Schizophrenia is as mysterious as it is devastating. No one knows just what happens within the brain to cause the disease’s characteristic hallucinations, delusions and cognitive deficits. Now researchers have identified a small region in the hippocampus where an early increase in activity—before symptoms become marked—might represent the beginning of the disease process. The results could lead to new targets for drug treatment and new ideas for strategies to prevent the disease.
Schizophrenia is often preceded by a “prodromal” phase, when individuals begin to exhibit symptoms but fall short of the criteria for a psychiatric diagnosis. They might, for instance, withdraw socially, or hear their names in the sound of the wind rather than an outright hallucination. Some studies suggest that treatment—including medication—during these early stages may delay the onset of full schizophrenia, reduce its severity or prevent it altogether.
But not all prodromal individuals go on to develop the disease—just 35 percent within 2.5 years, says Thomas McGlashan, a professor of psychiatry at Yale University who works with such patients. In the face of this uncertainty, most clinicians believe the risks of side effects from treatment outweigh potential benefits and have adopted a conservative wait-and-see approach. “For the ‘false positives,’ which might be the majority, you’d be unnecessarily giving powerful agents that can have severe side effects,” McGlashan says.
To investigate why the prodromal phase progresses to schizophrenia in only one out of three patients, researchers from Columbia University used a high-resolution variant of functional magnetic resonance imaging (fMRI) to compare the brains of 18 people with established schizophrenia with 18 healthy controls. In the disease group, they found increased blood flow, suggesting higher levels of activity, in the orbitofrontal cortex and in a small section—the CA1 subfield—of the hippocampus. In the dorsolateral prefrontal cortex, meanwhile, blood flow decreased.
Reported by Carl Sherman
The DANA Foundation
September 2009 issue of Archives of General Psychiatry
Submitted by Anna