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Motor cortex plasticity in Parkinson's disease and levodopa-induced dyskinesias.
Brain. 2006 Apr; 129(Pt 4):1059-69.B

Abstract

Experimental models of Parkinson's disease have demonstrated abnormal synaptic plasticity in the corticostriatal system, possibly related to the development of levodopa-induced dyskinesias (LID). We tested the hypothesis that LID in Parkinson's disease is associated with aberrant plasticity in the human motor cortex (M1). We employed the paired associative stimulation (PAS) protocol, an experimental intervention involving transcranial magnetic stimulation (TMS) and median nerve stimulation capable of producing long-term potentiation (LTP) like changes in the sensorimotor system in humans. We studied the more affected side of 16 moderately affected patients with Parkinson's disease (9 dyskinetic, 7 non-dyskinetic) and the dominant side of 9 age-matched healthy controls. Motor-evoked potential (MEP) amplitudes and cortical silent period (CSP) duration were measured at baseline before PAS and for up to 60 min (T0, T30 and T60) after PAS in abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles. PAS significantly increased MEP size in controls (+74.8% of baseline at T30) but not in patients off medication (T30: +0.07% of baseline in the non-dyskinetic, +27% in the dyskinetic group). Levodopa restored the potentiation of MEP amplitudes by PAS in the non-dyskinetic group (T30: +64.9% of baseline MEP) but not in the dyskinetic group (T30: -9.2% of baseline). PAS prolonged CSP duration in controls. There was a trend towards prolongation of CSP in the non-dyskinetic group off medications but not in the dyskinetic group. Levodopa did not restore CSP prolongation by PAS in the dyskinetic group. Our findings suggest that LTP-like plasticity is deficient in Parkinson's disease off medications and is restored by levodopa in non-dyskinetic but not in dyskinetic patients. Abnormal synaptic plasticity in the motor cortex may play a role in the development of LID.

Authors+Show Affiliations

Division of Neurology and Toronto Western Research Institute, University Health Network, University of Toronto, Toronto, Ontario, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16476674

Citation

Morgante, Francesca, et al. "Motor Cortex Plasticity in Parkinson's Disease and Levodopa-induced Dyskinesias." Brain : a Journal of Neurology, vol. 129, no. Pt 4, 2006, pp. 1059-69.
Morgante F, Espay AJ, Gunraj C, et al. Motor cortex plasticity in Parkinson's disease and levodopa-induced dyskinesias. Brain. 2006;129(Pt 4):1059-69.
Morgante, F., Espay, A. J., Gunraj, C., Lang, A. E., & Chen, R. (2006). Motor cortex plasticity in Parkinson's disease and levodopa-induced dyskinesias. Brain : a Journal of Neurology, 129(Pt 4), 1059-69.
Morgante F, et al. Motor Cortex Plasticity in Parkinson's Disease and Levodopa-induced Dyskinesias. Brain. 2006;129(Pt 4):1059-69. PubMed PMID: 16476674.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Motor cortex plasticity in Parkinson's disease and levodopa-induced dyskinesias. AU - Morgante,Francesca, AU - Espay,Alberto J, AU - Gunraj,Carolyn, AU - Lang,Anthony E, AU - Chen,Robert, Y1 - 2006/02/13/ PY - 2006/2/16/pubmed PY - 2006/4/18/medline PY - 2006/2/16/entrez SP - 1059 EP - 69 JF - Brain : a journal of neurology JO - Brain VL - 129 IS - Pt 4 N2 - Experimental models of Parkinson's disease have demonstrated abnormal synaptic plasticity in the corticostriatal system, possibly related to the development of levodopa-induced dyskinesias (LID). We tested the hypothesis that LID in Parkinson's disease is associated with aberrant plasticity in the human motor cortex (M1). We employed the paired associative stimulation (PAS) protocol, an experimental intervention involving transcranial magnetic stimulation (TMS) and median nerve stimulation capable of producing long-term potentiation (LTP) like changes in the sensorimotor system in humans. We studied the more affected side of 16 moderately affected patients with Parkinson's disease (9 dyskinetic, 7 non-dyskinetic) and the dominant side of 9 age-matched healthy controls. Motor-evoked potential (MEP) amplitudes and cortical silent period (CSP) duration were measured at baseline before PAS and for up to 60 min (T0, T30 and T60) after PAS in abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles. PAS significantly increased MEP size in controls (+74.8% of baseline at T30) but not in patients off medication (T30: +0.07% of baseline in the non-dyskinetic, +27% in the dyskinetic group). Levodopa restored the potentiation of MEP amplitudes by PAS in the non-dyskinetic group (T30: +64.9% of baseline MEP) but not in the dyskinetic group (T30: -9.2% of baseline). PAS prolonged CSP duration in controls. There was a trend towards prolongation of CSP in the non-dyskinetic group off medications but not in the dyskinetic group. Levodopa did not restore CSP prolongation by PAS in the dyskinetic group. Our findings suggest that LTP-like plasticity is deficient in Parkinson's disease off medications and is restored by levodopa in non-dyskinetic but not in dyskinetic patients. Abnormal synaptic plasticity in the motor cortex may play a role in the development of LID. SN - 1460-2156 UR - https://www.unboundmedicine.com/medline/citation/16476674/Motor_cortex_plasticity_in_Parkinson's_disease_and_levodopa_induced_dyskinesias_ L2 - https://academic.oup.com/brain/article-lookup/doi/10.1093/brain/awl031 DB - PRIME DP - Unbound Medicine ER -