Behavior of the H-reflex in humans following mechanical perturbation or injury to rostral spinal cord.

In humans H-reflexes are suppressed during early spinal shock. In animals rostral cord injury results in loss of segmental reflexes within seconds. If H-reflexes persist under general anesthesia, can they be used to monitor the integrity of the rostral cord? In part I of this study, we recorded H-reflexes intraoperatively in 25 patients to elucidate general anesthesia effect. In 23 subjects, H-reflexes were consistently elicited, and within +/- 13% of the normalized group mean amplitude. In part II, we recorded H-reflexes in 31 patients during spinal cord surgery to elucidate H-reflex behavior immediately following rostral spinal cord injury. In 6, abrupt suppression of the H-reflex coincided with cord injury. In 4 of 6, suppression was transient and less than 50% of baseline; none of these patients developed neurological deficits. In 2, suppression exceeded 90% and persisted throughout surgery; both patients developed profound deficits. We conclude that (1) the H-reflex can be consistently elicited under general anesthesia in most patients, (2) rostral cord injury rapidly suppresses the H-reflex, and (3) the degree and duration of H-reflex suppression reflects the severity of the injury.

Spinal motoneuron excitability after acute spinal cord injury in humans.

BACKGROUND: Few studies in humans have assessed the ability of Ia afferent and antidromic motor volleys to activate motoneurons during spinal shock. Hence, little is known about the excitability state of the spinal motoneuron pool after acute spinal cord injury (SCI) in humans. METHODS: In 14 patients with acute SCI involving anatomic levels T10 and above, we performed clinical and electrophysiologic studies early after injury (within 24 hours in seven subjects) and on day 10, 20, and 30 postinjury. Maximal H:M ratios, F-wave persistence, and tendon tap T-reflexes were recorded. Sixteen normal subjects and eight chronic SCI patients served as control subjects. RESULTS: Ten of 14 patients had spinal shock (complete paralysis, loss of sensation, absent reflexes, and muscle hypotonia below the injury) at the time of initial evaluation. F-waves were absent in patients with spinal shock, reduced in persistence in patients with acute SCI without spinal shock, and normal in persistence in patients with chronic SCI. H-reflexes were absent or markedly suppressed in patients with spinal shock within 24 hours of injury but recovered to normal amplitudes within several days postinjury. This recovery occurred despite absence of F-waves that persisted for several weeks postinjury. Deep tendon reflexes were proportionally more depressed in spinal shock than were H-reflexes. All patients had elicitable H-reflexes for days or weeks before the development of clinical reflexes. CONCLUSIONS: Rostral cord injury causes postsynaptic changes (hyperpolarization) in caudal motoneurons. This hyperpolarization is a major physiologic derangement in spinal shock. The rise in H-reflex amplitude despite evidence of persistent hyperpolarization is due to enhanced transmission at Ia fiber-motoneuron connections below the SCI. Finally, the observation that the stretch reflex is proportionally more depressed than the H-reflex is consistent with fusimotor drive also being depressed after SCI.