Using functional brain imaging, National Institute of Mental Health scientists for the first time have linked two key, but until now unconnected, brain abnormalities in schizophrenia. They have shown that the less patients' frontal lobes activate during a working memory task, the more the chemical messenger dopamine, thought to underlie the delusions and hallucinations of schizophrenia, rises abnormally in the striatum, a relay station deep in the brain. Together with other evidence, this suggests that the excess dopamine activity that antipsychotic drugs quell may be driven by a defect in the prefrontal cortex, the brain's executive control center. Andreas Meyer-Lindenberg, M.D., and Karen Berman, M.D., report on their PET (positron emission tomography) study, published online January 28, 2002, in Nature Neuroscience.
The most disabling form of mental illness, schizophrenia affects one percent of the adult population, typically in young adulthood, with hallucinations, delusions, social withdrawal, flattened emotions and loss of social and personal care skills. Although the cause of the disorder remains a mystery, studies that shed light on the role of dopamine in schizophrenia hold promise for advancing understanding and, ultimately, improving treatments.
The researchers used two different types of radioactive tracers in the same scanning sessions with 6 patients and 6 healthy controls to simultaneously monitor two different types of brain activity. A radioactive form of oxygen revealed where blood flowed, and hence what parts of the brain were active, during the experimental task. A radioactively-tagged chemical precursor of dopamine indicated activity of this chemical messenger. The PET scanner employs an array of radiation detectors to get a fix on the destinations of the tracers, producing color-coded, quantitative images of the activity being measured.
The scans were taken while patients performed an abstract reasoning / w
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Contact: Jules Asher
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27-Jan-2002