Action tremor with alternating activity in antagonist muscles.

Action tremors due to alternating activity in antagonist muscles create different clinical manifestations. Tremors range in frequency from 2.5 to 7 Hz and may be brought out by either posture or goal-directed movement. Using physiologic criteria, tremors can be divided into groups with possible pharmacologic implications.

Physiological mechanisms of rigidity in Parkinson's disease.

Electromyographic responses of triceps surae and tibialis anterior produced by dorsiflexion stretch were studied in 17 patients with Parkinson's disease. Most patients showed increased muscular activity when attempting to relax. A few patients showed an increase of short-latency reflexes when relaxed and when exerting a voluntary plantarflexion prior to the stretch. Many patients showed long-latency reflexes when relaxed and all but one showed long-latency reflexes with voluntary contraction; and these reflexes were often larger in magnitude and longer in duration than those seen in normal subjects. Unlike the short-latency reflex, the long-latency reflex did not disappear with vibration applied to the Achilles tendon. The long-latency reflexes and continuous responses to slow ramp stretches were diminished at a latency similar to the beginning of long-latency reflexes when the stretching was quickly reversed. Dorsiflexion stretch also frequently produced a shortening reaction in tibialis anterior. Of all the abnormal behavior exhibited by the Parkinsonian patients only the long-latency reflex magnitude and duration correlated with the clinical impression of increased tone. The mechanism of the long-latency reflex to stretch which is responsible for rigidity is not certain, but the present results are consistent with a group II mediated tonic response.

Stretch reflexes of triceps surae in patients with upper motor neuron syndromes.

Electromyographic responses of triceps surae to dorsiflexion stretch were studied in 47 patients with a variety of lesions producing an upper motor neuron syndrome. The short latency spinal reflexes, both when the patient was at rest and when he was exerting a voluntary plantarflexion, were frequently enhanced in magnitude and the rate of increase with acceleration was also enhanced. Long-latency reflexes were uncommon at rest. With background force long-latency reflexes were present unless the short latency reflex was very large. Long latency reflexes often were normal, but in some patients they were either excessively larger or even of abnormal shape with prolonged continuous activity. The clinical assessment of the ankle jerk correlated with the magnitude of the short latency reflex. The clinical assessment of tone correlated with the magnitude of the short latency reflex, the magnitude of the long latency reflex and the duration of the long latency reflex. There appear to be multiple physiological mechanisms underlying the clinical phenomenon of spasticity.

Treatment of action tremor in multiple sclerosis with isoniazid.

Four patients with disabling action tremor in the setting of MS were treated with isoniazid (800 to 1200 mg per day). All patients showed significant improvement of the tremor, allowing more functional use of their extremities. To the best of our knowledge, this is the only medical treatment for this type of tremor.