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.
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-positivepatients, 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-positivepatients 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.
Authors: April D Thames; Philip Sayegh; Kevin Terashima; Jessica M Foley; Andrew Cho; Alyssa Arentoft; Charles H Hinkin; Susan Y Bookheimer Journal: Neurobiol Dis Date: 2015-10-17 Impact factor: 5.996
Authors: Talia M Nir; Neda Jahanshad; Christopher R K Ching; Ronald A Cohen; Jaroslaw Harezlak; Giovanni Schifitto; Hei Y Lam; Xue Hua; Jianhui Zhong; Tong Zhu; Michael J Taylor; Thomas B Campbell; Eric S Daar; Elyse J Singer; Jeffry R Alger; Paul M Thompson; Bradford A Navia Journal: J Neurovirol Date: 2019-02-14 Impact factor: 2.643
Authors: Ase B Andersen; Ian Law; Karen S Krabbe; Helle Bruunsgaard; Sisse R Ostrowski; Henrik Ullum; Liselotte Højgaard; Annemette Lebech; Jan Gerstoft; Andreas Kjaer Journal: J Neuroinflammation Date: 2010-02-14 Impact factor: 8.322
Authors: Mike Sathekge; Ingeborg Goethals; Alex Maes; Christophe van de Wiele Journal: Eur J Nucl Med Mol Imaging Date: 2009-04-07 Impact factor: 9.236