It is unclear whether depression is a cause or consequence of progressive cognitive decline. Bassuk et al (SEE ARTICLE) assessed the relationship between depressive symptoms and subsequent cognitive performance in a cohort of community-dwelling elderly subjects followed up for 12 years. Depressive symptoms strongly presaged future cognitive losses among respondents evincing mild to moderate cognitive difficulties at baseline but were not associated with onset or rate of decline among initially cognitively intact persons. Because depression seems to be a reaction to rather than a risk factor for cognitive decline, these findings should restrain expectations that treatment for depression will delay dementia onset in elderly patients.
A Commentary by Meyers and Bruce is included.
In a magnetic resonance imaging study of schizophrenic patients, their siblings, and controls, Cannon et al (SEE ARTICLE) found that gray matter reduction in schizophrenia reflects genetic influences that predispose to the disorder (and/or shared environmental factors), while ventricular enlargement reflects primarily nonshared etiologic influences and/or factors secondary to the illness or its treatment.
Verbal memory deficits are common in schizophrenia. However, these deficits have repeatedly been found in the context of generalized cognitive dysfunction, suggesting that they result from a more basic cognitive deficit such as inattention. Wexler et al (SEE ARTICLE) divided patients with schizophrenia into those who passed and those who failed a test of attentional competence. Patients who passed had deficits in verbal memory but performed normally on more difficult nonverbal tests. These results suggest that general performance factors such as motivation, attention, or global memory are not the basis for verbal memory deficits in schizophrenia.
Some patients with schizophrenia have great difficulty remembering words they hear despite having normal attentional skills and normal memory for nonverbal material such as musical tones. Stevens et al (SEE ARTICLE) used functional magnetic resonance imaging to study brain activation in patients with schizophrenia and in healthy controls while they performed word-memory and tone-memory tasks. During the word-memory task, the patients had much lower activity than controls in the left inferior frontal gyrus, a brain region associated with language production.
Our understanding of the neurobiological deficits underlying attention-deficit/hyperactivity disorder (ADHD) is limited. Silberstein et al (SEE ARTICLE) examined the topography of the steady-state visually evoked potentials (SSVEP) in subjects with ADHD and normal control groups of young boys while they performed a visual vigilance task. Normal controls demonstrated significantly reduced SSVEP latency at right prefrontal sites during the task, while subjects with ADHD failed to demonstrate this latency reduction. These findings suggest that ADHD is associated with a reduced capacity to activate the right prefrontal cortex in a vigilance task.
Alcoholics and their offspring have defective brain opioid activity resulting in abnormal reinforcement following ethanol ingestion. Wand et al (SEE ARTICLE) found that, compared with the offspring of non–alcohol-dependent persons, offspring from families with a high density of alcohol-dependent members have increased sensitivity to opioid receptor blockade. These findings lend further support to the contention that children of alcoholics have diminished brain opioid activity.
A review by Schulberg et al (SEE ARTICLE) of recent research conducted with depressed primary care patients determined that antidepressant medications and psychotherapy are equally efficacious with an ambulatory medical population.
Current guidelines for the treatment of depression recommend 4 to 9 months of continuation antidepressant therapy following symptom remission to allow more complete episode resolution. Using Medicaid data, Melfi et al (SEE ARTICLE) found that adherence to these recommendations reduced the likelihood of relapse or recurrence.
In a collaboration between cognitive-behavioral therapists and psychopharmacologists, Heimberg et al (SEE ARTICLE) examined the relative efficacy of the monoamine oxidase inhibitor phenelzine and cognitive-behavioral group therapy for social phobia. Both treatments resulted in response rates superior to pill placebo and attention placebo conditions after 12 weeks of acute treatment, although phenelzine was associated with a faster onset of therapeutic effect and greater anxiety reduction on some measures than group therapy.
