physical punishment and humiliation during sex may be display- ing guilt about their sexual urges, whereas those who find administering punishment sexually exciting may be overcoming feelings of inadequacy by seeking power over others.

Although they are difficult to prove, these psychodynamic hypotheses seem at least superfi- cially plausible, and they do not exclude the possibility that paraphilic behavior is learned. A complete explanation for paraphilias may need to include both conditioning and psychody- namic components. Because most people with a paraphilic disorder are men, biological fac- tors will need to be incorporated as well. Finally, as already noted, substance use may provide the disinhibition that allows people to act on their paraphilic urges. In other words, like most disorders, the paraphilias will almost certainly turn out to be the result of social, psychologi- cal, and biological factors. (See Part 3 of Peter Hall’s case in the appendix.)

Treatment Clinical psychologists have always considered the paraphilias difficult to treat (Konrad, Welke, & Opitz-Welke, 2015). This is not surprising given that most people who undergo treatment are convicted sex offenders—men with the most severe, and most antisocial, paraphilias. People with mild paraphilias are rarely detected, let alone treated. Felons who participate in treatment are usually motivated by the promise of early release from jail, or they attend treatment after release as a parole requirement. Few are intrinsically motivated to change. Some, like Peter Hall, may not even admit that their behavior is disordered or harmful to oth- ers. Most treatment research has been aimed at “difficult to treat” sex criminal paraphiliacs, especially people with pedophilic disorder (see Balon, 2013, for example).

Even when clients are motivated to change, psychological treatments may not be up to the task (Walton & Chou, 2015). Psychodynamic therapy, based on insight and interpretation, has not been successful at “curing” paraphilias, nor has the most commonly applied form of behavior therapy—aversive conditioning. The idea behind aversive conditioning is to asso- ciate paraphilic objects with negative stimuli, thereby transforming their sexually arousing properties into aversive ones (Sarver & Gros, 2014). For example, to treat a person with a fetish for women’s shoes, therapists pair a painful stimulus, such as an electric shock, with one of the fetishist’s favorite shoes. Eventually, instead of sexual arousal, the sight of the shoe should elicit fear. Treating a pedophile is similar; an aversive stimulus is administered while the client looks at a photograph of a child (Zucker et al., 2015).

Because aversive conditioning is designed to be unpleasant (that is why it is called aver- sive), treatment dropouts are common. To make aversive conditioning more palatable, some

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therapists have used covert sensitization, in which aversive stimuli are presented, not directly (as in electric shock), but in the imagination (Walton & Chou, 2015). For example, a client may be asked to imagine approaching a child and then, as the client becomes aroused, to conjure up an image of being caught in a sexual act with the child by disgusted relatives. Unfortunately, neither aversive conditioning nor covert sensitization, on their own, produces a significant reduction in paraphilic behavior.

In an attempt to improve treatment outcomes, clinicians have devised cognitive-behavioral (multimodal) treatment programs (Calleja, 2013). In addition to aversive conditioning, these treatments may include cognitive restructuring, desensitization (to overcome the anxiety produced by social and sexual situations), stress management, and skills training designed to help clients develop social relationships.

In cases of incest, family therapy may be employed to help family members come to grips with the perpetrator’s behavior. Relapse prevention may be used to help people recognize and avoid situations most likely to stimulate their paraphilic behavior (Calleja, 2013; Walton & Chou, 2015).

There is evidence that cognitive-behavioral treatment reduces the likelihood that paraphilic behavior will be repeated (Sarver & Gros, 2014), but relapses still occur, especially among pedophiles with a long history of sex offenses and whose victims are boys rather than girls. Because of the relatively high likelihood of relapse, certain treatment options might appear to be rather drastic to some people. Chemical castration with drugs is one such treatment option for repeat sex offenders (Konrad, Welke, & Opitz-Welke, 2015). For example, they may be given Depo-Provera (medroxyprogesterone), a birth control drug that reduces the level of the male sex hormone testosterone (Assumpção, Garcia, Garcia, Bradford, & Thibaut, 2014). Lowering testosterone levels reduces sex drive and makes erections more difficult to achieve. In some cases, antidepressants, antipsychotics, and tranquilizers can have similar effects (Assumpção et al., 2014). Because the drugs simply lower sex drive while leaving sexual inter- ests unchanged, clients are likely to return to their paraphilic behaviors once these drugs are discontinued. For this reason, drugs should be supplemented with psychological treatment.

The balancing argument given to justify such severe treatment is the even greater harm suf- fered by the victims of sex offenders, especially children. Victims of sex crimes may develop anxiety disorders (including posttraumatic stress disorder) and depression. Some may turn to abusing substances for solace. Many will develop some type of sexual problem themselves. Proponents argue that by preventing sex crimes, sexual predator laws (despite their stigmatiz- ing brutality) produce more good than harm. (See Part 4 of Peter Hall’s case in the appendix.)

Prevention Because treatment is difficult and relapse a significant problem, many experts believe that prevention, especially of sex crimes, is the best way to use our scarce economic and health resources (Daro, 1994; Reppucci, Land, & Haugaard, 1998). Primary prevention efforts have so far been limited to censoring paraphilic pornography. The idea is that pornographic mate- rials may have two negative effects: (a) They may provoke naive viewers into modeling unac- ceptable behaviors that, if reinforced through orgasm, may lead to the development of sexual disorders, and (b) they may stimulate people who already have antisocial sexual fantasies

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to act them out (Lasher & Stinson, 2017). In a society that values freedom of speech, a complete ban on pornography is impossible to achieve. About the best we can hope for is to keep pornography away from minors. Additionally, it is unclear whether pornogra- phy has as strong an effect on antisocial sex- ual behavior as many people believe (Lasher & Stinson, 2017). For both reasons, banning pornography has received less attention from psychological researchers than have various forms of secondary prevention. Recent research has outlined, however, one example of a successful primary prevention program: Prevention Project Dunkelfeld, which targets potential offenders. This pro- gram was established in Germany in 2005 to provide free and confidential treatment for individuals with pedophilic disorder who wanted therapeutic help. One service offered by this program is an anonymous hotline num- ber to call in case they feel they may commit a pedophilic act (Levine & Dandamudi, 2016). Would this program work as well in the United States? Can we presume that a treatment pro- gram that works well in another country would work as well, or better, in the United States?

One approach to secondary prevention uses school programs and public service announce- ments to warn children of potential dangers and to encourage them to report suspicious people or incidents (Lasher & Stinson, 2017; Levine & Dandamudi, 2016). A more extreme approach to secondary prevention is to keep sexual offenders locked away so that they can- not offend again. Several states have “sexual predator” laws that permit the legal authorities to conduct civil commitment proceedings for about-to-be-released prisoners deemed likely to repeat a sex offense. The outcome of these proceedings can be indefinite involuntary incar- ceration in a mental hospital (Grudzinskas & Henry, 1997). Theoretically, people who have served their complete prison terms may remain in custody indefinitely. In practice, this rarely happens; most offenders are released eventually. To limit their opportunity to repeat their crimes and to allow members of the community to protect themselves and their children, many jurisdictions require police to register sex offenders and to inform community mem- bers when a registered sex offender moves into their neighborhood (Lasher & Stinson, 2017).

12.2 Sexual Dysfunctions The chapter on sexual dysfunctions is new to the DSM–5. In the DSM–IV–TR, sexual dysfunc- tions were included in the chapter on sexual and gender identity disorders. Sexual dysfunc- tions interfere with an individual’s ability to perform sexual acts. As are most of the disorders described in this book, sexual dysfunctions are mainly exaggerations of common problems. At one time or another, practically everyone will have some problem performing a sex act. Fatigue, illness, stress, depression, and substance intoxication (alone or in combination) can make us either uninterested in sex or unable to perform sexually. When these everyday occurrences become persistent enough to disturb an individual or a relationship, the DSM–5 considers

AP President Bill Clinton signed Megan’s Law into effect in 1996. The law provides the pub- lic with access to certain information on the whereabouts of sex offenders so that residents may protect themselves and their children.

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them to be dysfunctions. Many of the dysfunctions are based on the work of Masters and John- son, whose description of the phases of the human sexual response cycle is addressed next.

Human Sexual Response Much of what we know today about the biological aspects of sexual behavior originated in the work of William H. Masters (1915–2001) and Virginia E. Johnson (1925–2013) in the 1960s (Masters & Johnson, 1967, 1970). They followed up Kinsey’s sociological research with direct observations of people engaging in sexual behavior under controlled laboratory conditions. Their work is not the last word, however. Later investigations have used increas- ingly sophisticated techniques, such as endoscopy and ultrasound imaging, to picture what really happens during sexual activity, especially during intercourse (Buisson, Foldes, Jannini, & Mimoun, 2010; Suh et al., 2004). These techniques have added much information to Mas- ters and Johnson’s original observations, although their main observations (described here) remain relatively unchallenged.

Masters and Johnson set out to describe how physical and psychological mechanisms work together to control sexual responsiveness. Before their observations, research attention was devoted primarily to understanding sexual genetics and anatomy. Their five phases of the sexual response cycle are described in the accompanying Highlight.

Highlight: Five Phases of the Sexual Response Cycle

1. Desire. A sexual cycle usually begins with desire, the motivation to engage in sexual activity. Desire can arise spontaneously or in response to a sexually arousing stimulus. In some cases, desire may not appear until sexual stimulation begins.

2. Excitement. The excitement phase begins with petting and foreplay, which causes sexual hormones to be secreted. Heart rate increases, and breathing becomes more rapid. The nipples become erect in women and in many men as well. Some women develop a sex flush, a body rash that deepens in color with their degree of sexual arousal. Blood flows to the genitals, causing the penis and the clitoris to swell and become red. The lining of the vaginal walls becomes lubricated.

3. Plateau. The genitals continue to fill with blood, and the muscles become tense. The penis becomes erect, and the testes enlarge and are pulled up into the scrotum. The clitoris retracts under its hood and the tissues of the vagina swell. Psychologically, feelings of sexual excitement increase. This stage can last for from a few minutes to several hours.

4. Orgasm. Females experience strong genital sensations and warmth spreading in the pelvic area, followed by rhythmic muscle contractions causing the vaginal walls, uterus, and rectal sphincter muscle to contract and expand. Males first feel the ejaculate coming, followed by muscle contractions in the penis that propel semen through the urethra and out the urinary opening. For both sexes, a psychological sensation of orgasm (pleasurable release) accompanies these muscle contractions.

5. Resolution. The body gradually returns to its prior unstimulated condition. For men, there is a refractory period in which they are unable to have another orgasm no matter how much they are stimulated. This period varies from less than an hour for some men to many hours for others, depending on their age, fitness, and a host of other factors. Women may have multiple orgasms with no apparent refractory period, but the ability to have multiple orgasms varies considerably from one woman to the next.

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The DSM–5 categorizes sexual dysfunctions according to the phase of the sexual response cycle that they affect: Disorders of sexual desire affect the initial phase, disorders that affect sexual arousal arise in the excitement and plateau phases, and disorders that affect orgasm mainly affect the orgasm phase. Most of the literature on sexual dysfunctions deals with het- erosexual couples. Similar sexual problems affect same-sex couples as well. However, for the sake of brevity, we will focus only on heterosexual couples in this chapter.

This chapter discusses each type of sexual dysfunction separately, but in practice they overlap and interact. For example, a person who cannot achieve an orgasm may lose the desire for sex and, hence, may wind up with both an orgasmic disorder and a disorder of desire. Such multiple dysfunctions are the rule rather than the exception. Also keep in mind that sexual dysfunctions are highly charged emotionally. Because sexual dysfunctions make it difficult or impossible for people to have or enjoy sexual relations, they may be extremely distressing to those who have them. Anger, fear, resentment, shame, guilt, and humiliation are frequently associated with sexual dysfunctions. If they persist, individuals may develop secondary disor- ders, particularly anxiety disorders and depression. These secondary disorders may be even more devastating to individuals and couples than are the sexual dysfunctions that trigger them.

Diagnosis Diagnosing a sexual dysfunction requires considerable clinical sensitivity. There is no objec- tive way to decide where normal behavior ends and a sexual dysfunction begins. For example, the failure to reach orgasm is not by itself a disorder. Many women, and some men, report satisfying sex lives without having orgasms. Failure to have an orgasm becomes a problem only if it causes distress or interpersonal difficulty. The same is true of all of the sexual dys- functions listed in the DSM–5; they are problems only when the people involved decide they are. Because sexual behavior is affected by physiology and mood, the DSM–5 requires that other potential disorders (such as depression), substance abuse, and general medical condi- tions be ruled out before deciding that a person is suffering from a sexual dysfunction. Before making a diagnosis, the clinician must also assess whether a person’s sexual performance is appropriate for his or her age (older people may require more stimulation than younger ones to become aroused or to reach orgasm). The clinician must also try to assess whether the person is getting adequate sexual stimulation. People with insensitive or inattentive partners may think they have a sexual dysfunction when they really have partners who don’t know how to fulfill them (or don’t care).

For each sexual dysfunction, the DSM–5 distinguishes between lifelong patterns that were present from the person’s first sexual activity and acquired ones that developed after a period of normal functioning. The latter are more likely to be the result of trauma or the second- ary effect of some other disorder. The DSM–5 also distinguishes generalized problems, which are not limited to certain types of stimulation, partners, or situations, from situational ones, in which the problems occur only with certain partners, certain types of stimulations, or in certain situations. The prognosis for situational problems is likely to be better than that for dysfunctions that occur in all sexual situations.

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Sexual Desire Disorders Desire is the complex set of feelings, cognitions, and fantasies that motivates people to engage in sex. Without desire, sex is little more than rubbing and friction. Women or men who, for whatever reason, lack desire for sex are said to have a sexual desire disorder. The DSM–5 describes two such disorders, one for each gender: male hypoactive sexual desire disorder and female sexual interest/arousal disorder.

If a man has male hypoactive sexual desire disorder, he has never had much interest in any type of real or fantasy sex, and this lack of interest may negatively affect his life. It also becomes more common with age (APA, 2013).

Although it is possible for male hypoactive sexual desire disorder to exist on its own, it rarely does. Disturbances in the other phases of the sexual response cycle—especially disturbances in sexual excitement or orgasm—frequently co-occur with male hypoactive sexual desire dis- order (Connor, 2011). In some cases, it is the inability to sustain sexual excitement or to reach orgasm that causes the person to lose interest in sex. Medical conditions, particularly those that cause pain during intercourse, various psychological disorders (depression and body dysmorphic disorder, to name two), and many drugs (including antidepressants) may also cause people to lose interest in sex.

Male hypoactive sexual desire disorder is one of the most common complaints of people who seek treatment for sexual problems (ISSM, 2011; Rosen & Leiblum, 1995); it affects approxi- mately 1.8% of men aged 16–44 (APA, 2013). Some people lack desire for any type of sexual activity. In other cases, a person may lack desire for some sex acts (intercourse, for example) but may desire others (such as masturbation). Men with male hypoactive sexual desire disor- der may not initiate sexual activity but may go along if the partner insists.

Like practically all behaviors, sexual desire forms a continuum. People who fall at the low extreme have little desire for sex. The majority, who fall in the middle of the continuum, have an intermediate level of desire. Those who fall at the high extreme have a strong desire for frequent sex. Interestingly, the DSM–5 does not contain a “hyperactive sexual desire disorder.” The authors of the DSM–5 may not believe that high levels of sexual desire can produce psy- chological problems.

Female sexual interest/arousal disorder represents the combining of sexual desire and arousal disorders into this single category. Unlike the male version, the criteria are far more specific here. The woman, for at least six months, has to show the following: absence or reduced interest in sexual activity; absent or reduced sexual or erotic thoughts or fantasies; none or reduced initiation of sexual activity and generally unresponsive to her partner’s ini- tiation attempts; absent or reduced sexual excitement or pleasure during sexual encounters at least 75% of the time; absent or reduced sexual interest or arousal in response to written, verbal, or visual erotic cues; and absent or reduced genital or non-genital sensations during sexual activity in at least 75% of sexual encounters (APA, 2013). The woman must demon- strate at least three of these criteria consistently over a six-month time period.

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Sexual Arousal Disorders Even when they desire to have sex, some people find it difficult to maintain the necessary level of arousal. That is, they have problems with the excitement phase of the sexual response cycle. The DSM–5 contains two sexual arousal disorders: female sexual interest/arousal dis- order and erectile disorder.

Women with female sexual interest/arousal disorder experience distress and personal dif- ficulty because they have absent, or significantly reduced, sexual interest or arousal (APA, 2013). The DSM–5 considers female sexual interest/arousal disorder to have psychological origins. Like the sexual desire disorders, arousal disorders can begin early in life or in adult- hood and can affect all sexual situations or just some. Not surprisingly, arousal disorders are usually accompanied by orgasm disorders—it is not normally possible to have an orgasm if one is not sufficiently aroused.

Erectile disorder is defined as an inabil- ity to attain or sustain an erection until the completion of a sex act. Erectile disorder replaced the older term impotence, which has false connotations (that the man is unable to have children or is an inadequate lover). Erectile disorder is the most com- mon reason men visit clinics for help with a sexual dysfunction. It also accounts for hundreds of thousands of doctor visits each year (Laumann, Paik, & Rosen, 1999). After age 40, more than half of all men have some degree of erectile difficulty from time to time. In general, older men need more stim- ulation and take longer to achieve an erec- tion than younger men. This is not a sign of

a psychological disorder but of normal aging (Gewirtz-Meydan & Ayalon, 2017). Substances (antihypertension drugs, alcohol, tranquilizers), medical disorders (diabetes, spinal injury), and psychological disorders (such as depression) may affect a man’s ability to attain or sus- tain an erection. However, the diagnosis of erectile disorder is normally reserved for men whose dysfunction appears to have a large psychological component. For example, males who have erections while masturbating or during sleep are physically capable of having erections; thus, their erectile dysfunction during sex is likely to have a psychological origin. They may feel guilty about sex or suffer from performance anxiety, for example. As in all sexual dys- functions, erectile disorder is diagnosed only when the dysfunction distresses the man or his partner.

Orgasmic Disorders Some people have the desire for sex, enjoy foreplay, and become excited but have consider- able difficulty achieving an orgasm. There may be physical reasons for this problem (medical conditions, substance intoxication) and psychological ones (such as performance anxiety). In some cases, both types of etiology are present simultaneously. An orgasmic disorder is

Creative Crop/Exactostock-1527 Sildenafil, popularly sold as Viagra, is com- monly used to treat male erectile disorder.

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diagnosed when psychological factors dominate. The DSM–5 describes two orgasmic disor- ders: female orgasmic disorder and premature (early) ejaculation.

Some women who have difficulty reaching orgasm lack interest in or are averse to sex in gen- eral. Such women are presumed to be uninterested in sex. However, there are women who are responsive to sexual stimuli as measured by self-report, vaginal lubrication, and genital swelling, but who nevertheless have great difficulty achieving an orgasm (Kaplan et al., 1996). Between 10% and 15% of women never experience an orgasm at all. Another 10% to 15% experience them only rarely. Because most of these women, and their partners, are not dis- tressed by their infrequent or nonexistent orgasms, they do not qualify for the diagnosis of female orgasmic disorder. By definition, this refers to a delay or absence of orgasm in some women following normal sexual excitation. It must also cause distress or interpersonal dif- ficulty (APA, 2013).

It is often difficult to determine whether a woman has an orgasmic disorder or whether she is just not getting the type or amount of stimulation she requires to achieve an orgasm. Women exhibit wide variability in the type and intensity of stimulation they require. Some women find intercourse sufficient stimulation to produce an orgasm, but many others do not. They are able to have an orgasm only when stimulated orally or manually. From a clinical viewpoint, a woman who fails to reach orgasm because she is not getting the stimulation she requires does not have an orgasmic disorder.

Premature (early) ejaculation refers to men who reach orgasm with minimal stimulation. For them, sex is over almost before it has begun. This reduces their satisfaction as well as the enjoyment of their partners. How quickly must a man reach orgasm for his ejaculation to be considered premature? There is no definitive answer. Some couples prolong intercourse for hours, whereas others are satisfied with a few minutes. In practice, ejaculation on insertion of the penis into the vagina or after a thrust or two is usually considered premature. The DSM–5 defines “premature” as ejaculation occurring within one minute following vaginal penetra- tion (APA, 2013). Even then, a man is considered to have a disorder only if he is personally distressed by his premature ejaculation or if it disturbs his partner. Premature ejaculation is common among young, relatively inexperienced men, especially those whose sex lives have been dominated by situations where speed may be important (to avoid discovery, for instance).

Genito-Pelvic Pain/Penetration Disorder Genito-pelvic pain/penetration disorder is a female-only disorder. It is marked by at least one of the following that must have been occurring for at least six months: difficulty with vaginal penetration during intercourse; vaginal or pelvic pain during intercourse or vaginal penetration attempts; fear or anxiety about vaginal or pelvic pain in anticipation of, during, or as a result of vaginal penetration; and marked tensing or tightening of the pelvic floor muscles during attempted vaginal penetration (APA, 2013, p. 437). Recurrent pain during intercourse is seen in approximately 15% of women in North America, but the prevalence of genito-pelvic pain/penetration disorder is unknown (APA, 2013). Pelvic pain during sex can vary from superficial to severe. In practically all cases, it causes distress to both the woman and to her partner. The disorder is diagnosed only when the pain is believed to have a strong psychological component. When the pain is solely the result of a substance, the person has substance/medication-induced sexual dysfunction.

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Genito-pelvic pain/penetration disorder can also be diagnosed when the perineal muscles surrounding the front part of the vagina contract involuntarily whenever vaginal penetration is attempted. The woman may have normal sexual desire and excitement and the ability to reach orgasm, but is unable to have intercourse. This can cause personal distress and dis- rupt relationships. The condition seems to be found most often in younger women who have negative attitudes toward sex and among victims of sexual abuse. This may be the result of a conditioned fear response to sex or may be the result of abuse or an insensitive lover.

Epidemiology and Course As we have seen, deciding whether a person has a sexual dysfunction takes considerable clini- cal skill. To make a diagnosis, the clinician must consider the person’s age, health, substance use, and cultural background and must determine whether the person is receiving the stimu- lation necessary to build excitement and reach orgasm. In addition, the clinician must assess the degree of distress produced by the dysfunction in the individual and, where appropriate, the distress produced in the individual’s partner.

Etiology Each phase of the sexual response cycle depends on an intricate balance of social, psychologi- cal, and physiological forces. Disruption in any of these forces may result in a sexual dysfunc- tion. Keep in mind, however, that the relationship between any single variable and a sexual dysfunction is never entirely predictable. If the sexual dysfunction is transitory and likely to disappear when the precipitating problem is resolved, the proper diagnosis is adjustment disorder. Adjustment disorders straddle the border between normality and pathology. They represent extreme but temporary reactions to everyday crises.

Once men begin having erectile problems, even occasionally, a vicious cycle may begin. The man begins to worry about his performance. His anxiety keeps him from becoming fully immersed in the sexual act. Instead, he takes on what Masters and Johnson call a spectator role—he watches his own reactions (“Am I developing an erection, or will I fail and be embar- rassed?”). As his anxiety becomes worse, the chances of erectile failure increase. This makes the man even more anxious, and the vicious cycle continues. See Figure 12.1 for more etio- logical factors.

Sexual Dysfunction

Lack of knowledge about sex

Depression

Adjustment reactions

Age-related changes

Substance use

Inadequate stimulation

Fear of intimacy

History of abuse

Relationship conflicts

Performance anxiety

Negative attitudes about sex

Low hormone levels

Figure 12.1: Etiological factors contributing to sexual dysfunction

Source: From S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 13.4, p. 583.

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Treatment Dysfunctions may be treated with physiological or psychological interventions. People whose sexual dysfunctions are caused by diseases such as diabetes may benefit from better treat- ment of their disease. People whose dysfunctions are the result of medications may benefit from having their medications reviewed and dosages adjusted. Getting people to stop using recreational drugs may also be helpful. In some cases, drug treatments may assist some peo- ple with sexual dysfunctions.

Drug Treatments Testosterone may help some men achieve and maintain erections (Block, Meiboom, Zaig, Sch- reiber, & Abramov, 2013). Hormone replacement therapy may help postmenopausal women maintain desire, reduce the pain of penetration or of vaginal intercourse, and provide an ade- quate level of vaginal lubrication. Although antidepressants may contribute to sexual dysfunc- tion, they may also help men with premature ejaculation to last longer. Women with tensing or tightening of the pelvic floor muscles during attempted vaginal penetration may be helped by a program in which metal rods (dilators) of gradually larger diameter are inserted into the vagina until the woman can relax the vaginal muscles sufficiently to accommodate a penis.

To assist men with erectile disorders, a series of operations was developed in which pumps were implanted into the penis and inflated when the man wished to have intercourse (Hunter, Goodie, Oordt, & Dobmeyer, 2017). These were soon supplanted by injectable drugs that pro- duced erections (Hatzimouratidis et al., 2016). Neither of these methods was particularly practical or pleasant, so they were rarely used. With the release of sildenafil (Viagra), as well as newer medications like tadalafil (Cialis) and vardenafil (Levitra), they have been rendered essentially obsolete. Viagra, which is successful at producing erections in most men with erectile disorder, has replaced practically all other drugs and surgical procedures. It is taken about one hour before the man plans to have sex, and its effects last for about four hours. Note that Viagra does not produce an erection by itself; it is still necessary for the man to be sexually stimulated. Rather, the drug increases blood flow to the penis, thereby allowing the stimulated man to produce an erection. Viagra seems to be effective for erectile disorders caused by medical conditions as well as for disorders whose origins are mainly psychological (Hatzimouratidis et al., 2016).

The drug has become so popular that it is even being used by men who do not meet the diagnostic criteria for erectile disorder but who believe it will enhance their performance (Gewirtz-Meydan & Ayalon, 2017). Despite its popularity, Viagra is not for everyone. Men with heart disease or circulatory disease who have not had sex for some time may find the strain of Viagra-induced sex too much for their weak hearts. Initially it was believed, and some research substantiated this, that anyone who took medicine that contains nitrates (such as nitroglycerin used for circulatory disease) might find that Viagra made their blood pres- sure drop suddenly to a life-threatening level (Kloner & Jarow, 1999). More recent research has demonstrated that, in fact, there is no convincing evidence of any major safety issue when a male uses Viagra (Hatzimouratidis et al., 2016). In addition, Hatzimouratidis et al. (2016) found no cause and effect relationship between Viagra and cardiovascular events. Finally, the researchers did not find any new safety risks relating to cardiovascular events or to drug interactions. This included synergistic effects (Hatzimouratidis et al., 2016). Cialis and Levi- tra produce results similar to Viagra (Hatzimouratidis et al., 2016). Although Viagra is clearly

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useful and popular, it is important to remember that the drug is not a cure (Segraves & Seg- raves, 1998). Take the drug away, and erectile dysfunction returns. Psychological treatments, by contrast, are aimed at ameliorating sexual dysfunctions and preventing their return.

Psychological Treatments Until the middle of the 20th century, the psychological treatment approach to sexual disor- ders was the same as for other psychological disorders. This was not only expensive and time consuming, but it also was rarely effective. In the 1950s, behavioral psychologists attempted to devise more efficient and effective treatments for sexual dysfunctions. Masters and John- son’s approach to treating sexual dysfunctions has been augmented and expanded over the years to form what is known today as sex therapy (Frühauf, Gerger, Schmidt, Munder, & Barth, 2014). Modern sex therapy consists of a combination of treatment techniques that include sex education, communication skills training, cognitive-behavioral therapy, couples’ therapy, and, when necessary, insight-oriented therapy (Frühauf et al., 2014). In some cases, sex therapy also includes treatment for associated psychological disorders, such as substance abuse, anxiety, or depression.

Although people with psychological disorders need treatment that is tailored to their individ- ual needs, there are some common factors that apply to most people with sexual dysfunction. First, treatment is almost always focused on couples, even though it is usually just one part- ner who has the identified problem. Second, educating couples about sex is crucial. Ignorance and misinformation about sex are important factors in almost every sexual dysfunction. (The accompanying Highlight debunks some common myths about sex.)

Highlight: Sex Myths

Although sexual dysfunctions and disorders have a multitude of interacting causes, ignorance about sex is almost always a contributor. Many of us are influenced by descriptions of sex in the media, which have contributed to unrealistic expectations and leave many people feeling inadequate. Some of the most common myths about sex are summarized here:

• Sex equals erection, intercourse, and orgasm. This common myth is one of the main causes of sexual performance anxiety. When people convince themselves that sexual fulfillment depends on reaching a goal (orgasm), deviations from reaching the goal, even temporary ones, are likely to lead to anxiety. In reality, erections, intercourse, and orgasms are unnecessary for pleasurable sex. Many couples report considerable satisfaction from kisses and caresses. Indeed, couples who learn to pleasure one another in circumstances where neither erections nor orgasms are required report more fulfilling sex lives than do those whose only goal is orgasm.

• When it comes to sex, men must take the lead. This Victorian-era view can interfere with the sexual enjoyment of both men and women. It can also keep a man from ever learning what his partner desires. A better approach is for partners to communicate their needs and desires and to share responsibility for initiating sexual activity.

• Men are always ready for sex. This is another anxiety-producing myth. Men who believe it become anxious whenever they fail to become excited immediately. In reality, men as well as women need to feel comfortable with their partner and with the situation in order to engage in pleasurable sex.

(continued)

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Without such information, people often hold themselves to impossible standards. Similarly, attitudes and maladaptive cognitions (“sex is dirty”) need to be countered before progress can be made. A third common factor in practically all treatment programs is the need to over- come embarrassment and guilt about one’s sexual needs and preferences. To accomplish this, individuals and couples in treatment may be asked to explore their bodies and to experiment with masturbation in order to identify what gives them pleasure. Once they discover their particular preferences, they must then learn to communicate these to their partners. For a fulfilling relationship, partners need to know what gives their lovers pleasure, and what does not.

Masters and Johnson developed sensate focus as a way of helping couples learn about the sex practices that give them pleasure. Sensate focus requires that one partner actively stimulate the other, who focuses on the pleasurable feelings being induced. The couples then switch roles, so that each takes a turn giving and receiving stimulation. As they learn more about what gives them pleasure and communicate this to one another, they gain confidence. Couples may also undergo cognitive restructuring to change mistaken attitudes and beliefs about sex. Gradually, the couple proceeds to genital caresses and stimulation. They do not move on to intercourse until they can do so untroubled by performance anxiety. Masters and Johnson reported success rates of around 80% for their treatment. Some studies have reported less spectacular results, but sensate focus is still the treatment of choice for most couples (Früh- auf et al., 2014).

Specific techniques have also been developed to deal with particular sexual dysfunctions. For example, the start-stop technique for treating erectile disorder begins with the partner’s caressing the man until he gets an erection and then stopping. When the erection disappears, the partner repeats the caresses until the man is once again erect and then stops. When this start-stop cycle is repeated many times, the man gains confidence in his ability to achieve erections. He learns that his erections occur naturally in response to stimulation (provided that he does not focus on his performance).

• Women are not aroused by erotic films and books. This is untrue. Many women find such materials stimulating—just have a look at the stories and pictures in magazines aimed at women.

• Normal women achieve orgasm every time they have sex. Again, this may happen in the movies and in erotic literature, but it is not the case in real life. Individual differences allow some women to reach orgasm more easily than others. Even those women who reach orgasm easily do not have orgasms every time they have sex. Multiple orgasms are rarer still.

• Menopause is the end of a woman’s sex life. Although women who do not receive hormone replacement therapy may experience vaginal dryness, which can cause pain during intercourse, this is easily rectified by the application of vaginal lubrication. Many postmenopausal women report that not having to worry about pregnancy makes sex more pleasurable than when they were younger.

• Sex should be spontaneous rather than planned. This may work in the movies, but in many people’s busy lives, sex does not take place without planning.

Highlight: Sex Myths (continued)

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Section 12.3 Gender Dysphoria

The treatment of premature (early) ejaculation may include a technique known as pause and squeeze. The male is stimulated until he signals that he feels orgasm coming. At that point, the partner stops stimulating the male and squeezes his penis—preventing orgasm. As this is repeated, ejaculation is gradually delayed. The couple then switches to vaginal stimulation in which brief periods of entry are followed by stopping until the male is able to engage in inter- course for a reasonable period of time without ejaculating. These specific techniques work best when they are embedded in a multimodal treatment program that includes not just sex therapy but also education and cognitive restructuring (Hunter et al., 2017).

12.3 Gender Dysphoria Our sense of ourselves as male or female is known as our gender identity. Most of the time, gender identity is consistent with physical anatomy. Con- sider, for example, the case of Billy Tipton, a trans- vestite jazz musician who married five wives and was found to be a biological woman only on death (Middlebrook, 1998). Born Dorothy in 1914, Tipton was raised at a time when jazz was a man’s world. To have a career, a female musician had no choice but to pretend to be male. Tipton’s impersonation must have been excellent because it fooled not only his fellow musicians but also his various wives. Exactly how Tipton managed sexually is something of a mystery, but his amazing life demonstrates that gender identity is a social and cultural construct that is only loosely related to the biological facts (McConaghy, 1997).

Description and Diagnosis Children may sometimes become confused about their gender identity. Some become con- vinced that their physical anatomy and their gender are in conflict. They may look like males, but emotionally they feel like females (or vice versa). According to the DSM–5, such people may have gender dysphoria. People with gender dysphoria report that, even as children, they felt trapped in the wrong body (Berlin, 2016). Males say they were too “pretty” to be boys, whereas girls report feeling masculine (McDermid, Zucker, Bradley, & Maing, 1998). Gender dysphoria—especially for females—is rare. For adult natal (at birth) males, the range is between 0.005% and 0.014%; for natal females, the range is from 0.002 to 0.003% (APA, 2013). In adolescence, the ratio of males to females is about equal, but in adults the ratio of males to females ranges from 1:1 to 6.1:1 (APA, 2013).

Boys with gender dysphoria may dress in female clothing and adopt behaviors associated with female sex roles. Some may even wish for their penises to disappear. Girls may act like boys. Such children may find themselves ostracized by their peers. Their loneliness may lead to depression and other psychological disorders. Children then reach adolescence still confused

AP Although jazz musician Billy Tipton, center, was biologically a woman, he spent most of his life passing as a man.

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Section 12.3 Gender Dysphoria

about their gender identity. When sexual maturity occurs during adolescence, their biological sex becomes glaringly obvious. They can no longer pretend to be the opposite gender. To fit in, some learn to repress their feelings and play the sex role appropriate to their anatomy. A small number find this impossible; they endure adolescence and enter adulthood still wish- ing they were the opposite sex. Some decide to alter their sex through surgery.

Note that boys with gender dysphoria are not transvestic fetishists (they do not cross-dress to become sexually aroused), nor are they always gay males (Berlin, 2016). Gay males rarely wish to change their biological sex.

Etiology The etiology of gender dysphoria is not clear (Berlin, 2016; Zucker et al., 2015). It appears that brains may be “masculine” or “feminine” irrespective of whether the person has mascu- line or feminine genitalia.

The notion that brains have a gender identity separate from the genitalia is also consistent with the observations made of people born with a condition once known as pseudohermaph- roditism (note that persons born with aspects of both female and male genitalia are rare, and that the condition may be corrected by surgery). An individual with a disorder of sex develop- ment (this has also been called intersex, but this term is less common) is a genetic male whose genitalia do not fully develop before birth. These individuals are born looking like females and are usually raised as girls. They wear dresses and are encouraged to play female roles. This suggests that gender identity is determined more by the “sex” of a person’s brain than the appearance of a person’s genitalia.

It has not been possible to demonstrate that all people with gender dysphoria have been exposed to opposite-sex hormones during fetal development. Some may have developed gen- der dysphoria for other reasons, such as the sexual trauma caused by abuse. In some cases, children who have the appearance of the opposite sex (pretty boys, tomboyish girls) may have been strongly reinforced for taking the opposite sex role (Fridell, Zucker, Bradley, & Maing, 1996; McDermid et al., 1998). Eventually, they may have simply come to accept that they are the opposite sex. At the present time, similar to many of the other disorders discussed throughout the text, the cause of gender dysphoria is most likely to be found in a combination of biological and psychological factors (Berlin, 2016).

Treatment There are two ways to treat gender dysphoria: change the person’s sex role identity to match his or her anatomy, or change the anatomy to match the identity. The first option involves an immense psychological effort, which is not often successful. Hence, the option of changing anatomy has been taken up by thousands of people. Treatment usually begins by having the person live as the other sex for a trial period. During this period, the person is carefully moni- tored for other psychological disorders. Changing the sex of someone with a psychological disorder other than gender dysphoria is neither ethical nor sensible. People who are helped to overcome another psychological disorder may decide that they are perfectly happy with their existing sexual anatomy.

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Chapter Summary

During the trial period, sex hormones are administered to produce many of the physical char- acteristics of the other sex. Specifically, men are given estrogen, which causes them to develop breasts and makes their body and facial hair disappear. Testosterone is given to females to deepen their voices, increase their muscle mass, and cause body and facial hair to develop. Some people stop at this point, content to live as if they were the other sex. Some go all the way and have sex-change surgery, during which external genitalia are removed. For men a vagina is created by inverting the penis into the abdominal cavity. Females are given artifi- cial penises, which may be augmented with pumps or other erection-imitating mechanical devices, since they do not produce the normal male sexual response. Most people are satis- fied with the results of their sex-change operations and go on to lead rewarding lives (Berlin, 2016). A small number, particularly those with other psychological disorders, continue to have problems.

Chapter Summary

Defining Abnormal Sexual Behavior • Acceptable sexual behavior is defined by cultural norms. Activities considered nor-

mal in one culture may be prohibited in another. • What is considered normal in the present time might not have been considered nor-

mal in the past. • Normal means that the behavior as a whole is accepted by society as being proper

and acceptable.

Paraphilic Disorders (Paraphilias) • The paraphilic disorders are characterized by unusual, disturbing, or harmful sexual

fantasies and urges about sex with nonhuman objects, sex that involves suffering on the part of oneself or one’s partner, or sex with children.

• Some paraphilic disorders are exaggerations of everyday behavior; others involve serious crimes. Note, however, that not all apparently sexual crimes are paraphilias.

• Despite their diverse range, paraphilic disorders share a common characteristic—in every case, sexual behavior has been disconnected from a loving, consensual rela- tionship with another adult.

• Because paraphilic disorders occur mainly in men, researchers have assumed that they must have some hereditary sex-linked cause, although no such etiology has been uncovered.

• There is some evidence that people with paraphilic disorders have childhood and adolescent experiences that may have distorted their sexual interests.

Sexual Dysfunctions • Sexual dysfunctions are difficulties in sexual performance. Dysfunctions may affect

any of the stages of human sexual response (desire, excitement, plateau, orgasm, resolution).

• Although they are described as separate disorders, sexual dysfunctions often occur together.

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Chapter Summary

• Diagnosing sexual dysfunction requires clinical sensitivity; the clinician must try to assess whether the person is getting adequate sexual stimulation.

• The DSM–5 includes two disorders of sexual desire, one for men and one for women: male hypoactive sexual desire disorder and female sexual interest/arousal disorder.

• Female orgasmic disorder is diagnosed when a woman has difficulty achieving orgasm.

• Premature (early) ejaculation applies to men who reach orgasm too quickly. • Genito-pelvic pain/penetration disorder involves pain during sexual intercourse

and/or tensing or tightening of the pelvic floor muscles during attempted vaginal penetration.

• For genito-pelvic pain/penetration disorder, the clinician must assess whether there are physiological causes or psychological causes leading to physiological symptoms.

• Sexual dysfunctions are common and are influenced by medical conditions, sub- stances, and psychological factors (especially performance anxiety).

• Many sexual dysfunctions require multimodal sex therapy—a combination of treatment techniques that includes sex education, communication skills training, cognitive-behavioral therapy, marital therapy, and insight-oriented therapy when necessary.

Gender Dysphoria • Our sense of ourselves as male or female is known as our gender identity. • People with gender dysphoria are not transvestic fetishists (they do not cross-dress

to become sexually aroused), nor are they gay. • Gender dysphoria may have hormonal origins, or it may be the result of early learn-

ing experiences. • Treatment involves changing the person’s sex role identity to match his or her

anatomy or changing the anatomy to match the identity (usually through surgery).

Critical Thinking Questions

1. Sexual sadism and sexual masochism disorder might be lifestyle choices or alterna- tive forms of achieving pleasure. For others these are seen as deviances and fetishes. Discuss your position on these two diagnosable conditions, being sure to provide detailed support for your position.

2. Many of the paraphilic disorders discussed do not respond well to treatment and are incurable. Knowing this, how would you treat someone with a paraphilic disorder? Should we attempt to treat such an individual, or are we “wasting” everyone’s time by making this attempt?

3. The FBI revised its (and thus the United States’) definition of rape in 2012, by removing gender specification, among other updates. How important is this change? Can a male be raped?

4. Let’s presume that you were asked to update Masters and Johnson’s research based on what we know today. Discuss which topics you would research, and describe the experiments you would devise to research these topics.

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Chapter Summary

Key Terms adjustment disorder An extreme but tem- porary reaction to an everyday crisis; these responses usually fade over time without intervention.

BDSM An acronym that stands for bond- age & discipline/dominance & submission/ sado-masochism.

desire The complex set of feelings, cogni- tions, and fantasies that motivates people to engage in sex.

erectile disorder An inability to attain or sustain an erection until the completion of a sex act.

exhibitionistic disorder A condition characterized by exposing one’s genitals to a stranger, sometimes accompanied by masturbation.

female orgasmic disorder In women, trou- ble reaching orgasm despite being sexually excited.

female sexual interest/arousal disor- der A problem that occurs when a woman experiences distress and personal diffi- culty because she lacks, or has significantly reduced, sexual interest or arousal.

fetishistic disorder Sexual gratification obtained using nonliving objects, such as shoes, bras, underpants, or leather cloth- ing, in fantasy or directly to achieve sexual gratification.

frotteuristic disorder Involves a male touching or rubbing up against females, usu- ally in crowded places.

gender dysphoria A discomfort with one’s assigned sex role.

genito-pelvic pain/penetration disor- der When a woman has difficulties with vaginal penetration during intercourse; pain during penetration attempts or during vaginal intercourse; or tensing or tightening of the pelvic floor muscles during attempted vaginal penetration, making penetration dif- ficult or impossible.

hypoxyphilia The practice of achieving sexual gratification by depriving oneself of oxygen by hanging from a noose or put- ting a plastic bag over one’s head to achieve sexual arousal or orgasm; also called asphyxiophilia.

male hypoactive sexual desire disorder A persistent lack of interest in any type of real or fantasy sex and a significant reduction or lack of physical arousal; this lack of interest negatively affects the man’s life.

paraphilic disorder (paraphilia) A condition characterized by intense sexual fantasies about, and urges to have (a) sex with nonhuman objects (bras or panties, for example), (b) sex that involves suffering on the part of oneself or one’s partner, or (c) sex with children.

5. We have discussed using medications to treat many disorders. In this chapter, we discuss Viagra and other medications. Discuss the pros and cons of using Viagra or one of the other medications listed to treat erectile disorder. In addition, what would your views be if a similar medication were available for females?

6. One method for treating gender dysphoria is surgery to change the individual’s geni- talia. Since this method is irreversible, discuss your views on this rather drastic form of treatment.

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Chapter Summary

pedophilic disorder Fantasizing about or engaging in sex with prepubescent children.

premature (early) ejaculation Orgasm after a brief period of stimulation, before the male (or the partner) wishes it.

rape The penetration, no matter how slight, of the vagina or anus with any body part or object, or oral penetration by a sex organ of another person, without the consent of the victim. The FBI’s updated definition removed the phrase “carnal knowledge of a female forcibly and against her will” from the previous definition.

sensate focus A form of sex therapy (though some view it as a technique); it requires one partner to actively stimulate the other, who focuses on the pleasurable feelings being induced. The couples then switch roles, so that each takes a turn giving and receiving stimulation.

sex therapy Treatment techniques that include sex education, communication skills training, cognitive-behavioral therapy, cou- ples’ therapy, and, when necessary, insight- oriented therapy.

sexual dysfunction Difficulty in performing sexual act(s).

sexual masochism disorder Sexual gratifi- cation that involves real or imagined humili- ation and suffering inflicted upon the self to achieve sexual excitation or orgasm.

sexual sadism disorder Fantasizing about inflicting or actually inflicting suf- fering or humiliation on another for sexual satisfaction.

transvestic fetishism Cross-dressing for sexual pleasure by heterosexual males.

voyeuristic disorder Sexual fulfillment and excitement gained by watching unsuspecting people disrobe or engage in sex.

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Use the Harvard Business Case, “The Ready-to-Eat Breakfast Cereal Industry in 1994” as the basis for answering the following questions:

Prior to the entry of private label producers, how would you classify demand (elastic, inelastic, unit elastic) for cereals produced by the Big Three? Support your answer by using details from the case and referencing the factors that influence the elasticity of demand

How would the entry of new private label producers impact the elasticity of demand for the Big Three’s products?

Identify both a variable cost and a fixed cost of cereal production

Minimum 2 scholarly Articles References.

Minimum of 500 Words, APA Format

Your paper will be submitted to Turnitin software, No plagiarism.

9 Personality Disorders

Ingemar Edfalk/Blend Images/SuperStock

Chapter Objectives

After reading this chapter, you should be able to do the following:

• Describe what “personality” means.

• Understand the evolution of a personality disorder.

• Explain how a personality can be disordered.

• Discuss the causes of personality disorders.

• Explain the differences among the various DSM–5 personality disorders.

• Explain how people with personality disorders can be helped.

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Evolution of a Personality Disorder: From Psychopath to Antisocial Personality Section 9.1

When we describe people who prefer spending a quiet night at home to attending a party as “introverted” or when we call ace fighter pilots “brave,” we are implying that their behavior is caused by their personality traits. (Why do fighter pilots take to the sky? Because they are brave.) Such trait-based explanations of behavior have an intuitive appeal: They fit our beliefs about human nature. Some people are naturally shy; others, gregarious. Some are timid; oth- ers are brave. This is the “popular” meaning of personality. For this chapter, we will use a more scientific definition of personality. According to the DSM–5, the sum of an individual’s traits constitutes his or her personality, a set of “enduring patterns of perceiving, relating to, and thinking about the environment and oneself, which are exhibited in a wide range of important social and personal contexts” (American Psychiatric Association [APA], 2013, p. 647).

Experience tells us that there is at least some consistency to people’s behavior and that mal- adaptive personality traits can cause distress. The DSM–5 considers people with these mal- adaptive personality traits to have a personality disorder: an enduring pattern of inner experience and behavior that deviates markedly from the expectations of an individual’s cul- ture. Although both the DSM–5 and the International Statistical Classification of Diseases and Related Health Problems (ICD-9-CM) include a diagnostic category for personality disorders, the idea that a personality can be disordered is steeped in controversy (Sutker, 1994; Widiger & Trull, 2007). For example, do career criminals really suffer from a personality disorder, or have they simply made a choice about how they wish to lead their lives? Experts have differ- ing opinions on this issue. They also disagree about which personality traits are debilitating enough to constitute a disorder. Perhaps the fundamental problem with personality disorders is that they have so little in common. The personality disorders covered in the DSM–5 include excessive shyness, self-absorption, and schizophrenic-like behaviors, and there seems little logical, empirical, or theoretical justification for grouping such disparate “disorders” into a single category.

In contrast to clinical disorders such as schizophrenia, personality disorders are supposed to arise from enduring character traits. Taken to extremes, practically any personality trait can impair social functioning and create problems. Shy people may lead restricted social lives; those who are extremely aggressive may get into trouble with the law. Because any person- ality trait, taken to extremes, can produce difficulties in living, some psychologists prefer to conceptualize personality disorders as the unlucky result of falling at the extreme of some personality trait—too shy, too hostile, too self-centered, and so on (Wakefield, 2012).

9.1 Evolution of a Personality Disorder: From Psychopath to Antisocial Personality

The idea that criminal behavior is inherited was a subject loathed by social reformers, who hoped to create a more caring society. What is the point of trying to improve the lot of disad- vantaged people if their destiny is genetically predetermined? In the 19th century, however, social reformers were in the minority. Most professionals followed psychiatrist Emil Kraepe- lin, who said that criminal behavior was largely genetic in origin. Kraepelin grouped people who lied, cheated, committed crimes, and harmed others into a diagnostic category he called

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Section 9.1 Evolution of a Personality Disorder: From Psychopath to Antisocial Personality

“constitutional psychopathic inferiority.” “Psychopaths” were people who behaved in an anti- social manner. The cause of their behavior was genetic (“constitutional”) and probably the result of some failure in evolutionary development (“inferiority”). Although Kraepelin admit- ted that individuals considered to be psychopaths in one culture—terrorists, for example— might be hailed as freedom fighters in another culture, he still believed that social causes were secondary to genetics in the etiology of antisocial behavior.

