Bowel dysfunction in neurologic disorders …

General Neurology

Updated 10.10.2024
Released 09.25.2007
Expires For CME 10.10.2027

Bowel dysfunction in neurologic disorders

Authors: Tamara B Kaplan MD, Manali S Sheth MD

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Editor: Steven L Lewis MD

Bowel dysfunction in neurologic disorders

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Introduction

Overview

Neurogenic bowel dysfunction is common in patients with neurologic conditions. Symptoms mainly include constipation and fecal incontinence. These symptoms significantly impact quality of life and can be physically, socially, and emotionally disabling for patients. This article will review the following:

	• The neural control of colonic function and defecation
	• Bowel dysfunction in selected neurologic diseases
	• Bowel dysfunction in specialized patient populations
	• Overview of workup and management of neurogenic bowel dysfunction

Key points

	• Bowel dysfunction in neurologic diseases results from disturbance in the complex neural control of colonic function and defecation.
	• Bowel dysfunction is common in patients with neurologic diseases and may have considerable impact on quality of life.
	• Bowel dysfunction should be recognized in the context of neurologic disease and can be managed with a number of pharmacologic and nonpharmacologic approaches.

Neurogenic bowel dysfunction

Neurogenic bowel dysfunction is the loss of normal bowel function due to nerve injury, neurologic disease, or congenital nervous system defects (49). It includes symptoms such as constipation, fecal incontinence, gut dysmotility, gastroparesis, and abdominal pain (36). This condition is common in neurologic disorders, such as spinal cord injury, multiple sclerosis, stroke, and Parkinson disease. Symptoms vary based on the underlying neurologic defect, immobility, medications, and chronicity. Bowel dysfunction severely impacts quality of life, often more significantly than loss of mobility (30; 31; 36).

Constipation. Constipation is often subject to individual perception and generally refers to infrequent bowel action and difficulty releasing stool. Other symptoms may be present, including bloating, fatigue, and abdominal pain (69). A more inclusive construct is the Rome III criteria, designed to identify chronic functional constipation without diarrhea, irritable bowel syndrome, and structural or biochemical causes. These criteria should be fulfilled for the previous 3 months, with symptom onset at least 6 months before the diagnosis of functional constipation (25).

Neurologic diseases can directly cause constipation through various mechanisms:

Impaired gut mobility (slow transit constipation). Neurologic conditions can lead to impaired gut mobility or gastroparesis, prolonging colon transit time (36). This results in excessive water absorption from the feces and reduced stool frequency.

Difficulty evacuating stool (outlet constipation or dyssynergic defecation). Constipation may also result from difficulty evacuating stool due to impaired sphincter relaxation. This can be compounded by weakness in the levator ani or abdominal muscles (20).

Other factors contributing to constipation include diet, medications, metabolic disorders, and gastrointestinal malignancy. Common medications causing constipation include opioids, anticholinergics (including some antidepressants and antipsychotics), dopaminergic agents, iron, calcium and aluminum antacids, calcium channel blockers, calcitonin gene-related peptide (CGRP) antagonists, and diuretics. Metabolic disorders, including hypothyroidism and hypercalcemia, can also lead to constipation. Furthermore, an abrupt or otherwise unusual history of bowel dysfunction may indicate a colorectal neoplasm, prolapse, rectocele, or other non-neurologic structural causes (18; 20).

Fecal incontinence. Fecal incontinence is defined as the involuntary loss of solid or liquid stool. Overall, fecal incontinence is less common than urinary incontinence, partly because the rectum is filled less frequently than the bladder, and stool is usually solid. Unfortunately, fecal incontinence significantly affects quality of life, and many patients report that these symptoms affect aspects of physical, mental, and sexual health as well as socialization and travel. Even infrequent fecal incontinence may curtail essential life activities and cause avoidance of social occasions. This may explain, in part, why patient-reported outcomes for bladder and bowel interventions for incontinence are limited to select heterogeneous studies (66).

Fecal incontinence is associated with several factors, including residence in a nursing home, urinary incontinence, older age, physical disability, poor general health, female gender (especially after childbirth), and previous anorectal surgery. Diarrhea, regardless of cause, is a strong risk factor for fecal incontinence. Chronic constipation or fecal impaction can lead to fecal incontinence and paradoxical or overflow diarrhea as liquid stool bypasses the blockage, often affecting the elderly or severely disabled. Causative conditions include diabetes, multiple sclerosis, spinal cord injury, stroke, and dementia (62; 36). Additionally, anal sphincter dysfunction, impaired anorectal sensation, and abnormal cognition can all contribute to incontinence.

Anal continence relies on proper rectal musculosensory function and the correct tone of the internal and external anal sphincters. The internal anal sphincter, made of smooth muscle, is regulated by the autonomic nervous system with excitatory sympathetic and inhibitory parasympathetic input. The external anal sphincter, composed of striated muscle, is under voluntary control via the pudendal nerve from the Onuf nucleus in the sacral ventral horn. In cases of complete spinal cord injury, voluntary control of the external anal sphincter is lost (68).

Anal rectal sensation is also crucial for continence. Loss of sensation, particularly in individuals with cauda equina lesions and a flaccid rectum, can lead to incontinence and fecal impaction (21).

Neural control of bowel function

Neural control of the colon is complex and relies on the interaction between the enteric nervous system and the central nervous system. Intrinsic to the wall of the gastrointestinal tract is an extensive network known as the enteric nervous system. This, in turn, is influenced by the CNS via peripheral autonomic and somatic connections. These interactions are reviewed in this section.

Enteric nervous system: structure, function, and neurotransmitters

The enteric nervous system is the largest unit of the peripheral nervous system, located within the walls of the gastrointestinal tract. The enteric nervous system comprises more neurons than the entire spinal cord. It is the basis of the primary reﬂex circuit that mediates both the ﬁlling and emptying of the distal colon and coordinates peristalsis, secretion, and absorption of luminal contents in the gut. The enteric nervous system neurons are organized into two groups: the myenteric plexus, which controls the smooth muscles of the gut, and the submucosal plexus, which regulates the secretomotor and sensory components of gut function (34).

