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This Month in Archives of General Psychiatry |

This Month in Archives of General Psychiatry FREE

Arch Gen Psychiatry. 2000;57(3):208. doi:10.1001/archpsyc.57.3.208.
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Is depression increasing? Murphy et alArticle report that the overall current prevalence of depression remained stable in a typical North American population during the years 1952 to 1992. Early in this period, rates were similar by sex but older people were more vulnerable than younger people. By the 1990s a redistribution occurred. Prevalence among women younger than 45 years increased while rates among older people decreased.

Epidemiology in psychiatry is plagued by wide variation in reported rates of disorders such as depression. Eaton et alArticle, in a follow-up of the Baltimore, Md, sample of the Epidemiologic Catchment Area study, suggest that a focus on a diagnostic threshold contributes to the variation. In comparing structured self-report interviews used in epidemiologic surveys with later in-depth assessments by psychiatrists, there was poor agreement for diagnosis but stronger agreement at the level of the syndrome and on ordinal measures of symptomatology.

Questions have been raised about lay-administered interviews in psychiatric epidemiology and whether they identify transient mood disturbances rather than clinical disorder. By comparing 2 different lay interviews administered to the same subjects, Murphy et alArticle indicate that such interviews are not as inadequate as critics suggest.

Commentaries by RegierArticle; Blazer and KaplanArticle are included.

Within the prefrontal cortex of schizophrenic subjects, studies have found alterations in markers of γ-aminobutyric acid (GABA) neurotransmission, including the synthesizing enzyme for GABA, glutamic acid decarboxylase (GAD67). However, it is unclear whether all GABA neurons are uniformly affected. Volk et alArticle report that GAD67 messenger RNA expression is relatively unaltered in the majority of prefrontal cortex GABA neurons, but is reduced below a detectable level in a subset of GABA neurons. Altered GABA neurotransmission in this subset may contribute to prefrontal cortex dysfunction in schizophrenia.

Purdon et alArticle compared the comprehensive neuropsychological status of 65 patients with early-phase schizophrenia before and after up to 1 year of double-blind treatment with olanzapine, risperidone, or haloperidol. In this first direct comparison of novel treatments, olanzapine resulted in greater benefits than risperidone or haloperidol.

To understand individual differences in risk of psychoactive substance use disorders, Kendler et alArticle assessed lifetime prevalence in male twin pairs. For any use and for cannabis and hallucinogen use, twin resemblance was due to both genetic and familial-environmental factors. Twin resemblance for heavy use, abuse, and dependence resulted from only genetic factors.

Increased activity of the brain chemical glutamate may occur in neuropsychiatric illnesses such as schizophrenia, depression, and Alzheimer disease. Anand et alArticle found that lamotrigine (an antiepilepsy medicine that decreases glutamate release) is able to reverse schizophrenialike symptoms and memory problems induced by low-dose ketamine in healthy humans. Drugs that decrease glutamate release should be further investigated for the treatment and prevention of psychiatric illnesses.

Relapse rates in schizophrenia are very high, ranging from 30% to 40% in 1 year after hopsital discharge, even for patients who are taking their antipsychotic medication. Herz et alArticle report results of a treatment program that emphasizes close monitoring for prodromal symptoms of impending relapse with prompt clinical intervention when they appear. Relapse and rehospitalization rates were reduced by approximately 50% during an 18-month period compared with a "treatment as usual" control group.

Alexopoulos et alArticle) observed that executive dysfunction, but not memory impairment, is associated with relapse and recurrence of geriatric depression and with fluctuations of depressive symptomatology after recovery of geriatric depression. These observations, if confirmed, will aid clinicians in identifying patients in need of vigilant follow-up.





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