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  Vol. 56 No. 12, December 1999 TABLE OF CONTENTS
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This Month in Archives of General Psychiatry

Arch Gen Psychiatry. 1999;56:1070.

The MTA Cooperative Group (SEE ARTICLE) randomly assigned 579 children with attention-deficit/hyperactivity disorder (ADHD) to 1 of 4 treatment strategies (14 months long): monthly medication management, intensive behavioral treatment, both treatments combined, or assessment and referral back to community providers. The combined treatment and medication management alone were well tolerated and yielded substantially greater gains than the behavioral and community treatments for core ADHD symptoms. For non-ADHD symptom outcomes, combined treatment provided systematic benefits over community-based care and modest additional advantages over single-treatment approaches.

Extending the main report, The MTA Cooperative Group (SEE ARTICLE) found that treatment outcome did not differ as a function of sex, prior medication, or disruptive comorbidity. Children with comorbid anxiety disorders, however, responded relatively better to treatments that included behavior therapy regarding parent-reported outcomes. Families receiving public assistance and in the medication-alone group decreased positive interactions with their children but responded particularly well to combination treatment regarding teacher-reported social skills. Treatment acceptance and attendance enhanced response to medication treatment.

A Commentary by Taylor is included. (SEE ARTICLE)

In the search for new and effective medications for the treatment of cocaine dependence, Romach et al (SEE ARTICLE) examined the role of dopamine D1-like receptors in the behavioral and mood effects of cocaine by evaluating the effects of a D1/D5 antagonist, ecopipam (SCH 39166), on subjective responses to intravenous cocaine. They found that the euphoric and stimulating effects of cocaine were significantly attenuated by ecopipam.

A Commentary by Koob is included. (SEE ARTICLE)

Katon et al (SEE ARTICLE) demonstrated that a multifaceted collaborative program targeted to patients whose depressive symptoms persisted 8 weeks after initiation of antidepressant medication by a primary care physician significantly improved adherence to antidepressants and depressive outcomes compared with usual care.

Heckers et al (SEE ARTICLE) compared schozophrenic patients with and without primary negative symptoms (classified as deficit and nondeficit syndromes) using positron emission tomography during a verbal memory task. Frontal cortex function during memory retrieval was more impaired in deficit schizophrenia, whereas hippocampal recruitment deficits were not different between the 2 schizophrenia groups.

Schizophrenic patients have reduced frontal lobe function, which may be one expression of genetic risk. O'Driscoll et al (SEE ARTICLE) investigated whether reduced frontal lobe function would also be found in relatives of schizophrenic patients with abnormal eye tracking, a putative marker of risk for schizophrenia. Relatives with normal tracking activated frontal cortex during eye tracking tasks, while relatives with abnormal tracking did not. Frontal dysfunction seems to underlie abnormal eye tracking, and may be a genetically mediated difference in brain function that is relevant to schizophrenia.

Raising blood glucose levels improves memory for adults with Alzheimer disease (AD), and also increases endogenous insulin levels, which may affect brain regions supporting memory. Craft et al (SEE ARTICLE) examined whether insulin was essential for glucose-induced memory enhancement by raising glucose levels while coadministering a somatostatin analog that inhibited insulin secretion. Raising glucose levels did not improve memory for patients with AD when insulin was suppressed with somatostatin, while infusing insulin or somatostatin alone improved memory. These results demonstrate that insulin is essential for memory enhancement previously thought to result solely from increasing glucose availability, and also suggest a therapeutic role for somatostatin in AD.

Using data from 2 epidemiologic studies, Breslau and Klein (SEE ARTICLE) examined potential explanations for the association between daily smoking and panic attacks and disorder. They report that daily smoking increased the risk for first occurrence of panic attacks and disorder; the risk was higher in active than past smokers. No significant increase in the risk of daily smoking was found in persons with prior panic attacks.

Perpectives on psychiatric practice in the new millennium by Sharfstein, Michels, and Tischler and Astrachan are included. (SEE ARTICLE) (SEE ARTICLE) (SEE ARTICLE)







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