J.P.R. Dick

The interpretation of electromyographic responses to electrical stimulation of the motor cortex in diseases of the upper motor neurone

The complexities of interpreting results of electrical stimulation of the motor cortex in pathological states are discussed and illustrated by reference to results from a variety of patients with diseases affecting the upper motor neurone (multiple sclerosis, cervical spondylosis and myelopathy, motor neurone disease, hemiparesis due to cerebral infarction, and hereditary spastic paraplegia). The abnormalities of the electromyographic (EMG) responses after anodal cortical stimulation consisted of delay in the latency to onset, dispersion or reduction in response size or even absence of EMG responses. These changes were not confined to any specific condition or pathology. Previous work has suggested that the sequence of events that follow anodal cortical stimulation involves repetitive excitatory inputs to spinal motoneurones and transmission across at least one central synapse. Accordingly, delayed latencies may not exclusively indicate slowing of motor conduction, while the absence of any response may not indicate complete failure of conduction in corticomotoneurone pathways.

ABNORMALITIES IN CENTRAL MOTOR PATHWAY CONDUCTION IN MULTIPLE SCLEROSIS

The technique of scalp stimulation of the motor cortex was used to demonstrate abnormalities in the corticomotoneuron pathway in multiple sclerosis. Unilateral or bilateral delays in corticomotoneuron conduction, dispersion of corticomotoneuron volleys, or both, were shown to occur in such patients. Changes may be seen even in patients with little clinical evidence of corticomotoneuron deficit.

The Bereitschaftspotential, l-DOPA and parkinson's disease

Bereitschaftspotentials (BPs) prior to extension movements of the index finger were studied in normal subjects and in patients with Parkinsons disease. In both, BPs were studied before and after L-DOPA therapy; in addition, the normal subjects were studied after dopamine antagonists. In both patients and normal subjects, L-DOPA caused an increase in the amplitude of the early part of the BP and of the point of peak negativity, just prior to EMG onset (N1) but it did not cause an increase of the late lateralized part of the BP (NS of Shibasaki); in normal subjects dopaminergic antagonists caused a decrease in the amplitude of the N1. Control experiments suggested that the change caused by L-DOPA was not the result of slower movement or poorer triggering when OFF drugs. For patients with Parkinsons disease there was no correlation between the change in their peak BP negativity (N1) after L-DOPA and their change in clinical mobility; in addition, there was no difference in the peak BP negativity of patients OFF therapy and that of age-matched normals, though there was a slight decrease in the amplitude of the early part of the BP for the patients with Parkinsons disease; this was the same part that had been enlarged by L-DOPA therapy. These findings suggest that the N1 is not affected by Parkinsons disease and that the effect of dopaminergic drugs on the N1 is mediated by actions on dopaminergic mechanisms elsewhere than in the striatum, perhaps in the cerebral cortex itself. The effect of L-DOPA will need to be taken into account in subsequent studies of the BP in Parkinsons disease.

Increase of the Bereitschaftspotential in simultaneous and sequential movements

The amplitude and duration of the Bereitschaftspotential were analysed in 9 normal subjects prior to four different motor tasks: (1) simple isotonic elbow flexion (flex), (2) simple isometric finger flexion (squeeze), (3) simultaneous performance of flex and squeeze, and (4) sequential performance of flex then squeeze. The Bereitschaftspotential was much larger and slightly longer in the simultaneous and sequential movements than in the same movements performed separately. The amplitudes of the Bereitschaftspotential were measured 150 and 75 ms prior to electromyographic (EMG) onset of the prime mover, and at the time of EMG onset. Changes in size were seen in all leads (FCz, Cz, C3, C4) and at all time points. It is suggested that the increase of the Bereitschaftspotential prior to complex arm movements reflects a greater activation of the supplementary motor area before simultaneous and sequential movements.

Motor strategies involved in the performance of sequential movements

SummaryThe present study analyses the strategies adopted by normal subjects when they are asked to make two separate movements as rapidly as possible one after the other. Five subjects performed the following sequential movements in their own time. 1) Squeeze an isometric force transducer between fingers and thumb to a force of 30 N and then flex the elbow of the same arm through 15°. 2) Squeeze the transducer with one hand and then flex the elbow of the other arm. 3) Perform an isotonic opposition of finger and thumb and then flex the elbow of the same arm. 4) First flex the elbow through 15, 30 or 45° and then squeeze the transducer. 5) Flex and then extend the elbow as rapidly as possible. In tasks 1–4 there was no correlation between the times taken to complete the two separate components of the sequence. Because of this we suggest that the two movements remained under the control of two separate motor programmes. In contrast, in task 5, the times taken for the two components were correlated and hence we suggest that in this case a single programme was used to perform the sequence. In tasks 1–3, in which the mean duration of the first movement was some 135–162 ms, there was a mean pause of about 85 ms before the start of the second movement. Subjects tended to chose a minimum inter-onset latency between the start of the first and the start of the second movement of a sequence of some 230 ms. The reason for this appeared to be that if subjects were encouraged to decrease their interonset latencies to less than 200 ms, the speed of the second movement decreased sharply. However, if the duration of the first movement was prolonged as in task 4, the second movement could be delayed, although there now was little or no pause between the two movements. We conclude that when a single motor programme is run, it is followed by a “relative refractory period”. If a second programme is run within this period, it cannot be executed without loss of speed. Switching from one motor programme to another is achieved with an optimal minimum delay of 200 ms. Sequential movements which are controlled by a single programme do not share this limitation.

Modulation of the long-latency reflex to stretch by the supplementary motor area in humans

Surface-recorded, electromyographic responses to 200-ms ramp stretches were studied in the wrist flexor muscles from both arms of a patient with clinical and radiographic evidence of infarction in the right supplementary motor area (SMA). They were compared with those from 8 age-matched control subjects. The latencies of the spinal component of the stretch reflex were slightly longer than normal in both arms of the patient (normal subjects: 28.5 +/- 2.6 ms; patient: 35 ms, right arm and 32 ms left arm). However, the amplitude and duration of the short-latency response were identical in both arms. The onset of the long-latency response to stretch was symmetrical in both the patients arms and was slightly later than normal (normal subjects 55.5 +/- 4.0 ms, patient: 72 ms right arm and 70 ms left arm); however, its duration was considerably prolonged in the arm contralateral to the SMA lesion (normal subjects: 44.8 +/- 6.0 ms; patient: 48 ms right arm. 105 ms left arm). These results are consistent with the hypothesis that the long-latency stretch reflex is mediated via a transcortical loop.