Neurogenic Bowel Dysfunction and Management

Disrupted autonomic control of the gastrointestinal (GI) tract is the primary cause for neurogenic bowel dysfunction, leading to delayed gastric emptying (Leduc et al. 2002Gondim et al. 2001Menter et al. 1997Rajendran et al. 1992Fealey et al. 1984) and poor colonic motility (Lynch & Frizelle 2006Fajardo et al. 2003). This results in prolonged bowel transit time (Brading & Ramalingam 2006Krogh et al. 2000Nino- Murcia et al. 1990Lynch et al. 2001), constipation (Faaborg et al. 2008Finnerup et al. 2008Lynch 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 fecal 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. 2007Cosman & 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. 2006Stiens 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 feces 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.

To achieve fecal continence and avoid constipation, management of neurogenic bowel dysfunction depends upon regular and frequent pre-emptive interventions to empty the bowel at a planned time and frequency. A strict routine using dietary manipulation, rectal stimulants, oral laxatives and physical interventions such as abdominal massage, digital rectal stimulation and manual evacuation of stool is required to establish control over this profoundly important bodily function. Such multifaceted programs are the most commonly used method of bowel management after SCI (Coggrave et al. 2009) but evidence to support these programs is lackingand much trial and error is involved in development of effective, individualized routines.

Rarely, dangerous complications like sigmoid volvulus, intestinal obstruction, perianal abscess and stercoral perforation may develop (Banwell et al. 1993). In addition, autonomic dysreflexia is a life threatening emergency to which individuals with SCI above the 6th thoracic vertebra are at risk. Bowel dysfunction is the second most common cause of autonomic dysreflexia, a disorder characterized by an abnormal reaction to stimuli below the level of the SCI, resulting in a massive rise in blood pressure that can lead to adverse events including brain haemorrhage and death. Common GI problems reported by up to 41% of individuals with SCI include abdominal pain and bloating, haemorrhoids and rectal prolapse (Correa & Rotter 2000). Prolonged bowel evacuation is also common, particularly in chronically injured individuals (Coggrave et al. 2009Kirk et al. 1997Lynch et al. 2000), this is as disabling as ineffective management and is associated with anxiety (Glickman & Kamm 1996). The prevalence of chronic GI symptoms increases with time after injury, suggesting that these problems are acquired and potentially preventable (Rajendran et al. 1992).

It is important to emphasize that each person with SCI is unique and that individual bowel programs (maintain continence, ensure completed within a timely manner, safe, etc.) need to be client-specific. The program will reflect not just residual bowel function but also the individual’s personal goals, lifestyle and social circumstances. The effectiveness of a bowel program should be reevaluated and modified as needed.

Upper Motor Neuron lesion Lower Motor Neuron lesion
Level >T10 vertebral or T12 spinal segment >T10 vertebral or T12 spinal segment
Time from cecum to anus Increased Increased
Motility of left colon Decreased Decreased
External anal sphincter Spastic paralysis Flaccid paralysis
Sympathetic output Absent with lesions > T6 spinal segment Retained
Symptoms Constipation

Difficulty with evacuation



Difficulty with evacuation


Fecal impaction Proximal colon Rectal
Autonomic dysreflexia Common Rare
Reflex defecation Present Not known