Many neurotransmitters are present in the enteric nervous system, including acetylcholine, norepinephrine, serotonin and other monoamines, GABA, glutamate, ATP, nitric oxide, substance P, enkephalins, somatostatin, neuropeptide Y, and vasoactive intestinal polypeptide (34; 42). The enteric nervous system can function autonomously, albeit less efficiently, if disconnected from the CNS. Intrinsic reflexes can sense bowel contents, propel material forward, and coordinate secretion and absorption.

Autonomic and peripheral nervous system influence. Gastrointestinal motility is regulated through parasympathetic, sympathetic, and somatic pathways.

Parasympathetic pathways
	• The vagus nerve innervates the gastrointestinal tract from the esophagus to the colon’s splenic flexure.
	• The descending colon, rectum, and internal anal sphincter are innervated by the pelvic nerve, originating from the S2-S4 region.
	• Parasympathetic stimulation promotes peristalsis, intraluminal secretion, and relaxation of the internal anal sphincter.
Sympathetic pathways
	• Sympathetic innervation of the colon involves the mesenteric (T5-T12) and hypogastric (L1-L3) nerves.
	• Sympathetic activation decreases colonic motility, reduces intraluminal secretion, and increases internal anal sphincter tone.
Somatic pathways
	• The pudendal nerve, from the S2-S4 region, innervates the external anal sphincter and puborectalis muscles.
	• These muscles contract to maintain continence and relax during defecation. The puborectalis muscle "kinks" the angle between the rectum and anal canal to prevent extrusion of contents.
	• The pudendal nerve also innervates the pelvic floor muscles, aiding in continence and defecation.
	• Sensory receptors in the anal canal and mechanoreceptors in the pelvic floor send signals through the pudendal nerve, facilitating reflexive muscle tone adjustment and conscious perception of anorectal contents.
	• The abdominal wall and diaphragm muscles help generate pressure gradients to propel rectal contents (28).

Brain control of defecation. The brain’s role in defecation is not fully understood. Animal studies suggest that the pelvic organ control center, also known as the Barrington nucleus or pontine micturition center, directs the functions of all pelvic organs, including the rectum (65). Fecal incontinence following brain lesions has been long described; however, the specific neuroanatomical mechanisms remain unclear.

The gut-brain axis involves bidirectional interaction between the intestine and CNS. The brain influences commensal organisms (enteric microbiota) indirectly via changes in gastrointestinal motility, secretions, and intestinal permeability or directly through signaling molecules from enterochromaffin cells, neurons, and immune cells (74).

Enterochromaffin cells regulate communication between the gut and the nervous system. Vagal afferent innervation provides a direct pathway for signaling to neuronal circuits, crucial for modulating pain, immune responses, emotions, and homeostasis (74).

Neurogenic bowel dysfunction in selected neurologic diseases

The following section focuses on a few disorders whose association with bowel dysfunction has been studied.

Spinal cord injury. Almost all patients with a spinal cord injury experience bowel dysfunction, with up to 95% of patients reporting constipation and 75% reporting fecal incontinence at least once per year (68; 36; 55). These symptoms have a significant impact on quality of life.

The pathophysiology of this process depends on the complex interplay of the enteric nervous system and autonomic nervous system. Given that parasympathetic innervation accelerates motility via the lower sacral roots (S2-S4) more distally in patients with spinal cord injury, the dysfunctional gut segment is usually the distal colon. Sympathetic innervation (T9-L2) slows intestinal transit. These neuroanatomical mechanisms help provide a framework for the different clinical patterns of bowel dysfunction observed in patients with spinal cord injury, as the level of spinal cord injury influences the symptoms of bowel dysfunction significantly (20; 75; 55).

Injury above the conus medullaris disrupts inhibitory signals, slowing gut transit and causing hypertonia and hyperreflexia in the hindgut below the splenic flexure. This leads to rectal hypertonia and decreased compliance and increases the risk of reflex defecation and fecal incontinence (75).

Cord injury within the conus or at the cauda equina results in the loss of excitatory sacral parasympathetic supply. In this case, the efferent limb of the reflex arc to the hindgut is interrupted, resulting in hypotonia and hyporeflexia (20).

The clinical symptoms include constipation primarily followed by fecal incontinence, though both commonly exist, especially in the acute phase. However, bowel symptoms change with time after spinal cord injury. Over a 10-year period, patients are more likely to experience constipation-related symptoms and less likely to experience fecal incontinence (33).

Spinal vascular malformations can cause bowel incontinence due to increased venous pressure from congenital or acquired shunts. This pressure disrupts the arteriovenous gradient, leading to venous congestion, reduced blood flow, and ischemic hypoxia in the spinal cord. Initially, arteriovenous malformations present with nonspecific, gradually worsening symptoms like gait issues, paresthesia, sensory disturbances, and radicular pain. Advanced stages may develop severe outcomes such as bowel and bladder incontinence, erectile dysfunction, and urinary retention, particularly in cases of congestive myelopathy (04). Successful treatment, either endovascular or surgical, generally enhances long-term recovery from myelopathic symptoms, including both bowel and bladder dysfunction in most patients (04).

Multiple sclerosis. Neurogenic bowel dysfunction is common in multiple sclerosis and affects 39% to 73% of patients, depending on the population studied (69; 35). More than 50% of patients with multiple sclerosis experience constipation, and a similar number may experience fecal incontinence at some point during the disease process (69; 22). These rates are considerably higher than in the general population. In a cohort of 56 patients diagnosed in the previous 2 to 5 years, 31% of patients reported constipation, 16% reported diarrhea, and 12% reported fecal incontinence (63). These symptoms correlated with lower quality-of-life ratings.

Bowel dysfunction may occur even before diagnosis or early in the disease course and is often one of the first symptoms to appear in patients (35). In data from 385 patients with multiple sclerosis from two tertiary care centers, 31.6% of patients reported bowel symptoms before diagnosis; constipation (43.9%) was most common, followed by diarrhea (31.8%), irritable bowel syndrome (21.7%), and fecal incontinence (2.5%) (35). Overall, the mean time between the first bowel symptom and the presenting multiple sclerosis event is 3.7 years (35).

