Does sacral posterior rhizotomy suppress autonomic hyper-reflexia in patients with spinal cord injury?

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Abstract

Objective

To study the occurrence of autonomic hyper-reflexia (AHR) after intradural sacral posterior rhizotomy combined with intradural sacral anterior root stimulation, performed to manage the neurogenic hyper-reflexic bladder, and to determine the pathophysiological basis of the uncontrolled hypertensive crisis after sacral de-afferentation.

Patients and methods

Ten patients with spinal cord injury operated using Brindley's method between September 1990 and February 1994 were reviewed. Systematic continuous non-invasive recordings of cardiovascular variables (using a photoplethysmograph) were made during urodynamic recordings and the pre- and post-operative vesico-urethral and cardiovascular data compared.

Results

Nine of the 10 patients were examined using a new prototype measurement system; one woman refused the last urodynamic assessment. Eight of the nine patients who presented with AHR before operation still had the condition afterward. There was a marked elevation in systolic and diastolic blood pressure during the urodynamic examination in all eight patients, despite complete intra-operative de-afferentation of the bladder in five. The elevation of blood pressure started during the stimulation-induced bladder contractions and increased during voiding in all cases. Five patients showed a decrease in heart rate during the increase in blood pressure. However, in three patients the heart rate did not change or even sometimes slightly increased as the arterial blood pressure exceeded 160 mmHg, when the blood pressure and heart rate then increased together.

Conclusions

These results confirm that even after complete sacral de-afferentation, AHR persisted in patients with spinal cord injury and always occurred during the stimulation-induced voiding phase. In cases of incomplete de-afferentation, small uninhibited bladder contractions without voiding occurred during the filling phase. The blood pressure then increased but never reached the value recorded during stimulation-induced micturition. Stimulation of afferents that enter the spinal cord by the thoracic and lumbar roots and that are not influenced by sacral rhizotomy could explain why AHR increases during urine flow. The distinct threshold of decreased heart rate by increasing blood pressure to > 160 mmHg focuses attention on the chronotropic influences of the sympathetic nerves in the heart by an exhausted baroreceptor reflex.

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