We're unable to sign you in at this time. Please try again in a few minutes.
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
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. 2011;68(9):868. doi:10.1001/archgenpsychiatry.2011.102.
Text Size: A A A
Published online

In a 5-year longitudinal study comparing the change in cortical thickness in schizophrenic patients and healthy subjects, van Haren et alArticle found excessive thinning over time in widespread areas of the brain, most pronounced bilaterally in the temporal cortex and in the left frontal area and progressing across the entire course of the illness. The excessive thinning of the cortex appears related to outcome and cumulative antipsychotic medication intake.

In a multimodal imaging study, Fusar-Poli et alArticle investigated subjects at clinical risk for psychosis and matched controls using functional magnetic resonance imaging while performing a verbal fluency task and proton magnetic resonance spectroscopy to measure brain regional glutamate levels. They found that altered prefrontal, hippocampal, and temporal function in subjects at high risk for psychosis is related to a reduction in thalamic glutamate levels, and this relationship is different from that in healthy controls.

Using positron emission tomography and a selective radioligand, [11C]P943, Murrough et alArticle examined serotonin type 1B receptor binding in patients with posttraumatic stress disorder and a trauma-control cohort and found abnormally low levels of receptor binding in both groups compared with healthy nontraumatized participants within a cortico-striatal-limbic circuit. They further report a significant inverse relationship between receptor binding and participant age at first traumatic experience, suggesting that age at trauma exposure is a critical factor in causing neurobiological alterations in trauma survivors.

In a highly traumatized, primarily African American cohort, Mehta et alArticle demonstrate that functional variants in FKBP5 are associated with biologically distinct subtypes of posttraumatic stress disorder. Using endocrine, gene expression, and genotypic data, this study illustrates that the inheritance of glucocorticoid receptor sensitivity–moderating polymorphisms within FKBP5 can determine specific types of hypothalamic-pituitary-adrenal axis dysfunction within posttraumatic stress disorder, as reflected in gene-expression changes of a subset of glucocorticoid receptor–responsive genes.

Melhem et alArticle examined the course of grief reactions in bereaved children as long as 33 months after the death of their parent from suicide, accident, or sudden natural death. Grief reactions were found to abate over time for most children; however, a subset showed increased or prolonged grief reactions, which in turn increased the risk for functional impairment and depression.

MojtabaiArticle found that compared with bereavement-unrelated depressive episodes of the same duration, bereavement-related episodes were associated with less impairment, fewer comorbidities, and a lower risk of future depressive episodes. The findings argue against the DSM-5 draft proposal to eliminate the bereavement exclusion criterion of major depressive episodes.

Logan et alArticle used latent class analysis to identify patterns of co-occurring health- and life-stress–related circumstances known to be risk factors for suicide among 28 703 suicide decedents from 12 US states. Nine distinct patterns of known risk factors were identified and all decedents were classified by these patterns.

Sinha et alArticle experimentally modeled stress and alcohol cue exposure in recovering alcoholic inpatients and controls and prospectively followed up the patients to assess relapse risk. Stress- and alcohol cue–induced craving, high resting anxiety, and adrenal sensitivity to corticotropin each predicted alcohol relapse and treatment outcome. High adrenal sensitivity more than doubled the risk of shorter time to relapse during recovery.

Brody et alArticle examined brain nicotinic acetylcholine receptor occupancy from exposure to secondhand smoke (SHS). Cigarette smokers and nonsmokers underwent positron emission tomography scanning before and after sitting in a car for an hour and undergoing exposure to a moderate level of SHS. This SHS exposure resulted in 19% occupancy of brain nicotinic acetylcholine receptors and was similar for smokers and nonsmokers.

Gomar et alArticle investigated the discriminative utility of different classes of biomarkers (cerebrospinal fluid and brain volumetric measures) and cognitive markers for their prediction of the conversion from mild cognitive impairment to Alzheimer disease within a 2-year period. Delayed verbal memory and middle temporal lobe cortical thickness were robust predictors of conversion. Conversion was driven less by changes in the neurobiological trajectory of the disease than by sharp declines in functional ability and, to a lesser extent, in executive function.

Li et alArticle examined the temporal relationship between late-life depression and development of dementia in a large community-based prospective cohort with initially nondemented participants aged at least 65 years. This study confirmed previous observations of an association between late-life depression and increased risk of dementia and provided additional evidence that late-life depression may be an early manifestation of dementia rather than increasing risk for dementia.

First Page Preview

View Large
First page PDF preview





Also 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.
Please click the checkbox indicating that you have read the full article in order to submit your answers.
Your answers have been saved for later.
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.


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

0 Citations

Related Content

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