Bowel dysfunction in multiple sclerosis is likely multifactorial and includes direct neurologic injury intrinsic to multiple sclerosis, as well as external factors, such as medication use, diet, immobility, depression, anxiety, fatigue, and cognitive and behavioral difficulties (99; 69; 35). Patients may have a combination of slowed colonic transit, overactive external anal sphincter, decreased voluntary sphincter control, and reduced anorectal sensation.

As with other neurologic diseases, neuroanatomic and pathophysiologic correlations of bowel dysfunction in multiple sclerosis are not well defined due to difficulty with study design and small sample size. A greater degree of disability, as measured by the Expanded Disability Status Scale, has been shown to correlate with rectal compliance but not with constipation or incontinence score measures. This suggests that these observed alterations in rectal compliance may be secondary to spinal cord involvement, though it does not directly translate to the severity of constipation or incontinence (70).

Finally, the gut microbiota in multiple sclerosis is an area of increased interest. Gut microbiota is the combination of bacteria, fungi, archaea, eukaryotes, and viruses that reside in the intestinal mucosa; these microorganisms may contribute to food digestion and fermentation, nutrient absorption, metabolic regulatory activity, intestinal barrier integrity, and protection against inflammation (64). Gut microbiota may influence the CNS and participate in its regulation through neurochemical changes. Multiple sclerosis has been associated with dysbiosis (disruption in the composition of the gut microbiota); thus, literature seeks to uncover and further elucidate this relationship (64). Studies have provided evidence of alterations at the levels of phyla and genera in patients with multiple sclerosis, such as an increase in Methanobrevibacter and Akkermansia and a decrease in Butyricimonas and Bifidobacterium, to name a few (40; 38; 64). Therefore, this lends to the idea that probiotic administration may contribute to anti-inflammatory effects in multiple sclerosis by reducing inflammatory and oxidative biomarker levels and, thus, delaying the progression and severity of multiple sclerosis (45). Nevertheless, this is still an area of ongoing research as a cause-effect relationship between multiple sclerosis and dysbiosis has not formally been established.

Stroke. Patients affected by stroke commonly experience neurogenic bowel dysfunction. Constipation affects 30% to 60% of patients post-stroke, and chronic fecal incontinence affects 15% of patients (24; 37).

Fecal incontinence often occurs after a stroke, particularly during the acute phase. For example, the Copenhagen Stroke Study of 935 patients found that 40% experienced fecal incontinence 2 weeks post-stroke, dropping to 9% 6 months later. Risk factors include older age, larger infarcts, and comorbidities like diabetes (60). Most patients with post-stroke fecal incontinence also suffered from urinary incontinence, which is a strong indicator of poor outcomes (14; 56).

A separate community-based study revealed that 15% of stroke survivors developed fecal incontinence 3 years post-stroke, which increased the likelihood of long-term care placement and mortality (37). Fecal incontinence at 3 months was linked to needing help with toileting and the use of anticholinergic medications, with factors like infarct size and location also influencing outcomes.

Constipation is also common post-stroke and is estimated to affect almost 50% of patients (51). Factors such as immobility, insufficient fluids, medications, or cognitive decline often play a significant role in constipation. Thus, stroke patients are often at increased risk for constipation due to immobility. However, stroke itself is an independent risk factor for constipation. For instance, in a study that compared patients with hemiplegic stroke to a group of patients with major orthopedic injuries (who were similarly immobile 3 months post-event), de novo constipation was significantly greater in the stroke group (30%) versus the orthopedic group (7%) (12). Even after correction for age, sex, mobility, and medications, the difference persisted.

Constipation and fecal incontinence after stroke may stem from disruptions in brain circuits controlling bowel functions, although these are not fully understood. Research suggests stroke-related microbiota imbalances may occur due to suppressed immunity, inflammatory responses, sympathetic activation, stress, and impaired intestinal motility (53; 97; 96).

Stroke patients are also at an increased risk of gastrointestinal bowel obstruction. Bowel obstruction in the setting of an acute stroke is associated with a higher incidence of intubation, venous thromboembolism, sepsis, acute kidney injury, gastrointestinal hemorrhage, transfusions, and hemorrhagic strokes. In a single study, the administration of thrombolytic therapy was associated with a 30% increased likelihood of gastrointestinal bowel obstruction, and secondary intracerebral hemorrhage was associated with a 49% increased likelihood of gastrointestinal bowel obstruction (77).

Parkinson disease. Constipation is common in Parkinson disease, and gastrointestinal symptoms may predate the clinical onset of the central neurologic disorder (07; 72). In a retrospective chart review, patients with Parkinson disease were more likely to have constipation documented over 20 years before motor onset versus age-matched controls (80). Given that lesions in the enteric nervous system occur in very early stages of the disease, there has been speculation that perhaps the enteric nervous system may actually be the entry point for an environmental factor that then initiates the pathological process of Parkinson disease (07).

One study showed that 37% of patients with Parkinson disease reported daily unsuccessful attempts at defecation (47). A sense of incomplete rectal emptying at evacuation was reported at least once per week by 23%, and 27% had bowel movements less than once every second day. The frequency of fecal incontinence is not increased in Parkinson disease.

The pathophysiology of bowel dysfunction in Parkinson disease is related to both dystonia of the striated pelvic floor muscles and prolonged colonic transit time (39). For instance, patients frequently experience emptying difficulties, straining, and stool outlet obstruction due to dystonia of striated muscles that are used to coordinate defecation. Voluntary squeeze of the external anal sphincter may be reduced in the off state, paralleling motor fluctuations (06). The puborectalis muscle fails to relax in many patients during defecation (29). The external anal sphincter has also shown inappropriate activity in Parkinson disease. Dystonia of the striated muscles of the pelvic floor and external anal sphincter explains the defecation dysfunction; this etiological factor is supported by the observation that pelvic floor dysfunction is alleviated with L‐dopa (20).

