Epidemiology

Gastrointestinal dysfunction is frequently seen in people with neurologic diseases who require rehabilitation. Besides the direct effects of neurologic disease on gut function, debility, insufficient fluid intake, and use of anticholinergics and other medications can play a huge role in the development of enteric problems. Digestive tract problems and neurogenic bowel problems in stroke, brain injury, multiple sclerosis, Parkinson disease, neuromuscular diseases, muscular dystrophy, dysautonomias, peripheral nerve injuries, SCI, myelomeningocele, and other neurologic disorders have been shown to be difficult and challenging to manage and can be a primary disabling and handicapping feature for patients. *

* References .

Impact

Living with nausea, vomiting, bloating, abdominal pain, constipation, diarrhea, or fecal incontinence profoundly affects the quality of life. It significantly affects nutrition, overall health, and sense of well-being. Loss of voluntary control over bowel function alters every facet of a person’s life at home, at work, and in the community. The ability to spontaneously regulate and direct bowel function is essential for participation in everyday activities at home, work, or school. It plays a major role in one’s ability to create and maintain relationships. It has a significant impact on activities such as recreation or travel. Problems with constipation and fecal incontinence can create considerable psychological, social, and emotional trauma.

Fecal incontinence decreases the return-to-home rates for patients with stroke. Almost one third of persons with SCI report or exhibit worsening of bowel function 5 years beyond their injury, with 33% developing megacolon, suggesting inadequate long-term management. Recent evidence has shown some improvement outcomes for SCI bowel management. Nursing home costs are higher for patients with fecal incontinence. When restoring normal defecation is not possible, social continence becomes the goal. Social continence is defined as predictable, scheduled, adequate defecations without incontinence at other times. It is often achievable by persons with neurogenic bowel dysfunction. Embarrassment and humiliation from fecal incontinence frequently result in vocational and social disability, and adds substantial costs to the care related to neurogenic bowel dysfunction.

Neuroanatomy and Physiology of the Gastrointestinal Tract

In the past two decades, there has been significant advancement in the science of neurogastroenterology. This includes new discoveries in the basic physiology of the gastrointestinal tract and interactions with the brain and spinal cord, autonomic and enteric nervous systems, and somatomotor system (pharyngeal muscles and swallowing, pelvic floor muscles and defecation, continence. and pelvic pain).

Normal functioning of the stomach and intestines entails coordination of muscle contraction, digestion and absorption of nutrients, and regulation of blood flow. The neural schema of the gastrointestinal tract is much more complex than previously thought. Neural control of the gastrointestinal tract is an extremely organized and integrated hierarchy of mechanisms that involve the central nervous system (CNS; brain and spinal cord), autonomic nervous system (sympathetic and parasympathetic), and the enteric nervous system (ENS) ( Figures 21-1 and 21-2 ).

Gastrointestinal function is coordinated by three nervous systems: somatic, autonomic, and the enteric nervous system intrinsic to the gut wall. ES , External sphincter; IS, internal sphincter.

Neurologic levels and pathways for the sympathetic, parasympathetic, and somatic nervous system innervation of the colon and anorectum. Not shown is the enteric nervous system, which travels along the bowel wall from the esophagus to the internal anal sphincter and forms the final common pathway to control the bowel wall smooth muscle.

Enteric Nervous System

The ENS is a distinct system that has its own set of neurons that coordinate sensory and motor functions. In the ENS, the ganglia are interconnected, which allows for integration and processing of data (as opposed to autonomic ganglia, which only serve as relay centers for stimuli transmitted from the CNS). There are three different types of neurons in the ENS based on function: sensory neurons, interneurons, and motor neurons. Sensory neurons perceive thermal, chemical, or mechanical stimuli and transform these sensations into action potentials that are conducted to the nervous system. Interneurons serve as conduits between the sensory and motor neurons. The numerous synapses between interneurons create a highly organized circuitry that processes sensory input from the gut and other parts of the nervous system and integrates and generates reflex responses to these stimuli. Motor neurons are the final common pathway. They receive and translate signals to the gut (mucosa, muscle, vasculature) that affect digestive, interdigestive, and emetic functions based on the transmitters released.

