ORIGINAL_INVESTIGATIONA_Brief_Measure_for_Assessing

ORIGINAL INVESTIGATION

A Brief Measure for Assessing Generalized Anxiety Disorder

The GAD-7

Robert L. Spitzer, MD; Kurt Kroenke, MD; Janet B. W. Williams, DSW; Bernd Löwe, MD, PhD

Background: Generalized anxiety disorder (GAD) is one of the most common mental disorders; however, there is no brief clinical measure for assessing GAD. The ob- jective of this study was to develop a brief self-report scale to identify probable cases of GAD and evaluate its reli- ability and validity.

Methods: A criterion-standard study was performed in 15 primary care clinics in the United States from No- vember 2004 through June 2005. Of a total of 2740 adult patients completing a study questionnaire, 965 patients had a telephone interview with a mental health profes- sional within 1 week. For criterion and construct valid- ity, GAD self-report scale diagnoses were compared with independent diagnoses made by mental health profes- sionals; functional status measures; disability days; and health care use.

Results: A 7-item anxiety scale (GAD-7) had good re-

liability, as well as criterion, construct, factorial, and pro- cedural validity. A cut point was identified that opti- mized sensitivity (89%) and specificity (82%). Increasing scores on the scale were strongly associated with mul- tiple domains of functional impairment (all 6 Medical Out- comes Study Short-Form General Health Survey scales and disability days). Although GAD and depression symp- toms frequently co-occurred, factor analysis confirmed them as distinct dimensions. Moreover, GAD and de- pression symptoms had differing but independent ef- fects on functional impairment and disability. There was good agreement between self-report and interviewer- administered versions of the scale.

Conclusion: The GAD-7 is a valid and efficient tool for screening for GAD and assessing its severity in clinical practice and research.

Arch Intern Med. 2006;166:1092-1097

O NE OF THE MOST COM- mon anxiety disorders seen in general medical practice and in the gen- eral population is gener-

alized anxiety disorder (GAD). The disor- der has an estimated current prevalence in general medical practice of 2.8% to 8.5%1-3

and in the general population of 1.6% to 5.0%.4-6 Whereas depression in clinical set- tings has generated substantial research, there have been far fewer studies of anxi- ety. In part, this may be because of the pau- city of brief validated measures for anxiety compared with the numerous measures for depression,7,8 such as the Primary Care Evaluation of Mental Disorders 9-item Pa- tient Health Questionnaire (PHQ).9-11 This situation is unfortunate, given the high prevalence of anxiety disorders, as well as their associated disability and the availabil- ity of effective treatments, both pharmaco- logical and nonpharmacological.12,13

Measures of anxiety are seldom used in clinical practice because of their length,

proprietary nature, lack of usefulness as a diagnostic and severity measure,14-17 and requirement of clinician administration rather than patient self-report.18,19 The goal of this study was to develop a brief scale to identify probable cases of GAD and to assess symptom severity. We conducted a study in multiple primary care sites to select the items for the final scale and to evaluate its reliability and validity.

METHODS

GAD SCALE DEVELOPMENT

We first selected potential items for a brief GAD scale. The initial item pool consisted of 9 items that reflected all of the Diagnostic and Statisti- cal Manual of Mental Disorders, Fourth Edition (DSM-IV) symptom criteria for GAD and 4 items on the basis of review of existing anxi- ety scales. A 13-item questionnaire was devel- oped that asked patients how often, during the last 2 weeks, they were bothered by each symp- tom. Response options were “not at all,” “sev-

Author Affiliations: Biometrics Research Department, New York State Psychiatric Institute and Department of Psychiatry, Columbia University, New York (Drs Spitzer and Williams); Regenstrief Institute for Health Care and Department of Medicine, Indiana University, Indianapolis (Dr Kroenke); and Department of Psychosomatic and General Internal Medicine, University of Heidelberg, Heidelberg, Germany (Dr Löwe).

(REPRINTED) ARCH INTERN MED/ VOL 166, MAY 22, 2006 WWW.ARCHINTERNMED.COM 1092

Downloaded From: https://jamanetwork.com/ on 03/30/2021

eral days,” “more than half the days,” and “nearly every day,” scored as 0, 1, 2, and 3, respectively. In addition, an item to assess duration of anxiety symptoms was included. Our goal was to determine the number of items necessary to achieve good reliability and procedural, construct, and diagnostic criterion validity.

PATIENT SAMPLE

Patients were enrolled from November 2004 through June 2005 from a research network of 15 primary care sites located in 12 states (13 family practice, 2 internal medicine) administered centrally by Clinvest, Inc (Springfield, Mo). The purpose of the project’s first phase (n = 2149) was to select the scale items and cutoff scores to be used for making a GAD diagnosis. The pur- pose of the second phase (n = 591) was to determine the scale’s test-retest reliability. In all, 2982 subjects were approached and 2739 (91.9%) completed the study questionnaire with no or minimal missing data. To minimize sampling bias, we ap- proached consecutive patients at each site in clinic sessions un- til the target quota for that week was achieved.

In the first phase, 1654 subjects also agreed to a telephone interview, and of these, a random sample of 965 were inter- viewed within 1 week of their clinic visit by 1 of 2 mental health professionals (MHPs)—a PhD clinical psychologist and a senior psychiatric social worker. In the study’s second phase, 591 subjects who had completed the research ques- tionnaire were sent a 1-page questionnaire that consisted of the 13 potential GAD scale items. Of these, 236 subjects returned the completed 1-page questionnaire with no or mini- mal missing data within a week of completing the research questionnaire at the clinic. The mean GAD scale score of sub- jects returning the questionnaire did not differ from that of subjects who did not return the questionnaire. The study was approved by the Sterling Institutional Review Board, Spring- field, Mo.

SELF-REPORT RESEARCH QUESTIONNAIRE

Before seeing their physicians, patients completed a 4-page ques- tionnaire that included the 13 items being tested for use in the GAD scale, as well as questions about age, sex, education, eth- nicity, and marital status; the Medical Outcomes Study Short- Form General Health Survey (SF-20),20,21 which measures func- tional status in 6 dimensions; and either the 12-item anxiety subscale from the Symptom Checklist-9016 (first study phase only) or the Beck Anxiety Inventory14 (second study phase only). Depression was assessed with the PHQ-8, which includes all items from the PHQ-9 except for the item about suicidal ide- ation; PHQ-8 and PHQ-9 scores are highly correlated and have nearly identical operating characteristics.22 Finally, patients com- pleted items regarding physician visits and disability days dur- ing the previous 3 months.

MHP INTERVIEW

The 2 MHPs conducted structured psychiatric interviews by telephone, blinded to the results of the self-report research ques- tionnaire. The interview consisted of the GAD section of the Structured Clinical Interview for DSM-IV,23 modified with sev- eral additional questions to assess in greater detail some of the GAD diagnostic criteria of DSM-IV. The resulting DSM-IV GAD diagnosis, with the DSM-IV 6-month duration criterion, was used as the criterion standard for assessing the validity of the new scale. The interview also included the 13 potential GAD scale items to test agreement between self-report and clinician administration (ie, procedural validity).24

DATA ANALYSIS

The best items for the GAD scale were selected by rank order- ing the correlation of each item with the total 13-item scale score in the sample of 1184 patients who did not undergo the MHP interview. Item-total score correlations were reexamined in 2 independent subsamples of the study population: the 965 pa- tients who underwent the MHP interview and the 591 pa- tients in the second phase of the study. In addition, we con- ducted receiver operating characteristic analyses with varying numbers of items in these 965 patients by using an MHP di- agnosis of GAD as the criterion standard. Divergent validity of each item was assessed by calculating the difference between the item correlations with the 13-item anxiety score and the PHQ-8 depression score. Convergent validity was assessed by examining correlations of the final version of the GAD scale with the Beck Anxiety Inventory and the anxiety subscale of the Symptom Checklist-90, even though neither scale is spe- cific for GAD.

To assess construct validity, we used analysis of covari- ance to examine associations between anxiety severity on the final GAD scale and SF-20 functional status scales, self- reported disability days, and physician visits, controlling for demographic variables. For criterion validity, we investi- gated sensitivity, specificity, predictive values, and likeli- hood ratios for a range of cutoff scores of the final scale with respect to the MHP diagnosis. To investigate whether anxi- ety as measured by the GAD-7 and depression as measured by the PHQ-8 reflect distinct dimensions, we assessed facto- rial validity by using confirmatory factor analyses. Finally, procedural validity and test-retest reliability were assessed by means of intraclass correlation.25

RESULTS

DESCRIPTION OF PATIENTS

The mean (SD) age of the patients was 47.4 (15.5) years (range, 18-95 years). Most (65%) were female; 80% were white non-Hispanic, 8% were African American, and 9% were Hispanic; 64% were married, 13% were divorced, and 15% were never married; and 31% had a high school degree or equivalent, whereas 62% had attended some college.

ITEM SELECTION FOR THE GAD SCALES

The GAD-7 (Figure 1) consists of the 7 items with the highest correlation with the total 13-item scale score (r = 0.75-0.85). Receiver operating characteristic analysis with this set of items showed an area under the curve (0.906) as good as scales with as much as the full 13-item set. These 7 items also had the highest rank correlations in the developmental sample (n = 1184) and the 2 replication samples (n = 965 and n = 591). The 2 core criteria (A and B) of the DSM-IV definition of GAD are captured by the first 3 items of the scale.26 Of note, 6 of the 7 items had the greatest divergent validity (ie, the highest difference between the item-total scale score correlation and item-PHQ-8 depression score correlation [� r = 0.16-0.21]). Because each of the 7 items is scored from 0 to 3, the GAD-7 scale score ranges from 0 to 21.

(REPRINTED) ARCH INTERN MED/ VOL 166, MAY 22, 2006 WWW.ARCHINTERNMED.COM 1093

Downloaded From: https://jamanetwork.com/ on 03/30/2021

RELIABILITY AND PROCEDURAL VALIDITY

The internal consistency of the GAD-7 was excellent (Cronbach � = .92). Test-retest reliability was also good (intraclass correlation = 0.83). Comparison of scores de- rived from the self-report scales with those derived from the MHP-administered versions of the same scales yielded similar results (intraclass correlation = 0.83), indicating good procedural validity.

DIAGNOSTIC CRITERION VALIDITY AND SCALE OPERATING CHARACTERISTICS

Table 1 summarizes the operating characteristics of the GAD-7 at various cut points. As expected, as the cut point increases, sensitivity decreases and specificity increases in a continuous fashion. At a cut point of 10 or greater, sen- sitivity and specificity exceed 0.80, and sensitivity is nearly maximized. Results were similar for men and women and for those aged less and those aged more than the mean age of 47 years. The proportion of primary care patients who score at this level is high (23%). A cut point of 15 or greater maximizes specificity and approximates a prevalence (9%) more in line with current epidemiologic estimates of GAD prevalence in primary care. However, sensitivity at this high cut point is low (48%). Most patients (89%) with GAD had GAD-7 scores of 10 or greater, whereas most patients (82%) without GAD had scores less than 10.

The mean (SD) GAD-7 score was 14.4 (4.7) in the 73 patients with GAD diagnosed according to the MHP and 4.9 (4.8) in the 892 patients without GAD. The preva- lence of GAD according to the MHP interview was 9% in women and 4% in men. In the entire sample of 2739 patients, the mean GAD-7 score was 6.1 in women and 4.6 in men.

Although the GAD-7 scale inquires about symptoms in the past 2 weeks, the criterion-standard MHP inter- view required at least a 6-month duration of symptoms consistent with DSM-IV diagnostic criteria for GAD. None- theless, the operating characteristics of the scale were good because most patients with high symptom scores had

chronic symptoms. Of the 433 patients with GAD-7 scores of 10 or greater, 96% had symptoms for 1 month or more, and 67% had symptoms for 6 months or more.

CONSTRUCT VALIDITY

There was a strong association between increasing GAD-7 severity scores and worsening function on all 6 SF-20 scales (Table 2). As GAD-7 scores went from mild to moderate to severe, there was a substantial stepwise de- cline in functioning in all 6 SF-20 domains. Most pair- wise comparisons within each SF-20 scale between suc- cessive GAD-7 severity levels were significant. The relationship between GAD severity and functional im- pairment was similar in men and women.

Figure 2 illustrates graphically the relationship be- tween increasing GAD-7 scale scores and worsening func- tional status. Decrements in SF-20 scores are shown in terms of effect size (ie, the difference in mean SF-20 scores, ex- pressed as the number of SDs, between each GAD-7 inter- val subgroup and the reference group). The reference group is the group with the lowest GAD-7 scores (ie, 0-4), and the SD used is that of the entire sample. Effect sizes of 0.5 and 0.8 are typically considered moderate and large be- tween-group differences, respectively.27

When the GAD-7 was examined as a continuous vari- able, its strength of association with the SF-20 scales was concordant with the pattern seen in Figure 2. The GAD-7 correlated most strongly with mental health (0.75), fol- lowed by social functioning (0.46), general health per- ceptions (0.44), bodily pain (0.36), role functioning (0.33), and physical functioning (0.30).

Table 3 shows the association between GAD-7 se- verity levels and 3 other measures of construct validity: self-reported disability days, clinic visits, and the gen- eral amount of difficulty patients attribute to their symp- toms. Greater levels of anxiety severity were associated with a monotonic increase in disability days, health care use, and symptom-related difficulty in activities and re- lationships. When the GAD-7 was examined as a con- tinuous variable, its correlation was 0.27 with disability days, 0.22 with physician visits, and 0.63 with symptom- related difficulty.

Convergent validity of the GAD-7 was good, as dem- onstrated by its correlations with 2 anxiety scales: the Beck Anxiety Inventory (r = 0.72) and the anxiety subscale of the Symptom Checklist-90 (r = 0.74). Consistent with re- sults of previous studies of anxiety and depression,4,28 the GAD-7 and Symptom Checklist-90 anxiety scales also strongly correlated with our depression measure, the PHQ-8 (r = 0.75 and r = 0.74, respectively). Nonetheless, measuring anxiety and depression was complementary rather than duplicative. We determined the prevalence of high anxiety and high depression symptom severity in our sample, defined as severe scores (�15) on the GAD-7 and PHQ-8 depression scales, respectively. In the 2114 patients who completed the GAD-7 and the PHQ-8, there were 1877 (88.8%) patients with neither high anxi- ety nor high depression, 99 (4.68%) with high anxiety only, 68 (3.2%) with high depression only, and 70 (3.31%) with high anxiety and high depression. Thus, more than half (99/169) of patients with high anxiety scores did not

GAD-7

7. Feeling afraid as if something awful might happen 0 1 2 3

Not at all

Several days

More than half the days

Nearly every day

Over the last 2 weeks, how often have you been bothered by the following problems?

0 1 2 31. Feeling nervous, anxious or on edge

0 1 2 32. Not being able to stop or control worrying

0 1 2 33. Worrying too much about different things

0 1 2 34. Trouble relaxing

0 1 2 35. Being so restless that it is hard to sit still

0 1 2 36. Becoming easily annoyed or irritable

Total Score

= Add Columns

+ +

If you checked off any problems, how difficult have these problems made it for you to do your work, take care of things at home, or get along with other people?

Not difficult at all

Somewhat difficult

Very difficult

Extremely difficult

Figure 1. The generalized anxiety disorder 7-item (GAD-7) scale.

(REPRINTED) ARCH INTERN MED/ VOL 166, MAY 22, 2006 WWW.ARCHINTERNMED.COM 1094

Downloaded From: https://jamanetwork.com/ on 03/30/2021

have high depression scores. Also, when patients had high anxiety and high depression scores, there was an addi- tive effect on the SF-20 mental health and social func- tioning scales, as well as self-reported disability days and health care use.

FACTORIAL VALIDITY

Principal component analysis of a set of 15 items that in- cludes the 8 depression items of the PHQ-8 and the 7 anxi- ety items of the GAD-7 indicated that the first 2 emer- gent factors had an eigenvalue greater than 1. Sixty- three percent of the total variance was explained by the first 2 factors. The varimax-rotated component-matrix clearly confirmed the original allocation of the items to the PHQ scales, with all depression items having the high- est factor loadings on 1 factor (0.58-0.75) and all anxi- ety items having the highest factor loadings on the sec- ond factor (0.69-0.81).

COMMENT

This study has several major findings. First, a 7-item anxi- ety scale—the GAD-7—is a useful tool with strong cri-

terion validity for identifying probable cases of GAD. Sec- ond, the scale is also an excellent severity measure as demonstrated by the fact that increasing scores on the GAD-7 are strongly associated with multiple domains of functional impairment and disability days. Third, al- though many patients had anxiety and depressive symp- toms, factor analysis confirms GAD and depression as dis- tinct dimensions.

This study reports the development and validation of a measure for evaluating the presence and severity of GAD in clinical practice, the GAD-7, one of the few GAD mea- sures that is also specifically linked to the DSM-IV (Text Revision) criteria.19,26 A score of 10 or greater on the GAD-7 represents a reasonable cut point for identifying cases of GAD. Cut points of 5, 10, and 15 might be interpreted as representing mild, moderate, and severe levels of anxi- ety on the GAD-7, similar to levels of depression on the PHQ-9.10 The GAD-7 may be particularly useful in as- sessing symptom severity and monitoring change across time, although its responsiveness to change remains to be tested in treatment studies.

Construct validity was demonstrated by the fact that increasing scores on the GAD-7 scale were strongly as- sociated with multiple domains of functional impair-

Table 1. Operating Characteristics of GAD-7 at Different Cutoffs*

GAD-7 Scale Score† Sensitivity, % Specificity, % PPV, % NPV, % LR� Prevalence, %

8 92 76 24 99 3.8 29 9 90 79 26 99 4.3 26

10 89 82 29 99 5.1 23 11 82 85 31 98 5.5 20 12 73 89 35 98 6.5 16 13 66 91 38 97 7.7 13 14 56 92 37 96 7.2 12 15 48 95 42 96 8.7 9

Abbreviations: GAD-7, generalized anxiety disorder 7-item scale; LR�, likelihood ratio for a positive test; NPV, negative predictive value; PPV, positive predictive value.

*In 965 patients who underwent structured psychiatric interview by a mental health professional to determine the presence of generalized anxiety disorder by using Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnostic criteria.

†The actual score is greater than or equal to the score shown.

Table 2. Relationship Between GAD-7 Severity Score and SF-20 Health-Related Quality of Life Scales*

Level of Anxiety Severity GAD-7 Scale Score

Mean (95% Confidence Interval) SF-20 Scale Score

Mental Social Role General Pain Physical

Minimal 0-4 (n = 1182) 82 (81-83) 91 (89-92) 84 (82-86) 68 (67-69) 71 (70-72) 84 (82-85)

Mild 5-9 (n = 511) 65 (64-66) 79 (77-81) 69 (66-73) 52 (50-54) 56 (54-58) 74 (72-76)

Moderate 10-14 (n = 264) 54 (52-55) 69 (66-71) 59 (54-63) 43† (40-45) 51† (48-54) 66† (63-69)

Severe 5-21 (n = 171) 41 (39-43) 55 (52-59) 46 (40-52) 39† (36-43) 47† (43-50) 61† (58-65)

Abbreviations: GAD-7, generalized anxiety disorder 7-item scale; SF-20, Medical Outcomes Study Short-Form General Health Survey. *SF-20 scores are adjusted for age, sex, race, education, and study site. Point estimates for the mean and 95% confidence intervals (±1.96 � standard error of

the mean) are displayed. Number of patients adds to 2128 because of missing data. Missing data for any subscale of SF-20 was less than 5%. †Pairwise comparisons within each scale that are not significant from one another. However, most pairwise comparisons of mean SF-20 scores with each

GAD-7 scale level within each scale are significant at P�.05 by using a Bonferroni correction for multiple comparisons.

(REPRINTED) ARCH INTERN MED/ VOL 166, MAY 22, 2006 WWW.ARCHINTERNMED.COM 1095

Downloaded From: https://jamanetwork.com/ on 03/30/2021

ment. Furthermore, there was a strong association with self-reported disability days and a modest association with increased health care use.

To facilitate assessment of change in severity of anxi- ety symptoms, the GAD-7 asks about recent symptoms (ie, in the past 2 weeks). However, most patients with high scores had chronic symptoms, which is why the op- erating characteristics proved good with use of our cri- terion-standard MHP interviews based on the conven- tional GAD duration criterion of 6 months. However, the National Comorbidity Survey showed that patients with episodes of 1 to 5 months do not differ greatly from those with episodes of 6 months or more in onset, persis- tence, impairment, comorbidity, parental GAD, or so- ciodemographic correlates.5 Kessler et al5 conclude that there is little basis for excluding these people from a di- agnosis. Notably, 96% of patients with GAD-7scores of 10 or greater in our primary care sample had symptoms of a month or more, whereas 67% had symptoms of 6 months or longer. It may be that in treatment trials in which response to therapy is evaluated, assessing GAD symptom change during a shorter time (eg, the past week) may be desirable.

The high comorbidity of anxiety and depressive dis- orders and the high correlation between depressive and anxiety measures is well known.17,29 Not surpris- ingly, our depression measure, the PHQ-8, strongly c o r r e l a t e d w i t h t h e G A D - 7 a n d t h e S y m p t o m Checklist-90 anxiety scales. Nonetheless, factor analy- sis confirmed the value of assessing anxiety and depression as 2 separate dimensions. In addition, a number of patients with high anxiety symptoms according to the GAD-7 did not have high depression symptom severity, and patients with increasing sever- ity of anxiety symptoms had corresponding greater impairment in multiple domains of functional status. Together, these findings indicate that using only a depression measure to identify depressed patients who may benefit from treatment will miss a clinically important part of the patient population with dis- abling anxiety who also would benefit from treatment.

Several limitations of our study should be noted. First, the GAD-7 scale focuses on only 1 anxiety disorder, al- though there are many patients with other anxiety dis- orders, such as social phobia and posttraumatic stress dis- order, who need clinical attention. However, GAD is one of the most common mental disorders seen in outpa- tient practice. Second, the GAD-7 provides only prob- able diagnoses that should be confirmed by further evalu- ation. Third, because our study was cross-sectional, prospective observational and treatment studies are needed to determine the responsiveness of the GAD-7 in assessing change across time. Because there is already evidence for the responsiveness of the PHQ-9 and PHQ-2 depression scales,30,31 future research also likely will dem- onstrate that the GAD-7 scale is useful in assessing changes in the severity of anxiety over time.

This study has a number of strengths, including its large sample size, diverse clinical settings, and its gen- eralizability to primary care, where most patients with anxiety and depression are treated.2 Also, the GAD-7 is efficient in that it is brief and can be completed entirely by the patient. This latter feature is particularly impor- tant, given the time constraints and competing de- mands for busy clinicians.32 Although the GAD-7 was de- veloped and validated in primary care, we expect that, like the PHQ-9 depression measure, the GAD-7 will have considerable utility in busy mental health settings and clinical research, which is especially important given the high prevalence and substantial disability associated with GAD.