Patients with Parkinson disease often experience prolonged colonic transit, due to two critical factors: (1) the reduced number of dopaminergic neurons in the colonic wall, and (2) the accumulation of Lewy bodies in the enteric ganglia (95; 84; 68). Disordered intrinsic and extrinsic innervation of the colon results in slowed motility and transit, producing constipation. Mean colon transit time was twice as long in patients with Parkinson disease as in spousal controls (29).

Overall, constipation in Parkinson disease is due to degeneration of the vagal dorsal motor nucleus and the enteric nervous system, leading to slowed gut motility. Additionally, Parkinson disease medications, such as dopamine agonists and anticholinergics, may also worsen constipation (95; 84; 43; 67; 39).

Observational studies have found that men with less than one bowel movement a day were 2.7 times more likely to develop Parkinson disease in later life than men with one bowel movement per day; this group of men with less than one bowel movement per day were 4.5 times more likely to develop Parkinson disease than men with over two bowel movements a day (01). This suggests that Parkinson disease may not just be a degenerative disorder of the CNS but also of the enteric nervous system.

Evidence links abnormal accumulations of alpha-synuclein aggregates in the periphery (gut), similar to those seen in the cortex, to dysfunction at every level of the gastrointestinal tract, including the esophagus, stomach, small bowel, colon, and rectum. At autopsy, non-parkinsonian older men with low bowel movement frequency were more likely to have incidental Lewy bodies in the substantia nigra and locus coeruleus (02).

Similar to other disease processes mentioned above, alterations in the gut microbiota have also been reported in Parkinson disease. The abundance of Prevotellaceae in the feces of patients with Parkinson disease was shown to be reduced by 77.6% compared with unaffected individuals, and the relative abundance of Enterobacteriaceae was positively associated with the severity of postural instability and gait difficulty (38).

Multiple system atrophy. Prominent autonomic dysfunction is a major feature of multiple system atrophy, another neurodegenerative condition associated with parkinsonism. Bowel dysfunction may occur early and be particularly severe. In many cases, multiple system atrophy can closely resemble idiopathic Parkinson disease. External anal sphincter electromyography has been proposed as a means of differentiating the two. Denervation-reinnervation changes in external anal sphincter electromyography are thought to be common in multiple system atrophy (due to degeneration of Onuf nucleus) and unexpected in early Parkinson disease. If present within 5 years of onset, such findings may suggest multiple system atrophy over Parkinson disease. However, the absence of early denervation is still consistent with multiple system atrophy (102). Conversely, sphincter denervation can be noted in longstanding Parkinson disease (52). Neurologists should, therefore, not rely on sphincter electromyography for a diagnosis.

Alzheimer dementia. Alzheimer disease, which is characterized by neurofibrillary tangles of Tau protein aggregates and plaques of amyloid beta peptide in the brain, is also associated with neurogenic bowel dysfunction. Transgenic murine models with a high accumulation of amyloid beta peptides showed significant alterations in muscarinic acetylcholine receptors, excretion parameters, histopathological structure, capability of mucin secretion, and endoplasmic reticulum stress response (44). As a result of the dysregulation of muscarinic acetylcholine receptors (that was similarly seen in humans), patients experience bowel dysfunction such as constipation.

Furthermore, diet and specific nutrients can modify the composition of the gut microbiota, influencing the production and aggregation of amyloid proteins through mechanisms of molecular mimicry, resulting in alteration of the gut-brain axis (38). Alterations in the gut microbiota composition have been thought to worsen neurodegeneration (and thus, Alzheimer disease) by way of worsened neuroinflammation and neural injury (46). Thus, patients experience greater bowel dysfunction. Although disruption of the muscarinic acetylcholine receptors and a shift in gut microbiota may contribute to neurogenic bowel dysfunction in Alzheimer disease, other metabolites, such as succinic acid, mannitol, 4‐hydroxybenzoic acid (DOPAC), and trimethylamine N-oxide (TMAO,) that are produced in these patients also contribute (94). Clinical studies performed on cerebrospinal fluid samples have demonstrated that TMAO may be relevant to the neurodegenerative changes in Alzheimer disease‐related tau pathology, thus confirming the role of the gut-brain axis in the pathophysiology of Alzheimer disease (94).

Peripheral nervous system disorders. Many disorders of the peripheral nervous system can lead to bowel dysfunction.

Autonomic neuropathies may alter gastrointestinal motility, producing constipation and sometimes diarrhea. Causes of autonomic neuropathy include diabetes, amyloidosis, HIV, porphyria, toxins, and acute inflammatory demyelinating polyradiculoneuropathy (27). The pathogenesis of bowel dysfunction in these disorders is not yet elucidated. Some diseases, such as amyloidosis and diabetes, may also alter gut function via nonneural means.

Diabetes mellitus is considered a risk factor for gastrointestinal symptoms, including constipation, gastroparesis, diarrhea, and fecal incontinence. Most agree that these symptoms are more common in people with diabetes compared to the general population, but the reported prevalence varies substantially by study (27).

Autonomic neuropathy has been proposed to explain bowel dysfunction in diabetes. However, many studies have noted a weak correlation between diabetic bowel dysfunction and autonomic and peripheral neuropathy. Other mechanisms have been postulated, such as metabolic derangements, intestinal bacterial overgrowth, and hyperglycemia. For instance, acute hyperglycemia alone may increase proximal gastric compliance, slow gastric emptying, and increase perceptions of fullness, nausea, and bloating (78; 27).

Bowel dysfunction arises in other disorders of the peripheral nervous system. Focal injury to pelvic or pudendal nerves from surgery, childbirth, or tumor infiltration may cause symptoms, especially when occurring bilaterally. Sacral polyradiculopathy of any cause can cause constipation or incontinence. Examples include cauda equina syndrome from a herniated lumbar disk, which typically requires immediate surgery, and polyradiculitis from cytomegalovirus in AIDS. Myotonic dystrophy is associated with diarrhea, constipation, and fecal incontinence. Other disorders, such as myasthenia gravis and amyotrophic lateral sclerosis, are notable for sparing the neurologic mechanisms involved in bowel function and continence; however, dysphasia, gastroparesis, and chronic intestinal pseudo-obstruction may occur.