Automatic feedback control is present in the ENS, with the neurons being in close proximity to the stomach and intestines. This can be manifested as reflex circuits that systematize reflex responses to sensory signals, integrative circuits that coordinate motor patterns (migrating motor complex, digestive activity, giant migratory contractions [GMCs]), or as a pattern-generating activity that is generated when a “command neuron” is actuated and a rhythmic, repetitive behavior occurs.

The ENS is the key to proper functioning of the entire gastrointestinal tract. This collection of highly organized neurons is situated in two primary layers: the submucosal (Meissner) plexus and the intramuscular myenteric (Auerbach) plexus. These plexuses have an estimated 10 to 100 million neurons, plus two to three glial cells per neuron. The ENS glial cells resemble CNS astrocytes, and are much less abundant than the 20 to 50 glial cells per neuron in the CNS. The coordination of segment-to-segment function is largely regulated by the ENS. The ENS also has its own blood-nerve barrier, similar to the blood-brain barrier of the CNS.

Enteric Nervous System Relationship to the Spinal Cord and Brain

Sensory information from vagal afferents in the ENS is relayed to the nodose ganglia (caudal ganglion of the vagus) and consequently to the nucleus tractus solitarius (NTS) and area postrema in the medullary area of the brainstem. The NTS and the area postrema send signals to the rostral centers in the brain. The brain processes the data and projects descending connections to the dorsal vagal complex. The brain also participates in vagovagal reflex circuits that continuously monitor and promptly modify responses to changes in the chemical, thermal, and mechanical environment in the whole gut (mostly in the esophagus, stomach, duodenum, gall bladder, and pancreas). Sensory stimulation through this vagal circuit does not appear to reach the level of consciousness.

Besides making connections with the NTS and the area postrema in the brainstem, vagal afferents synapse with the dorsal motor nucleus of the vagus (DVN) and the nucleus ambiguus, creating the dorsal vagal complex. The incoming sensory information is integrated and shared with the forebrain and brainstem by the dorsal vagal complex. Brain coordination and influences (conscious and nonconscious) are translated to the dorsal vagal complex, where the DVN and nucleus ambiguus represent the efferent arm of the reflex pathway. It is the final common pathway from the brain responsible for precise control of muscle, glandular, and circulatory responses of the gastrointestinal tract. Multiple neurotransmitters are involved in the intricate conduction of impulses between the neuronal circuits in the dorsal vagal complex. Approximately 30 are identified and consist of acetylcholine, biogenic amines, amino acids, nitric oxide, and peptides.

Spinal afferents (splanchnic and pelvic) send sensory impulses to the dorsal root ganglia (or prevertebral sympathetic ganglia), which are then conducted to the dorsal horn (laminae I, II, V, and X) of the spinal cord and the dorsal column nuclei. The dorsal column is thought to play a greater role in nociceptive transmission of messages from the gut than the spinothalamic or spinoreticular tracts. The conscious perception of pain in the digestive tract is largely mediated through spinal afferents. The spinal cord modulates the conduction of neural messages (both nociceptive and nonnociceptive) to the higher brain. Other somatic and visceral sensory stimuli from the vagina, uterus, bladder, colon, and rectum are also conveyed through the dorsal horn and dorsal column in the spinal cord. Likewise, somatic afferents supply sensory input from the muscles of the pelvic floor through the pudendal nerve to the sacral region of the spinal cord.

Brain centers modulate the nociceptive impulses from the bowel that are relayed to the dorsal horn of the spinal cord. These descending pathways are facilitative or inhibitory or both, based on the visceral stimulus, and can alter the perception of pain in the digestive tract. The neurotransmitters serotonin, noradrenalin, and dopamine are released by these descending pathways as they synapse with the spinal cord.

