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