Over the years, Kraepelin’s category was shortened (by dropping “constitutional” and “inferiority”) to psychopath, defined as a person who lacks empathy, does not fear punishment, and will continue to break the law even if capture and punishment are likely. The first DSM, published in 1952, abandoned the term psychopath entirely. Instead, it referred to a sociopathic person- ality. This change in nomenclature signified the dominance of social theories of antiso- cial behavior: Criminals are made, not born.

Moral Insanity Revived The term sociopath never entirely replaced psychopath. Indeed, psychopath was still a widely used diagnostic term when Hervey Cleckley published The Mask of Sanity in 1976. Cleckley’s psychopaths were antisocial people who appeared “normal,” even to professionals, but whose normality was really only a superficial “mask of sanity.” Beneath the surface, Cleckley argued, psychopaths were deeply disturbed.

Because of their mask of sanity, psychopaths initially make a good impression. They can be friendly, intelligent, and show no overt signs of a mental disorder. Yet they lead highly aber- rant lives. They have dismal social relationships and disordered work histories, and they are often unreliable. On an impulse, they may give up a successful career to follow some momen- tary whim. Their projects, both legal and illegal, often turn out badly because, despite their intelligence, they fail to plan ahead. When confronted with evidence of their misbehavior, psy- chopaths first try to blame others. When this fails, they may admit their misdeeds and feign regret, but their remorse and concern for their victims are not genuine, and their misbehavior is often repeated. Punishment does not deter them. In fact, psychopathic people engage in antisocial behavior even when they are almost certain to be caught and punished. It is as if they cannot see the future. When they are apprehended, psychopaths remain self-centered. Some have even been known to ask employers for references after being fired for stealing.

The subject of this chapter’s case study, Eric Cooper, has many of the characteristics of Cleck- ley’s psychopaths.

Ross Dolan/Glenwood Springs Post Independent/AP Images Commonly, pyschopaths can be sociable, yet they often lack empathy. Serial killer Ted Bundy was often characterized as being charismatic and friendly.

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The Case of Eric Cooper: Part 1

Excerpt from the Assessment of Eric Cooper by the Court Psychologist MUNICIPAL COURT

Psychological Assessment

Date: December 4, 2011

Client: Eric Cooper

Instruments

Minnesota Multiphasic Personality Inventory–2 (MMPI-2) Thematic Apperception Test (TAT) Wechsler Adult Intelligence Scale (WAIS-IV) Psychopathy Checklist–Revised (PCL-R) Clinical interview

Psychologist: Dr. Aaron Lusted

Referral: Judge Warren

Reason for Referral: Judge Warren requested this presentencing report on Eric Cooper, a 30-year-old man who has been previously convicted of several crimes, including robbery and assault.

Behavioral Observations: Although the client was cooperative and friendly, he rarely made direct eye contact. Also, despite his general good mood, he would swear out loud and pound the table whenever he missed any questions on the intelligence test. There were no signs of delirium or alcohol intoxication, and the client was able to complete all tests with little prompting. The client reported that he had tried to rob a bank, while drunk, in order to pay his bills. He expressed concern that a guard was hurt during the attempted robbery and said he was pleased that no permanent damage was done. He asked whether there was a cure for his problem but when asked what his problem was, he said, “Bad luck, mostly.”

Social History: [See Document 10.3, Social Work Report.]

Intellectual Assessment: The client’s scores on the WAIS-IV intelligence test place him in the above-average range of intelligence. His scores on the verbal scales were higher, in general, than his scores on the performance scale. This is not surprising in someone with the client’s educational achievement.

Personality Assessment: The validity scales of the MMPI-2 were all in the average range, indicating that the test profile could be safely interpreted. The main feature of the profile was an elevated score on the psychopathic deviate scale. The client’s responses revealed a self-centered person, whose own feelings always take precedence over those of other people, and a person who lacks empathy for the feelings and rights of others. He also has a strong tendency to act impulsively. . . . The client’s TAT responses reflected a preoccupation with violence—there were numerous references to death, blood, and corpses—but no mention about how the characters in the story might respond or be affected by the violence. It was as if the client could not imagine what might be going through the heads of his own characters. . . . The client’s responses to the PCL-R (which assesses manipulative behavior and impulsivity) were those found among people who have been labeled “psychopaths”— people who lack empathy and are likely to use violence to achieve their goals.

(continued)

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Cleckley’s Etiological Hypothesis: An Inability to Feel Emotions For Cleckley, the failure to learn from experience was a central clue to the cause of psycho- pathic behavior. To explain why psychopathic people failed to profit from experience, Cleck- ley hypothesized that they are unable to experience normal emotions. They pretend to feel regret, affection, and fear, but they are really like actors, who simulate emotions they are not really experiencing. Because they do not feel anxiety about future punishment, psychopaths continue to commit antisocial acts for which they have been punished in the past (Crego & Widiger, 2015; Silverstein, 2007; Zuckerman, 1999).

DSM–IV Abandons Psychopathy The experimental data collected over the decades are remarkably consistent with Cleckley’s clinical observations (Hare, 1996; Hare & Neumann, 2006). People who meet his definition of a psychopath act on their immediate instincts and seem not to fear punishment. Not sur- prisingly, they are continuously in trouble. Despite these intriguing, and largely consistent, research findings, the DSM–IV abandoned both the term psychopath and the term sociopath, replacing them with antisocial personality disorder, which remains in the DSM–5. The DSM– IV deliberately replaced Cleckley’s psychopath—a clearly deviant person—with a diagnostic category that is so general it can accommodate practically anyone who behaves in an antiso- cial manner. Moreover, the new diagnostic criteria omit the hallmark of Cleckley’s concept of psychopathy—an inability to feel emotions.

Why the change? The main reason is the DSM–5’s attempt to make its diagnostic criteria as objective as possible. The DSM–5 criteria for antisocial personality disorder focus on

The Case of Eric Cooper: Part 1 (continued)

Based on the test results, behavioral observations, and my clinical interview, it appears that the client is a person who has little empathy for or understanding of other people. He thinks mainly of himself, his needs, and his feelings. He is prepared to use violence to meet his needs, no matter how simplistic or complex they may be. He will use violence if someone has something he needs (money or food or alcohol), or something he wants but cannot afford (an automobile). Because he lacks empathy, the client is almost certain to have trouble in personal relationships. In addition, his self-centered attitude as well as his impulsiveness and willingness to use violence are likely to bring him into continued conflict with the law.

Diagnostic Considerations: The client meets the DSM–5 criteria for antisocial personality disorder; he also meets many of the criteria for borderline personality disorder. In addition, he seems to have a pattern of substance abuse. He recently experienced stress from business problems, but his global functioning is only mildly impaired, and he is capable of a high level of psychological functioning.

Alcohol use disorder Antisocial personality disorder (possible borderline personality disorder as provisional secondary diagnosis)

See appendix for full case study.

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observable behaviors (such as impulsivity) and omit those that refer to presumed etiologies (such as a failure to feel emotions). The hallmark of the DSM–5’s antisocial personality dis- order is a flagrant disregard for the rights of other people. People with antisocial personality disorder are often irresponsible, impulsive, and untrustworthy. Although the objective crite- ria strived for in the DSM–5 are an improvement over the subjective diagnostic criteria some- times used in the past, it is curious that such a consistent body of psychological research has had so little effect on modern diagnostic practice.

Because only three of seven criteria need be met for the diagnosis of antisocial personality disorder, the DSM–5 criteria can encompass the behaviors of, among others in no particular order, con artists, thieves, career criminals, charlatans, corrupt politicians, even devious used car salespeople. Because the category is so broad, it tells us remarkably little about a person’s behavior. People with an antisocial personality disorder can have markedly different demean- ors. Some can be charming; others may be surly and aggressive. In other words, despite its status as a disorder of “personality,” the antisocial personality label tells us little about a per- son’s temperament; it is just a shorthand way of saying that a person engages in a habitual pattern of irresponsible behavior. Often, this behavior brings the person in contact with the law (Crego & Widiger, 2015). Nevertheless, it is important to note that an antisocial personal- ity is not the equivalent of criminality. Not all criminals have a psychological disorder and not all people who have antisocial personality disorder are criminals (Crego & Widiger, 2015).

For a diagnosis of antisocial personality disorder, there must be evidence of a conduct dis- order in childhood and an adult pattern of antisocial behavior that is evident by age 15. By insisting on such a lifelong pattern, the DSM–5 seems to have moved back in the direction of Kraepelin’s “constitutional psychopath,” who is either born antisocial or who develops such tendencies early in life. In practice, the initial onset of antisocial behavior is difficult to docu- ment (Ogloff, 2006). Objective information about a person’s childhood is rarely available, ret- rospective reports by others are often unreliable, and people suspected of being antisocial cannot be trusted to give an accurate history of their own lives. Despite these uncertainties, the idea that people who are “psychopathic” are different from birth, or at least early child- hood, is sometimes used to argue that they cannot help their actions—that they are simply suffering from an illness.

Prevalence and Course of Antisocial Personality Disorder Between 0.2% and 3.3% of the general population, mainly men, meet the DSM–5 criteria for antisocial personality disorder (APA, 2013; Zimmerman, Favrod, Trieu, & Pomini, 2005). Although the preponderance of men diagnosed with antisocial personality disorder may reflect a difference between the sexes, it may also be the result of stereotypical sex roles or of the clinician’s own biases (Castro, Carbonell, & Anestis, 2011). In our society, men are expected to be aggressive and to take more risks than women (see Figure 9.1). Men may be socially reinforced for behaving in ways consistent with at least some of the diagnostic crite- ria for antisocial personality disorder.

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Percentage with violence in stories

C o

u n

tr y

Canada

England

0 5 10 15 20 25 30 35 40 45 50

Japan

Sweden

Mexico

France

Korea

Northern Ireland

United States

Australia

New Zealand 38.7%

37.8%

32.6%

30.2%

29.0%

28.7%

27.2%

24.2%

19.9%

19.3%

18.6%

Figure 9.1: Are some cultures more antisocial than others?

In a cross-cultural study, teenagers were asked to write stories describing how imaginary characters would respond to various conflicts. About one third of the respondents from New Zealand, Australia, Northern Ireland, and the United States described violent responses, compared to less than one fifth of the subjects from Korea, Sweden, and Mexico.

Source: Adapted from Archer and McDonald (1995), as appearing in R. J. Corner, Abnormal Psychology, 6th ed. New York: Worth Publishers, 2007, Figure 16.3, p. 473. Reprinted by permission.

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By the DSM–5’s definition, antisocial personality disorder usually has its origins in adoles- cence, but it may begin even earlier (APA, 2013; Krastins, Francis, Field, & Carr, 2014). In fact, poor impulse control and aggressiveness as a child are important predictors of antisocial personality disorder later in life (Krastins et al., 2014).

A typical sequence is for an impulsive prepubescent boy to be labeled as a “conduct problem” in school. In adolescence, the same boy is labeled “delinquent,” and in early adulthood, he is diagnosed as antisocial (Krastins et al., 2014). Girls usually show fewer problems before adolescence (Javdani, Sadeh, & Verona 2011). About 10% of children have conduct disorder; of that group, 75% are male (Nock, Kazdin, Hiripi, & Kessler, 2006). Those with conduct disor- der are more likely to be diagnosed with antisocial personality disorder in later life (Krastins et al., 2014; Lahey, Loeber, Burke, & Applegate, 2005).

The highest prevalence of antisocial personality disorder is among men aged 25 to 44 years. In middle and old age, the incidence of antisocial personality disorder declines. It is not clear whether this means the disorder diminishes with age or whether people with antisocial per- sonality disorder fail to live past middle age (Hare, McPherson, & Forth, 1998; Oltmanns & Balsis, 2011). We do know that many die young from suicide, homicide, accidents, and sub- stance abuse (National Collaborating Centre for Mental Health, 2010).

Causes of Antisocial Personality Disorder Many researchers do not believe that there is a gene that makes a person a criminal. The mod- ern view is that genetics and environment both contribute to every type of behavior, includ- ing antisocial behavior. In this section, we will examine some of the ways in which heredity, biology, and experience interact to produce antisocial behavior (see Figure 9.2).

Dysfunctional, abusive family environment

Genetic tendency toward low arousal

and sensation seeking

Exposure to antisocial models in real life and in

the media

Antisocial Personality

Figure 9.2: Risk factors for antisocial personality disorder

Source: From S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 10.3, p. 437.

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Genetics Considerable evidence points to a genetic element in antisocial behavior, particularly when the antisocial behavior includes aggression. This evidence includes a higher concordance for antisocial traits among identical siblings than among nonidentical siblings (National Col- laborating Centre for Mental Health, 2010) and the finding that adopted children grow up to resemble their antisocial biological parents more than their non-antisocial adopted parents.

All of the simple explanations that have been offered to date (for instance, that antisocial behavior is the result of an extra male chromosome) have proved to be blind alleys (Har- mon, Bender, Linden, & Robinson, 1998). All researchers agree that the mechanism by which antisocial behavior is inherited is likely to be complicated (National Collaborating Centre for Mental Health, 2010). One popular theory is that low levels of serotonin possibly contribute to violent antisocial behavior (National Collaborating Centre for Mental Health, 2010). A com- plication for this hypothesis is that some of the variables that affect serotonin levels may, by themselves, cause antisocial behavior. For example, disadvantaged people, whose diets are poor, may have low serotonin levels. Their poverty also puts them at high risk of engaging in antisocial behavior. Is it their low serotonin that causes their antisocial behavior, or is it their poverty? Perhaps it is both.

There is a pressing need to clarify the ways in which genes affect antisocial behavior. Oppo- nents view genetic research as racially motivated, an attempt to redefine social problems in biological terms. They fear that genetic research will be used to stigmatize some minority groups as “born criminals.” Stigmatizing minorities is a danger, of course, but such an out- come can be avoided by properly educating the public about the meaning of genetic find- ings. Banning research on the genetics of antisocial personality disorder for political reasons would make it impossible for researchers to get a complete picture about how genetics and environment interact to produce antisocial behavior.

Sensation Seeking A hypothesis with a long history in psychology suggests that antisocial personality disor- der is the result of low emotional arousal (Schoorl, 2015). The idea is that low arousal is an aversive state that people naturally try to escape. They do this by seeking the stimulation and excitement that comes from dangerous, often antisocial, behavior (Schoorl, 2015). Of course, stimulation seeking need not always lead to antisocial behavior. Successful business- people, mountain climbers, and even scientists may also crave stimulation, but their behavior is not antisocial. Clearly, sensation seeking alone is not a sufficient explanation for why some people develop antisocial personality disorder. We must also explain why such people seek stimulation in socially disapproved ways. One likely place to look is in early childhood family experiences.

Family Dynamics Psychodynamic theorists attribute antisocial and most other personality disorders to an absence of trust in other people (National Collaborating Centre for Mental Health, 2010). This loss of trust, which results from a lack of love during infancy, leads to emotional detachment. Children grow up unable to empathize with others; as a result, they become self-absorbed.

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The evidence for this view is the frequent finding of dysfunctional backgrounds in the histo- ries of people with antisocial personality disorder (National Collaborating Centre for Mental Health, 2010). Again, however, there are many people who grow up with abuse who do not develop antisocial personality disorder, so family dynamics, on their own, are not a sufficient etiological explanation.

Modeling and Media Many lifelong habits, including antisocial ones, are first developed in childhood. For this rea- son, a childhood spent with criminal models is an ideal training ground for children to learn antisocial behavior (Paris, 2001). More often, however, exposure to antisocial behavior is not direct, but through the media. Children see crimes, including violent ones, on television, in the movies, and of course on the Internet; they can even “perpetrate” a pretend form of violence

by playing computer games.

Certainly, some evidence indicates that the number of hours spent watching media vio- lence is a predictor of aggression, both in children and later in life (Coker et al., 2015). But it is only one of many predictors, and not a very strong one at that. The correla- tion between aggression among males and the time spent watching violent television programs in the United States is 0.25. In Australia it is 0.13, and in Finland, 0.22 (cor- relations can range from 1.0 to –1.0; num- bers such as those here are not significant because they are too weak to have statistical significance; Huesmann, Moise, & Podolski, 1997). These correlations are too small to explain or predict violence on their own

(Barrett, 1997). Perhaps aggressive kids are more likely to watch violent videos and play violent computer games. To make things even more complicated, there are strong counterex- amples to the relationship between media violence and actual violence. Japan, for instance, is famous for its violent pornographic comics and gory cartoons, yet it has a much lower inci- dence of violent crime than other countries (NationMaster, 2017).

The evidence boils down to this: Violence in the media is not a sufficient explanation for child- hood violence. Censorship of media violence may reduce violence among some susceptible children (at the risk of violating everyone else’s right to free speech), but it is unlikely to elimi- nate what is really a complicated social problem that has multiple causes.

Treatment of Antisocial Personality Disorder Few adults with antisocial behavior seek treatment, and even fewer are motivated to change. In general, treatments tend to be ineffective (National Collaborating Centre for Mental Health, 2010). The most common “treatment” for people with antisocial personality disor- der is incarceration in a correctional facility. But incarceration is notoriously unsuccessful

Ingemar Edfalk/Blend Images/SuperStock Does violence in the media contribute to childhood violence? Researchers have conducted numerous studies on this topic, but the results have not pinpointed an exact cause.

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at rehabilitating most individuals, and repeat offenses are common. Psychological treatment does not usually thrive in involuntary settings such as prisons, yet there have been controlled studies showing the effectiveness of behavior therapy and behavioral staff training programs in reducing antisocial behavior, especially violence, by persons in institutions (Brazil, Van Dongen, Maes, Mars, & Baskin-Sommers, 2016). Clinicians have also had some success in reducing violence using antipsychotic and antidepressant medications, but more evidence is needed (Brazil et al., 2016). Given the difficulties encountered in treating antisocial personal- ity disorder after it is established, some psychologists have emphasized prevention instead (National Collaborating Centre for Mental Health, 2010). Prevention programs are usually aimed at children and adolescents from high-risk backgrounds (abused children, children in single-parent families, and children from marginal neighborhoods). These programs include parent training and school-based counseling programs, among others.

Highlight: The Slender Man Stabbings

On May 31, 2014, a horrific case shocked the relatively small city of Waukesha, Wisconsin. Two 12-year-old girls, Anissa Weier and Morgan Geyser, lured their best friend, 12-year- old Payton (Bella) Leutner, into the woods after a birthday sleepover at Geyser’s house. Weier and Geyser allegedly stabbed Leutner 19 times, purportedly to impress the fictional character Slender Man. By sacrificing Leutner, they believed that their families and they would be spared the Slender Man’s fatal wrath. After being stabbed, Leutner crawled to a road and lay on a sidewalk where a cyclist found her and called 911. She was rushed to a hospital, at which point she was close to death. Miraculously she recovered after being hospitalized for six days and later returned to school.

How could two 12-year-old girls, who were raised in evidently loving households where they did not lack basic needs, stab their best friend and leave her for dead? What could have led them to do such a thing? Although the case has a spectacular aspect to it that made major news headlines, an examination of some of the released facts provides a clearer picture of what might have occurred. Geyser purportedly had mental health issues since she was a very young child, according to her mother. What is not widely known is that her father has schizophrenia, currently in remission as of this writing. Weier was bullied extensively in school and would be drawn to unusual, often bizarre websites while withdrawing in her room.

Still, do these few facts (there are many others, of course) help to explain how two young girls could find themselves facing at least 60 years in prison? More relevant to the facts presented in this chapter, what if one or both also had premorbid indicators (warning signs) of a personality disorder? Neither girl can be diagnosed with a personality disorder because they are not yet 18. But does the inability to diagnose them prevent us from properly treating the girls? It seems not, as Geyser is in an inpatient psychiatric unit under court order, after being diagnosed with early-onset schizophrenia, and is doing reasonably well. Weier’s trial concluded in September 2017. A jury determined that she was mentally ill at the time of the attack, so Weier will avoid prison. Her attorney, Maura McMahon, said during closing

(continued)

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Highlight: The Slender Man Stabbings (continued) arguments that Weier was lonely and depressed after her parents divorced and she latched onto Geyser. Once they became friends, they became obsessed with Slender Man, developing a condition called shared delusional disorder. Although not a DSM–5 diagnosis (the term in the DSM–5 is delusional symptoms in partner of individual with delusional disorder), this means that Weier ended up believing the Slender Man delusions that Geyser kept telling her about. The defense argued that Geyser’s delusions provided content for Weier’s delusions. This decision means that Weier will be sent to a psychiatric hospital rather than prison. A plea agreement states that she has to spend at least three years at a hospital before further determination is made. Geyser’s trial was scheduled to begin in October 2017 but in late September, she reached a plea deal. The terms of the deal state that Geyser will be evaluated by doctors, and based on the doctors’ testimony a judge will determine how long she will remain in a state mental hospital.

This case raises many interesting questions: Why can’t we diagnose someone under age 18 with a personality disorder, even when it seems likely the signs and symptoms are present? Can we help someone who believes that fictions like Slender Man are real and who will go as far as attempting to kill another person? Although we can hypothesize that since Geyser’s father has schizophrenia, she may have inherited its diathesis, what about Weier? Is this the behavior of two misguided 12 year olds? Why didn’t anyone pick up on Geyser’s warning signs earlier, before it was too late? Or Weier’s? Would you be able to work with someone who has difficulty separating fantasy from reality, not knowing the difference between “right” and “wrong”? How important is it to stop bullying once it is detected? For the moment, these questions must remain hypotheses to a case that, sadly, has echoes in many school shootings and other tragic incidents, in which bullying and other possible premorbid indicators of a future personality disorder, or other kind of mental illness, are missed, downplayed, or ignored.

Milwaukee Journal Sentinel/GettyImages Anissa Weier (left) and Morgan Geyser (right) developed shared delusional disorder and believed that they were being threatened by a fictional bogeyman called Slender Man.

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9.2 Diagnosing Personality Disorders All personality disorders begin to become apparent during adolescence or early on in adult- hood, although some do not make their first appearance until adulthood (APA, 2013). Once these disorders appear, they change little over the years, and they affect behavior in numer- ous situations.

Some personality disorders—antisocial personality disorder, for example—do not normally cause the individuals who have them personal distress. Instead, other people, especially their victims, feel the anguish. In such cases, diagnosis depends not on the self-perceptions of the individuals concerned but on the effects of their behavior on others. This is not unusual in abnormal psychology.

Categories Versus Dimensions Because each of us can be described by noting where we fall on one or more personality traits, or “dimensions,” some psychologists have advocated a dimensional approach to diagnos- ing personality disorders. Instead of employing the “exclusional” diagnostic categories of the DSM–5—a person either meets the diagnostic criteria for a personality disorder or does not meet them—the dimensional approach to diagnosis describes people using a standard set of personality dimensions. The DSM–5 includes the dimensional model in Section III, “Emerging Measures and Models.” This section includes proposed diagnostic criteria for this new model. Perhaps this model will replace the current personality disorders model in the DSM’s next revision (see the accompanying Highlight).

Highlight: Personality Disorder Trait Specified (PDTS)

The APA (2013) has come up with an alternative dimensional approach to be considered in a possible DSM–5 update. A core component of this approach is the diagnosis of personality disorder trait specified (PDTS). Individuals would receive this diagnosis if one or more of their traits significantly impaired their functioning in everyday life. Psychologists and other helping professionals would identify and list the traits that were impaired, as well as rate the severity of the impairment. The five groups of traits are as follows:

• Negative affectivity: People who display this trait have and experience negative emotions frequently and intensely. They will demonstrate at least one of the following traits: emotional lability (unstable emotions), anxiousness, separation insecurity, submissiveness, hostility, perseveration (repeating certain behaviors despite repeated failures from prior attempts), depression, suspiciousness, and restricted affectivity (lack of affect).

• Detachment: These people often avoid social interactions, often withdrawing from them. They will demonstrate one of the following traits: withdrawal, intimacy avoidance, anhedonia (inability to feel pleasure or get pleasure from pleasurable things), depression, restricted affectivity, and suspiciousness.

(continued)

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The advantage of the dimensional approach is that it avoids pigeonholing people into narrow categorical boxes, thereby allowing them to be described in richer and more complex ways. Over the years, several attempts have been made to develop dimensional systems for describ- ing personality (Cloninger, Bayon, & Przybeck, 1997; Widiger & Trull, 2007). These have not had wide consensus because psychologists have not been able to agree on which personality dimensions to use for this purpose (Widiger, 1991). One more widely accepted model is the five-factor model. People are rated on the following dimensions, and the combination deter- mines the reasons why we are all so different: extroversion, agreeableness, conscientious- ness, neuroticism, and openness to experience (Costa & McCrae, 2005; Goldberg, 1993).

Types of Personality Disorders Following the DSM–5, this chapter divides the personality disorders into three clusters. Clus- ter A includes the paranoid, schizoid, and schizotypal personality disorders. Individuals who fall into Cluster A appear odd or eccentric. Cluster B includes the antisocial, borderline, histri- onic, and narcissistic personality disorders. Individuals in Cluster B are dramatic, emotional, and erratic. Cluster C includes the avoidant, dependent, and obsessive-compulsive person- ality disorders. Individuals in Cluster C are anxious and fearful. It is not uncommon for the same person to be simultaneously diagnosed with personality disorders from more than one cluster (APA, 2016; Phillips & Gunderson, 1996; Skodol, 2005).

The precise number of personality disorders and the names of these disorders have varied from one version of the DSM to the next. Although the DSM–5 has settled on the 10 personal- ity disorders listed in Table 9.1, keep in mind that these disorders represent only a sample of the total number of potential personality disorders.

Highlight: Personality Disorder Trait Specified (PDTS) (continued)

• Antagonism: These individuals will behave in ways that will put them in confrontation with others. They will demonstrate one of the following traits: manipulativeness, deceitfulness, grandiosity, attention seeking, callousness, and hostility.

• Disinhibition: These individuals behave impulsively without reflecting on potential future consequences. They will demonstrate one of the following traits: irresponsibility, impulsivity, distractibility, risk taking, and lack of rigid perfectionism.

• Psychoticism: These individuals have unusual and bizarre experiences. They will demonstrate one of the following traits: unusual beliefs and experiences, eccentricity, and cognitive and perceptual dysregulation (odd or unusual thought processes or sensory experiences) (APA, 2013).

An individual would qualify for a PDTS diagnosis if he or she has significant impairment in any of these five groups of traits, or in only one of the traits listed in any of the groups. As mentioned earlier, this approach and diagnosis are currently in review for the next revision of the DSM–5. What is your opinion about this dimensional approach?

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Diagnostic Reliability Clinicians have difficulty deciding which personality disorder diagnosis is appropriate for which individual. The problem is that the same diagnostic criteria can be applied to suppos- edly different disorders. Clinicians have no trouble agreeing that a person has poor social rela- tions (one of the diagnostic criteria), but they do not agree about whether a person with poor social relations should be classified as having a borderline, schizoid, or avoidant personality disorder (each of which is marked by the same criterion—poor social relations). Therefore, diagnostic reliability (the consistency of a measuring device, here referring to the DSM–5) is rather poor. Similarly, hostility (another of the diagnostic criteria) is easy to recognize, but of little discriminatory value because it is a feature of more than half the personality disorders.

Also, given the overlapping diagnostic criteria, it is not surprising that, as mentioned ear- lier, there is high comorbidity among personality disorders (APA, 2013). In fact, choosing between two or more personality disorders may be so difficult that clinicians may find it easier to simply give people both diagnoses.

Diagnostic Validity The predictive value of the personality and impulse-control disorders is somewhat uncertain. Here we would examine validity, that is, does the DSM–5 measure what it claims to measure? In addition, does the DSM–5 have eternal validity, meaning do the diagnostic criteria general- ize to many individuals? Knowing that someone has a personality disorder tells us little about

Table 9.1 DSM–5 personality disorders

Diagnostic Term Primary Personality Characteristics

Cluster A

Paranoid personality Distrust and suspicion of others, poor social relations

Schizoid personality Restricted range of emotions and unstable relationships

Schizotypal personality Eccentric behavior, including cognitive distortions

Cluster B

Antisocial personality Disregard of the rights of other people

Borderline personality Unstable relationships, poor self-image, impulsivity

Histrionic personality Excessive emotional display and the pursuit of attention

Narcissistic personality Grandiose feelings of superiority

Cluster C

Avoidant personality Socially sensitive, inhibited, feelings of inadequacy

Dependent personality Submissive and needing the care of others

Obsessive-compulsive personality Preoccupation with order and control

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Section 9.3 Cluster A: Paranoid, Schizoid, and Schizotypal Personality Disorders

how different personalities develop. Predicting how a person will behave in any situation requires that we understand not only the person’s personality but also the social situation in which the behavior takes place (Sherman et al., 2015).

Diagnostic Biases Clinicians must be on the alert for potential biases in themselves when making any diagno- sis, but personality disorders lend themselves to diagnostic biases. For example, dependence, submissiveness, and allowing one’s life to be directed by a spouse are all signs of a dependent personality disorder. However, they are also traits encouraged in females by many societies. If women adopt the dependent social role expected by their social group, are we really justified in calling their behavior a personality disorder? And gender biases are not the only ones that clinicians must avoid. Unless clinicians are careful, their evaluation of other people may also be biased by their own beliefs about or perceptions of social class, ethnicity, age, and educa- tion. As discussed in the following sections on specific personality disorders, each of these variables can bias clinical judgments about who is suffering from a personality disorder.

9.3 Cluster A: Paranoid, Schizoid, and Schizotypal Personality Disorders

Cluster A personality disorders are marked by eccentricity, not to the point of losing touch with reality, but enough for the individual to be perceived by others as odd. The disorders included in Cluster A all share at least a superficial similarity with schizophrenia. Indeed, Cluster A personality disorders have sometimes been construed as milder versions or pre- cursors of schizophrenia (Via et al., 2016). There is considerable overlap among the Cluster A personality disorders, making it difficult for clinicians to differentiate among them (APA, 2013; Via et al., 2016).

Paranoid Personality Disorder People with paranoid personality disorder lack trust in others and constantly fear that their friends may be disloyal or unfaithful. Consequently, people with paranoid personality disorder avoid revealing their thoughts and feelings. Often, others perceive them as being hypersensitive. Those with this disorder may interpret even innocuous events (omission of their name from a roster, for example) as a sign that others are plotting against them. Any offers of assistance are taken as criticisms that the person is unable to cope on his or her own. Because they react to these perceived insults with anger, people with paranoid personality disorder are perceived by others as hostile.

At one time, paranoid personality disorder was viewed as a milder form of schizophrenia, but there are important differences between the two conditions. In contrast to people with

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schizophrenia, those with paranoid personality disorder do not have delusions, hallucina- tions, or other forms of thought disorder (APA, 2013). Instead, they are characterized mainly by their suspicion of other people. Today, most clinicians believe that paranoid personality disorder is at best only a distant member of schizophrenia spectrum and other psychotic dis- orders (Triebwasser, Chemerinski, Roussos, & Siever, 2013).

Sometimes, several people with paranoid personality disorder band together into groups with others who share their paranoid beliefs. Of course, seemingly “paranoid” people may have real enemies, so this diagnosis should not be applied lightly to political or economic refugees or to people whose backgrounds may have actually included conspiracies and prejudice. Some crit- ics have argued that paranoid personality disorder should have been removed from the DSM– 5, as there is not enough empirical data to support its inclusion (Triebwasser et al., 2013).

Etiology Paranoid personality disorder first becomes apparent in childhood and seems to occur more often in males than females (APA, 2013). It affects between 0.5% and 4.4% of the general population (APA, 2013; O’Connor, 2008; Triebwasser et al., 2013). Because both traumatic brain injury and substance abuse may produce paranoid symptoms, care should be taken to exclude both possibilities when making the diagnosis (Gauba, Thomas, Balhara, & Desh- pande, 2016).

Treatment Few people with paranoid personality disorder seek psychological treatment; they are too suspicious of therapists. Those who do find their way into treatment may receive psychody- namic psychotherapy, cognitive-behavioral therapy, and medication. Unfortunately, none of these approaches to treatment have met with much success (Triebwasser et al., 2013).

Schizoid Personality Disorder Schizoid personality disorder consists mainly of negative rather than positive symptoms. As was discussed in Chapter 8, positive and negative do not refer to “good” and “bad” aspects. Rather, positive symptoms refer to something added to an individual’s behaviors or personal- ity (like a delusion), whereas negative symptoms refer to an absence of something or some kind of behavior that typically is present (for example, proper hygiene or speech). That is, the defining feature of schizoid personality disorder is not a delusion, obsession, or thought disorder—it is the lack of social relationships (Triebwasser, Chemerinski, Roussos, & Siever, 2012). People with schizoid personality disorder prefer solitary pursuits and spend much of their time alone (see the accompanying Highlight). They have flat affect (a limited range of emotions) and are indifferent toward the opinions of others. Because of their social isolation, people with schizoid personality disorder are socially inept and appear self-absorbed, cold, and aloof (Triebwasser et al., 2012).

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Section 9.3 Cluster A: Paranoid, Schizoid, and Schizotypal Personality Disorders

To keep schizophrenia and schizoid personality dis- order separate, the DSM–5 rules out schizoid per- sonality disorder in people with schizophrenia (or any other psychotic disorder). It is also important that diagnosticians consider a person’s social situ- ation. For example, the diagnosis of schizoid per- sonality disorder is inappropriate for people who have recently migrated from one culture to another. Although immigrants may show the signs of a schiz- oid personality disorder (immigrants often take a while to settle into their new surroundings), it would be unwise to make a diagnosis until they have had the opportunity to adjust to their new environ- ment. Finally, the diagnosis should be reserved for people in distress, not for people who prefer and adjust well to living as “loners.”

Etiology Although the term simple schizophrenia was once used to describe people with schizoid personal- ity disorder, it, like paranoid personality disor- der, is probably only a distant (at best) member of the spectrum of schizophrenia-related disorders

Mrk movie/Marka/SuperStock Some people have diagnosed Batman with schizoid personality disorder due to his solitary tendencies and aloof persona.

Highlight: Veronica’s Sunday

Veronica is a 32-year-old woman who works during the week as a security guard at a bank. This excerpt from a letter written by Veronica’s sister, with whom she lives, to their mother, is a description of a typical Sunday in the life of this woman with a schizoid personality disorder:

Dear Mom,

I hope you are well, and over your cold. I am doing OK, but I’m worried about Veronica. I have been keeping a close eye on her as you suggested, but she seems to be getting even more withdrawn. Let me tell you about Sunday. Veronica got up at 8:30 and switched on the television. She watched for an hour while still in bed. She then had some juice and coffee while watching a news show on television. At around 10:30, she fed Kat [the cat]. She sat and watched the cat eat for a while and then spent 45 minutes washing and ironing her clothes. She organized her drawers and then had a shower and got dressed. By this time, it was noon. Her next activity was to sit on a chair directly in front of a window and read the newspaper that we get delivered. After about an hour of this, Veronica once again turned on the television. She watched a talk show, and then she went outside for a walk. When she returned home, she ate a tiny dinner and watched television until late, when she fell asleep. She did not utter a word to me, or anyone else, all day. . ..

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Section 9.3 Cluster A: Paranoid, Schizoid, and Schizotypal Personality Disorders

(Fulton & Winokur, 1993; Laulik, Chou, Browne, & Allam, 2013; Maier, Lichtermann, Minges, & Heun, 1994). Schizoid personality disorder is no more common among the relatives of peo- ple with schizophrenia than it is among the relatives of people without schizophrenia. Like paranoid personality disorder, it is more likely to be found among the relatives of depressed people than of schizophrenic people.

Psychodynamic (and most behavioral) theorists blame rejecting and abusive parents for causing their offspring to shun other people (Laulik et al., 2013; Sperry, 2003). The trouble with this hypothesis is that precisely the same etiology is applied to paranoid personality dis- order. What psychodynamic theorists do not explain is why some rejected children withdraw and develop a schizoid personality disorder, whereas others react with anger and become paranoid. Based on the restricted range of affect often displayed by people with schizoid per- sonality disorder, cognitive theorists have hypothesized that their symptoms are the result of some deficit in processing emotional information (Smith, 2006; Triebwasser et al., 2012).

Treatment People with schizoid personality disorder rarely seek treatment; they are too disengaged from others to care and too threatened by close relationships to get involved in psychother- apy (Mittal, Kalus, Bernstein, & Siever, 2007; Triebwasser et al., 2012). Those who do find their way into treatment usually suffer from some associated condition, such as substance abuse or depression. For those who receive treatment, psychoanalytic therapy focuses on working through the trauma produced by early rejection, whereas cognitive-behavioral ther- apy attempts to teach people the social skills they need to interact with others. There have been case reports of successful psychological treatment of schizoid personality disorder in young people (Gooding, 2016; Herlihy, 1993), but, for most people, psychotherapy has pro- duced only limited success (Belcher et al., 1995) and medications have not proved much bet- ter (Gooding, 2016; Koenigsberg et al., 2002).

Schizotypal Personality Disorder Like people with schizoid personality disorder, those with schizotypal personality disor- der are loners who are unable to form relationships with other people or are uninterested in doing so. They prefer solitary activities to those involving others, and, like people with schizoid personality disorder, they are often perceived as cold and unemotional. There are also similarities between schizotypal personality disorder and paranoid personality disorder. Both disorders are marked by suspicion of the motives of others and by ideas of reference, the belief that unrelated comments and events pertain to those with the disorder.

Clearly, the schizotypal personality disorder shares symptoms with both the schizoid and the paranoid personality disorders, but it differs in an important respect: Schizotypal per- sonality disorder is hypothesized to be related to, and like, schizophrenia (Koenigsberg et al., 2005; Thames & Lilienfeld, 2015). People with schizotypal personality disorder have peculiar thoughts, rambling speech, odd appearance, and eccentric behaviors. Put simply, schizotypal personality disorder seems to be a mild form of schizophrenia that occurs in approximately 0.6% to 3.9% of the population (APA, 2013; Bollini & Walker, 2007; Rosell et al., 2014; Thames & Lilienfeld, 2015).

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Section 9.3 Cluster A: Paranoid, Schizoid, and Schizotypal Personality Disorders

Etiology Because of the similarity between schizotypal disorder and the schizophrenia spectrum of disorders, researchers have tried to apply the diathesis-stress etiological model of schizo- phrenia to schizotypal personality disorder. Certainly, the diathesis appears to be similar. Schizotypal personality disorder is most commonly found in families with schizophrenic rela- tives (Thames & Lilienfeld, 2015), and people with schizotypal personality disorder exhibit attentional deficits similar to those seen in people with schizophrenia (Bollini & Walker, 2007; Thames & Lilienfeld, 2015). The similarities between the two disorders do not end there. Both schizophrenia and schizotypal personality disorder have also been linked to higher than average levels of dopamine as well as to enlarged brain ventricles (Bollini & Walker, 2007; Fervaha & Remington, 2013).

Treatment As it is with schizophrenia, psychotherapy is of limited value in schizotypal personality disor- der (Ewing, Falk, & Otto, 1996; Ryan, Macdonald, & Walker, 2013). The most successful treat- ment approaches mirror those used in schizophrenia—skills training (McKay & Neziroglu, 1996; Ryan et al., 2013) and antipsychotic medication (Bollini & Walker, 2007; Ryan et al., 2013). See Table 9.2 for a comparison of Cluster A personality disorders and schizophrenia.

Table 9.2 Comparison of Cluster A personality disorders and schizophrenia on selected characteristics

Disorder Characteristics

Negative Symptoms (e.g., blunt affect)

Paranoid Ideas

Family Members With Schizophrenia

Positive Symptoms (e.g., thought disorder)

Schizophrenia Yes Yes Yes Yes

Cluster A Personality Disorders

Paranoid personality disorder

Yes

Schizoid personality disorder

Yes Yes

Schizotypal personality disorder

Yes Yes Yes

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Section 9.4 Cluster B: Antisocial, Borderline, Histrionic, and Narcissistic Personality Disorders

9.4 Cluster B: Antisocial, Borderline, Histrionic, and Narcissistic Personality Disorders

People with Cluster B personality disorders tend to be self-absorbed. They find it difficult to empathize with others because they spend so much time and energy on themselves. In addi- tion, they exaggerate the importance of everything that happens to them, usually in a theat- rical and overly dramatic way. Because of their excessive self-concern and melodramatics, people with Cluster B personality disorders find it difficult to establish and maintain interper- sonal relationships (APA, 2013). Antisocial personality disorder has already been discussed, so this section focuses on the remaining three Cluster B disorders: borderline, histrionic, and narcissistic personality disorders.

Borderline Personality Disorder Clinicians and researchers who work from different paradigms have used the term border- line in several different ways: (a) to refer to people whose behavior fell at some hypotheti- cal border between “neurotic” mood disorders and psychotic ones, (b) as a general term for the symptoms caused by mild brain damage, and (c) to describe people whose poor social relations are marked by manipulative suicide attempts (Gunderson, Zanarini, & Kisiel, 1995; Ogden & Prokott, 2013; Tyrer, 1994).

In an attempt to give systematic meaning to the term borderline, the DSM–5 has chosen to emphasize instability and impulsivity. According to the DSM–5, people with borderline per- sonality disorder are insecure because they have a morbid fear of abandonment. They want to form close relationships, and, initially at least, they succeed. But their need for attention and reassurance eventually becomes too overwhelming and their relationships break down. This is a recurring cycle—other people begin as perfect friends and evolve into enemies; there is no in-between. This tendency to categorize people as entirely good or entirely bad is known in psychoanalytic circles as “splitting.”

When relationships deteriorate, people with borderline personality disorder may threaten to harm themselves just to keep the connection going. If this does not work (and it rarely does), they may actually carry out their threats by mutilating or even killing themselves (Ogden & Prokott, 2016; Sherry & Whilde, 2008). In addition to self-harm, people with borderline personality disorder may engage in various forms of imprudent behavior—reckless driving, unsafe sex, gambling, and substance abuse (Schub & Kornusky, 2016; Sherry & Whilde, 2008). Indeed, their moods tend to swing widely depending on the state of their interpersonal rela- tionships. When these are going well, they may be elated, friendly, and good company. When their relationships are going badly, they become depressed, sullen, and aggressive.

Etiology There is considerable overlap between the symptoms of antisocial personality disorder and those of borderline personality disorder. There are some differences as well. Although people with both diagnoses are impulsive, reckless, unable to form stable relationships, and often hostile, borderline personality is also associated with a morbid fear of abandonment.

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Borderline personality disorder occurs in anywhere from 1.6% to 5.9% of the general popu- lation (APA, 2013; Sherry & Whilde, 2008), with about 75% being female. As we have seen, sex differences in the incidence of a disorder can have many explanations. In the case of bor- derline personality disorder, social factors, especially sex role expectations, seem to play an important part (Becker, 1997; Hoertel et al., 2014). Through the process of socialization, simi- lar etiological factors wind up producing somewhat different disorders. For instance, it is possible that the underlying causes of antisocial and borderline personality disorders are similar but that women are socialized to be more frightened of being alone and to turn their aggression inward in the form of suicidal gestures rather than outward toward others (Hoer- tel, Peyre, Wall, Limosin, & Blanco, 2014; Paris, 1997). Of course, social roles change from one society to another, so it is important to keep in mind that practically all of the research and clinical reports concerning borderline personality disorder come from developed countries such as the United States. Traditional societies, such as those found in developing countries, have different sex roles. For example, in some societies, women are almost guaranteed sup- portive relationships through a network of mutual family and community obligations. Per- haps this is the reason such societies have a low incidence of borderline personality disorder (Paris, 1996; Paris & Lis, 2012).

Borderline personality disorder has been attributed to parental loss or abuse in childhood (Ogden & Prokott, 2016; Sansone, Levitt, & Sansone, 2005) or to posttraumatic stress later in life (Ogden & Prokott, 2016; Zlotnick, 1997). In both cases, psychological trauma is thought to produce a fear of further loss and a subsequent fear of abandonment (Ogden & Prokott, 2016; Sherry & Whilde, 2008). Although this seems a plausible theory, it is hardly specific to bor- derline personality disorder. Parental loss and abuse are found in the backgrounds of many psychological disorders. A similar lack of specificity may be found in the various biological explanations offered for borderline personality disorder—genetics, low levels of serotonin (Norra et al., 2003; Ogden & Prokott, 2016), thyroid dysfunction (Klonoff & Landrine, 1997; Sinai et al., 2015), and brain structures either being unusually small or being overactive or underactive (Donegan et al., 2003; Visintin, Voci, Pagotto, & Hewstone, 2016); all occur in other disorders as well.

Treatment There have been many attempts to develop treatments for borderline personality disor- der, but none has proved especially successful. Psychoanalytic psychotherapy concentrates on analyzing the transference relationship that develops between patient and therapist. That is, in psychoanalysis, it is essential to establish a patient-analyst relationship in which the patient responds to the analyst as though the analyst is or was an important figure (for example, father, mother) in the patient’s life. The goal of treatment is to use the transference relationship as a model to show people the way in which they undermine their interpersonal relationships (Gabbard et al., 1994; Horwitz, 1996; Stoffers et al., 2013). A strong patient- therapist transference may also help people with borderline personality disorder to learn to trust others. As you can imagine, however, building a transference relationship and analyzing a client’s interpersonal functioning is difficult with people whose relationships are character- istically turbulent. Following their usual pattern, patients with borderline personality disor- der begin by idealizing the therapist as a potential savior and later, through splitting, turn this completely around so that the therapist becomes a money-seeking charlatan. In such cases,

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analyzing the transference relationship takes some time, with many regressions along the way (Bender & Oldham, 2005; Stoffers et al., 2013).

Although cognitive-behavioral therapy may assist people with borderline personality disor- der to lead more effective lives (Stoffers et al., 2013; Waldo & Harman, 1998), people with this disorder may find it difficult to complete a course of therapy. They may drop out of treat- ment at the first sign (real or imagined) that the therapist is neglecting them. To help such clients follow through with treatment, clinicians may first try to increase a client’s emotional stability. For example, emotional awareness training, in which people with borderline per- sonality disorder are given practice in recognizing their emotions (as well as those being experienced by others) and then taught ways to control their emotions, may help clients to cope with the stress of cognitive and behavioral interventions (Oldham, 2006; Stoffers et al., 2013). Therapists, too, must make certain adjustments. For example, they must learn to deal with the manipulative behavior of clients who are hypersensitive to criticism and are always imagining that they are being rejected.

Cognitive-behavioral therapists may employ a multimodal treatment strategy known as dia- lectical behavior therapy. This approach combines group and individual therapy, support- ive counseling, and a behavioral contract (usually an agreement not to harm oneself) with skill training aimed at improving and maintaining relationships (Linehan & Dexter-Mazza, 2008; Stoffers et al., 2013). Support may also be given to friends and family members who need to learn what to expect and how to deal with a person who has a borderline personality disorder (Gale, 2016).

In addition to psychological treatment, the entire spectrum of psychoactive drugs has been used to treat borderline personality disorder, usually in conjunction with some form of psy- chological therapy (Ogden & Prokott, 2016; Soloff, 2005). The most effective drugs are antide- pressants (especially the SSRIs), which seem to reduce the impulsivity, depression, and rage that destroy relationships (Binks et al., 2006; Ogden & Prokott, 2013).

Histrionic Personality Disorder Histrionic personality disorder is a direct descendant of the 19th-century concept of hysteria. People with this disorder do not have conversion symptoms, though. They are mainly motivated by the need to be the center of attention (Bates, 2016; Skodol, 2005). To gain the notice they crave, people with this disorder may act seductively, dress in eccentric clothes, or act in a loud and bois- terous fashion. People with a histrionic per- sonality disorder actively seek compliments and are easily upset by criticism. Because of their melodramatic displays, histrionic peo- ple are viewed as shallow and phony.

RubberBall/SuperStock People with histrionic personality disorder desire to be the center of attention.

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Section 9.4 Cluster B: Antisocial, Borderline, Histrionic, and Narcissistic Personality Disorders

Etiology Histrionic personality disorder appears to have a prevalence of 1.84% to 3% in the general population (APA, 2013; Bates, 2016; O’Connor, 2008) and affects men and women equally (Bates, 2016; O’Connor, 2008).

