What do the basal ganglia tell premotor cortical areas?

The defects in execution of simple single arm movements at one joint, and of complex arm movements simultaneously or sequentially at two joints, in Parkinson's disease are analysed as a clue to the formal functions of the basal ganglia in human motor control. Slowness in execution of single movements, due to failure to scale the size of the initial electromyographic burst of activity in the agonist, is one characteristic abnormality. However, patients with Parkinson's disease are also shown to have added difficulty with complex motor tasks. When they attempt to undertake a hand 'squeeze' at the same time as an elbow 'flex', both movements are even slower. When they try to perform an elbow flex as quickly as possible after a hand squeeze with the same or opposite arms, the second movement is slowed and the interval between movements is prolonged. Similar movement abnormalities have been found in patients with Huntington's disease-even in those with chorea alone, and irrespective of drug therapy-and in a patient with an infarct involving the right supplementary motor area. These observations suggest that the basal ganglia in humans are required to set up the correct motor programmes to execute complex simultaneous and sequential movements. It is suggested that the basal ganglia, acting on a read-out of existing sensorimotor cortical activity, direct the premotor cortical areas to select the correct parameters of the motor programmes required for subsequent motor action.