Habib F I, Inghilleri M, Badiali D, Corazziari E
Department of Clinical Science, University La Sapienza, Rome, Italy.
Ital J Gastroenterol Hepatol. 1999 Oct;31(7):574-9.
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.
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.
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).
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.
便秘患者中可能出现的阴部神经病变被认为是由于排便时反复用力导致盆底下降的结果。然而，可能导致反复用力排便的腹盆腔协同失调与盆底神经生理病理改变之间的关系尚未完全阐明。
本研究旨在评估32例慢性特发性便秘患者的肛门外括约肌神经生理改变、排便改变模式与排粪造影盆底生理之间的关系。
在肌电图检查中，19%的受调查对象发现有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%的受调查对象存在协同失调（肛门外括约肌与腹部肌肉共同收缩）。不同肌电图模式的患者在排便改变症状、排便频率、手法辅助排便的使用、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排粪造影结果改变显著相关：慢性神经源性病变和腹盆腔协同失调时静息肛管直肠角减小（p<0.01）；存在慢性神经源性病变时盆底过度下降（p<0.05）。
在慢性便秘患者中，排便改变症状似乎与腹盆腔协同失调和/或肛门外括约肌慢性神经源性病变无关，且与排粪造影改变无任何关联。这些结果表明，除腹盆腔协同失调和慢性神经源性病变外，其他因素也可导致排便时用力，且这两种改变具有不同的发病机制。