The secondary somatosensory cortex and, to a lesser extent, the paralimbic and limbic areas (anterior insular, anterior and posterior cingulate, prefrontal and orbitofrontal cortices) mediate emotional, volitional, and psychological responses to sensory input from the gut. These are manifested by abdominal pain, anorexia, nausea, vomiting, hyperphagia, constipation, or diarrhea. The somatosensory cortex regulates the awareness and recognition of pain, and the paralimbic and limbic areas contribute to the cognitive and affective aspects of pain.

Data from the brain and descending vagal pathways are conducted to the spinal cord, and then with the preganglionic neurons in the thoracolumbar area (modulates the sympathetic response) and the sacral area (modulates the parasympathetic response). Sympathetic or parasympathetic output is translated to the neurons in the ENS circuitry, which can be excitatory or inhibitory to motor neurons, gastric or digestive glands, and secretory mechanisms.

Gastrointestinal Neuromotor System

The muscles of the gastrointestinal tract carry out essential functions throughout the gut, including propulsion, grinding, mixing, absorption, storage, and disposal. The gut wall is composed of “self-excitable” smooth muscles that contract in an all-in-one manner. It spontaneously responds to stretch and can be independent of neural or endocrine control. The interstitial cells of Cajal act like a pacemaker and allow propagation of electrical slow waves into the circular muscle layer, which generates spontaneous muscle contraction. It acts like an electrical syncytium where action potentials are conducted in three dimensions from one smooth muscle fiber to another through gap junctions.

The gastrointestinal tract muscles respond to influences of the vagal efferents and the ENS microcircuitry based on excitatory or inhibitory innervation of motor neurons. Contraction is mediated by the release of excitatory neurotransmitters by vagal afferents at the neuromuscular junctions, acetylcholine (at the muscarinic receptor), and substance P (at the neurokinin-1 receptor). Conversely, the release of nitric oxide, adenosine triphosphate, and vasoactive intestinal peptide from the inhibitory motor neurons (which express the serotonergic 5-HT ₁ receptor) impedes contractile activity and facilitates relaxation. The aboral direction of propulsive activity throughout the digestive tract is achieved by segmental inactivation of inhibitory motor neurons distally. Contraction can only occur in the segments where the inhibitory motor neurons are inactivated. With passing of the food bolus or stool, the esophageal and internal anal sphincters (IASs) (smooth muscle sphincters), and inhibitory motor neurons are usually shut off and are inactivated. During vomiting, however, the inhibitory motor neurons are deactivated and propulsive forces work in the opposite direction.

The sympathetic and parasympathetic nervous systems seem to modulate the ENS, rather than directly controlling the smooth muscles of the bowel. The smooth muscles of the bowel also have their own electromechanical automaticity, which is directly modulated by the inhibitory control of the ENS. Sympathetic nervous system stimulation tends to promote the storage function by enhancing anal tone and inhibiting colonic contractions, although little clinical deficit occurs from bilateral sympathectomy. Parasympathetic activity enhances colonic motility, and its loss is often associated with DWE, including impactions and functional obstructions, such as Ogilvie pseudoobstructive syndrome.

The ENS and sympathetic postganglionic neurons transmit excitatory or inhibitory messages to secretomotor neurons. These secretomotor neurons release acetylcholine and vasoactive intestinal polypeptide when there is excitatory activation from paracrine stimulation by mucosal and submucosal cells such as enterochromaffin cells, mast cells, and other immune and inflammatory cells. Acetylcholine and vasoactive intestinal polypeptide are released at the neuroepithelial and neurovascular junctions. This promotes secretion into the gut of water, sodium chloride, bicarbonate, and mucus drawn from the intestinal glands. In addition, dilatation and increase in blood flow occurs with release of nitric oxide from vascular endothelium. Inhibitory influence reduces neuronal firing from secretomotor neurons by hyperpolarization of membranes. Sympathetic release of norepinephrine from nerve endings of the alpha ₂ -noradrenergic receptors inhibits secretomotor actuation, preventing the release of excitatory neurotransmitters. As a result, there is a decrease in secretion of water and electrolytes into the lumen and a congruent shunting of blood from the splanchnic to systemic circulation.

