Assessment of autonomic dysreflexia in patients with spinal cord injury.
OBJECTIVES AND METHODS: To assess the impairment of supraspinal control over spinal sympathetic centres and the occurrence of autonomic dysreflexia in patients with spinal cord injury. Autonomic dysreflexia is caused by the disconnection of spinal sympathetic centres from supraspinal control and is characterised by paroxysmal hypertensive episodes caused by non-specific stimuli below the level of the lesion. Therefore, patients with spinal cord injury were examined clinically and by different techniques to assess the occurrence of autonomic dysreflexia and to relate disturbances of the sympathetic nervous system to episodes of autonomic dysreflexia. RESULTS: None of the paraplegic patients, but 59% (13/22) of tetraplegic patients (91% of the complete, 27% of the incomplete patients) presented signs of autonomic dysreflexia during urodynamic examination. Only 62% of the tetraplegic patients complained about symptoms of autonomic dysreflexia. Pathological sympathetic skin responses (SSRs) of the hands were related to signs of autonomic dysreflexia in 93% of cases. No patient with preserved SSR potentials of the hands and feet showed signs of autonomic dysreflexia, either clinically or during urodynamic examination. Ambulatory blood pressure measurements (ABPMs) indicated a loss of circadian blood pressure rhythm (sympathetic control) but preserved heart rate rhythm (parasympathetic regulation) only in patients with complete tetraplegia. Pathological ABPM recordings were seen in 70% of patients with symptoms of autonomic dysreflexia. CONCLUSIONS: The urodynamic examination was more sensitive in indicating signs of autonomic dysreflexia in patients with spinal cord injury, whereas SSR allowed the assessment of the degree of disconnection of the sympathetic spinal centres from supraspinal control. Using ABPM recordings the occurrence of episodes of autonomic dysreflexia over 24 hours and the effectiveness of therapeutical treatment can be assessed.