This Month in Archives of General Psychiatry FREE

The long-term course of obsessive-compulsive disorder is insufficiently known. Skoog and SkoogArticle report on 144 patients followed up for 47 years from onset. Improvement was observed in 83%, including complete recovery in 20% and sublinical symptoms in 28%. Early age of onset, having both obsessive and compulsive symptoms, low social functioning at baseline, and an early chronic course were correlated with a poorer outcome.

A commentary by Price et al is included.

Using high-resolution magnetic resonance imaging and a large control group, Velakoulis et alArticle have identified bilaterally smaller hippocampi in chronic schizophrenia and first-episode psychosis. Preliminary results suggest that smaller hippocampi are present in both first-episode schizophrenia and affective psychosis. Thus, these changes are present from the onset of psychotic illness.

The planum temporale lies on the superior and posterior surface of the temporal lobe. On the left, it is thought to be a biological substrate of language and has been implicated in schizophrenia. Kwon et alArticle conducted a magnetic resonance imaging study and found that schizophrenic patients, as compared with controls, showed reduced left planum temporale gray matter volume and a consequent reversal of normal planum asymmetry.

Eye tracking dysfunction in schizophrenia has been consistently observed, but not completely understood. Because the brain regions responsible for processing visual motion signals are implicated in smooth pursuit eye movements, Chen et alArticle measured thresholds for detecting differences in target velocity. The thresholds of many schizophrenic patients were up to 10 times higher than those of normal controls, although other aspects of visual perception were preserved. Relative insensitivity to velocity is characteristic of schizophrenia and may be responsible for eye tracking dysfunction.

Velocity judgments are impaired in schizophrenic patients. Chen et alArticle examined how this perceptual deficit is related to abnormal smooth pursuit eye movements among schizophrenic patients by measuring pursuit eye movements to targets that move predictably as well as unpredictably. They found that reduced velocity sensitivity is related to poor initiation and maintenance of smooth pursuit eye movements. Functional impairments in brain centers that regulate velocity sensitivity, such as the middle temporal area, may be components of the abnormal smooth pursuit associated with schizophrenia.

In the first twin study to investigate the full range of psychotic disorders using operational diagnoses, Cardno et alArticle have shown a substantial genetic contribution to schizophrenia, schizoaffective disorder, and mania. The size of the genetic effect was similar across these disorders.

Using a special dietary manipulation, Smith et alArticle found that a sudden decrease in plasma tryptophan caused an acute temporary relapse of bulimia nervosa in women who had suffered from the disorder but who had recovered. Dieting-induced decreases in brain serotonin may be a biological trigger for bulimia in vulnerable individuals.

G proteins play a pivotal role in postreceptor information transduction and have been previously implicated in the pathophysiology of mood disorders. Avissar et alArticle determined immunoreactivities of G subunit proteins by Western blotting of mononuclear leukocyte membranes and report that untreated patients with atypical winter depression showed significantly reduced levels of Gsα and Giα proteins. Remission of the seasonal depressive symptoms following light treatment or during the summer correlated with normalization of G protein levels.

Pfefferbaum et alArticle used magnetic resonance spectroscopic imaging to assess the integrity of cortical gray matter in patients with Alzheimer disease (AD) and healthy elderly and young individuals. Both AD patients and healthy elderly subjects had substantial gray matter volume deficits as compared with healthy young subjects, but only AD patients had reduced gray matter concentrations of n-acetyl compounds, a marker of living neurons. Choline concentration, a possible indicator of cellular degeneration, increased with age and increased even further with AD. These biochemical changes were linked to poorer cognitive function in healthy elderly subjects and AD patients.