Author/Editor		Kojović, Maja; Bologna, Matteo; Kassavetis, Panagiotis; Murase, N.; Palomar, FJ; Berardelli, A.; Rothwell, John C.; Edwards, Mark J.; Bhatia, Kailash P.
Title		Functional reorganization of sensorimotor cortex in early Parkinson disease
Type		članek
Vol. and No.		Letnik 78, št. 18
Publication year		2012
Volume		str. 1441-1448
ISSN		0028-3878 - Neurology
Language		eng
Abstract		OBJECTIVE: Compensatory reorganization of the nigrostriatal system is thought to delay the onset of symptoms in early Parkinson disease (PD). Here we sought evidence that compensation may be a part of a more widespread functional reorganization in sensorimotor networks, including primary motor cortex. METHODS: Several neurophysiologic measures known to be abnormal in the motor cortex (M1) of patients with advanced PD were tested on the more and less affected side of 16 newly diagnosed and drug-naive patients with PD and compared with 16 age-matched healthy participants. LTP-like effects were probed using a paired associative stimulation protocol. We also measured short interval intracortical inhibition, intracortical facilitation, cortical silent period, and input/output curves. RESULTS: The less affected side in patients with PD had preserved intracortical inhibition and a larger response to the plasticity protocol compared to healthy participants. On the more affected side, there was no response to the plasticity protocol and inhibition was reduced. There was no difference in input/output curves between sides or between patients with PD and healthy participants. CONCLUSIONS: Increased motor cortical plasticity on the less affected side is consistent with a functional reorganization of sensorimotor cortex and may represent a compensatory change that contributes to delaying onset of clinical symptoms. Alternatively, it may reflect a maladaptive plasticity that provokes symptom onset. Plasticity deteriorates as the symptoms progress, as seen on the more affected side. The rate of change in paired associative stimulation response over time could be developed into a surrogate marker of disease progression in PD.