Abstract
Normal bowel physiology is a complex system that is under the combined control of intrinsic and extrinsic nervous systems that regulate intestinal mucous secretion, blood flow, and motility. Regardless of the specific neurologic condition or injury, disruptions along many portions of that extrinsic system, particularly within the central nervous system, will result in altered bowel functioning, known as a neurogenic bowel. This chapter describes that interplay between neurologic processes and bowel pathophysiology. The results of inadequately managed neurogenic bowel can have significant morbidity. The 2014 Cochrane review of this topic describes an effective management program for neurogenic bowel management as involving the “modulation of stool consistency, promotion of stool transit through the bowel, and effective reflex or manual evacuation of the stool from the rectum at an appropriate time and place.” This chapter discusses currently available diagnostic, treatment, and management options to optimize bowel care for individuals affected by neurogenic bowel.
Definition
A neurogenic bowel has been defined as “a life-altering impairment of gastrointestinal and anorectal function resulting from a lesion of the nervous system that can lead to life-threatening complications.” Neurologic dysfunction results in several gastrointestinal end-organ problems, including prolonged colonic transit time, reduced anorectal sensibility, and lack of voluntary control of the external anal sphincter associated with a dyssynergic response. These problems have an extensive impact on quality of life and frequently affect individuals with neurologic conditions, including spinal cord injury (SCI), multiple sclerosis (MS), cerebral palsy, spina bifida, stroke, and Parkinson disease. The quality and severity of colorectal dysfunction following an SCI depends on the degree of completeness and level of the SCI. Severity of bowel dysfunction after SCI correlates with high level of lesion, increased degree of completeness of injury, and longer duration of injury. As many as 95% of individuals with SCI may need some intervention to initiate defecation, and bowel dysfunction has been reported to affect lifestyle or life activities in 41% to 61% of persons living with SCI.
Bowel Innervations and Gastrointestinal Motility
Unlike the bladder, small and large bowels have a large degree of intrinsic regulation via the intrinsic enteric nervous system (ENS). The ENS is composed of the submucosal plexus and the myenteric plexus, which are located between the circular and longitudinal layers of smooth muscle in the wall of the intestines. The submucosal plexus regulates mucosal secretion and blood flow, while the myenteric plexus coordinates intestinal motility. The colon also receives extrinsic innervation from somatic as well as parasympathetic and sympathetic nerves. The vagus nerve arises intracranially and provides parasympathetic innervations from the esophagus to the splenic flexure of the colon, modulating the ENS to increase colonic motility. The vagus nerve is spared in spinal cord lesions ( Fig. 139.1 ). 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. Sympathetic innervations are supplied by the superior and inferior mesenteric (T9-T12) and hypogastric (T12-L2) nerves. This sympathetic system modulates the ENS to decrease colonic contractions. The somatic pudendal nerve (S2-S4) innervates the pelvic floor.
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. 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 produce transmission from cell to cell. Most intestinal muscle displays autorhythmicity that causes colonic wall contractions.
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 ENS and the activation of myenteric intrinsic primary afferent neurons are 5-HT 3 mediated. Signaling to the central nervous system is also predominantly 5-HT 3 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 ENS, which coordinates all segmental motility and some propagated movement.
A 2017 study documented the important interconnection between the intrinsic and extrinsic nervous systems of the intestines by demonstrating that impaired extrinsic innervation results in major neuromuscular alterations of the colon. These include loss of myenteric neurons, decreased nerve fiber density in the myenteric plexus, and disruption of the network of signaling cells around the myenteric plexus.
Normal defecation is the result of a complex interaction between muscles, nerves, and central nervous system. For normal defecation, there must be a mass movement of colonic contents associated with relaxation of internal and external anal sphincters. 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. 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.
Neurogenic Bowel
A neurogenic bowel occurs when there is a dysfunction of the colon or rectosigmoid due to impaired extrinsic nervous control. The ENS remains intact after an SCI. 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.
A lesion above the conus medullaris causes an upper motor neuron bowel syndrome or hyperreflexic 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. These changes result in 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 neurogenic bowel, constipation is usually a major consequence. 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 cause obstructed defecation or fecal incontinence. 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 or pelvic floor dyssynergic response. This is not a true dyssynergia because 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
Neurogenic bowel results in a wide spectrum of gastrointestinal symptoms: incontinence, constipation, hemorrhoids, abdominal pain, abdominal bloating, fecal impaction, rectal bleeding, rectal prolapse, anal fissure, nausea, autonomic dysreflexia, and prolonged evacuation. These symptoms and/or the fear of these symptoms negatively impact quality of life and may lead to social isolation. Hospitalization for an intestinal complication such as constipation, volvulus, impaction, or megacolon is twice as frequent in individuals with a neurogenic bowel versus those without this condition.
Physical Examination
For the management of neurogenic bowel, an individual evaluation 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 SCI. 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. 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. The occurrence and/or fear of unplanned or uncontrolled bowel evacuation can lead to social isolation, significant vocational challenges, and depression.
Diagnostic Studies
Colonic motor activity comprises four main components: myoelectric activity, 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. Although the direct assessment of colonic contractile activity can be achieved through colonic manometry, this procedure is only slowly gaining clinical acceptance, notably in children. Other novel methods are also available; two techniques exist for the routine assessment of colonic (or whole gut) transit, both of which involve irradiation of the subjects: radiopaque markers and radionuclide scintigraphy. Wireless (telemetric) motility capsules with magnetic markers to obviate irradiation are currently being tried, but they need further validation before being incorporated into general clinical practice. Together with assessment of rectal evacuation and rectal sensation, studies of colonic transit should form the cornerstone of investigation of chronic idiopathic constipation in patients with functional or partial neurologic impairment. These investigations have led to the conceptualization of constipation in three broad and overlapping categories: normal-transit constipation, slow-transit constipation, and evacuation disorders.
Anorectal Dyssynergia
For the precise diagnosis of anorectal dyssynergia, particularly in incomplete or functional lesions, anorectal manometry along with simultaneous electromyography of the external anal sphincter is important to distinguish between functional constipation and obstructed constipation due to a neurologic lesion. It is also important to evaluate impairment due to an incomplete lesion (e.g., MS, pudendal nerve lesion after childbirth, lumbar disc disease, back injury, or spinal tumor). Defecography, nerve stimulation and pudendal latency, ultrasonography, and magnetic resonance imaging may also be required for better understanding of gastrointestinal dysfunction. Defecography detects structural abnormalities and assesses functional information on the movement of the pelvic floor and the organs that it supports; conversely, excessive descent (descending perineum syndrome) can also be a pathophysiologic mechanism of constipation. Defecography can also help complement anorectal manometry studies in ruling out slow transit and other causes of constipation. Magnetic resonance imaging or pelvic floor sonography can further complement the studies.
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