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Microneurographic studies were made of normal human muscle spindle afferent activity to evaluate the role played by these endings, and by the segmental stretch reflex, in various types of physiological tremor. Primary endings are sufficiently sensitive to respond to the minute tremulous movements normally seen in contracting muscles. Human muscle spindle endings appear to possess the same non-linear sensitivity to small stretches as has been reported for cat muscle spindles. The findings also support the notion that the segmental stretch reflex plays an important role in enhanced physiological tremor, in so far as it tends to synchronize the motor outflow in such a way as to produce rhythmical contractions properly timed to reinforce the mechanical resonant properties of muscle spindle endings, the stretch reflex also serves to damp the larger oscillations of finger or hand which result from a brisk tap or muscle twitch. There is no evidence for alpha-gamma co-activation in these enhanced physiological tremors.

Blink reflexes were obtained in a total of 34 different patients with cerebrovascular lesions; 28 were studied within 1 week of the ictus and 11 were eventually restudied. In 13, the latency of the first component of the reflex on the clinically involved side was significantly delayed (greater than 1.5 msec). This was an acute phenomenon that usually resolved within the first week after the ictus, correlated clinically with the severity of the hemiparesis and decrease in tone, and may be seen with lesions restricted to the pyramidal tract. The second component was absent in 17 of 34 patients during the early phase after stroke, and was associated with a decreased corneal response. These changes, which reflect decreased excitability of certain brainstem structures (rather than a lesion within those structures), are therefore potentially important for documenting CNS pathophysiology.

In view of recent evidence that physiological tremor can be enhanced by positive feedback via the segmental stretch reflex, several manoeuvres and procedures were employed to enhance the finger and hand tremor of healthy subjects--the purpose being to determine if tremorogenic effects, at least in part, are due to increase efficacy of the stretch reflex servo. Mechanical events during tremor (and during voluntary or electrically induced muscle twitches) were recorded together with EMG activity from wrist and finger flexor muscles and discharges from primary spindle endings in these muscles. Physiological tremor can be enhanced not only by manoeuvres which increase the gain of segmental stretch reflexes (Jendrassik manoeuvre) but also by manoeuvres which increase the contrast in spindle firing during stretch versus shortening phases of tremor, thus enhancing reflex modulation. Effects of the latter type can be achieved by procedures which alter mechanical twitch properties of extrafusal fibres (isoproterenol infusions and fatigue) and by procedures which involve application of spindle stimuli acting preferentially during stretch phases of tremor movements (muscle vibrations). Physiological tremor, which can be temporarily enhanced by an externally applied muscle perturbation, also becomes accentuated by those small "pseudo-myoclonic" jerks which occur in all normal subjects attempting to perform slow, smooth movements.

One type of flexor reflex, that recorded from the tibialis anterior muscle in response to electrical stimulation of the sole of the foot, was studied in normal subjects and patients with several neurological disorders. Normally this reflex consists of two components, the second of which is related to the actual withdrawal. The first component, normally of lower threshold, is difficult to evoke in patients with chronic spinal cord or discrete cerebral lesions, whereas it has an unusually low threshold and is very clearly seen in those with Parkinson's disease. In patients with spinal cord disease, the exaggerated flexor reflexes are seen at long latencies after relatively small stimuli. During the early phase of recovery from spinal transection, both components may be seen and are, therefore, spinal in origin. Studies of patients with the sensory neuropathy of Friedreich's ataxia suggest that the afferent fibres responsible for these flexor reflexes are the small myelinated fibres. Recovery curves demonstrate very long-lasting changes in flexor reflex excitability in normal subjects and patients with `spasticity' from spinal lesions. This differs in patients with `spasticity' from lesions rostral to the brain-stem. Examples in man of such physiological phenomena as reciprocal inhibition, local sign, habituation, temporal and spatial summation are discussed.