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Am J Psychiatry 2004;161:A74-A74. doi:10.1176/appi.ajp.161.7.A74

Hint: money doesn’t hurt. The stimulant methylphenidate increased brain levels of dopamine, a neurotransmitter involved in motivation, in healthy people performing a mathematical task rewarded by money. Volkow et al. (p. 1173) found, however, that dopamine did not increase when the participants viewed scenic pictures or when they worked the math problems without methylphenidate, even though dopamine is sensitive to environmental stimulation. This interaction of methylphenidate and the math task suggests that methylphenidate amplifies the intrinsic cognitive salience of the activity. The subjects were more likely to describe the task as "interesting" or "exciting" after methylphenidate administration than after placebo, and these ratings correlated with the dopamine changes. Methylphenidate may increase attention by enhancing the saliency of the task and thus increasing the interest it elicits. Nonpharmacological ways of increasing salience—for instance, making schoolwork more interesting—might be worth a try.

Nutritional deficiency, liver dysfunction, and abnormal brain structure are common among alcoholics. Whether these conditions are related to each other and to long-term abstinence was evaluated by Pfefferbaum et al. (p. 1190). Men with chronic alcoholism in an inpatient treatment program had abnormal red blood cell and liver enzyme values after 1 week of sobriety. Red blood cell count, hemoglobin, and hematocrit correlated with the brain volumes of white matter and lateral ventricles, but liver function was not related to brain volume. At discharge, after 3 additional weeks of abstinence, the blood and ventricular volume measurements improved. These discharge values for red blood cell count, hemoglobin, and hematocrit were higher in the 17 men who stayed sober during the following 2–12 months than in the 22 men who relapsed. Hematological measures may help in identifying mechanisms of relapse and developing pharmacological treatments for alcoholism.

Many people try cigarettes but do not become smokers. Figuring out who does is especially important in adolescence, when the habit often begins. Genetic variations in dopamine transmission can enhance nicotine’s physiological reward. Depression also contributes to adolescent smoking. Audrain-McGovern et al. (p. 1224) examined the influences of depression and two dopamine-related genes on the progression of smoking between grades 9 and 11. Among students who had already taken at least one puff, the number of SLC6A3 10-repeat alleles did not affect smoking progression. However, each A1 allele of the gene for the dopamine 2 receptor, DRD2, nearly doubled the odds of progressing to either greater experimentation or current smoking. Depressive symptoms magnified this effect. These findings suggest that identifying adolescents with depressive symptoms and providing rewarding alternatives to smoking may improve mood and reduce the likelihood of smoking.

The dysfunctional brain activity in patients with eating disorders could be a response to food specifically or to all emotionally salient stimuli. Uher et al. (p. 1238) compared brain activation in women with anorexia nervosa, women with bulimia nervosa, and healthy women as they viewed photographs of food, emotionally aversive photographs of nonfood items, and neutral photographs. Responses specific to the food pictures differed between each group of women with eating disorders and the healthy women in the medial orbitofrontal cortex and anterior cingulate. Anorexia nervosa and bulimia nervosa differed from each other in activation of the lateral and anterior prefrontal cortex. The orbitofrontal cortex and anterior cingulate are a convergence zone for processing of emotional information and are implicated in obsessive-compulsive and mood disorders. These diagnoses often occur alongside eating disorders in patients and families, pointing to common neural mechanisms.

Brain damage involving the prefrontal cortex, particularly the region above the eyes (orbitofrontal cortex), often produces dramatic behavioral changes that lead to social problems. What is the mechanism for this aberrant behavior? Mah et al. (p. 1247) examined social perception—the ability to interpret social interactions from nonverbal cues. When asked questions about interpersonal relations in videotapes of real-life interactions, patients with orbitofrontal lesions scored lower than healthy subjects. However, so did subjects with lesions in dorsolateral regions of the prefrontal cortex. Also, greater dorsolateral damage correlated with worse overall performance and poorer detection of lies. These findings demonstrate disruption of fundamental social processes in patients with prefrontal damage and cast a new light on the dorsolateral prefrontal cortex, which traditionally has been associated with higher, nonsocial cognitive functions.F1

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