Cognitive deficits among outpatients with stable schizophrenia are thought to account for functional disability. In a 2-year randomized trial, Hogarty et al (SEE ARTICLE) compared the novel cognitive enhancement therapy with a state-of-the-art enriched supportive therapy. At 1 year, cognitive enhancement therapy demonstrated greater improvement than enriched supportive therapy in the neuropsychological domains of processing speed and neurocognition. By 2 years, significant improvement in social cognition, social adjustment, and style of thinking were also observed.
Fu et al (SEE ARTICLE) studied antidepressant treatment–related changes in brain function in a controlled, longitudinal study of patients with major depression. Using an event-related functional magnetic resonance imaging paradigm designed to activate brain systems for sad facial affect processing, treatment was found to attenuate activation in the left amygdala and ventral striatum and enhance prefrontal cortical response to discriminable degrees of sadness. Symptomatic improvement following 8 weeks of treatment with fluoxetine hydrochloride was correlated with brain functional changes in the anterior cingulate and cerebellum.
In a national sample of 42 932 respondents, Hasin and Grant (SEE ARTICLE) studied the occurrence of DSM-IV alcohol dependence with and without alcohol abuse. A substantial proportion of those with current or lifetime dependence did not manifest abuse symptoms, especially women and minorities. Using abuse as a screen for dependence in epidemiologic and primary care settings will differentially underestimate dependence in traditionally underserved groups. In genetic studies, the presence or absence of abuse may represent heterogeneous dependence phenotypes.
Liu et al (SEE ARTICLE) used random-effects models to estimate the genetic effects on the development of alcohol dependence in a twin study. Forty-nine percent of the variation in the age of diagnosis of alcohol dependence and 42% of the variation in the transition period between regular use and diagnosis could be explained by genetic factors, suggesting a substantial heritable basis for alcohol dependence along its developmental course, including age at diagnosis and the transition period.
Johnson et al (SEE ARTICLE) show that the glutamate antagonist topiramate not only promotes abstinence and reduces the "symptom" of drinking in alcoholics but also enhances their quality of life and decreases the harmful psychosocial consequences of drinking. Nonabstinent alcoholics drinking below the "safe level" with psychosocial improvement should be treated as being in "partial remission" and may be candidates for long-term topiramate treatment—with the expectation that the continuing psychosocial gains would, ultimately, lead to abstinence.
Using an ambulatory monitor, Hoehn-Saric et al (SEE ARTICLE) measured self-reports and physiological recordings in patients without an anxiety disorder, with panic disorder, and with generalized anxiety disorder during normal daily activities. Patients with anxiety disorder showed increased sensitivity to bodily changes. Diminished autonomic flexibility, observed in both anxiety conditions, may be the result of dysfunctional information processing during heightened anxiety that fails to discriminate between anxiety-related and neutral inputs.
Hicks et al (SEE ARTICLE) tested whether familial resemblance for externalizing disorders was due to a general or disorder-specific mode of transmission from parents to offspring. The sample consisted of 542 families that participated in the Minnesota Twin Family Study and included the biological mother and father and their twin offspring. The transmission of a general vulnerability to all the externalizing disorders accounted for the majority of familial resemblance, and this general vulnerability was highly heritable (h2 = 0.80).
In a randomized, controlled experiment, Parker et al (SEE ARTICLE) demonstrate that moderately stressful early experiences strengthen socioemotional and neuroendocrine resistance to subsequent stressors in monkeys. This preclinical model offers opportunities to enhance the prevention of stress-related disorders by elucidating the etiology of stress resistance.
Poor infant health is a major concern in many developing countries, and its determinants are not fully understood. Rahman et al (SEE ARTICLE) studied a community-based cohort of 320 infants from birth to 1 year and found that maternal depression in the antenatal and postnatal periods predicted poorer growth and higher risk of diarrhea in these infants. Because depression in women in developing countries is common, the findings may have public health implications.
