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From the University of Mississippi Medical Center, Department of Neurology (Dr. Leis), Jackson, MS; Division of Restorative Neurology and Human Neurobiology (Drs. Kronenberg, Stetkarova, and Stokic), Baylor College of Medicine, Houston, TX; and P & A Consultants (Dr. Paske), Missouri City, TX.
M.F. Kronenberg is at the Innsbruck University Hospital, Innsbruck, Austria. I. Stetkarova is at the Postgraduate Medical School, Prague, Czech Republic.
Supported in part by the Vivian L. Smith Foundation for Restorative Neurology, Houston, TX.
Received June 13, 1995. Accepted in final form October 18, 1995.
Address correspondence and reprint requests to Dr. A. Arturo Leis, University of Mississippi Medical Center, Department of Neurology, EEG/EMG, 2500 North State Street, Jackson, MS 39216-4505.
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.
NEUROLOGY 1996;47: 231-237
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