–0.5

–1.0

–1.5

–2.0

–2.5 Mental Social General Role Pain Physical

SF-20 Scale

Ef fe

ct S

iz e

Mild Moderate Severe

Figure 2. Relationship between anxiety severity as measured with the generalized anxiety disorder 7-item (GAD-7) scale and decline in functional status as measured with the 6 subscales of the Medical Outcomes Study Short-Form General Health Survey (SF-20). The decrement in SF-20 scores is shown as the difference between each GAD-7 scale severity group and the reference group (ie, those with GAD-7 scale scores of 0 to 4). Effect size is the difference in group means divided by the SD.

Table 3. Relationship Between GAD-7 Anxiety Severity Score and Disability Days, Symptom-Related Difficulty, and Clinic Visits*

Level of Anxiety Severity GAD-7 Scale Score

Mean No. of Disability Days

(95% CI)†

Mean No. of Physician

Visits (95% CI)†

Percentage of Symptom-

Related Difficulty‡

Minimal 0-4 (n = 1182) 3.9 (3.0-4.7) 1.2 (1.1-1.3) 15.0

Mild 5-9 (n = 511) 7.5 (6.2-8.7) 1.7 (1.5-1.9) 5.5

Moderate 10-14 (n = 264) 10.7 (8.9-12.4) 2.2 (1.9-2.5) 13.7

Severe 15-21 (n = 171) 16.8 (14.6-19.1) 2.4 (2.0-2.8) 47.4

Abbreviations: GAD-7, generalized anxiety disorder 7-item scale; CI, confidence interval.

*All pairwise comparisons between each GAD-7 scale severity level are significant at P�.05 by using a Bonferroni correction for multiple comparisons, with the exception of mean physician visits at moderate vs severe GAD-7 score severity levels.

†Disability days refers to number of days in the past 3 months that the patients’ symptoms interfered with their usual activities. Physician visits also refers to the past 3 months. Both are self-reported, and means are adjusted for age, sex, race, education, study site, and number of physical disorders. Number of patients adds to 2128 because of missing data. Missing data were less than 5%.

‡Response to single question: “How difficult have these problems made it for you to do your work, take care of things at home, or get along with other people?” The 4 response categories are “not difficult at all,” “somewhat difficult,” “very difficult,” and “extremely difficult.” Symptom-related difficulty in this table refers to patients reporting “very” or “extremely” difficult.

(REPRINTED) ARCH INTERN MED/ VOL 166, MAY 22, 2006 WWW.ARCHINTERNMED.COM 1096

Downloaded From: https://jamanetwork.com/ on 03/30/2021

Accepted for Publication: January 2, 2006. Correspondence: Robert L. Spitzer, MD, Department of Psychiatry, New York State Psychiatric Institute, Unit 60, 1051 Riverside Dr, New York, NY 10032 (RLS8 @Columbia.edu). Funding/Support: The development of the GAD-7 scale was underwritten by an unrestricted educational grant from Pfizer Inc (New York, NY). Dr Spitzer had full ac- cess to the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analy- sis. Acknowledgment: Mark Davies, MS, assisted in the sta- tistical analysis. Jeffrey G. Johnson, PhD, assisted in data collection and commented on early drafts. Diane Engel, MSW, also assisted in data collection.

REFERENCES

1. Olfson M, Fireman B, Weissman MM, Leon AC, Sheehan DV, Kathol RG. Mental disorders and disability among patients in a primary care group practice. Am J Psychiatry. 1997;154:1734-1740.

2. Roy-Byrne PP, Wagner A. Primary care perspectives on generalized anxiety disorder. J Clin Psychiatry. 2004;65(suppl 13):20-26.

3. Leon AC, Olfson M, Broadhead WE, et al. Prevalence of mental disorders in pri- mary care: implications for screening. Arch Fam Med. 1995;4:857-861.

4. Wittchen HU, Zhao S, Kessler RC, Eaton WW. DSM-III-R generalized anxiety dis- order in the National Comorbidity Survey. Arch Gen Psychiatry. 1994;51:355- 364.

5. Kessler RC, Brandenburg N, Lane M, et al. Rethinking the duration requirement for generalized anxiety disorder: evidence from the National Comorbidity Sur- vey Replication. Psychol Med. 2005;35:1073-1082.

6. Kessler RC, Keller MB, Wittchen HU. The epidemiology of generalized anxiety disorder. Psychiatr Clin North Am. 2001;24:19-39.

7. Williams JW, Pignone M, Ramirez G, Perez SC. Identifying depression in pri- mary care: a literature synthesis of case-finding instruments. Gen Hosp Psychiatry. 2002;24:225-237.

8. Löwe B, Spitzer RL, Gräfe K, et al. Comparative validity of three screening ques- tionnaires for DSM-IV depressive disorders and physicians’ diagnoses. J Affect Disord. 2004;78:131-140.

9. Spitzer RL, Kroenke K, Williams JB; Patient Health Questionnaire Primary Care Study Group. Validation and utility of a self-report version of PRIME-MD: the PHQ primary care study. JAMA. 1999;282:1737-1744.

10. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen Intern Med. 2001;16:606-613.

11. Löwe B, Gräfe K, Zipfel S, Witte S, Loerch B, Herzog W. Diagnosing ICD-10 de- pressive episodes: superior criterion validity of the Patient Health Questionnaire. Psychother Psychosom. 2004;73:386-390.

12. Fricchione G. Clinical practice: generalized anxiety disorder. N Engl J Med. 2004; 351:675-682.

13. Westen D, Morrison K. A multidimensional meta-analysis of treatments for de- pression, panic, and generalized anxiety disorder: an empirical examination of the status of empirically supported therapies. J Consult Clin Psychol. 2001; 69:875-899.

14. Beck AT, Epstein N, Brown G, Steer RA. An inventory for measuring clinical anxi- ety: psychometric properties. J Consult Clin Psychol. 1988;56:893-897.

15. Zimmerman M, Mattia JI. A self-report scale to help make psychiatric diag- noses: the Psychiatric Diagnostic Screening Questionnaire. Arch Gen Psychiatry. 2001;58:787-794.

16. Derogatis LR, Lipman RS, Rickels K, Uhlenhuth EH, Covi L. The Hopkins Symp- tom Checklist (HSCL): a measure of primary symptom dimensions. Mod Probl Pharmacopsychiatry. 1974;7:79-110.

17. Bjelland I, Dahl AA, Haug TT, Neckelmann D. The validity of the Hospital Anxiety and Depression Scale: an updated literature review. J Psychosom Res. 2002; 52:69-77.

18. Hamilton M. The assessment of anxiety states by rating. Br J Med Psychol. 1959; 32:50-55.

19. Antony MM, Orsillo SM, Roemer L, eds. Practitioner’s Guide to Empirically Based Measures of Anxiety. New York, NY: Kluwer Academic/Plenum Publishers; 2001.

20. Stewart AL, Hays RD, Ware JE Jr. The MOS short-form general health survey: reliability and validity in a patient population. Med Care. 1988;26:724-735.

21. Ware JE, Sherbourne CD. The MOS 36-item short-form health survey (SF-36), I: conceptual framework and item selection. Med Care. 1992;30:473-483.

22. Kroenke K, Spitzer RL. The PHQ-9: a new depression diagnostic and severity measure. Psychiatr Ann. 2002;9:1-7.

23. First MB, Spitzer RL, Williams JBW, Gibbon M. Structured Clinical Interview for DSM-IV (SCID). Washington, DC: American Psychiatric Association; 1995.

24. Pinto-Meza A, Serrano-Blanco A, Penarrubia MT, Blanco E, Haro JM. Assessing depression in primary care with the PHQ-9: can it be carried out over the telephone? J Gen Intern Med. 2005;20:738-742.

25. Deyo RA, Diehr P, Patrick DL. Reproducibility and responsiveness of health sta- tus measures: statistics and strategies for evaluation. Control Clin Trials. 1991; 12:142S-158S.

26. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR (Text Revision). 4th ed. Washington, DC: American Psy- chiatric Association; 2000.

27. Kazis LE, Anderson JJ, Meenan RF. Effect sizes for interpreting changes in health status. Med Care. 1989;27:S178-S189.

28. Carter RM, Wittchen HU, Pfister H, Kessler RC. One-year prevalence of sub- threshold and threshold DSM-IV generalized anxiety disorder in a nationally rep- resentative sample. Depress Anxiety. 2001;13:78-88.

29. Clark DA, Steer RA, Beck AT. Common and specific dimensions of self-reported anxiety and depression: implications for the cognitive and tripartite models. J Abnorm Psychol. 1994;103:645-654.

30. Löwe B, Unützer J, Callahan CM, Perkins AJ, Kroenke K. Monitoring depression treatment outcomes with the Patient Health Questionnaire-9. Med Care. 2004; 42:1194-1201.

31. Löwe B, Kroenke K, Gräfe K. Detecting and monitoring depression with a 2-item questionnaire (PHQ-2). J Psychosom Res. 2005;58:163-171.

32. Klinkman MS. Competing demands in psychosocial care: a model for the iden- tification and treatment of depressive disorders in primary care. Gen Hosp Psychiatry. 1997;19:98-111.

(REPRINTED) ARCH INTERN MED/ VOL 166, MAY 22, 2006 WWW.ARCHINTERNMED.COM 1097

Downloaded From: https://jamanetwork.com/ on 03/30/2021

Akeira Stewart Jacksonville Campus Professor Littlefield 03/18/2021

Infertility in Women  Introduction

A. Introductory Sentence: Type Here

B. Background/Contextual Info Point 1: Type Here

C. Background/Contextual Info Point 2: Type Here

D. Background/Contextual Info Point 3: Type Here

E. Background/Contextual Info Point 4: Type Here

F. Background/Contextual Info Point 5: Type Here

G. Summary of Points/Transitional Statement: Type Here

H. Thesis: Infertility rates are rising in women. Women should be more educated on

the different factors that play a part in infertility such as, poor nutrition, problems

with menstrual cycles, and polycystic ovary syndrome.

_________________

I. Main Point 1: Type Section Title Here

A. Topic Sentence: Type Here

1. Define/Explain the Point: Type Here

B. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

C. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

D. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

E. Connection/Transition to Next Section: Type Here

II. Main Point 2: Type Section Title Here

A. Topic Sentence: Type Here

1. Define/Explain the Point: Type Here

B. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

C. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

D. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

E. Connection/Transition to Next Section: Type Here

III. Main Point 3: Type Section Title Here

A. Topic Sentence: Type Here

1. Define/Explain the Point: Type Here

B. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

C. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

D. Support Sentence (Evidence): Type Here

1. Support Sentence (Explain Importance of Evidence): Type Here

E. Connection/Transition to Next Section: Type Here

____________________

 Conclusion

A. Paraphrased Thesis: Type Here

B. Paraphrased Point 1: Type Here

a. Subpoint if necessary: Type Here

C. Paraphrased Point 2: Type Here

a. Subpoint if necessary: Type Here

D. Paraphrased Point 3: Type Here

a. Subpoint if necessary: Type Here

E. Closing Remarks/Point: Type Here

Working References

The references should be placed on their own page. Make sure your spacing is correct! For more

information about creating your references page, refer to the APA manual style guide. The

Purdue University Online Writing Lab (OWL) website can be found by clicking here. An

example of a completed APA paper written in 7th edition style can be found by clicking here. A

https://owl.english.purdue.edu/owl/resource/560/05/

https://docs.google.com/document/d/1pTz0W_C8IREaRgvShXvzHQuApE0MNOqFTUa7yaA-6wc/edit?usp=sharing

guide designed for Jersey College students can be viewed by clicking here. An example of a

completed sentence outline assignment can be viewed by clicking here. The grading rubric for

this assignment can be accessed by clicking here.

https://drive.google.com/file/d/11Cy8qg5PblLhp-3mDuLrJuK344z89OOD/view?usp=sharing

https://docs.google.com/document/d/1F4hJxF9M_FGjyUiGKLIY2n2hs2IQyW7LYHlyf-eHbts/edit?usp=sharing

https://docs.google.com/document/d/1WOKV5Ftn-_fQnS4JVZYdQJ7GYb2ZlCmFHExhxNsUUl8/edit?usp=sharing

O ne personal copy m

ay be printed

15J Clin Psychiatry 2001;62 (suppl 11)

Nature and Course of GAD

eneralized anxiety disorder (GAD) has, until re- cently, been a relatively poorly understood disorder.

EPIDEMIOLOGY OF GAD

A number of critical clinical and research issues affect the reliability and understanding of GAD studies. Most cli- nicians and clinical epidemiologists are familiar with the clinical syndrome of generalized anxiety characterized by excessive worrying and marked symptoms of hypervigi- lance and anxiety as the essential aspects of what was for- merly labeled anxiety neurosis before the 1980s. However, confusion exists concerning the diagnostic criteria for GAD as a distinct and treatable psychiatric disorder. Indeed, few primary care physicians are aware that specific diagnostic criteria and diagnostic tools exist. Research into GAD in the past has also been complicated by the use of different definitions. The concept and diagnostic criteria of GAD have changed significantly since its formal introduction in DSM-III in 1980, several times in the subsequent revisions, and, to date, there are still differences in the understanding of GAD between Europe and the United States. These dif- ferences are predominantly due to the use of differing di- agnostic criteria: in Europe the use of the 10th International Classification of Diseases (ICD-10) prevails, whereas in the United States and in research the Diagnostic and Sta- tistical Manual of Mental Disorders (DSM) is preferred.

Historically, the study of GAD has been further hindered by methodological difficulties occurring during research. For example, few reliable assessment methods have been available until recently. Considerable developmental work during the 1990s resulted in more appropriate diagnostic modules,5 although the instruments that are in use still dif- fer in their conceptual backgrounds, which can result in variability in their findings. Some measures are polythetic,

Generalized Anxiety Disorder: Nature and Course

Hans-Ulrich Wittchen, Ph.D., and Jürgen Hoyer, Ph.D.

Generalized anxiety disorder (GAD) is a chronic and highly prevalent disorder in the adult popula- tion, yet it remains a relatively poorly understood condition. Clinicians may be familiar with the symptoms of enduring excessive worrying, anxiety, and hypervigilance that are characteristic of GAD, but may not necessarily recognize that these are usually symptoms of a distinct psychiatric dis- order. Despite changes in diagnostic criteria, estimates of prevalence for GAD are remarkably consis- tent across epidemiologic studies. Lifetime prevalence in the general population is estimated at 5% (DSM-III and/or DSM-III-R criteria), with rates as high as 10% among women aged 40 years and above, and cross-sectional rates among primary care attenders are about 8%, making GAD the most prevalent anxiety disorder in primary care. The age at onset of GAD differs from that of other anxiety disorders: prevalence rates are low in adolescents and young adults but increase substantially with age. Females are at greater risk than males, and the disorder is correlated with being unemployed or a housewife or having a chronic medical illness. GAD is frequently associated with comorbid depres- sion and other anxiety and somatoform disorders. Significant GAD-specific disability occurs even when comorbidity is not present. (J Clin Psychiatry 2001;62[suppl 11]:15–19)

G The recent increased interest in the condition has stemmed from the finding that GAD is the second most frequent dis- order in primary care after depression,1–3 the availability of reliable diagnostic criteria and instruments,4 and the devel- opment of new treatments for this condition. However, a number of concerns remain regarding the nosology of GAD as a separate psychiatric condition. Questions have been raised concerning the diagnostic validity of standard crite- ria, the prevalence in the general population, and in particu- lar, the meaning and implications of comorbid anxiety and depressive disorders frequently seen in clinical settings. Other key concerns are whether the disorder causes GAD- specific disabilities and whether the impairments are due to comorbid conditions. This review explores the nature of GAD by examining current research into its epidemiology (prevalence rates in both the general population and in pri- mary care are considered), onset, course, risk factors, and associated comorbidity and impairment.

From the Institute of Clinical Psychology and Psychotherapy, Technical University of Dresden, Dresden and Max Planck Institute of Psychiatry, Munich, Germany.

Presented at the meeting “Focus on Generalized Anxiety Disorder,” held by the International Consensus Group on Depression and Anxiety, March 30–31, 2000, in Cape Town, South Africa. The Consensus Meeting was supported by an unrestricted educational grant from SmithKline Beecham Pharmaceuticals.

Reprint requests to: Professor Hans-Ulrich Wittchen, Max Planck Institute of Psychiatry, Clinical Psychology and Epidemiology Unit, Kraepelinstr.2, 80804 Munich, Germany (e-mail: [email protected]).

O ne personal copy m

ay be printed

16 J Clin Psychiatry 2001;62 (suppl 11)

Wittchen and Hoyer

for example, the Structured Clinical Interview for DSM (SCID)6 and the World Health Organization’s Composite International Diagnostic Interview (CIDI),7 both designed specifically for administration of the apportionalized DSM criteria. On the other hand, others are of a syndromal na- ture, for example, the Clinical Interview Schedule (CIS)8

and the Schedules for Clinical Assessment in Neuropsy- chiatry (SCAN),9 resulting in differing rates.

As a consequence of these issues, direct cross-study comparisons are difficult, especially when interpreting findings not based on the same diagnostic system or instrument (DSM-III-R, DSM-IV, or ICD-10 criteria). Therefore, clear epidemiologic evidence for prevalence and risk factors for GAD has, until recently, been poor.

Prevalence of GAD Despite the fact that there have been many changes

in the diagnostic criteria for GAD during recent years, re- ported lifetime prevalence estimates in the general popula- tion (Table 1) are remarkably stable, compared with the considerable variance observed with other psychiatric dis- orders, such as depression and panic disorder, over a simi- lar age span. Based on more recent studies, the most likely lifetime prevalence rates for GAD in the general popula- tion are 5% using DSM criteria and may be slightly higher when using the wider ICD-10 criteria (6.5%). Current and 12-month prevalence rates for GAD are also reported in Table 1; these estimates depend largely on the rigidity of the definition of point prevalence and are subject to more variation than lifetime prevalence estimates. The most likely current prevalence rate in the general population seems to be in the range of 2% to 3% (DSM criteria).

The National Comorbidity Survey (NCS),24 performed in a representative sample of the U.S. general population (aged 15–54 years), is the largest study to report epidemio- logic findings for GAD to date.16 Using CIDI/DSM-III-R criteria in more than 8000 respondents, a lifetime preva- lence estimate of 5.1% (3.6% in males and 6.6% in fe- males) and a 12-month prevalence rate of 3.1% (2.0% in males and 4.3% in females) were reported. The lifetime prevalence estimate is in relatively good agreement with the findings of several other large epidemiologic studies that have been conducted throughout the world in recent years (see Table 1). The 12-month prevalence rate found by the NCS should be regarded with caution, however, since the CIDI is designed to gather lifetime prevalence rates and did not assess the presence of all of the disorder’s criteria in the preceding 12 months and thus might include a high proportion of people with lifetime GAD who have only had some significant signs of the disorder during the previous month. The 12-month prevalence estimates of threshold GAD were recently found to be lower in the German National Health Interview and Examination Sur- vey, Mental Health Supplement (GHS).23 This study used the slightly stricter DSM-IV criteria (which use the addi- tional criteria of difficulty controlling the worrying and a restricted range of associated symptoms), which increase the duration criterion from 1 month to 6 months compared with DSM-III-R, to examine GAD and other disorders in a representative sample of the German population (over 7200 adults). Using a 12-month version of the Munich- CIDI,25 the 12-month prevalence rate for GAD (meeting all DSM-IV criteria) was found to be 1.5% (1.0% in men and 2.1% in women). If, however, lifetime GAD cases with still

Table 1. Prevalence of Generalized Anxiety Disorder in General Population Surveysa

Source Diagnostic Criteriab Lifetime Prevalence, % 12-Month Prevalence, % Current Prevalence, %

Weissman et al,10 United States RDC … … 2.5 Angst et al,11 Zurich, Switzerland DSM-III … 3.8 … Blazer et al,12

ECA study, Durham, NC DSM-III 6.6 3.6 1.2 ECA study, St Louis, Mo DSM-III 6.6 2.9 1.3 ECA study, Los Angeles, Calif DSM-III 4.1 2.0 1.4

Stefansson et al,13 Iceland DSM-III 21.7 … … Chen et al,14 Shatin, Hong Kong DSM-III 7.8 males … …

11.1 females Faravelli et al,15 Florence, Italy DSM-III-R 5.4 … 2.8 Wittchen et al,16 DSM-III-R 5.1 3.1 1.6 NCS, United States Offord et al,17 Ontario, Canada DSM-III-R … 1.1 … Feehan et al,18 Dunedin, New Zealand DSM-III-R … [1.8] … Canals et al,19 Spain DSM-III-R … … [0] Wittchen et al,20 Munich, Germany DSM-IV [0.8] [0.5] … Jenkins et al,21 Great Britain ICD-10 … … 6.4 Bhagwanjee et al,22 South Africa DSM-IV … … 3.7 Carter et al,23 GHS, Germany DSM-IV … 1.5 … aAdapted, with permission, from Carter et al.23 Abbreviations: DSM = Diagnostic and Statistical Manual of Mental Disorders, ECA = Epidemiologic Catchment Area, GHS = German National Health Interview and Examination Survey, ICD = International Classification of Diseases, NCS = National Comorbidity Survey, RDC = Research Diagnostic Criteria. Prevalence rates in brackets indicate that the sample comprised only adolescents. bAll studies using DSM-III used 1-month instead of 6-month criteria (as used in DSM-III-R and DSM-IV).

O ne personal copy m

ay be printed

17J Clin Psychiatry 2001;62 (suppl 11)

Nature and Course of GAD

existing 12-month subthreshold GAD syndromes are counted as well—as was the case in the NCS study—an almost identical 12-month rate of 3.6% (2.4% in men and 4.9% in women) was confirmed. In addition, the disorder was found significantly more frequently in women than in men (odds ratio [OR] = 2.1, p < .05). The investigators also determined prevalence rates for subthreshold expressions of GAD by using different time criteria for duration, such as worrying for at least 1 month (7.8%) or worrying for at least 3 months (4.1%), and concluded that long periods of anxious worrying associated with subthreshold GAD symptoms are much more widespread in the community than threshold GAD.

When prevalence data from the NCS and GHS are ex- amined by age, it is clear that for both lifetime and 12- month prevalence rates, the lowest rates for GAD occur in the younger age groups and the highest rates are found in the older study participants (Figure 1).16,23 In the GHS,

the likelihood of receiving a diagnosis of GAD increased significantly with age (18–34 vs. 35–65 years: OR = 1.0, p < .05) when controlling for differences in gender, with point prevalence rates up to 4.4% in women aged 45 or older. These findings are consistent with the lower preva- lence rates for GAD recorded in studies of adolescents and young adults (see Table 1).

