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Electrophysiologic and Positron Emission Tomography Findings

Hans-Jürgen von Giesen, MD; Christina Antke, MD; Harald Hefter, MD, PhD; Frank Wenserski, MD; Rüdiger J. Seitz, MD; Gabriele Arendt, MD

Arch Neurol. 2000;57:1601-1607.

Background  We tested whether metabolic abnormalities in the prefrontal-striatal circuitry as demonstrated by positron emission tomography (PET) were present in patients seropositive for human immunodeficiency virus type 1 (HIV-1) with HIV-1–associated minor motor deficits as demonstrated by quantitative motor testing.

Patients  We examined 19 HIV-1–positive patients, covering the range from normal results of quantitative motor testing to clearly pathologic psychomotor slowing indicative of HIV-1–associated minor motor deficits. None fulfilled the clinical criteria for HIV-1–associated dementia. Results were compared with those of 15 healthy volunteers.

Methods  All subjects underwent clinical examination, routine magnetic resonance (MR) imaging, and electrophysiologic motor testing at the time of PET.

Results  Seven HIV-1–positive patients showed significant hypermetabolism in the basal ganglia. Nine patients showed a significant frontomesial hypometabolism.

Conclusions  The data of our cross-sectional study strongly suggest a characteristic time course in the development of HIV-1–associated minor motor deficits. Hypermetabolism in the basal ganglia is associated initially with normal motor performance. Moderate motor slowing appears at a later stage when basal ganglia hypermetabolism drops toward hypometabolism. More severe functional deficits and highly pathologic motor slowing become manifest when hypometabolism is most widespread in the basal ganglia. This stage leads to dementia.

From the Departments of Neurology (Drs von Giesen, Antke, Hefter, Seitz, and Arendt) and Diagnostic Radiology (Dr Wenserski), Heinrich-Heine-University, Düsseldorf, Germany.

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