Disrupted autonomic control of the gastrointestinal (GI) tract is the primary cause for neurogenic bowel dysfunction, leading to delayed gastric emptying (Leduc et al. 2002; Gondim et al. 2001; Menter et al. 1997; Rajendran et al. 1992; Fealey et al. 1984) and poor colonic motility (Lynch & Frizelle 2006; Fajardo et al. 2003). This results in prolonged bowel transit time (Brading & Ramalingam 2006; Krogh et al. 2000; Nino- Murcia et al. 1990; Lynch et al. 2001), constipation (Faaborg et al. 2008; Finnerup et al. 2008; Lynch et al. 2000), and postprandial (after eating a meal) abdominal distension (Stone et al. 1990a). Left unmanaged, individuals with neurogenic bowel dysfunction will experience profound constipation and fecal impaction as effective spontaneous evacuation does not occur. In addition, lost or impaired anorectal sensation and voluntary motor control lead to unpredictable feacal incontinence. The neurogenic changes are compounded by reduced mobility, polypharmacy and poor dietary intake. Furthermore, bowel dysfunction following SCI is associated with episodes of autonomic dysreflexia (Furusawa et al. 2007; Cosman & Vu 2005).
The colon and anorectum are innervated by the sympathetic and parasympathic autonomic nervous system with somatic innervation to the external sphincter as shown in Figure 1. In addition the gastrointestinal tract has an enteric nervous system divided into the submucosal (Meissner’s) and myenteric (Auerbach’s) plexuses. The enteric system controls gut secretions, blood flow and muscular activity giving the colon its inherent ability to produce peristalsis. While the autonomic and somatic neural input is disrupted in SCI, the enteric system remains intact.
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 while injury at the conus medullaris and cauda equina results in lower motor neuron (LMN) bowel syndrome (Singal et al. 2006; Stiens et al. 1997).
The upper motor neuron bowel, or hyperreflexic bowel, is characterized by increased colonic wall and anal tone. Voluntary (cortical) control of the external anal sphincter is lost or impaired and the sphincter remains tight, thereby promoting retention of stool. However, fecal incontinence can and does occur. Although there is loss of supraspinal control, the nerve connections between the spinal cord and the colon remain intact; therefore, there is preserved reflex coordination and stool propulsion. The upper motor neuron bowel syndrome is typically associated with constipation and fecal retention at least in part due to external anal sphincter over activity (Stiens et al. 1997). Stool evacuation in these individuals occurs in response to stimulation of reflex activity, such as presence of faeces in the rectum, a suppository, enema, or digital rectal stimulation causing rectal distension.
The lower motor neuron bowel, or areflexic bowel, is characterized by the loss of centrally-mediated (spinal cord) peristalsis and loss of reflex activity, resulting in slow stool propulsion and impaired reflex stool evacuation. A segmental colonic peristalsis occurs only due to the activity of the enteric nervous system, which is slower and less efficient than the centrally-mediated peristalsis. The result is increased bowel transit times with the production of drier and round- shaped stool. Lower motor neuron 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 puborecatlis and levator ani muscles; coordinated actions of these striated muscles are important in maintaining continence.
Completeness of injury also has a significant impact on bowel function in individuals with SCI. Those with an incomplete injury may retain some sensation of rectal fullness and some ability to control evacuatory function. However, residual rectal sensation may be abnormal and motor control impaired, resulting in fecal urgency or constipation due to disordered defaecation reflexes. Careful assessment is required.