Treatment Although people with histrionic personality disorder may seek treatment, they make difficult clients. They tend to use the therapeutic environment as another opportunity to “be on center stage” and present exaggerated versions of their problems (Bates, 2016; Gutheil, 2005). Group treatment is generally not possible for people with histrionic personality disorder because of their need to monopolize the therapist’s attention. Nor are histrionic people good candidates for insight-oriented therapy (self-awareness and understanding of the influence of the past on their present behavior); they find it impossible to accept any but their own interpretations of their behavior. Perhaps the best therapeutic approach is to concentrate on helping people with this disorder to separate important problems from trivial ones, and to teach them how to pay attention to others. There are no specific drug treatments for histrionic personality disorder, although drugs may be used to treat any comorbid disorders (such as major depres- sive disorder; Bates, 2016; Grossman, 2004).

Narcissistic Personality Disorder According to Greek mythology, Narcissus was a boy of legendary beauty who fell in love with his own reflection in the waters of a pond. He stared at his reflection until he wasted away to a flower. From this story, Freud derived the word narcissistic, meaning a person who is con- sumed with self-love. Freud’s use of the term has evolved into the DSM–5 diagnosis of nar- cissistic personality disorder. People with this disorder are characterized by their strong sense of superiority. They consider themselves to be important and demand special treat- ment. People with this disorder are often rude because they view rules and common courtesy as meant for others (Kealy, Goodman, Rasmussen, Weiderman, & Ogrodniczuk, 2017; Miller, Campbell, & Pilkonis, 2007). Like people with histrionic personality disorder, narcissistic people crave attention. They dream of achieving positions that will gain them the power and attention they seek. More often, however, narcissistic people exaggerate their own successes and envy the achievements of others. Beneath the surface, narcissistic people are so plagued by self-doubt that, even when they have reached a goal, they remain unsatisfied because suc- cess never brings them the level of adulation they desire.

Etiology In psychodynamic terms, narcissism starts in childhood. We are all narcissistic as children because the world seems to revolve around us. When we are hungry, someone feeds us; when we are cold, someone always caters to our needs. One of the most important tasks facing chil- dren during the process of socialization is learning that there are other people in the world, with their own feelings and needs. Learning to empathize with others is a skill that develops

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Section 9.5 Cluster C: Avoidant, Dependent, and Obsessive-Compulsive Personality Disorders

through childhood and the teenage years, so we must be wary of applying the DSM–5 criteria to young people (APA, 2013). However, by early adulthood, a narcissistic personality disorder should become clear. Once such a disorder develops, it tends to be ongoing (Bates & Neff, 2017; Ronningstam, 1998). Narcissistic personality disorder affects about 0% to 6.2% of the general population (APA, 2013), mainly males.

Treatment Both psychodynamic and cognitive-behavioral approaches to the treatment of narcissistic personality disorder focus attention on helping people to become more realistic in their goals and to find satisfaction and fulfillment in the normal events of daily life (Beck, Freeman, & Davis, 2004; Kealy et al., 2017). Training in recognizing and empathizing with the emotions of others is an important adjunct goal of treatment. As in many other personality disorders, drugs may be used to treat some symptoms or for comorbid disorders (Bateman, Gunderson, & Mulder, 2015; Joseph, 1997).

9.5 Cluster C: Avoidant, Dependent, and Obsessive-Compulsive Personality Disorders

The disorders in Cluster C share the characteristics of fearfulness and worry (Alpert et al., 1997; Laulik et al., 2013). In contrast to the anxiety disorders, however, Cluster C personality disorders tend to have an earlier onset, no clear cause, and a stable lifelong course (O’Donohue, Fowler, & Lilienfeld, 2007). Cluster C disorders include avoidant personality disorder, depen- dent personality disorder, and obsessive-compulsive personality disorder. Research support for the various etiological hypotheses is very limited. At the same time, treatments for these disorders appear to be modestly to moderately helpful—considerably better than for other personality disorders.

Avoidant Personality Disorder People with avoidant personality disorder are shy and socially uncomfortable. Unlike people with schizoid personality disorder, people with avoidant personality disorder would prefer to be sociable, but they avoid social contact because they fear embarrassment and criticism. In practice, it is difficult to separate avoidant personality disorder from social phobia (Prerost, 2016; Ralevski et al., 2005). When social anxiety is long-standing, the diagnoses are probably interchangeable. Because shyness and social reticence are developmentally appropriate for young children (and because some cultural groups encourage social timidity for one or both sexes), a client’s age and culture should be taken into account when making this diagnosis (APA, 2013). Avoidant personality disorder occurs in around 2.4% of the general population, and it affects men and women in equal numbers (APA, 2013; O’Connor, 2008; Prerost, 2016). It is often found in conjunction with the diagnosis of unipolar depression (APA, 2013; Prerost, 2016). Cognitive-behavioral treatments aimed at reducing social anxiety can also help people with avoidant personality disorder to lead fuller lives (Beck, 2016; Emmelkamp et al., 2006).

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Etiology Avoidant personality disorder is similar to social anxiety disorder in a number of ways, and may be comorbid with it (see, for example, Eikenaes et al., 2013). Both disorders present with a fear of humiliation and low self-confidence. However, there appears to be a key dif- ference between the two disorders: People with social anxiety disorder mainly fear social circumstances, whereas people with avoidant personality disorder fear close social relation- ships (Lampe & Sunderland, 2013). Others believe that the two disorders are very similar and therefore should be combined (Eikenaes et al., 2013).

Treatment One of the main issues with treating individuals with avoidant personality disorder is keeping them in treatment. This should not be a surprise, as many of the patients begin to avoid the sessions. This is not necessarily resistance but is based on the patient’s not trusting the clini- cian, and fearing being rejected by the clinician. An important aspect of treatment is therefore for the clinician to gain the patient’s trust (Colli et al., 2014; Leichsenring & Salzer, 2014). Typically, clinicians will treat avoidant personality disorder the same way they treat social anxiety disorder, and the success rate is usually moderate to good (Kantor, 2010; Porcerelli et al., 2007). As you might expect, psychodynamic therapists try to help the patients recognize and resolve their unconscious conflicts (Leichsenring & Salzer, 2014). Cognitive therapists, among other aspects, will work with patients to help them change their upsetting, irrational beliefs and thoughts, carry on in the face of painful emotions, and improve their self-image (Beck et al., 2004; Rees & Pritchard, 2013). Behavioral therapists will provide social skills training as well as exposure therapy, gradually requiring patients to increase their day-to-day interpersonal interactions (Herbert, 2007). Group therapy can be especially successful, as it provides the patient a chance to practice interpersonal interactions in a safe environment (Herbert et al., 2005).

Dependent Personality Disorder People with dependent personality disorder have a strong need to be taken care of by someone else, preferably someone important (Bornstein, 2005; Disney, 2013; Skodol, 2005). To fulfill this need, they tend to be submissive to the demands of their chosen caretaker, act- ing, at times, as if they were helpless to look after themselves. Like people with histrionic per- sonality disorder, those with dependent personality disorder have a strong need for approval. However, dependent people are timid, whereas histrionic people actively seek attention. Like people with borderline personality disorders, dependent people worry about being aban- doned. Instead of reacting with rage, however, dependent people become submissive. Finally, both avoidant and dependent personality disorders are characterized by feelings of inad- equacy, but avoidant people tend to withdraw, whereas dependent people seek to develop relationships with people who can care for them.

Dependent personality disorder affects anywhere from 0.6% to 2.5% of the general popula- tion (APA, 2013; Grant et al., 2004). The DSM–5 asserts that the disorder affects both sexes with only a small bias toward females (APA, 2013). This sex difference probably reflects the cultural stereotype of the dependent woman. Because young children are expected to be dependent and because some cultural groups foster dependent behavior among females,

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Section 9.5 Cluster C: Avoidant, Dependent, and Obsessive-Compulsive Personality Disorders

caution should be taken in applying this diagnosis to children or to members of some cultural groups (APA, 2013).

Etiology Although the precise causes of dependent personality disorder are not known, it is thought to begin with a fearful temperament (a genetic disposition) that evokes overprotectiveness from parents (Disney, 2013; Sperry, 2003). Illness in childhood, abandonment, and traumatic loss can produce a similar overprotectiveness. Children may resent this attitude but may learn to submit rather than challenge their parents.

Treatment Few people seek treatment for dependent personality disorder. However, some may find their way into therapy for an associated anxiety or depressive disorder (Disney, 2013; Skodol, Gal- laher, & Oldham, 1996). In psychodynamic treatment, the therapist uses the transference relationship first to form a bond with the client and then to teach the person how to separate. The idea is that, through the transference experience, the person will learn more effective modes of relating to others (Disney, 2013; Sperry, 2003). Cognitive therapists try to help their dependent clients to recognize the faulty cognitions that produce their lack of self-confidence (Disney, 2013; Freeman, 2002). Behavioral therapists use assertiveness training to enhance self-esteem by providing dependent clients with a nonsubmissive mode of relating to others. Relaxation training may also be helpful in reducing anxiety. Although people with this disor- der usually go along with their therapist’s treatment suggestions (they are submissive people, after all), they are still difficult to treat because of their need for constant reassurance.

Long-term treatment is probably not a good idea with dependent people because it may make them overly dependent on their therapist. Support and self-help groups could be useful places for clients to practice new skills learned in therapy (provided, of course, that clients partici- pate in the group and do not simply let others do all the talking). Drugs may be prescribed for the anxiety and depression often experienced by people with dependent personality disorder (Disney, 2013; Fava et al., 2002), but care should be taken because clients may use drug over- doses as a way of manipulating other people.

Obsessive-Compulsive Personality Disorder It is rather easy, based on the name among other aspects, to confuse obsessive-compulsive disorder (OCD) with obsessive-compulsive personality disorder. OCD behaviors fall along a continuum from relatively mild to severe (Stein & Hollander, 1997; Vorstenbosch et al., 2012). Obsessive-compulsive personality disorder (OCPD) behaviors fall at the mild end of the continuum. People who have this disorder do not display true obsessions or even severe compulsions. Instead, they are characterized by a perfectionistic attitude toward daily life (APA, 2013). People with this disorder try to maintain a rigid control over their routines and, when possible, the behavior of other people. They accomplish the latter by insisting on a tight adherence to rules and schedules. They feel that their approach to all matters is the only correct one, and they tend to deny that other people might have reasonable alterna- tive views. Not surprisingly, they are viewed by others as moralistic, rigid, and stubborn. The

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Section 9.5 Cluster C: Avoidant, Dependent, and Obsessive-Compulsive Personality Disorders

disorder seems to be more common among white, educated, married males and has a prevalence in the community of about 2.1% to 7.9% (APA, 2013; Bartz, Kaplan, & Hol- lander, 2007).

Etiology As for many of the personality disorders, research on the etiology of OCPD is limited. A number of theories link OCPD with OCD even though there may in fact be little simi- larity between the two conditions. As you might expect, Freudian concepts are heavily represented.

Freudian theorists suggest that people with OCPD are anal retentive. This is due to very strict toilet training by the individual’s par- ents during the anal stage. Therefore, they

become anal retentive and fixated in the anal stage. They develop a lot of anger, which is repressed; in order to control this anger and stay in control, they withhold their feces. The end result is that they become extremely orderly and restrained (Millon, 2011). Cognitive theorists, as you might guess, believe that illogical and irrational thinking maintains OCPD (Beck et al., 2004; Weishaar & Beck, 2006).

Treatment People with OCPD do not usually believe there is anything wrong with them. Because of this they are not likely to seek treatment unless they are also suffering from a comorbid condi- tion. This is often an anxiety disorder or unipolar depression. They may seek treatment if a close friend or family member insists on it (Bartz et al., 2007). Part of the treatment process, therefore, might involve the clinician’s trying to establish rapport and trying to convince the patient to stay in treatment (Colli et al., 2014).

In therapy, Freudians would try to help patients recognize and accept their insecurities and personal limitations. Cognitive therapists would again focus on helping patients to change their irrational, all-or-nothing thinking, as well as their perfectionism, procrastination, and chronic worrying. The response rate to both modalities is usually quite good (Svartberg & McCullough, 2010; Weishaar & Beck, 2006).

ABC Photo Archives/GettyImages Felix Ungar (left) of The Odd Couple is a notorious neat freak, always mopping, cleaning, and picking up dust bunnies. He is always immaculately dressed. Does he have OCPD?

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Chapter Summary

Evolution of a Personality Disorder • Personality disorders constitute distinct diagnostic categories; a person either

meets the criteria for a personality disorder or does not meet them. • Alternatively, people may be described by where they fall on a variety of personal-

ity dimensions. The dimensional approach provides richer descriptions and avoids pigeonholing people into narrow categories.

• Unfortunately, there are many possible personality dimensions, and no one knows which ones are appropriate for describing people.

Diagnosing Personality Disorders • Clinicians often disagree about personality disorder diagnoses because of overlap-

ping criteria. • Borderline, schizoid, and avoidant personality disorders are all marked by poor

social relations. • To make diagnosis easier, clinicians often simply give people more than one person-

ality-disorder diagnosis. • In some cases, personality-disorder diagnostic criteria reflect cultural and gender

stereotypes.

Antisocial Personality Disorder • The hallmark of antisocial personality disorder is a flagrant disregard for the rights

of other people. • The disorder is found mainly in males, it affects between 0.2% and 3.3% of the

population, and its incidence decreases with age. • Like much human behavior, antisocial personality disorder begins in childhood,

especially among children from abusive or discordant families. • Few people with antisocial personality disorder are motivated to seek treatment.

Cluster A: Paranoid, Schizoid, and Schizotypal Personality Disorders • Cluster A personality disorders are marked by eccentricity, not to the point of losing

touch with reality, but sufficient for the individual to be perceived by others as odd. • Psychological treatments for Cluster A disorders mirror those used in schizophre-

nia—social skill training and antipsychotic medication.

Cluster B: Antisocial, Borderline, Histrionic, and Narcissistic Personality Disorders

• People with Cluster B personality disorders are self-absorbed. They find it difficult to empathize with others, and they exaggerate the importance of everything that happens to them in a theatrical and overly dramatic way.

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Chapter Summary

• Because of their excessive self-concern and melodramatics, people with Cluster B disorders find it difficult to establish and maintain interpersonal relationships.

• These disorders are difficult to treat but may sometimes respond to therapy, particu- larly a mixture of psychodynamic and cognitive-behavioral treatment.

• Drugs are also used in treatment but mainly for associated conditions or specific symptoms.

Cluster C: Avoidant, Obsessive-Compulsive, and Dependent Personality Disorders

• The disorders in Cluster C share many characteristics with the anxiety disorders, such as fearfulness and worry, and they tend to co-occur with depression.

• Cluster C personality disorders tend to have no clear cause and a stable lifelong course.

Critical Thinking Questions

1. Personality disorders are chronic and difficult to treat. What makes these disorders so difficult to treat?

2. Antisocial personality disorder appears to be associated with criminal tendencies or behaviors. Discuss the possible connection between the two.

3. Narcissistic personality disorder was under consideration for removal from the DSM–5 as a diagnostic category. Discuss some possible reasons for this consideration.

4. Individuals with a Cluster B personality disorder often do not come into treatment voluntarily. Let’s assume you had someone with antisocial personality disorder in treatment who hated being there. How would you go about treating him or her?

5. Imagine that your coworker has a narcissistic personality disorder. What types of issues do you think you might encounter in working with him or her?

Key Terms antisocial personality disorder A Clus- ter B disorder; the key characteristic is a flagrant disregard for the rights of other people. People with antisocial personality disorder are often irresponsible, impulsive, and untrustworthy.

avoidant personality disorder A Cluster C disorder; people with avoidant personality disorder are shy and socially uncomfort- able. They would prefer to be sociable, but they avoid social contact because they fear embarrassment and criticism.

borderline personality disorder A Cluster B disorder; people with borderline personal- ity disorder are insecure because they have a morbid fear of abandonment. They tend to be self-injurious and have short-term, intense interpersonal relationships.

dependent personality disorder A Cluster C disorder; people with this disorder have a strong need to be taken care of by someone else, preferably someone important. They tend to be submissive to the demands of their chosen caretaker, acting, at times, as if they were helpless to look after themselves.

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Chapter Summary

dialectical behavior therapy A treatment approach for borderline personality dis- order that combines group and individual therapy, supportive counseling, and behav- ioral contracting with skill training aimed at improving and maintaining relationships.

dimensional approach This system for diagnosing personality disorders describes people using a standard set of personality dimensions.

histrionic personality disorder A Clus- ter B disorder; these individuals are moti- vated mainly by the need to be the center of attention. People with this disorder may act seductively, dress in eccentric clothes, or act in a loud and boisterous fashion.

narcissistic personality disorder A Cluster B disorder; these individuals have a strong sense of superiority. Those with the disorder consider themselves to be impor- tant and demand special treatment, and they are often rude because they view rules and common courtesy as meant for others.

obsessive-compulsive personality disor- der A Cluster C disorder; people who have this disorder are characterized by a per- fectionistic attitude toward daily life. They try to maintain a rigid control over their routines and, when possible, the behavior of other people.

paranoid personality disorder A Cluster A disorder; individuals with the disorder avoid revealing their thoughts and feelings and may interpret even innocuous events as a sign that others are plotting against them.

personality The sum of an individual’s traits.

personality disorder An enduring pattern of inner experience and behavior that devi- ates markedly from the expectations of an individual’s culture.

personality disorder trait specified (PDTS) A personality disorder currently under consideration for inclusion in a future DSM–5 revision. Individuals would receive this diagnosis if one or more of their traits significantly impaired their functioning in everyday life.

psychopath A person who lacks empathy, does not fear punishment, and will continue to break the law even if capture and punish- ment are likely.

schizoid personality disorder A Cluster A disorder; people with this disorder have negative rather than positive symptoms. The defining feature of schizoid personal- ity disorder is not a delusion, obsession, or thought disorder—it is the lack of social relationships.

schizotypal personality disorder A Cluster A disorder; those with this disorder are considered “loners” who are unable to form relationships with other people or are uninterested in doing so. They are often perceived as cold and unemotional.

shared delusional disorder Not a DSM–5 diagnosis (the DSM–5 term is delusional symptoms in partner of individual with delusional disorder); refers to a condition in which an individual’s delusions provide content for another person, thus fostering that person’s delusions.

transference relationship In psychoanaly- sis, establishing a patient-analyst relation- ship in which the patient responds to the analyst as though the analyst is or was an important figure (for example, father, mother) in the patient’s life.

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8 Schizophrenia Spectrum and Other Psychotic Disorders

Marcus Butt/Ikon Images/SuperStock

Chapter Objectives

After reading this chapter, you should be able to do the following:

• Describe and explain how schizophrenia is diagnosed.

• Describe and explain what causes schizophrenia.

• Describe and explain how schizophrenia is treated.

• Describe the other schizophrenia spectrum and psychotic disorders and differentiate them from schizophrenia.

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Schizophrenia is among the most catastrophic of all psychological disorders, with a lifetime prevalence ranging from about 0.3% to 0.7% (American Psychiatric Association [APA], 2013) and about 2.5 million cases in the United States alone (Lambert & Kinsley, 2005). This means that approximately 1 of every 100 people in the world suffers from schizophrenia during his or her lifetime (Lindenmayer & Khan, 2012; Long et al., 2014). One meta-analysis shows the worldwide lifetime prevalence at 0.48% (Simeone, Ward, Phillip, Collins, & Windish, 2015). According to the National Institute of Mental Health (2010), an estimated 24 million people worldwide are afflicted with the disorder. It typically strikes young adults, who may suffer for decades as schizophrenia wrecks their social relationships, impairs their thinking and health, and robs them of the ability to enjoy life. Schizophrenia also represents a massive drain on society’s resources. Many patients cannot work, many require public assistance, and most require expensive treatment (Wu et al., 2005). Faced with numerous difficulties, not only psy- chological and behavioral but also economic, many individuals with schizophrenia attempt suicide (at least 25% to 50% may attempt it, and about 4% to 13% may successfully complete it; Lee, Lee, Koo, & Park, 2015). These tragic deaths add to the guilt and pain already borne by the families of individuals with schizophrenia. However, with proper intervention, family involvement in treatment, better education (especially through mass media), and perhaps most important, early identification, many individuals with schizophrenia can lead meaning- ful lives.

Schizophrenia falls under the category of schizophrenia spectrum disorders. The other disor- ders in this category are discussed later in this chapter. The signs and symptoms of schizo- phrenia are not simply more extreme forms of everyday behavior, as with anxiety, depressive, or bipolar and related disorders. Some of the symptoms associated with schizophrenia are rarely, if ever, encountered in daily life. Still, it is important to remember that no matter how bizarre their behavior, people with schizophrenia are human beings who experience love, hurt, joy, grief, and all the other human emotions and feelings. To help us keep in mind the human side of the tragedy that is schizophrenia, this chapter refers frequently to the story of Jennifer Plowman. Let’s begin with Part 1 of her case study.

8.1 The Genesis of Schizophrenia We can all identify with people who are depressed or anxious. Most of us have been there ourselves, in the sense that at some time or another we have all experienced the “blues” or felt nervous and worried about events occurring in our daily lives. There is nothing baffling or impenetrable about depression, or anxiety, or even mania. Schizophrenia is different. Schizo- phrenia is not a personality disorder (these will be discussed in Chapter 9), and as discussed in Chapter 5, it is definitely not a dissociative disorder, such as dissociative identity disorder. People with schizophrenia behave in ways that most of us find incomprehensible. They may believe that other people can read their thoughts or that friends and neighbors are engaged in elaborate plots against them. In different historical periods, people who have displayed these behaviors have been given pejorative labels such as “mad,” “crazy,” “insane,” and “lunatic,” but such behaviors can be more accurately and appropriately categorized as symptoms of a group of disorders known as the psychoses, disorders characterized by gross distortions of reality.

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The Case of Jennifer Plowman: Part 1

Transcript of a Commitment Hearing for Jennifer Plowman COUNTY COURT

COURT TRANSCRIPT

Marion County

Presiding: Hon. Richard Harding

JUDGE: You are requesting that your daughter, Jennifer, be involuntarily committed to University Hospital? Are you represented by legal counsel?

ANNE PLOWMAN: No, Your Honor. I can’t afford a lawyer.

JUDGE: I can see that you receive public assistance.

ANNE PLOWMAN: I do not want my daughter to wait for public assistance. Jenny refuses to go to the hospital on her own, and she desperately needs help.

JUDGE: Why do you say this?

ANNE PLOWMAN: Jenny has not left the house for days. She has not washed or changed her clothes. She just sits in her room. Sometimes I hear her talking to herself. Other times I can hear her laughing and swearing. Jenny says that she cannot come out of her room because people can read her thoughts. Your Honor, she desperately needs help.

JUDGE: Has she threatened you or anyone else?

ANNE PLOWMAN: No.

JUDGE: Has she harmed herself ?

ANNE PLOWMAN: She won’t wash or change her clothes.

JUDGE: But has she tried to hurt herself, cut herself, or something similar?

ANNE PLOWMAN: No. She says that there is nothing wrong with her.

JUDGE: I do not want to deprive Jenny of her liberty unless there is some good reason. Jenny is a 21-year-old adult. If she is not dangerous to herself or anyone else, then she should choose for herself whether she needs treatment.

ANNE PLOWMAN: Please, Your Honor. I’m so worried. Isn’t there something you can do to help?

JUDGE: Perhaps we can talk her into going voluntarily into University Hospital. If not, I will commit her, but only for 72 hours so that she may be examined by Mental Health Services. Once I receive their report, I will decide how to proceed.*

*Note: The requirements for involuntary commitment vary from state to state. In general, they include the presence of a mental illness, dangerous behavior toward self or others, grave disability, and the need for treatment. A person can be involuntarily committed for 72 hours and must be released if there are no reason(s) to retain the individual.

See appendix for full case study.

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Emil Kraepelin (1856–1926) devised a classification system for psychotic conditions. After examining a group of hallucinating and delusional patients, he distinguished between two types of psychotic disorders. In the first type, serious mental symptoms began in adolescence or early adulthood and followed a deteriorating course. In the second type, symptoms fol- lowed a cyclical course in which periods of remission alternated with psychotic episodes. Kraepelin named the cyclic psychosis manic-depressive disorder. Kraepelin called the continu- ously deteriorating psychosis dementia praecox (translated from Latin, means “premature dementia”). Kraepelin believed that the deterioration he observed in dementia praecox was the result of a progressive organic brain syndrome that began early in life.

In contrast to Kraepelin, Swiss psychiatrist Eugen Bleuler (1857–1939) rejected the idea that the course of a disorder, alone, could ever distinguish one psychosis from another. Bleuler pre- ferred to classify psychological disorders on the basis of their characteristic signs and symp- toms, rather than on their course and outcome (Bleuler, 1911/1952). The DSM–5 adopted Bleuler’s approach.

Bleuler proposed that the name dementia praecox be replaced with schizophrenia, a term derived from the Greek words for “split” (schizo) and “mind” (phrene). It is important not to confuse Bleuler’s concept of schizophrenia with dissociative identity disorder (formerly called multiple person- ality disorder, as discussed in Chapter 5). Bleuler’s “split” was not among personali- ties but among cognitions within a single personality. In schizophrenia, thoughts become split (disconnected) from one another. People race from one idea to the next, often with no obvious connection. Bleuler believed that a “loosening of asso- ciative threads” among cognitions was the common link among a set of heterogeneous disorders that he loosely grouped together and called the “schizophrenias.”

Bleuler’s symptoms for schizophrenia included hallucinations (sensory experi- ences in the absence of external stimuli), delusions (unsubstantiated beliefs), odd motor movements, and bizarre behavior. For example, individuals with schizophre- nia might walk around in public wearing a lion’s pelt in the middle of summer and talk- ing to themselves, or they might sit in the middle of a busy street beating the ground

Vlue/iStock/Thinkstock The term schizophrenia derives from the Greek words for “split” (schizo) and “mind” (phrene) in order to demonstrate the disconnected, or split, thoughts that occur within the mind.

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with drumsticks. They might be combative or easily agitated. Bleuler always referred to “the schizophrenias” rather than simply to “schizophrenia.” He insisted on the plural because he believed that several different but related disorders were responsible for psychotic behav- ior. Although this chapter uses the more common singular term schizophrenia, Bleuler was undoubtedly correct; schizophrenia is far from a homogeneous diagnostic category.

Signs and Symptoms The DSM–5 diagnostic criteria for schizophrenia are relatively narrow (see Table 8.1). Yet, despite this narrowing, there is no single symptom or set of symptoms that describes all people with schizophrenia. The schizophrenic syndrome is heterogeneous (mixed or var- ied or different; homogeneous means “the same”) in the presentation of symptoms, course, response to treatment, and outcome. These differences among people may mean that Bleuler was correct: Schizophrenia is not a single disorder but a syndrome or series of disorders with different etiologies and outcomes (Cuesta & Peralta, 2016).

In addition to schizophrenia, the DSM–5 describes seven other psychotic disorders, each of which shares some characteristics with schizophrenia (see Table 8.2).

Table 8.1 Main DSM–5 diagnostic criteria for schizophrenia

A. Characteristic symptoms: two (or more) of the following, each present for a significant portion of time during a one-month period (or less if successfully treated). At least one of these must be (1), (2), or (3): 1. Delusions 2. Hallucinations 3. Disorganized speech (frequent derailment or incoherence) 4. Grossly disorganized or catatonic behavior 5. Negative symptoms (diminished emotional expression or avolition)

B. For a significant portion of the time since the onset of the disturbance, level of functioning in one or more major areas, such as work, interpersonal relations, or self-care are markedly below the level achieved prior to the onset (or when the onset is in childhood or adolescence, failure to achieve expected level of interpersonal, academic, or occupational functioning).

C. Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less if successfully treated) that meet criterion A (active-phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or two or more symptoms listed in criterion A present in an attenuated form (for example, odd beliefs or unusual perceptual experiences).

D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either (1) no major depressive or manic episodes have occurred concurrently with the active- phase symptoms; or (2) if mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods.

E. The disturbance is not due to the direct physiological effects of a substance (for example, a drug of abuse or a medication) or another medical condition.

F. If there is a history of autism spectrum disorder or a communication disorder of childhood onset [see Chapter 11], the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations, in addition to the other required symptoms of schizophrenia, are also present for at least a month (or less if successfully treated).

Source: APA (2013, p. 99).

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At first glance, it might appear to the untrained eye that all schizophrenia spectrum and other psychotic disorders are similar, if not almost identical. After all, most, if not all, include hal- lucinations and delusions among their diagnostic criteria. However, this is not the case. The accompanying Highlight briefly examines two disorders that appear similar to schizophrenia but are not.

Although the DSM–5 contains diagnostic criteria for each of the schizophrenia spectrum and other psychotic disorders, researchers have tended to neglect the other disorders in favor of schizophrenia. For this reason, this chapter focuses on schizophrenia, although the other disorders are mentioned when appropriate.

Positive Versus Negative Symptoms Schizophrenic symptoms are divided into two main categories: positive and negative. In this context, positive and negative do not mean good or bad. Instead they mean the presence (posi- tive) or absence (negative) of something. Positive symptoms reflect an excess or distortion of normal cognitive and emotional functions; negative symptoms reflect a reduction or loss of normal functions. The most common positive symptoms are delusions, hallucinations, dis- organized speech and thinking, inappropriate affect, and bizarre motor movements. The neg- ative symptoms are loss of initiative, lack of emotional expression, and impoverished speech.

Although the distinction between positive and negative symptoms may have some practical value in predicting who will respond to treatment, it is a rather crude dichotomy (Velligan et al., 1997). Positive symptoms can occur in people who have major depressive disorder,

Table 8.2 Main DSM–5 psychotic disorders

Schizophrenia: A psychotic disturbance lasting more than six months that includes one or more of the following: delusions, hallucinations, disorganized speech, or odd movements.

Schizophreniform disorder: A disorder with symptoms similar to schizophrenia but with a shorter duration (between one and six months).

Schizoaffective disorder: A combination of a mood disorder and symptoms similar to those found in schizophrenia.

Delusional disorder: A disorder characterized by at least one month of delusions that are not bizarre in character and with none of the other symptoms of schizophrenia.

Brief psychotic disorder: A disturbance in which psychotic symptoms last for less than one month.

Psychotic disorder due to another medical condition: A disturbance in which psychotic symptoms develop directly from a medical condition, such as a seizure disorder (epilepsy), migraine headaches, or multiple sclerosis.

Substance/medication-induced psychotic disorder: A disorder in which psychotic symptoms are the result of substance abuse or exposure to a toxin.

Catatonia: A disorder in which the individual displays at least three symptoms including stupor (no psychomotor activity), waxy flexibility (slight resistance to a professional’s attempt to change the individual’s body position), and mutism (no or very little verbal response).

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bipolar I disorder, delusional disorder, and schizoaffective disorder, among other conditions. In schizophrenia, positive symptoms do not seem to be closely related to one another. Some people with schizophrenia have only one positive symptom; others have many. Similarly, neg- ative symptoms are not specific to schizophrenia (they are also found in depressive, and bipo- lar and related disorders). Approximately 60% of individuals with schizophrenia exhibit pos- itive symptoms such as hallucinations and delusions (Lindenmayer & Kahn, 2006), whereas approximately 41% display at least two negative symptoms (Patel et al., 2015).

Delusions Delusions are odd or unusual ways of thinking that lie outside the realm of reality or do not have rational explanations. To be considered a potential symptom of schizophrenia, a delu- sion must be contrary to a person’s background and must not be held by members of the person’s cultural or ethnic group. For example, members of a cult who believe that the world will come to an end on a certain date are probably not showing signs of schizophrenia. By

Highlight: Differentiating Among Schizophrenia and Schizoaffective and Delusional Disorders

In schizoaffective disorder the individual must have a major mood episode (this means a major depressive or manic episode) along with criterion A of schizophrenia (delusions, hallucinations, disorganized speech, negative symptoms, and/or grossly disorganized or catatonic behavior; see Table 8.1). In addition, the delusions or hallucinations must be present for at least two weeks while a depressive or manic episode is not present. Third, the manic or depressive episode must be present for most of the total length of the active portion of the mental illness (APA, 2013). In other words, the individual must have symptoms of schizophrenia as well as a major mood episode during the illness, unlike schizophrenia, where a major mood episode has not occurred with the active-phase symptoms. In addition, schizoaffective disorder is rather rare, affecting 0.3% of the population, making it a third as likely to occur as schizophrenia (APA, 2013). Although it is difficult to differentiate schizoaffective disorder from schizophrenia, one need only assess if the criteria are being met for a manic or a major depressive episode during the majority of the active phase of the illness. If so, then one is most likely seeing schizoaffective disorder.

Delusional disorder differs from schizophrenia in one key aspect: Criterion A for schizophrenia has never been met. If hallucinations are present, they are not a prominent feature and are related to the delusion’s theme (for example, an individual who constantly hears voices saying that his or her every move is being closely watched and recorded in association with the delusion of persecution). In addition, the individual’s functioning is not very bizarre or odd. Also, if the individual has manic or major depressive episodes, they are brief. Delusional disorder is less common than schizophrenia and is a bit rarer than schizoaffective disorder, occurring in about 0.2% of the population.

Perhaps the most important differentiation among these three disorders is that schizophrenia is the most debilitating of the three disorders, oftentimes defying treatment progress or success. Individuals with schizophrenia often end up among the nation’s homeless population.

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contrast, educated middle-class Americans who believe that mice are scientifically advanced aliens who were sent to colonize the Earth and destroy humanity most probably are.

According to her mother, Jennifer Plowman believed that “people” could “read her mind.” This belief was explored by Dr. Stuart Berg, the psychologist who evaluated Jennifer on her second day in the hospital. Part of their discussion appears here.

The Case of Jennifer Plowman: Part 3

Transcript From an Interview Between Dr. Berg and Jennifer Plowman DR. BERG: Jenny, your mother says that you refused to leave your house. How come?

JENNIFER: Come, lum, rum is a drink that sailors like.

DR. BERG: But, why did you refuse to go outside?

JENNIFER: I am fine. Why do I need to be here? The walls protected me at home.

DR. BERG: From what?

JENNIFER: Selegonite cannot get out of lead. There is lead in the bed and the walls and halls. Outside, they can get through.

DR. BERG: Who can get through?

JENNIFER: They can hear my thoughts. Without the lead, they leak out, and they can hear them. I can hear them laughing. They find out what I am thinking, and they laugh at their success.

DR. BERG: You believe that lead in the walls of your house keeps people from reading your mind. While you are outside of the house, without the lead to protect you, people will read your thoughts and laugh when they manage to get what they want.

JENNIFER: Yes. Like Superman. I know the secret because I am a rocket scientist. I have flown to space. I can develop new rockets that run on special minerals. I am too smart for this place. I should be at home.

Additional Transcript of Jennifer Plowman’s “Background Chatter” at Her Intake Interview Men need sex. I have had sex 10,000 times. That window is in the room because you want patients to know the color of the world. I know the president. He lives in town. I didn’t like his movie. He just wants to win the Academy Award. His movie is my life. I made a movie once. It had lots of stars. The cameraman was my friend. The sound technician was excellent. Where are the mics and cameras hidden? Is this logomouth here to get me nervous? My father died last year, leer, jeer, tears on my pillow, pain in my heart over you, what can I do? There is nothing wrong with me, you know. I don’t know why I am here. I’m fine.

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Although Jennifer’s delusions are relatively vague and incoherent, this is not always the case (Maher & Spitzer, 1993). For some individuals with schizophrenia, delusions can be system- atic, be elaborate, and have a common premise. Persecutory delusions (also called paranoid delusions) are beliefs held by people who insist that someone is out to get them. Thought insertion delusions (sometimes called delusions of influence) are a category of delusion in which people believe thoughts are being inserted into their heads. Grandiose delusions, when people believe they have some extraordinary talent or power, are also relatively com- mon. For example, they may think they can control the weather or the stock market, or that they are Christ or Bill Gates.

In Capgras syndrome, people believe that someone they know has been replaced by a dou- ble (Moschopoulos, Kaprinis, & Nimatoudis, 2016), and in Cotard syndrome, the individual believes he or she is dead (Cannas et al., 2017). Both of these kinds of delusions are very rare. Incorrect but plausible delusions (for example, “my assistant is plotting to get my job”) may also be seen in individuals with schizophrenia, but bizarre delusions have greater diagnostic value. The problem with plausible delusions is that they may not be delusions at all. After all, even delusional people can have enemies.

Interestingly, most people with schizophrenia find it difficult to believe that others consider their ideas hard to believe and perhaps even outlandish. They cling to their beliefs even in the face of compelling negative evidence.

Delusions vary in the extent to which they disrupt everyday functioning. Some individuals with schizophrenia are totally preoccupied with their odd beliefs, whereas others are only minimally impaired. In fact, you may never even know that some people have delusions because they are perfectly rational and can get along well except when someone brings up the subject of their delusion. For example, one person might believe that she is a religious demi- god, or perhaps Batwoman, who will save her city from being overrun with crime. Another might believe that he is a famous artist and paint, and display his works on the sidewalk for all to enjoy, even though to a trained eye they are just scrawls on canvas. Something to consider: Do these kinds of delusions pose a danger to the individual or to others? Keep this question in mind as we continue the discussion.

Hallucinations We all have sensory illusions. If you’re alone in your house at night, you may think you hear a burglar when there is no one around. Walking across campus, you think you hear your name being called, and yet there is no one there. These experiences do not mean that you have schizophrenia. It is only your imagination “playing tricks.” In contrast, people who have schizophrenia consider such sensory illusions quite real.

Hallucinations are perceptions that occur without any external stimuli. Auditory hal- lucinations, such as hearing external voices,

Thomas J Peterson/Exactostock-1672/SuperStock Some individuals with schizophrenia believe that people can read their minds, or insert thoughts into their heads, common delusions. To guard against this, they may cover their head with tin foil.

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are the most common type, occurring in as many as 70% to 80% of individuals with schizo- phrenia (Chhabra et al., 2016; Gram-Henriksen, Raballo, & Pamas, 2015). Different cultures tend to produce different hallucinations: Visual, olfactory (particularly rotten odors), and tactile (touch) hallucinations (such as the feeling that bugs are crawling under one’s skin) are associated with schizophrenia in the United States (Bauer et al., 2011; Larøi et al., 2014). Another example of a culture-specific hallucination involves an Amazonian people called the Bororo. In this culture, the novice shaman is identified when he has a dream of soaring high above the earth, like a vulture, and seeing the fiery cloud of smoke that indicates an attacking illness (Larøi et al., 2014). To the person with active schizophrenia, these voices, odors, and sounds are not imaginary; they are real.

Imaging techniques have given researchers insight into what is going on in the brains of people when they hallucinate. One study found that the part of the brain most active during schizo- phrenic auditory hallucinations is the area responsible for speech production, not the brain area responsible for speech comprehension (Donata-Wolf et al., 2011). This finding suggests that when people with schizophrenia hallucinate, they are not “hearing” voices in their brain but instead are reporting their own thoughts. In effect, they are listening to their own voices and thoughts and cannot differentiate these from someone else talking to them (Chhabra et al., 2016).

Disorganized Speech As you can see from the earlier interview excerpts, Jennifer Plowman’s speech was distinctly odd. She made up words, such as selegonite (these are known as neologisms). She also jumped from one topic to the next, a phenomenon known as thought derail- ment. Jennifer also linked words together according to their sound, as in “come, lum, rum.” These sound- based sequences are known as clang associations. Like Jennifer, people with schizophrenia often give irrelevant responses to questions, a phenomenon known as tangentiality. When the disorganization becomes extreme, the result is word salad, a mass of disconnected words (for example, “I saw a rat earlier yet it really smells in here yabba glick morch blargh”). In contrast to Jennifer, many people with schizophrenia speak very little; others are exces- sively literal or concrete.

The incoherent speech produced by Jennifer, and other people with schizophrenia, is often taken as a sign of an underlying “thought disorder” (Wens- ing et al., 2017). However, disorganized speech is not found in all people with schizophrenia, nor is it unique to schizophrenia. It may also be present dur- ing the manic phase of bipolar I disorder, although the disorganized speech and communication typi- cally is much more severe and common in schizo- phrenia (Wensing et al., 2017; Yalincetin et al., 2017).

Remik44992/iStock/Thinkstock Schizophrenia patients may create their own words, called neologisms, and jump from one topic to the next, a phenomenon classified as thought derailment. Disorganized speech is also linked to the manic phase of bipolar disorder, but it is more severe in schizophrenia patients.

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For an example of Jennifer’s odd speech, look at Part 3 of Jennifer’s case study, in the section on delusions. It contains a transcript of what Dr. Kahn called Jennifer Plowman’s “background chatter,” recorded during Jennifer’s intake interview. The excerpt illustrates what Bleuler meant by a breakdown in associations. Note how Jennifer jumps from one idea to the next and how the word year produces the clang associations leer, jeer, and tear, which then conjures up an old song lyric.

Inappropriate and Flat Affect Many people with schizophrenia display what is called inappropriate affect: Emo- tions that are inappropriate or not properly fit to the current situation, such as laughing when one is very nervous (see, for instance, Gard et al., 2011). For example, if they are told, in a worst-case scenario, that their entire family was murdered in a grotesque way, they would smile or perhaps laugh. Similarly, if they were told they won a huge amount in Powerball they might cry, not tears of happiness but sadness (to know for certain what the tears meant, you would have to ask the person). They also might exhibit inappropriate mood shifts during a short timeframe. These shifts should not be confused with bipolar I or II disorder, as the mood changes are rapid and do not involve a shift from mania to depression.

Flat affect refers to having a blank facial expression that is devoid of emotion. Flat affect is also reflected in a monotonous speaking voice with few inflections. People with schizo- phrenia lose pleasure in previously enjoyable activities (anhedonia, a symptom also found in depression).

There is evidence that affective symptoms are associated with a poorer prognosis and are more common in men (Gur et al., 2006). In one interesting yet dated study, home movies of children who develop schizophrenia later in life show that they displayed fewer positive emo- tions than their siblings years before the appearance of their schizophrenia (Walker, Grimes, Davis, & Smith, 1993).

Disorganized or Catatonic Behavior (Catatonia) Left alone, some people with schizophrenia may not move a muscle for hours. At such times, they seem indifferent to events going on around them. This condition is known as cata- tonic stupor. Catatonic stupor may be accompanied by waxy flexibility, in which people with schizophrenia place or allow their limbs to be placed in uncomfortable positions (sitting with their hands on their heads, for example). They seem able to maintain these uncomfortable positions for long periods without apparent distress. Schizophrenia can also produce aimless,

Purestock/Thinkstock People with schizophrenia may spend most of their time alone and withdrawn from social activities.

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repetitive activity, such as pacing the floor or rocking back and forth in a chair (catatonic frenzy). These repetitive movements may be accompanied by odd mannerisms, such as facial grimaces. Catatonic behavior (catatonia) can also be displayed in bipolar disorder (especially bipolar I) as well as in depressive disorders, especially major depressive disorder. As we will see, catatonic schizophrenia used to be considered a subtype of schizophrenia. These sub- types were eliminated in the DSM–5.

The range of schizophrenic behavior is fairly wide: Patients may imitate other people’s move- ments, act like robots, or refuse to cooperate with even simple requests (negativism). Many people with schizophrenia neglect their personal hygiene, and some behave in socially unac- ceptable ways (shouting obscenities, for instance). Note that Tourette’s disorder will also pro- duce this phenomenon, yet Tourette’s begins in childhood and does not involve hallucinations and delusions.

Social Withdrawal and Lethargy Most people with schizophrenia spend their time alone, withdrawn from normal social activities. This further distances them from reality and seems to lead to or increase deficits in interpersonal skills (Ten- hula & Bellack, 2008). Indecisiveness, ambivalence, and apathy are among the most debilitating negative symptoms of schizophrenia because, put together, they rob people of the energy they need to keep up with the activities of everyday life.

Phases of Schizophrenia Individuals with schizophrenia typically go through several phases in the course of the disorder. Progress through the phases can vary widely from person to person.

Prodromal Phase The prodromal phase precedes the disorder and is marked by deterioration from some higher level of functioning. Friends and relatives almost always notice personality changes—flattened affect, social withdrawal, and other negative symptoms—well before any positive symptoms appear.

Mary Evans Picture Library/Everett Collection A 19th century depiction of someone demonstrating catatonia.

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Active Phase In contrast to those in the prodromal phase, patients in the active phase do not seem to be aware that they are behaving strangely. They deny that their peculiar ideas are delusional or that their sensory experiences may only be hallucinations. Because they are shunned by oth- ers, and partly for self-protection, most schizophrenic people withdraw into their own lonely and isolated worlds. The active phase can persist for weeks, months, or even years.

Residual Phase In most cases, active symptoms eventually respond to treatment. However, a minority of patients never get beyond the active phase. Their course is said to be “continuous.” Usually, negative symptoms and mild levels of positive symptoms persist in the residual phase. When negative symptoms alternate with active-phase positive symptoms, the course of the disorder is said to be “episodic.” In single episodes, the active phase is followed by a period in which there are either no symptoms or only negative ones.

Additional Symptoms and Signs In addition to the characteristic symptoms listed in criterion A, the DSM–5 includes several other important diagnostic criteria (see Table 8.1). First, the symptoms must affect the per- son’s work or social life, or, in the case of a child or adolescent, the symptoms must cause a failure to achieve the age-expected level of interpersonal, academic, or occupational function- ing. Second, the symptoms must persist for at least six months, including prodromal, active, and residual. In the prodromal and residual phases, only negative symptoms, or two or more symptoms in criterion A, may appear in a less severe form. The main effect of the six-month diagnostic criterion is to restrict schizophrenia to chronic cases, as in Kraepelin’s original formulation.

Kraepelin proposed three subtypes of schizophrenia, all of which were in use until publica- tion of the DSM–5. These subtypes are catatonic, paranoid, and disorganized (formerly known as hebephrenic, which means silly and immature emotionality). These subtypes were elimi- nated due to their limited diagnostic stability, low reliability, and poor validity (APA, 2013). Instead, an eight-item severity specifier is used, as measured by a psychosis rating scale (a checklist) completed by the clinician. The DSM–5 notes that the specifier’s use is optional (APA, 2013). In sum, schizophrenia is now considered a spectrum disorder, meaning that its severity can range from not present to present and severe, depending on the symptoms dis- played and their duration.

The DSM–5 also requires that schizoaffective disorder and depressive or bipolar disorder with psychotic features be ruled out before a person can be diagnosed as having schizo- phrenia. When a major depressive episode or manic episode is present with schizophrenic symptoms for a major portion of the active and residual phases, then the correct diagnosis is schizoaffective disorder, not schizophrenia. Finally, the DSM–5 criteria require that schizo- phrenia be kept separate from autism spectrum disorder or a communication disorder of childhood onset. Oftentimes people confuse schizophrenia with autism spectrum disorder. There are two critical differences: Autism spectrum disorder onsets in childhood, and people with autism spectrum disorder do not have hallucinations or delusions.

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Section 8.2 Prevalence and Course of Schizophrenia

8.2 Prevalence and Course of Schizophrenia

Incidence As explained in Chapter 5, the incidence of a dis- order is technically defined as the number of new cases that appear during a given period of time. Most incidence estimates are obtained by counting the number of new cases seen at treatment facilities (usually mental hospitals, but also doctors’ offices and counseling centers) over the period of a year. This approach assumes that all cases are seen at these treatment centers and that the clinicians who work in them are perfectly accurate diagnosti- cians. However, neither assumption is likely to be true. Hospitalization is less common today than in the past, and many people with schizophrenia live among the homeless and never come into contact with a mental health facility. In developing coun- tries and in the poorer parts of industrialized coun- tries, many people with schizophrenia lack access to treatment services. For those who do get to treat- ment, there is no guarantee that they will be diag- nosed accurately.

Using the standard DSM and International Statis- tical Classification of Diseases and Related Health Problems (ICD) criteria for schizophrenia, incidence rates are remarkably similar around the world. A review of 50 epidemiological studies (Warner & de Girolamo, 1995) conducted in both developing and developed countries, with many different age groups and clinicians, found the incidence of schizophrenia to be between 0.21 and 0.24 new cases per 1,000 people per year (Comer, 2007).