Physiology of Normal Defecation

The colon is a reservoir for food waste until it is convenient for elimination. It also acts as a storage device as long as the colonic pressure is less than that of the anal sphincter mechanism. Fecal elimination occurs when colonic pressure exceeds that of the anal sphincter mechanism. Another function of the colon is to reabsorb fluids (up to 30 L/day can be reabsorbed from the large and small bowel walls with typically only 100 mL of water loss in feces). The colon also reabsorbs gases (90% of the 7 to 10 mL of gases produced by intracolonic fermentation is absorbed rather than expelled). The colon also provides an environment for the growth of bacteria needed to assist in digestion, and also serves to absorb certain bacterial breakdown products. The layers of the colon wall are depicted in Figure 21-3 .

A transverse section of the gut, showing the enteric plexus and the distribution of adrenergic neurons. Note the ganglionic plexuses of Auerbach and Meissner. The deep muscular plexus contains a few ganglia, the subserosal contains an occasional ganglion, and the mucosal plexus shows none. The adrenergic fibers are all extrinsic and arise from the prevertebral sympathetic ganglia. The adrenergic fibers are distributed largely to the mesenteric, submucous, and mucosal plexuses and to blood vessels.

(From Goyal RK, Crist JR: Neurology of the gut. In Sleisenger MH, Fordtram JS, editors: Gastrointestinal disease, Philadelphia, 1989, WB Saunders, pp 21-52, with permission.)

The rectum is usually empty until just before defecation. Perception of rectal contents and pressures is essential for signaling voluntary contraction of the anal sphincter. Normal defecation begins with reflexes triggered by rectosigmoid distention produced by approximately 200 mL of feces ( Figure 21-4 ). A rectorectal reflex occurs in which the bowel proximal to the distending bolus contracts and the bowel wall distally relaxes, serving to propel the bolus further caudad. Reflex relaxation of the internal sphincter and stretching of the puborectalis muscle also occurs, which is enhanced by, but does not require, an extrinsic nerve supply. This relaxation, called the rectoanal inhibitory reflex, correlates with the urge labeled “the call to stool.” One can then volitionally contract the levator ani to open the proximal anal canal and relax the external sphincter and puborectalis muscles. This allows a straighter, shorter, and more open anorectal passage (see Figure 21-4 ), which permits the bolus to pass. Increasing the intraabdominal pressure by squatting and by the Valsalva maneuver assists bolus elimination. For 90% of normal individuals only the contents of the rectum are expulsed, whereas 10% will clear the entire contents of the left colon from the splenic flexure distally.

A, Defecation is prevented by a statically increased tone of the internal anal sphincter (IAS) and puborectalis, as well as by the mechanical effects of the acute anorectal angle. Dynamic responses of the external anal sphincter (EAS) and puborectalis to rectal distention reflexes or increased intraabdominal pressures further impede defecation. B, To initiate defecation, the puborectalis muscle and EAS relax while intraabdominal pressure is increased by the Valsalva maneuver, which is facilitated by squatting. The levator ani helps reduce the acute anorectal angle to open the distal anal canal to receive the stool bolus. C, Intrarectal reflexes result in continued IAS relaxation and rectal propulsive contractions, which help expel the bolus through the open canal.

(From Schiller LR: Fecal incontinence. In Sleisenger MH, Fordtran JS, editors: Gastrointestinal disease, Philadelphia, 1993, WB Saunders, pp 934-953.)

One can elect to defer defecation, however, by volitionally contracting the puborectalis muscle and EAS. The reflexive IAS relaxation subsequently fades, usually within 15 seconds, and the urge resolves until the IAS relaxation is triggered again. The rectal wall accommodates to the bolus by decreasing its wall tension with time, resulting in less sensory input and less reflex triggering from that particular accommodated bolus. This continence and reflex process is somewhat analogous to the function of the striated external urethral sphincter in volitional control of urinary voiding (see Chapter 20 ).