GAD, in common with panic disorder, is unique among anxiety disorders in that patients commonly present to primary care physicians for treatment.2 An international World Health Organization study used ICD-10 criteria with the CIDI to assess GAD and estimated the current preva- lence of GAD to be approximately 8% of all primary care attendees.1 A more recent reanalysis confirmed these re- sults by using more sophisticated analyses, finding a mean current prevalence rate of 7.9%.2 This study also found a wide range of prevalence rates across the participating countries, for example, 3.8% in Italy and 14.8% in Greece, possibly owing to differences in the way that countries and regions organize the provision of primary care services. It is noteworthy that this study suggests that the point preva- lence rate of GAD is considerably higher in primary care than that reported in the general population (see Table 1), suggesting that GAD patients are high utilizers of primary care resources. This is in contrast to social anxiety disor- der and most other anxiety disorders, for which the point prevalence in the general population is much higher than in primary care and subjects are unlikely to present to their family doctor owing to the nature of the condition.26

COURSE OF GAD

The presentation of GAD in primary care is similar to that of other anxiety disorders in that patients are unlikely to present directly and openly with complaints of anxiety symptoms.1 In fact, it is most likely that patients with GAD will present with somatic and sleeping problems.

The pattern of onset with GAD is different from that seen with other anxiety disorders; whereas most anxiety disorders clearly develop before the age of 20 years,27

prevalence rates for GAD in adolescents and young adults are usually low and then increase substantially with age.23

Notably in the GHS,23 few cases of full-blown DSM-IV GAD occurred before the age of 25 years. This was par- ticularly true among men. There was also a strong increase in the incidence of GAD later in life: for women, this oc- curred after the age of 35 years, whereas in men, the in- crease occurred after the age of 45 years. Furthermore, among respondents with at least 3 months of worrying, older subjects (aged 35–65 years) were more likely than younger subjects (aged 18–34 years) to have reported that their worrying had lasted for at least 6 months (OR = 3.94, p < .05). Thus, older people worry more and for longer periods of time than their younger counterparts. These findings are supported by a community study in over 3100

Figure 1. Prevalence of Generalized Anxiety Disordera

15–24

25–34

35–44

≥ 45

Total

Prevalence (%)

A g e G

ro u p (

0 2 4 6 8 10 12

2 2.5

1.5 6

7.1 4.7

5.9 7.2

4.6

6.9 10.3

3.6

5.1 6.6

3.6

Total Females Males

A. Lifetime Prevalence (CIDI and DSM-III-R criteria)b

aAbbreviations: CIDI = Composite International Diagnostic Interview, DSM = Diagnostic and Statistical Manual of Mental Disorders. bData from the National Comorbidity Survey.16 cData from the German National Health Interview and Examination Survey, Mental Health Supplement.23

18–24

25–34

35–44

≥ 45

Total

Prevalence (%)

A g

e G

ro u

p (

2.3 1.1

2.8 0.8

4.4 2.2

3.5 1.5

3.6 1.5

0 2 4 6 8

Including Subthreshold (DSM-III-R) Threshold (DSM-IV)

B. Twelve-Month Prevalence (Munich-CIDI and DSM-IV criteria)c

O ne personal copy m

ay be printed

18 J Clin Psychiatry 2001;62 (suppl 11)

Wittchen and Hoyer

older adults (aged 55–85 years), which found that GAD was the most frequent anxiety disorder in this elderly population (7.3%).28

Results from the GHS23 also show that the 12-month prevalence of extended worrying (worrying for at least 1 month) is lower in younger than in older participants. How- ever, worrying for long periods of time carries the same risk of developing full syndromal DSM-IV GAD irrespective of the age group.

GAD is a chronic condition in adults with a waxing and waning course. In younger patients, the course is more vari- able. Full and partial 6-month remission rates among life- time cases have shown that only one third of all patients with GAD have spontaneous remission.16

GAD is frequently associated with other psychiatric disorders. In the NCS, approximately two thirds of current (1-month) DSM-III-R GAD cases fulfilled criteria for at least one other disorder.16 GAD is frequently associated with depression or other anxiety disorders but it is only in- frequently associated with substance abuse disorders.16,23

At the same time, however, it is noteworthy that these seemingly extremely high rates of comorbidity were shown to be not remarkably different from those of other disorders, such as panic disorder and bipolar disorder.23,29

Comorbidity especially with major depressive disorder has been shown to significantly lower the probability of diagnosis and treatment of GAD and to increase disability and impairment.30 (For further discussion of comorbidity in GAD, see the article by Stein in this supplement.31)

CORRELATES AND RISK FACTORS FOR GAD

The NCS16 and GHS23 have both shown that the preva- lence of GAD increases with age and that the disorder is more common in females than in males. In addition, a number of significant correlates for GAD have been iden- tified. These include being previously married (separated, widowed, or divorced), not working, or being a house- wife.16 The NCS was also able to conclude that urbanicity, income, education, and religion lack significant associa- tion with GAD.16

Although GAD is more prevalent in women than in men and occurs more frequently in the unemployed or those that work at home than in employed people, only 16.9% of cases of GAD are found in nonworking home- makers. Even among females with GAD, the proportion of housewives does not exceed 25%.23 Therefore, GAD is not a disorder that is solely found in housewives.

BURDEN OF GAD

The NCS found that there is a considerable degree of impairment, professional help-seeking, and medication us- age to relieve symptoms in people with GAD, whether or not they had a comorbid mental disorder.16 To assess the

disability and impairment caused by pure GAD, analyses of data from studies that control for comorbid disorders, which may affect quality of life, have been implemented. Kessler and coworkers32 conducted a combined analysis of 2 U.S. general population studies (NCS16 and Midlife De- velopment in the United States Survey32) to assess whether DSM-III-R–defined GAD is itself associated with impair- ment or whether the impairment is due to comorbid depres- sion or other comorbid disorders. Assessing the proportion of patients with at least 1 day of disability/impairment in the past month, the authors showed that the impairment as- sociated with GAD alone is not only marked, but is equiva- lent in magnitude to the impairment caused by major de- pression. The highest levels of impairment were seen when GAD co-occurred with major depression.

A similar, more elaborate, recently published analysis, which included a wider range of impairment and disability measures, assessed disability in individuals with pure DSM-IV–defined GAD and GAD comorbid with major de- pression.30 The analysis used data from the GHS obtained from the Work Productivity and Activity Impairment ques- tionnaire (WPAI)33 and the 36-item short-form (SF-36).34

Impairment was defined as number of days completely lost plus number of days limited in the past month. Approxi- mately 48% of patients with comorbid GAD and major depression, 34% of those with pure GAD, and 21% of those with pure major depression had at least 6 days impaired over the past month. This study also considered disability in terms of reduction in work productivity. Approximately 11% of the respondents with GAD and no major depres- sion and 8% of those with major depression and no GAD reported a reduction of at least 50% in activity during the past month; more than 50% and 30% of those respective patients reported some reduction in activity. Thus, GAD is associated with considerable impairment even when no comorbid depression is present.

Since GAD is highly prevalent in the primary care set- ting, patients with the disorder are likely to be high users of primary care health services, both in terms of the num- ber of visits and the proportion contacting primary care providers because of problems associated with the disor- der. GAD is a disabling condition in primary care,35,36 and the associated social disability is as severe as that seen with chronic somatic diseases.2

CONCLUSION

GAD is a highly prevalent psychiatric disorder. The lifetime prevalence rate for GAD in the general population is approximately 5% using DSM-III and/or DSM-III-R criteria and possibly slightly higher (approximately 6.5%) using ICD-10 criteria. In primary care, the point preva- lence rate is approximately 8%, making GAD the most frequent anxiety disorder in primary care and the second most frequent psychiatric disorder after depression. In

O ne personal copy m

ay be printed

19J Clin Psychiatry 2001;62 (suppl 11)

Nature and Course of GAD

common with most other anxiety disorders, GAD more of- ten affects women than men, particularly in higher age groups. Unlike other anxiety disorders, GAD rarely occurs in childhood, making it unlikely that GAD is merely a temperament variant, personality trait, or disorder.

GAD is a persistent disorder with a waxing and waning course; only one third of lifetime GAD sufferers in the community experience spontaneous full remission. In the community, GAD also has high, although not necessarily higher, rates of comorbidity with depression and other anxiety disorders compared with the rates of comorbidity found with panic disorder or bipolar disorders. Even in the absence of comorbid disorders, GAD is as disabling as de- pressive disorders in terms of reduced work productivity and social impairment and is associated with increased use of health care services. GAD is a chronic, prevalent, and impairing psychiatric disorder that requires prompt recog- nition and effective treatment.

REFERENCES

1. Üstün TB, Sartorius N, eds. Mental Illness in General Health Care: An In- ternational Study. Chichester, UK: John Wiley & Sons Ltd; 1995

2. Maier W, Gaensicke M, Freyberger HJ, et al. Generalized anxiety disorder (ICD-10) in primary care from a cross-cultural perspective: a valid diag- nostic entity? Acta Psychiatr Scand 2000;101:29–36

3. Roy-Byrne P, Katon W, Broadhead WE, et al. Subsyndromal “mixed” anx- iety-depression in primary care. J Gen Intern Med 1994;9:507–512

4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. Washington DC: American Psychiatric Association; 1994

5. Wittchen H-U, Kessler R, Zhao S, et al. Reliability and clinical validity of University of Michigan-CIDI DSM-III-R generalized anxiety disorder. J Psychiatr Res 1995;29:95–110

6. Spitzer RL, Williams JBW, Gibbon M, et al. The Structured Clinical Inter- view for DSM-III-R (SCID), 1: history, rationale, and description. Arch Gen Psychiatry 1992;49:624–629

7. World Health Organization. Composite International Diagnostic Interview (CIDI) Version 1.0. Geneva, Switzerland: World Health Organization, Di- vision of Mental Health; 1990

8. Brugha TS, Bebbington PE, Jenkins R, et al. Cross validation of a general population survey diagnostic interview: a comparison of CIS-R with SCAN ICD-10 diagnostic categories. Psychol Med 1999;29:1029–1042

9. Wing JK, Babor T, Brugha T, et al. SCAN: Schedules for Clinical Assess- ment in Neuropsychiatry. Arch Gen Psychiatry 1990;47:589–593

10. Weissman MM, Myers JK, Harding PS. Psychiatric disorders in a US urban community: 1975–1976. Am J Psychiatry 1978;135:459–462

11. Angst J, Dobler-Mikola A, Scheidegger P. A panel study of anxiety states, panic attacks, and phobia among young adults. Presented at the Research Conference on Anxiety Disorders, Panic Attacks and Phobia; December 9, 1982; Key Biscayne, Fla

12. Blazer DG, Hughes D, George LK, et al. Generalized anxiety disorder. In: Robins LN, Regier DA, eds. Psychiatric Disorders in America: The Epi- demiologic Catchment Area Study. New York, NY: The Free Press; 1991: 180–203

13. Stefansson JG, Lindal E, Bjornsson JK, et al. Lifetime prevalence of spe- cific mental disorders among people born in Iceland in 1931. Acta Psychiatr Scand 1991;84:142–149

14. Chen C, Wong J, Lee N, et al. The Shatin Community Mental Health Sur- vey in Hong Kong: major findings. Arch Gen Psychiatry 1993;50:125–133

15. Faravelli C, Guerinni Degl’Innocenti BG, Giardinelli L. Epidemiology of anxiety disorders in Florence. Acta Psychiatr Scand 1989;79:308–312

16. Wittchen H-U, Zhao S, Kessler R, et al. DSM-III-R generalized anxiety disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1994; 51:355–364

17. Offord DR, Boyle MH, Campbell D, et al. One-year prevalence of psychi- atric disorder in Ontarians 15–64 years of age. Can J Psychiatr 1996;41: 559–563

18. Feehan M, McGee R, Raja SN, et al. DSM-III-R disorders in New Zealand 18-year-olds. Aust N Z J Psychiatry 1994;28:87–99

19. Canals J, Domenech E, Carbajo G, et al. Prevalence of DSM-III-R and ICD-10 psychiatric disorders in a Spanish population of 18-year-olds. Acta Psychiatr Scand 1997;96:287–294

20. Wittchen H-U, Nelson CB, Lachner G. Prevalence of mental disorders and psychosocial impairments in adolescents and young adults. Psychol Med 1998;28:109–126

21. Jenkins R, Lewis G, Bebbington P, et al. The National Psychiatric Morbid- ity surveys of Great Britain: initial findings from the household survey. Psychol Med 1997;27:775–789

22. Bhagwanjee A, Parekh A, Paruk Z, et al. Prevalence of minor psychiatric disorders in an adult African rural community in South Africa. Psychol Med 1998;28:1137–1147

23. Carter RM, Wittchen H-U, Pfister H, et al. One-year prevalence of sub- threshold and threshold DSM-IV generalized anxiety disorder in a nation- ally representative sample. Depress Anxiety 2001;3:78–88

24. Kessler RC, McGonagle KA, Zhao S, et al. Lifetime and 12-month preva- lence of DSM-III-R psychiatric disorders in the United States: results from the National Comorbidity Survey. Arch Gen Psychiatry 1994;51:8–19

25. Wittchen H-U, Pfister H, eds. Manual und Durchfuehrungsbeschreibung des DIA-X-M-CIDI. Frankfurt, Germany: Swets & Zeitlinger; 1997

26. Lecrubier Y, Wittchen H-U, Faravelli C, et al. A European perspective on social anxiety disorder. Eur Psychiatry 2000;15:5–16

27. Wittchen H-U, Lieb R, Schuster P, et al. When is onset? investigations into early developmental stages of anxiety and depressive disorders. In: Rapoport JL, ed. Childhood Onset of “Adult” Psychopathology: Clinical and Research Advances. Washington, DC: American Psychiatric Press; 1999:259–302

28. Beekman AT, Bremmer MA, Deeg DJ, et al. Anxiety disorders in later life: a report from the Longitudinal Aging Study Amsterdam. Int J Geriatr Psy- chiatry 1998;13:717–726

29. Kessler RC. The epidemiology of pure and comorbid generalized anxiety disorder: a review and evaluation of recent research. Acta Psychiatr Scand Suppl 2000;406:7–13

30. Wittchen H-U, Carter RM, Pfister H, et al. Disabilities and quality of life in pure and comorbid generalized anxiety disorder and major depression in a national survey. Int Clin Psychopharmacol 2000;15:319–328

31. Stein DJ. Comorbidity in generalized anxiety disorder: impact and implica- tions. J Clin Psychiatry 2001;62(suppl 11):29–34

32. Kessler RC, DuPont RL, Berglund P, et al. Impairment in pure and comor- bid generalized anxiety disorder and major depression at 12 months in two national surveys. Am J Psychiatry 1999;156:1915–1923

33. Reilly MC, Zbrozek AS, Dukes EM. The validity and reproducibility of a work productivity and activity impairment instrument. Pharma- coeconomics 1993;4:353–365

34. Ware JE, Sherbourne CD. The MOS 36-item short-form health survey (SF-36), 1: conceptual framework and item selection. Med Care 1992;30: 473–483

35. Ormel J, Von Korff M, Üstün B, et al. Common mental disorders and dis- ability across cultures: results from the WHO collaborative study on psy- chological problems in general health care. JAMA 1994;272:1741–1748

36. Schonfeld WH, Verboncoeur CJ, Fifer SK, et al. The functioning and well- being of patients with unrecognized anxiety disorders and major depressive disorder. J Affect Disord 1997;43:105–119

Table of Contents
Discussion

Mental Health Stigma: Society, Individuals, and the Profession

Brian K. Ahmedani, Ph.D., MSW School of Social Work, Michigan State University, [email protected]

Abstract Mental health stigma operates in society, is internalized by individuals, and is attributed by health professionals. This ethics-laden issue acts as a barrier to individuals who may seek or engage in treatment services. The dimensions, theory, and epistemology of mental health stigma have several implications for the social work profession.

Key Terms Mental Health; Psychiatric Conditions; Stigma; Treatment Engagement; Social Work Ethics

1. Introduction In 2001, the World Health Organization (WHO) reported that an estimated 25 percent of the worldwide population is affected by a mental or behavioral disorder at some time during their lives. This mental and behavioral health issue is believed to contribute to 12 percent of the worldwide burden of disease and is projected to increase to 15 percent by the year 2020 (Hugo, Boshoff, Traut, Zungu-Dirwayi, & Stein, 2003). Within the United States, mental and behavioral health conditions affect approximately 57 million adults (National Institute of Mental Health [NIMH], 2006). Despite the high prevalence of these conditions, recognized treatments have shown effectiveness in mitigating the problem and improving individual functioning in society. Nonetheless, research suggests that (1) individuals who are in need of care often do not seek services, and (2) those that begin receiving care frequently do not complete the recommended treatment plan (Corrigan, 2004). For example, it has been estimated that less than 40 percent of individuals with severe mental illnesses receive consistent mental health treatment throughout the year (Kessler, Berglund, Bruce, Koch, Laska, Leaf, et al, 2001).

There are several potential reasons for why, given a high prevalence of mental health and drug use conditions, there is much less participation in treatment. Plausible explanations may include (1) that those with mental health or drug use conditions are disabled enough by their condition that they are not able to seek treatment, or (2) that they are not able to identify their own condition and therefore do not seek needed services. Despite these viable options, there is another particular explanation that is evident throughout the literature. The U.S. Surgeon General (1999) and the WHO (2001) cite stigma as a key barrier to successful treatment engagement, including seeking and sustaining participation in services. The problem of stigma is widespread, but it often manifests in several different forms. There are also varying ways in which it develops in society, which all have implications for social work – both macro and micro-focused practice.

This text may be freely shared among individuals, but it may not be republished in any medium without express written consent from the authors and advance notification of White Hat Communications

NIH Public Access Author Manuscript J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

Published in final edited form as: J Soc Work Values Ethics. 2011 ; 8(2): 4-1–4-16.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

In order to understand how stigma interferes in the lives of individuals with mental health and drug use conditions, it is essential to examine current definitions, theory, and research in this area. The definitions and dimensions of stigma are a basis for understanding the theory and epistemology of the three main ‘levels’ of stigma (social stigma, self-stigma, and health professional stigma).

2. Stigma Definitions & Dimensions The most established definition regarding stigma is written by Erving Goffman (1963) in his seminal work: Stigma: Notes on the Management of Spoiled Identity. Goffman (1963) states that stigma is “an attribute that is deeply discrediting” that reduces someone “from a whole and usual person to a tainted, discounted one” (p. 3). The stigmatized, thus, are perceived as having a “spoiled identity” (Goffman, 1963, p. 3). In the social work literature, Dudley (2000), working from Goffman’s initial conceptualization, defined stigma as stereotypes or negative views attributed to a person or groups of people when their characteristics or behaviors are viewed as different from or inferior to societal norms. Due to its use in social work literature, Dudley’s (2000) definition provides an excellent stance from which to develop an understanding of stigma.

It is important to recognize that most conceptualizations of stigma do not focus specifically on mental health or drug use disorders (e.g., Crocker, Major, & Steele, 1998; Goffman, 1963). Stigma is relevant in other contexts such as towards individuals of varied backgrounds including race, gender, and sexual orientation. Thus, it is important to provide a definition of mental disorders, which also include drug use disorders, so that it can be understood in relationship to stigma. While each mental health and drug use disorder has a precise definition, the often cited and widely used Diagnostic and Statistical Manual of Mental Disorders (4th Ed., Text Revision [DSM-IV-TR]; American Psychiatric Association [APA], 2000) offers a specific definition of mental disorder which will be used to provide meaning to the concept. In this text, a mental disorder is a “clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress or disability or with a significantly increased risk of suffering death, pain, disability, or an important loss of freedom,” which results from “a manifestation of a behavioral, psychological, or biological dysfunction in the individual” (APA, 2000, p. xxxi). While this definition provides a consistent base from which to begin understanding how stigma impacts individuals with mental health and drug use disorders, it is important to recognize the inherent danger in relying too heavily on specific mental health diagnoses as precise definitions (Corrigan, 2007), which is why the term is being used just as a basis for understanding in this context.

The next important step is to understand the constructs underlying the concept of stigma. These constructs detail the multiple pathways through which stigma can develop. Building from Goffman’s initial conceptualization, Jones and colleagues (1984) identified six dimensions of stigma. These include concealability, course, disruptiveness, peril, origin, and aesthetics (Feldman & Crandall, 2007; Jones et al, 1984). In addition, Corrigan and colleagues (2001; 2000) identified dimensions of stability, controllability, and pity. It is important to understand that these dimensions can either present independently or simultaneously to create stigma. Further, stigma is more than a combination of these elements impacting each person as an individual, since stigma is believed to be common in the structural framework of society (Feldman & Crandall, 2007).

The first dimension of stigma is peril – otherwise known as dangerousness. Peril is often considered an important aspect in stigma development, and it is frequently cited in the research literature (Corrigan, et al, 2001; Feldman & Crandall, 2007; Angermeyer &

Ahmedani Page 2

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

Matschinger, 1996). In this instance, the general public perceives those with mental disorders as frightening, unpredictable, and strange (Lundberg, Hansson, Wentz, & Bjorkman, 2007). Corrigan (2004) also suggests that fear and discomfort arise as a result of the social cues attributed to individuals. Social cues can be evidenced by psychiatric symptoms, awkward physical appearance or social-skills, and through labels (Corrigan, 2004; Link, Cullen, Frank, & Wozniak, 1987; Corrigan, 2007). This particular issue highlights the dimension of aesthetics or the displeasing nature of mental disorders (Jones, et al, 1984). When society attributes, upon a person or group of people, perceived behaviors that do not adhere to the expected social norms, discomfort can be created. This often leads to the generalization of the connection between abnormal behavior and mental illness, which may result in labeling and avoidance. This also may be why society continues to avoid those with mental and behavioral disorders whenever possible (Corrigan, Markowitz, Watson, Rowan, & Kubiak, 2003).

Another dimension of stigma that is often discussed in the research on stigma is origin. As in the definition provided earlier, mental and behavioral disorders are often believed to, at least in-part; develop from biological and genetic factors – i.e., origin (APA, 2000). This has direct implications for the dimension of controllability (Corrigan, et al, 2001). Within this dimension, it is often believed in society that mental and behavioral disorders are personally controllable and if individuals cannot get better on their own, they are seen to lack personal effort (Crocker, 1996), are blamed for their condition, and seen as personally responsible (Corrigan, et al, 2001).

A recent report by Feldman and Crandall (2007), found that individuals with disorders such as pedophilia and cocaine dependence were much more stigmatized than those with disorders such as posttraumatic stress disorder. This supports the controllability hypothesis in which pedophilia and cocaine dependence could be viewed as more controllable in society than a disorder believed to be caused by a traumatic experience (PTSD). It also supports the pity dimension, in which disorders that are pitied to a greater degree are often less stigmatized (Corrigan, et al, 2000; Corrigan, et al, 2001). In this case, individuals within a culture or society may have more sympathy for disorders that are perceived as less controllable (Corrigan, et al, 2001).

Concealability, or visibility of the illness, is a dimension of stigma that parallels controllability, but also provides other insight into the stigmatization of mental and behavioral disorders. Crocker (1996) suggests that stigmatized attributes such as race can be easily identified, and are less concealable, allowing society to differentiate and stigmatize based on the visibility of the person. This is supported by research that shows that society attributes more stigmatizing stereotypes towards disorders such as schizophrenia, which generally have more visible symptoms, compared to others such as major depression (Angermeyer & Matschinger, 2005; Lundberg, et al, 2007).