Age of Onset The typical age of onset for the psychotic symptoms of schizophrenia (hallucinations, delu- sions, and negative symptoms) is between the late teenage years and mid-30s. As the DSM–5 notes, onset prior to adolescence is rare (APA, 2013). One study noted that the average age of onset for schizophrenia is between 15 and 25 for men and between 15 and 30 for women, with negative symptoms making their appearance around four years before the first hospi- tal admission (Eranti, MacCabe, Bundy, & Murray, 2013; Huang et al., 2017; Lewine, 1991). According to the APA (2013), the first psychotic episode appears in men in their early to mid-20s, and in women in their late 20s. By the age of 60, the cumulative incidence for men and women is equal, and almost no new cases of schizophrenia are identified after age 60

Mrk movie/Marka/SuperStock The film A Beautiful Mind (2001) was based on the life of John Nash and showcased not only Nash’s mathematic genius but also his struggle with paranoid schizophrenia.

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(Gottesman, 1991). Thus, although men show signs of schizophrenia earlier in life, women eventually catch up. The finding of an earlier onset for men, which was first noted by Kraepelin, has been con- firmed many times (APA, 2013; Howard, Castle, Wessely, & Murray, 1993; Reicher, Maurer, Loffler, & Fatkenheuer, 1991). A more recent study found that the sex difference in the age of onset is negligible or perhaps even absent in developing countries, when certain known risk factors are taken into consid- eration (such as birth complications and family his- tory; van der Werf et al., 2013). The earlier onset for males does not seem to be related to diagnostic pro- cedures, nationality, occupational status, or help- seeking differences between the sexes (Warner & de Girolamo, 1995). Instead, the striking cross-cul- tural similarity of the sex difference in age of onset points toward a biological explanation (Eranti et al., 2013). It has been suggested, for example, that the female hormone estrogen may reduce vulnerability to schizophrenia (Huang et al., 2017; Kulkarni et al., 2015; van der Werf et al., 2013) and has potential use for treatment (Kulkarni et al., 2015).

Prognosis We now know that Bleuler was correct—some patients do recover, perhaps as many as 25% or more (Roe & Davidson, 2008), and even severely affected patients may improve (Breier, Schreiber, Dyer, & Pickar, 1991; Hegarty, Baldessarini, Tohen, Waternaux, & Oepen, 1994). The best predictors of outcome are the level of premorbid functioning and the severity of symptoms in the active phase (Diaz-Caneja et al., 2015). Given two people with good pre- morbid functioning, the one whose symptoms are predominantly negative is likely to have a poorer outcome than the one with mainly positive symptoms (Diaz-Caneja et al., 2015).

Although the prognosis for those with schizophrenia is less pessimistic than Kraepelin thought, it is still not very good. Many will relapse more than once and will have remaining or irregular symptoms for the rest of their lives (Emsley, Chiliza, Asmal, & Harvey, 2013). The relapse rate is worst for those whose first episode occurred at a young age, probably because they never had the opportunity to develop adequate coping skills (Gomez-Revuelta et al., 2017). Life expectancy is also lower among people with schizophrenia. This is partly the result of a high rate of suicide (Kredentser, Martens, Chochinov, & Prior, 2014) and partly from deaths aris- ing from cold weather exposure among the schizophrenic homeless. In addition, individuals with schizophrenia may be at increased risk for cardiovascular disease, respiratory disorders, diabetes, tuberculosis, and other infectious diseases (Kredenster et al., 2014). On the other hand, one earlier, rather dated study revealed that 60% of those with schizophrenia who do manage to survive into middle and old age have a good chance of a reasonable quality of life free of active symptoms (Torrey, 2001).

BananaStock/BananaStock/Thinkstock Many people with schizophrenia may not have access to a mental health facility and live among the homeless.

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Section 8.3 Etiology of Schizophrenia: Genetics

Cultural Considerations The cultures of developing countries may be more accepting of different or deviating behav- ior than those of developed countries. For this reason, observers in developing countries (for example, Tunisia) may rate the same schizophrenic behavior as more tolerable than observ- ers in developed countries, such as Germany (Angermeyer et al., 2015). Overall, outcomes are better in developing countries than in the developed world, perhaps because of the greater tolerance of psychotic behavior in developing areas (Hopper, Harrison, Janca, & Sartorius, 2007). Vahia and Vahia (2008) found that, according to World Health Organization data, 25 million individuals with schizophrenia who live in developing countries (India and Nige- ria, for example), have better recovery rates than those who live in Western and other devel- oped countries, such as Germany. The hypothesis here, again, is that in developing countries the environments tend to be more supportive and therapeutic than in, say, the United States. More family may be available via extended family, less critical judgments might occur, and family may be more willing, and more available, to help out. For example, the Nigerian culture, according to Matsumoto and Juang (2008), tends to be more accepting of hearing voices than are Western cultures.

8.3 Etiology of Schizophrenia: Genetics One possible reason why the prevalence of schizophrenia is so similar from one country to the next is that it is an inherited condition. Franz Kallman (1938) examined the family mem- bers of more than 1,000 people with schizophrenia, all of whom were patients in a Berlin psy- chiatric hospital. He found that the more severe a person’s disorder, the more likely it was that a member of the person’s family would also show signs of a mental disorder. Decades later, a Danish study reported on a 30-year follow-up of 207 high-risk children, whose mothers were schizophrenic, and 104 low-risk children, whose family members showed no signs of mental illness (Mednick & Schulsinger, 1968). Thirty-one members of the high-risk group developed schizophrenia, whereas only two members of the low-risk group developed it. Over the years, there have been numerous investigations into the genetics of schizophrenia. The vast major- ity of these studies have confirmed the connection between genetics and schizophrenia. (To read more about Jennifer Plowman’s family background and to see if schizophrenia runs in her family, see Part 4 of her case in the appendix.)

Twin Studies Twin studies are one way to try to separate the effects of heredity from those produced by the environment. Specifically, if environmental factors determine who develops schizophrenia, we would expect the rate of concordance for schizophrenia between monozygotic (identi- cal) twins who are reared together to be similar to that for dizygotic (fraternal) twins reared together (monozygotic twins have the same genes, whereas dizygotic twins share only about 50% of their genes). By contrast, if genetics play a larger role, we should expect to find a higher concordance rate among monozygotic twins (who share both their genes and their environments) than among dizygotic twins.

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Section 8.3 Etiology of Schizophrenia: Genetics

Twin studies have produced mixed results. Still, the majority of studies have found that mono- zygotic twins have much higher concordance rates for schizophrenia than do dizygotic twins (about a 33% chance for monozygotic twins versus about a 7% chance for dizygotic twins; Hilker et al., 2017). This suggests that genetics is a more important determinant of schizo- phrenia than is the environment. However, it is always possible that schizophrenia may be present in some form from birth (congenital) without being genetic. For example, the antipsy- chotic medications given to pregnant women with schizophrenia may produce an abnormal intrauterine environment, which may affect the brain development of their children. It is pos- sible that such children may be predisposed to develop schizophrenia in response to stress. Alternatively, a virus during pregnancy could affect neurological development and make chil- dren susceptible to schizophrenia (Lambert & Kinsley, 2005; Torrey, 2001). Both of these con- genital causes would produce a higher concordance among twins than among other siblings because twins are exposed to the same intrauterine environment (Davis & Phelps, 1995).

To separate congenital from genetic causes of schizophrenia, Gottesman and Bertelsen (1989) studied the children of monozygotic twins where only one twin had schizophrenia. They found that the probability of finding schizophrenia in the next generation is 17%. It did not matter whether it was a parent who had schizophrenia or a parent’s identical sibling (an aunt or uncle). In both cases, the probability of a child’s developing schizophrenia was the same, 17% (see Figure 8.1). This is a striking finding. Children of parents without schizophre- nia whose aunts or uncles had schizophrenia have the same probability of developing schizo- phrenia as their cousins, whose parents actually had schizophrenia. This study suggests that genetics rather than events during pregnancy are responsible. The identical twin aunts and uncles who did not have schizophrenia seem to be “carriers” who pass on the condition to their children.

If schizophrenia were entirely a function of heredity, we would expect to find a concordance of 100% among identical twins because they share all of their genes. Yet, despite the wide- spread evidence for the inheritance of schizophrenia, no study has produced a concordance rate of 100% among monozygotic twins. Therefore, it seems obvious that factors other than genetics must be involved. Perhaps being raised by a mentally ill parent or alongside a sibling with schizophrenia determines who among those with “schizophrenic genes” will develop the disorder and what form it will take. In other words, if a child’s biological mother had schizophrenia and the child’s adoptive family was dysfunctional, the child would be more likely to “contract” schizophrenia (Tienari, Wahlberg, & Wynne, 2006; the quotes are ours). This hypothesis is consistent with the results of a case study of one set of quadruplets, the Genain sisters. All four developed schizophrenia between the ages of 22 and 24. This seems compelling evidence for the genetic transmission of schizophrenia. Yet there were differ- ences among the girls. Even though they shared 100% of their genes, each sister had a differ- ent course, symptoms, and outcome (Rosenthal, 1963). For example, two of the four sisters were floridly psychotic, showing severe symptoms, whereas the other two were much better adjusted. One of the four sisters eventually married and had children, two had fluctuating good periods and bad periods during which they had to be hospitalized, and the fourth sister spent her life in the hospital. These differences suggest that differences in the sisters’ respec- tive environments influenced the way they expressed their genetically identical disposition toward schizophrenia, even though their environments were quite similar.

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Adoption Studies Heston (1966) found that the risk of schizophrenia among the offspring of mothers with schizophrenia who were adopted early in life was 16.6%. This figure is not much different from the average morbid risk for children raised by their own mothers diagnosed with schizo- phrenia (Gottesman, 1991). In other words, being raised by a mother with schizophrenia does not increase the risk of developing schizophrenia. Over the years, other adoption studies have confirmed that the children of mothers with schizophrenia tend to resemble their biological mothers in terms of behaviors and traits more than their adoptive ones (Tienari et al., 2006).

One possible confounding variable in this research is the effect of adoption itself. Perhaps being adopted predisposes a person to develop schizophrenia. The implication is that being

Percentage

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Parents

0 5 10 15 20 25 30 35 40 45 50

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Dizygotic twins

Siblings with 1 schizophrenic parent

Offspring of 2 schizophrenic parents

Monozygotic twins

Figure 8.1: Risk of developing schizophrenia for relatives of people with schizophrenia

Source: Adapted from Gottesman and Shields (1972), as appearing in S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 9.1, p. 389.

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Section 8.3 Etiology of Schizophrenia: Genetics

raised by a parent with schizophrenia does not increase the probability of developing the dis- order. Further support for this idea comes from the finding that identical twins who are raised apart have the same concordance rates for schizophrenia as do those who are raised together by their natural parents (Gottesman, 1991).

Markers Underlying genotypes (the specific genetic makeup of an individual) are often reflected in phenotypic traits (behaviors or observable characteristics of an individual) known as mark- ers. These markers are present not only in people with schizophrenia but also in their rela- tives. Prospective studies, in which people with the supposed markers are followed longitudi- nally to see if they develop schizophrenia, can help researchers pinpoint the specific genetic causes of schizophrenia. Two potential cognitive markers for schizophrenia are attentional dysfunction and eye-tracking abnormalities.

Attentional Dysfunction Kraepelin (1919) viewed distractibility as one of the most common features of dementia praecox. Because attentional deficits not only run in fami- lies but also appear before any schizophrenic-like symptoms, they may reflect a genetic vulnerability to schizophrenia. For example, an inability to focus attention impairs a person’s ability to perceive affect (Combs & Gouvier, 2004) and engage in appropri- ate social functioning. However, because most of the family members who exhibit attentional deficits will never show any schizophrenic symptoms, sen- sory deficits alone are clearly not sufficient to cause schizophrenia; other factors must also be involved.

Eye Movement (Tracking) Dysfunction In his clinical descriptions, Kraepelin noted that people with dementia praecox had difficulty track- ing a moving stimulus, such as a pendulum. Instead of smooth eye movements from side to side, Krae- pelin’s patients had frequent, jerky eye movements. Kraepelin’s observations have been repeated many times over the decades. On each occasion, patients with schizophrenia were found to have eye-tracking abnormalities, whereas only a small number of peo- ple without schizophrenia displayed any eye-track- ing problem (Demler et al., 2016). These abnormali- ties in eye movement are also apparent in people at risk of developing schizophrenia (Demily et al., 2016). Specifically, about 35% of the relatives of people with schizophrenia have similar abnormalities (Lenzenweger, McLachlan, & Rubin,

Zoonar RF/Zoonar/Thinkstock Behaviors or observable character- istics are known as markers, and researchers have identified eye- tracking abnormalities as a potential cognitive marker for schizophrenia. Kraepelin discovered that patients with dementia praecox had difficulty following a moving stimulus, like the pendulum shown here.

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Section 8.4 Etiology of Schizophrenia: Nongenetic Risk Factors

2007). Imaging studies seem to indicate the presence of some defect in the frontal lobes of at least some people with schizophrenia (Mubarik & Tohid, 2016; Watanabe, Urakame, Hongo, & Ohtsubo, 2014).

How Many Genes Are Involved in Schizophrenia? On average, children get half their genes from their mother and half from their father. This means that, if schizophrenia is the result of a single dominant gene, we should expect to find that 50% of children with one schizophrenic parent develop schizophrenia. The actual figure is only 17%, however.

Also, if schizophrenia is the result of a single dominant gene, then it might be possible to identify its specific chromosomal location. However, researchers have not yet been able to replicate initial positive findings that have pointed toward potential “schizophrenic” genes (Hamilton, 2008). There is always the chance that researchers are seeking something that does not exist. There may not be a schizophrenic gene. Instead, schizophrenia may be poly- genic, the unlucky result of inheriting a number of interacting genes (Gottesman, 1991; Har- rison & Weinberger, 2005).

There are several reasons to believe that schizophrenia is polygenic. Polygenic inheritance would explain why only 17% of the offspring of a parent with schizophrenia develop the con- dition. (The probability of inheriting more than one schizophrenia-related gene is lower than the probability of inheriting only one.) Polygenic inheritance may also account for schizo- phrenia’s varied course and symptoms, which seem too diverse to be caused by a single domi- nant gene. Finally, when several genes are responsible for a condition, we would not expect any single genetic marker to be present in all cases, and they are not.

Whether schizophrenia is caused by one gene or many, there is little doubt that nongenetic factors play an important role. An inherited vulnerability is not sufficient on its own to pro- duce schizophrenia. Nongenetic factors must also be present. The best explanation is one derived from the diathesis-stress model. That is, the symptoms of schizophrenia are the result of an interaction between genetic and nongenetic factors. (See the accompanying Highlight.)

8.4 Etiology of Schizophrenia: Nongenetic Risk Factors It is possible to identify risk factors associated with a greater vulnerability to schizophrenia. In the sections that follow, we will examine several nongenetic risk factors that have been proposed to make schizophrenia disorders more likely to onset or to recur.

Viral Infection The idea that schizophrenia is the result of a brain infection comes partly from observing the rapid increase in the number of diagnosed cases during the 19th century. Schizophrenic-like conditions were considered rare in the 18th century, but their incidence increased dramati- cally in the late 1800s (Warner & de Girolamo, 1995). It is possible that some biological event

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(the birth of a new virus, for example) occurred sometime in the 1800s, producing the mod- ern condition we know as schizophrenia (Hare, 1988).

The notion that schizophrenia may be the result of a virus that affects brain development in the fetus is consistent with the findings of research on fingerprints. When only one identi- cal twin has schizophrenia, he or she has significantly greater or fewer fingerprint ridges than the twin without schizophrenia. This suggests that some process has interfered with the normal biological development of the twin with schizophrenia (Van Os, Fananas, Cannon, Macdonald, & Murray, 1997).

Although some researchers have found a relationship between maternal exposure to viral epidemics during pregnancy and later development of schizophrenia in offspring (Khanda- ker, Zimbron, Lewis, & Jones, 2013), others have failed to confirm such a relationship (Selten & Termorshuizen, 2017). One possible reason for the discrepant results is uncertainty about whether a specific woman contracted a virus during pregnancy. Just because an epidemic

Highlight: The Face of Schizophrenia You surely recognize this face: The Joker, perhaps the comics’ most famous villain. Why is his picture here? Good question! Is this how schizophrenia appears: a man in clown makeup who kills people solely for pleasure? The Joker does not hallucinate, but is he delusional? Do people with schizophrenia kill because they enjoy it? What about John Nash, whose life was the basis for the film A Beautiful Mind? Does the film present a true and accurate portrayal of someone

with schizophrenia? If you’ve seen the film One Flew Over the Cuckoo’s Nest, do you think Jack Nicholson’s character has schizophrenia? If you had no knowledge of this disorder, what would you think after seeing those movies and knowing about The Joker? Interviews with Batman’s current head writers have called The Joker a psychotic killer, a psychotic clown, and a schizophrenic clown. How accurate are these portrayals? If you’re familiar with Batman, chances are you know about The Joker’s girlfriend, Harley Quinn. Did you know she is considered psychotic, yet in her former life she was a psychiatrist? How often do psychiatrists develop schizophrenia?

The questions raised here are all relevant yet difficult to answer. Many of the Highlight boxes focus on how the media portray the disorders discussed in the text. Invariably it seems as though the media portray people with these disorders as raving madmen and madwomen, killers like Leatherface from the Texas Chainsaw Massacre movies or Jason Voorhees from Friday the 13th, or characters like The Joker. Is this just what most people expect? Is portraying people who have schizophrenia as chainsaw killers simply good for ticket sales or television ratings? Or do writers truly believe that these portrayals are accurate depictions of mental illness? What did you think before you took this class and began reading the text?

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occurred in an area does not mean that every pregnant woman who lived in the affected area contracted the illness. One study that used doc- tors’ records to substantiate that specific pregnant women had contracted influenza failed to find any increase in the prevalence of schizophrenia among the offspring of affected mothers, even after a period of 30 years (Crow & Done, 1992). Unfortu- nately, this negative finding does not settle the mat- ter completely because it remains possible that an infection other than influenza (or the drugs used by expectant mothers to combat illness) produced a delayed effect on the fetus.

Looking at the viral issue in a different way, researchers have published dozens of articles on the season of birth of people with schizophrenia. Most report an excess of births in late winter or early spring, which means that their mothers were pregnant during the winter virus season (Meyer, Feldon, Schedlowski, & Yee, 2005; Tamminga, Shad, & Ghose, 2008). The most common view is that the excess of late winter/early spring births among those with schizophrenia is the result of viruses such as influenza, which are more common dur- ing winter. Specifically, viral exposure at a critical

period of prenatal development may be causing subtle brain damage, which, in turn, pro- duces a vulnerability to schizophrenia (Stahl, 2007). In particular, respiratory infections dur- ing the second trimester are associated with an increased risk of schizophrenia spectrum and other psychotic disorders (Brown et al., 2000).

One way to test this coincidental relationship is to examine season of birth in the Southern Hemisphere, where January and February are summer months and winter occurs in July and August. If more individuals with schizophrenia are born in July and August in the Southern Hemisphere, then the “coincidence” explanation is not likely to be correct. Unfortunately, the results of studies conducted in Australia and South America are equivocal; some find an excess of schizophrenic births in the winter months of July and August; others do not (Lewis, 1992).

Life-Stress Studies that have followed people with schizophrenia over time have often found that active- phase episodes are preceded by significant life-stress (Docherty, Feldon, Schedlowski, & Yee, 2009). For instance, it is possible that the stress of being homeless contributes to the devel- opment of schizophrenia. Alternatively, though, people with schizophrenia may be unable to look after themselves and therefore become homeless. Some researchers have found sup- port for the hypothesized link between the immune system and schizophrenia, positing that a weak or weakened immune system may make one more susceptible (Ripke et al., 2014).

Dan ionut Popedcu/Hemera/Thinkstock The study of fingerprints has given researchers insight into the formation of schizophrenia. If one identical twin has schizophrenia, he or she will have greater or fewer fingerprint ridges than the twin without schizophrenia.

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One particular form of social stress that has received special attention is the stigma of being labeled “schizophrenic.” Goffman (1961) and Scheff (1966) have argued that once people are labeled as such, they are forced into a “sick” social role. They are denied employment, consid- ered incapable of looking after themselves, and subjected to treatment (sometimes against their wishes). Eventually, such people come to believe that they are sick and act accordingly. Although it is important not to discount the social stigma associated with being labeled schizophrenic, few researchers today believe that hallucinations, delusions, and other schizo- phrenic behaviors are simply the result of having been called schizophrenic.

Demographic and Socioeconomic Status Schizophrenia has been associated with several intriguing demographic and socioeconomic findings (see Figure 8.2). For example, schizophrenia is more common among people born and raised (up to the age of 15) in large cities than among people brought up in rural areas or small towns (Kirkbride et al., 2006; Lewis, Davis, Andreasson, & Allebeck, 1992). New immigrants have higher than average prevalence rates and so do divorced and single people (Cantor-Graae & Selten, 2005; Eaton, 1985). It is easy to explain why schizophrenia is more common among single than among married people—people with schizophrenia simply do not make good mar- riage prospects. Social class is a particularly important variable in schizophrenia research. It is a standard finding that schizophrenia is more common among those in the lower social and economic groups (Lambert & Kinsley, 2005; Werner, Malaspina, & Rabinowitz, 2007).

Economic status

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Figure 8.2: Socioeconomic class and schizophrenia

Lower- and lower-middle-class people in the United States are more likely than wealthy people to experience schizophrenia.

Source: From R. J. Corner, Abnormal Psychology, 6th ed. New York: Worth Publishers, 2007, Figure 14.1, p. 412. Reprinted by permission.

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Section 8.4 Etiology of Schizophrenia: Nongenetic Risk Factors

Traditionally, two theories have been put forward to account for the relationship between social class and schizophrenia. The previously mentioned social drift theory blames the debilitating effects of mental illness. People with schizophrenia are impaired in their ability to compete economically, so they “drift” down the socioeconomic ladder. In other words, the social drift theory argues that membership in the lower social classes is simply an offshoot of having schizophrenia.

Social stress theory proposes a direct causative role for social class. According to social stress theory, poor people are exposed to more economic and social problems than are those who are better off. However, in developing countries, the better educated are under greater social stress with industrialization because they must learn to become part of a new and unfa- miliar economic system, whereas the poor are left to their traditional subsistence living. This extra stress may be responsible for a higher prevalence of schizophrenia among the upper socioeconomic groups in those countries.

Family Communication Early on, many adherents of psychoanalytic theory harbored the belief that family interac- tions were somehow responsible for psychoses. The so-called schizophrenogenic mother, for example, was thought to produce schizophrenia by her cold, domineering, and aloof attitude toward her children (Fromm-Reichmann, 1948; Hartwell, 1996). Parents of schizophrenic children were accused of sending confused messages to their offspring. For example, moth- ers might scold their children for speaking without permission and then accuse them of not wanting to share their thoughts with their parents. Such messages allegedly place children in a psychological “double-bind” from which they cannot escape except by schizophrenic breakdown (Bateson, 1959; Wynne & Singer, 1963). The evidence for this theory was always tenuous, however (Willick, 2001). Few researchers even bothered to study parent-child inter- actions. After all, it is always possible that the causal direction is the other way around—psy- chologically disturbed children affect the communication style of their parents. These blame- the-family theories placed an additional burden of guilt on parents, and there is no research to support either of these two concepts.

Although these early communication-based hypotheses were overstated, we do know that stressful family relationships influence the course of schizophrenia (Boye, Bentsen, & Malt, 2002; Schiffman et al., 2001, 2002). Patients discharged to their own homes are more likely to return to the hospital or have an exacerbation of their symptoms if family members are hostile, critical, and/or overbearing.

Brain Structure and Function If viruses and birth injuries play a causative role in schizophrenia, they probably exert

Utah778/iStock/Thinkstock Brain imaging studies on patients with schizophrenia have shown that the most common brain abnormality is enlarged lateral ventricles.

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their effects by causing some form of brain damage (Gilmore & Murray, 2006). Brain imaging studies have attempted to identify these injuries. The most commonly reported abnormality is enlarged lateral ventricles (the cavities on each side of the brain that are filled with cerebro- spinal fluid; Raz & Raz, 1990). The ventricles of people with schizophrenia have been found to be enlarged even before treatment, so the defect is not the result of receiving antipsychotic medication (Belger & Dichter, 2006; Lawrie, McIntosh, Hall, Owens, & Johnstone, 2008). The problem is that we do not have any good theory for why people with enlarged ventricles should develop the negative (or any other) symptoms of schizophrenia (Staal et al., 2001). Enlarged ventricles tell us only that these people’s brains have failed to develop normally.

Enlarged ventricles are not the only observed abnormality in people with schizophrenia. Researchers have also reported that people with schizophrenia have a smaller hippocampus and amygdala than people without schizophrenia. The hippocampus and the amygdala are part of the brain’s limbic system, a part of the brain that is thought to be concerned with cog- nition and emotion (Barker et al., 2016).

Brain Chemistry Although the idea that body chemistry affects behavior goes back about 1,900 years, modern attempts to link schizophrenia to brain chemistry date to the 1950s. For at least the last 30 years, researchers have focused on and implicated serotonin, glutamate, and dopamine in schizophrenia (for example, Javitt & Laruelle, 2006; Tan et al., 2007). However, most research- ers have focused on dopamine. Their research can be summarized by three important findings:

1. If taken over a long period of time, antipsychotic medications known as phenothi- azines may produce symptoms similar to those found in the movement disorder Parkinson’s disease (that is, tremors and jerky movements). We know that Parkin- son’s disease results from the destruction of dopamine-producing neurons. It is pos- sible, therefore, that antipsychotic medications work because they somehow reduce dopamine activity in the brain.

2. The drug L-dopa, which is used to treat Parkinson’s disease, works by increasing dopamine activity. Because L-dopa can produce some of the positive symptoms of schizophrenia, this is further evidence that some schizophrenic symptoms are related to increased dopamine activity.

3. Finally, because some types of antipsychotic medications ameliorate the positive symptoms of schizophrenia (and seem to work by reducing dopamine activity in the brain), it seems reasonable to conclude that excess dopamine activity is somehow responsible for the positive symptoms.

Put simply, drugs known to increase dopamine activity seem to provoke schizophrenic symp- toms, whereas drugs that reduce dopamine activity tend to ameliorate them.

The evidence does not demonstrate conclusively that people with schizophrenia have a higher level of dopamine activity than others. Instead, it seems that people with schizophrenia have more dendritic dopamine receptors than do people without schizophrenia (see Figure 8.3). These excess receptors make them more responsive to dopamine, even though their overall levels of dopamine are no different from those of people without schizophrenia. Before we con- clude that extra dopamine receptors are somehow responsible for schizophrenic symptoms,

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however, there is one complication. Some antipsychotic drugs themselves can increase the number of dopamine receptors. Because most people with schizophrenia receive drug treat- ment, it is possible that the excess number of dopamine receptors observed by researchers is caused by drug treatment and, therefore, could not be responsible for the initial development of schizophrenic symptoms.

D5D4

D2 D3

Low expression

Background color

Neocortex

Hippocampus

Caudate Putamen

Nucleus accumbens Retrorubral

field Ventral

tegmental area

Pars compacta of the substantia nigra

Entorhinal cortex

Key

High expression

2 2

3 3

5 5

Figure 8.3: Areas of dopamine receptor activity

Five dopamine receptors have been identified to date. As shown, each one is more common in some parts of the brain than others. The D2 receptor is particularly implicated in schizophrenia.

Source: From S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 9.4, p. 402.

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Even if we could provide definitive evidence for an overabundance of dopamine receptors among untreated people with schizophrenia, the relationship between schizophrenia and dopamine would still be ambiguous. For example, among those patients who do respond to medication, it usually takes anywhere from five days to six weeks before any improve- ment is noticed (Rosenbaum et al., 2005). Yet conventional antipsychotic medications have an immediate effect on dopamine activity. The lag before symptoms improve and the finding that some people do not improve at all suggest that schizophrenic symptoms reflect more than just dopamine activity. Perhaps it is the balance among different neurotransmitters that is important in schizophrenia rather than the absolute level of any particular neurotransmit- ter (Bach, 2007).

8.5 Treatment Let us establish one main point at the outset: There is no cure for schizophrenia—no pill, no operation, and no psychotherapy. Nevertheless, the quality of life of people with schizophre- nia can be improved by medical, psychological, and social interventions.

Hospitalization and Milieu Treatment For at least 100 years, mental hospitals were considered to be the best place to treat psychotic individuals. Not only could drug and psychological treatment be delivered in the hospital, but the hospital environ- ment (or milieu) itself was thought to have beneficial effects of its own. Patients were sheltered from the everyday world, while doctors, nurses, and other staff created a culture in which patients interacted socially and gained a sense of independence by participating in ward government. Milieu treatment was considered to be an impor- tant factor in patient outcome. Even today, most people with schizophrenia spend at least some time in a hospital milieu pro- gram, although long-term hospitalization has fallen out of favor. In 1830, approxi-

mately 200 mentally disturbed people were hospitalized in the United States. By the 1950s, the number was 500,000. The numbers of hospitalized patients did not begin to fall off until the 1960s, when antipsychotic medications made it possible for people with schizophrenia to live outside the hospital. People who had spent most of their lives in mental hospitals were discharged in a process known as deinstitutionalization, the result of an act passed by Con- gress in 1963. This act, known as the Community Mental Health Act, provided funding to cre- ate community mental health centers.

UNITED ARTISTS/SuperStock Ken Kesey’s 1962 novel, One Flew Over the Cuckoo’s Nest, compared mental hospitals to jails and portrayed the institutionalized as citizens robbed of their freedom. Many people who spent most of their lives in mental hospitals were discharged after Congress passed the Community Mental Health Act in 1963.

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There were two general ideas driving deinstitutionalization (Scull, 1989). The first was the belief that mental patients are better cared for in their home communities, where they are known and where they can participate in everyday life. The second idea grew out of 1960s radical politics. Mental hospitals were portrayed as tools by which the state robbed citizens of their freedom. Books and movies such as One Flew Over the Cuckoo’s Nest portrayed men- tal hospitals as no different from jails. Hospitals were alleged to create more problems than they solved. What was formerly supposed to be a therapeutic milieu came to be seen as a repressive regime that enforced rigid conformity to rules and made patients apathetic, pas- sive, withdrawn, and helpless. Deinstitutionalization became a romantic crusade to give back to “oppressed” patients their rights and their freedom. Arguing that care should be provided in the least restrictive environment possible, the courts began to require that patients who could survive outside the hospital be discharged.

Ironically, however, the deinstitutionalization movement, which saw as one of its missions the restoration of freedom to hospitalized mental patients, produced a situation in which people were simply allowed to wallow on the streets or in jails. One psychiatrist summarized the situation by saying, “Freedom to be insane is an illusory freedom, a cruel hoax perpe- trated on those who cannot think clearly by those who will not think clearly” (Torrey, 1988, p. 34). Meanwhile, little has been done to improve the situation. What has become clear is that people who cannot look after themselves, who may be violent, or who do not have access to the services they require to live in the community need protection. The best place for them is probably in a hospital, at least during the active phase of their disorders.

Somatic Treatments Perhaps the most important development in the somatic treatment of schizophrenia took place in the 1940s with the development of antihistamines. These drugs were found not only to relieve the symptoms of allergies such as hay fever but also to be useful in preparing people for surgical procedures. Antihistamines made people sleepy and less anxious. Attempts to maximize the tranquilizing effects of antihistamines in the 1950s resulted in the discovery of chlorpromazine (Thorazine) followed by other phenothiazines. The phenothiazines were the first neuroleptic drugs (neuroleptic is derived from an ancient Greek term meaning “take hold of nerves”). They act by blocking certain dopamine receptors. The phenothiazines were soon followed by the butyrophenones (haloperidol [Haldol]) and the thioxanthenes (thiothix- ene [Navane]).

Studies have shown neuroleptic drugs to be effective in reducing the positive symptoms of schizophrenia, but they have a smaller effect on the negative symptoms (Julien, 2008). Neu- roleptics seem to be equally effective for people from different racial backgrounds (Levin- son & Simpson, 1992), although people of Asian origin may require lower doses than other people (Lin et al., 1989). Some people respond to one neuroleptic; some to another (Virani, Bezchlibnyk-Butler, & Jeffries, 2009). This is a bit mysterious because the neuroleptic drugs in each category are very similar to one another (Kane & Marder, 1993). Unfortunately, some people with schizophrenia do not respond to any neuroleptics at all (around 25%) and others respond only partially (Julien, 2008).

Even among those who do respond, neuroleptics present a risk because of their potential side effects (see the accompanying Highlight). The most troubling are the motor side effects that

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arise in the extrapyramidal neural pathways that connect the spinal cord to the brain. These include a shuffling walk, expressionless face, writhing, and other various odd movements. These side effects may be controlled by lowering the dosage or by administering additional drugs (Pereira & Albert, 2017).

To reduce the probability of a relapse, individuals with schizophrenia are often kept on neu- roleptic medication for long periods (Rosenbaum et al., 2005). Because patients sometimes choose to discontinue their neuroleptic medication when they are feeling better, neuroleptics may also be administered by periodic injections rather than as tablets or pills. This is done to ensure that the patients comply with medication protocols and, in effect, to take dosing con- trol away from the patient. Long-term neuroleptic treatment, whether by injection or tablet, is associated with a movement disorder known as tardive dyskinesia (Salem, Pigott, Zhang, Zeni, & Teixeira, 2017). The symptoms include facial grimaces, jerky movements, lip chewing, and a host of other tics and odd movements. Tardive dyskinesia is often irreversible, particu- larly in women (Salem et al., 2017).

Atypical neuroleptics, which work on serotonin as well as dopamine, have a lower probability of producing extrapyramidal symptoms while also having equal or better therapeutic effects (Divac, Prostran, Jakovcevski, & Cerovac, 2014). One of these is clozapine (Clozaril). This drug seems to reduce symptoms in patients who do not respond to traditional neuroleptics (Dem- ler, Morabito, Meyer, & Opler, 2016). Clozaril has one serious problem, though—it produces a potentially lethal blood condition known as agranulocytosis in about 1% of patients (Demler et al., 2016). In agranulocytosis, there is a dramatic lowering in the number of white blood cells and a consequent loss of immune function. People become prone to infections that they cannot fight off. For this reason, frequent white blood cell counts are required so that treat- ment may be discontinued before an infection takes hold. Table 8.3 lists several atypical anti- psychotic medications.

Highlight: Is the Treatment Worse Than the Disorder?

A common question students ask, and one you should consider, is the following: Is the treatment for schizophrenia, specifically the use of antipsychotic medications, worse than the disorder itself ? As you have just read, antipsychotic medications can produce significant side effects, sometimes leading to suicidal behaviors. Is this more problematic than perhaps hallucinations and/or delusions?

Another question: The medications control and reduce, perhaps eliminating, these symptoms. They do not, however, cure schizophrenia. We saw the same situation in Chapter 6, in our discussion of bipolar I and II. Does it make sense, then, for patients to take these medications when they do not cure schizophrenia?

There is a saying among many oncologists (cancer specialists): We can kill the cancer, but sometimes the patient dies also. Can that occur with schizophrenia? Should we, and psychiatrists, think carefully before prescribing, or advocating, medication use?

Finally, let’s assume that you were an individual with schizophrenia who was high functioning (that is, you have insight into your symptoms and can verbalize this). Suppose your health care provider recommended that you take Thorazine based on your medical history. How would you respond?

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Psychological Treatment Few, if any, psychologists believe that schizophrenia can be cured by psychotherapy alone. Instead, the aim of psychological interventions is to delay relapse and to improve the quality of life for people with schizophrenia and for those who care for them.

Initially talk therapy was not very successful with individuals with schizophrenia. An inter- esting example is provided by Frieda Fromm-Reichmann (1950). She would tell her patients that they could continue to stay in their world and stay there as long as they wished, in effect condoning the disorder. She believed, and wrote, that eventually the patients would accept, trust, and grow attached to her and begin to talk to her about their problems (Fromm-Reich- mann, 1950). Today, talk therapy is successful much more often than in Fromm-Reichmann’s time (Miller et al., 2012; Swartz et al., 2012). In combination with antipsychotic medications, cognitive-behavioral therapy and family therapy help patients to relieve thought and per- ceptual disturbances and help them to make behavioral changes and cope with life’s various stressors. Let’s examine each of these.

Cognitive-Behavioral Therapy Cognitive-behavioral techniques are based on the premise that people with schizophrenia have hallucinations due to biology. Patient try to make sense of these sensations and conclude that the hallucinations are coming from external sources, that people are out to get them, that people are putting thoughts into their head, and so on (Hagen et al., 2011; Howes & Murray, 2014). Techniques that can be used include educating patients about the biological causes of their hallucinations, and helping the patients learn to identify which situations (usually

Table 8.3 Atypical (second-generation) antipsychotic medications

Common U.S. Trade Name Generic Name

Abilify aripiprazole

Saphris asenapine maleate

Clozaril clozapine

Fanapt iloperidone

Latuda lurasidone

Zyprexa olanzapine

Symbyax olanzapine/fluoxetine

Invega paliperidone

Seroquel quetiapine

Risperdal risperidone

Geodon ziprasidone

Source: U.S. Food and Drug Administration

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stressful) set off the hallucinations. The clinician can also work with patients to challenge the hallucinations, for example, asking patients what would occur if they did not follow the voice’s orders? This helps to weaken the hallucinations’ power. Clinicians might also teach patients to more accurately interpret their hallucinations. Patients may conclude, “It’s not a real voice; it’s my illness.” Patients can also be taught to use relaxation techniques and to be distracted from the hallucinations when they occur. This can reduce any physical arousal that occurs, reducing the patient’s stress (Veiga-Martínez et al., 2008). The main issue is that these techniques do not eliminate the hallucinations, though they may reduce their frequency.

Family Therapy According to Tsai et al. (2011), more than 50% of those who are recovering from schizophre- nia live with their families. Not surprisingly, a patient’s recovery may be strongly influenced by the behavior and reactions of his or her relatives at home (Macleod et al., 2011). People with schizophrenia who feel positive toward their relatives do better in treatment (Okpokoro et al., 2014). Research has demonstrated that patients in recovery who live with relatives who are very critical, emotionally overinvolved, and hostile, similar to Minuchin’s enmeshed fam- ily, often have a much higher relapse rate than those living with more positive and supportive relatives. Some researchers have also discovered that family members may be very upset by the social withdrawal and unusual behaviors of a relative with schizophrenia (Friedrich et al., 2014; Quah, 2014).

Typically, clinicians will attempt to involve family members in the treatment of schizophrenia. This should include guidance, education about the disor- der, and emotional support and empathy (Burbach, Fadden, & Smith, 2010). Communication patterns often are examined and if need be worked on to improve them.

Expressed emotion refers to the frequency and quality of negative emotions, such as anger or hos- tility, expressed by family members that often lead to a high relapse rate with individuals with schizo- phrenia. Research has shown that relapse is at least in part determined by how people with schizophre- nia are received by their immediate families when they are discharged from the hospital (Ritsner & Gibel, 2007). Treatment programs usually begin by educating families and other caregivers about schizophrenia and what types of behavior they should expect. They are also taught about anti- psychotic medications and their side effects. Fam- ily assistance is enlisted in helping patients to stay on their medication because noncompliance is an important determinant of relapse (Saba, Mekaoui, Leboyer, & Schurhoff, 2007).

digitalskillet/iStock/Thinkstock Expressed emotion may contribute to a higher relapse rate of individuals with schizophrenia. Treatment programs educate family members and caregivers about schizophrenia and what types of behavior to expect.

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Chapter Summary

Token Economies Token economies are behavior modification programs used in psychiatric hospitals to rein- force desired behaviors (making one’s bed, for example). In these programs, staff reward each occurrence of a desired behavior with a token, which can be exchanged for privileges such as time watching television. Patients who disrupt others or who act inappropriately are not rewarded and may even be fined. Some research has found these programs to be effective (Combs, Basso, Wanner, & Ledet, 2008).

Social Skills and Cognitive Training Individuals with schizophrenia who spend long periods in hospitals (or out of the hospital but removed from social interaction) may lack social skills (Ridgeway, 2008). They need to learn the specific skills required to hold a conversation, go through a job interview, express their feelings, and maintain relationships. This is supplied by clinicians either on an inpatient or outpatient basis (Ridgeway, 2008).

In sum, a combination of antipsychotic medications, psychological treatment that includes family support, and social skills training, among other approaches, allows us to best treat schizophrenia. Current research continues to focus on antipsychotic medications as well as ways to more effectively treat this disorder (Conley et al., 2005).

Chapter Summary

The Genesis of Schizophrenia • Schizophrenia is the most common of the schizophrenia spectrum disorders (disor-

ders characterized by gross distortions of reality). • The precise definition of schizophrenia has varied over the decades. • The DSM–5 diagnostic criteria for schizophrenia require that two of five symptoms

be present (positive symptoms include delusions, hallucinations, disorganized speech, and grossly disorganized or catatonic behavior, whereas negative symptoms include limited speech and flat affect). At least one of the symptoms must include hallucinations, delusions, or disorganized speech.

• The diagnosis also requires evidence of a decline from a previous level of function- ing and the presence of disturbed behavior over a period of at least six months.

Course • The course of schizophrenia is divided into three stages: prodromal, active, and

residual. • The syndrome’s first appearance is usually in adolescence or early adulthood, with

alternating active and residual phases over many years.

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Chapter Summary

Etiology of Schizophrenia • The evidence from family, twin, and adoption studies suggests that there is a genetic

factor that determines vulnerability to schizophrenia; however, the inherited trait appears to have variable expression (relatives may not be schizophrenic but may have related disorders).

• Because even identical twins have a concordance of less than 50%, it seems clear that heredity is not a sufficient explanation for schizophrenia. Heredity must interact with other causal factors.

• Among the many risk factors that have been related to schizophrenia are season of birth, social class, life-stress, and expressed emotion in families.

• Etiology has been attributed to brain damage and neurochemical abnormalities (in dopamine, for example).

Treatment • Milieu treatment in hospitals, once the therapeutic mainstay, is now mostly limited

to brief stays during the active phase of the disorder. • Deinstitutionalization has resulted in an emptying out of psychiatric hospitals. • Schizophrenia is usually treated with drugs, although medications (both old and

new) may have serious side effects.

Critical Thinking Questions

1. Reread the case of Jennifer Plowman. Jennifer was adopted by parents who evidently have no history of mental illness and who raised her in a supportive environment. Jennifer’s biological mother, however, had schizophrenia. Discuss which causal factor(s) of schizophrenia Jennifer’s case supports. Justify your response.

2. Jennifer Plowman’s mother asked the court to commit her daughter to a psychiat- ric hospital, which meant she could be held for 72 hours for observation. The judge was initially reluctant to do so. Discuss the pros and cons of this, and also discuss whether you think “forcing” someone into a hospital or into treatment would be effective.

3. Scientists and practitioners have been researching and trying to understand schizo- phrenia better for decades now, yet successful treatment remains difficult. Give some reasons why this is the case.

4. How would you differentiate between a delusion and an actual belief ? That is, would you classify someone who claims to receive messages from a deity (for example, Christ) as having delusions? Why or why not?

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Chapter Summary

Key Terms active phase The phase in schizophrenia in which symptoms are present.

Capgras syndrome A condition in which an individual with schizophrenia believes that someone he or she knows has been replaced by a double; one type of delusion.

catatonic stupor A condition in which some people with schizophrenia do not move a muscle for hours. At such times, they seem indifferent to events going on around them.

chlorpromazine Known more commonly as Thorazine; the first antipsychotic medica- tion, developed in the early 1950s.

Cotard syndrome A type of delusion in which an individual with schizophrenia believes that he or she is dead.

deinstitutionalization A movement during which psychiatric patients were released from hospitals to be cared for in their home communities, where they are known and where they can participate in everyday life.

delusions Unsubstantiated beliefs; a symp- tom of schizophrenia.

dementia praecox The term that Kraepelin used to denote what he called the “continu- ously deteriorating psychosis”; this is analo- gous to schizophrenia.

expressed emotion The frequency and quality of negative emotions, such as anger or hostility, expressed by family members that often lead to a high relapse rate with schizophrenic patients.

flat affect Little to no emotional expression.

grandiose delusions A person’s beliefs that he or she has some extraordinary talent or power.

hallucinations Perceptual experiences in the absence of external stimuli.

inappropriate affect Emotions that are inappropriate or not properly fit to the cur- rent situation, such as laughing when one is very nervous.

milieu treatment Therapy for schizo- phrenic individuals in a psychiatric hospital with a complete daily program; designed to provide the patient optimal support.

negative symptoms Signs of schizophrenia that reflect a reduction or loss of normal functions, including loss of initiative, lack of emotional expression, and impoverished speech.

neuroleptic drugs Another term for phenothiazines, a class of antipsychotic medications.

persecutory delusions Also called para- noid delusions; a person’s beliefs that some- one is out to get him or her.

phenothiazines A class of antipsy- chotic medications; Thorazine is the most well-known.

polygenic inheritance A condition in which an individual inherits more than one gene that may be a causal factor for schizophrenia.

positive symptoms Signs of schizophrenia that reflect an excess or distortion of normal cognitive and emotional functions, including delusions, hallucinations, and bizarre motor movements.

prodromal phase The phase that precedes schizophrenia; marked by a deterioration from some higher level of functioning.

psychoses Disorders characterized by gross distortions of reality.

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Chapter Summary

residual phase The phase in schizophre- nia in which only negative symptoms, or mild versions of the positive symptoms, are present.

risk factors Features, genetic or otherwise, that are associated with a greater vulnerabil- ity to schizophrenia.

schizophrenia A psychotic disorder typi- cally characterized by hallucinations, delu- sions, and a loss of contact with reality.

social drift theory A theory proposing that schizophrenia affects a person’s social and economic condition; people with schizo- phrenia are impaired in their ability to compete economically, so they “drift” down the socioeconomic ladder.

social stress theory A theory proposing a direct causative role for schizophrenia: Poor people are exposed to more eco- nomic and social problems than are those who are better off and therefore are more likely to become schizophrenic. Although they also need to have a predisposition for schizophrenia, their social situation makes it more likely that symptoms will present themselves.

tardive dyskinesia A movement disorder with symptoms that include facial grimaces, jerky movements, lip chewing, and many other tics and odd movements.

thought insertion delusions Sometimes called delusions of influence; a person’s beliefs that thoughts are being inserted into his or her own head.

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7 Sleep-Wake and Eating Disorders

fpwing/iStock/Thinkstock

Chapter Objectives

After reading this chapter, you should be able to do the following:

• Describe the stages of the normal sleep cycle.

• Know and describe the main differences between the major sleep-wake disorders.

• Understand the main ways to treat sleep disorders.

• Know and describe the main feeding disorders.

• Know and describe the major differences between anorexia nervosa, bulimia nervosa, and binge-eating disorder.

• Describe some of the methods used to treat eating disorders.

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7.1 An Introduction to Sleep-Wake Disorders: The Normal Sleep Cycle

We sleep close to 3,000 hours per year, which means that we spend about one third of our lives asleep. However, according to the National Sleep Foundation (2017), about 40% of people in the United States don’t get enough sleep, and lack of proper sleep can lead to health problems (Depner, Stothard, & Wright, 2014; Liu, 2016; Schochat, Cohen-Zion, & Tzischinsky, 2013).

The normal human sleep cycle consists of four different stages of sleep, one of which involves rapid eye movement (REM) and three of which do not (non-REM, or NREM, sleep). The cycle begins with NREM Stage 1, which begins shortly after you fall asleep. In this stage, which lasts from 1 to 10 minutes, you are lightly asleep. However, you can quickly and somewhat easily return to being fully awake. Although you are asleep, you may wake up from this stage feeling like you didn’t sleep at all. The next stage is NREM Stage 2. This stage lasts about 20 minutes and is characterized by a slowing heart rate and a decrease in body temperature. You spend about 45% of your sleep time in NREM Stage 2 sleep. Your body reduces its activity to prepare you to go into a deep sleep, and it becomes harder to wake you up. Typically, NREM Stages 1 and 2 are referred to as light sleep. NREM Stage 3 comes next. This stage is the combination of what was previously separated into Stage 3 and 4 sleep and typically starts 35 to 45 minutes after falling asleep. Your brain waves slow down and become larger. In this stage, you will sleep through most potential sleep disturbances (noises and movements) without showing any reaction. If by some chance you actually wake up during NREM Stage 3 sleep, there is a good chance that you will feel disoriented for the first few minutes. Sometimes this stage is referred to as “slow-wave sleep” or “delta sleep.”

