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Defective Utilization of Sensory Input as the Basis for Bradykinesia, Rigidity and Decreased Movement Repertoire in Parkinson’s Disease: A Hypothesis
Published online by Cambridge University Press: 18 September 2015
Abstract
From a review of the anatomical relationships and single unit activity in the components of the basal ganglia related to limb movement, it is concluded that the major outflow from basal ganglia circuits is via the motor cortex (area 4). Recent results of recording from area 4 neurons revealed that they preferentially “encode” the higher derivatives of movement, i.e. acceleration and jerk. In the parkinsonian (PK) patient and in the monkeys treated with l-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), EMG responses to imposed loads show a markedly increased gain of the “M2” component which depends upon the integrity of area 4 and which correlates with the severity of PK rigidity.
The above observations are considered, along with those of others (demonstrating prolonged movement times, a decreased “repertoire” of voluntary movements fractionation of voluntary movements’, inability in tracking movements without visual input, and failure to improve performance in PK’s) in relation to a model of the interactions between sensory input and motor programs. Using this model, it is hypothesized that the above PK movement deficits, as well as rigidity, can be accounted for by abnormal processing of the mechanoreceptor sensory input utilized in the generation and execution of movements. The MPTP treated monkey is suggested as a model in which to directly test the hypothesis.
- Type
- 2. Physiology of the Basal Ganglia and Pathophysiology of Parkinson’s Disease
- Information
- Canadian Journal of Neurological Sciences , Volume 11 , Issue S1: Current Concepts and Controversies in Parkinson’s Disease , February 1984 , pp. 136 - 143
- Copyright
- Copyright © Canadian Neurological Sciences Federation 1984
References
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