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[脊髓中枢性损伤中的逼尿肌无活动。交感神经源性抑制性反射亢进假说]

[Detrusor inactivity in central spinal cord lesions. Hypothesis of inhibitory hyperreflexia of sympathetic origin].

作者信息

Labat J J, Le Coguic G, Mathé J F, Buzelin J M

出版信息

J Urol (Paris). 1982;88(8):527-30.

PMID:7161513
Abstract

In connection with two observations of suprasacral complete spinal cord patients showing a clear sublesional spasticity and paradoxically and inactive and unreactive detrusor, the authors discuss the mechanisms that are usually considered: vesical distension, sacral peripheric neurogenic lesion, reflex inhibition of the detrusor of somatic origin. They express the hypothesis of an inhibition hyper-reflex of sympathetic origin, reversible under phenoxybenzamine treatment, consider the urodynamic evaluation and the therapeutic treatment and compare this type of neurogenic vesical dysfunction to that of the spinal shock.

摘要

关于两例骶上完全性脊髓损伤患者的观察,这些患者表现出明显的损伤平面以下痉挛,以及矛盾的、无活性和无反应性的逼尿肌,作者讨论了通常被认为的机制:膀胱扩张、骶部周围神经源性损伤、躯体源性逼尿肌反射抑制。他们提出了交感神经源性抑制性高反射的假说,该假说在苯氧苄胺治疗下可逆,考虑了尿动力学评估和治疗,并将这种类型的神经源性膀胱功能障碍与脊髓休克的情况进行了比较。

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