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From the Departments of Neurology (Drs. Chang, Ernst, Leonido-Yee, and Singer) and Radiology (Drs. Ernst and Walot), University of California Los Angeles School of Medicine, Harbor–UCLA Medical Center, Torrance, CA.
Address correspondence and reprint requests to Dr. Linda Chang, Department of Neurology, 1000 W. Carson Street, B-4, Harbor–UCLA Medical Center, Torrance, CA 90509.
OBJECTIVE: To investigate the relation between biochemical alterations and disease severity in HIV–cognitive motor complex (HIV–CMC).
BACKGROUND: HIV–CMC encompasses both the milder form (HIV–minor cognitive motor disorder [HIV–MCMD]) and the more severe form (HIV–dementia). There is no validated marker to monitor disease severity noninvasively.
METHODS: A total of 54 patients with HIV–CMC (20 with HIV–MCMD, 34 with HIV–dementia) and 29 seronegative healthy volunteers were evaluated for cerebral metabolite abnormalities using proton (1H) MRS in the frontal cortex, frontal white matter, and basal ganglia.
RESULTS: The three subject groups showed different concentrations of myoinositol (MI; p = 0.0005) and choline-containing compounds (CHO; p = 0.004) in the frontal white matter. HIV–dementia patients had metabolite changes in all three brain regions whereas HIV–MCMD patients had abnormalities in the frontal white matter only. HIV–CMC patients had elevated MI (p < 0.0001) and CHO (p = 0.004) levels with increasing AIDS dementia complex stage, and N-acetyl compounds (NA) were decreased only in moderate to severe stages of dementia. Furthermore, CD4 count and CSF viral load, but not plasma viral load, showed significant effects on cerebral metabolite concentrations, which in turn showed significant effects on the HIV–dementia scale.
CONCLUSIONS: In early stages of HIV–CMC, frontal white matter showed evidence of glial proliferation (with elevated MI and CHO levels) and cell membrane injury (with increased CHO levels), but no significant neuronal injury (with normal NA concentrations). HIV–MCMD and HIV–dementia patients have different neurochemical abnormalities. Because these biochemical alterations are related to clinical disease severity, they may be useful surrogate markers for noninvasive quantitative assessment of brain injury in patients with HIV–CMC.
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