Incomplete spinal cord injury: neuronal mechanisms of motor recovery and hyperreflexia.
OBJECTIVE
To understand neuronal mechanisms of motor recovery and hyperreflexia after incomplete spinal cord injury (SCI), and their role in rehabilitation.


METHODS
Reviewed and compared clinical, neurophysiologic, and neuropathologic data from human SCI patients with behavioral, neurophysiologic, and neuroanatomic data from animals to postulate underlying neuronal mechanisms.


RESULTS
A postulation that two neuronal mechanisms-receptor up-regulation and synapse growth-act sequentially, to explain the gradual appearance of motor recovery after incomplete SCI. These same mechanisms may also act in spinal reflex pathways to mediate hyperreflexia caudal to SCI.


RESULTS
After incomplete SCI, walking ability and hyperreflexia often develop. Initially, cord neurons are hyperpolarized and less excitable because of loss of normal descending facilitation; this is spinal shock. Then, gradually, voluntary movement recovers and hyperreflexia develops. Early (hours to days), these changes develop simultaneously, suggesting a common postsynaptic mechanism-likely, an increase in postsynaptic receptor excitability, possibly receptor up-regulation. Late (weeks to months), recovery and reflex changes occur at a slow rate, are no longer simultaneous, and are long-lasting, which suggests a presynaptic mechanism, such as local synapse growth in spared descending pathways and in reflex pathways. This presumed synapse growth is seemingly enhanced by active use of the growing pathway. Also, developing hyperreflexia appears to limit motor recovery.


CONCLUSIONS
These observations suggest that rehabilitation for incomplete SCI should (1) increase activity in spared descending motor pathways, (2) initially use reflex facilitation or central nervous system stimulants to assist spared descending inputs in depolarizing cord neurons, and (3) later minimize reflex input, when spared descending inputs can depolarize cord neurons without reflex facilitation. Better understanding of neuronal mechanisms that underlie motor recovery after incomplete SCI promises better outcomes from rehabilitation.
D000818:Animals; D006181:H-Reflex / Q000502:physiology; D006801:Humans; D007103:Immobilization; D009046:Motor Neurons / Q000502:physiology*; D009410:Nerve Degeneration; D012021:Reflex, Abnormal / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology* / Q000534:rehabilitation*; D013569:Synapses / Q000502:physiology; D013997:Time Factors