Speakman C T, Kamm M A
Sir Alan Parks Physiology Unit, St Mark's Hospital, London.
Gut. 1993 Feb;34(2):215-21. doi: 10.1136/gut.34.2.215.
Changes of denervation in the anal sphincter striated and smooth muscle in patients with neurogenic faecal incontinence are well established. This study aimed to determine if there is also a more proximal visceral autonomic abnormality. Thirty women with purely neurogenic faecal incontinence (prolonged pudendal nerve latencies and an intact sphincter ring) and 12 patients with neuropathic changes together with an anatomical disruption were studied. Two control groups consisted of 18 healthy volunteer women and 17 women with normal innervation but an anatomically disrupted sphincter. Rectal sensation was assessed using balloon distension and electrical mucosal stimulation, and anal sensation by electrical stimulation. Rectal compliance was studied to determine whether sensory changes were primary or caused by altered rectal wall viscoelastic properties. Anal canal pressure changes in response to both rectal distension and rectal electrical stimulation were measured to assess the intrinsic innervation of the internal anal sphincter. Patients with neurogenic incontinence alone had impaired rectal sensation to distension (53.1 v 31.5 ml, p < 0.05, neurogenic v controls) and to electrical stimulation (24.4 v 14.8 mA, p < 0.005). Patients with neurogenic incontinence and sphincter disruption also showed impaired sensation compared with healthy controls (55.8 ml v 31.5 ml, p < 0.05 and 22.9 mA v 14.8 mA, p < 0.05). Patients with only a disrupted sphincter had normal visceral sensation to both types of testing. Both rectal compliance and the response of the internal anal sphincter to rectal distension and electrical stimulation were normal in all patient groups. This study suggests that there is a visceral sensory abnormality in patients with neurogenic incontinence which is not caused by altered rectal compliance. As evaluated in this study the intrinsic innervation of the internal anal sphincter is not affected in this process.
神经源性大便失禁患者肛门括约肌横纹肌和平滑肌的去神经改变已得到充分证实。本研究旨在确定是否还存在更靠近端的内脏自主神经异常。对30名单纯神经源性大便失禁的女性(阴部神经潜伏期延长且括约肌环完整)和12名伴有神经病变及解剖结构破坏的患者进行了研究。两个对照组分别由18名健康志愿者女性和17名神经支配正常但括约肌解剖结构破坏的女性组成。通过气囊扩张和黏膜电刺激评估直肠感觉,通过电刺激评估肛门感觉。研究直肠顺应性以确定感觉变化是原发性的还是由直肠壁粘弹性特性改变引起的。测量直肠扩张和直肠电刺激时肛管压力变化,以评估内括约肌的内在神经支配。仅患有神经源性失禁的患者对扩张(53.1对31.5 ml,p<0.05,神经源性组对对照组)和电刺激(24.4对14.8 mA,p<0.005)的直肠感觉受损。与健康对照组相比,患有神经源性失禁和括约肌破坏的患者也表现出感觉受损(55.8 ml对31.5 ml,p<0.05和22.9 mA对14.8 mA,p<0.05)。仅括约肌破坏的患者在两种测试中的内脏感觉均正常。所有患者组的直肠顺应性以及内括约肌对直肠扩张和电刺激的反应均正常。本研究表明,神经源性失禁患者存在内脏感觉异常,且不是由直肠顺应性改变引起的。如本研究评估,在此过程中内括约肌的内在神经支配未受影响。