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NEUROLOGY 1992;42:623
© 1992 American Academy of Neurology

Electrophysiologic changes in lumbar spinal cord after cervical cord injury

Mindy L. Aisen, MD, William Brown, MD, FRCP (C) and Michael Rubin, MD, FRCP (C)

Burke Rehabilitation Center, Cornell University Medical College, White Plains, NY (Dr. Aisen)
Division of Neurology, University Hospital, London, ON, Canada (Dr. Brown)
Department of Neurology, The New York Hospital, Cornell University Medical College, New York, NY (Dr. Rubin).

Spontaneous activity on the EMG examination is traditionally ascribed to disease of the lower motor neuron when present in muscles well below the level of para- or quadriplegia despite the absence of any detectable peripheral nerve injury. It is uncertain whether it reflects transient paralysis of transmission (related to clinical spinal shock) or irreversible postsynaptic damage. We performed serial EMG studies of lower extremities and paraspinal muscles on eight young, previously healthy adults, commencing 2 to 9 weeks after acute cervical cord injury. All had stimulated single-fiber EMG (SFEMG) studies at 6-month intervals to determine whether irreversible postsynaptic damage of the anterior horn cell had occurred. MRI and nerve conduction excluded patients with evidence of distal cord injury or peripheral neuropathy. All patients had spontaneous activity in all muscles tested, persisting after spinal shock had resolved. Jitter was present on SFEMG in three of eight patients 6 months after injury. Four of five patients retested 12 months after injury had abnormal jitter, including three who initially had normal SFEMG studies. We conclude that there is electrophysiologic evidence of trans-synaptic distal cord dysfunction following acute spinal cord injury. SFEMG studies suggest that anterior horn cell dropout occurs during the 1st year after injury.

Address correspondence and reprint requests to Dr. Mindy L. Aisen, The Burke Rehabilitation Center, Cornell University Medical College, 785 Mamaroneck Avenue, White Plains, NY 10605.

Supported by a grant from the American Paralysis Association.

Received May 21, 1991. Accepted for publication in final form August 21, 1991.




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