The final three dimensions, course, stability, and disruptiveness, also may have some similarities among each other and compared to the others presented. Course and stability question how likely the person with the disability is to recover and/or benefit from treatment (Corrigan, et al, 2001; Jones, et al, 1984). Further the disruptiveness dimension assesses how much a mental or behavioral disorder may impact relationships or success in society. While disorders are frequently associated with an increased risk for poverty, lower socioeconomic status and lower levels of education (Kohn, Dohrenwend, & Mirotznik, 1998), the stability and disruptiveness of the conditions have implications as to whether an individual will be able to hold down a successful job and engage in healthy relationships, as evidenced by differences in stigma based on social class status. This demonstrates that if disorders are less disruptive, in which case they may be perceived as more stable, they are also less

Ahmedani Page 3

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

stigmatized (Corrigan, et al, 2001). This also expresses that some flexibility exists within each type of mental or behavioral disorder, as each diagnosed person is not stigmatized to the same extent (Crocker, 1999). Figure 1 depicts stigma as a latent variable constructed from the dimensions discussed above.

3. Levels of Stigma: Theory & Epistemology Illustrating the constructs underlying the formation of stigma helps us understand three specific levels of stigma – social stigma, self-stigma, and professional stigma. In this context, ‘levels’ does not refer to a hierarchy of importance for these varied stigmas, but rather to represent different social fields of stigma that can be differentiated from each other. In addition, further definition and theory behind these three ‘levels’ of stigma must be presented. First, stigmatized attitudes and beliefs towards individuals with mental health and drug use disorders are often in the form of social stigma, which is structural within the general public. Second, social stigma, or even the perception that social stigma exists, can become internalized by a person resulting in what is often called self-stigma. Finally, another, less studied level of stigma is that which is held among health professionals toward their clients. Since health professionals are part of the general public, their attitudes may in part reflect social stigma; however, their unique roles and responsibility to ‘help’ may create a specific barrier. The following theories are presented as an aid to understanding how each ‘level’ of stigma may develop in society.

Social Stigma The first, and most frequently discussed, ‘level’ is social stigma. Social stigma is structural in society and can create barriers for persons with a mental or behavioral disorder. Structural means that stigma is a belief held by a large faction of society in which persons with the stigmatized condition are less equal or are part of an inferior group. In this context, stigma is embedded in the social framework to create inferiority. This belief system may result in unequal access to treatment services or the creation of policies that disproportionately and differentially affect the population. Social stigma can also cause disparities in access to basic services and needs such as renting an apartment.

Several distinct schools of thought have contributed to the understanding of how social stigma develops and plays out in society. Unfortunately, to this point, social work has offered limited contributions to this literature. Nonetheless, one of the leading disciplines of stigma research has been social psychology. Stigma development in most social psychology research focuses on social identity resulting from cognitive, behavioral, and affective processes (Yang, Kleinman, Link, Phelan, Lee, & Good, 2007). Researchers in social psychology often suggest that there are three specific models of public stigmatization. These include socio-cultural, motivational, and social cognitive models (Crocker & Lutsky, 1986; Corrigan, 1998; Corrigan, et al, 2001). The socio-cultural model suggests that stigma develops to justify social injustices (Crocker & Lutsky, 1986). For instance, this may occur as a way for society to identify and label individuals with mental and behavioral illnesses as unequal. Second, the motivational model focuses on the basic psychological needs of individuals (Crocker & Lutsky, 1986). One example of this model may be that since persons with mental and behavioral disorders are often in lower socio-economic groups, they are inferior. Finally, the social cognitive model attempts to make sense of basic society using a cognitive framework (Corrigan, 1998), such that a person with a mental disorder would be labeled in one category and differentiated from non-ill persons.

Most psychologists including Corrigan and colleagues (2001) prefer the social cognitive model to explain and understand the concept of stigma. One such understanding of this perspective – Attribution Theory – is related to three specific dimensions of stigma

Ahmedani Page 4

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

including stability, controllability, and pity (Corrigan, et al, 2001) that were discussed earlier. Using this framework, a recent study by these researchers found that the public often stigmatizes mental and behavioral disorders to a greater degree than physical disorders. In addition, this research found stigma variability based on the public’s “attributions.” For example, cocaine dependence was perceived as the most controllable whereas ‘mental retardation’ was seen as least stable and both therefore received the most severe ratings in their corresponding stigma category (Corrigan, et al, 2001). These findings suggest that combinations of attributions may signify varying levels of stigmatized beliefs.

Sociologists have also heavily contributed to the stigma literature. These theories have generally been seen through the lens of social interaction and social regard. The first of these theorists was Goffman (1963) who believed that individuals move between more or less ‘stigmatized’ categories depending on their knowledge and disclosure of their stigmatizing condition. These socially constructed categories parallel Lemert’s (2000) discussion on social reaction theory. In this theory, two social categories of deviance are created including primary deviance, believing that people with mental and behavioral disorders are not acting within the norms of society, and secondary deviance, deviance that develops after society stigmatizes a person or group. Similarly, research demonstrating that higher levels of stigmatization are attributed towards individuals with more “severe” disorders (Angermeyer & Matschinger, 2005) also resembles these hierarchical categories and the disruptiveness and stability dimensions of stigma.

Furthermore, Link and Phelan clearly illustrated the view of sociology towards stigma in their article titled Conceptualizing Stigma (2001). Link and Phelan (2001) argue that stigma is the co-occurrence of several components including labeling, stereotyping, separation, status loss, and discrimination. First, labeling develops as a result of a social selection process to determine which differences matter in society. Differences such as race are easily identifiable and allow society to categorize people into groups. The same scenario may occur when society reacts to the untreated outward symptoms of several severe mental illnesses; i.e., Schizophrenia. Labels connect a person, or group of people, to a set of undesirable characteristics, which can then be stereotyped. This labeling and stereotyping process gives rise to separation. Society does not want to be associated with unattractive characteristics and thus hierarchical categories are created. Once these categories develop, the groups who have the most undesirable characteristics may become victims of status loss and discrimination. The entire process is accompanied by significant embarrassment by the individuals themselves and by those associated with them (Link & Phelan, 2001).

While social psychology and sociology are the primary contributors to the stigma literature, other disciplines have provided insight as well. Communications, Anthropology, and Ethnography all favor theories that revolve around threat. In Communications literature, stigma is the result of an “us versus them” approach (Brashers, 2008). For example, the use of specific in-group language can reinforce in-group belongingness as well as promote out- group differentiation (Brashers, 2008). This is referenced in research on peer group relationships such that youth often rate interactions with their same-age peers more positively than with older adults (whether family members or not) (Giles, Noels, Williams, Ota, Lim, Ng, et. al., 2003). This can also be applied to those with mental disorders in that individuals in the out-group (mental disorders) are perceived less favorably than the non-ill in-group.

Anthropology and Ethnography also prefer the identity model. From this perspective, the focus is on the impact of stigma within the lived experience of each person. Stigma may impact persons with mental illnesses through their social network, including how it exists in the structures of lived experiences such as employment, relationships, and status. Further,

Ahmedani Page 5

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

the impact of stigma is a response to threat, which may be a natural or tactical self- preservation strategy. However, it only worsens the suffering of the stigmatized person (Yang, et al, 2007). It is important to note again that while many disciplines have been leaders in social stigma theory, social work-specific literature has been mostly void of discussion on this topic. This is particularly unusual, since stigma is an obvious factor that impacts the lives of social work clients on a daily basis.

Self-Stigma Crocker (1999) demonstrates that stigma is not only held among others in society but can also be internalized by the person with the condition. Thus, the continued impact of social/ public stigma can influence an individual to feel guilty and inadequate about his or her condition (Corrigan, 2004). In addition, the collective representations of meaning in society – including shared values, beliefs, and ideologies – can act in place of direct public/social stigma in these situations (Crocker & Quinn, 2002). These collective representations include historical, political, and economic factors (Corrigan, Markowitz, and Watson, 2004). Thus, in self-stigma, the knowledge that stigma is present within society, can have an impact on an individual even if that person has not been directly stigmatized. This impact can have a deleterious effect on a person’s self-esteem and self-efficacy, which may lead to altered behavioral presentation (Corrigan, 2007). Nonetheless, Crocker (1999) highlights that individuals are able to internalize stigma differently based on their given situations. This suggests that personal self-esteem may or may not be as affected by stigma depending on individual coping mechanisms (Crocker & Major, 1989).

Similarly, other theories have provided insight into the idea of self-stigma. In modified labeling theory, the expectations of becoming stigmatized, in addition to actually being stigmatized, are factors that influence psychosocial well-being (Link, Cullen, Struening, Shrout, & Dohrenwend, 1989). In this context, it is primarily the fear of being labeled that causes the individual to feel stigmatized. Similarly, Weiner (1995) proposed that stigmatized beliefs provoke an emotional response. This can be interpreted from the standpoint of the afflicted individual, such that he or she may feel stigmatized and respond emotionally with embarrassment, isolation, or anger.

Health Professional Stigma It may seem unlikely that social workers and other health professionals would carry stigmatized beliefs towards clients; especially those whom they know are affected by a variety of barriers to treatment engagement. Nonetheless, recent literature is beginning to document the initial impact of health professional stigma (Nordt, Rössler, & Lauber, 2006; Volmer, Mäesalu, & Bell, 2008). While limited evidence exists specifically on social worker attitudes, pharmacy students who desire more social distance towards individuals with Schizophrenia are also less willing to provide them medications counseling (Volmer, et al, 2008). In addition, one Swiss study (psychiatrists, nurses, and psychologists) found that mental health professionals did not differ from the general public on their desired social distance from individuals with mental health conditions (Nordt, et al, 2006). Other studies have also come to similar conclusions (Lauber, et al, 2006; Tsao, Tummala, & Roberts, 2008; Sriram & Jabbarpour, 2005; Ücok, Polat, Sartorius, Erkoc, & Atakli, 2004). Clients have also reported feeling ‘labeled’ and ‘marginalized’ by health professionals (Liggins & Hatcher, 2005). Individuals with mental illnesses may not even receive equivalent care (compared to non-mentally ill patients) in general health settings once health professionals become aware of their mental health conditions (Desai, Rosenheck, Druss, & Perlin, 2002).

Theory on health professional stigma is very limited, but some literature does provide insight into its possible development. In one way, stigma by health professionals may

Ahmedani Page 6

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

develop very much the same as the social stigma evident in the general public. Social workers may develop their own biases from their upbringing or even from burnout in their own working roles, particularly when working with individuals who have severe and persistent mental illnesses (Acker & Lawrence, 2009). Nonetheless, some indications suggest that health professional stigma may also develop in a unique way. For instance, social workers and other health professionals, similar to persons in the general public, experience their own mental health and drug use problems and often have friends or family members who experience these same issues (Siebert, 2004; Fewell, King, & Weinstein, 1993). Individuals may also self-select into a helping profession due in part to these experiences (Stanley, Manthorpe, & White, 2007). When social workers and other health professionals deal with mental health and drug use problems they may experience burnout and/or become more or less likely to recognize similar problems among their clients (Siebert, 2003). Some research suggests that mental health conditions are more prevalent among helping professionals than in the general public (Schemhammer, 2005). This problem has also been shown to impair professional social work practice behaviors (Siebert, 2004; Sherman, 1996). For example, Siebert (2003) found that social workers who used marijuana were less likely to recognize marijuana use as a problem among their clients.

The counter-transference that can develop as a result of personal experiences or behaviors may impact clients who may be vulnerable when participating in treatment and may not have the appropriate resources to determine when they are not being treated adequately (Siebert, 2004; Hepworth, Rooney, & Larsen, 2002; Rayner, Allen, & Johnson, 2005). Clients may also be disenfranchised by the treatment process and become more likely to end current treatment and less likely to seek treatment in the future. This creates a barrier to the overall well-being of individuals by preventing adequate treatment, but it also may impact the acknowledgement of their disorder. Overall, health professionals may not provide adequate intervention, early detection, or community referral options for individuals with mental or behavioral disorders (Gassman, Demone, & Albilal, 2001; Tam, Schmidt, & Weisner, 1996), because of their own stigmatizing beliefs and personal histories (Siebert, 2004; 2005).

4. Implications for Social Work While it is apparent that stigma (all three levels) impacts individuals’ lives, there are also several implications for stigma and health professionals. These implications are placed into context within social work practice, education, policy, and research. In practice, social workers make up between 60–70 percent of mental health professionals in the United States (Proctor, 2004). While their roles may vary in different countries, they can nonetheless be important participants in mitigating stigma across the world. Since social workers often provide gatekeeping and triage functions in their roles, they are among the first to be in contact with individuals with psychiatric conditions (Hall, et al, 2000). Their attitudes and treatment preferences in practice settings can thus either promote or disenfranchise treatment seeking among their clients.

Social workers may be able to address issues of stigma within themselves by recognizing and embracing values and personal biases. This may be a difficult transformation that requires significant personal work and/or therapy. They may also be able to work with their clients on issues of stigma through their treatment provisions, triage roles, and outreach efforts. Nonetheless, the National Association of Social Workers (NASW) Code of Ethics mandates that professionals promote self-determination, client rights, self-realization, empowerment, social justice, and the dignity and worth of every person (National Association of Social Workers [NASW], 1999). These specific professional values pointedly

Ahmedani Page 7

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

call social workers to work to mitigate their own levels of stigma and work with others to dispel levels of social stigma and self-stigma.

While social workers have the opportunity to work with individuals, they also work with families. One additional way social workers may seek to mitigate social stigma on a micro- level is via the family. Family therapy may help relatives understand psychiatric conditions and how they can help/support the afflicted individual (Lefley, 1989). Some research suggests that more attention to families of individuals with mental health conditions is needed (Thornicroft, Brohan, Kassam, & Lewis-Holmes, 2008). If social workers are able to support an individual’s support system (family), it may help improve treatment seeking and treatment engagement for that person. Several studies have demonstrated the positive impact between family interventions and treatment engagement by the afflicted individual (Copello, Velleman, & Templeton, 2005; Adeponle, Thombs, Adelekan, & Kirmayer, 2009; Glynn, Cohen, Dixon & Niv, 2006). While this does not replace group work or individual work with a particular client, families may be among the most stigmatizing groups towards the afflicted person (Lee, Lee, Chiu, & Kleinman, 2005), and improved efforts towards the family system may be helpful.

On a macro level, social workers can also be instrumental in leading larger targeted educational efforts aimed at reducing stigma. Targeted programs have shown effectiveness in challenging misconceptions, improving attitudes, and reducing social distance (Thornton &Wahl, 1996; Esters, et al, 1998; Corrigan, et al, 2001). One such program, lead by the network of the World Psychiatric Association, has focused on individuals that impact the larger structural attitudes of stigma such as medical personnel, police officers, and journalists (Thornicroft, et al, 2008s). Large macro-level stigma campaigns that can be facilitated by social workers include public advertisements, targeted educational efforts, and advocacy for agency change. Occasionally, other systematic changes need to accompany these targeted efforts (Pinfold, Huxley, Thornicroft, Farmer, Toulmin, & Graham, 2003), but they have shown effectiveness and are important in mitigating stigma around the world. Nonetheless, more interventions and strategies must be developed to mitigate stigma in society.

Another important way to impact stigma is by educating individuals that have an opportunity to make a difference – i.e., social work education. For instance, when individuals have contact with those with mental illnesses, stigma can be diminished (Corrigan, et al, 2001). This may be the result of stereotypical beliefs about psychiatric conditions that are consistent with dimensions of stigma such as dangerousness or aesthetics (see, Jones, et al, 1984). Exposing social workers to these population groups may increase their willingness to treat the afflicted clients. This can be implemented through the field practicum experience at the undergraduate and graduate level. Education on stigma also fits into the practice sequences (macro- and micro- level), elective courses on substance abuse, and clinical diagnosis and assessment courses. Nonetheless, Bina and colleagues (2008) found that improving the knowledge and education of social workers about clients with drug use conditions will increase their interest in working with that population in practice. Furthermore, social work educational research has demonstrated that training social workers improves the likelihood that they will intervene, assess, and provide treatment for persons in an afflicted population, seek employment in that area, and feel confident and competent about their work (Amodeo, 2000).

Stigma is a global issue, and efforts to mitigate stigma through policy may be another effective strategy. On the macro-level, social workers can be very influential in advocating for policy change. Corrigan and colleagues (2001) suggest that policy change is one of the three strategies to mitigate stigma in society. For instance, stigma may impact lawmakers

Ahmedani Page 8

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

and permeate throughout government. One of the most important reasons why mental health care is not adequate is due to a lack of resources. In this case, it appears that economic factors may play a role in access to treatment. However, there is also a low priority placed on mental health within government and other funding bodies to support services (Knapp, Funk, Curran, Prince, Grigg, & McDaid, 2006). The WHO (2003) showed that while neuropsychiatric conditions make up 13 percent of the global burden of disease, only a median 2 percent of health care budgets in countries around the world are appropriated for mental illness. The lack of governmental support combined with the lack of support from other funding bodies (insurance companies) can in part be attributed to stigma (Knapp, et al, 2006). The debate about mental health parity in the United States is another example. Insurance companies in the U.S. have traditionally not funded mental health treatment to the same degree as general physical health illnesses (U.S. Surgeon General, 1999), which promotes that devaluation of mental illness in society. These disparate policies also act as a barrier to afflicted individuals and their ability to access social work services. Social workers and other policy makers can advocate for change in society. Social workers can be specifically instrumental in this process as they often serve disadvantaged populations such as those with mental illnesses, and should work to assist with the needs of their clients.

Social workers, as social scientists, are in position to develop research programs that seek to understand and influence stigma. More research is needed to understand the impact of different cultural traditions, attitudes, values, and beliefs on stigma, as it may vary between and within countries. This is also true among health professionals and their attitudes towards treating individuals in their community. As social scientists that practice and conduct research with different client populations, social workers have the ability to measure stigma among not only different race/ethnicity groups, but also in relation to individuals’ sexual orientation, gender, and age. In addition, limited research has specifically addressed the dimensions of stigma as discussed in the theoretical literature (Corrigan, et al, 2000; Jones, et al, 1984). More precise measures are needed to adequately assess stigma, across its varying dimensions and levels. The use of current stigma-related measures such as the Psychiatric Disability Attribution Questionnaire (Corrigan, et al, 2001) and the development of alternative scales to measure health professional stigma are needed to address dimensions of stigma across all three levels simultaneously. Also, larger studies of health professional stigma are needed, to understand how the attitudes of health professionals, and specifically social workers, influence treatment engagement and access.

5. Conclusions Mental health conditions are pervasive around the world. In addition, the burden of these conditions is expected to grow over the next 20 years (Mathers & Loncar, 2006). Unfortunately, few individuals receive the psychiatric treatment they need, as individuals often do not seek services and frequently do not remain in care once they begin. The WHO (2001) has suggested that stigma is one of the largest barriers to treatment engagement, even though treatment has shown to be effective, even in low income countries (Patel, et al, 2007). While stigma remains evident in society, within individuals themselves, and among health professionals, the ethical problem of health professional stigma places an additional barrier on clients who seek needed mental health services.

Acknowledgments This work was partially supported by a National Institute of Drug Abuse (NIDA) Institutional Training Award Grant (T32DA021129). The content in this manuscript is the sole responsibility of the author and does not necessarily represent the official views of NIDA.

Ahmedani Page 9

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

References Acker GM, Lawrence D. Social work and managed care. Journal of Social Work. 2009; 9(3):269–283.

Adeponle AB, Thombs BD, Adelekan ML, Kirmayer LJ. Family participation in treatment, post- discharge appointment and medication adherence at a Nigerian psychiatric hospital. The British Journal of Psychiatry. 2009; 194:86–87. [PubMed: 19118334]

American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th Ed., Text Revision). Washington, D.C: Author; 2000.

Amodeo M. The therapeutic attitudes and behavior of social work clinicians with and without substance abuse training. Substance Use Misuse. 2000; 35(11):1507–1536. [PubMed: 10993386]

Angermeyer MC, Matschinger H. Have their been any changes in the public’s attitudes towards psychiatric treatment? Results from representative population surveys in Germany in the years 1990 and 2001. Acta Psychiatrica Scandinavica. 2005; 111(1):68–73. [PubMed: 15636596]

Angermeyer MC, Matschinger H. The effect of violent attacks by schizophrenic persons on the attitude of the public towards the mentally ill. Social Science & Medicine. 1996; 43:1721–1728. [PubMed: 8961416]

Bina R, Harnek-Hall DM, Mollette A, Smith-Osbourne A, Yum J, Sowbel L, et al. Substance abuse training and perceived knowledge: predictors of perceived preparedness to work in substance abuse. Journal of Social Work Education. 2008; 44(3):7–20.

Brashers, D. Marginality, Stigma, and Communication. In: Donsbach, W., editor. The International Encyclopedia of Communication. Blackwell Publishing; 2008. Retrieved on November 18, 2008, from Blackwell Reference Online: http://www.blackwellreference.com/subscriber/tocnode? id=g9781405131995_chunk_g978140513199518_ss6-1

Copello AG, Velleman RDB, Templeton LJ. Family interventions in the treatment of alcohol and drug problems. Drug and Alcohol Review. 2005; 24:369–385. [PubMed: 16234133]

Corrigan PW. The impact of stigma on severe mental illness. Cognitive and Behavioral Practice. 1998; 5:201–222.

Corrigan PW. How stigma interferes with mental health care. American Psychologist. 2004; 50(7): 614–625. [PubMed: 15491256]

Corrigan PW. How clinical diagnosis might exacerbate the stigma of mental illness. Social Work. 2007; 52(1):31–39. [PubMed: 17388081]

Corrigan PW, Markowitz FE, Watson AC. Structural levels of mental illness stigma and discrimination. Schizophrenia Bulletin. 2004; 30:481–491. [PubMed: 15631241]

Corrigan P, Markowitz F, Watson A, Rowan D, Kubiak MA. An attribution model of public discrimination towards persons with mental illness. Journal of Health Behavior. 2003; 44(2):162– 179.

Corrigan PW, River LP, Lundin RK, Penn DL, Uphoff-Wasowski K, Campion J, et al. Three strategies for changing attributions about severe mental illness. Schizophrenia Bulletin. 2001; 27(2):187– 195. [PubMed: 11354586]

Corrigan PW, River LP, Lundin RK, Wasowski KU, Campion J, Mathisen J, et al. Stigmatizing attributions about mental illness. Journal of Community Psychology. 2000; 28(1):91–102.

Crocker, J. Stigma. In: Antony, SR.; Hewstone, M., editors. The Blackwell Encyclopedia of Social Psychology. Blackwell Publishing; 1996. Retrieved November 18, 2008 from Blackwell Reference Online: http://www.blackwellreference.com/subscriber/tocnode? id=g9780631202899_chunk_g978063120289921_ss1-54

Crocker J. Social stigma and self-esteem: Situational construction of self-worth. Journal of Experimental Social Psychology. 1999; 35:89–107.