Bowel dysfunction in selected patient populations

Children and adolescents. Although the above text focuses mostly on adult patients, it is important to note that neurogenic bowel dysfunction may also affect the pediatric population, including children and adolescents (59). Bowel dysfunction may be related to neurologic causes (including the above), anatomical malformations, functional disorders, or digestive tract etiologies (59). In most cases, pediatric neurogenic bowel dysfunction is secondary to spinal bifida, though other common etiologies include multiple sclerosis, transverse myelitis, sacral agenesis, cerebral palsy, muscular dystrophy, Down syndrome, or traumatic brain or spinal cord injury (59). The pathophysiology behind neurogenic bowel dysfunction is similar to the pathway described in adult patients, and symptoms similarly depend on the location of injury or disease. Again, supraconal disorders tend to result in upper motor neuron symptoms or “spastic” bowels, whereas infraconal lesions lead to lower motor neuron symptoms or “areflexic” bowels (20; 59).

Menopausal women. Although menopausal women do not necessarily have exclusively neurogenic bowel dysfunction, it is worth mentioning that this population very commonly experiences significant bowel dysfunction, and it is often difficult to differentiate between neurogenic causes and non-neurogenic causes of bowel dysfunction. Menopause typically occurs between ages 50 and 55, though usually starts around the age of 40; in a study of 228 women (170 postmenopausal, 58 premenopausal), a significantly higher percentage of post-menopausal women endorsed bowel dysfunction, and 94% of women reported irritable bowel symptoms, alternating between constipation and diarrhea (89). Similarly, a significantly higher proportion of post-menopausal women reported abdominal pain and sought medical attention for their bowel complaints (89). About 9.4% of women require at least monthly laxative use, whereas pre-menopausal rates are closer to 1% to 5% (26; 89). Unfortunately, although hormone replacement therapy may be useful in reducing some symptoms related to menopause (such as sexual dysfunction or hot flashes), there is some evidence that such therapy may actually increase the rates of bowel dysfunction, specifically fecal incontinence; thus, such therapies should be used with caution (93; 85). There is ongoing work on differentiating between bowel dysfunction due to neurologic conditions (such as multiple sclerosis) and bowel dysfunction due to menopause, though there is large speculation that the symptoms and pathophysiological processes overlap significantly.

General assessment and diagnosis

When a patient presents with symptoms concerning for bowel dysfunction, a thorough history is the most critical test to complete. A complete bowel history should be obtained from the patient and any caregivers. Bowel habits before injury or disease onset should be explored, especially in patients with Parkinson disease, where bowel dysfunction may precede neurologic symptoms (68; 07).

Current symptoms should be assessed, including frequency of bowel movements, stool consistency, fecal incontinence or urgency episodes, maneuvers required for bowel management (eg, digital anorectal stimulation), and laxative or antidiarrheal usage (31). Score systems, such as the Cleveland constipation score (03) and St Mark’s incontinence score (91), may help quantify symptoms. However, there is varying consensus on which measurement or scoring tool is most helpful, as there are limitations to each system (87). Past medical history, including any coexisting gastrointestinal disorders such as irritable bowel syndrome, history of pelvic organ prolapse, and surgical procedures involving the gastrointestinal tract, should be assessed. All of these factors are relevant and may affect treatment outcomes (31). A medication history can also reveal constipating agents, such as antimuscarinics or drugs used for spasticity, such as baclofen (69). Finally, a detailed history regarding limitations in quality of life is critically important as symptoms of neurogenic bowel dysfunction have a substantial negative impact on quality of life, social integration, and personal independence (30).

In addition to taking the above history, a validated symptom-based score for neurogenic bowel dysfunction is a useful tool for all providers to complete (48). This tool, developed out of Denmark, identifies the symptoms that most affect a patient’s quality of life and has acceptable reproducibility and validity. There are ten questions in total, and based on a patient’s response, the severity of bowel dysfunction can be graded (48). This score can be found here: Neurogenic Bowel Dysfunction Score (48).

A 2-week bowel diary, with a log of patient-recorded liquid intake, stool frequency, consistency, urge sensations, and leakage, can be helpful to characterize daily habits, accurately quantify symptoms, and evaluate a bowel management routine (87).

Although a thorough physical examination is important to evaluate for underlying pathology, digital rectal examination is one of the most critical tests to perform in patients. A digital rectal examination allows a crude assessment of anal sensation, tone, and squeeze (31). Given the sensitive nature of the digital rectal examination, clinicians should consider using a chaperone during this examination. Laboratory testing is usually only warranted when causes such as anemia, infection, dehydration, or malnutrition are suspected as the etiology of bowel dysfunction. Stool sampling may be performed to evaluate for cancer, parasites, or other infections (75).

In terms of imaging, an abdominal x-ray may be warranted to evaluate for fecal impaction, intestinal obstruction, or perforation; more nuanced imaging may be necessary pending the results of the x-ray but is not always required in the assessment of these patients (75). Specialized anorectal physiology tests (typically initiated by gastrointestinal medicine specialists) may be indicated for patients with severe or persistent symptoms. The most frequent test includes colonic transit studies; these are done with an abdominal x-ray at a fixed time a few days after a patient ingests a radio-opaque marker (31). There are many protocols that then look for delayed or slowed transit through the colon. Another frequently performed test is anorectal manometry. This test is performed by placing a water-based catheter balloon system into the digital rectum and then withdrawing it through the anal canal; this test is used to measure somatovisceral anorectal sensation, anal sphincter pressures, and the integrity of the anal sphincters (69; 31). Less frequently performed tests include endoanal ultrasonography, electromyography, or sensory tests (31).

