Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus

doi:10.1017/CBO9780511544873.019

18 - Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus

from Part I - Basic aspects of neurodegeneration

Published online by Cambridge University Press: 04 August 2010

Anthony E. Lang and

Rocco Agostino and

M. Flint Beal: Affiliation:
Cornell University, New York
Anthony E. Lang: Affiliation:
University of Toronto
Albert C. Ludolph: Affiliation:
Universität Ulm, Germany
Antonio Currà: Affiliation:
Department of Neurological Sciences and I.N.M. Neuromed IRCCS, University of Rome “La Sapienza”, Italy
Rocco Agostino: Affiliation:
Department of Neurological Sciences and I.N.M. Neuromed IRCCS, University of Rome “La Sapienza”, Italy
Alfredo Berardelli: Affiliation:
Department of Neurological Sciences and I.N.M. Neuromed IRCCS, University of Rome “La Sapienza”, Italy

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Summary

Introduction

Movement disorders are a disease group related to functional or structural abnormalities of the basal ganglia.

The term “basal ganglia” refers to the following structures: the striatum (caudate and putamen), globus pallidus (internal and external segments, GPi and GPe), subthalamic nucleus, and substantia nigra (SN) (SN pars compacta, SNpc, and SN pars reticulata, SNpr). The striatum receives connections from specific cortical areas and from the SNpc; the basal ganglia output nuclei, the GPi and SNpr, exert an inhibitory effect on the thalamus. Diminished phasic activity in the GPi/SNpr disinhibits the thalamus thus facilitating cortical motor areas, whereas increased phasic activity in the GPi/SNpr causes the opposite effect. The GPi–SNpr inhibition of the thalamus is modulated through two parallel pathways. According to the classical model of basal ganglia functioning (Albin et al., 1989; Alexander & Crutcher, 1990; Alexander et al., 1990; De Long, 1990; Parent & Hazarati, 1995; Wichmann & De Long, 1996) the first is an inhibitory “direct” pathway that originates in the striatum and projects directly onto the GPi/SNr; the second is an “indirect” inhibitory pathway that crosses the GPe and subthalamic nucleus to project indirectly onto the GPi/SNpr. Activation of the direct pathway tends to disinhibit the thalamus. Activation of the indirect pathway disinhibits the subthalamic nucleus thereby increasing GPi/SNpr excitation thus resulting in increased thalamic inhibition: the two parallel circuits have an opposing action on the GPi/SNr and hence on the thalamus.

Type: Chapter
Information: Neurodegenerative Diseases
Neurobiology, Pathogenesis and Therapeutics
, pp. 227 - 250

DOI: https://doi.org/10.1017/CBO9780511544873.019 [Opens in a new window]

Publisher: Cambridge University Press

Print publication year: 2005

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