Electromyographic responses to sudden wrist extension were recorded from the forearm and finger flexor muscles in 10 patients with Huntington's disease (HD) and in 10 normal controls. Stretch reflexes were characterized by a short-latency (SL) and a long-latency (LL) component both in patients and controls. Latency, duration, and size of the SL component were not different in the two groups, whereas the LL component was delayed in latency and reduced in size in HD patients. Increasing the stretch repetition rate from 0.1 to 0.4 cycles/s did not affect the SL component of either group, whereas the LL stretch reflex was reduced in size and duration in normal controls, but not in HD patients. These findings suggest an impairment of the “gain” mechanisms of the sole LL component, responsible for a desaturation of this component. This study supports the hypothesis that LL stretch reflexes are mediated by a transcortical long loop, possibly damaged in HD.