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Self-medication is the most frequently suggested para- digm to explain the high rate of comorbidity between anxiety and substance use. Although anxiety disorders, including GAD, are common in alcoholic patients, pa- tients with GAD are less likely to self-medicate with al- cohol and other substances than are patients with panic disorder and social phobia. However, up to two-thirds of patients receiving treatment for alcohol problems re- port clinically significant anxiety, including GAD (Grant et al. 2005). In most cases GAD develops after the alcohol problem. Alcohol and other substance with- drawal states are indistinguishable from the autonomic symptoms of GAD. Prolonged exposure to alcohol and other substances can lead to the same gastrointestinal, acid-base, and sleep disturbances described by patients with GAD.

Conclusion

GAD is a challenging diagnostic and treatment di- lemma. Notwithstanding changing diagnostic criteria, epidemiological surveys suggest that the disorder is one of the most prevalent psychiatric conditions. While cli- nicians attempt to identify response patterns, course, and predictors of response in rigorous double-blind studies, neuroscientists focus on the neurochemistry and neuroanatomy of select features of DSM categories, such as the excessive worry seen among individuals with GAD. The synthesis of the results of basic and clinical neuroscience and DSM-based treatment and epidemi- ological studies will likely improve our understanding of the nature of GAD and lead to better treatment.

Key Clinical Points

• Generalized anxiety disorder is distinct and common, but the severe disability associated with it is still underappreciated.

• The diagnosis of GAD can be made reliably, even in the presence of many comor- bid conditions.

• The epidemiology and symptoms of GAD are likely to differ significantly by age and gender.

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Recommended Readings

Kessler RC, Berglund P, Demler O, et al: Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry 62:593–602, 2005

Moffitt TE, Harrington H, Caspi A, et al: Depression and generalized anxiety disorder: cumulative and sequential

comorbidity in a birth cohort followed prospectively to age 32 years. Arch Gen Psychiatry 64:651–660, 2007 Papp LA: Generalized anxiety disorder: evaluation and treat-

ment, in Treatment Companion to the DSM-IV-TR Case Book. Edited by Spitzer RL, First MB, Gibbon M, et al. Washington, DC, American Psychiatric Publishing, 2004, pp 137–142

Rickels K, Rynn M: Overview and clinical presentation of generalized anxiety disorder. Psychiatr Clin North Am 24:1–17, 2001

Spitzer RL, Kroenke K, Williams JB, et al: A brief measure for assessing generalized anxiety disorder: the GAD-7. Arch Intern Med 166:1092–1097, 2006

173

Pathogenesis of Generalized

Anxiety Disorder

Jeffrey D. Lightfoot, Ph.D.

Steven Seay Jr., M.S.

Andrew W. Goddard, M.D.

G

eneralized anxiety disorder (GAD) is a relatively new diagnosis that was first defined in the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (American Psychiatric Association 1980). GAD is char- acterized by excessive and uncontrollable anxiety and worry and is often considered the most “basic” anxiety disorder because its core features manifest in other anxi- ety disorders (Brown et al. 2001). Although individuals with GAD do not differ from healthy individuals with re- gard to the content of their worries, they tend to grossly overpredict the occurrence of negative outcomes (Barlow 1988; G. Butler and Mathews 1987). Physical symptoms associated with GAD include motor tension and vigi- lance (Brawman-Mintzer et al. 1994; Marten et al. 1993), and individuals with GAD commonly report irri- tability, feelings of restlessness, muscle tension, fatigabil- ity, and sleep and concentration difficulties (Marten et al. 1993). In this chapter, we review biological and psycho- social factors that are thought to play a role in the devel- opment and maintenance of the disorder. The biological section includes contributions from genetics, neuro- chemistry, and neurophysiology, and the psychosocial section explores intrapsychic, social, and learning ac- counts of the disorder. We then attempt to integrate these main areas to provide an etiological model of GAD.

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