Motor Cortical Plasticity in Parkinson’s Disease

Abstract

In Parkinson’s disease (PD), there are alterations of the basal ganglia (BG) thalamocortical networks, primarily due to degeneration of nigrostriatal dopaminergic neurons. These changes in subcortical networks lead to plastic changes in primary motor cortex (M1), which mediates cortical motor output and is a potential target for treatment of PD. Studies investigating the motor cortical plasticity using non-invasive transcranial magnetic stimulation (TMS) have found altered plasticity in PD, but there are inconsistencies among these studies. This is likely because plasticity depends on many factors such as the extent of dopaminergic loss and disease severity, response to dopaminergic replacement therapies, development of l-DOPA-induced dyskinesias (LID), the plasticity protocol used, medication, and stimulation status in patients treated with deep brain stimulation (DBS). The influences of LID and DBS on BG and M1 plasticity have been explored in animal models and in PD patients. In addition, many other factors such age, genetic factors (e.g., brain derived neurotropic factor and other neurotransmitters or receptors polymorphism), emotional state, time of the day, physical fitness have been documented to play role in the extent of plasticity induced by TMS in human studies. In this review, we summarize the studies that investigated M1 plasticity in PD and demonstrate how these afore-mentioned factors affect motor cortical plasticity in PD. We conclude that it is important to consider the clinical, demographic, and technical factors that influence various plasticity protocols while developing these protocols as diagnostic or prognostic tools in PD. We also discuss how the modulation of cortical excitability and the plasticity with these non-invasive brain stimulation techniques facilitate the understanding of the pathophysiology of PD and help design potential therapeutic possibilities in this disorder.

Investigation of Motor Cortical Plasticity and Corticospinal Tract Diffusion Tensor Imaging in Patients with Parkinsons Disease and Essential Tremor

“…The PAS-induced LTP-like MEP increase is thought to serve as a model of heterosynaptic plasticity at the systems level [6, 16]. It was found significantly reduced in PD patients off medication [30].…”

Effects of subthalamic nucleus stimulation on motor cortex plasticity in Parkinson disease

“…[8][9][10][12][13][14] There are several possible mechanisms of how dopamine deficiency leads to reduced motor cortex plasticity in patients with PD who are off medication. [8][9][10][12][13][14] There are several possible mechanisms of how dopamine deficiency leads to reduced motor cortex plasticity in patients with PD who are off medication.…”

Dopamine-dependent changes of cortical excitability induced by transcranial static magnetic field stimulation in Parkinson’s disease

“…12) – whereas only few studies investigated cortical plasticity induced by inhibitory NIBS techniques 13–15 . A key observation is that inhibitory cortical plasticity – induced by continuous theta-burst stimulation (cTBS) – can be observed in treated non-dyskinetic patients after overnight withdrawal of dopaminergic medication (OFF) but is disrupted by acute levodopa administration (ON) 15 .…”