ABNORMAL BASAL GANGLIA OUTFLOW IN PARKINSONS-DISEASE IDENTIFIED WITH PET - IMPLICATIONS FOR HIGHER CORTICAL FUNCTIONS

Citation
Am. Owen et al., ABNORMAL BASAL GANGLIA OUTFLOW IN PARKINSONS-DISEASE IDENTIFIED WITH PET - IMPLICATIONS FOR HIGHER CORTICAL FUNCTIONS, Brain, 121, 1998, pp. 949-965
Citations number
69
Categorie Soggetti
Neurosciences,"Clinical Neurology
Journal title
BrainACNP
ISSN journal
00068950
Volume
121
Year of publication
1998
Part
5
Pages
949 - 965
Database
ISI
SICI code
0006-8950(1998)121:<949:ABGOIP>2.0.ZU;2-7
Abstract
In this study we examined the effects of striatal dopamine depletion o n cortical and subcortical blood flow changes during two tasks known t o involve frontostriatal circuitry. Regional cerebral blood how was me asured in six patients with moderate Parkinson's disease and in six ag e-matched control subjects while they performed easy and difficult ver sions of a modified Tower of London planning task and a mnemonic varia nt of this task that required shortterm retention and reproduction of problem solutions, as well as a control condition that involved identi cal visual stimuli and motor responses. Relative to control conditions , the planning task was associated with an increase in cerebral blood flow centred on the internal segment of the right globus pallidus in t he age-matched control subjects, and a decrease in the same region in the patients with Parkinson's disease. A similar inverse relationship between the task-specific blood flow change observed in the control gr oup and that observed in the Parkinson's disease patients was not foun d in any other subcortical or cortical area examined, including region s of the dorsolateral frontal cortex known to be involved in this task . When blood flow in the spatial working memory task was examined, a s imilarly specific dissociation between the two groups of subjects was observed at similar coordinates in the right pallidum. We conclude tha t striatal dopamine depletion disrupts the normal pattern of basal gan glia outflow in Parkinson's disease and consequently, affects the expr ession of frontal-lobe functions by interupting normal transmission of information through frontostriatal circuitry.