Crocker, J.; Lutsky, N. Stigma and the dynamics of social cognition. In: Ainlay, SC.; Becker, G.; Coleman, LM., editors. The dilemma of difference: A multidisciplinary view of stigma. New York: Plenum Press; 1986.

Crocker J, Major B. Social stigma and self-esteem: The self-protective properties of stigma. Psychological Review. 1989; 96:608–630.

Crocker, J.; Major, B.; Steele, C. Social stigma. In: Fiske, S.; Gilbert, D.; Lindzey, G., editors. Handbook of social psychology. Boston: McGraw-Hill; 1998.

Ahmedani Page 10

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

http://www.blackwellreference.com/subscriber/tocnode?id=g9781405131995_chunk_g978140513199518_ss6-1

http://www.blackwellreference.com/subscriber/tocnode?id=g9780631202899_chunk_g978063120289921_ss1-54

Crocker, J.; Quinn, DM. Psychological Consequences of Devalued Identities. In: Brown, R.; Gaertner, S., editors. Blackwell Handbook of Social Psychology: Intergroup Processes. Blackwell Publishing; 2002. Retrieved from Blackwell Reference Online on November 18, 2008 from http:// www.blackwellreference.com/subscriber/tocnode? id=g9781405106542_chunk_g978140510654214

Desai MM, Rosenheck RA, Druss BG, Perlin JB. Mental disorders and quality of diabetes care in the Veterans Health Administration. American Journal of Psychiatry. 2002; 159(9):1584. [PubMed: 12202281]

Dudley JR. Confronting stigma within the services system. Social Work. 2000; 45:449–455. [PubMed: 11029900]

Esters LG, Cooker PG, Ittenbach RF. Effects of a unit of instruction in mental health on rural adolescents’ conceptions of mental illness and attitudes about seeking help. Adolescence. 1998; 33:469–476. [PubMed: 9706332]

Feldman DB, Crandall CS. Dimensions of mental illness stigma: What about mental illness causes social rejection. Journal of Social and Clinical Psychology. 2007; 26(2):137–154.

Fewell CH, King BL, Weinstein DL. Alcohol and other drug use among social work colleagues and their families: Impact on practice. Social Work. 1993; 38:565–570. [PubMed: 8211315]

Gassman RA, Demone HW, Albilal R. Alcohol and other drug content in core courses: Encouraging substance abuse assessment. Journal of Social Work Education. 2001; 37(1):137–145.

Giles H, Noels KA, Williams A, Ota H, Lim T, Ng SH, et al. Intergenerational communication across cultures: Young people's perceptions of conversations with family elders, non-family elders, and same-age peers. Journal of Cross-Cultural Gerontology. 2003; 18:32.

Glynn SM, Cohen AN, Dixon LB, Niv N. The potential impact of the recovery movement on family interventions for Schizophrenia: Opportunities and obstacles. Schizophrenia Bulletin. 2006; 32(3): 451–463. [PubMed: 16525087]

Goffman, E. Stigma: Notes on the Management of Spoiled Identity. Englewood Cliffs NJ: Prentice Hall; 1963.

Hall MN, Amodeo M, Shaffer HJ, Vander Bilt J. Social workers employed in substance abuse treatment agencies: A training needs assessment. Social Work. 2000; 45(2):141–155. [PubMed: 10710987]

Hepworth, DH.; Rooney, RH.; Larsen, J. Direct social work practice: Theory and skills. 6th ed.. Pacific Grove, CA: Brooks/Cole; 2002.

Hugo CJ, Boshoff DEL, Traut A, Zungu-Dirwayi N, Stein DJ. Community attitudes toward and knowledge of mental illness in South Africa. Social Psychiatry and Psychiatric Epidemiology. 2003; 38:715–719. [PubMed: 14689176]

Jones, EE.; Farina, A.; Hastorf, AH.; Markus, H.; Miller, DT.; Scott, RA. Social stigma: The psychology of marked relationships. New York: Freeman; 1984.

Kessler RC, Berglund PA, Bruce ML, Koch R, Laska EM, Leaf PJ, et al. The prevalence and correlates of untreated serious mental illness. Health Services Research. 2001; 36:987–1007. [PubMed: 11775672]

Knapp M, Funk M, Curran C, Prince M, Grigg M, McDaid D. Economic barriers to better mental health practice and policy. Health Policy and Planning. 2006; 21(3):157. [PubMed: 16522714]

Kohn, R.; Dohrenwend, BP.; Mirotznik, J. Epidemiologic findings on selected psychiatric disorders in the general population. In: Dohrenwend, BP., editor. Adversity, Stress, and Psychopathology. New York, NY: Oxford University Press; 1998. p. 235-284.

Lauber C, Nordt C, Braunschweig C, Rössler W. Do mental health professionals stigmatize their patients. Acta Psychiatrica Scandinavica. 2006; 113:51–59. [PubMed: 16445483]

Lee S, Lee MTY, Chiu MYL, Kleinman A. Experience of social stigma by people schizophrenia in Hong Kong. The British Journal of Psychiatry. 2005; 186:153–157. [PubMed: 15684240]

Lefley HP. Family burden and family stigma in major mental illness. American Psychologist. 1989; 44(3):556–560. [PubMed: 2648907]

Lemert, E. How we got where we are: An informal history of the study of deviance. In: Lemert, C.; Winter, M., editors. Crime and deviance: Essays and innovations of Edwin. Lanham: Rowman & Littlefield; 2000.

Ahmedani Page 11

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

http://www.blackwellreference.com/subscriber/tocnode?id=g9781405106542_chunk_g978140510654214

Liggins J, Hatcher S. Stigma toward the mentally ill in the general hospital: a qualitative study. General Hospital Psychiatry. 2005; 27(5):359–364. [PubMed: 16168797]

Link BG, Cullen FT, Frank J, Wozniak JF. The social rejection of former mental patients: Understanding why labels matter. American Journal of Sociology. 1987; 92:1461–1500.

Link BG, Cullen FT, Struening EL, Shrout PE, Dohrenwend BP. A modified labeling theory approach in the area of mental disorders: An empirical assessment. American Sociological Review. 1989; 54:100–123.

Link BG, Phelan JC. Conceptualizing stigma. Annual Review of Sociology. 2001; 27:363–385.

Lundberg B, Hansson L, Wentz E, Bjorkman T. Sociodemographic and clinical factors related to devaluation/discrimination and rejection experiences among users of mental health services. Social Psychiatry Psychiatric Epidemiology. 2007; 42:295–300.

Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med. 2006; 3(11):e442. [PubMed: 17132052]

National Association of Social Workers. Code of ethics of the National Association of Social Workers. DC: Author; 1999.

National Institute of Mental Health [NIMH]. The Numbers Count: Mental Disorders in America. 2006. Retrieved on June 18, 2010 from http://www.nimh.nih.gov/publicat/numbers.cfm#Intro

Nordt C, Rössler W, Lauber C. Attitudes of mental health professionals toward people with Schizophrenia and Major Depression. Schizophrenia Bulletin. 2006; 32(4):709. [PubMed: 16510695]

Patel V, Araya R, Chatterjee S, Chisholm D, Cohen A, De Silva M, et al. Treatment and prevention of mental disorders in low-income and middle-income countries. The Lancet. 2007; 370(9591):991– 1005.

Pinfold V, Huxley P, Thornicroft G, Farmer P, Toulmin H, Graham T. Reducing psychiatric stigma and discrimination: Evaluating an educational intervention with the policy force in England. Social Psychiatry and Psychiatric Epidemiology. 2003; 38:337–344. [PubMed: 12799785]

Proctor EK. Research to inform mental health practice: Social work’s contribution. Social Work Research. 2004; 28:195–197.

Rayner GC, Allen SL, Johnson M. Countertransference and self-injury: A cognitive-behavioural cycle. Journal of Advanced Nursing. 2005; 50(1):12–19. [PubMed: 15788061]

Schemhammer E. Taking their own lives – The high rate of physician suicide. New England Journal of Medicine. 2005; 352(24):2473. [PubMed: 15958803]

Sherman MD. Distress and professional impairment due to mental health problems among psychotherapists. Clinical Psychology Review. 1996; 16(4):299–315.

Siebert DC. Denial of AOD use: An issue for social workers and the profession. Health and Social Work. 2003; 28(2):89–97. [PubMed: 12774530]

Siebert DC. Depression in North Carolina social workers: Implications for practice and research. Social Work Research. 2004; 28(1):30–40.

Siebert DC. Help seeking for AOD misuse among social workers: Patterns, barriers, and implications. Social Work. 2005; 50(1):65–75. [PubMed: 15688681]

Sriram TG, Jabbarpour YM. Are mental health professionals immune to stigmatizing beliefs? Psychiatric Services. 2005; 56:610. [PubMed: 15872176]

Stanley N, Manthorpe J, White M. Depression in the profession: Social workers� experiences and perceptions. British Journal of Social Work. 2007; 37:281–298.

Tam TW, Schmidt L, Weisner C. Patterns in the institutional encounters of problem drinkers in a community human services network. Addiction. 1996; 91(5):657–670. [PubMed: 8935251]

Thornicroft G, Brohan E, Kassam A, Lewis-Holmes E. Reducing stigma and discrimination: Candidate interventions. International Journal of Mental Health Systems. 2008; 2:3. [PubMed: 18405393]

Thornton JA, Wahl OF. Impact of a newspaper article on attitudes toward mental illness. Journal of Community Psychology. 1996; 24:17–24.

Tsao CIP, Tummala A, Roberts LW. Stigma in mental health care. Academic Psychiatry. 2008; 32(2): 70. [PubMed: 18349322]

Ahmedani Page 12

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

http://www.nimh.nih.gov/publicat/numbers.cfm#Intro

Ücok A, Polat A, Sartorius N, Erkoc S, Atakli C. Attitudes of psychiatrists towards patients with Schizophrenia. Psychiatry and Clinical Neurosciences. 2004; 58:89–91. [PubMed: 14678463]

U.S. Surgeon General. Rockville, Maryland: Center of Mental Health Services, National Institute of Mental Health; 1999. Mental health: A report of the U.S. Surgeon General.

Volmer D, Mäesalu M, Bell JS. Pharmacy students’ attitudes toward and professional interactions with people with mental disorders. International Journal of Social Psychiatry. 2008; 54(5):402–413. [PubMed: 18786902]

Weiner, B. Judgements of Responsibility: A foundation for a theory of social conduct. New York: Guilford Press; 1995.

World Health Organization [WHO]. Investing in mental health. Geneva, Switzerland: WHO; 2003.

World Health Organization, WHO. World Health Report 2001. Mental health: new understanding, new hope. WHO: Geneva, Switzerland; 2001.

Yang LH, Kleinman A, Link BG, Phelan JC, Lee S, Good B. Culture and stigma: Adding moral experience to stigma theory. Social Science & Medicine. 2007; 64:1524–1535. [PubMed: 17188411]

Ahmedani Page 13

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

Figure 1. The dimensions of stigma

Ahmedani Page 14

J Soc Work Values Ethics. Author manuscript; available in PMC 2011 December 29.

N IH

-P A

A uthor M

anuscript N

IH -P

A A

uthor M anuscript

N IH

-P A

A uthor M

anuscript

C O N T I N U I N G M E D I C A L E D U C A T I O N

The Diagnosis and Treatment of Generalized Anxiety Disorder Borwin Bandelow, Reinhard J. Boerner, Siegfried Kasper, Michael Linden, Hans-Ulrich Wittchen, Hans-Jürgen Möller

SUMMARY Background: Generalized anxiety disorder (GAD) is a com- mon and serious disease with a lifetime prevalence of 4.3% to 5.9%. It is underdiagnosed in primary care.

Methods: Recommendations on the treatment of GAD are given on the basis of all available findings from pertinent randomized trials, retrieved by a selective search of the literature.

Results: Among psychotherapeutic techniques, various kinds of cognitive behavioral therapy (CBT) have been found useful in controlled trials. The drugs of first choice include selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephine reuptake inhibitors (SNRIs), and the calcium-channel modulator pregabalin. Tricyclic antidepressants are also effective but have more adverse effects than SSRIs. Although benzodiazepines are effective anxiolytic agents for short-term use, they should not be given over the long term because of the danger of addic- tion. Buspirone, an azapirone, was found to be effective in a small number of trials, but the findings across trials are inconsistent. The response rate of GAD to CBT in published studies lies between 47% and 75%, while its response rate to drug treatment lies between 44% and 81%.

Conclusion: The treatment of GAD with CBT and drugs is evidence-based and has a good chance of improving the manifestations of the disorder.

►Cite this as: Bandelow B, Boerner RJ, Kasper S, Linden M, Wittchen HU, Möller HJ: The diagnosis and treatment of general ized anxiety disorder. Dtsch Arztebl Int 2013; 110(17): 300–10. DOI: 10.3238/arztebl.2013.0300

G eneralized anxiety disorder (GAD) is a common and disabling disease. The ICD-10 diagnostic criteria for GAD are listed in Box 1 and eBox 1: It is characterized by worries based on extant dangers (e.g., of a spouse having an auto - mobile accident) whose likelihood is overestimated and whose negative consequences are viewed as catastrophic. Worries can rapidly generalize to multiple areas of everyday experience in sufferers from GAD, including health, family relationships, and their occupational or financial situation (or that of persons close to them). These worries typically in- duce defensive and avoidant behavior; for example, any activities held to be dangerous, such as travel, may be postponed or simply not undertaken. Somatic manifestations of anxiety arise, often leading to ex- tensive medical diagnostic evaluations (1).

The differential diagnosis includes somatic dis- orders, including neurological ones, but mainly other psychiatric conditions, and, in particular, other anxiety disorders. Among these, panic disorder in- volves periodic attacks of physical and emotional manifestations of anxiety, such as palpitations, short- ness of breath, a sensation of tightness in the chest, diaphoresis, feelings of helplessness, and pares- thesias. It is often combined with agoraphobia. Patients with panic disorder worry mainly about the potential consequences of such attacks for their health, or about a supposed somatic illness under - lying them; unlike patients with GAD, they do not worry that other persons close to them might become ill. In social anxiety disorder, the sufferer’s worries and fears are limited to social situations in which he or she might be observed or criticized. 40% to 67% of patients with GAD also suffer from depression (e1, e2). In such cases, if the patient’s worries are

Department of Psychiatry and Psychotherapy, University Medical Center Göttingen: Prof. Dr. med. Bandelow, Dipl.-Psych.

Psychiatric Department of the Christian General Hospital Quakenbrück Dr. med. Dr. scient. pth. Dipl.-Psych. Boerner

Medical University of Vienna, Department of Psychiatry and Psychotherapy: Prof. Dr. med. Kasper

Department of Behavioral and Psychosomatic Medicine at the Rehabilitation Centre Seehof, Teltow/Berlin: Prof. Dr. med. Linden

Institute of Clinical Psychology and Psychotherapy, Dresden University of Technology: Prof. Dr. med. Wittchen

Psychiatric Clinic of the Ludwig-Maximilians-University, Munich: Prof. Dr. med. Möller

Generalized anxiety disorder GAD is characterized by worries based on extant dangers (e.g., of a spouse having an automobile accident) whose likelihood is overestimated and whose negative con - sequences are viewed as catastrophic.

300 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10

M E D I C I N E

accompanied by such manifestations as mood fluctuations (regularly worse in the morning), early morning awakening, guilt feelings, or suicidal ideation, it must be determined whether depression is affecting the patient more severely than GAD. It may also be diffi- cult to differentiate GAD from a somatoform disorder with varying bodily symptoms that have no organic correlate, such as palpitations, shortness of breath, dysphagia, or unexplained abdominal discomfort. Such patients repeatedly demand medical evaluation and, unlike GAD patients, often reject a psycho - somatic explanation of their problems. Some of the avoidable errors in the diagnosis of GAD are listed in Box 2.

Epidemiological surveys of the general population have shown that GAD has a lifetime prevalence of 4.3% to 5.9% and a 12-month prevalence of 0.2% to 4.3% (2, 3). Among patients in general medical prac- tice, the one-month prevalence is 7.9% to 9 % (4). GAD is twice as common in women as in men. It is most often seen in persons aged 45 to 59, with a lower peak in persons aged 30 to 44 and a decline after age 60 (5). If untreated, GAD usually takes a chronic course, with most patients still suffering from its symptoms six to twelve years after the diagnosis is made. Only two out of five affected persons find their way to appropriate treatment (7).

Causes The causes of GAD are not yet well understood. Traumatic life experiences, faulty conditioning, ge - netic influences, and neurobiological dysfunction are considered to be potential etiological factors for GAD and other anxiety disorders (8). GAD tends to cluster in families (9). Twin studies have shown a moderate hereditary influence (10), which is, how- ever, less intense than in other anxiety disorders, e.g., panic disorder. The neurobiological factors under discussion include disturbances of various neurotransmitter systems (serotonin, epinephrine/ nor epinephrine, GABA) (11–13). Structural and functional neuroimaging of GAD patients has revealed abnormalities in the amygdala, the dorsomedial pre- frontal cortex, and other brain areas (e3–e6).

Treatment The following recommendations are based on an evalu- ation of all randomized controlled trials of treatment for GAD that we were able to retrieve by a literature

Lifetime prevalence Generalized anxiety disorder (GAD) is a common and serious disease with a lifetime prevalence of 4.3% to 5.9%. It is underdiagnosed in primary care.

The causes of GAD Traumatic life experiences, faulty conditioning, genetic influences, and neurobiological dys- function are considered to be potential etiologi- cal factors for GAD and other anxiety disorders.

BOX 1

The diagnosis of generalized anxiety disorder according to ICD-10 ● Tension, worries, and fears about everyday events and problems for at least

six months, with the following symptoms and signs: – vegetative manifestations such as increased heart rate, diaphoresis, tremor,

or dry mouth – symptoms in the chest or abdomen (respiratory symptoms, feeling of tight-

ness, chest pain, abdominal discomfort) – mental symptoms (dizziness, derealization, fear of losing control, fear of

dying) – general symptoms (hot or cold flashes, paresthesiae) – symptoms of tension (muscle tension, agitation, foreign-body sensation in

throat) – other, nonspecific symptoms (exaggerated startle response, lack of concen-

tration, irritability, difficulty falling asleep) Patients are tormented by constant worries,e.g., that they (or their loved ones) might have an accident or become ill. Activities that are perceived as dangerous are avoided or postponed. Patients also worry about the fact that they are always worrying (“meta-worries,” e.g., “All this worrying is sure to give me an ulcer“).

BOX 2

Avoidable errors in the diagnosis of anxiety disorders ● In primary care, 45% of anxiety disorders are not recognized as such (23). ● Anxiety disorders are often misdiagnosed because the patients present with

somatic complaints: for 87% of patients with generalized anxiety disorder, the primary symptom is not anxiety, but rather pain or sleep disturbance (24, e110).

● Patients with GAD are often considered to have some type of mental distur - bance, but two-thirds are not diagnosed as having either any anxiety disorder or GAD, and thus do not receive appropriate treatment (1).

● In patients with depression, a coexisting anxiety disorder is often missed and therefore not treated (24).

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10 301

M E D I C I N E

search; the latter involved both automated searching in databases (Medline and the Web of Science database of ISI Web of Knowledge) and a manual search. A struc- tured evaluation of each trial for correctness of method (size of study population, blinding, randomization, sta - tistics, instruments, etc.) was performed according to the recommendations of the Scottish Intercollegiate Guidelines Network (SIGN, www.sign.ac.uk). The trials evaluated here include all of those that were

analyzed for the guidelines of the World Federation of Societies for Biological Psychiatry (2008) (14) along with 21 further randomized controlled trials that have appeared since these guidelines were published. As will become clear below, some of the trials of drug treat- ment or of psychotherapy had negative or inconclusive results. Only treatments that were found to be effective in a majority of trials in which they were tested are recommended here.

Cognitive behavioral therapy The goal of treatment is for the patient to develop the ability to recognize, eliminate, and correct his or her dysfunctional (faulty, one-sided) assump- tions and thoughts in order to behave more appro- priately in various situations.

Demonstration of efficacy The efficacy of CBT has been demonstrated in many randomized clinical trials. A number of trials showed CBT to be superior to being placed on a waiting list or to treatment with psychological placebo conditions.

BOX 3

The components of cognitive behavioral therapy (CBT) for generalized anxiety disorder* ● Nonspecific effects

– Establishment of a robust therapeutic relationship – Discussion of all of the patient’s problems and his or her

life story, rather than focusing exclusively on symptoms ● Psychoeducation

– Information about the disorder – Explanation of the somatic manifestations of anxiety as a

natural fight-or-flight response – Explanation of the rationale for treatment – Recommendation of suitable information brochures and

self-help materials ● Cognitive strategies

– Reevaluation of unrealistic assumptions about the utility and disadvantages of worries

– Development of a realistic assessment of the probability that various types of problems will have negative conse- quences, and of the amount of suffering this will cause

– Putting the type and frequency of the patient’s worries in perspective (“What do other people do in this situation?”)

– Examining catastrophic expectations with homework exercises involving prediction of what will come next (identification of “worry chains”)

– Recognition of negative fluency (What opportunities do I have for positive or negative thinking?)

– Distancing onself from worries and controlling them (practicing the ability to anticipate positively; inner self-distancing dialogues)

– Dealing with problems caused by perfectionism and the inability to tolerate uncertainty

– Working on meta-worries (“I am worried that my constant worrying will give me an ulcer”)

– Building up resources (“Are there any areas of life in which I have no worries?”)

● Exposure – Patients are instructed to try not to engage in safety

behavior (e.g., telephoning their children to make sure they are healthy). The tendency to put off activities perceived to be dangerous, such as travel, is also therapeutically addressed.

– In sensu exposure to particular things about which the patient is worried

● Emotional regulation – Muscle relaxation techniques

● Problem-solving techniques – Practicing problem-solving strategies to lessen

inappropriate approaches to problems (worrying) – Establishment of goals and life plans, participation in

enjoyable activities, increased perception of emotional well-being

*modified from (26, 27)

302 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10

M E D I C I N E

Psychotherapy Cognitive behavioral therapy (CBT)—Cognitive be- havioral theories start from the presumption that anxiety disorders, like other mental disorders, are caused in part by distorted, illogical, or unrealistic cog- nitions (e7). The goal of treatment is for the patient to develop the ability to recognize, eliminate, and correct his or her dysfunctional (faulty, one-sided) assumptions and thoughts in order to to cope more appropriately

with various situations (e8–e10). Psychoeducation, confrontational techniques (e.g., in sensu exposure to the things the patient fears, e.g., anticipated ca - tastrophic events) (e11, e12), and problem-solving techniques are further components of CBT. The cre- ation of a robust therapeutic relationship is, of course, another important element of behavioral therapy. The therapeutic components of CBT for GAD are summa - rized in Box 3 (e10, e11).

Internet-based cognitive behavioral therapy Internet-based CBT involves either pure self- therapy with the aid of various materials or else self-therapy enhanced by brief contacts with therapists by e-mail or telephone.