The final stage of a normal sleep cycle is called REM Stage 4. The first REM sleep stage lasts around 10 minutes and usually happens after having been asleep at least 90 minutes. Your eyes move rapidly in all directions during REM sleep, almost as though you are watching a movie. Typically, REM stages get longer and longer as the night goes by. Dreams (and night- mares) usually happen during the last REM stage, which can last an hour and is the deepest. This stage is also known as “paradoxical sleep.” One reason for this: Even though your brain is quite active during the stage, most of your muscles are paralyzed (Chieh, 2015).

The two main types of sleep disorders are the dyssomnias (irregularities or abnormalities in the amount, quality, or timing of sleep) and the parasomnias (sleep disturbances that result from unusual or abnormal events that occur when one is asleep, typically during the night). Psychological factors can play an important role in these disorders. Parasomnias can occur during both REM and NREM sleep. Somnambulism (sleepwalking) and enuresis (bedwetting) occur during the REM stage. We will describe the major sleep-wake disorders in the next two sections.

7.2 Dyssomnias Dyssomnias are disorders that affect the initiation or maintenance of sleep, which includes nighttime wakefulness, or excessive sleepiness. They include insomnia disorder, hyper- somnolence disorder, narcolepsy, breathing-related sleep disorders, and circadian rhythm sleep-wake-disorders.

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Insomnia Disorder Insomnia involves a disturbance in the amount, quality, or timing of sleep that occurs at least three nights per week for at least 3 months (American Psychiatric Association [APA], 2013). The most com- mon sleep-wake disorder is insomnia, called insomnia disorder in the DSM–5. Insomnia disorder is characterized by difficulty fall- ing asleep, maintaining sleep, or not feel- ing rested after normal amounts of sleep, occurring at least three nights per week for at least three months (American Psy- chiatric Association [APA], 2013). Difficulty maintaining sleep is defined in the DSM–5 as having frequent awakenings or problems returning to sleep after awakening. Overall, about one third of all adults report some symptoms of insomnia, and about 6% to 10% meet the diagnostic criteria for insomnia disorder (APA, 2013; Morin & Jarrin, 2013). The National Sleep Foundation estimates that almost 50% of the U.S. population experiences some symp- toms of insomnia during a given year (Morin & Jarrin, 2013). Typically these individuals go through the day quite sleepy and may have difficulty performing tasks, especially those that require memory and recall. This can also be dangerous as individuals may get sleepy while driving. Insomnia might be a result of the individual being under too much stress and being unable to cope, or perhaps being depressed or anxious. Insomnia can occur only on some nights but not others, or it can have a more chronic pattern, lasting weeks to many months, or even lasting a lifetime after onset.

Hypersomnolence Disorder (Hypersomnia) Hypersomnolence disorder is characterized by excessive sleepiness even though the indi- vidual may have slept at least seven hours (this qualifies as a lot of sleep for many people these days). If a person has slept for more than nine hours per day and does not feel refreshed, this qualifies as hypersomnolence. To qualify for the diagnosis, this problem must occur at least three times a week for at least three months. Typically, the individual will have difficulty getting out of bed or may take frequent daily naps. Unlike insomnia, which occurs twice as often in women (Pallesen, Sivertsten, Nordhus, & Bjorvatn, 2014; Taylor, Bramoweth, Grieser, Tatum, & Roane, 2013), hypersomnolence occurs more frequently in men (Billiard & Sonka, 2016).

Narcolepsy What if an individual quickly and unexpectedly falls asleep and goes directly into REM sleep? Narcolepsy is marked by sudden and repeated “attacks” of REM, or dream-state, sleep that may be accompanied by a brief loss of muscle tone, called cataplexy. The individual might fall asleep during a conversation or an important presentation, or might fall asleep without

OcusFocus/iStock/Thinkstock Insomnia affects nearly 50% of the U.S. population every year.

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warning while driving. Like the other dyssomnias already discussed, the individual must have, minimally, episodes three times per week for at least three months. Narcolepsy tends to be rare, affecting about 0.02% to 0.04% of the population (APA, 2013; Partinen et al., 2014). It seems that the sudden REM sleep attacks may be set off by strong emotional events such as extreme excitation, happiness, or anger. In addition, it is now known that narcolepsy is caused by an orexin (hypocretin) deficiency (APA, 2013). Orexin, also called hypocretin, is a neurotransmitter that regulates and is involved with arousal, wakefulness, and appetite. The most common form of narcolepsy, involving cataplexy, is caused by a lack of hypocretin in the brain due to destruction of the cells that produce it.

Breathing-Related Sleep Disorders Breathing-related sleep disorders are caused by sleep-related breathing difficulties that lead to excessive sleepiness or insomnia. Individuals who suffer from these disorders have interrupted sleep many times during the night and do not feel rested even when they get more than the typical amount of sleep (eight hours). These disorders are subdivided into obstructive sleep apnea hypopnea, central sleep apnea, and sleep-related hypoventilation. In obstructive sleep apnea hypopnea, the individual may stop breathing for as long as 30 sec- onds many times during the night, with minimally five obstructive apneas or hypopneas per hour of sleep. This may occur hundreds of times during the night, but the victim is unaware that it is occurring. Typically the individual is significantly overweight and will be a loud snorer. Obstructive sleep apnea hypopnea is associated with obesity, or being minimally 30 pounds overweight, as defined by the National Institutes of Health (Drager, Toreiro, Polotsky, & Lorenzi-Filbo, 2013), and may also be associated with increasing age (Franklin & Lindberg, 2015). Obstructive sleep apnea hypopnea can also be associated with trauma (Tamanna, Parker, Lyons, & Ullah, 2014), and it can lead to increased blood pressure and may lead to a stroke. Typically, this disorder is more common in males (Peppard et al., 2013).

Central sleep apnea is the occurrence of at least five central apneas per hour of sleep. It needs to be diagnosed via polysomnography. Polysomnography, also called a sleep study, records the individual’s brain waves, blood oxygen level, heart rate and breathing, as well as eye and leg movements. Polysomnography usually is done at a sleep disorders unit within a hospital or at a sleep center. Typically this is done at night so that the test can record the individual’s nighttime sleep patterns, but it can be performed during the day to accommodate those who work at night. An important function of this test is that it can be used to help adjust the treatment plan for an individual who has already been diagnosed with a sleep disorder (Mayo Clinic, 2017).

Finally, in sleep-related hypoventilation, which also must be diagnosed via polysomnography, the individual has decreased respiration while asleep, as demonstrated by elevated carbon dioxide levels (APA, 2013).

Circadian Rhythm Sleep-Wake-Disorders Circadian rhythm sleep-wake disorders refers to a series of sleep-wake problems in which individuals have difficulty sleeping at the times required for work, school, or other aspect of their lives. Typically this occurs when individuals do shift work; they may work two normal

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days in a row, then work three days during the night (Wright, Bogan, & Wyatt, 2013). The sleep disturbance leads to excessive sleepiness, insomnia, or both (APA, 2013). One easy way to treat this disorder, at least in theory, is to encourage the individual to get a job that has consistent working hours.

Etiology Insomnia disorder can have a variety of causes. First, people who have insomnia disorder may not become sleepy until much later at night because their body temperature doesn’t drop enough for them to fall asleep (Miller et al., 2015). Drug and alcohol usage can also contribute to insomnia disorder, as can changes in light, noise, or temperature. Psychological factors can also play a role, specifically stressful events occurring during the day (LeBlanc et al., 2007). Individuals may also misperceive how much sleep they need. In addition, they may not fully appreciate how disruptive interrupted sleep is. Insomnia disorder can also be a learned behavior. For example, the individual may associate the bed and bedroom with nega- tive thoughts or feelings related to frustrations falling asleep; therefore, bedtime sets off anxi- ety reactions (Stepanski, 2006).

Breathing-related sleep disorders can also contribute to insomnia disorder. Another etiologi- cal factor may be our always-on world—when most of us spend large amounts of time using smartphones and other electronic devices.

One interesting causal factor can be daytime naps—a common way that people try to make up for lost sleep at night. These naps can interrupt sleep the next night as the body’s natu- ral rhythms are upset. In addition, a person may think that daytime naps are a good way to compensate for lost sleep and so may anticipate the naps and, subsequently, be unable to fall asleep or have sleep disruptions at night.

Some of the sleep-wake disorders run in families, which is not a causal factor, as such, but might offer a research direction in the future (Gehrman, Keenan, Byrne, & Pack, 2015). In fact, some research has shown that 39% of people who had hypersomnolence disorder had a fam- ily history of it (Guilleminault & Pelayo, 2000). Narcolepsy may also run in families (Ohayon, 2016).

Treatment The most commonly used medical treatments for sleep-wake disorders that include insom- nia involve prescribing medications, specifically the benzodiazepines or related medica- tions. These medications include zolpidem (Ambien) and zaleplon (Sonata), two examples of short-acting drugs. Longer-lasting drugs include flurazepam (Dalmane), a benzodiazepine. Short-acting drugs are often preferred as they will have stopped working by morning and will not produce daytime drowsiness. These drugs do have negative effects though. Benzo- diazepines can cause excessive sleepiness and can lead the individual to become dependent on them. They are also designed for short-term use; long-term use can lead to dependence. Ambien, in particular, has been documented to cause sleepwalking-related problems in some people (Pagel, 2014), and nocturnal eating episodes in others (Pagel, 2014; Paulke, Wunder, & Toennes, 2015).

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Stimulants such as amphetamine or Ritalin are often prescribed for narcolepsy or hyper- somnolence disorder (Lopez, Arnulf, Drouot, Lecendreux, & Dauvilliers, 2017). For breath- ing-related sleep disorders, such as obstructive sleep apnea hypopnea, weight loss is often strongly recommended, but individuals given this advice are typically unsuccessful at con- quering their disorder because they often fail to lose weight or maintain weight loss (Sanders & Givelber, 2006). Mechanical devices to improve breathing during sleep, or to reposition the tongue or jaw during sleep, have also been tried, again typically with little success because of the discomfort these methods produce. One assistive mechanical device, which is quite cum- bersome, is called a continuous positive airway pressure (CPAP) machine. A CPAP machine delivers just enough air pressure to a mask to keep the upper airway passages open while the user is asleep, thus assisting breathing and making sleep apnea and poor sleep less likely. This can also be used to prevent very loud snoring, a result of sleep apnea as well as of being morbidly obese (Qaseem, Barry, Denberg, Owens, & Shekelle, 2013).

Simple environmental treatments (altering the environment to make changes in the individu- al’s behaviors) for sleep disorders include making bedtimes several hours later than normal and using bright light to help fool the brain into thinking it’s earlier than normal, known as phototherapy (Dagan, Borodkin, & Ayalon, 2006).

Relaxation techniques, described in Chapter 3, have been used to successfully treat insomnia disorder (Zacharie, Lyby, Ritterband, & O’Toole, 2016). Stimulus control techniques have also been used with greater success in treating insomnia disorder (Harvey et al., 2014). In this tech- nique, the individual is asked to use the bed for only two things: sleep and sex. This, of course, is easier said than done, as many people read, watch television, and also eat in bed. In effect, we ask the individual to redefine the purpose of the bed and the bedroom. Our constantly being connected to smartphones or tablets can also be a problem, especially before bedtime. Studies have shown that the light from screens in the evening alters sleepiness and alertness, and suppresses melatonin levels (Chang, Aeschbach, Duffy, & Czeisler, 2015). Reducing time spent using these lighted screens before bedtime might help decrease insomnia.

Finally, establishing a good sleep hygiene program, taking steps during the day and before bedtime to ensure a good night’s sleep, is also effective. Avoiding caffeine and nicotine well before bedtime, setting a regular bedtime for each night, and making sure the bedroom is the proper temperature each night are some of the preventive measures that seem to be effective (Irish, Kline, Gunn, Buysse, & Hall, 2015).

7.3 Parasomnias The DSM–5 parasomnias include non–rapid eye movement sleep arousal disorders (sleep ter- ror and sleepwalking types) and nightmare disorder.

Non–Rapid Eye Movement Sleep Arousal Disorders, Sleep Terror Type Non-rapid eye movement sleep arousal disorder, sleep terror type is not related to nightmares (dreams arousing feelings of intense fear, horror, and distress) as sleep terror

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disorder occurs during NREM sleep, whereas night- mares occur during REM sleep. Typically sleep ter- rors affect children and cause them to awaken with a frighteningly loud scream. The child will have a rapid heart rate, be very upset, and often be sweat- ing profusely. Typically, sleep terrors appear in children, disappear in adolescence, and affect up to 6% of children at one time or another (APA, 2013). Oddly enough, children do not recall sleep terrors (Tinuper, Bisuli, & Provini, 2012). Sleep terrors affect about 2% to 4% of adults (Carrillo-Solano, Leu-Semenescu, Golmard, Groos, & Arnulf, 2016).

Non–Rapid Eye Movement Sleep Arousal Disorders, Sleepwalking Type Non-rapid eye movement sleep arousal disor- ders, sleepwalking type (sometimes called som- nambulism when it recurs) is primarily a childhood disorder that, surprisingly to most people, occurs during NREM sleep (APA, 2013). It typically occurs during the first few hours of sleep (the first third of sleep). Affected individuals will usually leave their

beds repeatedly during the night and walk around without being conscious of doing so or being able to recall doing so later, once awake. It is not dangerous to awaken a sleepwalker, but if left alone, the individual will typically return to bed. Statistics vary, but anywhere from 2% to 5% of children have repeated episodes (APA, 2013) and up to 40% of children may have at least one episode (APA, 2013). Stress and extreme fatigue may be related to sleep- walking (APA, 2013). Sleepwalking usually ends by the time a child reaches age 15. Like night terrors, this disorder affects about 2% to 4% of adults (Carrillo-Solano et al., 2016).

Nightmare Disorder We mentioned nightmares earlier, but when do nightmares become nightmare disorder? According to the DSM–5, the extended and unfortunately well-remembered dreams of night- mare disorder usually have themes of “avoiding threats to survival, security, and physical integrity” and “generally occur during the second half of a major sleep episode” (APA, 2013, p. 404). Typically the individual will awaken rapidly and do so repeatedly following a night- mare. Nightmare disorder tends to affect women slightly more so than men (Sandman et al., 2013).

Etiology and Treatment We still know little about the etiology and treatment of parasomnias (Owens & Mohan, 2016; Tinuper et al., 2012), and currently there are few recommended treatments for these

Creatas Images/Creatas/Thinkstock Contrary to popular myth, it is not usually considered dangerous to awaken someone who is sleepwalking.

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disorders. One efficacious method used to treat and eliminate sleep terrors in children is scheduled awakenings, in which the parent is told to wake the child about 15 to 20 minutes before each sleep terror episode is expected to begin (Kuhn & Elliot, 2003; Mindell, Kuhn, Lewin, Meltzer, & Sadehet, 2006). The same method can be used with adults. Typically adults can go to a sleep disorders clinic, where their sleep patterns and behaviors can be observed and measured (for example, with an electroencephalograph, or EEG). Behavior modification techniques can be used, as well as psychotherapy to see if the nightmares have recurring themes. An efficacious method is for someone observing an individual having nightmares or night terrors to take notes and record the themes, if the individual can recall the nightmares or night terrors on waking (Owens & Mohan, 2016).

In sum, we still do not know a lot about sleep disorders, but we do know that many indi- viduals in the United States do not get enough sleep, making problems more likely to occur. Research continues into these somewhat puzzling disorders.

7.4 Feeding Disorders Like all animals, humans must eat regularly and properly in order to stay physically and psy- chologically healthy, to survive, and to thrive. Individuals who have a feeding or an eating disorder may eat too much in too short a timeframe, or they may eat too little and thus lose a significant amount of weight, becoming dangerously underweight for their height or age. (See the accompanying Highlight for a look at eating disorders in a modern context.) Alternatively, they may eat nonnutritive or nonfood substances, such as wood shavings or lead paint chips.

Highlight: Eating Disorders and the Internet

The possibilities are quite strong that you have heard of pro-anorexia (pro-ana) and pro- bulimia (pro-mia) websites. An Internet search will reveal a lot of them. What are these sites about? Generally speaking, they promote anorexia nervosa and bulimia nervosa as lifestyle choices as well as diet options. The creators of these sites see nothing wrong with these behaviors. For example, a 16-year-old blogger shared this piece of advice: “Wear a rubber band around your wrist and snap it when you want to eat. Food = pain.” Most people would agree that this statement promotes unhealthy, potentially lethal behavior. But what about the women who think this is normal? How can we hope to help them and provide treatment to them if they see these kinds of statements online, promoted as normalcy? These sites also equate amenorrhea as a measure of successful weight loss, whereas the DSM–IV–TR saw this as a diagnostic criterion for anorexia nervosa. Clearly there are different perspectives here.

Pro-mia websites are the same, except they focus on bulimia nervosa, not anorexia nervosa. Many people are not aware that such sites exist, yet once they view them, for the most part, they become disturbed by what they read. In the United States, freedom of speech is a fundamental right, but perhaps the creators of these kinds of sites should think about the consequences of the behaviors they are promoting. Some social media sites have attempted to ban or restrict such sites, but they usually just pop up elsewhere. What is your perspective?

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Pica Pica is an unusual eating disorder that occurs in people across socioeconomic groups, ages, and genders (Stiegler, 2005), although it may be more prevalent among women, children, and those of lower socioeconomic status (Delaney et al., 2015; Kelly, Shank, Bakalar, & Tanofsky- Kraff, 2014). The name pica comes from the Latin word for “magpie,” a bird known to eat practically anything. This is precisely the problem in pica. People with this disorder have been known to eat dirt, laundry starch, chalk, buttons, paper, cigarette butts, matches, sand, soap, toothpaste, and many other supposedly inedible substances. The main DSM–5 diagnostic cri- teria for pica appear in Table 7.1. Note that it is important to consider cultural practices when making this diagnosis. Members of cultures that sanction the consumption of odd substances, such as clay, are not suffering from a psychological disorder.

The prevalence and cause of pica are unknown. Psychological theories tend to be vague (for example, “fixation at the oral stage of development”). Physiological explanations are not much better. Most are based on the idea that diet deficiencies (too little iron or zinc, for example) cause a craving for anything containing these missing minerals. Yet most of the items craved by people with pica do not actually supply the missing minerals.

Rumination Disorder and Avoidant/Restrictive Food Intake Feeding Disorder The DSM–5 includes two other feeding disorders usually found in infants or young children: rumination disorder and avoidant/restrictive food intake feeding disorder. Rumination dis- order is marked by regurgitation of food, whereas avoidant/restrictive disorder of infancy is manifested by inadequate eating. Both disorders are diagnosed only when there is no clear medical condition causing the symptoms, and little is known about the prevalence or etiology of either one (APA, 2013; Delaney et al., 2015).

Table 7.1 DSM–5 diagnostic criteria for pica

A. Persistent eating of nonnutritive, nonfood substances over a period of at least one month. B. The eating of nonnutritive, nonfood substances is inappropriate to the developmental level of the

individual. C. The eating behavior is not part of a culturally supported or socially normative practice. D. If the eating behavior occurs in the context of another mental disorder (e.g., intellectual disability

[intellectual developmental disorder], autism spectrum disorder, schizophrenia) or medical condition (including pregnancy), it is sufficiently severe to warrant additional clinical attention.

Specify if: In remission: After full criteria for pica were previously met, the criteria have not been met for a sustained period of time.

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7.5 Eating Disorders What do Lady Gaga, Demi Lovato, Paula Abdul, Fiona Apple, Oprah, and the late Princess Diana have in common? All of these women had an eating disorder, in most cases bulimia nervosa (described later in this section). To their credit, many if not most of them have been or were open about their struggles.

Eating disorders refer to extreme distur- bances in eating behavior. Two core features of eating disorders are an obsession with losing weight and a morbid fear of gaining weight. The hallmark characteristic of eat- ing disorders is the desire for, and perhaps obsession with, getting thin or remaining thin. In this section we will examine the two most common eating disorders, anorexia nervosa and bulimia nervosa. Anorexia nervosa is marked by an obsessive and irrational fear of gain- ing weight, with a resultant major reduction in food intake (known as restriction), so much so that the individual loses a significant amount of body weight (APA, 2013). Those suffering from bulimia nervosa may be obsessed with maintaining weight by binging (out-of-control eating) and then using an inappropriate compensatory behavior (such as fasting or using laxatives) to prevent weight gain (APA, 2013).

We will also briefly examine binge-eating disorder (BED), which was first identified in the 1990s and was under further review in the DSM–IV–TR. This disorder has now been included as a diagnosis in the DSM–5 (APA, 2013). Individuals with BED experience marked distress as a result of their binging. However, binging is not then followed by inappropriate compensa- tory behaviors, defined as purging or restriction (that is, self-starvation) as it is with other eating disorders. (See the comparison of eating disorders in Figure 7.1).

In this chapter, we frequently focus on women when discussing anorexia nervosa and buli- mia nervosa. We do so simply because these disorders overwhelmingly affect females; per- haps as many as 90% to 95% of individuals with anorexia nervosa and bulimia nervosa are female (Smink, van Hoeken, Oldehinkel, & Hoek, 2014). Data point to the lifetime prevalence of anorexia nervosa as ranging anywhere from 0.5% to 2% of the female population in West- ern countries; some researchers estimate that the prevalence is closer to 0.3% (Litmanen, Fröjd, Marttunen, Isomaa, & Kaltiala-Heino, 2017). Another study suggests that as many as 5% of women develop bulimia from ages 14 to 15 (Kjelsas, Bjornstrom, & Gotestam, 2004), and a more recent estimate puts the rate of bulimia in men at about one-tenth the rate in women (APA, 2013). This discrepancy leads researchers to hypothesize that gender and/or gender roles may somehow be involved in the development of eating disorders. It has also been hypothesized that hormones and estrogen levels may be involved (Getzfeld, 2006).

Anna Celadina/Hemera/Thinkstock Eating disorders are often caused by an obsessive or irrational fear of gaining weight.

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Figure 7.1: Similarities and differences among eating disorders

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Table 12.6, p. 543.

Has missed at least three menstrual periods Obsessed with food and odd eating rituals Binges Exercises excessively Gains weight Expresses dissatisfaction with appearance Considers binging beyond control Vomits or uses drugs to purge calories Disappears into bathroom for long periods (to purge)

Weight less than 85% of expected weight Considers self fat even though severely underweight

*Binge-eating/purging subtype

Symptom Anorexia nervosa

Bulimia nervosa

Binge-eating disorder

X* X

X X X

Eating disorders did not attract much research until the 1960s (Fairburn & Brownell, 2002; Striegel-Moore & Smolak, 2001). More important, anorexia nervosa and bulimia nervosa did not appear in the DSM until the DSM–III (APA, 1980). Due to the late acknowledgment of eat- ing disorders in the research community, the scientific and research information that we have on bulimia and anorexia nervosa is somewhat limited. It is remarkable that we know as much as we do about these disorders given the relatively short period of time in which they have been scientifically investigated. Before we examine anorexia nervosa, let’s meet Paula Ames in Part 1 of her case study.

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The Case of Paula Ames: Part 1

Paula, a 31-year-old single Caucasian female, is an undergraduate student in liberal arts at a major university. Paula’s height is approximately 5’6” and she was initially reluctant to share her weight with her psychologist. Paula works as a waitress full time in order to pay her tuition and to make ends meet. Paula was pleasant during the sessions but often seemed rather tense and on edge. She kept checking her watch, and she wore long sleeves even though it was summer.

Excerpt From Transcript of Treatment Session Conducted by Dr. Brian Philipps With Paula Ames Brian Philipps, Ph.D. Psychologist

Transcript of Treatment Session: Paula Ames

Client: Paula Ames

Therapist: Dr. Brian Philipps

DR. PHILIPPS: What brings you to therapy today, Paula?

PAULA: I need to finally shut certain people up, especially my Mom and my fiancé. They have really been driving me crazy about my eating. It’s not like I do anything odd; most women diet before their wedding. My wedding is in a few months, and I need to fit into my dress. I need to lose a few pounds, but I do like my food. I’m also not the biggest fan of crowds . . . I don’t do well in social situations . . . everyone always seems to be staring at me, so we are trying to keep the number of guests down.

DR. PHILIPPS: I would like to try and understand why your family and future husband might, as you say, be concerned about your eating. Would you be able to describe your diet for me?

PAULA: Well, I’m tall—5’6”—and I weigh . . . do you need to know exactly, because I can tell you exactly. Like, I know how to calculate accurately as I bought a very expensive scale. I weigh 92 pounds and that is too much. I want to be a beautiful bride, so I need to lose about maybe 5 more pounds to get into the best dress I can afford. This is my day, my fairytale. Cinderella wasn’t fat like I am. I look at my arms and see the flesh hanging off . . . blech.

DR. PHILIPPS: I see. And would you be able to describe your eating behaviors?

PAULA: I eat . . . What is it with you people? Food is not a problem for me. I told you I need to get to the proper size before my wedding. I’m a flabby Patty right now, and a flabby bride won’t do. My fiancé will leave me at the altar if I don’t lose a bit more.

DR. PHILIPPS: Could you perhaps be more specific about your eating behaviors? For example, what do your meals look like on a daily basis? How would you say you manage your weight?

PAULA: Manage my weight? Not real well as you can see. I eat normal meals, cereal at breakfast, sandwich for lunch, yogurt for dinner, maybe iceberg lettuce. Always drink water, as that’s the healthiest, or tea plain. No coffee or coffee specialty drinks. I need to keep my calories down, no more than 500 a day tops; 300 is much better, of course.* Sometimes I exercise to keep the weight off or to lose the weight. But I can handle food; it’s not a weird thing for me.

See appendix for full case study.

*Note: The suggested calorie count for females is anywhere between 1,500 and 2,000 calories per day.

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Anorexia Nervosa Anorexia nervosa literally means “nervous loss of appetite,” though this is misleading as the individual usually maintains an appetite. Three DSM–5 criteria need to be met for a diagnosis of anorexia nervosa.

First, individuals must refuse to maintain their minimally normal body weight for their age, sex, developmental trajectory (expected height), and physical health. This is defined as a weight that is less than that which is minimally normal (in the DSM–IV–TR this was defined as body weight less than 85% of that expected for individuals of the same age and height; APA, 2013) or for children and adolescents, a weight that is less than is minimally expected of them (APA, 2013). The “85%” criterion was removed from the DSM–5.

Second, individuals must have an intense fear of gaining weight or becoming fat, even though they are obviously at a significantly low weight (APA, 2013). This is a crippling fear, perhaps obsessive in nature, that limits the individual’s life so much that he or she becomes com- pletely focused on either not gaining any additional weight or perhaps trying to lose even more weight. Not only is there a heightened fear of weight gain, but the individual’s behavior ensures he or she will not gain weight. (See the accompanying Highlight.)

Highlight: Body Dissatisfaction

“Tell me what you don’t like about yourself ”—this question opened every episode of Nip/ Tuck, a television drama about plastic surgeons that ran from 2003 to 2010. Although the series slanted toward the bizarre, it made some important points about people and society in general. Wouldn’t every person asked this question be able to reel off a whole list of body dissatisfactions? Is there something wrong with not liking aspects of yourself ? If you look at the data, you can see that the number of plastic surgeries increased by about 4% from 2015 to 2016 (from 1,715,224 total procedures to 1,780,987; American Society of Plastic Surgeons, 2017). The top three procedures were breast augmentation, liposuction, and nose reshaping (rhinoplasty). Evidently a large number of people in the United States do not like aspects of themselves.

Yet body dissatisfaction, paired with obsessions over celebrities such as the Kardashians, Taylor Swift, and so many others, can lead to devastating outcomes. Seeking surgery after surgery in the pursuit of mythical perfection—or developing unhealthy eating habits that can lead to a full-blown eating disorder—carries grave risks. Perhaps helping professionals can promote the concept that you are okay just the way you are, and that it’s okay to be dissatisfied with a feature or two. It takes all kinds to make up the world, and not everyone can look alike. Maybe such an approach could lead to a decrease in eating disorders—and in unnecessary plastic surgeries as well.

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The third criterion is the denial of the seriousness of the low body weight or a disturbance in how the individual experiences or perceives her or his weight or shape (APA, 2013). Individu- als will usually see themselves as quite obese even though it is obvious to everyone else that they are seriously malnourished (Farrell, Lee, & Shafran, 2005). Denial appears to be a key component of eating disorders. This can be denial of the individual’s actual shape or denial of the seriousness of the problem.

The DSM–5 lists two subtypes of anorexia nervosa. The main difference between these two subtypes involves how individuals with anorexia nervosa manage to maintain their abnor- mally low weight, or how they continue to lose weight. The restricting type is characterized by individuals being meticulous, perhaps obsessive, about how much food they eat at a given time, and what their caloric intake is at each meal or on a daily basis. Typically, these individu- als will first cut out sweets and other foods perceived as “fattening” (APA, 2013). Individuals do not regularly engage in binge-eating or purging behavior (APA, 2013). The binge-eating/ purging type is characterized by individuals regularly engaging in binge-eating or purging behavior such as self-induced vomiting or the misuse of laxatives, diuretics, or enemas (APA, 2013). The individuals feel like they cannot control the binging behavior. Binges are typically smaller than those seen in individuals with bulimia, and purging happens more often than it does with bulimia, typically after every meal (Agras, 1987). It has been estimated that about 50% of all individuals with anorexia nervosa binge and purge. Note also that for anorexia to be diagnosed with either subtype, the symptoms must be active for a period of at least three months (APA, 2013; Smink et al., 2014).

Eating disorders, particularly anorexia nervosa, are the most lethal of all of the mental dis- orders, including unipolar depression (Franko et al., 2013). In the past, some research dem- onstrated that approximately 20% of individuals with anorexia nervosa died from medical complications related to their disorder; at least 50% of these were suicides (Chavez & Insel, 2007; Mehler & Brown, 2014). Other studies state that the death rate from anorexia ner- vosa is approximately 2% to 6% (Kask et al., 2016; Suokas et al., 2013), although a certain percentage of those deaths were due to suicide. Getzfeld (1999) hypothesized that females with anorexia nervosa may be engaging in a form of suicide, slowly disappearing and wast- ing away. Psychologically, they are detached, focused solely on their body image and their weight, or lack thereof, and physically detaching themselves from life.

Bulimia Nervosa Whereas anorexia nervosa affects between 0.5% and 2% of all women in Western- ized countries (Ekern, 2014; Smink et al., 2014; Stice, Burger, & Yokum, 2013), buli- mia nervosa, literally “hunger of an ox,” affects between 2% and 5% of the popu- lation (Ekern, 2014). Bulimia nervosa is characterized by the individual eating an unusually large amount of food at a single sitting and then using inappropriate com- pensatory behavior(s) to rid the body of the excess calories. An individual suffering from

vadimguzhva/iStock/Thinkstock People with the restricting type of anorexia nervosa become meticulous about the amount of food they eat on a daily basis.

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bulimia nervosa will often binge on 3,000 to as many as 6,000 calories in a single sitting and then compensate by purging through vomiting or using laxatives, or by fasting (APA, 2013). Although the average calorie count for a binge, which might occur as often as 30 times per week, is about 3,400 calories, binges may reach as high as 10,000 calories. Consider that a McDonald’s Big Mac sandwich has 560 calories. A binge of approximately 3,000 calories is equivalent to eating about 5.5 Big Macs in one sitting; a binge of about 10,000 calories would be the same as consuming 18 Big Macs, also in one sitting.

Bulimia nervosa is diagnosed by using five DSM–5 criteria. First, these individuals must have recurrent episodes of binge eating (where they eat much more during a specific time period than most people would under similar circumstances [APA, 2013] and believe they have no control over this behavior). They feel that they cannot stop their eating or control what they are eating or how much they are eating.

Second, the individual must engage in recurrent inappropriate compensatory behaviors, which means they must engage in self-induced vomiting or misuse of diuretics (medications that increase urination), laxatives, or enemas. These are all examples of purging behaviors. The goal of a purge is to eliminate all of the food that was consumed during the prior binge. It is only a purge if the food is somehow forced out of the body by inappropriate compensatory behaviors. (A person who unintentionally vomits is not purging.) Inappropriate compensa- tory behaviors are behaviors designed to counterbalance and counteract the effects of the binge. They are designed to ensure that the individual with bulimia does not in fact gain any weight, but they also serve to give the individual the illusion of self-control. Their purging seems to alleviate any anxiety caused by the fear of gaining weight. Another way that the individual can eliminate the food is through fasting or exercising excessively, such as exercis- ing at least three hours a day every day, presuming that he or she is not a professional ath- lete or in training for a competition such as the Olympics (APA, 2013). Some people call this behavior “exercise bulimia nervosa.” Unfortunately, the DSM–5 does not define the terms excessively or misuse, which can be problematic as it is left up to clinicians and psychologists to interpret these terms.

Third, the binging and purging, or other inappropriate compensatory behavior, must occur on average at least once per week over a three-month period. Fourth, the individual’s self-evaluation must be unduly influenced by their body weight and shape (APA, 2013). These people place extreme and excessive emphasis on body weight and shape to the point where it seems to become an obsession. (Obsessions were discussed in Chapter 3.) In fact, only about 3% of the women with bulimia in one dated study were not obsessed (our word) with their body’s weight and shape (Garfinkel, 1992).

Stockbyte/Stockbyte/Thinkstock One way individuals with bulimia nervosa eliminate the food consumed during binging is through excessive exercise, which often means exercising several hours every day.

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Binge-Eating Disorder (BED) Binge-eating disorder (BED) involves binging episodes similar to those found in bulimia ner- vosa but without the inappropriate compensatory behaviors (for example, purging and self- starvation). In effect, the main, and some might say only, diagnostic criterion for BED is recur- rent episodes of binge eating that occur on average at least once per week for three months, identical to the first criterion for bulimia nervosa. A critical difference between BED and buli- mia nervosa is that the DSM–5 definition for BED does not include inappropriate compensa- tory behaviors being demonstrated by the individual, a criterion of bulimia nervosa (APA, 2010, 2013). In addition, BED cannot be comorbid with anorexia nervosa or bulimia nervosa (APA, 2013). The DSM–5 diagnostic criteria for BED are summarized in Table 7.3. (Which of the eating disorders do you think Paula Ames has? See Part 2 of her case in the appendix.)

The fifth DSM–5 criterion states that bulimia nervosa does not occur solely during episodes of anorexia nervosa (APA, 2013). We must be able to distinguish between bulimia nervosa and anorexia nervosa, as treatment modalities differ significantly, especially the often recom- mended and/or required medical interventions.

The DSM–5 diagnostic criteria for bulimia nervosa are summarized in Table 7.2. Table 7.2 DSM–5 diagnostic criteria for bulimia nervosa

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: 1. Eating, in a discrete period of time (e.g., within any two-hour period), an amount of food that is definitely

larger than most people would eat during a similar period of time and under similar circumstances. 2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or

control what or how much one is eating). B. Recurrent inappropriate compensatory behaviors in order to prevent weight gain (e.g., self-induced vomit-

ing; misuse of laxatives, diuretics, enemas, or other medications; fasting; or excessive exercise). C. The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week

for three months. D. Self-evaluation is unduly influenced by body shape and weight. E. The disturbance does not occur exclusively during episodes of anorexia nervosa.

Table 7.3 DSM–5 diagnostic criteria for binge-eating disorder

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following: 1. Eating, in a discrete period of time (for example, within any two-hour period), an amount of food

that is definitely larger than most people would eat during a similar period of time and under similar circumstances.

2. A sense of lack of control over eating during the episode (for example, a feeling that one cannot stop eating or control what or how much one is eating).

B. The binge-eating episodes are associated with three (or more) of the following: 1. Eating much more rapidly than normal. 2. Eating until feeling uncomfortably full. 3. Eating large amounts of food when not feeling physically hungry. 4. Eating alone because of being embarrassed by how much one is eating. 5. Feeling disgusted with oneself, depressed, or very guilty after overeating.

C. Marked distress regarding binge eating is present. D. The binge eating occurs, on average, at least once a week for three months E. The binge eating is not associated with the recurrent use of inappropriate compensatory behaviors as in

bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa.

Source: APA (2013, p. 350).

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Etiologies of Eating Disorders Researchers have uncovered several factors they believe influence the emergence of eating disorders in general, or anorexia nervosa or bulimia nervosa specifically, and developed theo- ries to explain these factors.

Sociocultural Factors Unlike many of the disorders in this book, both bulimia nervosa and anorexia nervosa seem to occur most often within specific Westernized countries, specific age groups, specific social classes, and most commonly in females.

Eating disorders may now be crossing racial boundaries (Perez, Ohrt, & Hoek, 2016; Solmi, Hotopf, Hatch, Treasure, & Micali, 2016). However, eating disorders have been viewed as by- products of Western cultures where the media—including television, Internet, and movies— “shape” people’s opinions of how a healthy body should appear, which, in this case, means thin (Ferguson, Muñoz, Garza, & Galindo, 2013). Anorexia nervosa is more common in industrial- ized societies, especially in those societies where Western media influence is pronounced, and where female thinness is seen as an ideal (Pike, Hoek, & Dunne, 2014). In nonindustrial- ized societies, or in societies where Western influence is minimal, a more rounded figure is preferred. In addition, eating disorders manifest themselves during adolescence and young adulthood for a simple reason: Society expects females to be thin. These women may be inter- nalizing this concept (Hoek, 2002; Hsu, 1990).

What does internalizing “thin is in” mean? What this means is that some women (and men) appear to be more vulnerable to mass media’s ideas of the ideal body shape and size, whereas others are less so. For men, this would be a shape that is lean yet muscular, with the so-called “six-pack” abdominal muscles made famous by Mike “The Situation” Sorrentino on the TV show The Jersey Shore or Zac Efron in the movie Baywatch (2017). For women, this would be a body that either has little body fat or else has impossible curves like Barbie, even in her newer, “more accurate” version. An individual’s ability to avoid developing a negative body image and negative self-statements, in addition to being able to avoid the pressure to either remain thin or to lose more weight, seems to be related to media exposure, how well the individual can handle environmental stressors, and the quality of the individual’s support systems (Stice, Schupak-Neuberg, Shaw, & Stein, 1994; Stice, Spangler, & Agras, 2001). (See the accompanying Highlight.)

Psychological Factors Even though familial and sociocultural factors surely play some role in the development of eating disorders, a number of psychological factors have also been implicated in their etiolo- gies. These include individuals striving for some kind of control in their lives, interoceptive awareness, separation problems, and body dissatisfaction.

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Striving for Control One trait that appears to be common among individuals with anorexia nervosa is that they tend to be perfectionists and have obsessive-compulsive tendencies. These in- dividuals struggle for control and perfection in every part of their lives and, therefore, also with their bodies. The lack of eating can perhaps be viewed as a way to gain con- trol over their lives and as a way to develop a sense of independence—an idea posited by Hilda Bruch (1973). Individuals may feel that their weight, and thus their appearance, is the only thing that they can control with- out parental or other outside influence or interference; anything less than perfection is considered to be a failure, especially by individuals with anorexia nervosa (Bruch, 1973; Pearlman, 2005).

Highlight: The Media, Anorexia Nervosa, and Bulimia Nervosa

In 2016 Sports Illustrated chose three women to be cover models for its annual swimsuit issue, which many people argue promotes subtle sexuality and female objectification, and not swimsuits. Suppose you received all three issues and you were an adolescent female. You would soon see that Haley Clauson, a “supermodel,” is topless and is quite thin. Ronda Rousey, a mixed martial arts former champion, appears in body paint, totally nude underneath. Ashley Graham, a “plus sized” supermodel, appears in a two-piece swimsuit. Why is Graham, who by standard modeling criteria is overweight and perhaps obese, wearing a two-piece swimsuit, while the others, who are a lot thinner, are not? What does this convey about body image as well as what is considered normal? What would your reactions be if Graham were topless or nude, with her body parts tastefully covered? Could she appear in ESPN’s The Body Issue, where famous athletes from all sports appear nude? Which woman would a teenager be most likely to identify with? The media promote certain body types and shapes as being aesthetic, sexy, and “normal,” while promoting others stereotypically. How often do you see someone who has curves like Graham playing a romantic role, or a lead, for example? In many shows and movies, such actresses usually portray funny, sarcastic supporting characters. Why can’t they be considered “sexy” or their bodies be seen as normal?

urfinguss/iStock/Thinkstock For many sufferers of anorexia nervosa, a lack of eating feels like a way of taking control over their lives and their bodies.

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Interoceptive Awareness Interoceptive awareness refers to an individual’s awareness of internal cues, including emo- tional states and hunger (Khalsa et al., 2015; Lavender et al., 2014). Individuals with anorexia nervosa may be more in touch with their appearance than with the fact that they feel sad, angry, happy, or disgusted. Because of this, they don’t recognize certain internal cues, such as hunger pangs. Researchers have found that some women without a high level of interoceptive awareness cannot recognize when they are sated (Viken, Treat, Nosofsky, McFall, & Palmeri, 2002). Earlier research noted that a lack of interoceptive awareness was able to predict the development of eating disorders as much as two years into the future (Leon, Fulkerson, Perry, & Early-Zald, 1995).

Body Dissatisfaction Body dissatisfaction is a key factor in both bulimia nervosa and anorexia nervosa. In both cases, the disorder is caused and perpetuated by the individuals wanting to change their bod- ies. However, individuals with anorexia nervosa are much more concerned with their appear- ance and are totally dissatisfied with their body shape, to the point of evidencing pathology. In other words, these individuals will continue to starve themselves even when their weight is dangerously low “just to lose a bit more” and to appear ever thinner. Individuals with bulimia, who may starve themselves as a method of staving off weight gain, will be of a normal weight or slightly overweight. They tend to be more concerned with pleasing others, are often more concerned with being attractive to others, and are more likely than individuals with anorexia nervosa to have sexual relationships (Striegel-Moore, Silberstein, & Rodin, 1993). Cultural influences in Western societies contribute to this body dissatisfaction by placing a very high value on a reed-thin body (Culbert, Racine, & Klump, 2015).

Biological Factors Like many of the psychological disorders, eating disorders seem to run in families and seem to have a genetic component (Culbert et al., 2015; Starr & Kreipe, 2014). In addition, low levels of serotonin activity have been linked to bulimia nervosa (e.g., Phillips et al., 2014; Starr & Kreipe, 2014), especially to binge eating of carbohydrates (Kaye et al., 2012). Sero- tonin is a neurotransmitter that is involved with information processing and coordination of motor skills, specifically movement. It is also involved with inhibition and restraint and helps to regulate aggression, sexual behaviors, and eating, which would include binging and purging. Irregular serotonin levels have been directly implicated in the etiology of unipolar depression (Gryglewski, Lanzenberger, Kranz, & Cumming, 2014) and in obsessive-compul- sive disorder (Lissemore et al., 2014), both of which are sometimes comorbid with eating disorders (Cederlöf et al., 2015; Godart et al., 2015), although it is unclear which condition manifests first (Getzfeld, 1992). This link between eating disorders and unipolar depression and obsessive-compulsive disorder can be substantiated by the fact that antidepressants that work to increase serotonin activity in the brain will, in many instances, reduce and/or elimi- nate bulimic symptoms (Milano et al., 2013).

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Some researchers believe that people with eating disorders have serotonin levels that are too high, and that this irregularity is present at birth (Kaye et al., 2005). By self-starvation or purging, the individual is, perhaps unconsciously, attempting to reduce these unusually high serotonin levels (Kaye et al., 2005).

The Psychoanalytic Perspective Psychoanalysts believe that people with bulimia nervosa see their families as rejecting of them, and they often engage in arguments and conflicts, whereas individuals with anorexia nervosa may see their families as being overly close (Fornari et al., 1999). Bruch (2001), whose work in studying and treating eating disorders was groundbreaking, noted that a dys- functional relationship between the mother and her child led to, among other things, a poor sense of independence and control, which eventually led to the child manifesting an eating disorder. She called this an ego deficiency in the child.

Bruch saw a dichotomy in how parents respond to their child’s needs. Effective parents feed their children when they are hungry, and comfort them when they are frightened, sad, or in pain. By contrast, ineffective parents do not properly attend to their children’s needs. For example, they might feel or determine that the child is hungry or in need of comforting while misinterpreting the child’s actual condition. They might feed the child when the child is in pain and needs comforting, or comfort the child instead of feeding him or her when the child is hungry. According to Bruch (1973), children raised in this fashion may be unaware of or confused about their internal needs (hunger, pain, and so on), leading to their being unable to correctly recognize and identify their emotions. Once children reach adolescence, their desire to become more independent understandably, and predictably, increases, but they feel as though they are unable to do so. In effect, they demonstrate reaction formation: Because they feel helpless and that they lack control, they instead do the opposite, which is they seek out excessive control over their body and eating behaviors. There is some support for this hypothesis (for example, Holtom- Viesel & Allan, 2014), as well as for Bruch’s point that individuals who have an eating disorder misperceive their internal cues (Lavender et al., 2014). Keep her points in mind, especially when we discuss treatment modalities.

The Behaviorist Perspective According to Bandura’s modeling theory (which states that a child who is interested in a model’s behavior and is able to repro- duce it will indeed do so), parents may be the cause of eating disorders in their chil- dren. Per Bandura’s theory, children whose parents are on a diet will notice how pre- occupied the parents are with their caloric intake and decide they too should get

Denver Post/Getty Images Hilde Bruch, a pioneer in the study and treat- ment of eating disorders.

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involved in this diet program. Additionally, parents may push their children to lose weight, whether to win a spot on the cheerleading team or simply to compete with the children’s thinner peers in school (Abraczinskas, Fisak, & Barnes, 2012). Recent research has also noted that mothers, fathers, and peers each played an important role in the development of girls’ bulimic symptoms by affecting their body dissatisfaction, which was related to later dieting behaviors, depressive symptoms, and bulimic symptoms (Blodgett-Salafia & Gondoli, 2010). The results suggested that peers were a stronger influence than mothers and fathers. (See Part 3 of Paula Ames’s case in the appendix.)

Treatment of Anorexia Nervosa Successful treatment for anorexia nervosa is rather limited (Hsu, 1990). In one study, approximately 10% to 20% of patients with anorexia nervosa remained at their pre- treatment weight during their posttreat- ment follow-ups (Haliburn, 2005). What this means is that many patients with anorexia nervosa do not respond well to treatment, which often includes inpatient hospitaliza- tion. For those who do initially respond to treatment, recovery may not last (Richard, Bauer, & Kordy, 2005).

Anorexia nervosa treatment includes two goals. The first, most immediate goal is to get the individual to gain back a certain amount of weight and to attempt to normal- ize her eating pattern. In life-threatening cases, this may need to occur in an inpatient setting. This type of intervention is war- ranted if patients absolutely refuse to eat or if their weight is significantly below where

it should be. This can lead to increased risk for cardiac arrest. If individuals refuse to eat, they would need to be force-fed via intravenous lines and/or via a tube down the throat. This can lead to an early treatment obstacle because the force-feeding may lead to distrust of treat- ment professionals, setting up an aversive condition. For a variety of reasons, not the least of which is to avoid setting up such a condition, treatment now typically occurs in an outpatient setting or in a day treatment hospital (see, for example, Raveneau et al., 2014).

One advantage of day treatment hospitals or, if the individual’s life is at risk, inpatient set- tings is that weight gain can be monitored carefully. The weight gain should be gradual, with a target of about two to three pounds per week, although this depends on the individual’s weight at treatment onset. In some instances, the individual might gain as much as a pound per day. There are several reasons the weight gain needs to be gradual and not sudden. Psy- chologically, rapid weight gain might scare the patient, and the patient might drop out of

Siri Stafford/Photodisc/Thinkstock Treatment for anorexia nervosa is not always successful, which can often lead to patients being hospitalized so that necessary weight gain may be carefully monitored.

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treatment, making the treatment goal act like a punishment. The APA (2000, 2013) also notes that if weight gain is rapid, the individual might suffer from constipation, abdominal pain, and bloating. The most commonly used weight restoration method is usually called a nutritional rehabilitation program. This includes nursing care, nutritional counseling, and a high-calorie diet to help the individual get back to normal eating and to help her gain weight (Leclerc et al., 2013). Typically, the calorie count will increase gradually until it reaches approximately 3,000 calories per day (Zerbe, 2010). These programs usually last from 8 to 12 weeks.

The second goal of treatment is to work on the psychological, social, and environmental issues that either may have caused or are somehow maintaining the disorder and thus interfering with recovery. Some of these issues include working with individuals to change their dysfunc- tional body image attitudes and working on the interpersonal problems they have in their lives (with, for example, family, friends, and significant others). The issue of loss of control of one’s eating is also addressed in therapy. Treatment is typically conducted through family therapy, self-help groups, or individual therapy.

