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This Month in Archives of General Psychiatry
November 2002

This Month in Archives of General Psychiatry

Author Affiliations

Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2002

Arch Gen Psychiatry. 2002;59(11):975-976. doi:10.1001/archpsyc.59.11.975

For forty years, Solomon SnyderArticle has been in the forefront of research in psychopharmacology. In this summary of his lecture given on the reception of the 2001 Institute of Medicine's Sarnat International Prize in Mental Health, he reviews critical discoveries about fundamental mechanisms involved in chemical neurotransmission that led to a better understanding of how psychotropic medications exert their effects to more recent identification of novel therapeutic targets.

For decades, Michael RutterArticle has led child psychiatry in applying scientific methods to study the role of development in the cause of psychiatric morbidity. In this summary of his lecture given on his reception of the 2001 Institute of Medicine's Sarnat International Prize in Mental Health, he reviews the advances in the fields of psychiatric genetics, psychosocial influence, and developmental processes that are illuminating the interplay between susceptibility genes and psychosocial adversity resulting in age-related changes in psychopathology.

Imaging studies have demonstrated gray matter volume decrements in schizophrenia. As clinical deterioration is greatest in the early stages of schizophrenia, one would expect gray matter to decrease progressively, particularly in first-episode patients. Cahn et alArticle have examined gray matter volumes at inclusion and after 1 year in 34 first-episode patients and 36 healthy comparison subjects. Gray matter volume progressively decreased in schizophrenia. Decrements were independently associated with poorer outcome and with higher doses of antipsychotic medication. This suggests that progressive loss of gray matter occurs in the early stages of schizophrenia and is related to the disease process and antipsychotic medication.

Doniger et alArticle compared subjects with schizophrenia and matched controls for their ability to recognize degrade of images of common objects, presented sequentially from more degraded to less. Recognition, known as perceptual closure, is associated with an event-related potential recorded over the visual association cortex. Schizophrenic subjects exhibited significant impairments in perceptual closure as well as the amplitude of the associated event-related potential when compared with controls. The results suggest an impairment of magnocellular functioning involved in image recognition but not in primary visual cortical functioning in schizophrenia.

Koro et alArticle found that olanzapine exposure was associated with increased risk of hyperlipidemia in schizophrenia patients. Subjects prescribed olanzapine exhibited more than a 3-fold increase in the odds of developing hyperlipidemia compared to conventional antipsychotic patients. In contrast, exposure to risperidone was not associated with increased odds of hyperlipidemia. The increased risk of hyperlipidemia among olanzapine users raises serious questions about the risk-benefit ratio for olanzapine use in schizophrenia patients. This is particularly true since schizophrenia patients tend to exhibit other major risk factors for cardiovascular events, such as smoking, sedentary lifestyle, diabetes mellitus, and weight gain.

Persons with generalized social phobia (GSP) fear and avoid interacting with others, and are hypersensitive to disapproval. Stein et alArticle used functional magnetic resonance imaging(fMRI) to study the neural circuitry of facial affect processing in persons with GSP. They find that compared with healthy subjects, persons with GSP display increased activation of the amygdala when processing disorder-salient stimuli (ie, angry or contemptuous faces). These findings are consistent with a role for differential amygdala functioning (also implicated in the pathophysiology of several other anxiety disorders) in the neurobiology of GSP.

In a prospective longitudinal study of a community sample over 20 years, Brook et alArticle found that earlier illegal drug use in adolescence was significantly associated with major depressive disorder, alcohol dependence, and substance use disorders in young adulthood, after taking into account other potential risks, including disadvantaged socioeconomic status, age, gender, and previous episodes of major depressive disorder and substance use disorders. Earlier alcohol use was associated with later major depressive disorder, alcohol dependence, and substance use disorders. However, earlier tobacco use was associated with later alcohol dependence and substance use disorders, but not with new episodes of major depressive disorder.

Ganguli et alArticle performed a 10-year prospective epidemiological study in a largely blue-collar cohort of 1064 adults aged 67 years and older. Predictors of mortality at 3-, 5-, and 10-year end points were older age, male sex, disability in instrumental activities of daily living, and number of regularly taken prescription drugs, all measured at baseline. Cognitive functioning predicted mortality only when disability in instrumental activities of daily living was excluded from the model. Depression by itself predicted mortality in the shorter (3-year and5-year) rather than the longer (10-year) term. However, in combination with poor self-rating of health, depression strongly predicted mortality at all end points.

Asarnow et alArticle investigated the hypothesis that first-degree relatives of probands with childhood-onset schizophrenia (COS) are at increased risk for specific neurocognitive impairments. They compared parents of COS probands, parents of patients with attention-deficit/hyperactivity disorder (ADHD), and parents of controls on 3 neurocognitive tasks. Rigorous cutting scores for performance on the 3 tasks robustly discriminated parents of COS subjects from those with ADHD or controls. This neurocognitive strategy may yield a higher level of diagnostic accuracy for use in genetic linkage studies.

Environmental contaminants polychlorinated biphenyls (PCBs) and dioxin-like chemicals are known to cause neurocognitive damage in children born to exposed mothers. In 1992-1995, Lai et alArticle followed118 children born to mothers exposed to PCBs and dioxin-like chemicals due to consumption of contaminated rice oil in 1978, and found that the exposed children had lowered IQs than controls as measured by the Wechsler Intelligence Scales for Children–Revised, and more behavioral problems than controls assessed by the Achenbach Child Behavior Checklist (CBCL) and the Rutter Child Behavior Scale A. It was concluded that prenatal exposure to these compounds produced long-lasting cognitive and behavioral sequelae.