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Proton MRS and Neuropsychological Correlates in AIDS Dementia Complex: Evidence of Subcortical Specificity

Received September 21, 2005; revised May 11, 2006; accepted June 12, 2006. Dr. Paul is affiliated with the Department of Behavioral Neuroscience, University of Missouri, St. Louis, Missouri. Dr. Yiannoutsos is affiliated with the Division of Biostatistics, Department of Medicine, Indiana School of Medicine, Indianapolis, Indiana. Dr. Miller is affiliated with the Department of Psychiatry and Biobehavioral Sciences, UCLA Semel Institute of Neuroscience, Los Angeles, California. Drs. Chang and Ernst are affiliated with the Department of Medicine, John A. Burns School of Medicine, Honolulu, Hawaii. Drs. Marra, Richards, and Jarvik are affiliated with the University of Washington, Seattle, Washington. Dr. Schifitto is affiliated with the University of Rochester Medical Center, Rochester, New York. Dr. Singer is affiliated with the Department of Neurology, UCLA, Los Angeles, California. Drs. Price and Meyerhoff are affiliated with the University of California, San Francisco, California. Dr. Kolson is affiliated with the University of Pennsylvania, Philadelphia, Pennsylvania. Dr. Ellis is affiliated with the Department of Neurology, University of California, San Diego Medical Center, San Diego, California. Dr. Gonzalez is affiliated with the Department of Radiology, Harvard Medical School, Boston, Massachusetts. Drs. Lenkinski and Navia are affiliated with the Departments of Neurology and Psychiatry, Tufts-New England Medical Center and Tufts University Medical School, Boston, Massachusetts. Dr. Cohen is affiliated with the Department of Psychiatry and Human Behavior, Brown Medical School, Providence, Rhode Island. Address correspondence to Dr. Paul, University of Missouri, St. Louis, One University Boulevard, Stadler 412, St. Louis, MO 63121; paulro{at}umsl.edu (e-mail).

Few studies have described the metabolic substrates underlying neuropsychological performance in HIV infection or examined the specificity of these relationships. The authors performed magnetic resonance spectroscopic and neuropsychological evaluations on 61 patients with AIDS dementia complex (stages 1–3) and 39 HIV-positive neurologically asymptomatic individuals. N-acetylaspartate, a marker of mature neurons, choline and myoinositol, both markers of gliosis, and creatine, a reference marker, were measured in the basal ganglia, frontal white matter, and parietal cortex. The neuropsychological evaluation consisted of tests that measured gross and fine motor skills, psychomotor function, information processing speed, and verbal memory. The authors examined performance on individual subtests and an aggregate Z score based on eight subtests (NPZ-8), adjusted for age and education. The NPZ-8 was significantly higher in subjects with greater N-acetylaspartate/creatine in the frontal white matter and was lower in subjects with higher myoinositol/creatine in the basal ganglia. Particularly strong associations were found between measures of gross and fine motor function, which correlated positively with N-acetylaspartate/creatine in the frontal white matter and negatively with myoinositol/creatine in the basal ganglia. Similarly, cognitive processing speed was negatively correlated with myoinositol/creatine in the basal ganglia. In contrast, there were no statistically significant relationships between brain metabolite levels in the parietal cortex and neuropsychological function. This study provides convincing evidence that neuropsychological impairment is associated with reduced markers of mature neurons and increased markers of gliosis in the basal ganglia and frontal white matter. Neural changes as reflected by these metabolite levels may prove useful in identifying individuals at risk for neuropsychological impairment. Prospective studies are needed to elucidate the evolution of these changes in the setting of antiretroviral therapy.

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