Deficits in sensorimotor control during precise hand movements in Huntington's disease.

OBJECTIVES: To investigate the performance of patients with Huntington's disease (HD) while manipulating objects using a precision grip. METHODS: The grip forces developed by the fingers were studied while subjects lifted an object of unpredictable weight in the hand. The ability to stabilize grip force after externally imposed weight change was also studied. RESULTS: Patients used higher grip forces than the normal subjects in both the lifting and holding phases, particularly with a lighter weight. Lift timing was slowed in the patients, most markedly with a lighter weight. Increased levels of inter-trial variation were observed only with a light weight. This indicates that the slowing in HD differs from that in Parkinson's disease, which remains constant regardless of object load, and that the slowing in HD is not due to involuntary antagonist muscle activity resulting from an underlying chorea. The grip force response to sudden weight change was normal, but appeared after a delay which increased at lower rates of weight change. CONCLUSIONS: Disturbances in precision grip timing and magnitude in HD may result from a reduced ability to process relevant tactile afferent input. The delay in the adaptive response suggests an increased threshold for detection of weight change in HD. Alternatively, this delay may arise from mediation of the response over an additional cerebellar pathway to compensate for damage to the basal ganglia.

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.