The external sphincter generally tenses in response to small rectal distentions via a spinal reflex, although reflexive relaxation of the external sphincter occurs in the presence of greater distentions. These spinal cord reflexes are centered in the conus medullaris and are augmented and modulated by higher cortical influences. When cortical control is disrupted, as by SCI, the external sphincter reflexes usually persist and allow spontaneous defection. During sleep the colonic activity, anal tone, and protective responses to abdominal pressure elevations are all decreased, whereas rectal tone is increased.

The “gastrocolonic response” or “gastrocolic reflex” refers to the increased colonic activity (GMCs and mass movements) in the first 30 to 60 minutes after a meal. This increased colonic activity appears to be modulated both by hormonal effects, from release of peptides from the upper gastrointestinal tract (gastrin, motilin, cholecystokinin) that increase contractility of colonic smooth musculature, and by a reduction in the threshold for spinal cord–mediated vesicovesical reflexes. Upper gastrointestinal receptor stimulation also results in increased activity in the colon, possibly because of reflexively increased parasympathetic efferent activity to the colon. The possibility of a purely ENS-mediated activation exists, although the small bowel and colon motor activities do not seem to be synchronized. In persons with SCI, the measured increase in colonic activity after a meal is blunted as compared with that in normal individuals. The gastrocolonic response is often used therapeutically, even in patients with SCI, to enhance bowel evacuation during this 30- to 60-minute postprandial time frame. Occasionally certain foods can serve as trigger foods that are especially likely to induce bowel evacuation shortly after consumption.

The resting anal canal pressure is largely determined by the angulation and pressure at the anorectal junction by the puborectalis sling and smooth muscle internal sphincter tone. Continence is maintained by the anal sphincter mechanism, which consists of the IAS, EAS, and the puborectalis muscle. Only approximately 20% of the anal canal pressure is attributable to the static contraction of the somatically innervated striated EAS. The EAS and puborectalis muscle are the only striated skeletal muscles whose normal resting state is tonic contraction. These muscles consist mainly of slow-twitch fatigue-resistant type I fibers (unlike the situation in nonupright animals such as the cat or dog, in which it consists of predominately type II fibers). Anal pressure can be increased volitionally by contracting the EAS and puborectalis muscles. Maximum volitional squeeze pressures, however, are not as high as can be generated reflexively against Valsalva pressure. The EAS is physically larger than the internal sphincter, and its contraction is under both reflex and volitional control. The volitional control is learned during the course of normal maturation. Normal baseline reflex action of the anorectal mechanism allows spontaneous stool elimination. The EAS is innervated by the S2 to S4 nerve roots via the pudendal nerve. The puborectalis muscle is innervated by direct branches from the S1 to S5 roots (see Figure 21-1 ). The remarkable degree of learned EAS coordination allows the selective discrete passage of gas while juggling a variable mixture of solids, liquids, and gases.

Pathophysiology of Gastrointestinal Dysfunction

A whole range of neurologic diseases affecting central, peripheral, and intrinsic enteric nervous innervation have been demonstrated to result in disorders in various segments of the bowel. These are predominantly characterized by disturbances in gastroesophageal, small or large intestinal motility, and sensation. Symptoms of dysphagia, vomiting, bloating, abdominal discomfort and pain, constipation, and incontinence have been described in individuals with neurologic ailments.

Exact and detailed pathophysiologic mechanisms of gastrointestinal dysfunction in the various neurologic diseases are not very well understood. Recent studies, however, have been able to identify various mechanisms of symptom production that might facilitate therapeutic strategies.

Upper Motor Neurogenic Bowel

Any destructive CNS process above the conus, from SCI to dementia, can lead to the upper motor neurogenic bowel (UMNB) pattern of dysfunction. Spinal cortical sensory pathway deficits lead to a decreased ability to sense the urge to defecate. Most persons with SCI, however, sense a vague discomfort when excessive rectal or colonic distention occurs. It has been reported that 43% have chronic complaints of vague abdominal distention discomfort that eases with bowel evacuation. These sensations might be mediated by autonomic nervous system afferent fibers bypassing the zone of SCI via the paraspinal sympathetic chain, or by means of vagal parasympathetic afferents.