Family therapy is most successful with adolescents who have had anorexia nervosa for less than three years, that is, with an early onset and a short duration (Rutherford & Couturier, 2007). The core problem is presumed to be the parents’ disagreement with, and perhaps denial of, the adolescent’s desire for autonomy. Mealtimes and thoughts about food and weight are typically dysfunctional within the individual’s family and are focused on in treatment. Family attitudes toward body shape, as well as any underlying conflicts, will be discussed. Typically, in family therapy, the therapist will work to get the individual out of the role of being a “sick” child and will work with the parents to confront their own issues and conflicts directly with each other and not through their children (Minuchin, Rosman, & Baker, 1978). One main goal is to get the family to work as a team to address the anorexic eating behaviors and to function better as a family unit in general. Whereas some studies note that family therapy appears to be one of the more successful treatment modalities for anorexia nervosa (Dare & Eisler, 2002; Lock & le Grange, 2005), many therapists will use this modality in combination with individual and group therapy as well as self-help groups.

Cognitive-Behavioral Therapy Cognitive-behavioral therapy (CBT) is often used in conjunction with other techniques pre- viously mentioned to treat anorexia nervosa. Therapists may work with individuals to help them learn more appropriate ways to exercise control, as anorexia nervosa is often caused in part by an individual’s wanting to feel in control. The individual’s attitudes about food, eating, and weight would also be examined in therapy. Typically these individuals view food as an enemy. Therapists would work on what are called faulty cognitions, sometimes called irra- tional beliefs. These are irrational or false beliefs that result in self-defeating behavior(s) that the person demonstrates. The individual’s cognitions are so faulty that they obscure the truth; thus, the individual believes in the falsehoods. Individuals’ self-esteem ends up even more damaged and self-destructive behaviors become entrenched (see, for example, Fair- burn & Cooper, 2014; Lask & Bryant-Waugh, 2000; McFarlane, Carter, & Olmsted, 2005).

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Psychotropic Medications Many professionals agree that medications should not be used in the treatment of anorexia nervosa because they tend to be rather ineffective (Watson & Bulik, 2013). Since many of these individuals are severely underweight, potential medication side effects could be more pronounced, leading to significant complications. Being malnourished or severely under- weight can change the amount of medicine in the individual’s body. Too much or too little can be dangerous. For example, tricyclic antidepressants (TCAs) may lead to heart arrhythmias, which can lead to cardiac arrest. In fact, antidepressants, in general, seem to be ineffective in treating anorexia nervosa (Suárez-Pinilla et al., 2015).

Treatment of Bulimia Nervosa The treatment of bulimia nervosa has been shown to have about a 40% success rate, defined as (a) eliminating or greatly reducing the cycle of binging followed by inappropriate compen- satory behavior, (b) eating normally, and (c) maintaining a normal weight for the individual’s height and age (Isomaa & Isomaa, 2014). Isomaa and Isomaa (2014) also noted that in follow-up research years after treat- ment ended, up to 85% of those with buli- mia nervosa have either fully or partially recovered. Approximately 30% to 50% will experience relapse (MacDonald, McFarlane, Dionne, David, & Olmsted, 2017). Treat- ment for bulimia nervosa is evidently much more effective than treatment for anorexia nervosa. There are two possible reasons for this. First, because bulimia nervosa is more common, more research has been done on its possible treatments. Antidepressants, especially the selective serotonin reuptake inhibitors (SSRIs) like fluoxetine (Prozac) and sertraline (Zoloft) may reduce and/or eliminate the symptoms, especially when combined with CBT (Bernacchi, 2017; Starr & Kreipe, 2014). Second, treatment is more effective because, unlike in anorexia ner- vosa, death due to bulimia nervosa remains relatively rare (Keel & Mitchell, 1997).

The most pressing goal of treatment for bulimia is to extinguish the binge/purge cycles and to reestablish good eating habits, working under the assumption that, at one point, the indi- vidual exhibited healthy or “normal” eating habits. The long-term goal is to examine, and perhaps bring to the surface of the conscious mind, the root causes of the individual’s bulimic behaviors.

callum redgrave-close/iStock/Thinkstock Antidepressants have shown positive results in reducing or eliminating the symptoms of bulimia nervosa.

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Behavioral Therapy Typically, behavioral techniques are used in conjunction with other therapeutic techniques such as cognitive methods and supportive techniques (Bernacci, 2017). A common technique is to ask patients to keep a food diary, which documents their daily meals, what they eat, and any changes they note in their feelings of hunger or fullness. The most important result of keeping a food diary is that it allows patients to objectively look at their eating patterns and behaviors, something that many individuals with bulimia do not (or perhaps cannot) do. In addition, and perhaps more important, this method allows individuals to recognize emo- tional eating. In other words, are any emotions triggering an eating binge, and do individuals eat as a result of an uneasy emotion, or because they are truly hungry?

Cognitive-Behavioral Therapy Cognitive-behavioral therapy focuses on teaching ways to resist the binge/purge impulses and notice the warning signs (Wilson, 2005). Christopher Fair- burn (1985), a major researcher in the field of buli- mia, created a three-step approach to treat bulimia nervosa that has been successful and is often used by today’s helping professionals. The main goal in the three-step approach is to look at individu- als’ eating behavior and to have them look at the consequences of binging. The helping professional examines the physical consequences of binging and purging with the patients and helps them under- stand how ineffective it is to use laxatives or vomit to control their weight. Dieting, especially extreme diets where the daily caloric intake is severely reduced, is also examined in either therapy or edu- cational sessions. These can occur individually or in groups. Next, an eating plan is set up in which many small meals are eaten each day, with no more than three hours between any meals. This planned eat- ing schedule will eliminate the bouncing back and forth between periods of overeating and purging, or restriction, that occur with bulimia nervosa (Fair- burn, 1985).

Next, the helping professional will examine the dysfunctional cognitions, or beliefs, that the individuals have about their appearance and dieting behaviors. Cognitive restructuring, helping patients to recognize and change negative thoughts that lead to binging and subse- quently purging, may be used at this point. The helping professional works with the individu- als to assist them as they discover these irrational thoughts and make plans to change these negative self-statements. Goals include raising the individuals’ self-esteem and helping them realize that they cannot be perfect all of the time.

Stockbyte/Stockbyte/Thinkstock Keeping a food diary allows individuals with bulimia to track patterns in their eating habits, which in turn can help uncover the source of the individuals’ bulimic behaviors.

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Finally, the helping professional will prepare patients for potential relapses and how to han- dle them. They will also work with patients to help them develop realistic beliefs and expec- tations about eating and weight-related issues. Research has demonstrated that these tech- niques lead to the elimination of bulimic symptoms in at least one third to as many as two thirds of individuals with the disorder (Agras, Walsh, Fairburn, Wilson, & Kraemer, 2000; Mitchell et al., 2002; Poulson et al., 2014).

Interpersonal Therapy Interpersonal therapy (IPT) may also be an effective treatment modality. IPT focuses on the individual’s current relationships, with particular focus on the family during weekly sessions over four to six months. Communication and problem-solving skills are worked on in order to improve individuals’ interpersonal relationships, and the focus is on what in their relation- ships led to the onset, maintenance, and relapse of bulimia nervosa (Bernacci, 2017; Kass, Rosenthal, Pottackal, & McGann, 2013; Tanofsky-Kraff, Shomaker, Young, & Wilfley, 2016). This therapeutic modality does not focus on the individual’s maladaptive eating behaviors but instead focuses on reducing interpersonal conflicts, especially within the individual’s family.

Psychotropic Medications Research has shown significantly positive outcomes for the use of antidepressants in treating bulimia nervosa (Hay & Claudino, 2012; Starr & Kreipe, 2014). The antidepressants typically used are SSRIs such as fluoxetine (Prozac), which have fewer side effects than others, increas- ing the likelihood of medication compliance. Prozac is the only medication approved by the FDA to treat the binges and inappropriate compensatory behaviors (specifically, purges) of bulimia nervosa. Other SSRIs, such as sertraline (Zoloft), also have proven to be effective.

Treatment of Binge-Eating Disorder A crucial component of making sure that individuals who diet do not regain the weight is to stop the binge eating (see, for example, Fisher et al., 2014). Cognitive-behavioral therapy and interpersonal therapy have both proved to be rather successful in treating BED (Amianto, Ottone, Daga, & Fassino, 2015; Brownley et al., 2016; Fisher et al., 2014; Grilo et al., 2014). Interestingly, using self-help procedures appears to be ineffective in the long-term in treating BED; more effective interventions are required (Fairburn & Murphy, 2015; Grilo et al., 2014). These results were similar to those for subjects who were in therapy groups. Another inter- esting study measured the effectiveness of Prozac in treating BED. Four experimental groups were formed: Prozac alone, placebo, CBT and Prozac, and placebo and CBT. Prozac alone, when compared with placebo alone, showed no significant difference in eliminating BED. When CBT was used in conjunction with Prozac and with placebo, both treatment modalities were more successful than Prozac alone or placebo alone. In fact, 73% of the subjects did not binge for one month after treatment concluded, which the researchers defined as remission (Ramacciotti et al., 2013). So, one can conclude that adding Prozac to CBT does not make the overall treatment more effective. (See Part 4 of Paula Ames’s case in the appendix.)

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Chapter Summary

A more recent treatment modality for BED is the use of lisdexamfetamine dimesylate (Vyvanse), a stimulant used to treat attention-deficit/hyperactivity disorder in children aged 6 years or older and adults. It was approved to treat BED in 2015. Common side effects are dry mouth, constipation, insomnia, and increased heart rate. Since Vyvanse is a stimulant, there is the potential for abuse and/or dependence. Interestingly, the anticonvulsant topira- mate (Topamax) has been found to reduce binge-eating episodes. Possible side effects include dizziness and kidney stones. Since Topamax is not an FDA-approved treatment for BED, if prescribed it will be off-label. This means that the psychiatrist can legally prescribe Topamax, but it has not been FDA approved to treat the condition for which it is being prescribed. What are your views on off-label prescribing?

Chapter Summary

Sleep Disorders • The two main types of sleep disorders are the dyssomnias and the parasomnias. • Insomnia disorder is characterized by a difficulty falling asleep, maintaining sleep,

or not feeling rested after normal amounts of sleep. • Narcolepsy, a rare condition, is marked by sudden and repeated “attacks” of dream

state (rapid eye movement, or REM) sleep that will also be accompanied by a brief loss of muscle tone, called cataplexy.

• In obstructive sleep apnea hypopnea, the individual may stop breathing for as long as 30 seconds many times during the night. This may occur hundreds of times dur- ing the night, and the victim is unaware that this is occurring.

• The parasomnias are characterized by sleep disturbances that result from unusual or abnormal events that occur during the night.

• Non–REM sleep arousal disorder, sleep terror type, which typically affects children and usually disappears in adolescence, is not related to nightmares, as sleep terrors occur during non-REM sleep.

• Non–REM sleep arousal disorder, sleepwalking type (called somnambulism when it is repeated), is primarily a childhood disorder, occurring during NREM sleep, that disappears around age 15.

Etiologies of Sleep-Wake Disorders • Causes of insomnia may include a failure of the body temperature to drop enough for

the individual to fall asleep; drug and alcohol use; changes in light, noise, or temper- ature; stressful events occurring during the day; fatigue; or a misperception of how much sleep is needed or of how disruptive interrupted sleep can be.

• Some of the sleep-wake disorders, including narcolepsy, run in families; however, this cannot be considered a causal factor.

• Sleep apnea may be associated with trauma.

Treatment of Sleep Disorders • The most commonly used treatment for insomnia is medication, specifically the ben-

zodiazepines (Dalmane) or related medications (such as Ambien). However, negative effects of benzodiazepines include excessive sleepiness and dependence.

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• Short-acting drugs are often the preferred medication choice as they will have stopped working by morning and will not produce daytime drowsiness.

• Stimulants are often prescribed for narcolepsy or hypersomnia. • For breathing-related sleep disorders, such as obstructive sleep apnea hypopnea,

weight loss is often strongly recommended. • Mechanical devices to improve breathing during sleep typically have little success

because of the discomfort they produce. • Simple environmental treatments include making bedtimes several hours later than

normal or using bright light to fool the brain into thinking it’s earlier. • Progressive relaxation techniques have been used with a limited amount of success. • Stimulus control techniques, limiting bedroom activities to sleeping and having sex,

have been used with greater success. • Establishing a good sleep hygiene program is also effective. • One method used to eliminate sleep terrors is scheduled awakenings.

Eating Disorders • People with eating disorders suffer from extreme disturbances in eating behavior

caused by an obsessive and irrational fear of gaining weight. • The individual may have an obsessive and irrational fear of gaining weight (anorexia

nervosa), or may be obsessed with maintaining their weight by binging and then using an inappropriate compensatory behavior to prevent weight gain (bulimia nervosa).

Anorexia Nervosa

• Anorexia nervosa, a condition that can be quite lethal and appears most often in women, is defined as an eating disorder in which the individual refuses to maintain proper body weight and weighs less than the minimally normal amount for their height and age.

• Individuals with anorexia nervosa have an intense fear of gaining weight or becom- ing fat even though they are severely underweight, and they deny the seriousness of the problem or cannot properly perceive how their bodies appear.

• Anorexia nervosa has two subtypes: the restricting type, characterized by the indi- vidual (during the current episode) not regularly engaging in binge-eating or purg- ing behavior, and the binge-eating/purging type, characterized by the individual (during the current episode) regularly engaging in binge-eating or purging behavior.

Bulimia Nervosa

• In bulimia nervosa, individuals binge eat and then expel the food from their bodies, either through purging or nonpurging behavior.

• Binging is characterized by individuals eating an amount of food during a certain period of time that is significantly larger than what most would eat during that time period and under similar circumstances, and by those individuals feeling as though they lack control over their eating binges.

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Binge-Eating Disorder (BED)

• In binge-eating disorder (BED), the individual binges without using compensatory behaviors.

Etiologies of Eating Disorders • One sociocultural factor associated with eating disorders that has been investigated

is Western values and the influence of Western media on what should be the ideal body type.

• Psychological causal factors that have been researched include control issues, a lack of interoceptive awareness, separation problems from the family, and body dissatis- faction issues.

• Biological causal factors that have been investigated include improper serotonin levels, among other hypotheses.

Treatment of Anorexia Nervosa • In treating anorexia nervosa, the immediate goal is to get affected individuals to gain

back a certain amount of weight and to attempt to normalize their eating patterns. • Interpersonal therapy, ideally using the family therapy modality, is also used, and

cognitive-behavioral techniques seem to be somewhat successful. Medications are not recommended for treating anorexia nervosa, as none has been proven successful.

Treatment of Bulimia Nervosa • The most pressing goal in treatment is to extinguish the binge/purge cycles and to

reestablish good eating habits. • The long-term goal is to examine, and perhaps bring to the surface of the conscious

mind, the root causes of the individual’s bulimic behaviors. • Standard modalities for treating bulimia include individual and family therapy, spe-

cifically cognitive-behavioral therapies and interpersonal behavior therapies. • Antidepressants, specifically the SSRIs Prozac and Zoloft, have been proven to be

quite successful in reducing the binge/purge cycles. • Tricyclic antidepressants (TCAs) have also proven to be effective, but their side-

effect profiles (and the potential for a lethal overdose) do not warrant their usage in lieu of SSRIs.

Treatment of Binge-Eating Disorder • Cognitive-behavioral therapy and interpersonal therapy have been successful in

treating BED. • Self-help procedures have not proven to be effective in the long term.

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Chapter Summary

Key Terms anorexia nervosa An eating disorder in which the individual avoids consuming food due to an unrealistic fear of gaining weight, even though the individual is seriously underweight at present. It literally means “nervous loss of appetite.”

avoidant/restrictive disorder A feeding disorder characterized by inadequate eating.

binge eating Eating within a specific time period an amount of food that is significantly larger than most people would eat during that time period under similar circum- stances; may range from 6,000 to upwards of 10,000 calories at one sitting.

binge-eating disorder (BED) Involves binging episodes similar to those found in bulimia nervosa but without the inappropri- ate compensatory behaviors (e.g., purging, self-starvation).

binge-eating/purging type A subtype of anorexia nervosa characterized by the indi- vidual, during the current episode, regularly engaging in binge-eating or purging behav- ior (that is, self-induced vomiting or the misuse of laxatives, diuretics, or enemas).

body image How an individual thinks he or she appears to others.

breathing-related sleep disorders An illness caused by sleep-related breathing difficulties that lead to excessive sleepiness or insomnia. These disorders are subdi- vided into obstructive sleep apnea hypop- nea, central sleep apnea, and sleep-related hypoventilation.

bulimia nervosa An eating disorder char- acterized by the individual’s eating and then expelling the food from the body. The indi- vidual is deathly afraid of gaining weight. It literally means “hunger of an ox.”

cataplexy A brief loss of muscle tone that often accompanies narcolepsy.

Critical Thinking Questions

1. A common treatment modality for insomnia disorder is prescribing medications to help the individual fall asleep. One problem with these medications is that it is rela- tively easy to become addicted to them. Discuss your views on using medications to treat insomnia disorder, noting both positive and negative outcomes of using them.

2. Some of the parasomnias, like non–REM sleep arousal disorder with sleep terrors and non–REM sleep arousal disorder with sleepwalking, tend to disappear by adult- hood. Discuss and explain some of the possible reasons for this.

3. Anorexia nervosa is a difficult disorder to comprehend. Give your perspective on what might cause adolescents to starve themselves to the point of death (in some instances), and discuss the most effective treatment methods for anorexia nervosa.

4. Bulimia nervosa is easier to understand and to treat than anorexia nervosa, and it is also more common. What might some of the reasons be for these differences?

5. BED is a new diagnosis in the DSM–5. Describe and discuss some reasons why BED is now a DSM–5 diagnostic category.

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central sleep apnea The occurrence of, minimally, five or more central apneas per hour of sleep.

circadian rhythm sleep-wake disorders A series of sleep-wake problems in which the individual has difficulty sleeping at the times required for their work, school, or other aspect of their lives.

cognitive restructuring A technique psy- chologists use to help their patients recognize and change negative thoughts that lead them to binge and subsequently purge, or to engage in other self-destructive behaviors.

continuous positive airway pressure (CPAP) A machine used in sleep apnea therapy. By delivering enough air pressure to a face mask, it keeps the upper airway pas- sages open while the user is asleep.

diuretics Medications that increase urination and therefore have a tendency to dry someone out and perhaps lead to weight loss.

dyssomnias Irregularities or abnormali- ties in the amount, quality, or timing of sleep. Included in this category are disor- ders initiating or maintaining sleep, which includes nighttime wakefulness, or excessive sleepiness.

eating disorders Illnesses that occur when an individual suffers extreme disturbances in eating behavior caused by an obsessive and irrational fear of gaining weight.

faulty cognitions Sometimes called irrational beliefs, these are irrational or false beliefs that result in self-defeating behavior(s), which can lead to self-destruc- tive or maladaptive behaviors.

food diary A written record of a patient’s daily eating habits, food intake, and so on, that is to be shared with a clinician on a weekly basis. Ideally the food diary will also include binges, purges, and the patient’s feelings when he or she eats.

hypersomnolence disorder A sleep-wake disorder characterized by excessive sleepi- ness even though the individual may have slept at least seven to nine hours.

inappropriate compensatory behav- iors Behaviors designed to counterbalance and counteract the effects of an eating binge. They are designed to ensure that the indi- vidual with bulimia does not in fact gain any weight; they also serve to help the individual regain self-control. The purging seems to alleviate any anxiety caused by the fear of gaining weight.

insomnia disorder An inability to sleep characterized by a difficulty falling asleep, maintaining sleep, or not feeling rested after normal amounts of sleep.

insomnia A disturbance in the amount, quality, or timing of sleep that occurs at least three nights per week for at least 3 months.

interoceptive awareness An individual’s awareness of his or her internal cues, includ- ing emotional states and hunger.

irrational beliefs Ways of thinking that can lead to self-destructive or maladaptive behaviors. One example would be the state- ment “I must be loved by everyone.” This is impossible, as no one person, real or ficti- tious, is loved by everyone.

narcolepsy A sleep disorder marked by sudden and repeated “attacks” of dream state (REM) sleep that will also be accom- panied by a brief loss of muscle tone, called cataplexy.

nightmare disorder The frequent occurence of extended and well- remembered dreams that usually have themes of avoiding threats to survival, secu- rity, and physical integrity. These dreams usually occur during the second half of a major sleep episode.

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Chapter Summary

nightmares Dreams that arouse feelings of intense fear, horror, and distress.

non–rapid eye movement sleep arousal disorder, sleep terror type A childhood disorder that occurs during NREM sleep. Sufferers experience sleep terrors and awaken screaming very loudly.

non–rapid eye movement sleep arousal disorders, sleepwalking type Primarily a childhood disorder that occurs during NREM sleep, typically during the first few hours of sleep. Affected individuals will usually leave their beds repeatedly during the night and walk around without being conscious of doing so or being able to recall doing so later once awake.

obesity Being minimally 30 pounds over- weight, as defined by the National Institutes of Health.

obstructive sleep apnea hypopnea A breathing-related sleep disorder during which the individual may stop breathing for as long as 30 seconds many times during the night.

orexin (hypocretin) A neurotransmitter that regulates and is involved with arousal, wakefulness, and appetite.

parasomnias Sleep disturbances that result from unusual or abnormal events that occur during the night.

pica A feeding disorder in which the indi- vidual will eat things such as dirt, laundry starch, and chalk.

polysomnography (sleep study) A test that records an individual’s brain waves, blood oxygen level, heart rate and breathing, as well as eye and leg movements in order to diagnose sleep disorders.

purge The elimination of all of the food that was consumed during a prior binge by an individual with anorexia or bulimia. It is only a purge if the food is somehow forced out of the body by inappropriate compensatory behaviors.

restricting type A subtype of anorexia ner- vosa characterized by the individual being meticulous, perhaps obsessive, about how much food he or she eats at a given time, and his or her caloric intake at each meal or on a daily basis. Such individuals do not regularly engage in binge-eating or purging behavior.

rumination disorder A feeding disorder marked by regurgitation of food.

sleep-related hypoventilation A sleep dis- order in which the individual has decreased respiration while asleep as demonstrated by elevated carbon dioxide levels; diagnosed by polysomnography.

sleep terrors A sleep disorder (but not a DSM–5 diagnostic category) that typically affects children and causes them to awaken with a frighteningly loud scream; the child will have a rapid heart rate, be very upset, and often be sweating profusely. Children do not recall sleep terrors.

somnambulism Recurrence of sleepwalk- ing episodes.

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5 Dissociative Disorders and Somatic Symptom and Related Disorders

Roman Barelko/Hemera/Thinkstock

Learning Objectives

After reading this chapter, you should be able to:

• Differentiate between dissociative and somatic symptom and related disorders.

• Describe what roles are played by unconscious thoughts and feelings in causing these disorders.

• Describe how helping professionals treat dissociative disorders.

• Differentiate among the different treatment methods, and theoretical perspectives, of dissociative identity disorder.

• Describe how helping professionals treat somatic symptom and related disorders.

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If anyone knows what it’s like to be paralyzed and still have feelings it’s me. I could use a few moments of oblivion. (Dr. Christian Troy to Dr. Liz Cruz, Nip/ Tuck)

Sigmund Freud believed that everyday memory lapses might be caused by the repression of troubling thoughts and feelings. By using examples from typical life situations, Freud hoped to demonstrate that repression is not an abnormal process but rather the ego’s routine way of defending itself against unacceptable thoughts and impulses. He maintained that every- day memory lapses and slips of the tongue obey the same psychological principles, and are explainable by the same theories, as psychological disorders. The difference between them is one of degree. Repression, a normal psychological process, causes a mental disorder when it becomes so pervasive that it interferes with either occupational or social functioning. This is consistent with one of the recurrent themes of this book—an acknowledgment of the conti- nuity between normal and abnormal behavior.

Over the years, theorists have challenged many of Freud’s views, but the idea that uncon- scious thoughts and emotions can produce psychological disorders still seems to prevail when it comes to the DSM–5 categories discussed in this chapter—dissociative disorders and somatic symptom and related disorders.

Although they are the most written about, and indeed fascinating, psychological disorders, we know surprisingly little about the etiology and treatment of the dissociative disorders and somatic symptom and related disorders. Dissociative disorders derive their name from their main symptom—the “disassociation” of the personality. (Dissociation here refers to the sepa- ration between the personality and the body. That is, the body is physically there while the mind is elsewhere.) Our personalities are the totality of our inner experiences and our behav- iors. Normally, the various parts of our personalities are glued together by our memories. In the dissociative disorders, our memories and sometimes our identities become detached (dissociated) from one another. We may forget the past or, in some cases, even who we are.

Somatic symptom and related disorders are marked by physical symptoms that mimic those produced by disease (somatic means “similar to the body”). They differ from the stress-related organic disorders discussed in Chapter 2 in that people with somatic symptom and related disorders have no obvious physical illness. Instead, the symptoms are viewed as physical manifestations of psychological (usually unconscious) problems. The absence of a physical illness also differentiates the dissociative disorders from organic brain disorders and syn- dromes that produce similar symptoms (these brain disorders are discussed in Chapter 10).

Although there are no obvious physical reasons for their symptoms, you should not conclude that people suffering from somatic symptom and dissociative disorders are deliberately fak- ing. People with dissociative disorders have real memory losses, and people with somatic symptom and related disorders really do believe that they are physically ill, are about to fall ill, or are physically deformed. People who intentionally pretend to be sick are classified as either malingering (pretending to be sick to avoid commitments or to gain some advantage) or suffering from a factitious disorder (in which people feign illness for no personal gain other than attention).

Following Freud’s early work, the dissociative and somatic symptom and related disorders were originally classified together as neuroses. The DSM–5 places them into separate chapters

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(as did the DSM–IV and DSM–IV–TR) because of their rather different clinical appearance. Here they are grouped together because of the apparent role played by unconscious processes in all three categories of disorder. Factitious disorder is also included because its superficial similarity to somatic symptom and related disorders presents clinicians with an important diagnostic challenge.

Let’s examine the case of Helen Fairchild, a woman whose lost past appears to have returned to haunt her.

The Case of Helen Fairchild: Part 1

Dr. Dorothy McLean’s Assessment and Preliminary Treatment Plan for Helen Fairchild Reason for Referral: Helen Fairchild was self-referred. She says that she is distracted, has no sexual desire, sometimes feels that life is not real, and has no memory of parts of her past.

Behavioral Observations and Brief History: Helen Fairchild, a 27-year-old female, reports feeling distressed for the past few months. Her husband of seven years left her three months ago and moved in with his administrative assistant. Helen says that she never had much interest in sex and found little enjoyment in intimacy. Since her husband left, Helen has developed recurrent stomachaches, dizziness, hot flushes, and headaches. She sought medical advice, but no physical cause was identified. Her family doctor prescribed painkillers for her headaches. She denies any illness or substance use.

Helen has found it difficult to concentrate and has been having trouble at work. She has not been completing tasks, has been missing appointments, and sometimes has missed whole days of work. On several occasions, she found herself driving in the country when she was supposed to be at work. On these occasions, she was unable to recall how she had gotten to the country or what she had done during the preceding hours. She finds this loss of memory distressing, especially since she also has few memories of her childhood. Sometimes she feels that life is not “real” and that she is simply “playing a role.” She says that she feels as if she is standing outside herself, watching herself go through the motions of everyday life.

Helen was carefully dressed and groomed. Although she seemed quiet, she was not weepy, nor did she seem particularly anxious. Although she was responsive to questions, she would lapse into silence and from time to time had to be prompted to respond. In general, she seemed to be a mildly depressed woman with a variety of physical complaints coupled with feelings of unreality and memory loss.

Diagnostic Considerations: Helen seems to be mildly depressed, but she also has distinct signs of dissociative disorders, such as depersonalization and amnesia. It is premature to make any specific diagnosis, but the following are possibilities:

Dissociative amnesia (rule out with dissociative fugue) Depersonalization/derealization disorder Somatic symptom disorder Major depressive disorder

(continued)

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5.1 Dissociative Disorders We will begin this section by examining amnesia (memory loss associated with psychologi- cal trauma) and fugue (when a person not only develops amnesia but also moves away from home and perhaps even adopts a new identity). We will then examine depersonalization/ derealization disorder. People with this disorder feel as if their body parts have changed in size, or they may have the impression that they are outside their bodies, viewing themselves from a distance. Finally, we will look at dissociative identity disorder, formerly known as mul- tiple personality disorder. In this disorder, two or more separate identities recurrently come forward to take charge of a person’s behavior. Each identity has its own characteristic person- ality, habits, and memories.

Amnesia and Fugue As Freud demonstrated, having memory slips is common. We all forget things: items on shop- ping lists, telephone numbers, birthdays, and anniversaries. However, when memory gaps are too great to blame on ordinary forgetfulness—when a person cannot recall important life events or even who she or he is, and when memory loss is associated with psychological trauma—then dissociative amnesia (psychogenic memory loss) may be suspected (Bailey & Brand, 2017).

There are two main types of amnesia. An inability to form new memories is known as antero- grade (forward) amnesia. Sufferers can remember events that occurred before a traumatic experience, but new events are forgotten shortly after they occur. For example, a person may remember everything that occurred before an automobile accident but not after the accident.

The Case of Helen Fairchild: Part 1 (continued)

No medical reason has been uncovered for memory loss, headache, and stomachache; could be signs of a somatic symptom disorder

Preliminary Treatment Plan: Before treatment progresses, Helen needs to be referred to a medical doctor. This is to rule out any possible neurological causes of her condition. Although Helen’s problems may be a reaction to her husband’s infidelity and abandonment, there are some troubling and puzzling aspects to this case. Helen has no interest in sex, and she has unexplained gaps in her childhood memories. She also seems to have “blank” periods when she cannot recall where she was or what she was doing. Putting these together, it may be possible that Helen has repressed sex-related childhood memories that have led her to fear sex. One possibility may be childhood sexual abuse. This would be consistent with her stomachache, which could be a “body memory” of what happened to her. Her dissociative symptoms may arise from the same source. Therapy will be targeted at uncovering evidence for such early abuse. Free association and hypnosis may help her to recover these memories. If such evidence is uncovered, Helen will be enrolled in a support group for trauma survivors. She will also need to confront her abuser.

See appendix for full case study.

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Each day, the person awakes believing that the accident took place the day before. Retrograde (backward) amnesia is exactly the opposite; events that took place before a traumatic event are forgotten. A person may not recall anything that happened before an automobile accident while remembering events that occurred after the accident. Almost all cases of dissociative amnesia are of the retrograde type.

In more severe cases, memory loss is generalized. Sufferers fail to recognize relatives and friends and cannot recall any details about their past before the traumatic event. Yet they still retain all their talents and abilities (they can still read, for example, or play the piano). Generalized retrograde amnesia occurs more frequently in Hollywood movies than in real life, but it is not entirely unknown in the clinic.

The DSM–5 also includes localized amnesia, when a person loses all memory of events that occur within a limited timeframe. When this kind of amne- sia occurs, it usually if not always happens after the individual experiences, directly or indirectly, a trau- matic, perhaps horrific event. In the HBO documen- tary Three Days of Terror: The Charlie Hebdo Attacks

(Reed & Hermann, 2015), one of the people interviewed who heard the cartoonists being massacred in the offices above stated that for many months he could not recall much about the events that occurred during that time. This forgotten period is called the amnestic epi- sode. The individual may have issues recalling the traumatic event but may be unaware of the memory problems. In the Charlie Hebdo case, things began to come to the survivor’s mind only after the documentary began filming. One could say that the mind was acting as a pro- tective device for the survivor so that he would not ruminate about the massacre. Localized amnesia is the most common form of amnesia.

Selective amnesia, the second most common form, occurs when the person remembers some, but not all, of the events that occurred during a particular timeframe. If the Charlie Hebdo survivor recalled the sounds of gunfire (which he did) as well as screams and then silence, but not more traumatic aspects and memories, this would be called selective amnesia.

In systematized amnesia, individuals lose memory for a specific category of information, such as all memories related to their family, aspects of when they were being abused as a child, aspects of a poor marriage, and so on (American Psychiatric Association [APA], 2013).

Finally, in continuous amnesia, forgetting continues into the present day and time. Survivors might not recall the actual events or, in the current example, what occurred before the terror- ists entered the Charlie Hebdo offices, but they might also not recall new experiences either.

When a person not only develops retrograde amnesia but also leaves home and adopts a new identity, the appropriate specifier is dissociative fugue. In extreme cases, a person may move to another town, assume a new name, start a new job, and even experience a change in personality. However, most fugues are not so dramatic. People do not begin entirely new lives; they simply wander away from home for brief periods (Loewenstein, 1991). The majority are

Imageegaml/iStock/Thinkstock Amnesia can affect memory in differ- ent ways. Retrograde amnesia affects a person’s ability to recall events prior to an amnesia-causing incident.

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soon found or return home on their own, claiming not to know why they left, where they had been, or what transpired in their absence (APA, 2013).

Distinguishing Amnesia and Fugue From Organic Brain Conditions Several types of brain damage can produce disorientation, flight, and memory loss. This is why it is vital to distinguish between organic brain conditions and the dissociative disorders. Unfortunately, this is not always easy. All of the symptoms associated with dissociative amne- sia and with dissociative fugue may also be produced by organic brain syndromes (Squire & Butters, 1992). To make matters even more complicated, brain injury and psychological trauma may go together. For example, a mugging or rape can easily result in both brain injury and psychological trauma.

Several clinical signs may help to distinguish organic from dissociative amnesia with dissocia- tive fugue: (a) Organic amnesias usually result from degenerative diseases that develop grad- ually, whereas dissociative amnesias come on suddenly; (b) organic amnesias are typically anterograde, whereas dissociative amnesias are almost always retrograde; (c) dissociative amnesia is associated with severe psychological stress; and (d) people with organic amnesias do not usually take on new identities. Sophisticated psychological and medical tests may be required to determine the cause of a memory loss and, even then, may sometimes produce vague results.

Etiology and Treatment of Amnesia and Fugue Because dissociative amnesia with dissociative fugue is rare, we did not initially know much about its family patterns and course (Pope, Poliakoff, Parker, Boynes, & Hudson, 2007). It seems to occur most often after a severe psychological trauma such as the death of a loved one, combat, or natural disasters such as an earthquake (McLeod, Byrne, & Aitken, 2004). However, more recent research demonstrated a clear link between childhood trauma and the development of dissociative symptoms in adulthood (Bailey & Brand, 2017). According to Dell (2017), 97% of the subjects who had dissociative identity disorder (discussed later in this chapter) reported an extensive history of childhood trauma. Many psychologists, irre- spective of their theoretical bent, view these and other forms of traumatic stress as the essen- tial cause of dissociative amnesia with dissociative fugue. Because of the close association between traumatic stress and dissociative symptoms, it is not surprising that amnesia and fugue frequently accompany posttraumatic stress disorder (as discussed in Chapter 2; Bailey & Brand, 2017).

A possible behavioral explanation for amnesia is derived from the notion of state-dependent learning (Bower, 1981; Dorahy & Huntjens, 2007; Sar, Dorahy, & Krüger, 2017). In a state- dependent learning experiment, participants learn different materials (two lists of words, for example) in two distinct mental states (say, one while sober and one while inebriated). Later, the participants are asked to remember words from each list while sober and again while inebriated. Typically, people in the sober state recall best the words they learned when sober and those in the inebriated state recall best the words they learned while inebriated. It would follow that the only way to recall these lost events is to once again subject the person to great stress. Clearly, this is an impossible hypothesis to test in any ethical experiment or treatment.

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The aim of psychoanalytic treatment is to help patients with dissociative amnesia with dis- sociative fugue to uncover the repressed material that caused them to lose their memories or wander off. Patients in psychoanalysis may be asked to free-associate, beginning with the last remembered events prior to the onset of amnesia or fugue. If this is not successful, they may be asked to tell their complete life stories in the hope that some retrieved memory might trig- ger the recall of relevant material (Fayek, 2002). In some cases, therapists may use hypnosis to uncover memories that are otherwise unavailable to consciousness.

Because they do not know that anything is wrong, people in fugue states rarely refer them- selves for treatment. Any treatment that does take place usually occurs after they recover their memories. For this reason, therapy for fugue is aimed at preventing future episodes. Cognitive and behavioral interventions, such as stress management and stress inoculation, may be particularly valuable because they provide people with more adaptive ways to cope with stress and conflict than by escaping their lives or forgetting who they are. (See Part 2 of Helen Fairchild’s case in the appendix.)

Depersonalization/Derealization Disorders In a depersonalization/derealization disorder, the sense of “self ” becomes dissociated from the rest of the personality. People with this disorder (previously called depersonaliza- tion disorder in the DSM–IV–TR) may believe that their hands and feet are too large or too small, or they may have the impression that they are outside their bodies viewing themselves from a distance. Sometimes they feel mechanical, as though they are robots. Derealization, the feeling that the world is not real or of living in a dream, is paired with depersonalization to form this current diagnosis.

Similar complaints may be found in people suffering from other psychological disorders. For example, people with schizophrenia may also complain that they are not “real.” In contrast to people with a depersonalization/derealization disorder, who realize that the world is still there and that they are not really robots, people with schizophrenia lose touch with reality. Some come to believe that they really are robots.

People who fall into trances during socially sanctioned religious or cultural rituals do not have a depersonalization/derealization disorder. However, a person who falls into a trance claiming to be “possessed,” and whose behavior differs markedly from that of other members of his or her culture, may well be suffering from a dissociative disorder.

Depersonalization/derealization disorder affects anywhere from about 0.8% of the U.S. pop- ulation (Johnson, Cohen, Kasen, & Brook, 2006) to as many as 2.8% of the population (APA, 2013). The lifetime prevalence is estimated at about 2% (APA, 2013). Depersonalization/ derealization disorder usually begins in the teenage years, and is associated with psychologi- cal trauma (APA, 2013); it also follows an unpredictable course, which waxes and wanes in response to life-stress.

We will next examine dissociative identity disorder, which combines elements of the other dissociative disorders. (See Part 3 of Helen Fairchild’s case in the appendix.)

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Dissociative Identity Disorder The modern era in the study of “multiple personality” began in 1908, when Morton Prince published The Dissociation of a Personality. Prince’s book was a biographical study of “Sally Beauchamp,” who consulted him because of headaches and blackouts. Under hypnosis, Sally revealed three personalities—the Saint, the Devil, and the Woman—each with individual feel- ings, tastes, and memories.

The popularity of the book The Three Faces of Eve (Thigpen & Cleckley, 1957), and the subsequent award-winning film, spawned a literary genre. Chris Sizemore, the real-life “Eve,” wrote her own book, A Mind of My Own (1989), in which she described a few more personalities not included in the movie. And this isn’t surprising given that personality infla- tion seemed to become characteristic of this disor- der. Each new patient seemed to present with more personalities than the last (Merskey, 1995).

Flora Rheta Schreiber (1975) described Sybil’s 16 alters, or alternative personalities, and Daniel Keyes (1981) catalogued Billy Milligan’s 24. As the number of personalities multiplied, some psycholo- gists became skeptical about their reality. As will be seen in this section, practically every aspect of dissociative identity disorder is the subject of intense controversy (Lalonde, Hudson, & Pope, 2002). (Sybil Exposed: The Extraordinary Story Behind the Famous Multiple Personality Case [Nathan, 2016] gives a different perspec- tive on this famous case, as you will see in the accompanying Highlight.)

20th Century-Fox Film Corp./Everett Collection The film The Three Faces of Eve por- trays the dissociative identity disorder of Chris Sizemore, the real-life Eve.

Highlight: Sybil: Fact or Fraud?

The case of Sybil Dorsett is indeed a fascinating one. Shirley Mason, the real Sybil, was the subject of Flora Rheta Schreiber’s 1973 best seller. The book was “pitched’ as the true story of a woman who suffered from dissociative identity disorder (called multiple personality disorder at that time). Within a few years of its publication, reported cases of multiple personality disorder increased geometrically, from fewer than 100 to thousands (Nathan, 2016). Shirley Mason grew up in the Midwest. Like many people, she had some emotional issues. At age 31 (in 1954), she decided to seek psychiatric help. Mason became unusually attached to her psychiatrist, Dr. Connie Wilbur, and she knew that Wilbur had a special interest in multiple personality disorder. According to Nathan (2016), Mason felt that she was not getting the proper attention from Wilbur.

During one of the sessions Mason said that she was Peggy, an alter, and started to act as though she had a number of different people inside of her. Wilbur believed that she had a noteworthy case, so she began seeing Mason frequently. Most important, she met up with Flora Rheta Schreiber to work on a book about Mason. As the sessions continued, Mason

(continued)

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Diagnosis of Dissociative Identity Disorder The main DSM–5 criteria for the diagnosis of dissociative identity disorder are summarized in Table 5.1. In dissociative identity disorder, each identity has its own characteristic personality, habits, and memories. When a particular identity is in control, the person acts accordingly— quiet when a shy personality is dominant, outgoing and brash when an extroverted person- ality is in control. One personality may be aware of the other’s existence, but more often, a personality is unaware of what is happening when another personality is in control.

Highlight: Sybil: Fact or Fraud? (continued)

became increasingly dependent on Wilbur for emotional and financial support. Due to transference, perhaps, Mason wanted to give Wilbur what she wanted. Wilbur began injecting Mason regularly with sodium pentothal (Pentothal), which was then being used to help people remember traumatic events that they had repressed. Under the influence of drugs and hypnosis, Mason uncovered her many personalities (Nathan, 2016).

Schreiber knew that Mason’s story was not entirely true and that Mason and Wilbur exaggerated details and even lied about some situations. Schreiber had a deadline and a contract and needed to complete the book. Schreiber panicked, since she was fearful that Mason had been lying, but it was too late to rescind the contract. Mason wrote a letter to Wilbur that Nathan found, stating that Mason was lying about all of the alters. Wilbur was too heavily invested in Mason to let her go and basically was “stuck,” as Mason’s story had ballooned out of control. Schreiber’s book was published in 1973. It sold 6 million copies and, in 1976, was made into a TV movie. People began to recognize Mason as the patient portrayed in the book and the film. She fled her life and moved into a home near Wilbur. She lived out of the spotlight until her death in 1998.

What is your perspective on Mason? Do you believe that she faked all of her alters to gain more attention from Wilbur? Is this “normal”? What are your views on Wilbur’s use of sodium pentothal? Could you see how Wilbur and Schreiber got “caught up” in the lies and got “stuck”? Knowing this, have your views on dissociative identity disorder changed?

Table 5.1: Main DSM–5 diagnostic criteria for dissociative identity disorder

A. Disruption of identity characterized by two or more distinct personality states, which may be described in some cultures as an experience of possession. The disruption in identity involves marked discontinuity in sense of self and sense of agency, accompanied by related alterations in affect, behavior, consciousness, memory, perception, cognition, and/or sensory-motor functioning. These signs and symptoms may be observed by others or reported by the individual.

B. Recurrent gaps in the recall of everyday events, important personal information, and/or traumatic events that are inconsistent with ordinary forgetting.

C. The symptoms cause clinically significant distress or impairment in social, occupational, or other impor- tant areas of functioning.

D. The disturbance is not a normal part of a broadly accepted cultural or religious practice. Note: In children, the symptoms are not better explained by imaginary playmates or other fantasy play.

E. The symptoms are not attributable to the physiological effects of a substance (e.g., blackouts or chaotic behavior during alcohol intoxication) or another medical condition (e.g., complex partial seizures).

Source: APA (2013, p. 292).

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Clinicians have claimed that alters can also differ physiologically: in handedness, visual acu- ity, blood pressure, autonomic arousal, and even in the illnesses they suffer (Sar et al., 2017). If such claims were true, they would give considerable force to the idea that different person- alities can inhabit the same body. In reality, the evidence for physiological differences among alters is vague at best (Miller & Triggiano, 1992). A 2006 study did find that the two electro- encephalograph (EEG; brain scan) records of one subject (alter 1 versus alter 2) were more different from one another than the two EEG records of a single control, but less different from one another than the EEG records of two separate controls. Most of the EEG variability between alters involved beta activity in the frontal and temporal lobes (Lapointe, Crayton, DeVito, Fichtner, & Konopka, 2006). It is more objective to say that people with dissociative identity disorder act as if their bodies are inhabited by several personalities. Also, note that a diagnosis of dissociative identity disorder requires the multiple personalities to persist over time. A temporary incident, or one brought on by substance abuse, does not qualify.

In addition to using the formal DSM–5 criteria to make a diagnosis, clinicians look for telltale signs that may signal the possibility of a dissociative identity disorder (Kluft, 1987; Putnam, 1989). For example, people who report finding letters in their own handwriting that they cannot remember writing and who complain of headaches and blackouts (as did Sally Beau- champ and Eve) may be harboring more than one personality. People who refer to themselves by different names or call themselves “we” are also suspect. Keep in mind, however, that the habit of using different names for different personalities is sometimes the result of a thera- pist’s suggestion (Kihlstrom, 2005).

The symptoms of dissociative identity disorder overlap those produced by other disorders, including schizophrenia (Putnam, 1997). Diagnostic instruments have been developed to aid diagnosis, but their validity is difficult to establish (Cardena, 2008). Still, dissociative identity disorder appears to be the most appropriate diagnosis in certain cases.

Is Dissociative Identity Disorder Becoming More Common? Dissociative identity disorder is usually diagnosed first in adolescence or early adulthood, although it may sometimes begin in childhood. It appears to be equally common in women and in men (APA, 2013), and the incidence of the disorder (the number of new cases that appear during a given period of time) has been rising since the 1940s. A review conducted in the 1940s found that only 76 cases had ever been reported in the literature (Taylor & Martin, 1944). By 1970, the number of published cases had grown to 100. The number reached 200 in the mid-1970s, 300 by 1980, and by the 1990s, cases in the thousands appeared (Kluft, 1991). The best estimate today is that in the United States dissociative identity disorder affects about 3.5% of psychiatric inpatients, about 2% to 3% of psychiatric outpatients, and 1% to 1.5% of the general population (Sar et al., 2017). (See the accompanying Highlight.)

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The reason for the high, and apparently increasing, incidence of dissociative identity disorder in the United States is not entirely clear. Freud originally attributed dissociative disorders to childhood sexual abuse. He saw them as ways to repress childhood traumas. However, Freud’s belief that his patients were sexually abused as children was abhorrent to his contemporaries, who pressured him considerably to retract the theory. Eventually, he took back his original theory and replaced it with the idea that children “fantasize” about sexual activity. C. A. Ross (1997) suggests that Freud may have been correct the first time around; sexual abuse is com- mon, and it does produce mental disorders, especially dissociative identity disorder. The ini- tial low number of dissociative identity disorder cases may have been due to a reluctance of clinicians to diagnose them rather than a low incidence of the disorders in the population. In other words, it is possible that Freud and other therapists avoided making the diagnosis of dissociative identity disorder because they simply did not want to accept the prevalence of the sexual abuse of children.

Ross’s theory has several virtues, perhaps the most important one being that there does seem to be a connection between dissociative identity disorder and childhood sexual abuse, which may lead to repression (Ross, 1997; Wang & Jiang, 2007). Nevertheless, there are other pos- sible explanations for the apparent increase in prevalence. High on the list are the continually changing diagnostic criteria (APA, 2013; Welburn, Fraser, Jordan, Cameron, Webb, & Raine, 2003). For example, although the DSM–IV–TR made, and the DSM–5 makes, a clear distinc- tion between dissociative identity disorder and schizophrenia, this has not always been the

Highlight: How Common Are Dissociative Experiences?

Probably more common than you think! Many people, according to one study (Steinberg & Schnall, 2000), see having a dissociative experience as a normal response to a stressful situation (parents divorcing, sexual assault, war, and so on). Johnson et al. (2006) found that in their nonclinical sample of 658 individuals, 9.1% had a dissociative disorder. There was no difference based on gender. Perhaps more important, Johnson et al. (2006) found that dissociative disorders have comorbidity with anxiety, depressive, and personality disorders. The dissociative experiences can be fleeting or more permanent. Although 9.1% of a nonclinical random sample seems like a large number, based on the statistical frequency model discussed in Chapter 1, anyone who has or had a dissociative experience would be diagnosed. However, as you can see, the people dealing with normal stressful situations still are in the statistical minority.

Making dissociative disorders more real and true can help people to understand the importance of getting a break from stressful events. In addition, the more that solid research is conducted on dissociative identity disorder, the faster an efficacious treatment will be discovered.

