Vallès Margarita, Mearin Fermín
Unit of Functional Digestive Rehabilitation, Institut Guttmann (affiliated with the Autonomous University of Barcelona), Badalona, Spain.
Dis Colon Rectum. 2009 Sep;52(9):1589-97. doi: 10.1007/DCR.0b013e3181a873f3.
Bowel dysfunction is a major problem in patients with spinal cord injury. Previous work has provided partial information, particularly about motor incomplete lesions. The purposes of this study were to evaluate the pathophysiologic features of neurogenic bowel in patients with motor incomplete spinal cord injury and to compare them with those in patients with motor complete lesions.
Fifty-four patients (59% men; mean age, 43 years) with chronic spinal cord injury and fecal incontinence and/or constipation were evaluated; 32 had motor incomplete lesions, and 22 had motor complete lesions. Clinical assessment, colonic transit time, and anorectal manometry were performed.
Colonic transit time was delayed similarly in patients with motor complete lesions and those with motor incomplete lesions. Anal squeeze pressure was present in most patients with motor incomplete lesions and absent in all patients with motor complete lesions. The cough-anal reflex was less frequent in patients with motor complete lesions with a neurologic level above T7 (P < 0.05). Rectal sensitivity was less severely impaired in those with motor incomplete lesions (P < 0.05). Most patients in both groups did not show anal relaxation during defecatory maneuvers. Rectal contractions and anal sphincter activity during distention of the rectum were detected more often in patients with motor complete lesions (P < 0.05).
Many severe pathophysiologic mechanisms are involved in neurogenic bowel, affecting patients with motor incomplete spinal cord injury similarly to those of patients with motor complete lesions with spinal sacral reflexes. The pathophysiologic mechanisms of constipation are obstructed defecation, weak abdominal muscles, impaired rectal sensation, and delayed colonic transit time; the mechanisms of fecal incontinence are impaired external anal sphincter contraction, uninhibited rectal contractions, and impaired rectal sensation. However, specific evaluation is required in individual cases.
肠道功能障碍是脊髓损伤患者的一个主要问题。既往研究提供了部分信息，尤其是关于运动不完全性损伤的信息。本研究的目的是评估运动不完全性脊髓损伤患者神经源性肠道的病理生理特征，并将其与运动完全性损伤患者的特征进行比较。
对54例慢性脊髓损伤且伴有大便失禁和/或便秘的患者（59%为男性；平均年龄43岁）进行评估；其中32例为运动不完全性损伤，22例为运动完全性损伤。进行了临床评估、结肠传输时间测定和肛肠测压。
运动完全性损伤患者和运动不完全性损伤患者的结肠传输时间均同样延迟。大多数运动不完全性损伤患者存在肛门挤压压力，而所有运动完全性损伤患者均无此压力。运动完全性损伤且神经平面高于T7的患者咳嗽-肛门反射较少见（P<0.05）。运动不完全性损伤患者的直肠敏感性受损程度较轻（P<0.05）。两组中的大多数患者在排便动作时未出现肛门松弛。直肠扩张时，运动完全性损伤患者更常检测到直肠收缩和肛门括约肌活动（P<0.05）。
神经源性肠道涉及许多严重的病理生理机制，对运动不完全性脊髓损伤患者的影响与对具有骶段脊髓反射的运动完全性损伤患者的影响相似。便秘的病理生理机制包括排便受阻、腹肌无力、直肠感觉受损和结肠传输时间延迟；大便失禁的机制包括肛门外括约肌收缩受损、直肠不受抑制的收缩和直肠感觉受损。然而，个别病例需要进行具体评估。