Summary of management and treatment options

The goal of neurogenic bowel management is to accomplish complete evacuation of the rectum regularly, thus reducing the risk of fecal impaction, urgency, and incontinence (101). Still, there is sparse research that identifies optimal treatment strategies for patients with neurogenic bowel dysfunction, and more research is needed.

Treatment of neurogenic bowel dysfunction should be tailored to the individual’s situation and symptom profile. The goal is to establish a bowel regimen and develop a routine that works for the patient. Some patients may opt for a more interventional approach, whereas others may choose to try conservative measures first. Management of neurogenic bowel is often described in a stepwise approach from more conservative measures to more invasive, but, in reality, patients often require a combination of interventions (31).

As described in detail below, neurologists should be familiar with basic management options for constipation. In severe cases, management may be best guided by specialists due to the complexities of the disease processes and symptoms. The approach to constipation has been summarized in previously published reviews (05). There is a lack of evidence guiding the management of constipation, specifically in patients with nervous system disease (19), though in recent years, there is increasing evidence on optimizing diet, a bowel regimen, biofeedback mechanisms, transanal irrigation, and neuromodulation for such patients with nervous system disease (69). Similarly, management of fecal incontinence can be complex, especially because constipation is often present as well, and treatment for one bowel symptom can often worsen the other. There are limited evidence-based guidelines for managing fecal incontinence, especially in patients with neurologic disease (19), though various treatments are discussed below.

The following treatment options aim to maximize bowel emptying to prevent fecal impaction and incontinence, minimize time spent toileting, and improve quality of life.

Conservative management

Lifestyle and dietary modifications. Stool consistency can be manipulated by modulating fiber and water intake. The goal is to balance having enough fiber to add bulk and soften stools but avoid bloating. Fiber supplements may help increase stool frequency but may be intolerable for some patients due to gas and bloating. In patients with slow-transit constipation, fiber may not relieve symptoms. Increased bulk may lead to fecal impaction in patients prone to intestinal obstruction related to severe colonic delay or immobility without adequate water intake.

Caffeine, alcohol, and food containing the sweetener sorbitol may loosen stool and should be used with caution in those with fecal incontinence (31).

Behavioral modifications. Bowel biofeedback is a technique that seeks to modify bowel function through behavioral changes using the assistance of an external device. This device allows visualization of a function (such as anal sphincter contraction) and, in turn, feeds it back to the patient, who can work on modifying it (69). In a randomized controlled trial, biofeedback therapy showed benefit in more than 70% of patients with functional outlet obstruction, but patients with neurologic disease were excluded (73). In a case-control study, patients with incomplete spinal cord injury had a similar significant response to biofeedback compared to functional anorectal disorder-matched controls (57). Biofeedback and pelvic floor retraining are free of morbidity and are shown to improve rectoanal coordination during defecation (69).

Other. Other nonpharmacologic measures include abdominal massage and Valsalva maneuvers, perhaps by promoting bowel movements. In a small study, patients with multiple sclerosis and constipation reported alleviation in constipation symptoms after abdominal massage for 4 weeks (58).

Pharmacological interventions

A number of medications can be used to treat the symptoms of neurogenic bowel dysfunction.

Pharmacological interventions to treat symptoms of neurogenic bowel dysfunction

(Contributed by Dr. Tamara Kaplan. From: Bashir A, Sizar O. Laxatives. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing, 2024.)

Laxatives, stool softeners, and receptor modulators. For mild constipation symptoms, there are three categories of agents: bulk-forming laxatives, stool softeners, and oral laxative agents.

Bulk-forming laxatives. Bulk-forming laxatives, such as psyllium seed, methylcellulose, calcium polycarbophil, and wheat dextrin, are commonly used for mild constipation symptoms (16). These laxatives are quite effective in increasing the frequency of bowel movements and softening stool consistency; they may be used alone or in conjunction with increased dietary fiber. Psyllium generally is the most effective (16).

Stool softeners. Stool softeners, such as docusate sodium or docusate calcium, attempt to lower the surface tension of stool and, therefore, allow more water to enter the stool and soften the stool. There are few side effects to stool softeners in general, but several systematic reviews concluded that stool softeners might actually be inferior to bulk-forming laxatives such as psyllium in managing constipation symptoms (10; 56).

Oral laxative agents. Oral osmotic laxatives, such as milk of magnesia, lactulose, sorbitol, and polyethylene glycol, are commonly used. They increase stool softness and frequency by preferentially retaining water in the intestinal lumen. Polyethylene glycol appears to be safe and effective, even with daily treatment for 6 months (23). In an 8-week randomized controlled trial, polyethylene glycol improved stool frequency and consistency in Parkinson disease but did not improve straining. The benefit was maintained in the second month, and patients tolerated it well (103). However, overuse can cause dehydration and electrolyte abnormalities in vulnerable patients. Based on data from the general population, osmotic laxatives are generally first-line therapy, and many start with an every-other-day or three-times-a-week regimen and then reassess (41).

When symptoms of constipation are more severe, second-line agents are often used in addition to the first-line agents listed above. These include stimulant laxatives, serotonin 5-HT4 receptor agonists (also known as prokinetic agents), chloride channel activators, guanylate cyclase-C agonists, and cholinesterase inhibitors.

Stimulant laxatives. Stimulant laxatives, such as bisacodyl or sennosides, activate contractions of the intestinal wall, thereby promoting transit. Data are limited on the use of these medications in patients with neurogenic bowel. Still, systematic reviews and meta-analyses have shown that these agents are helpful in those with chronic constipation or idiopathic constipation (54; 41).