If you had a dissociative experience, how would you react? Would you see this as a cry for help, or as a manifestation of a mental disorder? Some people say these experiences are a means to cope with traumatic experiences. What do you think?

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case. Blackouts, memory lapses, and feeling under the control of another person are all com- mon among people with schizophrenia (APA, 2000, 2013; Getzfeld, 2006). It is possible that some people who meet today’s DSM–5 diagnostic criteria for dissociative identity disorder would have been diagnosed with schizophrenia in the past (Turkington & Harris, 2001). As the schizophrenia diagnosis became more precise, people who formerly fell into that cate- gory were given the diagnosis of dissociative identity disorder instead, thereby increasing its incidence.

There does seem to be a modern tendency to look for multiple personalities. Putnam (1992), for example, argues that Anna O. was not suffering from “hysteria,” as Breuer and Freud believed, but was really a case of dissociative identity disorder. Others believe that Anna O. was suffering from bipolar disorder or a grief reaction brought about by her father’s termi- nal illness (Borch-Jacobsen, 1996). It pays to be suspicious about this rush to find multiple personalities. Books and movies such as The Three Faces of Eve provide an easily accessible script for anyone who wants to assume the role of a person with a dissociative identity disor- der. As already noted, clinicians may unwittingly reinforce such role playing by encouraging people to give names to their various personalities and then by addressing each one by name (Kihlstrom, 2005).

Etiology and Treatment of Dissociative Identity Disorder Although they differ in detail, all schools of psychology attribute dissociative identify disor- der to traumatic experiences. As already noted, these experiences often involve physical and sexual abuse, as well as psychological and emotional abuse, usually by an attachment figure such as the mother or father, or the primary caregiver (Sar et al., 2017). According to psy- choanalytic theory, these anxiety-producing memories are successfully repressed, and a new personality is created to take “responsibility” for all of the “forgotten” feelings and memories (Turkington & Harris, 2001).

Not everyone who is abused as a child develops a dissociative identity disorder, however, so other factors must be involved. Eugene Bliss (1986) has suggested that one such extra factor is a susceptibility to “self-hypnosis” (the ability to put oneself into a hypnotic state). Bliss stated and believed that dissociative identity disorder is an example of the individual self-hypnotizing in order to cope with childhood abuse (Dell, 2017). We know that hypnosis can be used to induce forgetting in suggestible people, and we also know that people with dissociative identity disorder are highly suggestible and easily hypnotized. Putting the two together, it is possible that people prone to dissociative identity disorder hypnotize them- selves into forgetting painful memories (Sar et al., 2017). An alternate personality is created to protect the abused child from direct involvement with sexual abuse. Future psychological problems are dealt with by creating additional personalities.

Psychodynamic therapy is devoted to helping people lift their repression and “work through” conflicts associated with early trauma. In the past, this has meant picking one of the person- alities and focusing on that personality’s memories.

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To avoid the continued spawning of personalities, modern treatments attempt to fuse a per- son’s various personalities into a single one (called fusion), typically while using hypnother- apy (Howell, 2011; Kluft, 2001). The hope is that the various personalities will become one when they share the same memories. The new whole personality can then be taught to cope with anxiety in ways other than by forming new personalities. There can be resistance to fusion, as some patients’ alters might see fusion as a form of death (Howell, 2011). Some clini- cians note that fusion has a high success rate (Dorahy et al., 2014; Howell, 2011).

Drugs may also be used to treat dissociative identity disorder. For example, because there is a high degree of comorbidity between dissociative identity disorder and other psychological problems, particularly depression and anxiety, antidepressants and antianxiety medications are often prescribed. Using drugs to get people to reveal matters that they would otherwise keep to themselves is as old as recorded history. The Latin proverb in vino veritas (wine brings truth) is but one example. Like alcohol, the barbiturates sodium amytal (Amobarbital) and sodium pentothal (Pentothal) release inhibitions, allowing people to reveal memories that would otherwise remain repressed. Unfortunately, such memories may be state dependent and forgotten once the drug wears off. Also, we cannot assume that drug-induced memories are always accurate.

Behaviorists view dissociative identity disorder as an extreme form of normal behavior. Each of us displays different behaviors and moods in different situations. These various roles and moods are elicited by environmental stimuli, but, in dissociative identity disorder, certain stimuli produce exceptionally dramatic changes in behavior and mood. For example, a person may behave in a hostile fashion whenever a police officer is present, even if the officer pres- ents no threat. Such a person may appear perfectly happy and at ease yet suddenly become belligerent and hostile when the police officer appears. The dramatic change makes it appear as if the person has more than one personality. Although plausible, this explanation seems oversimplified. For example, it does not explain why one personality is often unaware of the existence of an alter.

Although the behavioral explanation for dissociative identity disorder seems inadequate, behavioral treatment may still be useful. For instance, teaching people with dissociative iden- tity disorder coping skills to help them deal with stress could reduce their need for alters. Behavioral therapists also use positive reinforcement to encourage clients to display their healthiest personality (Cronin et al., 2014; Kohlenberg, 1973).

The many theories and cases we have discussed suggest a highly variable outcome. In some cases, dissociative identity disorder may last for years and be highly resistant to treatment (Coons, 1986), whereas in other cases considerable progress can be made (Coons & Bowman, 2001; Dorahy et al., 2014; Howell, 2011; Kluft, 2001). Treatment is less likely to be success- ful the longer a dissociative identity disorder exists; therefore, the individual is less likely to recover without treatment (Maldonado & Spiegel, 2003). Consequently, early diagnosis and intervention are recommended to prevent a more resistant condition from developing. (Does Helen Fairchild have dissociative identity disorder? See Part 4 of Helen Fairchild’s case in the appendix.)

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Section 5.2 Somatic Symptom and Related Disorders

5.2 Somatic Symptom and Related Disorders The DSM–5 describes five somatic symptom and related disorders: somatic symptom dis- order, illness anxiety disorder, conversion disorder (functional neurological symptom disor- der), psychological factors affecting other medical conditions, and factitious disorder. Two broader categories are also included in the DSM–5 chapter: other specified somatic symptom and related disorder, and unspecified somatic symptom and related disorder (APA, 2013). As you will see, there are important differences among these disorders, but there is also a general unifying theme—all of the somatic symptom and related disorders are construed as physical manifestations of psychological (usually unconscious) problems (Phillips, Fallon, & King, 2008).

Somatic Symptom Disorder Somatic symptom disorder, along with illness anxiety disorder, used to be grouped under a single category, hypochondriasis. People who suffer from somatic symptom disorder become extremely distressed by, and have their lives disrupted by, bodily (somatic) symp- toms they experience. Sometimes the symptoms have a known cause and sometimes they do not. Regardless, the person’s worries and concerns are out of proportion to the seriousness of the bodily issue (for example, thinking the slightest pimple is cancer or that a momentary cough means tuberculosis). The person also has a significant amount of anxiety about his or her health and symptoms and spends an excessive amount of time and energy focusing on these symptoms or health issues. These issues must last at least six months before a diagno- sis can be made (APA, 2013). If the individual’s symptoms predominantly involve pain, the diagnosis is specified as with predominant pain. The predominant pain pattern seems to be somewhat common, and it occurs more commonly in women than in men (Nickel, Ademmer, & Egle, 2010). This pattern usually occurs after an accident or an illness that causes signifi- cant genuine pain.

Illness Anxiety Disorder As mentioned previously, illness anxiety disorder, along with somatic symptom disorder, used to be known as hypochondriasis. People with illness anxiety disorder are always anxious about their health. Either they are obsessive about health-related behaviors (for example, checking their heart rate every minute, taking their temperature on the hour, or repeatedly checking their body for signs of illness), or they demonstrate extreme unhealthy avoidance (avoiding doctor’s appointments or hospitals). These individuals persist in their misinter- pretations no matter what friends and physicians tell them. Most do not recognize that these concerns are excessive and disproportionate, but some do. This preoccupation must last at least six months, but the specific feared illness may change over time (APA, 2013). The care- seeking type often visits doctors or undertakes medical tests or procedures, whereas the care-avoidant type rarely uses medical care. Illness anxiety disorder affects 1% to 5% of the U.S. population (Abramowitz & Braddock, 2011).

Illness anxiety disorder seems to have a common etiology with many anxiety disorders. The individual acquires these illness fears via classical conditioning or perhaps modeling (Marshall et al., 2007). According to cognitive theorists, because these individuals are hypersensitive to

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bodily cues and threatened by them, they misinterpret them for illness symptoms (Witthöft & Hiller, 2010). Treatment modalities for illness anxiety disorder are similar to those used to treat obsessive-compulsive disorder. Sometimes antidepressants can be helpful in easing the anxiety (Bouman, 2008). Cognitive therapists will work with individuals so that they can iden- tify and change the beliefs about illness that are reinforcing the disorder (Hedman et al., 2011).

Conversion Disorder Freud and Breuer’s famous patient, Anna O., had among her many symptoms a false preg- nancy. Hysteria was once considered to be a physical, usually a neurological, disease. How- ever, after Breuer and Freud published their studies on hysteria, professional opinion began to change. Today, it is generally agreed that hysteria is a psychological condition. According to Freud’s theory, repressed sexual conflicts are “converted” into physical symptoms, which represent these conflicts in a disguised form. Hysterical paralysis of the hand, for example, may be a symbolic representation of guilt over masturbation. Although the term hysteria is no longer used and Freud’s influence is much reduced, echoes of the past may still be heard in the DSM–5’s name for hysteria—conversion disorder (classified for the first time as func- tional neurological symptom disorder; APA, 2013). Sufferers complain of paralysis, blind- ness, deafness, seizures, odd tingling sensations, and anesthesias (loss of feeling). Note that sexual symptoms are excluded because they fall into a separate diagnostic category.

Sometimes, conversion symptoms may be bizarre. Individuals may complain of being unable to hear when lying down but report that they hear perfectly when sitting upright. They may claim to be unable to speak loudly, only softly. A common complaint is globus hystericus, the feeling of having a lump stuck in one’s throat (Finkenbine & Miele, 2004). An interesting symptom of a conversion disorder is called glove anesthesia, in which numbness begins at the wrist and goes down to the fingertips in an even pattern. Real neurological conditions or damage typically do not spread out evenly like that, nor do they occur so abruptly. The indi- vidual might also demonstrate la belle indifference, a naive, inappropriate calmness or lack of concern in the face of perceptions by others of one’s disability. This is often seen in those with conversion disorder (Farlex, 2012).

More commonly, however, conversion symptoms mimic those of real illnesses. They can be differentiated from physical illness because laboratory tests and examinations are nega- tive and because there is no long-term physical deterioration or improvement as might be expected with a genuine medical condition. See Table 5.2 for the main DSM–5 diagnostic cri- teria for conversion disorder.

Table 5.2: Main DSM–5 diagnostic criteria for conversion disorder (functional neurological symptom disorder)

A. One of more symptoms of altered voluntary motor or sensory function. B. Clinical findings provide evidence of incompatibility between the symptom and recognized neurological

or medical conditions. C. The symptom or deficit is not better explained by another medical or mental disorder. D. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or

other important areas of functioning or warrants medical evaluation.

Source: APA (2013, p. 318).

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When making the diagnosis of conversion disorder, it is important to consider a person’s social and cultural environment (Alexander, Joseph, & Das, 1997). In some evangelistic church services, people may fall into a trance or have “seizures.” Because they are culturally accepted parts of such religious ceremonies, these symptoms are not signs of a conversion disorder.

Medical disorders such as multiple sclerosis, myasthenia gravis (progressive muscular weak- ness), and others may produce strange symptoms (for example, numbness or abnormal sen- sations in any bodily area, problems moving arms or legs and/or walking, tremors in one or more arms or legs, and/or weakness in one or more arms or legs that are easily confused with conversion disorders). About 10% to 15% of people originally diagnosed as having a conversion disorder turn out to have a physical disease (Binzer & Kullgren, 1998; Hurwitz & Pritchard, 2006), and sometimes these misdiagnosed medical conditions lead to tragic out- comes (Bokey, 1993; Jones & Barklage, 1990). For example, Jones and Barklage (1990) found two patients who had been misdiagnosed with conversion disorder. In further medical evalu- ations, one was discovered to have a brain lesion that led to seizures, and the second was found to have a ruptured brain tumor. Research has revealed that conversion disorder has become less common (Kirmayer, Looper, & Taillefer, 2003), but this may be explained by the misdiagnosis of patients in the past. Clearly, it is important to be cautious when concluding that a person’s symptoms result from a conversion disorder. Figure 5.1 exemplifies another way of distinguishing conversion disorder from problems of a physical origin.

Figure 5.1: Neural innervation (neural arousal of an organ, muscle, or gland)

Patterns of neural innervation (a) and typical areas of anesthesias in patients suffering from a conversion disorder (b). Conversion disorders can sometimes be detected because the physical symptoms make no anatomical sense. If numbness has a psychogenic rather than a neurological origin, areas of pain insensitivity may not correspond to the actual structure of the nervous system.

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 7.1, p. 297.

a b

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Prevalence, Family Patterns, and Course Although Breuer, Freud, and their contemporaries treated many people with conversion dis- orders, modern clinicians rarely see a case. Psychoanalytic psychologists consider the appar- ent decrease in the prevalence of conversion disorders evidence for Freud’s view that such disorders are the result of repressed sexual conflicts. They argue that Freud’s turn-of-the- century Vienna was sexually inhibited and that today’s more open attitude toward sex has eliminated the main cause of conversion disorders. Because the few sexual taboos that do remain today apply more to women than to men (as they also did in Freud’s time), we should expect to find a higher prevalence of conversion disorders among women than men. This is indeed the case (Abbey, 2005). In the United States, most cases occur in people from rural areas, especially among those with little education, low income, and fundamentalist religious backgrounds (Binzer, Andersen, & Kullgren, 1997; Kirmayer et al., 2003).

Etiology and Treatment Psychoanalysts view conversion disorders as manifestations of repressed conflicts in the symbolic form of somatic symptoms (Brown, Schrag, & Trimble, 2005). Symptoms provide a primary gain to the person with a conversion disorder—they keep unacceptable conflicts at bay. For example, people with conflicts about expressing anger may develop hysterical mute- ness. Symptoms also provide a secondary gain in the form of sympathy and attention. It is important to keep these two types of gain separate (van Egmond, 2003). Psychoanalytic treatment is aimed mainly at the primary gain. It involves uncovering conflicts, showing how they contribute to the apparent illness, and helping people to express their psychological needs in less debilitating ways. In addition, the emotional catharsis that comes from releas- ing repressed sexual energy, combined with new insights into one’s behavior, is supposed to help people give up their symptoms.

Psychoanalytic treatment for secondary gain is subsidiary. It is aimed at removing the attention and sympathy that reinforce the “sick” role. In contrast, behavioral and cognitive clinicians focus almost entirely on secondary gain (Blanchard, 1994). They believe that a conversion disorder is most likely to develop when (a) an individual is under stress, (b) the person knows enough about an illness to mimic its symptoms, and (c) there is some reinforcement (secondary gain) for being “sick.” The person need not consciously pretend to be sick. Symp- tom formation can take place outside of awareness.

In theory, systematic desensitization should reduce situational anxiety, thereby alleviating the source of somatic complaints. In practice, however, desensitiza- tion alone is rarely sufficient to overcome a conver- sion disorder. People with conversion disorders are reluctant to admit that their problems might be psy- chological. They rarely undergo systematic desensiti- zation because they avoid referrals to mental health professionals. Instead, they prefer to make the rounds of medical practitioners. For many people, remaining ill is preferable to making such an admission. Bogus medical treatments (in which people are prescribed

Jupiter Images/Creatas/Thinkstock Symptoms of conversion disorder often provide the sufferer with a secondary gain, such as sympathy or attention, that reinforces the “sick” role.

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placebo pills) may help such people by giving them a face-saving way of attributing their improve- ment to medical rather than psychological treatment (Price, Finniss, & Benedetti, 2008).

People who have successfully avoided responsibility because of “illness” have had their symptoms strongly reinforced. Overcoming their habitual “avoidance through sickness” might require family therapy targeted not just at the “patient” but also at those people in the person’s social environment who are reinforcing and maintaining the conversion symptoms (Brazier & Venning, 1997). None of this is possible, of course, until the therapist overcomes the main obstacle—getting people with conversion disorder into treatment in the first place.

5.3 Factitious Disorder In 1784, Rudolf Erich Raspe published Baron Munchausen’s Narrative of His Marvelous Travels and Campaigns in Russia. Raspe described the life of Baron Karl Friedrich Hieronymous von Münchausen, allegedly a retired Russian army officer, who traveled from town to town spin- ning wild and unsubstantiated stories of his heroism, including detailed descriptions of his extensive battle wounds. In honor of Raspe’s hero, Munchausen syndrome became the name applied to people who wandered from hospital to hospital pretending to be ill (Zuger, 1993). Though this disorder was removed from the DSM–5, it appeared in the DSM–IV–TR, which called Munchausen syndrome a factitious disorder—a condition in which people pretend to be sick. The first extensive study of factitious disorder appeared in 1951; it has also been called “thick chart syndrome” and “hospital hopper syndrome” (Yates & Feldman, 2016).

As indicated earlier, people with factitious disorder should not be confused with those who malin- ger. People who are malingering also fake their symptoms, but they always have a clear reason for doing so. They may wish to avoid jury duty or a final examination, or they may be attempting to pro- vide evidence for a lawsuit. Malingering may even be a way of keeping fed and warm for the winter. Malingering is not always unhealthy—hostages who pretend to be sick to escape from their captors have good reason to malinger. Factitious disorder, by contrast, is more difficult to explain. Sufferers pretend to be sick without any obvious reward or incentive (other than attention); they may have a desire to receive attention or care, may gain a sense of control from deceiving health care profes- sionals, or may gain a “rush” from undergoing medical procedures (Yates & Feldman, 2016).

The primary DSM–5 diagnostic criterion for factitious disorder is pretending to be ill or intention- ally manufacturing symptoms or both. Diagnosis can be particularly complicated when parents use their children as “proxies” for their own factitious disorders (Ayoub, 2006; see accompanying Highlight on Gypsy Blanchard). In such cases, it is often difficult to tell whether the child is really ill or whether the parents are falsifying their child’s symptoms (Feldman, 2004; Yates & Feldman, 2016). This is called factitious disorder imposed on another in the DSM–5 (APA, 2013).

In both subtypes, individuals may use drugs and other substances to enhance their symptoms. People with factitious disorder often present their illness in dramatic terms: “I barely made it here alive. One more day and I probably would have died.” Because their speech is filled with medical terms and they know about clinical routines, their presentation is usually sufficiently realistic to get them admitted to a hospital. Indeed, the medical histories of people with factitious disorder often contain multiple hospitalizations, numerous tests, and even surgical procedures (Fry & Ger- gel, 2016). In one notorious case, a woman with factitious disorder had both her breasts removed because of suspected cancer (McDaniel, Desoutter, Firestone, & McDonnell, 1992).

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Section 5.3 Factitious Disorder

Once their illness is proven false, people with factitious disorder quickly develop “complica- tions” or new symptoms. When they are finally forced to leave the hospital, they simply turn up at another. Deciding whether a symptom is real or phony requires considerable skill. The diagnosis should be made only when all medical explanations for a symptom are eliminated or when there is clear evidence that a symptom has been manufactured.

Although factitious disorder is relatively rare in both sexes, the available evidence suggests that it occurs quite more often among women than among men (Yates & Feldman, 2016). The disorder seems to begin in early adulthood and is typically difficult to treat. Although the subject of much speculation (Plassmann, 1994), there are no generally accepted etiological theories or treatment programs for factitious disorder (Fry & Gergel, 2016). Many professionals are reluctant to expend their energies on people who are faking their symptoms, so factitious disorder has received little clinical attention. However, some treatment success has been reported using a combination of behavioral, cognitive, and SSRI antidepressants (Fry & Gergel, 2016). As they do with the other somatic symptom and related disorders, placebos allow people with factitious disorder to save face by attributing their recovery to medical treatment rather than having to admit that they were never really physically ill. (See Part 5 of Helen Fairchild’s case in the appendix.)

Highlight: The Strange Case of Gypsy Blanchard

In July 2016, Gypsy Rose Blanchard was sentenced to 10 years in prison after pleading guilty to second-degree murder in the stabbing death of her mother, Clauddine “Dee Dee” Blanchard. Gypsy had effectively been her mother’s prisoner since she was three months old. According to various reports, Gypsy was confined to a wheelchair, had a feeding tube inserted into her stomach, had her head shaved by her mother to fake cancer, and was raised as though she had intellectual disabilities, to name just a few things her mother did to her.

Gypsy eventually found a boyfriend online who urged her to murder her mother, which she did. Experts seem to agree that this is a case of factitious disorder imposed on another, more commonly called Munchausen’s syndrome by proxy (though this latter term is not in the DSM–5 and therefore is not a diagnostic term). The diagnostic criteria include falsifying physical or psychological symptoms or disease(s) in another person; presenting the other person, identified as the victim (Gypsy, in this case), as ill or impaired; and exhibiting the deceptive behavior even when external rewards are absent (APA, 2013). The perpetrator receives this diagnosis, not, as is often believed, the victim. The prevalence is unknown and unclear, but the APA (2013) estimates that about 1% of the U.S. population displays factitious disorder. It is hard to identify because of the deceptiveness of the perpetrator.

What is most interesting about Gypsy’s case is the volume of solid evidence that supports this diagnosis in her late mother. She took Gypsy to the hospital on a regular basis, and somehow no one suspected anything during all of these stays. Many perpetrators engage in this behavior for sympathy and emotional gratification, though Blanchard’s mother also seemed to be doing it for donations, free trips, and other fraudulent means of making money.

Gypsy’s mother convinced her ex-husband that Gypsy at three months needed a respirator, she let her teeth rot, and she confined her to a wheelchair, telling her she couldn’t walk. Does this sound like a typical mother’s behavior to you? Some observers believe that factitious disorder imposed on another is not a mental illness, but surely Gypsy’s case represents a form of horrific child abuse, at the very least. Suppose you were given the case of Gypsy for a pretrial diagnosis and assessment. How would you handle these tasks, and how would you react upon hearing her stories? Could you remain objective?

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Chapter Summary

Chapter Summary We know surprisingly little about the etiology and treatment of the dissociative disorders, the somatic symptom and related disorders, and factitious disorder, even though they are among the most written about psychological disorders. One reason for this is reluctance on the part of clinicians and researchers to become involved with people who may be malingering.

Dissociative Disorders

Dissociative Amnesia with Dissociative Fugue

• Dissociative amnesia involves memory loss. • When a person not only develops amnesia but also moves away from home and per-

haps even adopts a new identity, the diagnosis is dissociative amnesia with dissocia- tive fugue.

• Most instances of dissociative amnesia with dissociative fugue are brief (hours or days).

• Many psychologists construe memory loss and fugue as ways of escaping traumatic stress.

• Because they do not know that anything is wrong, people in fugue states rarely refer themselves for treatment.

• Treatment usually takes place after the person recovers and is aimed at preventing future episodes.

Depersonalization/Derealization Disorder

• People with depersonalization/derealization disorder feel as if their body parts have changed in size, or they may have the impression that they are outside their bodies, viewing themselves from a distance.

• Sometimes they feel mechanical, as though they are robots. • The onset of the disorder is usually sudden and associated with stress. • The treatment literature is sparse and inconclusive.

Dissociative Identity Disorder

• In dissociative identity disorder, formerly known as multiple personality disorder and still incorrectly called this by some people today, two or more separate identi- ties recurrently come forward to take charge of a person’s behavior.

• Each identity has its own characteristic personality, habits, and memories. • Dissociative identity disorder is more common in women than in men, and it also

seems to run in families. • All schools of psychology attribute dissociative identity disorder to traumatic experi-

ences, particularly childhood physical and sexual abuse. • Other causal factors may include the ability to put oneself into a hypnotic state. • Some cases of dissociative identity disorder are clearly frauds. • Treatment attempts to fuse disparate personalities into a single person.

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Chapter Summary

Somatic Symptom and Related Disorders

Somatic Symptom Disorder

• Somatic symptom disorder is characterized by multiple physical complaints span- ning several bodily systems, with no medical explanation and without conscious faking.

• In females, somatic symptom disorder typically begins in late adolescence, whereas males are diagnosed later following a history of interpersonal problems.

• Few clients consent to participate in psychological treatment, so there is little data on treatment efficacy.

Conversion Disorder (Functional Neurological Symptom Disorder)

• Conversion disorder—pseudomedical complaints in otherwise healthy people—gets its name from Freud’s theory that the energy associated with unconscious conflicts is “converted” into physical symptoms.

• These symptoms may sometimes be bizarre, but usually they mimic real illnesses. • Treatment may require family therapy targeted not just at the “sick” person but also

at those people in the person’s social environment who are reinforcing the conver- sion symptoms.

• The longer that conversion symptoms are present, the poorer the prognosis.

Factitious Disorder • People with factitious disorder pretend to be sick. • Unlike people who are malingering, people with factitious disorder pretend to be

sick without obvious reward. • Parents may even falsify the symptoms of their children. • Although they use different terminology, the major paradigms take a remarkably

similar view and recommend comparable treatments. • Clearly, there is much left to learn about these puzzling disorders.

Critical Thinking Questions

1. The chapter states that many psychologists view dissociative amnesia with dissocia- tive fugue as resulting from trying to “escape” from traumatic stress. What types of traumatic stress do you imagine could cause these conditions?

2. We briefly discussed dissociative identity disorder and noted that, even though it appears to be increasing in prevalence, many psychologists still question its exis- tence. Give your opinion on this subject.

3. Give your views on conversion disorder. How should mental health professionals approach patients who present with this problem?

4. Some research has revealed that those with conversion disorder are victims of child- hood sexual abuse; the conversion symptoms allow them to handle the underlying trauma. Give your views on this perspective.

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Chapter Summary

5. Review the Highlight on Gypsy Blanchard. How realistic do you think her side of the story is, that is, is she making most of this up? Some reports have said that she is an accomplished “liar” like her late mother was, and is doing so to manipulate the media and gain reduced prison time. What do you think? Additionally, we are com- pelled to ask again: What kind of mother could do this to her child?

Key Terms alters Alternative personalities seen in dis- sociative identity disorder.

amnestic episode A forgotten period of time in a dissociative state, in which, for many months, the individual cannot recall much about the events that occurred during that time.

care-avoidant type A subtype of illness anxiety disorder in which the individual rarely uses medical care.

care-seeking type A subtype of illness anxiety disorder in which the individual often visits doctors or undertakes medical tests or procedures.

continuous amnesia In a dissociative disorder, when forgetting continues into the present day and time. The individual might not recall the actual events, but he or she might not recall new experiences, either.

conversion disorder (functional neuro- logical symptom disorder) A disorder in which sufferers complain of paralysis, blind- ness, deafness, seizures, odd tingling sensa- tions, and anesthesias.

depersonalization/derealization dis- order A disorder that involves someone feeling like their sense of “self ” has become dissociated from the rest of their personality.

derealization The feeling that the world is not real or of living in a dream.

dissociative amnesia Memory loss caused by psychological, not physiological, factors.

dissociative disorders Disorders that are identified by the disassociation of the per- sonality; memories and sometimes identi- ties become detached (“dissociated”) from one another.

dissociative fugue A disorder in which a person not only develops retrograde amne- sia (forgets things that happened in the past) but also leaves home and adopts a new identity.

dissociative identity disorder Formerly known as multiple personality disorder, a disorder in which a person acts as if his or her body is inhabited by several personali- ties, with only one appearing at a time.

factitious disorder A disorder in which a person feigns illness for no personal gain other than attention.

factitious disorder imposed on another A disorder in which the person feigns illness in his or her child, falsifying the child’s symp- toms. This was previously called Munchau- sen’s syndrome by proxy.

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Chapter Summary

fusion Used in treating dissociative identity disorder; a clinician’s attempt to fuse a per- son’s various personalities into a single one.

glove anesthesia A symptom of a conver- sion disorder; numbness begins at the wrist and goes down to the fingertips in an even pattern. Real neurological conditions or damage typically do not spread out evenly like that nor do they occur so abruptly.

hypochondriasis The former term used to cover somatic symptom disorder and illness anxiety disorder.

illness anxiety disorder A disorder in which the person is always anxious about his or her health. The person either is obsessive about health-related behaviors or demonstrates extreme unhealthy avoidance (avoiding doctor’s appointments or hospi- tals). Individuals with this disorder persist in their misinterpretations no matter what friends and physicians tell them.

la belle indifference In a conversion disorder, a naive, inappropriate calmness or lack of concern in the face of perceptions by others of one’s disability.

localized amnesia When a person loses all memory of events that occur within a limited timeframe.

malingering When a person pretends to be sick to avoid commitments or to gain some advantage.

Munchausen syndrome The name origi- nally applied to people who wandered from hospital to hospital pretending to be ill.

primary gain In a conversion disorder, when symptoms keep unacceptable conflicts at bay.

secondary gain In a conversion disorder, when symptoms gain an individual sympa- thy and attention.

selective amnesia Occurs when the person remembers some, but not all, of the events that occurred during a particular timeframe.

somatic symptom disorder Psychologi- cal disorder marked by physical symptoms that mimic those produced by disease, even when no physiological disease is present.

state-dependent learning Learned mate- rial is recalled more easily if the individual is in the state in which the material was originally learned (e.g., intoxicated).

systematized amnesia Occurs when people lose memory for a specific category of information, such as all memories related to their family, aspects of when they were being abused as a child, aspects of a poor marriage, and so on.

with predominant pain A specifier for somatic symptom disorder; used if the indi- vidual’s symptoms predominantly involve pain.

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4 Substance-Related and Addictive Disorders

Lee O’dell/Hemera/Thinkstock

Learning Objectives

After reading this chapter, you should be able to:

• Explain what psychoactive substances are.

• Explain why psychoactive substances are so popular.

• Analyze the potential dangers of using psychoactive substances.

• Explain how substance-related disorders are treated.

• Discuss ways that substance-related disorders can be prevented.

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Section 4.1 Psychoactive Substances: Some Basic Information

4.1 Psychoactive Substances: Some Basic Information Chemicals that alter moods or behavior have been used for thousands of years by people from just about every culture and society. This chapter is concerned with why so many people use these psychoactive substances, the problems such substances can cause, how to help people who want to stop using substances, and how to prevent people from taking them up in the first place. Psychoactive substances—chemicals that alter our moods or behavior—touch every aspect of modern life; they affect the way we live, work, relax, and die. In the United States, the total cost of substance abuse in 2016 (the most recent year for which estimates are available) was more than $400 billion in lost workplace productivity (in part due to prema- ture mortality), health care expenses, law enforcement and other criminal justice costs (for example, drug-related crimes), and losses from motor vehicle crashes (U.S. Department of Health and Human Services [USDHHS], 2016). Furthermore, about three quarters of the costs associated with alcohol use were due to binge drinking, and about 40% of those costs were paid by the government, emphasizing the huge cost of alcohol misuse to taxpayers (USDHSS, 2016). This value represents both the use of resources to address health and crime conse- quences as well as the loss of potential productivity from disability, death, and withdrawal from the workforce.

There is no precise boundary between social drinking and alcohol abuse. Like many psy- chological problems, substance-related disorders are often just extreme cases of common behaviors. How common? Recent data reported by the Center for Behavioral Health Statistics and Quality (CBHSQ, 2015) reveal that slightly more than half of Americans aged 12 or older (139.7 million, or 52.7%) reported some amount of alcohol use. This refers to general use of alcohol—a beer with pizza or a glass of wine at dinner, for example. A bit more than two out of every five people aged 12 or older (60.9 million, or 40%) participated in binge drinking at least once in the past 30 days (CBHSQ, 2015). For males, binge drinking is defined as the consumption of five or more alcoholic drinks in a row on at least one occasion during the pre- ceding two-week period; for females, it refers to the consumption of four or more drinks dur- ing that time period (Bartel et al., 2017). The rates in 2009 and 2010 were similar (23.7%). Finally, heavy drinking was reported by 6.2% of the population aged 12 or older, or 16.3 mil- lion people (CBHSQ, 2015).

More disturbingly, data provided by the National Survey on Drug Use and Health (NSDUH) showed that in 2014, “17 million persons aged 12 or older were classified with an alcohol use disorder. This represented 6.4 percent of the population” (CBHSQ, 2015).

Psychoactive substances form a spectrum. At one end are everyday substances, such as the caffeine found in coffee, soft drinks, and tea. At the other end of the spectrum are illicit and potentially dangerous substances, such as opiates (for example, heroin). A variety of other substances lie between these two extremes.

Robert Jones presents an interesting example of an individual who may—or may not—have a drinking problem. Let’s meet him before we continue.

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Section 4.1 Psychoactive Substances: Some Basic Information

The Case of Robert Jones: Part 1

Robert (or Bob as he prefers to be called) is a 48-year-old African American male who has been married for 30 years to Paula. He has two children, aged 16 and 5. When Bob came to us, he was well dressed, presented pleasantly and appropriately, and had a friendly demeanor. He was not entirely sure why he was sent to the clinic, but he was sure that it was a mistake.

“I’ve got no idea what’s going on here. The cops stopped me one night after work. Both were African Americans, and they knew me. They’ve seen me in town, at church. They told me I was weaving all over the road, and they wanted to make sure I was okay. Of course I was okay! I’ve been driving for over 30 years and never had an accident, never had a ticket! They asked me twice if I’d been drinking. I don’t drink, well, not that much anyway. They thought I was drunk! Would I drive drunk? I’ve got two kids, one a teenager who’ll be driving soon herself. I told them no, and then they asked me to step out of the car as they wanted me to do some things for them . . . .”

Bob continued his story for us during his initial intake interview. “This was so insane! I’ve got a graduate degree. I’m an upstanding citizen. The cops asked me to walk a straight line, to touch the tip of my nose with the index finger of each of my hands. That wasn’t good enough! Then they asked me if I’d been drinking—again—and then they asked me to blow into a tube in this little machine. I wasn’t sure I needed to do this, but I’d heard if you refuse to do this you’re immediately arrested. Where’s the ‘innocent until guilty’ here?” Bob decided that he’d better go along with the officers’ request and he did, but he complained the whole time. The end result was shocking to him, to say the least: “They said I was drunk! My . . . BAR . . . or something like that [we corrected him and explained that this was his blood alcohol concentration (BAC)] was .20.”

BAC refers to the percentage of alcohol that is in the body as compared to the total blood supply. A BAC of 0.08 is equivalent to about four drinks consumed per hour for an average- sized individual.

“That meant zip to me, so they told me it seemed like I’d had about 10 drinks. 10 drinks! That’d make me a rummy, a lush! I only drink beer anyway. 10 beers in one hour! That’d kill me much less anyone else!”

We confirmed the BAC results on Bob’s paperwork, sent to us by his probation officer. She sent him to us as part of his plea bargain in order to avoid jail time. Bob believed that he had no reason to be in our office. “Why don’t you concentrate on the real problems out there— the murderers, lying politicians, and the drunks that kill people while driving—huh? I’m a hardworking family man; I don’t belong in here with the winos and the loony tunes.” We pointed out the conditions of his probation and gave him the option to leave. Bob thought about this for a while and then finally stood up to leave.

See appendix for full case study.

Because the DSM–5 includes many substance-related disorders, it is not possible to review each one here. Instead, this chapter emphasizes the common features of psychoactive sub- stance use by focusing on the four substances most frequently used by American college stu- dents: caffeine, nicotine, alcohol, and cannabis (marijuana). Let’s start by surveying the physi- cal and psychological effects of each of these substances.

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Section 4.1 Psychoactive Substances: Some Basic Information

Caffeine If you need proof that practically everyone uses psychoactive substances at one time or another, just consider caffeine. It is practically everywhere. The only way you can avoid it is to shun coffee, tea, Red Bull, many popular soft drinks, cocoa, and chocolate. Even then, you may not succeed because caffeine is also found in headache, diet, and cold medications. Today, coffee remains the world’s most popular source of caffeine (see Figure 4.1 for other common sources).

Figure 4.1: Common sources of caffeine

Source: Data from Consumer Reports, “What Caffeine Can Do for You and to You,” Consumer Reports on Health, 9(1997), pp. 97, 99–101, as appearing in S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 6.1, p. 238.

Caffeine (mg)

0 25 50 75 100 125 150 175 200

Espresso, 2 oz Regular coffee, brewed, 6 oz Instant coffee, 6 oz

Coffee

Jolt Cola, 12 oz Mountain Dew, 12 oz Surge, 12 oz Coca-Cola Classic, 12 oz Pepsi, 12 oz Java Water, 12 oz Water Joe, 12 oz Java Juice, 12 oz XTC Juice, 12 oz

Soft drinks

Black tea, 6 oz Green tea, 6 oz

Tea

Aspirin-free Excedrin Anacin NoDoz maximum strength NoDoz

Medications

S o

u rc

e o

f c a ff

e in

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Section 4.1 Psychoactive Substances: Some Basic Information

Action Caffeine belongs to a class of chemicals called stimulants, whose main psychoactive effect is to make us more alert. Within 45 to 60 minutes after you drink a cup of coffee or munch on a chocolate bar, caffeine is absorbed from the stomach and the intestines. Once in the blood- stream, it causes blood pressure, pulse rate, and stomach acid production to increase. In the nervous system, caffeine acts as an antagonist to the neuroinhibitor adenosine (Kaster et al., 2015). Antagonists are chemicals that reduce the potency of other chemicals. In contrast, agonists are chemicals that increase the potency of other chemicals (for example, fluoxetine [Prozac] is a serotonin agonist). Caffeine is also a powerful diuretic because it increases the excretion of liquid from the body.

Health Effects Although it is widely used and generally regarded as safe, caffeine may still have adverse effects on health (de Mejia & Ramirez-Mares, 2014). For example, it increases the production of stomach acid, which may worsen digestive disorders and can cause acid reflux (“heartburn”). Insomnia, poor sleep, and anxiety are other potential results of overuse of caffeine. Excessive continual coffee consumption can also lead to bone loss, increased blood pressure, and lower bone density, meaning that fractures are more likely (Chaudhary, Grandner, Jackson, & Chakra- vorty, 2016; de Mejia & Ramirez-Mares, 2014). Some researchers, however, found that coffee consumption does not lead to ulcers or acid reflux (Papakonstantinou et al., 2016).

Psychological Effects Because caffeine is a stimulant, many people consume drinks containing it to combat drowsi- ness, increase alertness, and boost energy. Paradoxically, many people also consume caffeine to relax. It is possible that the relaxing effect of caffeine is not the result of its chemical action but of expectancies (what people expect when they use a drug or substance) and social rein- forcements. If we expect caffeine to be relaxing, it probably will be.

Nicotine Nicotine is the primary psychoactive ingredient in tobacco, a plant that has grown in the Americas for centuries. Let’s look at a few statistics to put tobacco use into perspective. Although tobacco usage has decreased over the past few years, in 2015 nearly 25.3% of high school students used some type of tobacco product, including 13% who reported cur- rently using at least two or more tobacco products (Singh, 2016). Among current high school users, smokeless tobacco was the product used most often during the past month (42%), followed by cigarettes

kolosigor/iStock/Thinkstock As with substances administered through a needle, our bodies react physiologically to nicotine within a matter of seconds.

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Section 4.1 Psychoactive Substances: Some Basic Information

(31.6%). Not surprisingly, e-cigarettes were used by about 15.5% of those surveyed (Neff et al., 2016). Cigar smoking was also common among high school students, at about 13.1% (Neff, Spiker, & Truant, 2015; Singh, 2016).

Action Nicotine is a powerful stimulant, so toxic that it has been used as a natural insecticide. A small amount instantly kills a variety of insects. In humans, nicotine is one of the fastest acting psy- choactive substances. Within seconds of a smoker’s puffing on a cigarette, nicotine reaches the smoker’s brain (Benowitz, 1996). It activates specific receptors in the midbrain that pro- duce increased arousal. The end result is similar to the one produced by caffeine—smoking makes people more alert and less drowsy.

Health Effects Carbon monoxide, the poisonous gas found in automobile exhaust emissions, is also present in cigarette smoke. It reduces the smoker’s oxygen supply, thereby affecting the heart and other circulatory organs. The organic chemicals suspended in smoke droplets, known as tar, contain several known carcinogens, or substances that can cause cancer. Many other danger- ous substances, such as formaldehyde (a well-known carcinogen) and nitric oxide (a poison- ous gas), are also found in tobacco smoke.

The effects of smoking on health have been known for decades. In 1948, researchers began a prospective study of more than 5,000 people living in Framingham, Massachusetts. Their aim was to identify the factors that contribute to heart disease. The now-famous Framingham Heart Study revealed a number of risk factors (characteristics, genetic or otherwise, that seem to be associated with an increased risk of disease onset or recurrence). Somewhat unex- pectedly, at least at the time, high among those risk factors was smoking (Dawber, 1980). The Framingham study was the first evidence that tobacco smoking was related to heart disease. It was followed by a study of 8,000 men of Japanese descent, which found that smoking is also a risk factor for stroke (Abbott, Yin, Reed, & Yano, 1986). Smokers have three times as many strokes as people who have never smoked. A 34-year follow-up of the Framingham study shows a continuing association between smoking and a range of diseases years after smoking ceases (Freund, Belanger, D’Agostino, & Kannel, 1993).

In addition to heart disease and stroke, smoking is a risk factor in respiratory diseases such as bronchitis and emphysema (Rigotti, 2013), in stomach ulcers, and in diseases of the mouth (Sood et al., 2014). Exposure to the smoke of other people’s cigarettes, pipes, and cigars (known as passive smoking) is also a health risk, especially for young children (Czogala et al., 2014). These researchers estimated that passive smoking kills more than 600,000 people worldwide every year, an astonishingly high figure (Czogala et al., 2014).

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Section 4.1 Psychoactive Substances: Some Basic Information

According to the World Health Organization (WHO), tobacco is the second leading cause of death around the globe. WHO estimates that 12% of all deaths among adults aged 30 or older are smoking related, which comes out to about 5 million people each year. This number is expected to grow to 8 million by 2030. Half of all smokers will die from their tobacco use (WHO, 2012). In 2015, WHO estimated that over 1.1 billion people smoked tobacco (WHO, 2012).

Although smoking is directly related to stroke, heart disease, diabetes, chronic obstructive pulmonary disease (COPD), and 12 types of cancer (Carter et al., 2015; Farsalinos et al., 2016), the best known link is the relationship between smoking and lung cancer (Carter et al., 2015).

Psychological Effects Despite nicotine’s arousing effects, most smokers, like most coffee drinkers, claim that they smoke to relax. Some research suggests that smoking may actually increase stress levels (Par- rott, 2000). Other studies reveal that smoking is relaxing and that smoking increases under stressful circumstances (Hughes, 2005). As with coffee drinking, the relaxing effects of ciga- rette smoking may be, at least in part, the result of expectancies and social reinforcement.

Personality may play a role in nicotine use. Despite the well-known health risks, millions of people continue to smoke. Hans Eysenck (1991) suggested that this phenomenon may be partly explained as a behavioral expression of the personality trait of extroversion. Accord- ing to Eysenck, extroverts are born with low levels of arousal. The experience of low arousal is perceived as unpleasant, so extroverts continuously seek stimulation—and smoking is a source of stimulation. Not all extroverts smoke, of course. There are other ways to raise arousal; some may drink lots of coffee. However, once extroverts start smoking (because of peer pressure, rebelliousness, or for some other reason), they are likely to continue because smoking provides the stimulation they crave (Hakulinen et al., 2015). In 2015, e-cigarettes were the most commonly used tobacco product among middle (5.3%) and high (16.0%) school students (Singh, 2016). During 2011–2015, significant increases in current use of e-cigarettes and hookahs occurred among middle and high school students. This finding is bothersome, but what is interesting is that the current use of conventional tobacco products such as cigarettes and cigars decreased during that timeframe. Many people falsely believe that e-cigarettes are healthier for you, and although ads may imply that this is the case, it is not true (Callahan-Lyon, 2014).

Nicotine, as a stimulant, belongs to the same class of substances as amphetamines, cocaine, and MDMA, which is also known as ecstasy or Molly (see Table 4.1).

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Section 4.1 Psychoactive Substances: Some Basic Information

Alcohol Alcohol (known more accurately as ethanol) is the second most commonly used psychoac- tive substance in the United States and perhaps in the world. It is estimated that 2 billion peo- ple worldwide use alcohol (WHO, 2011). Globally, 45% of the world’s population has never consumed alcohol (35% of men and 55% of women).

Alcohol is found in wine, liquor, spirits, beer, cider, and many cold medications. Unlike smok- ing, alcohol use is positively correlated with educational attainment. College graduates drink more than those who ended their education after high school (although college students with low marks drink more than high-performing students; Ansari, Stock, & Mills, 2013; Quinn & Fromme, 2011). International comparisons suggest considerable cross-cultural variability in

Table 4.1: Examples of stimulants (other than caffeine and nicotine)

Name Description

Amphetamine A synthetic (manufactured) compound that comes in legal prescription versions and ille- gal street versions, such as “speed.” Amphetamine powder can be inhaled (“snorted”) or injected. Amphetamines enhance neurotransmitter concentration, especially norepineph- rine and dopamine. This increased concentration produces alertness and arousal. Origi- nally intended as an asthma medication, amphetamines still have several medical uses. For example, drugs such as dextroamphetamine (Adderall) and methylphenidate (Ritalin) may be prescribed for people with attention-deficit/hyperactivity disorder (discussed in Chapter 11); and because they suppress appetite, they are sometimes used as diet aids. Large doses of amphetamines can also be fatal.

Cocaine Derived from the South American coca plant, cocaine, or coke, comes in several forms and was once an ingredient in Coca-Cola (Musto, 1992). Cocaine produces stimulatory effects similar to those produced by amphetamines. Also like amphetamines, cocaine can be injected, snorted, or smoked in forms known as free-base and crack. Cocaine acts to enhance the action of dopamine and other neurotransmitters, thereby increasing arousal while producing a variety of psychological effects including (after prolonged use) paranoia, anxiety, panic attacks, and even a psychotic disorder (Yudofsky, Silver, & Hales, 1993). Withdrawal does not seem to produce symptoms unless cocaine use extends over a consid- erable period, usually defined as six months or longer (Gawin & Kleber, 1992). Similar to amphetamines, cocaine can be fatal in large doses (Harlow & Swint, 1989). In 2010, about 1 million people had cocaine dependence in the United States (NSDUH, 2011).

MDMA MDMA (3, 4-methylenedioxymethamphetamine), also known as ecstasy, is technically a stimulant but is often considered to be a hallucinogen as it produces hallucinogenic effects. This drug is often used in clubs and at raves as it provides users with a boost in energy that allows them to go on dancing for extended time periods. MDMA has no medicinal effects and can lead to many physical problems, including increased blood pressure and heart rate, which can lead to cardiac arrest (Ksir, Hart, & Oakley, 2008). The popular nickname Molly (slang for “molecular”) often refers to the supposedly “pure” crystalline powder form of MDMA, usually sold in capsules. Sometimes the capsule is “cut” with another substance (meaning that another substance in addition to MDMA is added in, often without the user’s or buyer’s knowledge). Other stimulants include cocaine, ketamine, methamphetamine, over-the-counter cough medicine, and synthetic cathinones (“bath salts”).

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Section 4.1 Psychoactive Substances: Some Basic Information

alcohol consumption depending on availability and cultural prohibitions (Erol & Karpyak, 2015; WHO, 2014).

In all ethnic groups, males are much more likely than females to be binge drinkers, although women appear to be closing the gap (Erol & Karpyak, 2015). This also puts women at risk for other drug use, where they also seem to be catching up to men (Clinkinbeard & Barnum, 2015). Even so, the gap between men and women still exists. Why might that be? First, blood levels of alcohol build up more quickly in women than in men of the same size because women have less of the enzyme—known as alcohol dehydrogenase (ADH)—that helps break down alcohol in the stomach before it enters the bloodstream (Erol & Karpyak, 2015). Note, how- ever, that Erol and Karpyak (2015) also found some reports that suggested this is not the case. Second, many women do not drink when they are pregnant because of the now well-known fact that alcohol can cause birth defects (Landgraf, Nothacker, Kopp, & Heinen, 2013).

Action Chemically, alcohol is a depressant. It lowers arousal and makes people drowsy (Yi, 1991). Some of the other depressants included in the DSM–5 are described in Table 4.2.

