Definition

Within the nervous system, there are peripheral, somatic, and autonomic (sympathetic and parasympathetic) contributions to the various organ-based functions. Related to the gastrointestinal system, several end-organ problems resulting from neurologic dysfunction include prolonged colonic transit time, reduced anorectal sensibility, and lack of voluntary control of the external anal and urethral sphincters, often associated with a dyssynergic response. The severity of colorectal dysfunction depends on the degree of completeness and level of the spinal cord injury [1,2]. However, specific evaluation is required in individual cases. These problems have an extensive impact on quality of life. Our study based on interviews of 125 consecutive male patients and 2 female patients with spinal cord injury showed that 27% of patients had chronic disabling gastrointestinal problems requiring alteration of their lifestyle; symptoms usually appeared 5 to 10 years after injury (P < .05) [3]. Severity of bowel dysfunction correlated with high level of lesion, completeness of cord injury, and longer duration of injury (≥ 10 years) [4,5].

Bowel Innervations and Gastrointestinal Motility

Unlike in the bladder, small and large bowel movements are mainly autonomous and may be influenced with some spinal cord lesions. The vagus nerve, which arises intracranially and provides parasympathetic innervations from the esophagus to the splenic flexure of the colon, is spared in spinal cord lesions (Fig. 138.1). The pelvic nerve carries parasympathetic fibers from S2-S4 to the descending colon and rectum. Some pelvic nerve branches travel proximally and innervate the transverse and ascending colon [6]. Sympathetic innervations are supplied by the superior and inferior mesenteric (T9-T12) and hypogastric (T12-L2) nerves. The somatic pudendal nerve (S2-S4) innervates the pelvic floor.

The intrinsic nervous system of the gastrointestinal tract, which includes Auerbach plexus, is situated in the colonic wall between the longitudinal and circular muscle layers. This nerve supply helps coordinate colonic wall movement and the advancement of stool through the colon. The behavior of the bowel can be controlled by the intrinsic innervations of the gut independently of input from the central nervous system.

The extrinsic nervous system also innervates the colon and includes the parasympathetic, sympathetic, and somatic nerves [4,5]. Peristaltic waves travel both toward and away from the ileocecal valve in the ascending colon; but in the descending colon, the waves travel mainly to push the contents to the anus [4]. The motility of the colon is performed by three primary mechanisms: myogenic, chemical, and neurogenic. The myogenic transmission of signals occurs between enteric smooth muscle cells that are interconnected by gap junctions, which produces transmission from cell to cell. Most intestinal muscle displays autorhythmicity that causes colonic wall contractions [4].

Chemical control is through the activity of neurotransmitters and hormones. The chemicals influence the promotion or inhibition of contractions through the action of the central nervous system or autonomic nervous system or by direct action on muscle cells. This activity can be triggered by luminal stimuli that are detected by nerves through epithelial intermediation. Epithelial enterochromaffin cells act as sensory transducers that activate the mucosal processes of both intrinsic and extrinsic primary afferent neurons through their release of 5-hydroxytryptamine (5-HT). Intrinsic primary afferent neurons are present in both the submucosal and myenteric plexuses. Peristaltic and secretory reflexes are initiated by submucosal intrinsic primary afferent neurons, which are stimulated by 5-HT acting at 5-HT_1P receptors. Serotonergic transmission within the enteric nervous system and the activation of myenteric intrinsic primary afferent neurons are 5-HT₃ mediated [6]. Signaling to the central nervous system is also predominantly 5-HT₃ mediated. The gut is thus the only organ that can display reflexes and integrate neuronal activity even when it is isolated from the central nervous system.

The neurogenic mechanism of colonic control is through the enteric nervous system, which coordinates all segmental motility and some propagated movement. The number of intrinsic neurons in the gut greatly exceeds the number of fibers in the vagus and splanchnic nerves. In humans, the enteric nervous system contains up to 100 million neurons, compared with only 2000 efferent fibers in the vagus nerve, suggesting that intrinsic nerves may direct most reflex and control activities and that the extrinsic innervations may serve only a modulatory function [7,8].

Normal defecation is the result of a complex interaction between muscles, nerves, and central nervous system. For a normal defecation, there needs to be a mass movement of colonic contents associated with relaxation of internal and external anal sphincters. Mass movement of colonic contents before defecation associated with internal sphincter relaxation has recently been shown to result from high-amplitude propagating contractions in children even with sigmoid dysmotility [9]. The colon absorbs fluids, electrolytes, and short-chain fatty acids; provides for growth of symbiotic bacteria; secretes mucus for lubrication of feces; and slowly propels stool toward the anus [10]. The contents in the distal colon are retained until bowel evacuation. Transport of contents may take 12 to 30 hours from the ileocecal valve to the rectum [2].