Colonic compliance and sphincter tone have been experimentally evaluated in patients with SCI. Studies of colonic compliance in response to a continuous infusion of saline initially suggested rapid pressure rises and a hyperreflexic response. More recent studies have demonstrated normal colonic compliance in patients with SCI who have UMNB. Passive filling of the rectum leads to increases in the resting sphincter tone. These increases are associated with increased external sphincter pressure development resulting from sacral reflexes that can be abolished by pudendal block. This form of rectal sphincter dyssynergia has unfortunately been labeled decreased colonic compliance, even though intermittent or slow filling in the rectum appears to be associated with normal bolus accommodation and pressure relaxation. This contrasts with the true decreased compliance found in ischemic or postinflammatory rectal bowel wall resulting from fibrosis, which cannot accommodate and relax regardless of flow rates.

Colonic motility and stool propulsion are known to be affected by SCI. De Looze, et al. used a questionnaire method to study patients with SCI levels above L2 and found that 58% of patients with chronic SCI had constipation (defined as two or less bowel movements per week or the requirement for digital evacuation). Only 30% ( P = 0.002) of patients with paraplegia below T10 and above L2, however, were prone to constipation. Actual stool propulsion was studied later by Krogh et al. using swallowed markers and serial radiographs. In patients with chronic SCI with supraconal lesions, transit times were significantly prolonged in the ascending, transverse, and descending colon and rectosigmoid. Total gastrointestinal transit time averaged 3.93 days (control group, 1.76 days) for chronic complete SCI above the conus. In an attempt to demonstrate a difference that may have been conferred by sympathetic innervation, mean total gastrointestinal transit times were compared for patients with lesions above T9 (2.92 ± 2.41 days), and from T10 down to L2 (2.84 ± 1.93 days). No statistically significant differences could be found even with comparison of transit times for individual colonic segments.

Patients with SCI who had complete upper motor neuron bowel lesions were studied during the acute phase (5 to 21 days) after SCI. These same patients were reevaluated 6 to 14 months later. Total gastrointestinal transit time was longer during the acute rather than the chronic phase. The upper motor neuron neurogenic colon tended to have slower transit throughout the colon with less severe rectosigmoid dysfunction. Patients with UMNB have spared reflex arc control of the rectosigmoid and pelvic floor. Internal sphincter relaxation upon rectal distention occurs in persons with SCI as well as in neurologically intact persons. Sufficient rectal distention might cause the external sphincter to completely relax, resulting in expulsion of the fecal bolus. Rectal sphincter dyssynergia does not necessarily correlate with bladder sphincter dyssynergia, but it often results in DWE. The protective vesicorectal reflex, in which the external sphincter pressure increases in response to increased intraabdominal pressure, is usually intact ( Table 21-1 ). Patients with UMNB also have normal or increased anal sphincter tone, intact anocutaneous (or anal wink) and bulbocavernosus reflexes, a palpable puborectalis muscle sling, and normal anal verge appearance ( Figure 21-5 ).

Table 21-1

Features of Colorectal Function in Normal Individuals and in Those With Upper Motor Neurogenic Bowel, Upper Motor Neurogenic Bowel With Posterior Rhizotomy, and Lower Motor Neurogenic Bowel

