Disturbances of precision grip in Huntington's disease.

Disturbed motor control of the fingers, as revealed by the response to unexpected loading of an object held in a precision grip, or to finger perturbation during isometric holding, has been studied in patients with Huntington's disease (HD) and in normal subjects. In normal subjects unexpected loading elicited a reflex response (mean latency 73 ms) in the first dorsal interosseus muscle (FDI). This was accompanied by a clear increase in grip force, reaching a maximum at 200 ms, which stabilised block position. Index finger perturbation led to a long-latency reflex response in the FDI of all normal subjects. No such response was seen in the HD patients. The response to object loading, in contrast, was present, but significantly delayed (mean onset 95 ms; P = 0.0135). The response was qualitatively normal, with grip force reaching a maximum at 220-230 ms. It is suggested that the absence of the long-latency stretch reflex and the delay in the response to loading in HD patients may represent a reduction in somatosensory input to the cortex caused by disruption of basal ganglia structures.

Changes in the short- and long-latency stretch reflex components of the triceps surae muscle during ischaemia in man.

1. In order to establish the afferent source responsible for the M1 and M2 stretch reflex components of the voluntarily activated human triceps surae muscle, mechanical reflex testing was applied before and during ischaemic blockade of the lower limb. This procedure is known to affect large, fast conducting afferent fibres earliest, specifically Ia afferents arising from muscle spindle afferents. 2. It was found that both the M1 and M2 components were eliminated at the same time, at a point when the P40 peak in the somatosensory evoked potential, produced from stimulation of fast conducting peripheral afferents, was also abolished. This evidence indicates that both reflex components are mediated by information carried by muscle spindle Ia afferents. 3. The M1 component was selectively increased in the early stages of ischaemia. The M2 response did not increase during this period, but showed a tendency to reduce in amplitude. This effect may arise as the result of increased recruitment of motor units in the M1 component reducing the number of units available for activation in the M2 response. 4. These results do not support the view that the M2 reflex component of the triceps surae muscle is mediated by secondary afferent information, but indicate, rather, that both the M1 and M2 components are mediated by Ia afferent information acting on spinal pathways.

Absence of frontal somatosensory evoked potentials in Huntington's disease.

A fast route for transmission of deep and cutaneous afferent information to the frontal cortex is well established in non-human primates. Whether the incoming cortical information gives rise to early frontal somatosensory evoked potentials (SEPs) in humans is still a matter of contention. We attempted to solve this question by investigating the topography of SEP generators evoked by median nerve stimulation in 30 healthy subjects and in 30 patients suffering from Huntington's disease, who are known to have reduced SEP amplitudes. Using an earlobe reference, SEPs were recorded with an array of either five surface electrodes over the contralateral parietal cortex or 32 electrodes distributed over the whole scalp. In normal subjects analysis of frontal potentials revealed an early positive (P22) and negative (N30) component which could not be explained by generators located in the parietal cortex. Apart from the reduction of parietal components (N20, P25) frontal P22 and N30 were diminished or absent in Huntington's disease patients. Frontal potentials were even reduced in those patients who had parietal SEP amplitudes within the range of normal subjects. These frontal changes are similar to those reported in other basal ganglia disorders. Basal ganglia dysfunction might therefore be associated with changes of frontal SEP components.