Neurogenic Bowel

A neurogenic bowel occurs when there is a dysfunction of the colon or rectosigmoid due to the lack of nervous control [11–13]. The enteric nervous system remains intact after spinal cord injury. However, depending on the level of the injury, different bowel problems and complications may arise. The lower motor neuron bowel syndrome or areflexic bowel results from a lesion affecting the parasympathetic cell bodies in the conus medullaris, cauda equina lesions, or damage to the pelvic nerves. No spinal cord–mediated peristalsis occurs, and there is slow stool propulsion. Only the myenteric plexus coordinates segmental colonic peristalsis, and a dryer, rounder stool shape occurs. Because of the denervated external anal sphincter, there is increased risk for incontinence. The levator ani muscles lack tone, and this reduces the rectal angle and causes the lumen of the rectum to open. The lower motor neuron bowel syndrome produces constipation and a significant risk of incontinence due to the lax external anal sphincter. A lesion above the conus medullaris causes an upper motor neuron bladder and bowel syndrome or hyperreflexic bladder and bowel. There is increased colonic wall and anal tone. The voluntary control of the external anal sphincter is lacking, and the sphincter remains tight, thereby retaining stool. The nerve connections between the spinal cord and the colon, however, remain intact; therefore, there is reflex coordination and stool propulsion. The upper motor neuron bowel syndrome with supraconal lesions in the spinal cord produces constipation and fecal retention at least in part owing to the hyperactivity of the external anal sphincter.

Pathophysiology of Constipation in Neurologically Impaired Patients

In neuropathic bowel, constipation is usually a major consequence [11–13]. The pathophysiologic mechanisms of constipation are obstructed defecation, weak abdominal muscles, impaired rectal sensation, and delayed colonic transit time. Both incomplete and complete lesions can have an obstructed defecation or fecal incontinence [14]. The mechanism for fecal incontinence is due to areflexic or atonic anal sphincter, uninhibited rectal contractions, poor rectal sensibility, and lack of anal sphincter tone and contraction (conus and cauda equina lesions).

During attempts to defecate, in some able-bodied persons with chronic constipation, there is also an inappropriate contraction (or failed relaxation) of the puborectalis and of the external anal sphincter muscles. This paradoxical contraction of the pelvic floor musculature during straining at defecation is also called pelvic floor dysfunction [14,15] or pelvic floor dyssynergic response. This is not a true dyssynergia because it can be relaxed with volitional control. The diagnostic criteria were elucidated in the Rome II report and include those for functional constipation plus at least two of three investigations among manometry, electromyography, and defecography showing inappropriate contraction of or failure to relax the pelvic floor muscles [14,15]. Patients can learn to relax the pelvic floor musculature with biofeedback to manage functional obstructed defecation. This dyssynergic response, therefore, needs to be distinguished from true detrusor anal sphincter dyssynergia due to neurologic impairment, in which biofeedback may not have any role for the functional improvement.

Symptoms

There is a high prevalence and wide spectrum of gastrointestinal symptoms after spinal cord injury. Abdominal bloating and constipation are usually related to specific spinal cord levels of injury [16]. The limited manner through which spinal cord–injured patients can manifest symptoms resulted in complaints that were characteristically vague [3]. The most common problems that impaired quality of life were poorly localized abdominal pain (14%) and difficulty with bowel evacuation (20%), hemorrhoids (74%), abdominal distention (43%), and autonomic dysreflexia. Twenty-three percent of our population required at least one admission to the hospital for a gastrointestinal complaint after their injury. The prevalence of chronic gastrointestinal symptoms increased with time after injury [3].

Physical Examination

For the rehabilitation of neurogenic bowel, an individual evaluation [17,18] is important with a careful rectal examination and anorectal neurologic testing to document degree of neurologic impairment. A neurologic examination can reveal the extent of the nerve damage and the completeness of the spinal cord injury. The abdomen should be inspected and palpated for distention, palpable fecal masses, increased abdominal muscle tone indicative of spasticity, and bowel sounds. The rectal examination can provide information about external anal sphincter tone, stool in the rectal vault, presence of hemorrhoids, cystocele in women, or masses, and it assesses the tone and ability to produce voluntary contraction of the puborectalis muscles.

The bulbocavernosus reflex assesses the integrity of the local spinal reflex arc; its absence along with poor anal tone indicates a conus or cauda equina lesion (lower motor neuron). It is also important to assess the patient’s strength in the upper and lower extremities, hand function, sitting balance, and ability to transfer; the length of the patient’s arms, legs, and trunk; and the patient’s weight. These factors are helpful to determine whether the patient can perform his or her own bowel program or whether assistance will be needed. Berkowitz and colleagues [19] found that 37% of all patients with spinal cord injury need assistance with bowel care. People with tetraplegia are more likely to need assistance than are people with paraplegia.

Functional Limitations

There is some degree of loss of voluntary control for bowel evacuation, constipation, unpredicted incontinence, abdominal distention, and associated discomfort, depending on the degree and level of completeness of the neurologic lesion.

Diagnostic Studies

Colonic and anorectal dysfunctions are recognized as the principal pathophysiologic mechanism underpinning chronic constipation and particularly obstructed constipation in neurologically impaired patients [20].

Colonic motor activity comprises four main components: myoelectric activity [21], phasic contractile activity, tonic contractile activity, and intraluminal transit. Specific methods are available for the assessment of each separate component, but no single investigation gives information about all four types of activity. In current clinical practice, evaluation of colonic motor function is almost exclusively limited to assessment of intraluminal pressure and transit time [22