Internet-based therapy: current evidence Internet-based therapy cannot now be recom- mended, as there have not been any trials com - paring it to traditional CBT, in which the patient and therapist are in personal contact.

BOX 4

Treatment recommendations for generalized anxiety disorder (GAD); accompanying psychotherapy is recommended in all cases ● Drugs of first choice

– SSRIs, e.g. escitalopram*1 10–20 mg or paroxetine*1 20–60 mg – SNRIs, e.g. duloxetine*1 60–120 mg or venlafaxine*1,*2 75–225 mg – pregabalin*1 150–600 mg

● Drugs of second choice – buspirone*1 15–60 mg, usually 30 mg – imipramine 75–200 mg, usually 100–150 mg – opipramol*1 100–300 mg, usually 200 mg – hydroxyzine*1 37.5–75 mg

For concomitant treatment with an antidepressant until the onset of the antidepressant effect, alprazolam*1 1.5–6 mg, usually 3 mg

● Procedure for patients who do not respond to standard pharmacotherapy No more than a partial response in 4–6 weeks

– raise dose and treat for a further 4–6 weeks No response at all in 4–6 weeks

– Change of drug (although an analysis of multiple studies of patients with GAD who did not respond to 2 weeks of SSRI treatment showed that only 38% went on to have a response by 8 weeks [28])

– Possible strategies for drug-switching (in the absence of relevant clinical studies): – switch to another drug of first choice (SSRI, SNRI, pregabalin) – switch to a drug of second choice (tricyclic antidepressant, buspirone, opipramol) – switch to a drug known from clinical trials to be effective against other anxiety disorders, but not yet adequately

tested against GAD (e.g., moclobemide, mirtazapine) – switch to quetiapine (off-label)

– Possible add-on strategies: – administration of pregabalin or olanzapine in addition to an SSRI or SNRI (e111; e112)

*1approved in Germany for the treatment of anxiety states/disorders *2Most of the available evidence is for the extended-release formulation of venlafaxine. SSRI, selective serotonin reuptake inhibitor; SNRI, serotonin-norepinephrine reuptake inhibitor.

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10 303

M E D I C I N E

The efficacy of CBT has been demonstrated in many randomized clinical trials. A number of trials showed CBT to be superior to being placed on a waiting list (e13–e19), and several studies comparing CBT to a “psychological placebo” showed that CBT has not only nonspecific psychotherapeutic effects, but also specific ingredients (e20–e23). The rate of response to behav - ioral therapy in therapeutic trials ranges from 47% to 75%, with varying definitions of a “response.”

In the last few years, a number of trials of Internet- based CBT have been carried out, involving either pure self-therapy with the aid of various materials or else self-therapy enhanced by brief contacts with therapists by e-mail or telephone (e24–e26). All but one of these trials revealed significant differences between CBT and being placed on a waiting list; in a single trial, neither Internet-based CBT nor Internet-based psychodynamic therapy was any more effective than being placed on a waiting list (e27). Internet-based therapy cannot now be recommended, as there have not been any trials com - paring it to traditional CBT, in which the patient and therapist are in personal contact. Moreover, Internet- based therapy is difficult to reimburse and is fraught with other medicolegal and ethical difficulties (for example, if the patient is suicidal).

Psychodynamic (depth-psychological/psycho ana - lytical) therapy—There are a number of approaches to the psychodynamic treatment of GAD. A special type of psychoanalytic focal therapy for GAD (e29, e30) has been developed on the basis of sup portive-expressive psychotherapy (e28). This type of treatment proceeds from the hypothesis that patients with GAD have inse- cure relationships and that their mental symptoms are caused by a central relational conflict. As in other types of psychodynamic conflict, the transference relation- ship is exploited for therapeutic purposes. Current psy- chodynamic treatment for GAD often consists of short- term therapy in which an active therapeutic attitude is preferred.

Our extensive literature search yielded only two evaluable randomized controlled trials of the effect of psychodynamic therapy for GAD. In one trial, behav - ioral therapy was found to be more effective than psy- chodynamic therapy, both acutely and in later follow- up (e31, e32). In the other trial, the authors concluded that psychodynamic therapy was about as effective as CBT; in fact, however, the numerical results they reported were markedly better for CBT, but the differ-

ences were not significant. Thus, in our view, this study was underpowered to demonstrate either thera- peutic equivalence or a therapeutic difference (e33, e34). The overall state of the evidence does not yet permit any concrete recommendation. Comparisons with waiting lists and active controls (psychological placebos) are also lacking.

Because of the lack of published data, nothing can yet be said about the possible efficacy of other types of psychodynamic therapy (psychotherapy based on depth psychology, long-term psychoanalysis, or others).

Drugs There have been many controlled trials of pharmaco- therapy for generalized anxiety disorder, with response rates ranging from 44% to 81% (e35, e36). The dosages used are given in Box 4. The advantages and disad - vantages of various classes of drugs and their adverse effects are listed in Table 1.

Whenever GAD is treated with drugs, the treating physician must continue to maintain an empathic and attentive psychotherapeutic relationship with the patient. Antidepressants often have adverse effects in the first few days of treatment before their therapeutic effect sets in; compliance with treatment can be increased by a pre - ventive preliminary discussion of the types of adverse effects that might arise, e.g., agitation at the beginning of treatment with selective serotonin reuptake inhibitors (SSRIs). Telling the patient in advance that antidepres- sants generally take time to work often obviates the need for benzodiazepines at the beginning for treatment. A proactive discussion of possible sexual dysfunction (e37) or weight gain (e38) has also proved useful in practice.

Selective serotonin reuptake inhibitors (SSRIs)—A number of controlled trials have demonstrated the ef - ficacy of the SSRIs escitalopram (e39–e45), paroxetine (e46–e49), and sertraline (e50–e52).

SSRIs are generally well tolerated. Adverse effects such as agitation, nervousness, and worsened anxiety may arise in the first few days or weeks of treatment and may impair compliance. After longer periods, sexual dysfunction may arise, or there may be with- drawal phenomena differing from those seen in ben- zodiazepine withdrawal (15). SSRIs should be taken in the morning to avoid nocturnal restlessness and insomnia at the start of treatment. The anxiolytic effect usually sets in with a latency of two to four weeks.

Empathic patient care Whenever GAD is treated with drugs, the treating physician must continue to maintain an empathic and attentive psychotherapeutic relationship with the patient. Antidepressants often have adverse effects in the first few days of treatment.

SSRIs and SNRIs Adverse effects such as agitation, nervousness, and worsened anxiety may arise in the first few days or weeks of treatment with these drugs and may impair compliance. Their anxiolytic effect usually sets in with a latency of two to four weeks.

304 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10

M E D I C I N E

Drugs of first choice • selective serotonin reuptake inhibitors (SSRIs) • serotonin-norepinephrine reuptake inhibitors

(SNRIs) • pregabalin

Drugs of second choice • tricyclic antidepressants (TCA) • buspirone • benzodiazepines • hydroxyzine • opipramol

TABLE

The advantages and disadvantages of drugs used to treat generalized anxiety disorder*1

*1modified from (13)

Drug

Drugs of first choice Selective serotonin reuptake inhibitors (SSRIs)

Serotonin- norepinephrine reuptake inhibitors (SNRIs)

Pregabalin

Drugs of second choice Tricyclic ¨¨ antidepressants (TCA)

Buspirone

Benzodiazepines

Hydroxyzine

Opipramol

Advantages

– No dependence – Safe in case of

overdose

– No dependence – Safe in case of

overdose

– Rapid onset of action – No cytochrome P-450 inter-

actions – Positive effect on sleep

– No dependence

– No dependence – Relatively safe in case of

overdose – Rapid onset of action – Relatively safe in case of

overdose

– No dependence – Rapid onset of action

– No dependence

Disadvantages

– Latency of action 2–6 weeks – At the start of treatment: agitation,

nervousness, increased symptoms of anxiety

– Possible cytochrome P-450 interactions

– Latency of action 2–6 weeks – At the start of treatment: agitation,

nervousness, increased symptoms of anxiety

– Possible cytochrome P-450 interactions

– Lack of concentration and drowsiness are common, particularly at the start of treatment

– No data available from long-term trials – latency of action 2–6 weeks – dangerous in case of overdose

– Less effective than other drugs in several clinical trials

– Latency of action 2–6 weeks – Dependence possible

– Few trials documenting efficacy – No long-term trials

– Very few trials documenting efficacy – No long-term trials – Latency of action 2–6 weeks

Adverse effects

Agitation, nausea, diarrhea, constipation, gastrointestinal symptoms, headache, decreased or increased appetite, weight loss, weight gain, diaphoresis, hot flashes, dry mouth, fatigue, tremulousness, sexual disturbances, nightmares, mania, withdrawal phenomena, and other adverse effects Agitation, sleep disturbances, nausea, loss of appetite, gastrointestinal symptoms, dry mouth, constipation, diaphoresis, headache, dizzinesss, palpita - tions, rise in blood pressure, drop in blood pressure, tremulousness, shaking chills, sexual disturbances, mania, disturbances of micturition, sensory disturbances, visual disturbances, confusion, and other adverse effects Somnolence, drowsiness, insomnia, euphoria, lethargy, confusion, memory disturbances, irritability, sexual dis - turbances, increased appetite, weight gain, dizzinesss, motor disturbances, tremulousness, sensory distur - bances, dysequilibrium, visual disturbances, vomiting, dry mouth, constipation, edema, and other adverse effects

Fatigue, dry mouth, hypotension, dizzinesss, tremulousness, diaphoresis, increased appetite, weight gain, disturbances of micturition, palpitations, visual disturbances, confusion, constipation, mania, withdrawal phenomena, and other adverse effects Somnolence, nausea, headache, nervousness, dizzinesss, oveerxcitement, diaphoresis, sweaty palms, and other adverse effects Fatigue, “hangover” on the following day, dizziness, prolonged reaction times, visual disturbances, unsteady gait, dysarthria, memory disturbances, forgetfulness, confusion, respiratory depression, paradoxical agitation, muscle weakness, weight change, danger of falling in elderly patients, and other adverse effects. In prolonged use: dependence After abrupt withdrawal: withdrawal phenomena (agitation, insomnia, feeling sick, nausea, vomiting, palpitations, drop in blood pressure, diaphoresis, tremulousness, muscle tension, and other symptoms) Somnolence, fatigue, insomnia, dry mouth, gastrointestinal symptoms, weight gain, concentration difficulties, tachycardia, arrhythmia, headache, abnormal liver function, and other adverse effects Fatigue, sedation,shortened reaction times, dry mouth, nasal congestion, hypotension, and other adverse effects

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10 305

M E D I C I N E

Serotonin-norepinephrine reuptake inhibitors (SNRIs)—A number of trials have demonstrated the efficacy of the SNRI venlafaxine (e35, e44, e53–e60); only one found it to be no better than placebo (e61). It is generally given in an extended release formulation. Duloxetine was effective against GAD in controlled trials (e56, e57, e62–e65). At the start of treatment with an SNRI, adverse effects such as nausea, agi- tation, or sleep disturbances may impair compliance. The anxiolytic effect sets in with a latency of two to six weeks, or sometimes even later.

Pregabalin—Multiple controlled trials have shown that pregabalin is effective against GAD (e36, e58, e66–e70). The anxiolytic effect arises rapidly: Sig- nificant efficacy is demonstrable from the fourth day of treatment onward (e67), with respect to both the mental and the physical symptoms of GAD (e54). Sleep disturbances improve (e67). Impaired concen- tration and drowsiness are the most common adverse effects.

Tricyclic antidepressants (TCA)—The findings of controlled trials support the use of imipramine to treat GAD (e71, e72). Especially at the beginning of treat- ment, TCAs can cause adverse effects such as intensi- fied anxiety, anticholinergic effects, sedation, or weight gain. Adverse effects are more common with TCAs than with the more recently introduced antide- pressants (SSRIs and SNRIs), and the latter should therefore be preferred. If these standard medications turn out to be ineffective or are poorly tolerated, TCAs may be a good treatment option. Their latency of effect is two to six weeks, or longer.

Benzodiazepines—A number of benzodiazepines have been investigated for efficacy against GAD: alprazolam (e71, e73–e76), diazepam (e69, e72, e73, e77–e84), lorazepam (e67, e68), and bromazepam (e85).

The anxiolytic effect appears as soon as treatment is begun. Benzodiazepines are considered safe, but they have a tranquilizing effect on the central nervous system, potentially causing sedation, dizziness, prolonged reaction times, and other problems. After prolonged treatment (i.e., four to eight months), as many as 40% of patients become dependent on the drug, especially if they are predisposed to dependency (16, 17); low-dose dependency is the usual type.

Tolerance, expressing itself in the need for a steadily increasing dose, is rare (18). Generally speaking, benzodiazepines should only be used in the acute phase of treatment (i.e., for four to eight weeks). They are usually given at the start of antidepressant treat- ment to tide the patient over until the antidepressant effect sets in. Their long-term use may be indicated in rare individual cases if other drugs are ineffective or poorly tolerated. Patients with a history of substance abuse should be excluded. It should also be borne in mind that benzodiazepines have little or no effect on the depressive symptoms that often accompany GAD.

Other drugs The 5-HT1A agonist buspirone has been found to be effective in a number of trials (e59, 74, e82–e84, e86–e88), but it was less effective than venlafaxine in one study (e59). In one trial, it was no better than placebo (e89).

A few controlled trials have demonstrated the ef - ficacy of hydroxyzine, an antihistamine drug (e85, e89–e91), but no recurrence-prevention trials have been conducted over a time span of six to twelve months. Hydroxyzine has not become established in the routine treatment of generalized anxiety disorder.

Opipramol, an anxiolytic drug chemically resem - bling the tricyclic antidepressants, was found to be more effective than placebo and just as effective as alprazolam in a three-armed trial (e76). No long-term trials have been reported.

Quetiapine, an atypical antipsychotic drug origi - nally developed for the treatment of schizophrenia, is also effective against GAD at a dose much lower than the usual anti-schizophrenic dose (e43, e92–e96). This drug, however, has not been approved for the treatment of GAD and can only be considered for use in patients for whom standard treatments have been ineffective or poorly tolerated. When giving this drug, physicians should be aware of its potential adverse effects, including the metabolic syndrome.

Agomelatin, a new antidepressant, is a melatonin agonist and 5-HT2C antagonist. It was more effective than placebo against GAD in one trial (e97), and a recurrence-prevention trial likewise showed its super - iority to placebo (e98). This drug has not yet been approved for the treatment of GAD. It can elevate the values of liver function tests; such tests are recommended before and during treatment with agomelatin.

Benzodiazepines Benzodiazepines are usually given at the start of antidepressant treatment to tide the patient over until the antidepressant effect sets in.

Homeopathic preparations Only one controlled trial of a homeopathic preparation has been carried out to date. The preparation was no more effective than placebo.

306 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10

M E D I C I N E

Herbal and homeopathic preparations In a single trial without placebo control, a standard- ized lavender-oil extract was found to be as effective as lorazepam (e99); this trial, however, had only 77 subjects and was inadequately powered for non- inferiority testing. Moreover, lorazepam was only given once daily (instead of three times), even though its half-life is relatively short; this may well have les- sened the benefit of treatment in the lorazepam arm of the trial. The placebo-controlled trials performed to date in persons with “sub-syndromic” anxiety dis- orders do, however, indicate a possible effect of lavender-oil extract (e100, e101) that would merit further study in trials comparing it to standard medications.

Only one controlled trial of a homeopathic prepara- tion has been carried out to date. The preparation was no more effective than placebo (e102).

Long-term and recurrence-prevention trials Generalized anxiety disorder often persists, needing long-term treatment. Recurrence-prevention trials over time spans of six to twelve months have shown SSRIs (escitalopram, paroxetine), SNRIs (venla - faxine, duloxetine), and pregabalin to be more effec- tive than placebo for long-term recurrence prevention. A meta-analysis on the treatment of GAD with anti - depressants showed robust treatment effects. These findings imply that the treatment should be continued for six to twelve months after the onset of improvement.

Before the treatment is entirely discontinued, the dose of the drug should be lowered slowly, in steps. Benzodiazepines are not recommended for long-term treatment except when other drugs or CBT have been ineffective.

In the trials of behavioral therapy, treatment was provided for a total of 8 to 28 hours; no trials have addressed the question whether longer treatment works any better than, or more durably than, shorter treatment. Experience suggests that severely affected patients may need to be treated for longer times.

Intractability For patients who do not respond to standard drug treatment, further treatment is recommended as sum- marized in Box 4.

The treatment of elderly patients Only a few trials have specifically dealt with patients over age 65. The efficacy of pregabalin and quetia-

pine in elderly patients with GAD was demonstrated in placebo-controlled trials (e103). In one trial, escita- lopram had a higher response rate than placebo (e41). An analysis of the elderly patients in four GAD trials led to the conclusion that duloxetine is effective (e104); an analysis of the elderly patients in five trials revealed that venlafaxine was more effective than placebo with respect to CGI (Clinical Global Impres- sion) score, but not in all primary measures of effec- tiveness (e105). In summary, pregabalin or duloxetine can be recommended for the treatment of elderly pa- tients. In intractable cases, quetiapine can be given off-label.

CBT has also been shown to be effective in elderly patients, albeit with a lesser treatment effect than in patients under age 65 (e18, e106–e109).

Comparison of psychotherapy with drug treatment Hardly any comparative data are available regarding psychotherapy versus pharmacotherapy for GAD. Two small trials (both of which had methodological problems) revealed no difference between the two, although the combination of CBT and diazepam was found to be more effective than diazepam alone (e13, e23). This finding cannot be applied to combinations of psychotherapy with the currently recommended drugs. As both forms of treatment are known to be effective and have comparable effect strengths, it seems that combining them is recommendable. The decision whether to treat a particular patient with psychotherapy, drugs, or both should be based both on considerations of efficacy and on the following important factors: the patient’s preference, the ad- verse effects of medication, the latency of effect, the severity of the patient’s condition, comorbidities, if any, cost, time, the availability of psychotherapy, and the qualifications of the therapist. In practice, drug treatment is often begun at once, while patients may have to wait several months to begin psychotherapy even in places with relatively high availability (20). If the patient is suffering from GAD in combination with comorbid depression, antidepressant medi- cation should not be omitted (21).

Acknowledgement We thank Prof. Hans-Peter Volz, Werneck, for reading the manuscript critically and giving us valuable advice.

Treating elderly patients with GAD Elderly patients with GAD can be treated with pregabalin or duloxetine.

Combination therapy As psychotherapy and drug treatment are both effective, a combination of the two can be recommended.

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10 307

M E D I C I N E

Conflict of interest statement Prof. Dr. Bandelow has received consultant’s fees from Lilly, Lundbeck, Ono, Otsuka, and Pfizer. He has received reimbursement of conference participation fees from Servier and Pfizer. He has received honoraria for lecturing at continuing medical education events from AstraZeneca, Boehringer-Ingelheim, Glaxo, Janssen, Lilly, Lundbeck, Pfizer, Servier, and Wyeth.

Dr. Boerner has received reimbursement of travel and accommodation costs and payment for preparing continuing medical education events from Pfizer. He has received consultant’s fees from Pfizer.

Prof. Kasper has received research support and lecture honoraria from, and has served on advisory boards or as a consultant for, AstraZeneca, CSC, Eli Lilly, Alkmers, Lilly, Lundbeck, Merck Sharp & Dohme (MSD), Neuraxpharm, Bristol Myers Squibb, GlaxoSmithKline, Pfizer, Organon, Janssen, Novartis, Pierre Fabre, Schwabe, Sepracor, Servier, and Wyeth.

Prof. Linden has received consultant’s fees and lecture honoraria from Pfizer, Lilly, Servier, and Janssen-Cilag. He has received payment from Servier for preparing scientific articles.

Prof. Wittchen has received reimbursement of conference participation fees and travel and accommodation costs from Pfizer. He has received payment for preparing continuing medical education events from Pfizer.

Prof. Möller has received consultant’s fees and payment for preparing continuing medical education events from Pfizer.

Manuscript submitted on 19 October 2012, revised version accepted on 13 March 2012.

Translated from the original German by Ethan Taub, M.D.

REFERENCES 1. Wittchen HU, Kessler RC, Beesdo K, Krause P, Hofler M, Hoyer J:

Generalized anxiety and depression in primary care: prevalence, recognition, and management. J Clin Psychiatry 2002; 63 (Suppl 8): 24–34.

2. Wittchen HU, Jacobi F: Size and burden of mental disorders in Eu- rope—a critical review and appraisal of 27 studies. Eur Neuro - psychopharmacol 2005; 15: 357–76.

3. Wittchen HU, Jacobi F, Rehm J: The size and burden of mental disorders and other disorders of the brain in Europe 2010. Eur Neuropsychopharmacol 2011; 21: 655–79.

4. Maier W, Linden M, Sartorius N: Psychische Erkrankungen in der Allgemeinpraxis. Ergebnisse und Schlußfolgerungen einer WHO- Studie. Dtsch Arztebl 1996; 93(18): 1202–1206.

5. Kessler RC, Berglund P, Demler O, Jin R, Merikangas KR, Walters EE: Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 2005; 62: 593–602.

6. Tyrer P, Seivewright H, Johnson T: The Nottingham Study of Neurotic Disorder: predictors of 12-year outcome of dysthymic, panic and generalized anxiety disorder. Psychol Med 2004; 34: 1385–94.

7. Kessler RC, Frank RG, Edlund M, Katz SJ, Lin E, Leaf P: Differences in the use of psychiatric outpatient services between the United States and Ontario. N Engl J Med 1997; 336: 551–7.

8. Bandelow B, Broocks A: generalized anxiety disorderen – Hypo- thesen zur Ätiologie. In: Bandelow B (ed.): Angst- und Panikerkran- kungen, 2nd edition. Bremen: UNI-MED, 2006: 105–108.

9. Noyes R Jr., Clarkson C, Crowe RR, Yates WR, McChesney CM: A family study of generalized anxiety disorder. Am J Psychiatry 1987; 144: 1019–24.

10. Hettema JM, Prescott CA, Kendler KS: A population-based twin study of generalized anxiety disorder in men and women. J Nerv Ment Dis 2001;189:413–20.cal basis of generalized anxiety dis- order.

11. Abelson JL, Glitz D, Cameron OG, Lee MA, Bronzo M, Curtis GC: Blunted growth hormone response to clonidine in patients with generalized anxiety disorder. Arch Gen Psychiatry 1991; 48: 157–62.

12. Tiihonen J, Kuikka J, Rasanen P, Lepola U, et al.: Cerebral benzo- diazepine receptor binding and distribution in generalized anxiety disorder: a fractal analysis. Mol Psychiatry 1997; 2: 463–71.

13. Bandelow B, Zohar J, Hollander E, Kasper S, et al.: World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the pharmacological treatment of anxiety, obsessive-compulsive and post-traumatic stress disorders – first revision. World J Biol Psychiatry 2008; 9: 248–312.

14. Lader M: Dependence and withdrawal: comparison of the benzo- diazepines and selective serotonin re-uptake inhibitors. Addiction 2012; 107: 909–10.

