Abstract
The long-term, chronic, paralysis resulting from spinal cord injury in the cat has been reversed by the use of an alpha 2-adrenergic receptor agonist, clonidine. Administration of this drug resulted in "normalization" of sensory-motor and autonomic dysfunctions. Preliminary studies of the clonidine in humans with traumatically injured spinal cord indicate that autonomic dysreflexia can be controlled and spasticity minimized. The data suggest that biochemical and pharmacologic manipulation of receptors may ameliorate paralysis following traumatic injury to the spinal cord as well as to the brain and brainstem.