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This Month in Archives of General Psychiatry
April 1998

This Month in Archives of General Psychiatry

Arch Gen Psychiatry. 1998;55(4):296. doi:10.1001/archpsyc.55.4.296

Distributing a national graduate medical education (GME) trust fund was the subject of an Institute of Medicine study for the House Ways and Means Committee. Herdman and StevensArticle describe the study's findings and recommendations and contrast them with the GME funding provisions enacted by Congress in the Balanced Budget Act of 1997. Similarities among the principles and provisions of the study and the Balanced Budget Act are noted, and some of the implications are discussed. This article should help readers to understand the concepts and details of GME funding and the directions in which it is moving. Commentaries relating the report to psychiatry have been prepared by Michels and Pardes.

The expanding use of antidepressants has been a focus of considerable public and professional controversy. Olfson et alArticle studied national trends in the prescription of antidepressants by outpatient psychiatrists. They found a sharp increase in the number of psychiatric outpatients who were prescribed antidepressant medications. Children, patients with less severe psychiatric disorders, and patients who were new to the prescribing psychiatrist experienced particularly large increases in antidepressant use.

A randomized controlled study in 87 patients with posttraumatic stress disorder (PTSD) by Marks et alArticle compared the outcomes of prolonged exposure (to avoid situations resembling the initial trauma), cognitive restructuring (to improve thinking patterns), exposure plus cognitive restructuring, and relaxation (control treatment). Results found that exposure alone and cognitive restructuring alone were each effective, combining the 2 treatments conferred no advantage, and each was better than relaxation.

The volitional control of the urge to tic for persons who have Tourette syndrome is a potentially important model of impulse control. Peterson et alArticle assessed brain activity changes associated with tic suppression in 22 subjects with Tourette syndrome using functional magnetic resonance imaging. Significant changes were seen in the cortical and subcortical brain regions that are thought to provide the attentional resources required to suppress unwanted behaviors and impulses. Correlations of brain activity changes with tic symptom severity were significant throughout subcortical brain regions, implicating these structures in the pathophysiology of Tourette syndrome.

In short-term studies, pattern analysis distinguishes "true drug" response to antidepressant medications from nonspecific response. Stewart et alArticle tested the utility of pattern analysis in identifying which patients with remitted major depression required continued medication to maintain their benefit. Patients with true drug initial responses required continued fluoxetine to maintain their improvement, while those with nonspecific initial response patterns had similar outcomes regardless of whether the drug was continued.

Neuroimaging studies of the living brain have revealed deficits in cortical volume of gray matter (the cell bodies) but not white matter (the cell connections) in patients with schizophrenia. Recently, using spectroscopic neuroimaging, Lim et alArticle found that the concentration of N-acetylaspartate, a marker of living neurons, was reduced in white but not gray matter. This observation suggests that the gray matter volume deficit does not reflect a neurodegenerative condition but that cell connectivity may be aberrant in schizophrenic patients.

There is growing preclinical evidence that the capacity of ethanol to block the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors contributes to its behavioral effects. Krystal et alArticle present new data indicating that ketamine, an NMDA antagonist, has ethanol-like effects in recently detoxified alcoholic patients. These data support the hypothesis that the NMDA antagonist actions of ethanol contribute to its cognitive and behavioral effects in humans.

Stress exposure can exacerbate psychiatric illness and produce signs of prefrontal cortex (PFC) dysfunction such as impaired concentration and response inhibition. As mild stress produces dopamine release in the PFC, Arnsten and Goldman-RakicArticle examined whether stress exposure impairs PFC function by excessive stimulation of dopamine receptors. Monkeys exposed to very mild stress exhibited a pattern of cognitive deficits resembling PFC dysfunction. These deficits were ameliorated by low doses of dopamine receptor antagonists or by agents that prevent stress-induced dopamine release, consistent with a hyperdopaminergic mechanism.