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Research article summary (published 30 Dec 2002):

The physiological basis of clinical deficits in Parkinson's disease.

Full Abstract

Despite the fact that Parkinson's disease (PD) is a relatively common neurological condition, the physiological derangements that result in its clinical features remain unclear. On combining findings from psychophysical, clinical and electrophysiological studies, an overriding theme is proposed that PD deficits are essentially quantitative rather than qualitative in nature. This may arise because the normal function of the basal ganglia is to activate neural processes selectively, providing appropriate diversion of "attentional" resources for decision-making aspects of motor tasks and appropriate "energising" of the executive aspects of such tasks. It is suggested that these concepts of attention, an idea stemming from psychophysical studies, and of energisation, which has derived from kinematic studies, may in fact reflect the same universal process of selective facilitation of particular processes and inhibition of others. In PD, without efficient facilitation, tasks may still be performed but less well than in normal individuals. Possible underlying mechanisms of basal ganglial function are discussed in the context of new findings on direct and indirect pathway actions and the role that oscillatory modulations may play in achieving selective facilitation is explored. Further investigation of disturbances of such mechanisms in PD may prove important in understanding the underlying pathophysiology of the condition.

 

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Author information

Author/s: McAuley, J H (JH);

Affiliation: Department of Neurology, Royal London Hospital, Whitechapel, London E1 1BB, UK. jhmcauley(-atsign-)clara.co.uk

Journal and publication information

Publication Type: Journal Article; Review

Journal: Progress in neurobiology (Prog Neurobiol), published in England. (Language: eng)

Reference: 2003-Jan; vol 69 (issue 1) : pp 27-48

Dates: Created 2003/03/14; Completed 2003/07/25; Revised 2005/11/16;

PMID: 12637171, status: MEDLINE (last retrieval date: 12/26/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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