Potential time course of human immunodeficiency virus type 1-associated minor motor deficits - Electrophysiologic and positron emission tomography findings

Citation
Hj. Von Giesen et al., Potential time course of human immunodeficiency virus type 1-associated minor motor deficits - Electrophysiologic and positron emission tomography findings, ARCH NEUROL, 57(11), 2000, pp. 1601-1607
Citations number
39
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ARCHIVES OF NEUROLOGY
ISSN journal
00039942 → ACNP
Volume
57
Issue
11
Year of publication
2000
Pages
1601 - 1607
Database
ISI
SICI code
0003-9942(200011)57:11<1601:PTCOHI>2.0.ZU;2-S
Abstract
Background: We tested whether metabolic abnormalities in the prefrontal-str iatal circuitry as demonstrated by positron emission tomography (PET) were present in patients seropositive for human immunodeficiency virus type 1 (H IV-1) with HIV-1-associated minor motor deficits as demonstrated by quantit ative motor testing. Patients: We examined 19 HIV-1-positive patients, covering the range from n ormal results of quantitative motor testing to clearly pathologic psychomot or slowing indicative of HIV-1-associated minor motor deficits. None fulfil led the clinical criteria for HIV-1-associated dementia. Results were compa red with those of 15 healthy volunteers. Methods: All subjects underwent clinical examination, routine magnetic reso nance (MR) imaging, and electrophysiologic motor testing at the time of PET . Results: Seven HIV-1-positive patients showed significant hypermetabolism i n the basal ganglia. Nine patients showed a significant frontomesial hypome tabolism. Conclusions: The data of our cross-sectional study strongly suggest a chara cteristic time course in the development of HIV-1-associated minor motor de ficits. Hypermetabolism in the basal ganglia is associated initially with n ormal motor performance. Moderate motor slowing appears at a later stage wh en basal ganglia hypermetabolism drops toward hypometabolism. More severe f unctional deficits and highly pathologic motor slowing become manifest when hypometabolism is most widespread in the basal ganglia. This stage leads t o dementia.