The treatment of spasticity in severely paralyzed patients undergoing rehabilitation constitutes a significant neurosurgical challenge that requires comprehensive management. In this study, 118 patients were treated with invasive modalities when medical therapy failed. The results of percutaneous radiofrequency foraminal rhizotomy were initially successful in 95% of the 77 patients who underwent this procedure; the rate of minor complications was 5%. This procedure was satisfactorily supplemented with percutaneous radiofrequency sciatic neurectomy in 32 of these 77 patients. Four myelotomies were performed with complete success and no major complications in patients in whom percutaneous techniques had proven inadequate. In 35 instances of focal spasticity and incomplete paralysis, intramuscular neurolysis by phenol injection was used. The success rate was 89%. In 9 patients with persistent recurrent spasticity of the lower limb, open tenotomies and peripheral neurectomies were done. Success was complete and without complications. Multiple modalities must be available for the comprehensive management of patients with paralytic spasticity. (Neurosurgery 26:300-306, 1990)
The treatment of spasticity in severely paralyzed patients undergoing rehabilitation constitutes a significant neurosurgical challenge that requires comprehensive management. In this study, 118 patients were treated with invasive modalities when medical therapy failed. The results of percutaneous radiofrequency foraminal rhizotomy were initially successful in 95% of the 77 patients who underwent this procedure; the rate of minor complications was 5%. This procedure was satisfactorily supplemented with percutaneous radiofrequency sciatic neurectomy in 32 of these 77 patients. Four myelotomies were performed with complete success and no major complications in patients in whom percutaneous techniques had proven inadequate. In 35 instances of focal spasticity and incomplete paralysis, intramuscular neurolysis by phenol injection was used. The success rate was 89%. In 9 patients with persistent recurrent spasticity of the lower limb, open tenotomies and peripheral neurectomies were done. Success was complete and without complications. Multiple modalities must be available for the comprehensive management of patients with paralytic spasticity.
Experiments were done on the inhibitory synapse of crayfish tonic muscle receptor organs (MROs) to determine whether gamma-aminobutyric acid (GABA) receptors would be affected by denervation or axotomy. It was found that severing the dorsal nerve containing the MRO sensory and inhibitory neurons usually induced, in 30 days or less, a dramatic transformation in the responses of MROs to ionophoretically applied GABA. In contrast to normal MROs which show only inhibitory responses to GABA, transformed MROs were substantially depolarized and excited by GABA application to numerous points found on the axon, soma, dendrites. Interspersed among the points of excitation, normal inhibitory points could still be found on the transformed cells. The results suggested that chronic lesions can induced structural changes in GABA receptors, whereby the Cl- ionophore is replaced by a cationic channel. It was possible to compare the effects of postsynaptic axotomy alone with those of postsynaptic plus presynaptic axotomy by testing MROs from animals whose ventral nerve cord was sectioned. These experiments suggested that interruption of the presynaptic neuron is an important factor in the transformation. It was not determined whether complete degeneration of the inhibitory synapse is necessary for the transformation, but the rapidity of the effect, coupled with the probability of long-term survival of synaptic contacts, suggested that complete degeneration was not necessary. Similarities were found in the GABA responses of transformed MROs and those MROs which normally receive no innervation, which are located in the sixth abdominal segment. These results support the idea that trophic regulation from inhibitory neurons is a factor in stabilizing the association of the Cl- ionophore with GABA receptor.
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