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PubMed · 9188135

Autonomic hyperreflexia revisited.

B Schurch·P A Knapp·A B Rossier
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Abstract

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.

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Autonomic Nervous System DiseasesBlood PressureFemaleHumansMaleParaplegiaQuadriplegiaReflex, AbnormalSpinal Cord InjuriesUrinary BladderUrinary Bladder, NeurogenicUrodynamicsJournal ArticleResearch Support, Non-U.S. Gov't

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B Schurch, P A Knapp, A B Rossier. 1997. Autonomic hyperreflexia revisited.. https://doi.org/10.1159/000282972

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Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients.

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.

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