Prokinetic agents. Numerous prokinetic agents can be used and often have serotonin agonist activity. Serotonin, including the 5-HT4 receptor subtype, has a role in both gastrointestinal smooth muscle relaxation and contraction, as well as visceral perception (83). Numerous agents that target this receptor have been approved by the US Food and Drug Administration for chronic idiopathic constipation. Prucalopride (Prudac™, Motegrity®) is a selective, high-affinity 5-HT4 agonist. It was efficacious over placebo in severe chronic constipation in three large, randomized controlled trials (15; 86; 71). An integrated analysis of six main clinical trials showed significantly more patients treated with prucalopride (27.8%) versus placebo (13.2%) who achieved an average of three or more spontaneous, complete bowel movements each week over the 12-week treatment period (15; 71); neurologic disease was excluded in the trial. However, in more recent years this has been used as a second-line treatment for constipation in patients with multiple sclerosis, though this recommendation is based on a small study over 4 weeks (69). Tegaserod (Zelnorm®) is another 5 HT-4 receptor agonist. Although it was originally approved by the FDA in 2002 for the short-term treatment of patients with constipation, concerns over cardiovascular ischemic adverse effects led to its withdrawal from the market in 2007. It was then reintroduced and approved by the FDA in 2019 at a dose of 6 mg twice daily in patients with constipation who do not have any history of cardiovascular ischemic events (83). Studies have shown that patients have a significant reduction in abdominal pain and an over 50% increase in stool frequency during treatment (83). As with other serotonin agonists, patients are often monitored and screened for depression, as there is a warning for increased suicide risk and attempts, though in the original tegaserod trial, there were no patients who attempted suicide (83).

Chloride channel agonists. Chloride channel agonists, such as lubiprostone, enhance chloride-rich intestinal fluid secretion into the lumen; this increased fluid secretion causes luminal distension, secondary peristalsis, and laxation (90). This was approved in the United States in 2008 for irritable bowel syndrome and idiopathic chronic constipation. The approval of lubiprostone was based on two placebo-controlled trials of nearly 500 patients who were assigned to either drug versus placebo for 4 weeks (90). Significantly more patients receiving treatment showed improvement in the number of spontaneous bowel movements. Subsequent open-label trials showed improvement of other symptoms, including abdominal bloating, discomfort, and constipation for 6 to 12 months (90); the main side effect was nausea in about 30% of patients, though this side effect was dose-dependent. To date, this drug has not been studied specifically in patients with neurologic diseases.

Guanylate cyclase-C agonists. Medications that target guanylate cyclase-C receptors are also used to alleviate bowel dysfunction symptoms, particularly constipation. Examples of these drugs include linaclotide and plecanatide. Linaclotide is a minimally absorbed 14-amino acid peptide; it acts as a selective agonist of the guanylate cyclase-C receptor on the luminal surface of intestinal enterocytes. It plays a critical role in the regulation and secretion of intestinal fluid (88). Linaclotide was approved in 2012 for the treatment of irritable bowel syndrome and chronic constipation after two phase 3 trials (50; 17). The most common side effect is diarrhea (82). Plecanatide has a mechanism of action similar to linaclotide and similar efficacy as well (82), and the most common side effect is diarrhea.

Cholinesterase inhibitors. Finally, pyridostigmine, a cholinesterase inhibitor, has also been shown to accelerate colonic transit time, but it is not approved for this purpose. Historical studies have shown that pyridostigmine reduces constipation in patients with Parkinson disease, autoimmune neuropathy (79), and diabetes with chronic constipation (09).

Suppositories. Rectal medications, including suppositories and enemas, are also key components of neurogenic bowel management. These medications help control the timing and predictability of a bowel movement and, thus, manage both constipation and fecal incontinence. Stimulant suppositories contain medication, such as bisacodyl, and stimulate bowel reflex. These suppositories are usually inserted 15 to 30 minutes before planned bowel emptying. In general, rectal bisacodyl will produce a bowel movement much faster (within an hour) compared to oral bisacodyl (6 to 12 hours). Lubricating suppositories that contain nonmedicated substances, such as glycerin, may also be helpful to hold water in the bowel, soften stool, and make it easier to pass. There is relatively little research on the use and effectiveness of suppositories and enemas in neurogenic bowel patients. Still, a small number of prospective controlled trials support their use and have noted that these agents decrease total bowel care time (41).

Non-pharmacological interventions

Pelvic floor physical rehabilitation. Pelvic floor rehabilitation includes pelvic floor muscle training, biofeedback, and volumetric training with rectal balloon catheters (81). The most utilized pelvic floor therapy is electromyographic biofeedback-guided pelvic floor muscle training that is typically done with a physical therapist. The goal is to improve pelvic floor and anal muscle sphincter muscle strength, tone, endurance, and coordination (81). A commonly used PFMT includes Kegel contractions to strengthen the transversus abdominus muscle. This is commonly done in conjunction with biofeedback exercises, which allow the patient to have a greater awareness of physiological functions (81). A popular biofeedback tool utilizes EMG; data are recorded through surface electrodes or via the use of intrarectal sensors. The biofeedback apparatus gives information about how strongly the muscles contract, and then the patient utilizes the learned pelvic floor exercises to try to more effectively control neurogenic bowel symptoms, such as fecal incontinence (81). In several trials that have studied this method, the overall consensus has been that patients have about a 50% to 66% improvement in symptoms using pelvic floor exercises and biofeedback, and this benefit can be long-term (81).

Digital rectal stimulation. Digital rectal stimulation involves the insertion of fingers into the rectum with a circular stimulation; this provides physical stimulation to the rectal wall and allows for bowel evacuation in patients with neurogenic bowel dysfunction (61). In two studies that used this as a primary intervention, there was a significant pressure rise in the anal canal due to digital rectal stimulation, which then caused bowel evacuation in a significant manner (61). Thus, this can be used as a non-pharmacologic intervention, often in conjunction with the pharmacologic modalities described above.

Transanal irrigation methods. Transanal irrigation is a second-line intervention for patients with neurogenic bowel dysfunction. It allows for the evacuation of stool by introducing lukewarm water into the colon and rectum through the anus and induces reflex colorectal voiding. A single-use cone or catheter is used to insert the water, and after the device is removed, the proximal colon and rectal contents are emptied (76). Regular usage helps to reestablish control over bowel function and allows the patient to time their evacuation better. A study that assessed the long-term use of transanal irrigation found that most patients continued treatment at long-term follow-up, and regular use was associated with lower rates of urinary tract infections, episodes of fecal incontinence, and stoma surgery as well as improved quality-adjusted life years compared to conservative management (32). Similarly, a systematic review showed significant improvement in patients using transanal irrigation compared to conservative measures; however, these positive results also must be balanced with high discontinuation rates (up to 57%) due to pain during application, side effects, and inefficacy (11; 76).

