In This Issue

Emotion-related hypoactivation in the brains of patients with schizophrenia is more nuanced than previously indicated. Patients studied by Ursu et al. (p. 276) had normal responses to facial expressions across the frontal cortex, basal ganglia, and amygdala. But when they were asked to recall the information after a delay (figure), they had decreased activation of the dorsolateral prefrontal cortex relative to comparison subjects. Patients accurately detected emotion expressions in others, but their memory of the emotion became disrupted, often because of the introduction of negative feelings even when their initial perception was positive. Gold's editorial (p. 237) suggests the need for compensatory cognitive strategies directed to this deficiency in emotional memory. Pinkham et al. (CME, p. 293) also found that persons with schizophrenia are able to discern emotions, even when a person is not looking directly at them, but they are generally hyporesponsive, particularly to anger and threat. They point out that diminished response to threat, typical of paranoid patients, suggests that they have difficulty in discriminating what is truly threatening.

Treatment of alcoholism with ondansetron in patients who have particular variants of two DNA sequences (“polymorphisms”) in the serotonin transporter gene was more effective than in patients with other genotypes. Ondansetron, a 5-HT₃ receptor antagonist, was effective only in patients with the LL promoter variant in the study by Johnson et al. (p. 265). Perlis in an editorial (p. 234) points out that this study is the first major clinical trial to assign patients to treatments based on genotype and thus is an important first step in genomic medicine for a psychiatric illness, a strategy that has been very effective for cancer chemotherapy.