Autonomic hyperreflexia revisited.
OBJECTIVE
To analyze autonomic hyperreflexia (AHR) associated with neurogenic bladder dysfunction in high spinal cord-injured patients.


METHODS
Sixty-five patients were examined using a new recording system. Seventeen suffered from a spinal cord lesion above the T5-T6 level and presented with neurogenic voiding disorders and AHR. Mean arterial pressure (MAP) changes were analyzed during 3 different urodynamic phases: bladder filling; isometric bladder contraction, and voiding.


RESULTS
Of the 17 tetraplegic and high paraplegic patients, 6 dropped out and 11 entered the study. Nine of these eleven patients displayed uninhibited bladder contractions and voiding. In these 9 cases MAP increased progressively during bladder contraction until a maximal bladder pressure was reached. An ongoing elevation of MAP was observed during voiding which returned to normal values within 5 min after micturition. In 2 patients detrusor-sphincter dyssynergia prevented voiding. As opposed to the 9 previously mentioned patients, maximal MAP occurred at or before the maximal bladder pressure in these 2 cases and decreased thereafter.


CONCLUSIONS
Evidence is presented that the posterior urethral receptors and their ascending pathway played a major role in the maintenance of AHR during micturition.
Schurch
B
B
Swiss Paraplegic Centre, University Hospital Balgrist, Zürich, Switzerland.
Knapp
P A
PA
Rossier
A B
AB
D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D010264:Paraplegia / Q000209:etiology / Q000503:physiopathology; D011782:Quadriplegia / Q000209:etiology / Q000503:physiopathology; D012021:Reflex, Abnormal / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000150:complications / Q000503:physiopathology*; D001743:Urinary Bladder / Q000294:innervation*; D001750:Urinary Bladder, Neurogenic / Q000209:etiology / Q000503:physiopathology*; D014563:Urodynamics / Q000502:physiology*