15. Schweizer E, Rickels K, De Martinis N, Case G, Garcia-Espana F: The effect of personality on withdrawal severity and taper outcome in benzodiazepine dependent patients. Psychol Med 1998; 28: 713–20.

16. Kan CC, Breteler MH, Zitman FG: High prevalence of benzodiaze - pine dependence in out-patient users, based on the DSM-III-R and ICD-10 criteria. Acta Psychiatr Scand 1997; 96: 85–93.

17. Rickels K: Benzodiazepines in the treatment of anxiety. Am J Psychother 1982; 36: 358–70.

18. Donovan MR, Glue P, Kolluri S, Emir B: Comparative efficacy of antidepressants in preventing relapse in anxiety disorders—a meta-analysis. J Affect Disord 2010; 123: 9–16.

19. Walendzik A, Lux G, Wasem J, Jahn R: Studie des Lehrstuhls für Medizinmanagement an der Universität Duisburg-Essen im Auftrag der Deutschen Psychotherapeuten-Vereinigung 2011.

20. Ballenger JC, Davidson JRT, Lecrubier Y, Nutt DJ, et al.: Consensus statement on generalized anxiety disorder from the international consensus group on depression and anxiety. Journal of Clinical Psychiatry 2001; 62(Suppl 11): 53–58.

21. DIMDI. ICD-10-GM 2009 – Systematisches Verzeichnis: Inter- nationale statistische Klassifikation der Krankheiten und verwandter Gesundheitsprobleme – 10. Revision – German Modification. Deut- sches Institut für Medizinische Dokumentation und Information (DIMIDI). In: Graubner B (eds.). Köln: Deutscher Ärzte-Verlag, 2008

22. Sartorius N, Üstün TB, Costa e Silva JA, Goldberg D, et al.: An inter- national study of psychological problems in primary care. Prelimi- nary report from the World Health Organization Collaborative Project on ’Psychological Problems in General Health Care’. Arch Gen Psychiatry 1993; 50: 819–24.

23. Wittchen HU, Kessler RC, Beesdo K, Krause P, Hofler M, Hoyer J: Generalized anxiety and depression in primary care: prevalence, recognition, and management. J Clin Psychiatry 2002; 63 (Suppl 8): 24–34.

308 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10

M E D I C I N E

24. Sartorius N, Ustun TB, Lecrubier Y, Wittchen HU: Depression co - morbid with anxiety: results from the WHO study on psychological disorders in primary health care. Br J Psychiatry Suppl 1996; 30: 38–43.

25. Bandelow B, Rudolf S, Reitt M, Wedekind D: Psychotherapie der Angsterkrankungen. In: Herpertz S, Schnell. K, Falkai P (eds.): Psychotherapie in der Psychiatrie. Stuttgart: Kohlhammer 2013.

26. Linden M: Generalisierte Angsterkrankungen. In: Batra A, Wass- mann R, Buchkremer G, (eds.): Verhaltenstherapie. Grundlagen, Methoden, Anwendungsgebiete. Stuttgart: Thieme Verlag, 2012.

27. Baldwin DS, Stein DJ, Dolberg OT, Bandelow B: How long should a trial of escitalopram treatment be in patients with major depressive disorder, generalised anxiety disorder or social anxiety disorder? An exploration of the randomised controlled trial database. Hum Psychopharmacol 2009; 24: 269–75.

Corresponding author Prof. Dr. med. Borwin Bandelow, Dipl.-Psych. Klinik für Psychiatrie und Psychotherapie der Universität Göttingen von-Siebold-Str. 5, 37075 Göttingen, Germany [email protected]

@ For eReferences please refer to: www.aerzteblatt-international.de/ref1713 eBox: www.aerzteblatt-international.de/13m300

Further information on CME

This article has been certified by the North Rhine Academy for Postgraduate and Continuing Medical Education. Deutsches Ärzteblatt provides certified continuing medical education (CME) in accordance with the requirements of the Medical Associations of the German federal states (Länder). CME points of the Medical Associations can be acquired only through the Internet, not by mail or fax, by the use of the German version of the CME questionnaire within 6 weeks of publication of the article. See the following website: cme.aerzteblatt.de Participants in the CME program can manage their CME points with their 15-digit “uniform CME number” (einheitliche Fortbildungsnummer, EFN). The EFN must be entered in the appropriate field in the cme.aerzteblatt.de website under “meine Daten” (“my data”), or upon registration. The EFN appears on each participant’s CME certificate. The CME unit “Specific immunotherapy—indications and mode of action“ (issue 9/2013) can be accessed until 2 June 2013. The CME unit “The prevention, diagnosis and treatment of premature labor” (issue 13/2013) can be accessed until 30 June 2013. For issue 21/2013, we plan to offer the topic “The diagnosis and treatment of giant cell arteritis”

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10 309

M E D I C I N E

Please answer the following questions to participate in our certified Continuing Medical Education program. Only one answer is possible per question. Please select the answer that is most appropriate.

Question 1 Which of the following manifestations are included in the definition of generalized anxiety disorder? a) Episodes of intense fear without any evident reason b) Fear of crowds c) Vegetative symptoms such as palpitations, diaphoresis, or

tremor d) Muscle tension e) Restless legs syndrome

Question 2 What are “meta-worries”? a) The coexistence of multiple anxiety disorders b) Long-term fears of losing one’s economic footing c) Worries about one’s own health, rather than that of loved

ones d) Fears that one may become ill from constant worrying e) The comorbidity of anxiety disorder and depression

Question 3 A 36-year-old dental hygienist is seen in a hospital emergency room. She has the following symptoms and signs: palpi- tations, shortness of breath, a feeling of tightness in the chest and neck, abdominal discomfort, trembling, diaphore- sis, dizziness, feeling faint, tingling paresthesias, and fear of dying. The general medical and neurological examination is normal, as are all relevant laboratory findings. What is the most likely diagnosis? a) Angina pectoris b) Pheochromocytoma c) Somatization disorder d) Generalized anxiety disorder e) Panic disorder

Question 4 Which of the following is a drug of first choice for the treatment of generalized anxiety disorder? a) Hydroxyzine b) Pregabalin c) Imipramine d) Opipramol e) Buspirone

Question 5 What is the typical latency of the anxiolytic effect of SNRIs? a) 1–2 weeks b) 2–4 weeks c) 2–6 weeks d) 6–8 weeks e) 8–10 weeks

Question 6 What is the most common adverse effect of pregabalin? a) Nausea b) Agitation c) Sexual dysfunction d) Somnolence e) Insomnia

Question 7 Which of the following types of psychotherapy has been best docu- mented as an effective treatment for generalized anxiety disorder? a) Long-term psychoanalysis b) Interpersonal therapy c) Catathymic imagery experience d) Client-centered talk therapy e) Cognitive behavioral therapy

Question 8 What is the response rate of generalized anxiety disorder to drug treatment in published trials? a) 11%–19% b) 22%–33% c) 44%–81% d) 85%–95% e) 100%

Question 9 A 42-year-old woman working as a caregiver for elderly patients complains of the following symptoms: racing heartbeat, irregular pulse, shortness of breath, headache, arthralgia, abdominal pain, diarrhea alternating with constipation, esophageal reflux, nausea, bloating, itching, burning, urinary frequency, muscle weakness, dysphagia, and sensory disturbances. Her symptoms frequently vary. Organic causes have been excluded. The patient cannot accept the judgment of numerous physicians that her symptoms have no bodily cause. She demands further medical evaluation and treatment. What is the most likely diagnosis? a) Anxiety combined with depression b) Hyperthyroidism c) Panic disorder d) Generalized anxiety disorder e) Somatoform disorder

Question 10 Which of the following is a typical technique in the treatment of generalized anxiety disorder with cognitive behavioral therapy? a) Practicing safety behavior b) Family constellation c) In sensu exposure to feared catastrophes d) Ignoring the bodily expressions of fear (natural fight-or-flight response) e) Resource deconstruction (“Is there anything I ought to worry more

about?”)

310 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17): 300−10

M E D I C I N E

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17) | Bandelow et al.: eReferences I

M E D I C I N E

C O N T I N U I N G M E D I C A L E D U C A T I O N

The Diagnosis and Treatment of Generalized Anxiety Disorder Borwin Bandelow, Reinhard J. Boerner, Siegfried Kasper, Michael Linden, Hans-Ulrich Wittchen, Hans-Jürgen Möller

e17. Dugas MJ, Ladouceur R, Leger E, Freeston MH, et al.: Group cognitive-behavioral therapy for generalized anxiety disorder: treatment outcome and long-term follow-up. J Consult Clin Psychol 2003; 71: 821–5.

e18. Mohlman J, Gorenstein EE, Kleber M, de Jesus M, Gorman JM, Papp LA: Standard and enhanced cognitive-behavior therapy for late-life generalized anxiety disorder: two pilot investigations. Am J Geriatr Psychiatry 2003; 11: 24–32.

e19. Dugas MJ, Brillon P, Savard P, Turcotte J, et al.: A randomized clinical trial of cognitive-behavioral therapy and applied relaxation for adults with generalized anxiety disorder. Behav Ther 2010; 41: 46–58.

e20. Borkovec TD, Mathews AM, Chambers A, Ebrahimi S, Lytle R, Nelson R: The effects of relaxation training with cognitive or non- directive therapy and the role of relaxation-induced anxiety in the treatment of generalized anxiety. J Consult Clin Psychol 1987; 55: 883–8.

e21. Borkovec TD, Costello E: Efficacy of applied relaxation and cog - nitive-behavioral therapy in the treatment of generalized anxiety disorder. J Consult Clin Psychol 1993; 61: 611–9.

e22. Linden M, Zubraegel D, Baer T, Franke U, Schlattmann P: Efficacy of cognitive behaviour therapy in generalized anxiety disorders. Results of a controlled clinical trial (Berlin CBT-GAD Study). Psychother Psychosom 2005; 74: 36–42.

e23. Power KG, Simpson RJ, Swanson V, Wallace LA: Controlled com- parison of pharmacological and psychological treatment of gen- eralized anxiety disorder in primary care. Br J Gen Pract 1990; 40: 289–94.

e24. Titov N, Andrews G, Robinson E, Schwencke G, et al.: Clinician- assisted Internet-based treatment is effective for generalized anxiety disorder: randomized controlled trial. Australian and New Zealand Journal of Psychiatry 2009; 43: 905–12.

e25. Robinson E, Titov N, Andrews G, McIntyre K, Schwencke G, Solley K: Internet treatment for generalized anxiety disorder: a random - ized controlled trial comparing clinician vs. technician assistance. PLoS One 2010; 5: e10942.

e26. Paxling B, Almlov J, Dahlin M, Carlbring P, et al.: Guided internet-de- livered cognitive behavior therapy for generalized anxiety disorder: a randomized controlled trial. Cogn Behav Ther 2011; 40: 159–73.

e27. Andersson G, Paxling B, Roch-Norlund P, Ostman G, et al.: Inter- net-based psychodynamic versus cognitive behavioral guided self-help for generalized anxiety disorder: a randomized con - trolled trial. Psychother Psychosom 2012; 81: 344–55.

e28. Luborsky L: Principles of Psychoanalytic Psychotherapy: A Manual for Supportive-Expressive (SE) Treatment New York: Basic Books, 1984.

e29. Crits-Christoph P, Wolf-Palacio D, Ficher M, Rudick D: Brief sup- portive-expressive psychodynamic therapy for generalized anxiety disorder. In: Barber JP, Crits-Christoph P, (eds.): Dynamic Therapies for Psychiatric Disorders. New York: Basic Books, 1995: 43–83.

e30. Leichsenring F, Leibing E: Supportive-Expressive (SE) Psycho - therapy: An Update. Current Psychiatry Reviews 2007; 3: 57–64.

eREFERENCES

e1. Brown TA, Marten PA, Barlow DH: Discriminant validity of the symptoms constituting the DSM-Iii-R and DSM-IV associated symptom criterion of generalized anxiety disorder. J Anxiety Disord 1995; 9: 317–28.

e2. Kessler RC, DuPont RL, Berglund P, Wittchen HU: Impairment in pure and comorbid generalized anxiety disorder and major de- pression at 12 months in two national surveys. Am J Psychiatry 1999; 156: 1915–23.

e3. Monk CS, Telzer EH, Mogg K, Bradley BP, et al.: Amygdala and ventrolateral prefrontal cortex activation to masked angry faces in children and adolescents with generalized anxiety disorder. Arch Gen Psychiatry 2008; 65: 568–76.

e4. Blair K, Shaywitz J, Smith BW, et al.: Response to emotional ex- pressions in generalized social phobia and generalized anxiety disorder: evidence for separate disorders. Am J Psychiatry 2008; 165: 1193–202.

e5. Nitschke JB, Sarinopoulos I, Oathes DJ, et al.: Anticipatory activation in the amygdala and anterior cingulate in generalized anxiety disorder and prediction of treatment response. Am J Psychiatry 2009; 166: 302–10.

e6. Schienle A, Ebner F, Schafer A: Localized gray matter volume abnormalities in generalized anxiety disorder. Eur Arch Psychiatry Clin Neurosci 2011; 261: 303–7.

e7. Beck J: Praxis der Kognitiven Therapie. Weinheim: PVU 1999.

e8. Becker ES, Hoyer J: Generalisierte Angststörung. Göttingen: Hogrefe 2005.

e9. Wells A: Metacognitive therapy for anxiety and depression. Guildford 2009.

e10. Bandelow B, Rudolf S, Reitt M, Wedekind D: Angststörungen. In: Herpertz S, Schnell K, Falkai P (eds.): Psychotherapie in der Psy- chiatrie. Stuttgart: Kohlhammer 2013.

e11. Becker ES, Margraf J: Generalisierte Angststörung. Ein Therapie- programm. Weinheim: Beltz 2002.

e12. Hoyer J, Beesdo K, Gloster AT, Runge J, Hofler M, Becker ES: Worry exposure versus applied relaxation in the treatment of generalized anxiety disorder. Psychother Psychosom 2009; 78: 106–15.

e13. Lindsay WR, Gamsu CV, McLaughlin E, Hood EM, Espie CA: A controlled trial of treatments for generalized anxiety. Br J Clin Psychol 1987; 26: 3–15.

e14. Butler G, Fennell M, Robson P, Gelder M: Comparison of behavior therapy and cognitive behavior therapy in the treatment of gen- eralized anxiety disorder. J Consult Clin Psychol 1991; 59: 167–75.

e15. Barlow DH, Rapee RM, Brown TA: Behavioral Treatment of Gen- eralized Anxiety Disorder. Behavior Therapy 1992; 23: 551–70.

e16. Ladouceur R, Dugas MJ, Freeston MH, Leger E, Gagnon F, Thibo- deau N: Efficacy of a cognitive-behavioral treatment for genera - lized anxiety disorder: evaluation in a controlled clinical trial. J Consult Clin Psychol 2000; 68: 957–64.

II Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17) | Bandelow et al.: eReferences

M E D I C I N E

e31. Durham RC, Murphy T, Allan T, Richard K, Treliving LR, Fenton GW: Cognitive therapy, analytic psychotherapy and anxiety management training for generalised anxiety disorder. Br J Psychiatry 1994; 165: 315–23.

e32. Durham RC, Fisher PL, Treliving LR, Hau CM, Richard K, Steward JB: Psychotherapy and anxiety management training for general - ized anxiety disorder: Symptom change, medication usage and attitudes to treatment. Behavioural and Cognitive Psychotherapy 1999; 27: 19–35.

e33. Leichsenring F, Salzer S, Jaeger U, Kachele H, et al.: Short-term psychodynamic psychotherapy and cognitive-behavioral therapy in generalized anxiety disorder: a randomized, controlled trial. Am J Psychiatry 2009; 166: 875–81.

e34. Salzer S, Winkelbach C, Leweke F, Leibing E, Leichsenring F: Long-term effects of short-term psychodynamic psychotherapy and cognitive-behavioural therapy in generalized anxiety disorder: 12-month follow-up. Can J Psychiatry 2011; 56: 503–8.

e35. Allgulander C, Hackett D, Salinas E: Venlafaxine extended release (ER) in the treatment of generalised anxiety disorder: Twenty-four- week placebo-controlled dose-ranging study. Br J Psychiatry 2001; 179: 15–22.

e36. Kasper S, Herman B, Nivoli G, van Ameringen M, et al.: Efficacy of pregabalin and venlafaxine-XR in generalized anxiety disorder: results of a double-blind, placebo-controlled 8-week trial. Int Clin Psychopharmacol 2009; 24: 87–96.

e37. Serretti A, Chiesa A: Treatment-emergent sexual dysfunction re- lated to antidepressants: a meta-analysis. J Clin Psychopharma- col 2009; 29: 259–66.

e38. Hasnain M, W Victor RV, Hollett B: Weight gain and glucose dys- regulation with second-generation antipsychotics and antidepres- sants: a review for primary care physicians. Postgrad Med 2012; 124: 154–67.

e39. Davidson JR, Bose A, Korotzer A, Zheng H: Escitalopram in the treatment of generalized anxiety disorder: double-blind, placebo controlled, flexible-dose study. Depress Anxiety 2004; 19: 234–40.

e40. Goodman WK, Bose A, Wang Q: Treatment of generalized anxiety disorder with escitalopram: pooled results from double-blind, placebo-controlled trials. J Affect Disord 2005; 87: 161–7.

e41. Lenze EJ, Rollman BL, Shear MK, Dew MA, et al.: Escitalopram for older adults with generalized anxiety disorder: a randomized controlled trial. JAMA 2009; 301: 295–303.

e42. Baldwin DS, Huusom AK, Maehlum E: Escitalopram and paroxe - tine in the treatment of generalised anxiety disorder: randomized, placebo-controlled, double-blind study. Br J Psychiatry 2006; 189: 264–72.

e43. Merideth C, Cutler AJ, She F, Eriksson H: Efficacy and tolerability of extended release quetiapine fumarate monotherapy in the acute treatment of generalized anxiety disorder: a randomized, placebo controlled and active-controlled study. Int Clin Psycho- pharmacol 2012; 27: 40–54.

e44. Bose A, Korotzer A, Gommoll C, Li D: Randomized placebo-con- trolled trial of escitalopram and venlafaxine XR in the treatment of generalized anxiety disorder. Depress Anxiety 2007.

e45. Allgulander C, Florea I, Huusom AK: Prevention of relapse in gen - eralized anxiety disorder by escitalopram treatment. Int J Neuro - psychopharmacol 2006; 9: 495–505.

e46. Pollack MH, Zaninelli R, Goddard A, et al.: Paroxetine in the treat- ment of generalized anxiety disorder: results of a placebo-con- trolled, flexible-dosage trial. J Clin Psychiatry 2001; 62: 350–7.

e47. Rickels K, Zaninelli R, McCafferty J, Bellew K, Iyengar M, Sheehan D: Paroxetine treatment of generalized anxiety disorder: a double-blind, placebo-controlled study. Am J Psychiatry 2003; 160: 749–56.

e48. Stocchi F, Nordera G, Jokinen RH, Lepola UM, et al.: Efficacy and tolerability of paroxetine for the long-term treatment of genera - lized anxiety disorder. J Clin Psychiatry 2003; 64: 250–8.

e49. Bielski RJ, Bose A, Chang CC: A double-blind comparison of escitalopram and paroxetine in the long-term treatment of genera lized anxiety disorder. Ann Clin Psychiatry 2005; 17: 65–9.

e50. Allgulander C, Dahl AA, Austin C, Morris PL, et al.: Efficacy of sertraline in a 12-week trial for generalized anxiety disorder. Am J Psychiatry 2004; 161: 1642–9.

e51. Brawman-Mintzer O, Knapp RG, Rynn M, Carter RE, Rickels K: Sertraline treatment for generalized anxiety disorder: a random - ized, double-blind, placebo-controlled study. J Clin Psychiatry 2006; 67: 874–81.

e52. Ball SG, Kuhn A, Wall D, Shekhar A, Goddard AW: Selective serotonin reuptake inhibitor treatment for generalized anxiety disorder: a double-blind, prospective comparison between paroxetine and sertraline. J Clin Psychiatry 2005; 66: 94–9.

e53. Rickels K, Pollack MH, Sheehan DV, Haskins JT: Efficacy of ex- tended-release venlafaxine in nondepressed outpatients with generalized anxiety disorder. Am J Psychiatry 2000; 157: 968–74.

e54. Nimatoudis I, Zissis NP, Kogeorgos J, Theodoropoulou S, Vidalis A, Kaprinis G: Remission rates with venlafaxine extended release in Greek outpatients with generalized anxiety disorder. A double- blind, randomized, placebo controlled study. Int Clin Psycho - pharmacol 2004; 19: 331–6.

e55. Lenox-Smith AJ, Reynolds A: A double-blind, randomised, place- bo controlled study of venlafaxine XL in patients with generalised anxiety disorder in primary care. Br J Gen Pract 2003; 53: 772–7.

e56. Hartford J, Kornstein S, Liebowitz M, Pigott T, et al.: Duloxetine as an SNRI treatment for generalized anxiety disorder: results from a placebo and active-controlled trial. Int Clin Psychopharmacol 2007; 22: 167–74.

e57. Nicolini H, Bakish D, Duenas H, Spann M, et al.: Improvement of psychic and somatic symptoms in adult patients with generalized anxiety disorder: examination from a duloxetine, venlafaxine extended-release and placebo-controlled trial. Psychol Med 2009; 39: 267–76.

e58. Montgomery SA, Tobias K, Zornberg GL, Kasper S, Pande AC: Efficacy and safety of pregabalin in the treatment of generalized anxiety disorder: a 6-week, multicenter, randomized, double- blind, placebo-controlled comparison of pregabalin and venlafax - ine. J Clin Psychiatry 2006; 67: 771–82.

e59. Davidson JR, DuPont RL, Hedges D, Haskins JT: Efficacy, safety, and tolerability of venlafaxine extended release and buspirone in outpatients with generalized anxiety disorder. J Clin Psychiatry 1999; 60: 528–35.

e60. Gelenberg AJ, Lydiard RB, Rudolph RL, Aguiar L, Haskins JT, Salinas E: Efficacy of venlafaxine extended-release capsules in nondepressed outpatients with generalized anxiety disorder: A 6-month randomized controlled trial. JAMA 2000; 283: 3082–8.

e61. Hackett D, Haudiquet V, Salinas E: A method for controlling for a high placebo response rate in a comparison of venlafaxine XR and diazepam in the short-term treatment of patients with gen - eralised anxiety disorder. Eur Psychiatry 2003; 18: 182–7.

e62. Koponen H, Allgulander C, Erickson J, Dunayevich E, et al.: Efficacy of Duloxetine for the Treatment of Generalized Anxiety Disorder: Implications for Primary Care Physicians. Prim Care Companion J Clin Psychiatry 2007; 9: 100–7.

e63. Rynn M, Russell J, Erickson J, Detke MJ, et al.: Efficacy and safety of duloxetine in the treatment of generalized anxiety disorder: a flexible-dose, progressive-titration, placebo-controlled trial. Depress Anxiety 2008; 25: 182–9.

e64. Allgulander C, Nutt D, Detke M, Erickson J, et al.: A non-inferiority comparison of duloxetine and venlafaxine in the treatment of adult patients with generalized anxiety disorder. J Psychopharma- col 2008; 22: 417–25.

e65. Davidson JR, Wittchen HU, Llorca PM, Erickson J, et al.: Duloxe - tine treatment for relapse prevention in adults with generalized anxiety disorder: a double-blind placebo-controlled trial. Eur Neuropsychopharmacol 2008; 18: 673–81.

e66. Pohl RB, Feltner DE, Fieve RR, Pande AC: Efficacy of pregabalin in the treatment of generalized anxiety disorder: double-blind, placebo-controlled comparison of BID versus TID dosing. J Clin Psychopharmacol 2005; 25: 151–8.

