Neural plasticity in functional restoration of brachial plexus injury
N. Tsuyama (National Rehabilitation Center for the Disabled, Tokorozawa, Japan)
For the cases of total brachial plexus injury of complete root avulsion type involving C5 to Th1, there was no possibility of nerve repair in the past. Since 1965 we started direct anastomosis of the Th3 and Th4 intercostal nerve cable to the musculocutaneous nerve at the site as near as possible the motor point of M.biceps brachii. The results were far better than we expected and the respiratory influence faded away with the time course of training. The functional conversion, or more accurately segregation, of the respiratory function to the volitional elbow flexor control will be shown with actual case presentations and the mechanism of this plasticity will be discussed.
SPINAL SPASTICITY: PATHOPHYSIOLOGY AND PHARMACOLOGICAL MANAGEMENT
R. M. Herman (Neurobiology Institute, Scottsdale, AZ, USA); S.C. D'Luzansky (Good Samaritan Regional Medical Center, Phoenix, AZ, USA)
The spinal form of spasticity reveals two basic reflex phenomena; (a) tonic rigidity and (b) phasic spasms. Function-limiting spasms, which occur spontaneously or by sensory stimulation, utilize pain pathways in the dorsal horn of the spinal cord and disinhibited intersegmental pathways, accounting for wide-spread motor discharges ('irradiation'). Increased activity of bladder afferents, projecting to the dorsal horn, increase the excitability of dorsal horn neurons and further promotes irradiation. Pharmacological management is directed at the chemoarchitecture of the dorsal horn neurons, particularly at receptors (GABA, alpha-adrenergic, opioid) which become up-regulated or supersensitive following a supraconal spinal cord lesion. Administration of intraspinal agents will be described for patients with intractable spasticity (i.e., patients refractory to per-oral agents).