	Normal	Upper Motor Neurogenic Bowel	Upper Motor Neurogenic Bowel With Posterior Rhizotomy	Lower Motor Neurogenic Bowel
Bowel dysfunction	Normal colon activity and defecation	Chronic intractable constipation, fecal impaction, reflex defecation with or without incontinence	Chronic constipation, no reflex defecation	Chronic constipation, fecal impaction maximal in the rectum
Transit time (cecum to anus)	12 to 48 hours	Prolonged >72 hours	Very prolonged unless sacral nerve stimulator used	Prolonged >6 days, especially left side of colon
Colonic motility at rest	GMCs approximately 4 per 24 hours	GMCs may be reduced in frequency	Reduced GMCs	Reduced GMCs
Colonic motility in facilitation response to stimuli	GMCs facilitated by defecation, exercise, and food ingestion	Less GMC facilitation by defecation, exercise, or food ingestion	Less GMC facilitation by defecation, exercise, or food ingestion	Less GMC facilitation by defecation, exercise, or food ingestion
Anal Sphincter Pressure (mm Hg)
Resting tone	>30	>30	Normal	Reduced
Volitional squeeze	>30 (up to 1800)	Absent	Absent	Absent
Rectal compliance	Normal	Normal but sigmoid compliance decreased	Normal or increased	Rectum dilated, increased distention volume, increased compliance
Rectal Balloon Distension
Effect on IAS	Normal rectoanal inhibitory reflex	Normal rectoanal inhibitory reflex	Normal rectoanal inhibitory reflex	Normal rectoanal inhibitory reflex
Effect on EAS	Causes contraction	Causes contraction	No contraction	No contraction
Sensory perception threshold	<20 mL volume	None	None	None
Stimulation of rectal contraction	Induced by balloon distention	Giant rectal contractions stimulated readily	Rectal contraction stimulation	Rectal contraction stimulation
Vesicoanal reflex	Present (>50 mm Hg)	Present	Absent	Absent
Valsalva Protective Reflex
Reflex defecation	Yes	Yes	Impaired	Impaired
Perianal sensation (cutaneous sensation of touch, pinprick)	Normal	No sensory perception	No sensory perception	Loss of perianal buttock sensation resulting from injury to sacral nerves
Anocutaneous reflex (“anal wink”)	Present	Present, may be increased	Absent	Absent as a result of injury to afferent or efferent sacral pathways
Bulbocavernosus reflex	Present	Present, may be increased	Absent	Absent
Anal appearance	Normal	Normal	Normal	Flattened, scalloped, attributable to loss of EAS bulk

 

EAS , External anal sphincter; GMCs , giant migratory contractions; IAS , internal anal sphincter.

From Banwell JG, Creasey GH, Aggarwal AM, Mortimer JT: Management of the neurogenic bowel in patients with spinal cord injury, Urol Clin North Am 20:517-526, 1993; Schiller LR: Fecal incontinence. In Sleisenger MH, Fordtran JS, editors: Gastrointestinal disease, Philadelphia, 1993, WB Saunders, pp 934-953.)

Upper motor neurogenic bowel presents an appearance similar to normal ( A, rear view; B, profile from above). Anal contour of the lower motor neurogenic bowel ( C, rear view; D, profile from above), with its atrophic external anal sphincter, shows a flattened, scalloped-appearing anal area.

Gastrointestinal Dysfunction in Common Neurologic Disorders

Comprehensive Evaluation

History

A comprehensive investigation for nausea, vomiting, bloating, early satiety, abdominal pain, diarrhea, constipation, and fecal incontinence must be completed. The gastrointestinal history should not only review for cardinal symptoms but should also address the patient’s general neuromuscular and gastrointestinal function. A detailed review of the patient’s bowel program includes an assessment of fluids, diet, activity, medications, and aspects of bowel care. Careful consideration must be given to drugs that seriously decrease gastrointestinal motility such as opiates, anticholinergics, tricyclics, antihistamines, calcium channel blockers, and phenothiazines. A review of the technique and outcome of bowel care should include a description of schedule, initiation method (chemical or mechanical stimulation), facilitative techniques, time requirements, and characteristics of stool results. The history should include premorbid bowel pattern information, such as defecation frequency, typical time(s) of the day, associated predefecatory activities, bowel medications and techniques or trigger foods, and stool consistency. It is important to elicit any history of premorbid gastrointestinal disease or dysfunction. The presence of gastrointestinal pain, warning sensations for defecation, sense of urgency, and ability to prevent stool loss during Valsalva activities such as laughing, sneezing, coughing, or transfers should be noted. Excessively large-caliber hard stool can be ascertained by a history of toilet plugging. The patient’s goals and willingness to alter previous bowel patterns or management need to be established. All aspects of impairment and disability that limit a person’s ability to maintain continence and volitionally defecate must be assessed within the perspective of the entire person. All aspects of personal performance should be addressed in person-centered rehabilitation, with the overall goal of maximizing independence in bowel management or direction of a bowel program.

