ParkinsonCanadaV1, Main, Exploration, bibRecord, 002E28

Short and long latency afferent inhibition in Parkinson’s disease

Identifieur interne : 002E28 ( Main/Exploration ); précédent : 002E27; suivant : 002E29

Short and long latency afferent inhibition in Parkinson’s disease

Auteurs : Alexandra Sailer [Canada, Allemagne] ; Gregory F. Molnar [Canada] ; Guillermo Paradiso [Canada] ; Carolyn A. Gunraj [Canada] ; Anthony E. Lang [Canada] ; Robert Chen [Canada]

Source :

Brain [ 0006-8950 ] ; 2003-08.

RBID : ISTEX:4514548BED7D27D07B6B0DEC184FE95B2F1DDCB8

Descripteurs français

Pascal (Inist)
- Cortex moteur, Homme, Nerf, Parkinson maladie, Stimulation, Stimulus magnétique.
Wicri :
- topic : Homme.

English descriptors

Abstract

Sensory abnormalities have been reported in Parkinson’s disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of ∼20 ms, and long latency afferent inhibition (LAI) at an ISI of ∼200 ms. We studied SAI and LAI in 10 Parkinson’s disease patients with the aim of assessing whether sensorimotor processing is altered in Parkinson’s disease. Patients were studied on and off medication, and the findings were compared with 10 age‐matched controls. Median nerve and middle finger stimulation were delivered 20–600 ms before TMS to the contralateral motor cortex. The motor evoked potentials were recorded from the relaxed first dorsal interosseous (FDI) muscle. SAI was normal in Parkinson’s disease patients off dopaminergic medications, but it was reduced on the more affected side in Parkinson’s disease patients on medication. LAI was reduced in Parkinson’s disease patients compared with controls independent of their medication status. LAI reduced long interval intracortical inhibition in normal subjects but not in Parkinson’s disease patients. The different results for SAI and LAI indicate that it is likely that separate mechanisms mediate these two forms of afferent inhibition. SAI probably represents the direct interaction of a sensory signal with the motor cortex. This pathway is unaffected by Parkinson’s disease but is altered by dopaminergic medication in Parkinson’s disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non‐dopaminergic manifestation of Parkinson’s disease.

Url:

https://api-v5.istex.fr/document/4514548BED7D27D07B6B0DEC184FE95B2F1DDCB8/fulltext/pdf

DOI: 10.1093/brain/awg183

Affiliations:

Allemagne, Canada

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Abbreviations: CS = conditioned stimulus; DNS = digital nerve stimulation; FDI = first dorsal interosseus; ISI = interstimulus interval; LAI = long latency afferent inhibition; LICI = long interval intracortical inhibition; MEP = motor evoked potential; MNS = median nerve stimulation; SAI = short latency afferent inhibition; SEP = somatosensory evoked potential; TMS = transcranial magnetic stimulation; TS = test stimulus; UPDRS = Unified Parkinson’s Disease Rating Scale</term>
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<front><div type="abstract" xml:lang="en">Sensory abnormalities have been reported in Parkinson’s disease and may contribute to the motor deficits. Peripheral sensory stimulation inhibits the motor cortex, and the effects depend on the interstimulus interval (ISI) between the sensory stimulus and transcranial magnetic stimulation (TMS) to the motor cortex. Short latency afferent inhibition (SAI) occurs at an ISI of ∼20 ms, and long latency afferent inhibition (LAI) at an ISI of ∼200 ms. We studied SAI and LAI in 10 Parkinson’s disease patients with the aim of assessing whether sensorimotor processing is altered in Parkinson’s disease. Patients were studied on and off medication, and the findings were compared with 10 age‐matched controls. Median nerve and middle finger stimulation were delivered 20–600 ms before TMS to the contralateral motor cortex. The motor evoked potentials were recorded from the relaxed first dorsal interosseous (FDI) muscle. SAI was normal in Parkinson’s disease patients off dopaminergic medications, but it was reduced on the more affected side in Parkinson’s disease patients on medication. LAI was reduced in Parkinson’s disease patients compared with controls independent of their medication status. LAI reduced long interval intracortical inhibition in normal subjects but not in Parkinson’s disease patients. The different results for SAI and LAI indicate that it is likely that separate mechanisms mediate these two forms of afferent inhibition. SAI probably represents the direct interaction of a sensory signal with the motor cortex. This pathway is unaffected by Parkinson’s disease but is altered by dopaminergic medication in Parkinson’s disease patients and may contribute to the side effects of dopaminergic drugs. LAI probably involves other pathways such as the basal ganglia or cortical association areas. This defective sensorimotor integration may be a non‐dopaminergic manifestation of Parkinson’s disease.</div>
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La maladie de Parkinson au Canada (serveur d'exploration)

Short and long latency afferent inhibition in Parkinson’s disease

Short and long latency afferent inhibition in Parkinson’s disease

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.