Advanced therapies

Neuromodulation and electrical stimulation. Sacral nerve stimulation, specifically of the S2-S3 nerve root, can be achieved via an implantable stimulator or peripherally via the tibial nerve (69). Nerve stimulation can reestablish neurogenic control and alleviate bowel dysfunction symptoms (100). Interventions may include sacral anterior root stimulation, sacral nerve stimulation, nerve rerouting, tibial nerve stimulation, dorsal genital nerve stimulation, and magnetic stimulation. Intradural sacral anterior root stimulation, which has the greatest efficacy for neurogenic bladder in select patients with spinal cord injury, may help with bowel symptoms in some patients (92). Sacral nerve stimulation with an implantable device was safe and effective in a prospective study of 120 subjects with chronic fecal incontinence (98), leading to the 2011 FDA approval of the InterStim® device (Medtronic; Minneapolis, MN) for chronic fecal incontinence in patients who failed or are not candidates for more conservative therapies. A small trial in spinal cord injury showed statistically significant improvement in total bowel care time using electrical stimulation of abdominal muscles compared with no electrical stimulation (MD 29.3 minutes, 95% CI 7.35 to 51.25) (18).

Surgical intervention. Surgical formation of a stoma is generally considered a last option, given that it is more invasive and irreversible. Even in a tertiary center with a strong presence of surgical referrals, only 5% of cases in this highly selected cohort justified surgical treatment (05). However, such surgical interventions are associated with improved quality of life and reduced bowel management time (13). Still, there is a significant risk of complications, such as rectal mucus discharge, postsurgical adhesions, and diversion colitis (31). Other surgical procedures include anal sphincteroplasty or artificial anal sphincter implantation. The evidence supporting these techniques is limited.

Summary

Neurogenic bowel dysfunction is highly prevalent in patients with neurologic conditions. Patients may experience constipation, fecal incontinence, or a combination of both. These symptoms can have a tremendous impact on quality of life. Assessment involves obtaining a comprehensive history of bowel habits and symptoms and may include more invasive physiological investigations. Treatment should be tailored to each patient and often involves a multidisciplinary approach.

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Tamara B Kaplan MD

Dr. Kaplan of Harvard Medical School received consulting fees from EMD Serono.
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Manali S Sheth MD

Dr. Sheth of Brigham and Women's Hospital received consulting fees from Sanofi.
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Editor

Steven L Lewis MD

Dr. Lewis of Lehigh Valley Fleming Neuroscience Institute has no relevant financial relationships to disclose.
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Former Authors

Praveen Dayalu MD
Jina Rachel Park MD
Howard W Sander MD
Amy A Pruitt MD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male=female
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Constipation: K59.0

Faecal incontinence: R15

Neurogenic bowel, not elsewhere classified: K59.2

Other and unspecified intestinal obstruction: K56.6
ICD-11: Constipation: ME05.0

Faecal incontinence: ME07

Obstruction of large intestine: DB30

Obstruction of small intestine: DA91

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Bowel dysfunction in neurologic disorders

Associated Disorders

Acute inflammatory demyelinating polyradiculoneuropathy
Acute traumatic spinal cord injury
Advanced Parkinson disease
Diabetic neuropathies
Lumbar spinal stenosis
- Medical complications of stroke
- Multiple sclerosis: clinical aspects
- Multiple sclerosis: treatment of its symptoms
- Multiple sclerosis: management
- Multiple system atrophy
- Myelomeningocele
- Neurologic complications of primary systemic amyloidosis
- Normal-pressure hydrocephalus
- Sacral agenesis
- Sjogren syndrome: neurologic complications
- Split cord malformation
- Parkinson disease
- Primary systemic amyloidosis: neurologic complications
- Pure autonomic failure
- Tethered spinal cord
- Transverse myelitis
- Vascular disorders of the spinal cord

Also Relevant

Anticholinergics
Cervical spondylotic myelopathy
Multiple sclerosis: treatment of its symptoms
Neurogastroenterology
Neurogenic bladder
- Rehabilitation of spinal cord injury
- Sexual dysfunction in neurologic disorders
- Urinary dysfunction in neurologic disorders

Clinical Categories

General Neurology

Bowel dysfunction in neurologic disorders …

Bowel dysfunction in neurologic disorders

Introduction

Overview

Key points

Neurogenic bowel dysfunction

Neural control of bowel function

Enteric nervous system: structure, function, and neurotransmitters

Neurogenic bowel dysfunction in selected neurologic diseases

Bowel dysfunction in selected patient populations

General assessment and diagnosis

Summary of management and treatment options

Conservative management

Pharmacological interventions

Non-pharmacological interventions

Advanced therapies

Summary

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Also in This Category

Brain death/death by neurologic criteria

Hepatic encephalopathy

Coma due to primary brainstem and diencephalic lesions

Transient visual loss

Neuroimaging in acute stroke

Sports activities: neurologic complications

Neurotechnology: brain-computer and brain-machine interfaces

Hyperventilation syndrome

Bowel dysfunction in neurologic disorders

Introduction

Overview

Key points

Neurogenic bowel dysfunction

Neural control of bowel function

Enteric nervous system: structure, function, and neurotransmitters

Neurogenic bowel dysfunction in selected neurologic diseases

Bowel dysfunction in selected patient populations

General assessment and diagnosis

Summary of management and treatment options

Conservative management

Pharmacological interventions

Non-pharmacological interventions

Advanced therapies

Summary

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Brain death/death by neurologic criteria

Hepatic encephalopathy

Coma due to primary brainstem and diencephalic lesions

Transient visual loss

Neuroimaging in acute stroke

Sports activities: neurologic complications

Neurotechnology: brain-computer and brain-machine interfaces

Hyperventilation syndrome

This is an article preview.
Start a Free Account
to access the full version.