Delayed and enhanced long latency reflexes as the possible cause of postural tremor in late cerebellar atrophy.

The pathophysiology of postural tremor was studied in 7 patients with cortical cerebellar atrophy, and compared with the responses of 14 healthy control subjects to the same tests. Both tibial nerves were simultaneously and selectively stimulated in the fossa poplitea. EMG was recorded from agonist gastrocnemius muscles and from the antagonistic anterior tibial muscles. Displacement of the centre of foot pressure, inclination of trunk and head in the anteroposterior direction, and the ankle angle were also measured. Patients and controls both exhibit a synchronized discharge in the anterior tibial muscle (antagonist) with a latency of 120 ms to stimulus onset (tib1). Tib1 is shown to be a segmental stretch reflex elicited by the contraction of the gastrocnemius (agonist). A later, presumed long-loop response occurs after another 120 ms both in gastrocnemii and anterior tibial muscles in the normal subjects. This latency, and the amplitude of the late reflex, are increased in the patient group. The synchronization of delayed long-loop reflexes and a stretch response of the gastrocnemius in response to tib1 terminate the first cycle of the postural tremor which thereafter continues by way of the same mechanism generating a contraction of the anterior tibial muscle. Postural tremor can thus be synchronized by a single bilateral electrical stimulus and can even be elicited in incipient cases of the disease. With further progression of the cerebellar atrophy the dominant frequency of the postural tremor decreases along with an increase of long-loop latencies.