Overview of generalized anxiety disorder: Epidemiology, presentation, and course

Brown University, Box G-BH, Duncan Building, Providence, RI 02912, USA.
The Journal of Clinical Psychiatry (Impact Factor: 5.5). 02/2009; 70 Suppl 2(Suppl 2):4-9. DOI: 10.4088/JCP.s.7002.01
Source: PubMed


Generalized anxiety disorder (GAD) was defined relatively recently, and the diagnostic criteria are still being refined. The essential feature of the disorder has changed from persistent anxiety to excessive worry, and the required symptom duration has changed from 1 month to 6 months. Additionally, exclusion criteria involving permissibility of the diagnosis in children and wording regarding the relationship of GAD with mood disorders have changed. Nosologic controversies still surround the criteria for excessive worry, symptom duration, the relationship between GAD and major depressive disorder, and the required number of associated symptoms. Alterations in the criteria have been suggested, but more research is needed on the validity of these proposed changes. Generalized anxiety disorder appears to be highly prevalent. In the United States, the lifetime prevalence of DSM-IV GAD is estimated to be about 5% and the current prevalence to be about 2% to 3%. The disorder is differentially prevalent across gender and ethnic and social groups. The course of GAD is chronic and can be exacerbated by poor family relationships, comorbid cluster C personality disorders, and comorbid Axis I disorders. Impairment and suicidal ideation are associated with GAD.

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    • "2005). GAD is a chronic and highly recurrent disease that is associated with significant impairments in quality of life and an increased risk of suicidality (Weisberg, 2009). GAD is frequently comorbid with other psychiatric disorders (Wittchen et al., 1994; Alonso et al., 2004), particularly major depressive disorder (MDD), which is present in two-thirds of patients with GAD at any time in their lives (Judd et al., 1998). "
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    ABSTRACT: To evaluate the effectiveness of pregabalin in patients with resistant generalized anxiety disorder (GAD) and severe depressive symptoms, we carried out a post-hoc analysis of a multicenter, prospective, and observational 6-month study. We included patients who were at least 18 years old, fulfilled the Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV) criteria for GAD, showed inadequate responses to previous courses of antidepressant treatment, had Montgomery-Asberg Rating Scale scores of at least 35, had not received pregabalin previously, and were prescribed pregabalin upon entry into this study. We included 1815 patients fulfilling the DSM-IV criteria for GAD, and 133 (7.3%) fulfilled the selection criteria for these analyses. Ninety-seven percent of the patients received pregabalin (mean dose: 222 mg/day) in combination with other psychotropics. The Hamilton Anxiety Scale total score was reduced by a mean of 20.3 points (95% confidence interval, 22.1-18.4) (57.2% reduction) at month 6. Pregabalin also ameliorated comorbid depressive symptoms, with a reduction in the mean score of the Montgomery-Asberg Rating Scale of 22.3 points (95% confidence interval, 24.2-20.4) (56.6% reduction). Our results suggest that pregabalin, as part of a combination regimen with antidepressants and/or benzodiazepines, might be effective for the treatment of patients with GAD who have shown inadequate response to previous antidepressants and have severe depressive symptoms.
    International clinical psychopharmacology 06/2015; 30(5). DOI:10.1097/YIC.0000000000000087 · 2.46 Impact Factor
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    • "A person with mild GAD can manage to keep a career and a social life, however, severe GAD can lead to failure at work and an avoidance of social situations. Women are at a greater risk for GAD than are men and a diagnosis of GAD is made when an individual three or more of the above symptoms almost daily for six consecutive months [10,11]. Panic disorder is sudden attacks of fear and a sense of impending doom. "
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    ABSTRACT: Drugs used to treat anxiety have many negative side effects including addiction, depression, suicide, seizures, sexual dysfunction, headaches and more. Anxiolytic medications do not restore normal levels of neurotransmitters but instead manipulate the brain chemistry. For example, selective serotonin reuptake inhibitors (SSRIs) prevent the reuptake of serotonin from the synapse allowing serotonin to remain in the area of activity for a longer period of time but does not correct the lack of serotonin production. Benzodiazepines, such as Valium and Xanax®, stimulate GABA receptors, thus mimicking the calming effects of GABA but again do not fix the lack of GABA production. Often, the brain becomes accustomed to these medications and they often lose their effectiveness, requiring higher doses or different drugs. In contrast to anxiolytic drugs, there are herbs and nutrients which can stimulates neurotransmitter synthesis and more naturally effect and even adjust brain chemistry in the absence of many of the side effects experienced with drugs. Therefore this paper explores several herbal and nutritional approaches to the treatment of anxiety.
    Medical science monitor: international medical journal of experimental and clinical research 04/2012; 18(4):RA40-8. DOI:10.12659/MSM.882608 · 1.43 Impact Factor
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    • "Generalized anxiety disorder is a common condition that is reported to have a current prevalence of 2–3 % and a lifetime prevalence of 5 % (Weisberg, 2009). The most widely used treatments for generalized anxiety disorder include the selective serotonin reuptake inhibitors and benzodiazepines (Baldwin et al. 2010 ; Davidson, 2009). "
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    ABSTRACT: Preclinical studies suggest that substance P acting at neurokinin 1 (NK1) receptors may be involved in stress responses and NK1 receptor antagonists show activity in tests of anxiety. These data raise the possibility that NK1 receptor antagonists could be potential anxiolytic treatments in humans. We evaluated this hypothesis clinically using the NK1 antagonist L-759274. This is a randomized, double-blind, placebo- and active-controlled, multicentre, proof-of-concept trial. Patients with generalized anxiety disorder were randomized 1:1:1 to 6 wk of treatment with 40 mg L-759274 (n=73), 1-6 mg lorazepam (n=69) or placebo (n=71). Efficacy was assessed using the Hamilton Anxiety Scale (HAMA). A positron emission tomography (PET) study was also performed in 16 healthy subjects to determine the relationship between NK1 receptor occupancy and plasma levels of L-759274 to verify adequate target engagement by the doses tested during the clinical trial. No statistically significant difference in mean change from baseline HAMA score at 6 wk was seen for L-759274 vs. placebo [difference=1.0 (95% confidence intervals (CI) -1.2 to 3.2), p=0.359] whereas the lorazepam group did show a significant improvement vs. placebo (difference=-2.7, 95% CI -5.0 to -0.4, p=0.020) and L-759274 (difference=3.7, 95% CI 1.5-6.0, p=0.001]. Results from the PET study indicated that the L-759274 dosing regimen used in the clinical trial likely provided high levels of NK1 receptor occupancy (>90%), supporting the view that it was an adequate proof-of-concept trial. The NK1 receptor antagonist L-759274 does not appear to be efficacious for the treatment of generalized anxiety disorder.
    The International Journal of Neuropsychopharmacology 03/2012; 16(1):1-11. DOI:10.1017/S1461145712000065 · 4.01 Impact Factor
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