ABSTRACT
PURPOSE: Neurogenic bladder dysfunction after spinal cord injury (SCI) is a major medical and social problem for which there is no definitive solution. After the successful establishment in animals of a skin-central nervous system-bladder reflex pathway for micturition we performed this procedure on 15 patients with SCI who had 3 years of followup. MATERIALS AND METHODS: A total of 15 male volunteers with hyperreflexic neurogenic bladder and detrusor external sphincter dyssynergia (DESD) caused by complete suprasacral SCI underwent limited hemilaminectomy and ventral root (VR) micro anastomosis, usually between the L5 and S2/3 VRs. The L5 dorsal root was left intact as the trigger of micturition after axonal regeneration. Mean followup was 3 years. All patients underwent urodynamic evaluation before surgery and during followup. RESULTS: Preoperative studies in patients with complete suprasacral SCI revealed hyperreflexic neurogenic bladders and DESD with some differences in storage function during infusion cystometrograms. Of the 15 patients 10 (67%) regained satisfactory bladder control within 12 to 18 months after VR micro anastomosis. Average residual urine decreased from 332 to 31 ml and urinary infection as well as overflow incontinence disappeared. Urodynamic studies revealed a change from detrusor hyperreflexia with DESD and high detrusor pressure to almost normal storage and synergic voiding without DESD. Impaired renal function returned to normal. Two patients (13%) who required a skin stimulator to evoke voiding following the VR anastomosis had partial recovery but more than 100 ml residual urine. One patient was lost to followup and 2 had failure. CONCLUSIONS: An artificial somatic-central nervous system-autonomic reflex arc can be established surgically to provide a novel method for controlling bladder function in patients with complete suprasacral SCI who have hyperreflexic bladder and DESD. Nerve impulses delivered from the efferent neurons of a somatic reflex arc can be transferred to initiate the response of an autonomic effector.
