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The Neurogenic Bowel After SCI

| Source: depts.washington.edu

The digestive tract is essentially a long tube that begins at the lips and ends at the anus. After food is swallowed, it moves through the esophagus to the stomach, which is basically a storage bag, and then on to the intestines or bowels, where nutrients are absorbed and waste is collected and prepared for elimination.

The absorption of nutrients occurs in the small bowels, which are made up of the duodenum, the jejunum, and the ileum. The caecum marks the entryway into the colon or large bowel, where digestive waste is stored before exiting the body.

The colon encircles the abdomen, starting on the right with the ascending colon, passing across the top with the transverse colon, and down the “s”-shaped sigmoid colon to the rectum, which opens at the anus.

The movement of feces through the colon is produced by coordinated muscular contractions of the colon walls called peristalsis. This motion is orchestrated by a bureaucracy of nerve cells at several different levels.

At the bottom is the myenteric (Auerbach’s) plexus, a network of nerves which are located between the circumferential and longitudinal bowel wall muscles and which direct local intestinal movement. In 1899, two English physiologists, W. M. Bayliss and E. H. Starling, reported that the intestines, even when removed from the body, have an inherent tendency to produce peristalsis toward the anus. This has become known as the “law of the intestine”. Whenever the intestine wall is stretched or dilated, the nerves in the myenteric plexus cause the muscles above the dilation to constrict and those below the dilation to relax, propelling material down the tube.

The next level of organization comes from autonomic nerves that travel from the brain and spinal cord to the colon. The ascending colon and the rest of the digestive tract that precedes it, as well as part of the transverse colon, receive messages through the vagus (“vagabond”) nerve, which starts at the brain and bypasses the spinal cord, following the esophagus into the abdomen. The pelvic parasympathetic nerves, or nervi erigentes, bring movement messages from the spinal cord (Sacral segments 2, 3, and 4) to the neurons in part of the transverse and all of the descending colon to propel feces out of the colon.

The highest level of control comes from the brain. Conscious perception of rectal distention permits discrimination between solid material and gas, and the decision to eliminate colonic contents in a socially acceptable manner. Messages relayed via the spinal cord produce voluntary relaxation of the pelvic floor and anal sphincter muscles, allowing defecation to occur. This process is aided by coordinated abdominal muscle contractions that increase intra-abdominal pressure and compress the colon.

Depending on its location, spinal cord injury (SCI) produces one of two different patterns of bowel dysfunction. An injury above the sacral segments of the spinal cord produces a “spastic”, or upper Motor Neuron (UMN), bowel, in which defecation cannot be triggered by conscious effort, but the spinal Reflex remains intact. The anal sphincter remains tight due to Spasticity of the pelvic floor.

An injury below the sacral segments that damages the nerves connecting the spinal cord to the colon results in a “relaxed”, or lower motor neuron (LMN), bowel, in which no spinal-cord-mediated reflex defecation can occur. Slow stool propulsion is coordinated by the myenteric plexus alone, and the anal sphincter has low tone, producing a sluggish stool movement and a dryer, rounder (scybalous) stool shape.

Study of patients with upper Motor Neuron SCI has been limited, but a number of Functional abnormalities have been described. Menardo et al. found that swallowed markers passing through the digestive tract in patients with SCI moved very slowly through the transverse and descending colon. However, surface electromyographic studies have demonstrated increased muscular activity in the colon after SCI. Without regular bowel movements to clear the stool, this activity may lead to increased intracolonic pressures and development of complications such as fecal impactions, diverticulosis (small out-pocketings of the colon), and Autonomic Dysreflexia (a sudden, severe increase in blood pressure in response to a noxious stimulus below the level of injury).

To achieve satisfactory bowel function after SCI, the Rehabilitation process emphasizes social continence of stool and predictable, efficient defecation. Without the ability to feel stool in the rectum or to voluntarily initiate Reflex defecation, a person with SCI must regularly assume the need for bowel movements and stimulate the reflex manually with a finger inserted in the rectum and/or with appropriate suppositories.

Persons with UMN injuries need a scheduled trigger of defecation daily or at least once every three days. The trigger is typically a suppository, enema, or mini-enema, which produces a mucosal contact stimulus that is transmitted to the Sacral spinal cord. The most common active ingredient in these preparations is bisacodyl, which activates mass colonic movement in 5-15 minutes. Sequential waves of colon peristalsis are then maintained by moving the finger in a circular motion inside the rectum (digital stimulation), which activates the law of the intestine, producing peristalsis above the finger, and also gently stretches the anus open, reducing the spastic tone and allowing the stool to pass.

