Parkinsonism and Epilepsy

  • Tamas L. Frigyesi
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 90)


Clinical observations indicate that parkinsonians do not, or only exceptionally, exhibit epileptic phenomena and vice versa (Scholz, 1957; Klee, 1975). Yakovlev reported (1928) that when epileptic patients develop parkinsonism, the epilepsy pari passu disappears. The exact neurophysiological mechanisms underlying these pathological conditions are poorly understood. Yet, it is apparent, that both of these diseases dominantly involve the sensorimotor system. Thus the question appears to be of more than heuristic importance as to why these two disease states are mutu ally exclusive. Whereas epilepsy readily lends itself to experimental approaches in the domain of electrophysiology, parkinsonism does not, because only its morphological and biochemical features but not its clinical symptomatology can be reproduced in experimental animals. The normal integration of sensorimotor activities, and the electrophysiological consequences of caudatal and nigral damage (established sites of pathology in parkinsonism) to such integrative processes, have extensively been explored in felines and subhuman primates (Fvigyesi, 1975a, 1975b); these studies yielded data which, when extrapolated to parkinsonism, suggested the nature of elementary processes which underlie, at least some symptoms of, parkinsonism (Frigyesi, 1971; Frigyesi, et al., 1974).


Motor Cortex Lower Trace Proprioceptive Feedback Thalamic Neuron Spike Discharge 
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Copyright information

© Plenum Press, New York 1977

Authors and Affiliations

  • Tamas L. Frigyesi
    • 1
  1. 1.Department of PhysiologyTexas Tech University School of MedicineLubbockUSA

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