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Войти в исследования Urologia internationalis · 1997
Autonomic hyperreflexia revisited.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Schurch B, Knapp P A, Rossier A B
Аннотация
PURPOSE: To analyze autonomic hyperreflexia (AHR) associated with neurogenic bladder dysfunction in high spinal cord-injured patients.
MATERIAL AND 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.
MATERIAL AND 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.