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This Month in Archives of General Psychiatry
November 2009

This Month in Archives of General Psychiatry

Arch Gen Psychiatry. 2009;66(11):1158. doi:10.1001/archgenpsychiatry.2009.157

Prata et alArticle examined the effect of a polymorphism in the dopamine transporter 1 gene on brain function during executive processing in healthy volunteers and patients with schizophrenia. They found that insular, cingulate, and striatal function is normally modulated by this genetic variation but that its effect in the dorsolateral prefrontal cortex and ventral striatum is altered in patients with schizophrenia.

Catatonia, a motor dysregulation syndrome, is often masked among mood disorders, stupors, postseizure states, metabolic and toxic states, encephalitis, and autism. It is commonly found in general medical and neurologic hospital services. Severe forms may be fatal if not recognized and effective treatments applied. Fink and TaylorArticle review their experience with the catatonia syndrome, finding it readily diagnosable and treatable and not restricted to schizophrenia.

Kocsis et alArticle describe a trial that compared continued next-step pharmacotherapy options with or without adjunctive augmentation with either the cognitive behavioral analysis system of psychotherapy or brief supportive psychotherapy in chronically depressed patients not achieving remission during an initial pharmacotherapy phase. Neither form of psychotherapy significantly improved outcomes over that in the pharmacotherapy regimen alone.

Harrison et alArticle used resting-state functional magnetic resonance imaging to provide evidence that functional connectivity in brain corticostriatal networks is altered in patients with obsessive-compulsive disorder. In particular, they found that heightened functional connectivity of the ventral caudate/nucleus accumbens and orbitofrontal cortex was associated with patients' symptom severity.

Xie et alArticle examined the effects of childhood adversity, adult traumatic events, 5-HTTLPR genotypes, and gene × environment interactions on the etiology of posttraumatic stress disorder. In both European American and African American groups, the short variant of 5-HTTLPR was found to interact with stressful life events to increase risk for posttraumatic stress disorder.

Cohen et alArticle examined the association of posttraumatic stress disorder and cardiovascular health status in a cohort of 1022 men and women with stable coronary heart disease. Participants with posttraumatic stress disorder had greater cardiac symptom burden, greater physical limitation, and worse quality of life. Posttraumatic stress disorder remained associated with worse cardiovascular health status even after adjusting for comorbid depression and for several objective measures of cardiac function.

In a neuroimaging study drawn from a larger community survey of Vietnamese ex–political detainees who were exposed to torture, Mollica et alArticle found higher rates of depression among those with traumatic head injury (THI) than those without THI exposure. Structural deficits in the prefrontotemporal brain were linked to THI exposure and associated with severity of depression.

Kwon et alArticle investigated a genetic association between SLC1A1 and atypical antipsychotic–induced obsessive compulsive symptoms in clinically stable patients with schizophrenia. Both single-nucleotide polymorphism and haplotype-based analyses indicate that sequence variations in SLC1A1 are significantly associated with susceptibility to atypical antipsychotic–induced obsessive compulsive symptoms.

In a large sample of adolescents, Lotfipour et alArticle found that prenatal exposure to maternal cigarette smoking influenced substance use behavior in association with the thickness of the orbitofrontal cortex. The relationship between the likelihood of drug experimentation and the orbitofrontal thickness was opposite in the exposed and nonexposed adolescents and moderated by BDNF genotype in the latter group.

Piper et alArticle conducted a randomized, double-blind, placebo-controlled comparative efficacy smoking cessation trial. One thousand five hundred four adults who smoked 10 or more cigarettes per day were randomized to 1 of 6 conditions: sustained-release bupropion, nicotine patch, nicotine lozenge, sustained-release bupropion plus nicotine lozenge, nicotine patch plus nicotine lozenge, or placebo. The nicotine patch plus lozenge group had the highest biochemically confirmed abstinence rates at 8 weeks (53.6%) and 6 months (40.1%) postquit.

Whether heritable traits at middle age contribute to late-onset Alzheimer disease was studied by van Exel et alArticle. Offspring with a parental history of Alzheimer disease more often had hypertension and an innate proinflammatory cytokine profile compared with offspring without a parental history of dementia, suggesting that these early risk factors contribute to Alzheimer disease.