You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 61 No. 1, January 2004 TABLE OF CONTENTS
  Archives
  •  Online Features
  This Month in Archives of General Psychiatry
 This Article
 •PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal

This Month in Archives of General Psychiatry

Arch Gen Psychiatry. 2004;61:12.

Gogtay et al (SEE ARTICLE) examined the diagnostic specificity of cortical gray matter (GM) loss by comparing patients with prospective childhood-onset schizophrenia (COS), patients with atypical psychosis, and healthy patients. The COS group had greater total and regional GM loss than both the atypical psychosis and control groups. Because patient groups had similar cognitive functioning, medications, and hospitalization, the striking GM loss appears intrinsic to early-onset schizophrenia.

Agerbo et al (SEE ARTICLE) examined the long-term association between schizophrenia, marital status, and labor market affiliation before and after the first inpatient episode using a population-based case-controlled design. Patients diverged from age-, sex-, and year-matched controls up to 19 years before and 25 years after their first hospital admission. This pattern was especially pronounced for men and for individuals who had more than 1 hospital admission.

Goldapple et al (SEE ARTICLE) examined brain changes associated with response to cognitive behavior therapy in a sample of patients with unipolar depression using positron emission tomography. Treatment response resulted in unique metabolic changes in the dorsal cingulate and medial frontal cortex not seen with pharmacotherapy. Changes in the prefrontal cortex and hippocampus were also present but were the inverse of those seen with medication. These specific brain changes may reflect a primary top-down mechanism of action for cognitive behavior therapy response within a more general depression-remission circuit.

Major depression is a frequent psychiatric complication among patients with traumatic brain injury. Jorge et al (SEE ARTICLE) prospectively assessed the clinical, neuropsychological, and structural neuroimaging correlates of major depression occurring after traumatic brain injury. Major depressive disorder was associated with executive dysfunction, negative affect, aggression, and prominent anxiety symptoms. In addition, neuroimaging findings suggest that prefrontal damage plays a significant role in the pathogenesis of this syndrome.

Fann et al (SEE ARTICLE) prospectively examined the risk of psychiatric illness in the 3 years following traumatic brain injury in a large staff-model health maintenance organization. Both moderate to severe and mild traumatic brain injury were associated with increased risk for subsequent psychiatric illness, especially in the first 6 to 12 months after traumatic brain injury. Prior psychiatric illness significantly modified the relationship between traumatic brain injury and subsequent psychiatric illness and was itself a significant predictor of subsequent psychiatric illness.

Freeman et al (SEE ARTICLE) examined associations between depressed mood and hormonal changes in the transition to menopause in a population-based cohort. The likelihood of depressive symptoms increased in the menopausal transition as identified by menstrual bleeding patterns and decreased following menopause. A significant inverse association of subject aggregate profiles of follicle-stimulating hormone with depressive symptoms provided strong corroborating evidence that the changing hormonal milieu contributes to dysphoric mood in this transition period.

London et al (SEE ARTICLE) assessed mood disturbances and regional cerebral glucose metabolism in newly abstinent methamphetamine abusers and healthy control subjects during the performance of a vigilance task. Methamphetamine abusers reported elevated depression and anxiety and had altered metabolism in brain structures implicated in mood disorders, suggesting that these regions are involved in affective dysregulation and may be an important target of intervention for methamphetamine dependence.

Canino et al (SEE ARTICLE) examined the prevalence rates and relationship of DSM-IV diagnoses to global impairment, demographic correlates, and service use in a representative sample of children and adolescents aged 4 to 17 years in Puerto Rico. Although 16.4% of the population had 1 or more of the DSM-IV disorders, rates were reduced to 6.9% when a measure of global impairment was added. Global impairment was more important in predicting service use than diagnosis.

Hampel et al (SEE ARTICLE) investigated the diagnostic performance of 3 different tau phosphorylation epitopes (p-tau231, p-tau181, and p-tau199) in the cerebrospinal fluid of patients with primary dementia disorders and healthy patients. Applied as single markers, p-tau231 and p-tau181reached specificity levels greater than 75% between the Alzheimer disease (AD) group and the combined non-AD group when sensitivity was set at 85% and higher. Discrimination between AD and dementia with Lewy bodies was maximized using p-tau181, whereas p-tau231 maximized group separation between AD and frontotemporal dementia.







HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2004 American Medical Association. All Rights Reserved.