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Basal Ganglia Metabolite Abnormalities in Minor Motor Disorders Associated With Human Immunodeficiency Virus Type 1
Hans-Jürgen von Giesen, MD;
Hans-Jörg Wittsack, PhD;
Frank Wenserski, MD;
Hubertus Köller, MD;
Harald Hefter, MD, PhD;
Gabriele Arendt, MD
Arch Neurol. 2001;58:1281-1286.
Background Minor motor disorders (MMDs) associated with human immunodeficiency virus type 1 (HIV-1) predict HIV-1 dementia and death. Little is known about the time course and neuropathologic mechanisms of HIV-1 MMDs.
Objective To investigate the relationship between HIV-1 MMDs, as assessed by psychomotor speed, and metabolic alterations in the basal ganglia, as detected by proton magnetic resonance spectroscopy.
Patients and Methods A total of 32 HIV-1–seropositive patients (10 with no MMD, 8 with incipient MMD, and 14 with sustained MMD, assessed through electrophysiologic testing of psychomotor speed including contraction times; 29 treated with highly active antiretroviral therapy) and 14 HIV-1–seronegative control subjects were examined for cerebral metabolite abnormalities in the basal ganglia by means of magnetic resonance spectroscopy.
Results The 3 patient groups showed significantly different ratios of myoinositol/creatine (P = .02) in the basal ganglia. Whereas patients with no MMD or incipient MMD showed normal ratios, patients with sustained MMD showed higher values for myoinositol/creatine as a sign of glial proliferation. No differences in N-acetyl compounds, indicative of neuronal loss, were found.
Conclusion Whereas metabolic alterations in the basal ganglia were not detected in patients with incipient HIV-1 MMD, patients with sustained HIV-1 MMD did have significantly altered metabolic spectra indicative of glial proliferation.
From the Departments of Neurology (Drs von Giesen, Köller, Hefter, and Arendt) and Diagnostic Radiology (Drs Wittsack and Wenserski), Heinrich Heine University, Düsseldorf, Germany.
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