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Clinical physiology of dopa dyskinesia.
Ann Neurol. 2000 Apr; 47(4 Suppl 1):S147-50; discussion S150-3.AN

Abstract

Levodopa-induced dyskinesias are clinically heterogeneous, both in appearance and timing with respect to dose. Electromyogram observations indicate that levodopa-induced dyskinesias are comprised of irregular bursts of either synchronous or asynchronous neuronal firing in antagonist muscles. Studies of the blink reflex and spontaneous blinking have provided useful neurophysiologic information on brainstem function that is sensitive to changes in brain dopamine concentrations. The blink rate is reduced in Parkinson's disease (PD) and increased with dopamine treatment. The blink rate in patients with levodopa-induced dyskinesias, however, has been shown to be faster than that in optimally treated PD patients and normal individuals. These results suggest that dyskinesias are associated with a relative hyperdopaminergic state. However, there appears to be no correlation of dopaminergic benefit to the parkinsonian symptoms, indicating perhaps that there are several dopaminergic systems, including one responsible for motor function and one for dyskinesia. Alternatively, it may be that the pattern of neural firing influences dyskinesias, while the average firing rate may be responsible for motor benefits.

Authors+Show Affiliations

Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1428, USA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

10762142

Citation

Hallett, M. "Clinical Physiology of Dopa Dyskinesia." Annals of Neurology, vol. 47, no. 4 Suppl 1, 2000, pp. S147-50; discussion S150-3.
Hallett M. Clinical physiology of dopa dyskinesia. Ann Neurol. 2000;47(4 Suppl 1):S147-50; discussion S150-3.
Hallett, M. (2000). Clinical physiology of dopa dyskinesia. Annals of Neurology, 47(4 Suppl 1), S147-50; discussion S150-3.
Hallett M. Clinical Physiology of Dopa Dyskinesia. Ann Neurol. 2000;47(4 Suppl 1):S147-50; discussion S150-3. PubMed PMID: 10762142.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clinical physiology of dopa dyskinesia. A1 - Hallett,M, PY - 2000/4/13/pubmed PY - 2000/4/29/medline PY - 2000/4/13/entrez SP - S147-50; discussion S150-3 JF - Annals of neurology JO - Ann Neurol VL - 47 IS - 4 Suppl 1 N2 - Levodopa-induced dyskinesias are clinically heterogeneous, both in appearance and timing with respect to dose. Electromyogram observations indicate that levodopa-induced dyskinesias are comprised of irregular bursts of either synchronous or asynchronous neuronal firing in antagonist muscles. Studies of the blink reflex and spontaneous blinking have provided useful neurophysiologic information on brainstem function that is sensitive to changes in brain dopamine concentrations. The blink rate is reduced in Parkinson's disease (PD) and increased with dopamine treatment. The blink rate in patients with levodopa-induced dyskinesias, however, has been shown to be faster than that in optimally treated PD patients and normal individuals. These results suggest that dyskinesias are associated with a relative hyperdopaminergic state. However, there appears to be no correlation of dopaminergic benefit to the parkinsonian symptoms, indicating perhaps that there are several dopaminergic systems, including one responsible for motor function and one for dyskinesia. Alternatively, it may be that the pattern of neural firing influences dyskinesias, while the average firing rate may be responsible for motor benefits. SN - 0364-5134 UR - https://www.unboundmedicine.com/medline/citation/10762142/Clinical_physiology_of_dopa_dyskinesia_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0364-5134&date=2000&volume=47&issue=4 Suppl 1&spage=S147 DB - PRIME DP - Unbound Medicine ER -