Bowel dysfunction in patients with motor complete spinal cord injury: clinical, neurological, and pathophysiological...

Abnormal bowel function is a key problem in patients with spinal cord injury (SCI). Previous works provided only partial information on colonic transit time (CTT) or anal dysfunction but did not identified a comprehensive neurogenic bowel pattern.

To evaluate clinical, neurological, and pathophysiological counterparts of neurogenic bowel in patients with motor complete SCI.

Fifty-four patients (56% men, mean age 35 yr) with chronic motor complete SCI (mean evolution time 6 yr) were evaluated: 41% with injuries above T7 (> T7) and 59% with injuries below T7 (< T7); patients were also classified according to the presence or not of sacral spinal reflexes. Clinical assessment, total and segmental CTT quantification, anorectal function evaluation by manometry, intrarectal balloon distension, and surface electromyography were performed.

Three different neuropathophysiological patterns were observed: Pattern A, present in > T7 injuries, characterized by very frequent constipation (86%) with significant defecatory difficulty and not very severe incontinence (Mean Wexner score 4.5); it was related to moderate delay in CTT (mainly in the left colon and recto-sigma), incapacity to increase the intra-abdominal pressure, and the absence of anal relaxation during the defecatory maneuvre; Pattern B, present in < T7 injuries with preserved sacral reflexes, characterized by not so frequent constipation (50%) but very significant defecatory difficulty and not very severe incontinence (Wexner 4.8); the pathophysiological counterpart was a moderate delay in CTT, capacity to increase intra-abdominal pressure, increased anal resistance during the defecatory maneuver, and presence of external anal sphincter (EAS) contraction when intra-abdominal pressure increased and during rectal distension; Pattern C, present in < T7 injuries without sacral reflexes, characterized by not very frequent constipation (56%) with less defecatory difficulty and greater severity of incontinence (Wexner 7.2); this was associated with severe delay in CTT (mainly in the left colon), capacity to increase intra-abdominal pressure, absence of anal resistance during the defecatory maneuver, and absence of EAS contraction when intra-abdominal pressure increased and during rectal distension.

In patients with motor complete SCI, we were able to define three different neuropathophysiological patterns that are associated with bowel function abnormalities and clinical complaints; this might be of help when designing therapeutic strategies.