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17) | Bandelow et al.: eReferences III

M E D I C I N E

e67. Pande AC, Crockatt JG, Feltner DE, Janney CA, et al.: Pregabalin in generalized anxiety disorder: a placebo-controlled trial. Am J Psychiatry 2003; 160: 533–40.

e68. Feltner DE, Crockatt JG, Dubovsky SJ, Cohn CK, et al.: A ran - domized, double-blind, placebo-controlled, fixed-dose, multi- center study of pregabalin in patients with generalized anxiety dis order. J Clin Psychopharmacol 2003; 23: 240–9.

e69. Rickels K, Pollack MH, Feltner DE, Lydiard RB, et al.: Pregabalin for treatment of generalized anxiety disorder: a 4-week, multi- center, double-blind, placebo-controlled trial of pregabalin and alprazolam. Arch Gen Psychiatry 2005; 62: 1022–30.

e70. Feltner D, Wittchen HU, Kavoussi R, Brock J, Baldinetti F, Pande AC: Long-term efficacy of pregabalin in generalized anxiety dis- order. Int Clin Psychopharmacol 2008; 23: 18–28.

e71. Hoehn-Saric R, McLeod DR, Zimmerli WD: Differential effects of alprazolam and imipramine in generalized anxiety disorder: somatic versus psychic symptoms. J Clin Psychiatry 1988; 49: 293–301.

e72. Rickels K, Downing R, Schweizer E, Hassman H: Antidepressants for the treatment of generalized anxiety disorder. A placebo-con- trolled comparison of imipramine, trazodone, and diazepam. Arch Gen Psychiatry 1993; 50: 884–95.

e73. Elie R, Lamontagne Y: Alprazolam and diazepam in the treatment of generalized anxiety. J Clin Psychopharmacol 1984; 4: 125–9.

e74. Enkelmann R: Alprazolam versus buspirone in the treatment of outpatients with generalized anxiety disorder. Psychopharma - cology 1991; 105: 428–32.

e75. Lydiard RB, Ballenger JC, Rickels K: A double-blind evaluation of the safety and efficacy of abecarnil, alprazolam, and placebo in outpatients with generalized anxiety disorder. Abecarnil Work Group. J Clin Psychiatry 1997; 58 Suppl 11: 11–8.

e76. Möller HJ, Volz HP, Reimann IW, Stoll KD: Opipramol for the treat- ment of generalized anxiety disorder: a placebo-controlled trial including an alprazolam-treated group. J Clin Psychopharmacol 2001; 21: 59–65.

e77. Fontaine R, Annable L, Chouinard G, Ogilvie RI: Bromazepam and diazepam in generalized anxiety: a placebo-controlled study with measurement of drug plasma concentrations. J Clin Psycho - pharmacol 1983; 3: 80–7.

e78. Ansseau M, Olie JP, von Frenckell R, Jourdain G, Stehle B, Guillet P: Controlled comparison of the efficacy and safety of four doses of suriclone, diazepam, and placebo in generalized anxiety disorder. Psychopharmacology (Berl) 1991; 104: 439–43.

e79. Rickels K, Schweizer E, DeMartinis N, Mandos L, Mercer C: Gepirone and diazepam in generalized anxiety disorder: a place- bo-controlled trial. J Clin Psychopharmacol 1997; 17: 272–7.

e80. Boyer WF, Feighner JP: A placebo-controlled double-blind multi- center trial of two doses of ipsapirone versus diazepam in gen - eralized anxiety disorder. Int Clin Psychopharmacol 1993; 8: 173–6.

e81. Rickels K, DeMartinis N, Aufdembrinke B: A double-blind, place- bo-controlled trial of abecarnil and diazepam in the treatment of patients with generalized anxiety disorder. J Clin Psychopharma- col 2000; 20: 12–8.

e82. Feighner JP, Merideth CH, Hendrickson GA: A double-blind comparison of buspirone and diazepam in outpatients with genera lized anxiety disorder. J Clin Psychiatry 1982; 43: 103–8.

e83. Jacobson AF, Dominguez RA, Goldstein BJ, Steinbook RM: Comparison of buspirone and diazepam in generalized anxiety disorder. Pharmacotherapy 1985; 5: 290–6.

e84. Ross CA, Matas M: A clinical trial of buspirone and diazepam in the treatment of generalized anxiety disorder. Can J Psychiatry 1987; 32: 351–5.

e85. Llorca PM, Spadone C, Sol O, Danniau A, et al.: Efficacy and safety of hydroxyzine in the treatment of generalized anxiety dis- order: a 3-month double-blind study. J Clin Psychiatry 2002; 63: 1020–7.

e86. Pollack MH, Worthington JJ, Manfro GG, Otto MW, Zucker BG: Abecarnil for the treatment of generalized anxiety disorder: a placebo-controlled comparison of two dosage ranges of abecarnil and buspirone. J Clin Psychiatry 1997; 58 Suppl 11: 19–23.

e87. Rickels K, Weisman K, Norstad N, Singer M, et al.: Buspirone and diazepam in anxiety: a controlled study. J Clin Psychiatry 1982; 43: 81–6.

e88. Strand M, Hetta J, Rosen A, Sorensen S, et al.: A double-blind, controlled trial in primary care patients with generalized anxi - ety— a Comparison between Buspirone and Oxazepam. Journal of Clinical Psychiatry 1990; 51: 40–5.

e89. Lader M, Scotto JC: A multicentre double-blind comparison of hydroxyzine, buspirone and placebo in patients with generalized anxiety disorder. Psychopharmacology-Berl 1998; 139: 402–6.

e90. Darcis T, Ferreri M, Natens J, Burtin B, Deram P: A multicentre double-blind placebo-controlled study investigating the anxiolytic efficacy of hydroxyzine in patients with generalized anxiety. Human Psychopharmacology: Clinical and Experimental 1995; 10: 181–7.

e91. Ferreri M, Hantouche EG, Billardon M: Interêt de l’hydroxyzine dans le trouble anxiété géneralisée: étude contrôle en double aveugle versus placebo. Encéphale 1994; 20: 785–91.

e92. Khan A, Joyce M, Atkinson S, Eggens I, Baldytcheva I, Eriksson H: A randomized, double-blind study of once-daily extended release Quetiapine Fumarate (Quetiapine XR) Monotherapy in patients with generalized anxiety disorder. J Clin Psychopharmacol 2011; 31: 418–28.

e93. Bandelow B, Chouinard G, Bobes J, Ahokas A, et al.: Extended- release quetiapine fumarate (quetiapine XR): a once-daily mono- therapy effective in generalized anxiety disorder. Data from a randomized, double-blind, placebo- and active-controlled study. Int J Neuropsychopharmacol 2010; 13: 305–20.

e94. Katzman MA, Brawman-Mintzer O, Reyes EB, Olausson B, Liu S, Eriksson H: Extended release quetiapine fumarate (quetiapine XR) monotherapy as maintenance treatment for generalized anxiety disorder: a long-term, randomized, placebo-controlled trial. Int Clin Psychopharmacol 2011; 26: 11–24.

e95. Magi K, Mezhebovsky I, She F, Datto C, Eriksson HA: Efficacy and tolerability of extended release quetiapine fumarate (quetiapine XR) monotherapy in elderly patients with generalised anxiety disorder (GAD) (Poster). World J Biol Psychiatry 2009; 10: 239.

e96. Altamura AC, Serati M, Buoli M, Dell’Osso B: Augmentative quetiapine in partial/nonresponders with generalized anxiety disorder: a randomized, placebo-controlled study. Int Clin Psycho- pharmacol 2011; 26: 201–5.

e97. Stein DJ, Ahokas AA, de Bodinat C: Efficacy of agomelatine in generalized anxiety disorder: a randomized, double-blind, place- bo-controlled study. J Clin Psychopharmacol 2008; 28: 561–6.

e98. Stein DJ, Ahokas A, Albarran C, Olivier V, Allgulander C: Agomela- tine prevents relapse in generalized anxiety disorder: a 6-month randomized, double-blind, placebo-controlled discontinuation study. J Clin Psychiatry 2012; 73: 1002–8.

e99. Woelk H, Schläfke S: A multi-center, double-blind, randomised study of the Lavender oil preparation Silexan in comparison to Lorazepam for generalized anxiety disorder. Phytomedicine 2010; 17: 94–9.

e100. Kasper S, Gastpar M, Muller WE, et al.: Efficacy and safety of silexan, a new, orally administered lavender oil preparation, in subthreshold anxiety disorder – evidence from clinical trials. Wien Med Wochenschr 2010; 160: 547–56.

e101. Kasper S, Gastpar M, Muller WE, et al.: Silexan, an orally ad - ministered Lavandula oil preparation, is effective in the treatment of ’subsyndromal’ anxiety disorder: a randomized, double-blind, placebo controlled trial. Int Clin Psychopharmacol 2010; 25: 277–87.

e102. Bonne O, Shemer Y, Gorali Y, Katz M, Shalev AY: A randomized, double-blind, placebo-controlled study of classical homeopathy in generalized anxiety disorder. J Clin Psychiatry 2003; 64: 282–7.

IV Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17) | Bandelow et al.: eReferences

M E D I C I N E

e103. Montgomery S, Chatamra K, Pauer L, Whalen E, Baldinetti F: Efficacy and safety of pregabalin in elderly people with general - ised anxiety disorder. Br J Psychiatry 2008; 193: 389–94.

e104. Davidson J, Allgulander C, Pollack MH, et al.: Efficacy and tolerability of duloxetine in elderly patients with generalized anxiety disorder: a pooled analysis of four randomized, double- blind, placebo-controlled studies. Hum Psychopharmacol 2008; 23: 519–26.

e105. Katz IR, Reynolds CF 3rd, Alexopoulos GS, Hackett D: Venlafaxine ER as a treatment for generalized anxiety disorder in older adults: pooled analysis of five randomized placebo-controlled clinical trials. J Am Geriatr Soc 2002; 50: 18–25.

e106. Stanley MA, Beck JG, Novy DM, Averill PM, et al.: Cognitive- behavioral treatment of late-life generalized anxiety disorder. J Consult Clin Psychol 2003; 71: 309–19.

e107. Stanley MA, Beck JG, Glassco JD: Treatment of generalized anxiety in older adults: A preliminary comparison of cognitive- behavioral and supportive approaches. Behavior Therapy 1996; 27: 565–81.

e108. Stanley MA, Wilson NL, Novy DM, et al.: Cognitive behavior therapy for generalized anxiety disorder among older adults in primary care: a randomized clinical trial. Jama 2009; 301: 1460–7.

e109. Wetherell JL, Gatz M, Craske MG: Treatment of generalized anxiety disorder in older adults. Journal of Consulting and Clinical Psychology 2003; 71: 31–40.

e110. Wittchen HU, Kessler RC, Beesdo K, Krause P, Hofler M, Hoyer J: Generalized anxiety and depression in primary care: prevalence, recognition, and management. J Clin Psychiatry 2002; 63 Suppl 8: 24–34.

e111. Rickels K, Shiovitz TM, Ramey TS, Weaver JJ, Knapp LE, Miceli JJ: Adjunctive therapy with pregabalin in generalized anxiety dis- order patients with partial response to SSRI or SNRI treatment. Int Clin Psychopharmacol 2012; 27: 142–50.

e112. Pollack MH, Simon NM, Zalta AK, et al.: Olanzapine augmentation of fluoxetine for refractory generalized anxiety disorder: a placebo controlled study. Biol Psychiatry 2006; 59: 211–5.

Deutsches Ärzteblatt International | Dtsch Arztebl Int 2013; 110(17) | Bandelow et al.: eBox I

M E D I C I N E

eBOX

Generalized anxiety disorder—definition according to the ICD-10 research criteria (abbreviated version)* Tension, worries, and fears about everyday experiences and problems lasting for at least six months, accompanied by at least four of the following types of symptoms (including at least one of symptoms 1–4):

● Vegetative symptoms 1. Palpitations, sensation of heartbeat, rapid heart rate 2. Diaphoresis 3. Fine or coarse tremor 4. Dry mouth

● Thoracic and abdominal symptoms 5. Respiratory symptoms 6. Feeling of tightness in the chest 7. Chest pain or discomfort 8. Nausea or abdominal discomfort

● Mental symptoms 9. Feeling dizzy, unsteady, faint or light-headed 10. Derealization or depersonalization 11. Fear of loss of control, going insane, or “cracking up” 12. Fear of dying

● General symptoms 13. Hot or cold flashes 14. Numbness or tingling

● Symptoms of tension 15. Muscle tension 16. Agitation and inability to relax 17. Feeling of being wound up, nervousness, emotional tension 18. Feeling of something sticking in the throat, dysphagia

● Other, nonspecific symptoms 19. Exaggerated startle response 20. Concentration difficulties, feeling of emptiness 21. Persistent irritability 22. Difficulty falling asleep because of worries

*modified from (22)

Client demographics:

1. 24 years old 2. Female (cisgender), heterosexual 3. Single, never married; currently lives with her boyfriend of 8 years 4. Identifies as catholic but says she is not “very religious” 5. 2 children (father is her boyfriend)

Clinical problems/symptoms and diagnoses of the client:

*PLEASE REFER TO The Diagnosis and Treatment of Generalized Anxiety Disorder ARTICLE TO SUPPORT THE DIAGNOSIS*

● The client explains that her worry occurs more often than not and has persisted for at least six months (not specific)

● The client also expressed feeling anxious when things do not go her way, or when there is a last minute change in existing plans (ex:boyfriend was supposed to pick up kids from school, he got stuck later than he anticipated so she had to pick them up and gets anxious about being late)

● The client expressed feelings of worthlessness, along with low energy levels as well as a significant difference in sleeping/eating patterns recently.

● Her main struggle is anxiety, which sometimes leads to other issues such as depression or difficulty managing her anger

● She expressed concerns that her anxiety and inability to control it has affected her relationships with her boyfriend and children. She did not recognize it as being a big issue until her oldest son expressed that she “stresses him out” about everything.

● General Presenting Concerns: anxiety, depression and anger ● Generalized Anxiety Disorder 300.02 (F41.1) : The client meets the Diagnostic Criteria

(ex: Excessive anxiety and worry, occurring more days than not for at least 6 months, concerning a number of events, Restlessness, feeling keyed up or on edge, The individual finds it difficult to control the worry etc.)

Pertinent clinical issues:

*PLEASE REFER TO Mental Health Stigma ARTICLE FOR THIS SECTION.*

● Client describes mental health as being a “taboo” subject in her family growing up therefore she had no formal Psychiatric history to report.

● She said that her boyfriend and some of her friends mocked her when she confessed to them that she was seeking treatment.

● The client is initially hesitant to share her reasons for seeking treatment.

● She pretends that everything is fine on the exterior appearance to others to avoid being made fun of, but on the inside she is experiencing a wide range of what are often negative emotions that she does not know how to handle in a healthy way.

Cognitive Behavioral Case Formulation and Treatment Plan:

The client demonstrated many symptoms of anxiety including difficulty concentrating, muscle tension,shaking, etc.She has never experienced a successful work history or marriage. She had always aspired to be successful and independent and a person who was competent and reliable and helpful to others but feels as if her getting pregnant at a young age “stoof in the way” of those aspirations.. She strongly values hard work but feels she is not achieving this. Her held values led to behavioral patterns related to depression and anxiety of holding high, and somewhat unrealistic, expectations for herself to “be completely independent.”. Her corresponding intermediate/schemas beliefs were: “I am worthless because I am not good at anything”, “I am not going to get through this rough period of my life”, “I worry about everything and am told that I overthink a lot” and “I have to hide my feeling aso people don’t say that I think too much.”

My client’s biggest struggle is her anxiety, which often leads to other problems such as depression or difficulty managing her anger. “Often chronic in nature, anxiety disorders are associated with severe impairments across interpersonal and occupational domains.” (Antony, M. M., & Stein, M. B. 2009, p. 4). She communicated worries that her anxiety and inability to control it have significantly affected her relationships with her boyfriend and children.

The client reports that she was a good student in High School, describing her grades as “A’s and B’s most of the time.” She graduated from High School, but has not yet attended college despite aspirations to do so. She explained that it has always been her dream to attend college and pursue a successful career but she reports that time restraints due to her having children at such a young age as well as financial problems are the main reasons for not attending college

The main aspects of “being put down” that the client reported from stemming from her relationship with her boyfriend and her friends..She reported factors such as name calling, aggression such as yelling and various forms of emotional abuse such as name calling and gas lighting. The client reports that she never felt “good enough” for her boyfriend, and as a result was always fearful of criticism.

The plan is to reduce The client's anxiety which would reduce the clients symptoms of depression and inability to control her anger as well as, improve her functioning and social interactions, and increase positive affect.

1). Unemployment/Get a job: Examined advantages and disadvantages of looking for a job in order for the client to feel a sense of independence. The client and the therapist evaluated and responded to hopeless automatic thoughts, “I am worthless because i do not have a job,” problem-solved how to update resume and look for a job; roleplayed job interview.

2). Avoidance/Re-engage in avoided activities: The client and the therapist came up with specific tasks around the house to do at specific times; did behavioral experiments to test his automatic thoughts (“I am not good at anything”) The therapist and the client evaluated and responded to automatic thoughts. These scheduled activities along with other activities that could help to bring a sense of pleasure. The therapist encouraged the client to give herself credit and appreciation for any task that she completed.

3).Communication skills with boyfriend/Investigate whether improved communication skills can help being “open” with a partner about anxiety. The client and the therapist practice communication skills such as assertion and performed behavioral experiments to test thoughts

4). Help the client cope with her depression and anxiety with interventions involving goal setting, self monitoring, and behavior modification.

5). Set up specific goals, with defined steps, to aid her in reaching the quality of life that she wants.

6). We also practiced the art of being present. This process involves the practice of mindfulness. The client is encouraged to soak everything in, down to every single detail. For example, when the client leaves for work in the morning, she is encouraged to slow down and take the time to observe things such as the weather, the sound of leaves or neighbor’s cars starting, etc.

7). Help the client learn how to accept accountability for her actions and decisions with positive and negative reinforcement, and reframing her negative automatic thoughts

Treatment depicted, therapeutic progress, and proposed interventions

The client and the therapist meet weekly for twelve weeks, then every other week for four weeks, then once a month for four months, for a total of 18 sessions over 8 months. We had standard 45-minute CBT sessions.

The Therapist and the client agreed that together, they work first on the following: (1) encouraging the client to get out of her house almost every day, even if it is to complete a small task (2) spending more time trying to communicate effectively to her partner what she is experiencing/going through (3) cleaning up her house because completing any task increased her sense of worthiness .(Later the client and the therapist worked on spending more time practicing self-awareness in order to help reduce the clients anxiety.. Once the client is functioning at a higher level and practicing coping skills for anxiety effectively, the client and the

therapist will work on finding employment for the client to feel more independent and accomplished.

The therapist will continue to monitor progress in the coming sessions.

Overall, the client showed a positive clinical response to CBT treatments. Further to that, she has shown a reduction in anxiety and depression. .She has responded positively and quickly to interventions

Instructions for Case Conceptualization Paper

● Choose a client you are seeing and complete a case conceptualization ● Do NOT use the actual name of the client. Refer to the client as “the client”, the therapist

as “the therapist” and other people as their relationship to the client (the client’s brother, partner, daughter, etc.).

● The paper should be written in third person, e.g., “The client reported…”, “the client’s therapist emphasized…” “it is recommended...” and be professional in tone and language (not casual language

● All sections should be in narrative form and complete sentences (not bullets). ● Length: 10-13 pages (double-spaced), excluding title page and references page. Times

New Roman 12-size font, 1-inch margins all around. APA style.

Use the following sections to cover relevant content. Use these exact headings provided below:

1. Client demographics (age, gender, ethnicity, family composition and relations, living situation, employment [& history], education, sexual orientation, marital status, etc. Do NOT include clinical diagnosis information or symptom descriptions in this section). Suggested length: 1-2 paragraphs.

2. Clinical problems/symptoms and diagnoses of the client. Describe and discuss all presenting symptoms and count them against the DSM-5 criteria for specific disorders, making a judgment if the criteria are met and what are the likely DSM-5 diagnoses. You have to briefly list each of the criteria for the proposed disorders and explain how they are met or not met, providing examples from the client clinical picture. The emphasis is on explaining how the criteria are met, not listing the full criteria. Provide as complete diagnoses as possible. Include a history of symptom development and progress, if available. Discuss what additional information may need to be collected for alternative possible diagnoses to be ruled in or out, if relevant. Suggested length: 2 pages.

3. Pertinent clinical issues, such as social environment of the client, existence or lack of social support, relationships with significant others (family of origin and own family), cultural/diversity issues, client strengths, any complicating factors, and prognosis. Suggested length: About 1 page.

4. Cognitive Behavioral Case Formulation and Treatment Plan. Provide a case formulation and treatment plan for this client case. Your case formulation and treatment plan should be based on your own diagnosis and understanding and formulation of client problems, Do your best to write the CBT working

hypothesis section based on client info and typical cognitions for their disorder (do not omit or downplay this section, it is very important). Include suspected schemas, if information is not clear. Please also check relevant chapters or articles about CBT for OCD, Panic Disorder, etc. Suggested length: 3 pages.

5. Treatment depicted, therapeutic progress, and proposed interventions.

(a) Discuss and critique the treatment taken place with the client), Give details about techniques used and provide a critical examination of the process and outcome of treatment shown. Discuss client response to treatment and relevant obstacles. Comment on therapeutic relationship issues and note any difficulties. Suggested length: 2 pages.

(b) Discuss what additional or modified CBT or other interventions you would recommend, based on your case conceptualization and client response on interventions used in the video. Your interventions should cover all clinical issues, not just the primary diagnosis. Include both cognitive and behavioral techniques. Provide specific examples of the specific content of the interventions targeting specific content of client problems. For example, list what case-specific client negative distortions and thoughts need to be addressed and what the alternative, realistic thoughts would be. Also, what specific behavioral interventions will address specific client problems. Discuss how diversity or cultural factors affect treatment and how interventions may need to be adapted, if relevant to this client. Lastly, discuss the research/evidence base of your proposed interventions (with citations of research supporting the use of the specific intervention for the specific disorders). Suggested length: 2 pages.

blog2

Get help from top-rated tutors in any subject.