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 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.

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.

Bowel dysfunction is a problem in patients with spinal cord injury. The sacral anterior root stimulator has been used for neurogenic bladder and has been claimed to be useful for neurogenic bowel. The purposes of this study were to analyze the clinical response of bowel function to the sacral anterior root stimulator and to evaluate physiologic factors that could determine its efficacy. Eighteen consecutive patients with spinal cord injury and an implanted sacral anterior root stimulator were evaluated. Clinical assessment, colonic transit time, and anorectal manometry were performed. Patients were evaluated before implantation of the sacral anterior root stimulator and clinically reevaluated after 12 months. Fewer patients required laxatives after implantation of the sacral anterior root stimulator. The mean number of methods used to evacuate was reduced from 2.1 to 1.5 (P < 0.05). Bowel movement frequency was higher (P < 0.05). Time devoted to defecation was reduced, although no statistical significance was achieved. Fecal incontinence did not change, but constipation was reduced (P < 0.05). Most patients reported being more satisfied with bowel function after implantation of the sacral anterior root stimulator. No correlation was found between objective and subjective responses to the sacral anterior root stimulator and manometric or colonic transit times before implantation. The sacral anterior root stimulator improves bowel function, and patient satisfaction with this treatment is high. Further studies are needed to evaluate the characteristics of stimulation parameters to achieve better results.

Kumru H, Benito J, Murillo N, et al. Effects of high-frequency repetitive transcranial magnetic stimulation on motor and gait improvement in incomplete spinal cord injury patients. Neurorehabil & Neural Repair. 2013;27:421-429. Original DOI: 10.1177/1545968312471901. The above article has been retracted because of substantial overlap with a previously published article in another journal.

Objective. To evaluate the efficacy of botulinum toxin (BTX-A) injection in the cricopharyngeus muscle in patients with neurological dysphagia caused by alteration in the upper esophageal sphincter (UES) opening and with preserved pharyngeal contraction. Material and methods. A prospective pilot study was undertaken in 10 patients (7 brain lesions and 3 cervical spinal cord injuries), with a minimum time-lapse of 6 months from neurological lesion to BTX-A injection. Dysfunction of the UES opening and the presence of pharyngeal contraction were diagnosed by videofluoroscopy (VDF) and esophageal manometry (EM). The BTX-A (100 U) injection was guided by endoscopy. Clinical, VDF, and EM follow-ups were carried out at 3 weeks, 3 and 6 months, and at 1 year post-injection. Results. Prior to treatment, 6 patients were fed by nasogastric tube. VDF showed impairment of the UES opening, residue in pyriform sinuses, and aspiration in all cases. During follow-up, there was a decrease in the number of patients that had aspiration: 3 patients at one year. During swallowing, EM showed a mean UES relaxation of 90% (range: 74.5–100%), residual pressure 3.2 mmHg (range: 0–13 mmHg) and pharyngeal amplitude 52 mmHg (range: 25–80 mmHg). At follow-up, a significant improvement in UES relaxation (98% (89–100%)) and pharyngeal contraction (97 mmHg (35–165 mmHg)) was observed. At 3 months, 6 patients were eating exclusively by mouth. Conclusions. One single injection of BTX-A in the UES has long-lasting effectiveness in patients with neurological dysphagia caused by alteration in the UES opening and with pharyngeal contraction. Nevertheless, a randomized control trial should be done to confirm these results and rule out the effect of potential spontaneous improvement of neurological injury.