Bowel function is a major physical and psychological problem for persons with spinal cord injury. Following a spinal cord injury, changes in bowel motility, sphincter control and gross motor dexterity interact to make bowel management a major life-limiting problem. In 2000, Lynch et al. surveyed 1200 persons with SCI and 1200 age and gender-matched controls to describe bowel function. For persons with SCI, their mean Fecal Incontinence Score (FIS) was significantly higher than controls. It was also noted that for persons with complete SCI, their mean FIS was significantly higher than those persons with incomplete SCI. Quality of life was affected by incontinence in 62% of SCI respondents compared with 8% of controls. Fecal urgency and time spent on bowel management were also significantly higher for persons with SCI. A significantly higher percentage (39%) of SCI respondents use laxatives compared to 4% of controls. The decreased ability to discriminate between gas and liquid for complete SCI patients also makes the chance for fecal incontinence more likely.

Depending on the level of injury, there are two distinct patterns in the clinical presentation of bowel dysfunction: injury above the conus medullaris results in upper motor neuron (UMN) bowel syndrome and injury at the conus medullaris and cauda equine results in lower motor neuron (LMN) bowel syndrome (Singal et al. 2006; Steins et al. 1997).

The UMN bowel syndrome, or hyperreflexic bowel, is characterized by increased colonic wall and anal tones. Voluntary (cortical) control of the external anal sphincter is disrupted and the sphincter remains tight, thereby promoting retention of stool. The nerve connections between the spinal cord and the colon, however, remain intact; therefore, there is preserved reflex coordination and stool propulsion. The UMN bowel syndrome is typically associated with constipation and fecal retention at least in part due to external anal sphincter activity (Steins et al. 1997).  Stool evacuation in these individuals occurs by means of reflex activity caused by a stimulus introduced into the rectum, such as an irritant suppository or digital stimulation.

LMN bowel syndrome, or areflexic bowel, is characterized by the loss of centrally-mediated (spinal cord) peristalsis and slow stool propulsion.  A segmental colonic peristalsis occurs only due to the activity of the intrinsic myenteric plexus, resulting in the production of drier and round- shaped stool. LMN bowel syndrome is commonly associated with constipation and a significant risk of incontinence due to the atonic external anal sphincter and lack of control over the levator ani muscle that causes the lumen of the rectum to open.

Completeness of injury also has a significant impact on bowel function in individuals with SCI.  Those with an incomplete injury may retain the sensation of rectal fullness and ability to evacuate bowels so no specific bowel program may be required.

Table 1: Clinical Presentations in Bowel Functions Following SCI (Singal et al. 2006)

Difficulties with bowel emptying are of concern to most persons with SCI. For the tetraplegic patient, loss of control over visceral function may be seen as more important than the ability to walk (Frost et al. 1993). Urinary problems in patients with SCI have been extensively studied, and with the advent of intermittent self-catheterization, electrical stimulation of the bladder and advances in diagnostic techniques, considerable improvements have been made in managing lower urinary tract and renal function. In contrast, the management of bowel disorders, and in particular, the intractable constipation that is so common in these patients, has remained essentially unchanged over the past two decades (MacDonagh et al. 1990).

Various researchers have shown that electrical stimulation of the somatic nervous system can bring about an alteration in visceral function in humans. Riedy et al. (2000) showed that short periods of electrical stimulation with perianal electrodes resulted in an increase in anal pressures. Bowel reflex centres within the sacral spinal cord may be released from descending inhibition after SCI and may be altered with somatic input (Frost et al. 1993). Electrical sacral root stimulation induces defecation in SCI patients and is currently under examination as a new therapy for fecal incontinence. In contrast to electrical stimulation, magnetic stimulation may produce similar results and is noninvasive (Morren et al. 2001). Morren et al. (2001) studied the effects of magnetic sacral root stimulation on anorectal pressure and volume in both fecal incontinence and SCI patients. Sun et al. (1995) investigated the role of spinal reflexes in anorectal function. Their subjects underwent anorectal manometry and electromyography, before and after having a sacral posterior rhizotomy performed by the same neurosurgeon. They found that all subjects lost conscious control of the external anal sphincter as well as  responses to intra-abdominal pressure and rectal distention. While the use of sacral root stimulation, either electrical or magnetic, seems to be producing positive results, further research is required.