Chronic neurogenic lesions of the external anal sphincter and abdomino-perineal dyssynergia in chronic constipation.

F I Habib, M Inghilleri, D Badiali, E Corazziari
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Abstract

Background: Neuropathy of the pudendal nerves which may be found in constipated patients has been considered the result of pelvic floor descent due to the repetitive acts of straining at stool. However, the relationship between abdominopelvic dyssynergia, which may lead to repetitive acts of straining and neurophysiopathologic alterations of the pelvic floor has not yet been fully elucidated.

Aim: Of this study was to assess the relationship between neurophysiologic alterations of the external anal sphincter, patterns of altered evacuation and defaecographic pelvic floor physiology in 32 patients with chronic idiopathic constipation.

Results: At electromyography partial muscle denervation, identified as chronic neurogenic lesions of the external anal sphincter, were found in 19% and dyssynergia (co-contraction of external anal sphincter and abdominal muscles) in 34% of the investigated subjects. Patients with different electromyography patterns did not differ as far as concerns symptoms of altered evacuation, bowel frequency, use of digital manoeuvres, age, and duration of symptoms. The presence of neurophysiologic alterations was significantly associated with altered defaecographic findings: reduced ano-rectal angle at rest in chronic neurogenic lesions and abdomino-pelvic dyssynergia (p < 0.01); excessive pelvic floor descent in the presence of chronic neurogenic lesions (p < 0.05).

Conclusions: In chronically constipated patients symptoms of altered defaecation do not appear to be related to abdomino-pelvic dyssynergia and/or chronic neurogenic lesion of the external anal sphincter and do not show any association with defaecographic alterations. These results suggest that straining at evacuation can be induced by additional factors other than abdomino-pelvic dyssynergia and chronic neurogenic lesions and that these two alterations have different pathogenetic mechanisms.

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慢性便秘的外肛门括约肌慢性神经源性病变和腹会阴协同障碍。
背景:阴部神经病变可能在便秘患者中发现,被认为是骨盆底下降的结果,由于反复的大便紧张行为。然而,可能导致重复劳损行为的腹盆腔协同障碍与盆底神经生理病理改变之间的关系尚未完全阐明。目的:本研究旨在评估32例慢性特发性便秘患者外肛门括约肌的神经生理改变、排空改变的模式和盆底生理缺陷的关系。结果:在肌电图上,19%的人发现部分肌肉失神经支配,被确定为肛门外括约肌的慢性神经源性病变,34%的人发现协同作用障碍(肛门外括约肌和腹肌共同收缩)。不同肌电图类型的患者在排便改变的症状、排便频率、手指操作的使用、年龄和症状持续时间方面没有差异。神经生理改变的存在与改变的缺陷表现显著相关:慢性神经源性病变和腹盆腔协同障碍患者静息时肛门直肠角降低(p < 0.01);存在慢性神经源性病变时盆底过度下降(p < 0.05)。结论:慢性便秘患者排便改变的症状似乎与腹盆腔协同作用障碍和/或肛门外括约肌慢性神经源性病变无关,也未显示与排便改变有任何关联。这些结果表明,除腹盆腔协同作用障碍和慢性神经源性病变外,排空时的紧张还可能由其他因素引起,这两种改变具有不同的发病机制。
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