Central motor processing in Huntington's disease a PET study

Repeated PET cerebral blood flow measurements using H2(15)O were performed in 13 patients with confirmed Huntington's disease and nine age-matched controls. The activation paradigm consisted of an externally triggered finger opposition task (1.5 Hz) with the dominant hand, the control condition...

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Bibliographic Details
Published in:Brain (London, England : 1878) England : 1878), 1997-09, Vol.120 (9), p.1553-1567
Main Authors: BARTENSTEIN, P, WEINDL, A, SPIEGEL, S, BOECKER, H, WENZEL, R, CEBALLOS-BAUMANN, A. O, MINOSHIMA, S, CONRAD, B
Format: Article
Language:English
Subjects:
Adult
Aged
Biological and medical sciences
Brain - metabolism
Brain - physiopathology
Cerebrovascular Circulation
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Female
Glucose - metabolism
Humans
Huntington Disease - diagnostic imaging
Huntington Disease - physiopathology
Male
Medical sciences
Middle Aged
Movement - physiology
Neurology
Reference Values
Rest
Tomography, Emission-Computed
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Summary:Repeated PET cerebral blood flow measurements using H2(15)O were performed in 13 patients with confirmed Huntington's disease and nine age-matched controls. The activation paradigm consisted of an externally triggered finger opposition task (1.5 Hz) with the dominant hand, the control condition being the auditory input. In the patients with Huntington's disease, impaired activity of the striatum and its frontal motor projection areas (rostral supplementary motor area, anterior cingulate and premotor cortex) could be demonstrated along with enhanced activity mainly in parietal areas during movement. The results suggest that the pathology of Huntington's disease causes impairment of the output part of the basal ganglia-thalamo-cortical motor circuit and may induce a compensatory recruitment of additional accessory motor pathways involving the parietal cortex.
ISSN:0006-8950
1460-2156
1460-2156
DOI:10.1093/brain/120.9.1553