0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
This Month in Archives of General Psychiatry |

This Month in Archives of General Psychiatry FREE

Arch Gen Psychiatry. 2009;66(11):1158. doi:10.1001/archgenpsychiatry.2009.157.
Text Size: A A A
Published online

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.

Figures

Tables

References

Correspondence

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.