Delayed initiation of voluntary movements after pyramidal lesions in man (author's transl)

Abstract

The reaction times for rapid movements in muscles of arm and leg were measured in 20 patients with unilateral lesions of the motor cortex and the internal capsule. Rapid unilateral and bilateral movements after an acoustic signal (click) on the pyramidally paretic side were compared with the normal side. In these patients and in 10 normal subjects, electromyographic and mechanical recordings from symmetrical muscles of both sides were compared. 2. All patients with pyramidal lesions showed in the case of unilateral movements a marked prolongation of motor latency in the affected muscles: compared to the normal side, the movement started 30-160 msec later in muscles contralateral to the lesion of the motor cortex. In contrast, normal subjects showed equal latencies on both sides with maximal differences of 10-20 msec. 3. When movements were executed bilaterally the latency prolongation in the pyramidally paretic muscles was markedly diminished or disappeared in later stages. In most patients the bilateral movements started simultaneously in the normal and the paretic muscles, except in 5 recent lesions of the contralateral motor cortex. 4. The significance of the findings is discussed in terms of the function of the human motor cortex in starting and controlling voluntary movements. It is assumed that the disappearance of latency prolongation when movements are executed bilaterally in patients with unilateral pyramidal lesions can be best explained by homolateral projections of uncrossed pyramidal fibres to the motoneurones. 5. These results, and other observations, suggest that the motor cortex starts and controls voluntary movements via rapidly conducting pyramidal fibres to the motoneurones. This occurs after a preprogramming and a readiness posture is established by other cerebral structures. The prolongation of motor latencies after motor cortex lesions is probably due to a disturbance in the rapidly conducting cortico-spinal projections to spinal motoneurones and interneurones.