A full meal before the Bowel program may increase colonic activity, although research has produced mixed results concerning whether this response (known as the gastrocolic reflex) is preserved after upper motor neuron SCI. Defecation may also be aided by increasing abdominal pressure through contractions of the abdominal muscles or the use of a tight elastic band around the abdomen.

Those with LMN injuries have more difficulty with their bowel programs due to the absence of spinal reflex peristalsis and low tone of the anal sphincter. The rectum must be cleared of stool more frequently, usually one or more times per day, to prevent accidents from stool that cannot be retained by the loose sphincter. Some patients wear tight underwear or bicycle pants to support the pelvic floor and help retain stool. The LMN bowel program usually consists of removing stool with the finger and using digital stimulation to increase peristalsis. Continence of stool is improved by eating a high-fiber diet (vegetable and fruit fibers absorb water and help keep the stool formed) and by using medications, often containing plant fibers such as psyllium hydromucilloid (Metamucil, Citrucel), to produce a drier stool.

Treatment techniques have changed little over the last 20 years, and major changes in the near future are unlikely. Recent research has focused on reducing the time required to complete a bowel program and on improving the ease of access for digital stimulation. Reviews of commode chair design and use assessments have led to suggestions for improvements such as adjustable seat heights, new seat cutout designs, and improved skin exposure for showering.

In preliminary studies conducted at the Seattle Veterans Affairs Medical Center, we have found that bisacodyl suppositories made with new media, such as polyethylene glycol, produce shorter bowel programs than those made with conventional vegetable oil. Persons with SCI often change their habits and techniques of bowel care after they leave inpatient rehabilitation, and we are developing a questionnaire to investigate the reasons for these changes and their effect on gastrointestinal function. Others have done animal studies using electrical stimulation of the nerves from the spinal cord to the colon, and have been successful in producing defecation in upper motor neuron injuries. More testing is needed before this technique is tried in humans.

A small number of persons with long histories of SCI and limited ability to independently manage their own bowel care have reported improvements in quality of life after colostomy. This surgical procedure creates a permanent opening between the colon and the surface of the abdomen to which a stool collection bag is attached. Colostomies sometimes become necessary because of fecal soiling of pressure sores (decubiti), continual stool Incontinence, or excessively long bowel programs. Colostomy enables many patients to manage their bowels independently, and colostomy management usually takes less time than bowel programs.

Prevention of complications of the neurogenic bowel begins with a balanced diet that includes plenty of liquids, fruit, and vegetables, since plant fibers absorb water and stimulate peristalsis, making it easier for the stool to be propelled without excessive intracolonic pressures. Supporting the pelvic floor with a gel or air cushion to distribute pressure over the entire perineal surface prevents the enlargement of hemorrhoids and maintains closure of the anal sphincter.

Following a regular schedule of bowel programs is important even if stool elimination does not occur each time. Missed bowel programs can contribute to the buildup in the colon of excessive stool that becomes dryer and more difficult to eliminate. This can overstretch the colon wall, reducing the effectiveness of peristalsis and resulting in longer bowel programs with poorer results.

Chronic daily use of oral stimulant laxatives, such as phenolphthalein, senna, bisacodyl, and cascara preparations, should be avoided because the bowel may develop a tolerance to them, making them less effective. Stool softeners, such as docusate sodium and mineral oil, are preferred for ongoing use because tolerance does not develop. Daily fiber supplements containing cellulose, polysaccharide, or psyllium can improve stool consistency if adequate fluid intake is maintained.

Hemorrhoids can be prevented through frequent digital stimulations to minimize the time necessary for the bowel program and by avoiding constipation.

VAMC SCI Gastrointestinal Research Group: Steven A. Stiens, MD; Margaret C. Hammond, MD; Richard Buhrer, RN, MN; Victoria Bozzacco, MN; Janet Loehr, ARNP; Glen House, MSIII.


1. Menardo G, Baujano G, Corazziari E, et al. Large bowel transit in Paraplegic patients. Dis Colon Rectum 1987;30:924-8.
2. Aaronson MJ, Freed M, Burakoff R. Colonic myoelectric activity in persons with spinal cord injury. Dig Dis Sci 1985;30:295-300.
3. Glick ME, Meshinpour H, Haldeman S, et al. Colonic Dysfunction in Patients with Thoracic Spinal Cord Injury. Gastroenterology 1984;86:287-94.
4. Gore RM, Mintzer RA, Calenoff. Gastrointestinal complications of spinal cord injury. Spine 1981 6:536-44.
5. Sun EA, Snape WJ, Cohen S, et al. The role of opiate receptors and cholinergic neurons in the gastrocolonic response. Gastroenterology 1982;82:689-93.
6. Connell AM, Frankel H, Guttmann L. The motility of the pelvic colon following complete lesions of the spinal cord. Paraplegia 1963;1:98-115.

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