In This Issue

Consumption of alcohol during pregnancy is a known risk factor for nervous system dysfunction in the offspring. In utero exposure of animals to nicotine, caffeine, ethanol, or stress has been related to neurobehavioral changes similar to symptoms of attention deficit hyperactivity disorder (ADHD). Whether prenatal exposure to these four conditions increases the risk of ADHD in humans was the subject of a literature review by Linnet et al. (p. 1028). The evidence is strongest for a connection between ADHD and prenatal smoking. Most studies indicated that prenatal smoking by the mother is associated with inattention and hyperactivity in the children, but few showed a dose-response effect. Unfortunately, the number and/or quality of studies on the other lifestyle issues preclude conclusions. The prevalence and long-lasting effects of ADHD, however, make a strong case for further high-quality investigations.

More than 50 years after the Holocaust, questions still remain about its long-term effects on children who survived. Also, have the survivors “passed on” the trauma to their offspring? Sagi-Schwartz et al. (p. 1086) studied attachment and trauma-related issues by matching Holocaust survivors with comparison subjects and by including three generations in 98 families. The Holocaust survivors immigrated to Israel as children after losing both parents during the Holocaust. At approximately age 65, these women suffered from more unresolved loss and from more anxiety and posttraumatic stress reactions than the comparison women, who had migrated from Europe to Israel before the war began. General adaptation did not suffer, however, and daughters of the two groups did not differ. Holocaust survivors may have been able to protect their daughters from their war experiences, although they themselves still suffer from the effects of the Holocaust. Early attachment may have been preserved by the survivors’ experience of several years of normal family life before the Holocaust and by imposition of the trauma from outside the family unit.

The neurotransmitter glutamate has repeatedly been tied to schizophrenia. Recently, structural evaluations have focused on the thalamus, which is critical to cognitive and emotional functioning. One abnormal aspect of glutamatergic functioning in the thalamus involves the NR₁ subunit of the N-methyl-d-aspartic acid (NMDA) receptor. Clinton et al. (p. 1100) further refined the search by examining three forms of the NR₁ subunit in the thalamus of deceased patients with schizophrenia. One type, expressed in DNA transcripts containing exon 22, was less abundant in the patients than in individuals without psychiatric illness. The measurements also included a set of intracellular molecules that modulate NMDA receptor activity and participate in signal transduction. Three of these proteins were expressed at higher levels in the schizophrenia group. Thus, glutamatergic abnormalities may involve not only glutamatergic neuroreceptors but also intracellular pathways involved in receptor signaling.

Depression and serious depressive symptoms are common among the elderly. Few cases are detected, and even with treatment the prognosis is only modest. The results include personal suffering, decline in functioning, greater use of medical services, and higher health care costs. As a step toward preventing depression in the elderly, Cole and Dendukuri (p. 1147) systematically reviewed studies of factors associated with new cases of depression over a median of 24 months. Twenty studies of elderly subjects in the community covered 43 variables. Meta-analysis identified five characteristics significantly associated with the onset of depression: bereavement, sleep disturbance, disability, prior depression, and female gender. Specific techniques are available for managing the first three conditions. On a larger scale, the five factors together can help identify elderly people at high risk of depression and guide population-based interventions.

After a stroke, cognitive problems are common and may be compounded by the depression that can accompany a stroke. Treatment of the depression often improves cognitive functioning as well, but for how long? To answer this question, Narushima et al. (p. 1157) reassessed depressed stroke patients 21 months after successful treatment of their depression. Both cognition and depression had improved during 3 months of antidepressant treatment, and they remained steady throughout the rest of the study. For nondepressed stroke patients, cognitive ability remained stable for the entire study period. At 2 years, the depressed and nondepressed groups had scores on the Mini-Mental State Examination that were nearly identical but were lower than the population-based norm. Since even nondepressed stroke patients suffer a cognitive decline, it is especially important to treat poststroke depression, which adds to cognitive dysfunction.

Images in Psychiatry (p. 1060)