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

Antonio Currà, Rocco Agostino, Alfredo Berardelli

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

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.

Original languageEnglish
Title of host publicationNeurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics
PublisherCambridge University Press
Pages227-250
Number of pages24
ISBN (Print)9780511544873, 052181166X, 9780521811668
DOIs
Publication statusPublished - Jan 1 2005

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Neurophysiology
Myoclonus
Dystonia
Huntington Disease
Dyskinesias
Levodopa
Thalamus
Parkinson Disease
Basal Ganglia
Subthalamic Nucleus
Globus Pallidus
Putamen
Movement Disorders
Motor Cortex
Substantia Nigra

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Currà, A., Agostino, R., & Berardelli, A. (2005). Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus. In Neurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics (pp. 227-250). Cambridge University Press. https://doi.org/10.1017/CBO9780511544873.019

Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus. / Currà, Antonio; Agostino, Rocco; Berardelli, Alfredo.

Neurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics. Cambridge University Press, 2005. p. 227-250.

Research output: Chapter in Book/Report/Conference proceedingChapter

Currà, A, Agostino, R & Berardelli, A 2005, Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus. in Neurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics. Cambridge University Press, pp. 227-250. https://doi.org/10.1017/CBO9780511544873.019
Currà A, Agostino R, Berardelli A. Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus. In Neurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics. Cambridge University Press. 2005. p. 227-250 https://doi.org/10.1017/CBO9780511544873.019
Currà, Antonio ; Agostino, Rocco ; Berardelli, Alfredo. / Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus. Neurodegenerative Diseases: Neurobiology, Pathogenesis and Therapeutics. Cambridge University Press, 2005. pp. 227-250
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