Physical Examination

The physical examination should include the gastrointestinal system and the associated parts of the musculoskeletal and nervous systems required for adequate management of the bowel program. The examination should be completed at the onset and then annually for SCI. The purpose of the examination is to detect functional changes, screen for complications, and identify any new masses or lesions.

The abdomen should be inspected for distention, hernias, and other abnormalities. Careful assessment for the presence or absence of bowel sounds should be done. Percussion and auscultation should precede palpation for masses and tenderness. With the abdomen relaxed, the examiner transabdominally palpates the colon for hard stool. Palpable hard stool should not be present on the right side of the abdomen (ascending colon). Gastroparesis, intestinal, and colonic pseudoobstruction present with an abdomen that is distended, tympanitic with hypoactive bowel sounds, and tender. This can be accompanied by autonomic dysreflexia in persons with SCI. The patient can show signs of malnutrition and dehydration, including loss of weight, pale skin, dry mucous membranes, poor skin turgor, orthostatic hypotension, and tachycardia.

The rehabilitation evaluation should be interdisciplinary in approach and include assessment not only for colon and pelvic floor dysfunction but also for impairments of other organs or systems that could affect rehabilitative strategies to make bowel care independent or prevent unplanned bowel movements.

Physical examination continues with inspection of the anus. A patulous, gaping orifice suggests a history of overdistention and trauma by a previous regimen. A normal anal-buttock contour (see Figure 21-5 ) suggests an intact EAS muscle mass, whereas its loss results in a flattened, fanned-out, scalloped-appearing anal region. The patient should perform a Valsalva maneuver while the examiner observes the anus and perineum for excessive descent. Perianal cutaneous sharp stimulation normally results in an externally visible anal sphincter reflexive contraction. This is the anocutaneous reflex, mediated by the inferior hemorrhoidal branch of the pudendal nerve (S2 to S5). Sensation to light touch is tested at the same time. The tone and voluntary squeeze strength of the EAS and tone of the IAS should be assessed. Integrity of the pelvic floor muscles can be examined by the ability to contract and relax. The length of the anus, where pressure is sensed, is normally 2.5 to 4.5 cm. The point where the pressure decreases marks the anorectal junction. Along the posterior wall, 1.5 to 2.5 cm from the anal verge, the puborectalis muscular sling can be palpated as a ridge that will push the finger forward as the patient resists defecation. No palpable ridge or push suggests puborectalis atrophy or dysfunction. A shortened length of anal pressure zone suggests EAS muscle atrophy. With the examiner’s finger in place, the bulbocavernosus reflex can be elicited by rapidly tapping or squeezing the clitoris or glans penis. The response can be delayed up to a few seconds in pathologic conditions. Insertion of the finger in the anal canal occasionally triggers IAS relaxation, but more often triggers a tightening squeeze that is efferently equivalent to the bulbocavernosus reflex. The patient is asked to volitionally squeeze the anus before removing the finger (“resist defecation”) to check for volitional EAS and puborectalis tone and control. In addition, the patient is asked to bear down and relax alternately to evaluate contraction, relaxation, and coordination of the pelvic muscles.

Diagnostic Testing

The history and physical examination provide most of the necessary information. The clinical cause of neurogenic bowel dysfunction in most patients who are referred to physiatrists is readily apparent. Additional objective laboratory testing can be helpful when the cause of fecal incontinence or DWE is obscure, the history appears doubtful, conservative interventions fail, or surgical interventions are contemplated. Table 21-2 lists some of the many tests available.

Table 21-2

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