Alcohol exerts a variety of effects on the central nervous system, but one of its most impor- tant is to reduce inhibition, which is controlled by the GABA neurotransmitter system (GABA stands for gamma-amino butyric acid; the “gamma” is typically abbreviated with the Greek letter for gamma). The result is that drinkers lose some degree of self-control. Alcohol dilates blood vessels, decreases blood pressure, lowers heart rate, and slows respiration. Although small amounts of alcohol are exhaled as vapor by the lungs, which can be measured by road- side Breathalyzers, most of the ingested alcohol goes to the liver, where it is gradually broken down (metabolized) and excreted. The average person can metabolize about one “standard drink”—the equivalent of one 12-ounce glass of beer, one 5-ounce glass of wine, or 1 ounce of 90-proof liquor—per hour. (We will discuss the BAC a bit later in this chapter.) Neither drinking black coffee nor splashing cold water on one’s face makes any difference in the rate at which alcohol is metabolized; there is no quick way to sober up.

Health Effects Drinking moderate amounts of alcohol, especially red wine, may reduce the likelihood of cor- onary heart disease (Chiva-Blanch, Arranz, Lamuela-Raventos, & Estruch, 2013). However, chronic use of alcohol can damage the heart and just about every other organ in the body (Shield, Parry, & Rehm, 2014; WHO, 2014). Alcohol irritates the digestive system, causing

ZzzVuk/iStock/Thinkstock Males are more likely to be binge drinkers than females, partly because women have less of the enzyme ADH (alcohol dehydrogenase) that helps break down alcohol in the stomach.

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inflammation and bleeding. Prolonged and intensive use of alcohol can turn the liver into nonfunctioning, fibrous tissue. This syndrome is known as cirrhosis. A very high blood alco- hol level can be fatal, although most people become unconscious before drinking enough to cause death.

Heavy drinking during pregnancy can put a fetus at risk of developing fetal alcohol syn- drome (FAS), which is marked by intellectual disabilities, hyperactivity, facial deformities, and growth deficiencies of internal organs and the body’s systems (Caputo, Wood, & Jabbour, 2016; Landgraf et al., 2013). A classification known as fetal alcohol spectrum disorders (FASD) includes FAS, partial FAS, alcohol-related neurodevelopmental disorder, and alcohol-related birth defects (Landgraf et al., 2013). Even when they consume the same amount of alcohol, African American women and female members of certain Native American tribes are more likely to have children with FAS than are members of other groups (Caetano, Vaeth, Chartier, & Mills, 2014). Their increased vulnerability appears to be the result of genetic differences in alcohol metabolism (Caetano et al., 2014; Gordis, 1991).

Psychological Effects Moderate amounts of alcohol make most people feel talkative and relaxed. Even though drinkers may relax, even modest amounts of alcohol can affect cognition (Starkey & Charlton, 2014). After a few drinks, we concentrate on only the immediate and the most obvious cues in our environment, ignoring complexities and long-term consequences. For example, you may feel like talking back to a professor or to your supervisor at work, but a sober consideration of the consequences will probably inhibit you from actually saying anything. Under the influ- ence of alcohol, however, you may not consider the long-term consequences and just lash out. This narrowing of focus to the immediate is called alcoholic myopia (Fairbairn & Sayette, 2013). This can lead to having unprotected sex and inappropriate, even dangerous, acts of aggression (Giancola, 2015; Kiene, Simbayi, Abrams, & Cloete, 2016), for example.

As the amount of alcohol in the bloodstream builds, vision becomes blurred, hearing grows less acute, and motor control begins to break down. It is these effects that make drinking and driving so dangerous. Indeed, alcohol was associated with around 29% of all automobile accident fatalities in 2015 (National Highway Traffic Safety Administration [NHTSA], 2016).

The level of cognitive and motor impairment produced by alcohol depends on its concentra- tion in the blood. Concentrations below 0.05% of blood by volume usually produce feelings of relaxation, with minimal cognitive or motor effects. Higher concentrations affect judgment and motor coordination. Figure 4.2 shows the relationship between blood alcohol concentra- tion (BAC) and body weight.

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Figure 4.2: Approximate blood alcohol concentration (BAC) and body weight

Source: P. M. Insel & W. T. Roth, Core Concepts in Health, 10th ed. Mountain View, CA: Mayfield Publishing Company, 2000, p. 254. Reprinted by permission.

1 hour

2 hours

3 hours

4 hours

1 hour

2 hours

3 hours

4 hours

1 hour

2 hours

3 hours

4 hours

1 hour

2 hours

3 hours

4 hours

1 hour

2 hours

3 hours

4 hours

1 hour

2 hours

3 hours

4 hours

Total drinks

0 1 2 3 4 5 6 7 8

1 hour

2 hours

3 hours

4 hours

Time from first drink

90–109 lb

(0.00%) Not impaired

(0.01–0.04%) Sometimes impaired

(0.05–0.07%) Usually impaired

(0.06 and up) Always impaired

110–129 lb

130–149 lb

170–189 lb

210 lb & over

150–169 lb

190–209 lb

BAC zones:

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Not only is judgment affected by alcohol, but so are the attributional processes required to interpret and control emotions (Giancola, 2013). For example, alcohol makes some people feel sexually aroused. Because their judgment is impaired, they may interpret innocent signs as indicating that another person feels the same way. Couple this with disinhibition, and it is not surprising that people influenced by alcohol may do things they would never do while sober. It is primarily alcohol’s disinhibiting effect that makes people believe that it is “stimu- lating,” even though it is a depressant. Excessive disinhibition can sometimes lead to aggres- sion (Giancola, 2013). Aggression, combined with impaired judgment, makes alcohol a factor in child abuse (Freisthler & Gruenewald, 2013), as well as in many suicides (Borges et al., 2017). See Table 4.2 for a summation of depressants other than alcohol.

Table 4.2: Depressants other than alcohol

Name Description

Sedatives, hypnotics (sleep- inducing drugs), and anxiolytics (antianxiety drugs)

Barbiturates (Seconal, Nembutal, and others) were first used in 19th-century Germany as sleeping aids. Benzodiazepines (e.g., Valium) are considered safer than barbiturates. The main effect of all sedative and anxiolytic drugs is to depress bodily functions. At low doses, these drugs are calming and promote sleep, but they can affect memory and interfere with psychosocial functioning (Warneke, 1991). The abrupt cessation of any of these drugs after prolonged use can cause neuro- logical symptoms, including seizures. Because alcohol, sedatives, and anxiolytics all affect the GABA system (McKim, 1991), mixing alcohol and these drugs produces a strong and potentially deadly effect (Fils-Aime, 1993).

Opioids Opioid is the general term for substances derived from the opium poppy plant. Known as opiates or narcotics, these include opium, morphine, and heroin; syn- thetic variants, such as methadone; and naturally occurring brain substances, such as beta-endorphins (Jaffe, 1991). All opioids are habit-forming. Although they may produce a brief feeling of elation, opioids are depressants (Barinaga, 1992). There is also evidence that opioids reduce the functioning of the immune system, thereby lowering resistance to disease.

Cannabis Cannabis is actually a short name for Cannabis sativa, a type of hemp plant that produces sev- eral psychoactive substances. Marijuana (also known as pot, weed, and many other names) is a mixture of the dried shredded flowers and leaves of the plant. Hashish is a sticky resin obtained from cannabis flowers. Cannabis users usually roll the substance into a cigarette known as a joint or smoke it in a pipe.

The psychoactive ingredient in marijuana is delta-9-tetrahydrocannabinol, usually called THC. Ordinary marijuana contains about 3% THC, but some types can contain 20 times as much. At such high doses, THC can produce distorted sensations and perceptions (hallucina- tions). Technically, this makes cannabis a hallucinogen, but, as previously noted, the DSM–5 classifies it in a separate category because perceptual distortions do not always accompany cannabis intoxication. Several hallucinogens are described in Table 4.3.

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Cannabis is one of the oldest crops cultivated by human beings (see Grinspoon & Bakalar, 1993, for one example of a detailed history of marijuana). Ten-thousand-year-old clay pots unearthed in Taiwan were found to have strands of hemp fiber in their decorations. For centu- ries, and until fairly recently, hemp fiber was a major source of rope, canvas, paper, and cloth (the first Levi’s jeans were made of hemp).

Action Within a few minutes of inhaling cannabis smoke, users experience dry mouth, rapid heart- beat, some loss of coordination, and slower reaction times. Blood vessels in the eyes expand, and blood pressure rises. Once in place, THC stimulates chemical reactions that produce the euphoria that users experience when they smoke cannabis.

Health Effects Many people use cannabis regularly with little obvious effect on their health. In fact, the most common physiological effects reported by cannabis users are feelings of thirst and hunger (“the munchies”). However, cannabis smoke contains many of the same ingredients as tobacco, so cannabis smoking can result in the same respiratory problems that cigarette

Table 4.3: Common hallucinogenic substances

Name Description

MDMA Widely known as ecstasy, MDMA has both hallucinogenic and amphetamine-like stimu- lating qualities. MDMA destroys neurons, especially those containing dopamine. It not only produces hallucinations but also a loss of motor control (Fischer, Lankford, & Galea, 1995).

Natural (plant-derived) substances

Psilocybin (found in certain mushrooms), DMT (from the bark of the South American virola tree), mescaline (a cactus derivative), and other naturally occurring hallucinogens produce varying degrees of cognitive distortions depending on their concentration and on users’ expectations. (People who expect to see changing colors or bright lights are more likely to experience these sensations than those without such expectations.)

LSD Lysergic acid diethylamide is one of the most powerful hallucinogens. The physical effects of LSD are similar to those of stimulants: increased heart rate and blood pressure, loss of appetite, sleeplessness, and dry mouth. LSD’s psychological effects depend on the amount ingested, individual differences, expectations, and the social context. Typical reactions include rapid mood swings, distortions in time, and hallucinations. Sensations become confused, and some people claim to “hear” colors and “see” sounds (a phenom- enon known as synesthesia). People who find such sensory experiences frightening label their experience a “bad trip” (American Psychiatric Association [APA], 2000).

PCP Because its profile of psychological effects differs from those of LSD and MDMA, the DSM–5 puts phencyclidine (PCP) in a different category. Yet PCP is also a powerful hal- lucinogen. Widely known as angel dust, PCP was developed in the 1950s as a surgical anesthetic. However, many people given PCP had hallucinations.

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smoking causes: cough, increased susceptibility to colds, and lung disease. In fact, because cannabis smokers try to keep the smoke in their lungs as long as possible, smoking a mari- juana joint may actually have a greater effect on respiratory health than smoking a cigarette. Cannabis also increases blood pressure and heart rate, so it may have particularly negative effects on people with heart or circulatory diseases (Hall & Degenhardt, 2013; Owen, Sutter, & Albertson, 2014; Volkow, Baler, Compton, & Weiss, 2014).

Over the past few years, many regular users of marijuana have either demonstrated mari- juana abuse or become physiologically dependent, meaning they develop a tolerance for it and demonstrate irritability and restlessness when they stop using (Hasin et al., 2015). The long-term effects of cannabis smoking on the pulmonary-respiratory system are not as clear (Hall & Degenhardt, 2013). The 2014 National Survey on Drug Use and Health provides the following statistics: “Marijuana was the illicit drug with the highest rate of past-year depen- dence or abuse in 2014, followed by pain relievers and cocaine. Of the 7.1 million persons aged 12 or older classified with illicit drug dependence or abuse in 2014, 4.2 million had mar- ijuana or hashish dependence or abuse (representing 1.6 percent of the total population aged 12 or older, and 63.0 percent of all those classified with illicit drug dependence or abuse), 1.9 million persons had pain reliever dependence or abuse, and about 913,000 persons had cocaine dependence or abuse” (CBHSQ, 2015).

Medical Marijuana Usage According to the National Institute on Drug Abuse (NIDA, 2017), medical marijuana refers to using the whole, unprocessed marijuana plant or its basic extracts to treat symptoms of ill- ness and other conditions. The U.S. Food and Drug Administration (2017) has not recognized or approved the marijuana plant as medicine. THC can increase appetite and reduce nau- sea, which are extremely important for chemotherapy patients. THC may also decrease pain, inflammation (swelling and redness), and muscle control problems. These problems may also be treated with opioids, which can become physiologically addicting. Although the marijuana plant is still not FDA approved as of this writing, its potential medicinal usages require further research so that we can ascertain if (and how) this plant can have medicinal value.

Psychological Effects The psychological effects of cannabis are highly variable. They depend on the amount of THC ingested, the expectations of the individual, and the social context. Some people feel noth- ing at all when they smoke marijuana. Most report feeling lazy, relaxed, and mildly elated (a state usually summarized as feeling “stoned”). Distorted perceptions (sights, sounds, time, and touch) have also been reported (Hadland, Knight, & Harris, 2016). Occasionally, can- nabis users experience sudden feelings of anxiety and have paranoid thoughts (Hadland et al., 2016). A 2016 meta-analysis estimated that cannabis use is statistically associated, in a dose-dependent manner, with an increased risk of the development of psychotic disorders, which might include schizophrenia (Marconi, Di Forti, Lewis, Murray, & Vassos, 2016). Dose- dependent refers to a relationship in which a change in the amount, intensity, or duration of exposure to marijuana is associated with a change in risk of a specified outcome, in this case an increased risk of developing psychotic disorders.

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Section 4.2 Why Are Psychoactive Substances So Popular?

4.2 Why Are Psychoactive Substances So Popular? Why do we use psychoactive substances? According to ethologists, scientists who observe natural behavior in humans and animals, substance use is a “displacement” activity, some- thing done in place of another behavior. For example, psychoanalysts view smoking as a way of obtaining oral gratification, a displacement for the breast. Such simple explanations, how- ever, hardly do justice to the complex web of factors controlling substance use.

Perhaps the most obvious reason for using a substance is to change our state of conscious- ness. If we need to get started in the morning or if we are having trouble concentrating on our work, a cup of coffee or a cigarette may help. Similarly, when we are tense, alcohol or canna- bis may help us to relax. In other words, we use psychoactive substances to produce specific psychological effects.

Although they are important, the psychological effects of substances are only part of the story. Substance use is the complex result of several interacting factors: exposure and availability, reinforcement, expectancies, social and cultural context, and biological variables.

Modeling, Exposure, and Availability Before we can use a substance, we must first know that the substance exists and, second, have access to it. In the case of caffeine, modeling is almost universal. Parents, friends, practically everyone uses caffeine in one form or another. Alcohol use is also widely modeled. Children can readily identify the smell of alcohol (beer, wine, or whiskey), and many associate alcohol with adults or with unpleasant results (Jayne & Valentine, 2017).

Because we see so many people using caffeine, alcohol, and nicotine, often in happy surround- ings, and because these substances are heavily promoted in the media and by peers, it is not surprising that most of us decide to give at least one of them a try. Contrast the familiarity and availability of caffeine, nicotine, and alcohol with our knowledge of and access to amphet- amines. Amphetamines are also stimulants, but they are not as widely used. Few of us see our parents or friends using them, and they can be obtained legally only with a doctor’s prescrip- tion. In addition, marijuana is legal in some countries but not in others. Therefore, people who have been exposed to marijuana will be more familiar with it and its usage than will those who live in countries where marijuana is illegal. Medical marijuana usage remains part of the national debate in the United States.

Reinforcement Modeling and availability might determine which substances we are most likely to try, but other factors determine whether we will keep using those we do try. One of the most impor- tant factors is the positive reinforcement we get from changing our mental state through the use of a substance (Posner, Amira, Algaze, Canino, & Duarte, 2016). These changes in mental state are perceived as pleasurable because they stimulate the brain’s “pleasure center,” the part of the brain that gives rise to subjectively pleasant feelings (Olds, 1956; Wise, 2013).

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Although the exact location of the pleasure center is a matter of debate, it seems to be closely related to the dopamine system (Wise, 2013). One of the reasons that people continue to use substances is to experience the reinforcing feelings produced when substances stimulate the brain’s pleasure center (see Figure 4.3).

Figure 4.3: The chemical process of dependence on nicotine

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 6.4, p. 86.

Receptor sites

Dopamine

Transmitting nerve cell

Nerve signal

Nerve ending

Receiver cell

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Section 4.2 Why Are Psychoactive Substances So Popular?

The reasons for using a substance may change over time. Consider cigarette smoking, for instance. Most of the time, people find their first experience unpleasant. The first few ciga- rettes may cause coughing, dizziness, nausea, even vomiting. It is amazing that anyone would wish to repeat the experience, especially since most adolescents know the health risks before they light up their first cigarette, though they typically underestimate the risk involved (Ambrose et al., 2014). Yet many go on to become smokers. One reason is peer group accep- tance. Teenagers whose siblings or friends smoke are more likely to begin smoking than are those with no peers to emulate or impress (Huang et al., 2014). Because smoking is followed by peer approval, as well as by desired changes in mental state, it is reinforced. Exactly the same group dynamics reinforce the use of alcohol, cannabis, and other substances. Social reinforcement is an important determinant of substance use because substances are an inte- gral part of social activity.

In addition to positive reinforcement, negative reinforcement (escape from an aversive state) also plays an important role in substance use. Feeling tired or unable to concentrate is an unpleasant feeling. If a cigarette or a cup of coffee dissipates our fatigue and makes us more alert, we will be reinforced to try the same “cure” again the next time we feel tired or dis- tracted. Similar negative reinforcement comes from substances that reduce feelings of anxi- ety and depression (SAMHSA, 2016).

Expectancies Expectancies also influence usage (Harrell et al., 2015). How can a substance like nicotine, which increases blood pressure, pulse rate, and arousal, help people relax and fall asleep? We have discussed part of the answer; increases in arousal are reinforcing for low-arousal people, and stimulants affect the brain’s pleasure center, releasing pleasurable endorphins, chemicals in the body that inhibit pain and produce pleasure. But there is another factor operating as well—cognitive expectancies. If we believe that a cup of tea will help us to sleep or that a cigarette will help us relax, then they probably will have these effects even though both tea and cigarettes contain stimulants. These expectancies about the effects of substances are the result of direct experience with a substance as well as exposure to parents, peers, and the media (Chisolm, Manganello, Kelleher, & Marshal, 2014).

Social and Cultural Context As stated, the reinforcement produced by peer group acceptance is an important determi- nant of substance use, but economic factors are also related to substance use (Karriker-Jaffe, 2013). For instance, people in lower socioeconomic classes have higher substance abuse rates (Andrabi, Khoddam, & Leventhal, 2017; Karriker-Jaffe, 2013). Substance use is a particularly serious problem for some ethnic groups. Therefore, understanding substance use, and help- ing people with substance-related problems, requires sensitivity to the ways in which cultural norms affect substance-related behavior (Otiniano-Verissimo, Grella, Amaro, & Gee, 2014).

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Biological Variables and Individual Differences Some people may be genetically vulnerable to suffer from drug abuse (Palmer et al., 2015). If they are exposed to certain substances, people with such predispositions are more likely than others to use again. For example, genetics certainly play a role in alcohol use (Verhulst, Neale, & Kendler, 2015). A possible mechanism for a predisposition to alcoholism is the dopamine 2 (D2) gene found on chromosome 11 (Bühler et al., 2015; Mbarek et al., 2015). About 66% of excessive alcohol users (people whose alcohol use has caused them problems) carry this gene, whereas it is present in only 20% of the rest of the population. The existence of the D2 gene does not mean that some people are born “alcoholics.” Other genes may be connected to substance-related disorders (see Bühler et al., 2015). Chromosomes 4 and 12 have also been implicated (Bühler et al., 2015; Mbarek et al., 2015). In addition, an individual with a D2 gene might never drink because of religious reasons, choice, a preexisting medical condition, or for some other reason. The same gene is also associated with other substances, including nico- tine and opioids, and with compulsive binge eating and gambling (Bühler et al., 2015; Clarke et al., 2014; Gyllai et al., 2014; Kessler, Hutson, Herman, & Potenza, 2016; Lobo et al., 2015; Schulte, Grilo, & Gearhardt, 2016).

Some people with the D2 gene may never develop substance-related problems because they have also inherited competing dispositions that counteract the effects of D2. For example, as many as half of all people of Asian descent lack one of the enzymes that helps break down alcohol in the liver. When they drink alcohol, they experience an “alcohol-flush syndrome” that includes a blushing red skin, dizziness, and nausea (Newman et al., 2013). The alcohol- flush syndrome may be unpleasant enough to prevent affected people from drinking, even if they have inherited the D2 gene.

It is important to note that one third of problem drinkers do not have the D2 gene. This sug- gests that there may be two different types of people who develop problems with alcohol: (a) those with the D2 gene and a family history of excessive drinking, who develop alcohol-related problems early in life, and (b) those without the gene, whose drinking problems develop late in life and whose social and occupational functioning is only mildly affected (Schuckit & Smith, 1996; Yoshino & Kato, 1996). Drinking in the second group seems mainly affected by environmental factors (exposure, social reinforcement), whereas drinking in the first group may be influenced more by genetics.

The United States’ Opioid Epidemic In 2015 (the latest year for which data are available), 12.5 million people misused prescrip- tion opioids (USDHHS, 2017). Of those, 2.1 million people misused prescription opioids for the first time, and 2 million people had prescription opioid use disorder. In addition, 33,091 people died from overdosing on opioids, including 15,281 whose deaths were attributed to overdosing on commonly prescribed opioids, an inordinately high number. In 2013, the opioid epidemic cost the United States $78.5 billion (USDHHS, 2017). These numbers are increasing yearly, indicating the existence of a significant opioid epidemic, and one that is not going away soon. The USDHHS notes that the misuse and abuse of prescription medications in the United States remains high, but few people are aware of the extent of the problem. As we will discuss later, the best methods to address the problems of misuse and abuse are increased education and prevention. We need to determine why the abuse rate continues to increase, and how we

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Section 4.3 Potential Problems of Sustained Substance Use

can educate preteens and teenagers about the dangers of these substances. Perhaps then we will see the opioid abuse rate and the resulting death toll decrease.

4.3 Potential Problems of Sustained Substance Use The average American consumes 200 mg of caffeine per day, the equivalent of two strong cups of brewed coffee. Of course, many people consume much more. High caffeine consumption can induce caffeine intoxication, which is marked by restlessness, excitement, an inability to sleep, flushed face, muscle twitching, and in especially severe cases, rambling speech, heart rate abnormalities, and agitation (APA, 2013). Very large doses can even be fatal. Alcohol and cannabis also produce well-documented intoxication syndromes (APA, 2013).

You may know people who show no signs of intoxication even after consuming significant amounts of alcohol and wonder why these people seem immune to its intoxicating effects. The answer is tolerance (the lessening of the body’s response to a drug after continued use). As a result of tolerance, individuals using a drug will find that they begin to need greater and greater amounts in order to achieve the same effects as before, or even to achieve a lesser effect. Three beers may be enough to produce intoxication in a nonuser, whereas a much larger amount may have little or no effect on a habitual beer drinker. People can develop tol- erance to most (but not all) substances.

How much substance users consume, and how often, is determined partly by the amount of a substance in the user’s body. For example, smokers adjust their habit to maintain a certain level of nicotine in their bodies. If the amount of nicotine falls below the desired level, smok- ers may become irritable, restless, distractible, and hungry (Soyster, Anzai, Fromont, & Pro- chaska, 2016). These symptoms are known as nicotine withdrawal (APA, 2013). The DSM–5 also contains diagnostic criteria for alcohol withdrawal, which is marked by tremor, sweating, nausea, and anxiety. In severe cases, people withdrawing from alcohol may experience dis- turbances in consciousness, including hallucinations (known as delirium tremens, or the DTs). Withdrawal symptoms may be so severe that people continue using a substance just to avoid the symptoms. In such cases, substance use is being maintained by a form of negative reinforcement.

Substance Use Versus Substance Abuse Substance use, by itself, is not a psychological disorder. Substances present a psychological problem only when they produce adverse consequences. Consuming a glass of wine with din- ner does not lead to adverse consequences for most people; thus, it is not a sign of a psycho- logical disorder. In contrast, drinking to the point of intoxication and missing classes several times a week for a number of weeks could be a sign of what the DSM–5 refers to as a sub- stance use disorder.

The DSM–IV–TR had separate categories for substance abuse and substance dependence. Sub- stance dependence criteria included tolerance and withdrawal as well as loss of control (the feeling that once an individual began using a substance, he or she was unable to stop, even if intending to do so). The DSM–5 combined both categories into a new category: substance

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Section 4.4 Overcoming Substance Use Disorders

use disorder (APA, 2013). This new category codes the substance use disorder on a spec- trum using the following specifiers: mild, moderate, and severe. In addition, the criterion that the individual had to have recurrent legal problems in order to qualify for the old substance abuse diagnosis has been eliminated from the DSM–5 (APA, 2013). It is now also somewhat more difficult to “qualify” for substance use disorder. To qualify for the DSM–IV–TR substance abuse diagnosis, an individual had to satisfy minimally one criterion. In the DSM–5, the indi- vidual must satisfy minimally two or more criteria. For the moderate subcategory, an indi- vidual must satisfy minimally four or more criteria, as opposed to satisfying three or more for the old substance dependence disorder.

Perhaps more important, a new criterion was added to the DSM–5 regarding substance use disorder: craving, or a strong desire or urge to use a substance (APA, 2013). Craving implies physiological dependence which can lead to loss of control as well as intoxication.

Substance Dependence Chronic substance abuse or misuse may lead to a substance use disorder. The DSM–5 uses the term dependence rather than addiction because the latter has pejorative connotations and, according to APA, has an uncertain definition (APA, 2013). According to the DSM–5, all catego- ries of substances except caffeine can produce a substance use disorder.

Once a substance use disorder forms (meaning that the individual may have developed a dependence on that substance), people begin to organize their lives around satisfying their craving. The chronic use of substances may also change body chemistry because many sub- stances replace the body’s natural chemicals. When substances are discontinued, the body takes a while to restart its natural production. In the interim, the person experiences with- drawal symptoms.

Not all substances produce physical signs of tolerance and withdrawal. The opposite is also true: Tolerance and withdrawal can exist without the craving for a substance that marks dependence.

Scientists once thought that people who abuse alcohol enter an inevitable downward spiral in which they become increasingly dependent (Jellinek, 1946), but we now know that alcohol abuse does not necessarily lead to dependence, or a substance use disorder (Wise & Koob, 2014). What is still not entirely clear is why some alcohol abusers become dependent, whereas others do not (Sobell & Sobell, 1993; Vaillant & Hiller-Sturmhofel, 1997). It is important to emphasize that dependence is much the same disorder whatever the substance involved. Dependence on multiple substances is known as polysubstance dependence, a common pat- tern among many substance-dependent individuals (Connor, Gullo, White, & Kelly, 2014).

4.4 Overcoming Substance Use Disorders Substance use is often a difficult pattern to break. Even people who are highly motivated to quit may not necessarily succeed. This section illustrates the problems people face in overcoming a substance use disorder and maintaining recovery and offers some proposed

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Section 4.4 Overcoming Substance Use Disorders

solutions. Because the use of nicotine and alcohol is so common, the main focus of this section is on these two substances, but the discussion also shows how lessons learned from helping people give up common substances may be applied to less frequently used substances.

Practically all treatment programs for substance dependence combine several different meth- ods, a strategy known as multimodal treatment. The general idea is to wean people away from a substance; help them manage their craving; and give them the skills necessary to cope with social stress, anxiety, and other potential causes of substance abuse.

Stages in Overcoming Substance Use Disorders As summarized in Figure 4.4, people with a substance use disorder are thought to go through a series of stages in the process of recovery from substance dependence. This model was orig- inally put forward by Prochaska and DiClemente (1983), to describe the process of quitting smoking, but it is applicable to practically any substance (see also Kougiali, Fasulo, Needs, & Van Laar, 2017). From not even thinking about ceasing substance use and not thinking that they have a substance dependence (the precontemplation stage), people move through the contemplation stage, in which they are thinking about ceasing usage and are beginning to think that they have a substance dependence, to the action stage, in which they actually quit. In the final stage, maintenance, they consolidate their treatment gains and attempt to avoid relapse. Most psychological treatment programs are aimed at the action stage, and the major- ity also address maintenance issues. (See Part 2 of Robert Jones’s case in the appendix.)

Figure 4.4: Lichtenstein and Glasgow’s stages of giving up a substance

Source: Adapted from S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 6.6, p. 261.

Precontemplation

Contemplation

Action

Maintenance

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Section 4.4 Overcoming Substance Use Disorders

Detoxification Once the action stage is reached, the first step in many treatment programs is detoxification, removal of the substance from the body. Smokers must stop smoking; alcohol-dependent peo- ple must stop drinking; heroin users must stop injecting or snorting.

To minimize withdrawal symptoms and maximize the probability that an individual will con- tinue treatment, detoxification is usually a gradual process (Sachdeva, Choudhary, & Chandra, 2015). Sometimes, people undergoing detoxification may be prescribed anxiolytics and anti- depressants to help with the stress of the withdrawal process (Sachdeva et al., 2015). Care must be taken, however, to limit the use of these drugs to ensure that people do not give up one substance only to start using another. Residential facilities (hospitals, drug treatment centers) often provide the safest environment for people undergoing withdrawal. However, inpatient treatment is more expensive than outpatient treatment, and there is little evidence that the extra expense necessarily produces better outcomes (Sachdeva et al., 2015). Most detoxifications today occur on an outpatient basis (Sachdeva et al., 2015). Inpatient treat- ment will offer better continuity for the patients, especially if they begin their treatment in a hospital. It also keeps the patient in an alcohol-free environment, lessening the relapse pos- sibility. In addition, one study demonstrated that relapse rates are high for those patients who do not receive a treatment follow-up to detoxification (Polydorou & Kleber, 2008).

Detoxification does not, by itself, constitute a treatment. Many substance-dependent people go through cycles of detoxification followed by abuse and dependence followed by detoxifica- tion again (McKay & Hiller-Sturmhoefel, 2011). To break this cycle, clinicians may prescribe a medication to block the action of the substance.

People who are dependent on alcohol (an alcohol use disorder) may be prescribed a drug called Antabuse. If they take Antabuse and then consume alcohol, they will become quite ill—their hearts will race, they will vomit violently, and they may break out in soaking sweats. In theory at least, people who take Antabuse will stop drinking alcohol to avoid becoming ill (Soyka et al., 2017). Unfortunately, these aversive treatments rely on the person actually tak- ing the Antabuse. A person who wants to drink without becoming sick needs only to stop tak- ing the Antabuse—and that is just what many people do (Winslow, Onysko, & Hebert, 2016).

Substance Replacement and Maintenance Some forms of substance use disorder may be so addictive that users settle for replacing a dan- gerous substance with a less dangerous one that they can stay on indefinitely. This is known as maintenance treatment. The most common drug maintenance program involves substitut- ing the synthetic opioid methadone for the more dangerous opioid heroin (D’Aunno, Pollack, Frimpong, & Wuchiett, 2014). Methadone needs to be taken once a day, requiring either a daily trip to a clinic or take-home dosages. Although maintenance treatment may help some people wean themselves off heroin, it is almost certain that participants in such programs will become dependent on methadone (McCance-Katz & Kosten, 2005). Methadone maintenance is still the primary treatment approach for opioid disorders, even as buprenorphine (Subutex) and nal- trexone (Vivitrol) have become more widely used (D’Aunno et al., 2014).

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Highlight: Celebrities and Substance Use Disorder

The list of famous people and celebrities who have died as a result of a substance use disorder is lengthy and continues to expand. In May 2017, Chris Cornell, Soundgarden’s frontman, killed himself by hanging. A recovering drug addict, he was taking the anxiolytic lorazepam (Ativan) and may have overdosed. Prince died of a drug overdose in 2016. Prince had espoused clean living and to many people’s knowledge did not smoke, drink, or use illicit substances. Michael Jackson overdosed on propofol (Diprivan) as well as various anxiolytics. Amy Winehouse, a British singer and songwriter, was just 27 when she died of alcohol poisoning. What is it about being famous (or in Jackson’s, Prince’s, and, to a lesser extent, Cornell’s cases, music superstars) that could lead these individuals to develop a substance use disorder? Perhaps the pressures of fame, touring, and always being in the public eye led them to develop significant anxiety, and they saw alcohol and substance misuse as a way to cope with the anxiety.

How about you? When you have a bad day, perhaps failing an exam for which you knew the material cold, how do you handle it? Do you say, “I need a drink,” and then have one. . .or three? Is this a normal way to alleviate stress? After all, alcohol has been around since the beginning of recorded history, and besides, what is so terrible about having a beer after a long and difficult day?

For Cornell, Jackson, and the others, perhaps the media’s never-ending stream of photos, information, and gossip led to their deaths, since famous people are in the public eye every waking moment. Maybe it was the pressure of performing, or of coming up with new songs and albums, that created their problems. Or perhaps the music world attracts individuals

who are prone to addiction: the addiction of fame, performing live, making millions of dollars at a young age, and being admired for their music and voices. Maybe these pressures, and the fear of losing everything quickly, led them to illicit substances.

We can only presume that these very talented individuals were suffering silently, perhaps burdened by their fame, and sought a way to disconnect, even for a short while. Sadly, if this is the case, the brief respite from reality and stress that substances provided became an addiction, leading eventually to their deaths.

Album/Album/SuperStock Michael Jackson overdosed on propofol in 2009.

Francesc Fàbregas/Album/SuperStock Prince passed away from an overdose in 2016.

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Section 4.4 Overcoming Substance Use Disorders

Self-Help Groups Self-help groups have a long history in the treatment of substance dependence. Alcoholics Anonymous (AA), for example, has been offering a self-help program around the world since 1935 (Nathan, 1993). Al-Anon is a related organization that provides support for the families of people dependent on alcohol (Timko, Young, & Moos, 2012). There are similar programs, such as Narcotics Anonymous, for people dependent on opioids and other substances (Miller, Gold, & Pottash, 1989). The AA program usually progresses through a series of 12 steps (see the accompanying Highlight). Alcohol-dependent people must first acknowledge their depen- dency, must then put their trust in a spiritual being (“a power greater than ourselves”), and must make amends to people whom they have harmed (Pagano et al., 2013). Because people are not randomly assigned to AA or a control group, it is not possible to conduct controlled clinical trials on the effectiveness of AA.

Relapse Prevention Most substance abuse treatment programs have high relapse rates. For example, practically all quit-smoking programs are successful at first, but after a time, 70% to 80% of participants begin smoking again. Some treatment programs attempt to improve on this by training peo- ple to deal with the potential causes of relapse before they occur. The main factor influencing relapse prevention and treatment efficacy seems to be treatment length. Longer, repeated, and more intense treatments produce better results than brief treatments (McKay & Hiller- Sturmhoefel, 2011). (See Part 3 of Robert Jones’s case in the appendix.)

Treatment of Substance Use Disorder (Substance Dependence): State of the Art Despite the best efforts of generations of psychologists, substance dependence remains difficult to treat. An 11-year follow-up study showed that 10.2% of men treated for heroin dependence were dead, 24.8% continued to use heroin, 46.6% were currently in treatment, and about 22% were involved with criminal activity (Teesson et al., 2015). More recent data reveal that, in the United States, the number of persons aged 12 or older needing treatment for an alcohol use problem was 18.0 million (6.9% of the population aged 12 or older; NSDUH, 2013). Even though the NSDUH report does not discuss the difficulty of preventing alcohol abuse or dependence relapse, practitioners and individuals with an alcohol abuse or depen- dence problem know the difficulty of maintaining recovery. In short, no single program seems to work for everyone.

Substance dependence is often associated with other psychological disorders (Lai, Clearly, Sitharthan, & Hunt, 2015). It is often difficult to determine whether substance abuse is the cause of another psychological disorder or its result, or both (Lai et al., 2015). In most cases, however, it is necessary to treat any serious psychological disorders before people can mod- erate their use of substances. The problems of mentally ill chemical abusers (MICAs) are especially severe, according to one study (Kutcher, Kachur, Marton, Szalai, & Jaunkalns, 1992). MICAs, who are most often young males, are generally poor, homeless, sickly, and likely to get into legal difficulties.

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Highlight: Some Thoughts on Alcoholics Anonymous (AA)

Chances are excellent that you have heard of Alcoholics Anonymous, or AA, sometimes called Friends of Bill W. on cruise ships and elsewhere (Bill Wilson, along with Dr. Bob Smith, founded AA). You may have some preconceived notions: that AA is for a bunch of drunks, that it’s an excuse to drink anonymously, that it’s only for men or ex-Navymen, that it’s only for alcoholics, that it espouses religion and if you’re not religious you cannot attend, or that it’s only for older people. All of these statements are unequivocally false. AA welcomes everyone: all genders and people of any ethnic, racial, or religious background, usually without an age floor (the lowest age allowed, within reason, of course). One does not need to have a

substance use disorder to attend. Open meetings are for people who want to learn about AA and for those who think they may have a substance use disorder or misuse a substance—in both cases, alcohol. Typically these meetings include a speaker who relates his or her story to the audience. The attendees may take turns discussing their connection to the night’s story or theme. Closed meetings are for those who have, or think they have, a substance use disorder. Typically these meetings have a leader who discusses a theme, speaks to how the theme relates

to himself or herself, and then goes around a table or the room to ask others what the theme means to them. There is never pressure to participate, nor to pay (meetings are free). A contribution “hat” may be passed, but it’s not mandatory to give. Most important, last names and even last initials are never used; the entire meeting is anonymous. Finally, although the 12 steps process has a religious overtone, AA itself is not a religious entity. According to the organization’s website, “A.A.’s Twelve Steps are a group of principles, spiritual in their nature, which, if practiced as a way of life, can expel the obsession to drink and enable the sufferer to become happily and usefully whole.”

As noted previously, AA and its relatives Al-Anon and Narcotics Anonymous have seemed to be effective in helping people to stay sober and clean. Many clinicians use these groups as a treatment adjunct (an addition to psychotherapy), and patients seem to appreciate feeling as though they are not alone.

AA is a worldwide organization and is still going strong after more than 80 years. What are your views on AA? Did you believe some of the myths shared at the beginning of this feature? Would you ever consider going to an open meeting to observe and learn?

Quoted text from www.aa.org.

KatarzynaBialasiewicz/iStock/Thinkstock

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Section 4.5 Prevention of Substance-Related Disorders

4.5 Prevention of Substance-Related Disorders Although they vary in their specifics, all clinical-based programs for substance dependence focus on the individual. The social forces maintaining substance abuse—peer pressure, lack of knowledge, advertising (in the cases of nicotine and alcohol), and legal restrictions—are rarely addressed. Clinical programs are also expensive; they involve multiple sessions, and only limited numbers of people can be treated at one time. In contrast, prevention programs have the potential to save money because keeping disorders from developing is usually cheaper than treating disorders after they develop. Prevention programs may benefit the most people who are unable to access or afford clinical treatment.

Legal Restrictions Perhaps the most straightforward approach to the primary prevention of substance abuse and dependence is to use the legal system. However, because legal restrictions on exposure to drugs have had limited success, public health authorities have argued that restricting access might be a more effective means of preventing substance abuse (Stockings et al., 2016).

One approach to restricting access is to ban substance use in certain settings. Smoking, which was once common in offices, restaurants, planes, and theaters, is now prohibited in most public areas. As the number of places where smoking is permitted decreases, smokers have fewer opportunities to pursue their habit. Thus, making smoking inconvenient may reduce its prevalence (Stockings et al., 2016).

Health Education Programs Although people who use substances are usually aware of the health risks, they tend to believe that these risks apply more to other people than to themselves (Gibbons, McGovern, & Lando, 1991). This feeling of invulnerability, which applies to adults as well as adolescents (Quadrel, Fischhoff, & Davis, 1993), may explain why people continue to use dangerous sub- stances even when they know they are harmful (Gibbons, Kingsbury, & Gerrard, 2012). The main value of health warnings (such as the surgeon general’s warning on cigarette packages or television commercials that talk about the perils of drug use) is in moving those who use substances from the precontemplation to the contemplation stage of the quitting process, at which point other, more powerful interventions take over.

Specific Educational Programs Global educational programs provide information about substances, but they do not address the factors that maintain substance use: peer pressure, mood changes, advertising, avoidance of withdrawal, and stress reduction. Specific educational interventions designed to teach those at risk how to resist these influences and temptations, and how to deal with stress and withdrawal, may have a greater chance of succeeding (Ksir et al., 2008).

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Chapter Summary

Worksite Programs As their name suggests, worksite programs are delivered to workers, and sometimes their families, at their places of employment. With the cooperation of employers, workers are given time off to attend these programs and may even be rewarded for success. In an attempt at secondary prevention, some employers also use chemical tests to screen employees for sub- stance use. However, such programs raise certain ethical problems involving consent and dis- closure of purpose (Forrest, 1997).

Highlight: Substance Use on the Big Screen

Do these titles sound familiar: Arthur, Fast Times at Ridgemont High, Harold and Kumar Go to White Castle? They are all Hollywood comedies that have as a central theme excessive alcohol or drug usage. In each film (and in far too many others to mention), the excessive usage is portrayed in a comedic fashion. To be sure, these films are quite funny, as comedies should be. But what kinds of messages do they send to the general public who watches them? In Fast Times, Sean Penn’s character, Spicoli, is perpetually stoned; the same is true for Kumar in that film series. Arthur is virtually always intoxicated.

Should the general public be laughing at individuals who, if they came into a psychologist’s office, would most likely be diagnosed with a substance use disorder? Is being perpetually stoned or drunk something that is funny, or is it dangerous? More important, let’s presume that the majority of the population does not understand what a substance use disorder is, and that these films (and similar television shows) are their primary exposure to the disorder. How could we make audiences understand that these comedic portrayals are fictitious, and that a real substance use disorder is not funny at all, but instead presents a risk to the person’s life, as well as to loved ones, family members, and innocent people, especially if the person chooses to drive while intoxicated?

An important component of a helping professional’s job is being an educator. We need to continue to educate the public about what a substance use disorder is, about how it truly presents itself, and, most important, that the situations and characters seen in movies, while amusing, are designed to make us laugh and are not accurate portrayals of the facts.

Chapter Summary

Psychoactive Substances: Some Basic Information • Practically everyone has used a psychoactive substance at some time in their lives.

These substances form a spectrum, from those that are commonly used, such as caf- feine, to highly dangerous drugs such as heroin and other opioids.

• Caffeine, nicotine, alcohol, and cannabis are the four psychoactive substances most commonly used by American college students.

• Caffeine is found in many drinks, as well as in headache, diet, and cold medications. Nicotine is the psychoactive ingredient in tobacco. Alcohol is found in wine, beer, spirits, and many medications. And cannabis is a type of hemp plant whose leaves may be ingested in a variety of ways.

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Chapter Summary

• Caffeine and nicotine are stimulants; they combat drowsiness, increase alertness, and help produce energy.

• Alcohol is a depressant, which slows body processes and induces sleep. • Cannabis has a variety of stimulant and depressant effects. It also has the potential

to produce sensory and cognitive distortions. • Although caffeine and nicotine may be dangerous to one’s health in large doses, they

have not been linked to any specific illness. • At higher doses, alcohol can cause serious health problems, and cannabis smoke

may be as dangerous as cigarette smoke. • Although both caffeine and nicotine are stimulants, many people claim to find them

relaxing. This may be a reflection of their ability to enhance the body’s natural opioids.

• Relaxation may also be the result of cognitive expectancies and social reinforcement. • A third possibility is that some personality types (extroverts) are chronically under-

aroused, a state they find unpleasant. Because stimulants increase their arousal to “normal” levels, they find these substances produce pleasant feelings.

Why Are Psychoactive Substances So Popular? • People begin to use substances such as nicotine, alcohol, and opioids partially

because of social conformity. • Certain personality traits—extroversion, for example—may also encourage people

to use substances.

Potential Problems of Sustained Substance Use • Using substantial amounts of many substances can result in intoxication. • Chronic use of substances may also produce tolerance, forcing users to continually

increase the amount they consume to achieve the same effect. • When one has a substance dependence, abruptly ceasing a habitually used substance

can produce the unpleasant symptoms characteristic of withdrawal.

Overcoming Substance Use Disorder • First, the person must decide to change. Next comes an active attempt to change.

Finally, the new behavior must be maintained. • Most psychological interventions are aimed at the action stage; many also target the

maintenance stage. • Practically all treatment programs aimed at substance abuse and dependence are

multimodal (they combine several treatment methods). • Sometimes, replacing one substance with another, less dangerous one (replacing

cigarettes with nicotine patches, for example) can assist the treatment process. • In addition to positive treatments, aversive conditioning has also been widely used

to help people who are dependent on substances.

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Chapter Summary

Prevention of Substance-Related Disorders • Public health interventions have the potential to reach many more people at much

less cost than psychological interventions. • Although they may be valuable in getting people to think about quitting, outright

prohibition and global educational programs have not proved successful in reducing substance dependence.

• Worksite programs and self-help strategies have the potential to help many people give up substances.

Critical Thinking Questions 1. Let’s assume that you are a regular coffee, tea, or cola drinker. How difficult would

it be for you to quit drinking “cold turkey,” that is, to stop drinking these beverages completely, with no treatment interventions?

2. Some people believe that a substance use disorder (substance dependence) is a moral flaw and is the fault of the dependent individual—that is, the individual can stop whenever he or she likes. What are your views on this perspective?

3. The chapter notes that some psychoactive substances cannot lead to physiological dependence. Discuss your views on this.

4. Alcoholics Anonymous (AA) has been around for more than 80 years, and, in spite of no solid research support, the organization seems to be successful. How can a self- help group where no therapy is provided help people stay sober and straighten out their lives?

5. Discuss your views on using psychoactive substances like methadone to treat opioid dependence.

6. We have mentioned elsewhere that psychotropic medications such as anxiolytics can be used to treat psychiatric disorders. It is possible to become dependent on some of these medications. What is your perspective on this? Is helping to treat a condition worth the risk of dependence?

Key Terms agonist A chemical that increases the potency of other chemicals.

alcohol (ethanol) The second most com- monly used psychoactive substance in the United States.

alcohol dehydrogenase (ADH) An enzyme that breaks down alcohol in the stomach and the liver.

alcoholic myopia Narrowing of focus to the immediate.

antagonist A chemical that reduces the potency of other chemicals.

binge drinking Consumption, for a male, of five or more alcoholic drinks in a row on at least one occasion during a two-week period; for a female, it is four or more drinks.

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Chapter Summary

caffeine A stimulant; the most commonly used psychoactive substance in the United States.

cannabis Marijuana or pot; a type of hemp plant that produces several psychoactive substances such as marijuana and hashish.

craving A strong desire or urge to use a substance.

delirium tremens (the DTs) A symptom of alcohol withdrawal, which can include hallu- cinations, disorientation, insomnia, physical discomfort, shaking, and nausea.

depressant A psychoactive substance that lowers arousal and makes people drowsy.

detoxification Removal of a substance from the body, usually done in an inpatient setting.

endorphins Chemicals in the body that inhibit pain and produce pleasure.

ethologists Scientists who observe natural behavior in humans and animals.

expectancies What people expect when they use a drug or substance.

extroversion A personality trait commonly found in people born with low levels of arousal. The experience of low arousal is perceived as unpleasant, so extroverts con- tinuously seek stimulation.

fetal alcohol syndrome (FAS) A disorder marked by intellectual disabilities, hyper- activity, facial deformities, heart defects, and organ malfunctions due to the mother’s excessive alcohol consumption during pregnancy.

hallucinogen A psychoactive substance that produces distorted sensations and per- ceptions (hallucinations).

lysergic acid diethylamide (LSD) A very powerful hallucinogen.

mentally ill chemical abusers (MICAs) Individuals, often young males, generally poor, homeless, sickly, and likely to get into legal difficulties, who misuse chemi- cal substances.

multimodal treatment Programs that combine several different methods to cure substance dependence.

nicotine A psychoactive substance found in cigarettes; it acts quickly and is addictive.

polysubstance dependence Dependence on multiple substances.

psychoactive substances Chemicals that alter a person’s moods or behavior.

risk factors Characteristics, genetic or otherwise, that seem to be associated with an increased risk of disease onset or recurrence.

stimulants Substances whose main psycho- active effects are to increase alertness.

substance use disorder (substance dependence) A condition in which the individual has a recurring pattern of substance-related difficulties. The more criteria the individual satisfies, the more likely the individual is physiologically dependent on that substance.

THC (delta-9-tetrahydrocannabinol) The psychoactive ingredient in marijuana.

tolerance The body’s response to a drug wherein it takes more (sometimes less) of a psychoactive substance to achieve the same effect.

withdrawal The physiological effects suf- fered by an individual once a psychoactive substance has been removed from the body.

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