The role of motor cortex in the pathophysiology of voluntary movement deficits associated with parkinsonism.
The characteristic motor deficits of parkinsonism result from dysfunction of the nigrostriatal dopaminergic system of the basal ganglia. These subcortical deficits must ultimately be expressed at the cortical and spinal motoneuron levels to result in the difficulty with initiation and execution of movements seen in parkinsonism. This article describes the neuronal activity of two motor cortical regions, the primary motor cortex (MI) and supplementary motor area (SMA), which receive the majority of basal ganglia outputs related to movement control through the ventral lateral thalamus. The kinematics and electromyographic characteristics of stimulus-initiated and self-initiated normal and parkinsonian movements are described, and the possible relation of SMA and MI task-related neuronal activity to the parkinsonian movement deficits is reviewed.
Watts
R L
RL
Department of Neurology, Emory University School of Medicine, Atlanta, Georgia.
Mandir
A S
AS
D000818:Animals; D004195:Disease Models, Animal; D004576:Electromyography; D000882:Haplorhini; D006801:Humans; D009044:Motor Cortex / Q000503:physiopathology*; D009069:Movement Disorders / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology*; D011930:Reaction Time; D014836:Volition