Central Nervous System

A variety of colorectal dysfunction can be attributed to lesions of the central nervous system. Those disorders that are seen most commonly in clinical practice will be discussed, namely cere-brovascular accidents, spinal cord injury, multiple sclerosis, Parkinson's disease, and spina bifida.

The impact of gastrointestinal (GI) complications after an episode of cerebrovascular accident is determined by the extent of the functional impairment related to the event. Initially after the event of a stroke, fecal incontinence is more frequent (31-40%) and is associated with the severity of the stroke; after 6 months, the frequency of fecal incontinence is reduced to 3% to 9%.34 The frequent association of constipation with disorders involving neuronal malfunction suggests that disruption of the neural modulation of colonic motility may play an important role in the development of constipation. In a study of 8.8 million Medicare patients in the United States, the closest associations were observed between constipation and neurologic diseases.35 A prospective study to determine the incidence of constipation was conducted on a population of 152 inpatients at a stroke rehabilitation center. The authors found that constipation occurred in 60% of the patients, and that the incidence of constipation was not related to age or gender but was strongly related to functional status of patients as assessed by the Barthel Index.36

The prevalence of individuals with spinal cord injury is estimated to be between 183,000 to 230,000, with approximately an 11,000 annual incidence.37 The pervasive effect of spinal cord injury on the individual involves many systems and results in a variety of impairments that limit adaptive compensation. The impact of gastrointestinal, specifically neurogenic bowel, dysfunction after spinal cord injury can be particularly life limiting.38 Neurogenic bowel dysfunction is defined as the life-altering impairment of gastrointestinal and anorectal function resulting from a lesion of the nervous system that can lead to life-threatening complications.39 These symptoms result from interruption of supraspinal control of the sacral parasympathetic supply to the colon, pelvic floor, and anal sphincters.40,41 In addition, paralysis and sensory deficits of the limbs can limit independence in the adaptive habits required to compensate for a neurogenic bowel.38

Among the plethora of complications associated with neurogenic bowel dysfunction, constipation and difficulty with evacuation have the strongest negative impact on the quality of life of the individual, as it affects as many as 80% of people with spinal cord injury.42 One of the main impediments in the management of neurogenic bowel dysfunction is that common therapeutic modalities used in addressing constipation, such as fiber therapy, do not lead to optimal results and may even exacerbate colonic impairment.43 Studies assessing the colonic transit in individu als after spinal cord injury, both with the use of colonic markers44 and colonic scintigraphic studies,45 have demonstrated that there is a significant delay in individuals with this injury as compared to healthy control groups. In both of these studies, it has been suggested that the significant delay occurs in the rectosigmoid and the descending colon, whereas the transverse, ascending colon, and cecum did not show any significant delays. The authors have suggested that this finding is likely due to the damage to the reflex arches between the colorectum and the sacral spinal cord, thus significantly reducing emptying of the rectosigmoid and descending colon during defecation.

Through the use of solid-state manometric catheters, Fajardo et al46 evaluated the colonic motor function of the colon of individuals with spinal cord injury and healthy controls. Ambulatory monitoring was made technically possible by attaching the manometric sensors on the colon through the use of endoclips.47 Prolonged colonic manometric recordings, that is, >24 hours, were made distal to the splenic flexure. The authors concluded that resting colonic motor activity, defined by the motility index, is significantly affected after spinal cord injury when compared to healthy subjects (8.3 ± 3.2 vs. 2.6 ± 0.6,p < .01).

It has been suggested in the literature that colonic motor dysfunction after spinal cord injury is impaired partly due to reduced postprandial colonic motor activity in these individ-uals.48,49 However, it has been demonstrated that although significantly reduced as compared to healthy subjects, there is a significant increase in the motility index of those individuals with spinal cord injury after meal ingestion (2.6 ± 0.6 vs. 4.6 ± 0.7, p < .01). The interesting finding in this study is that there appears to be regional variation in the postprandial response of the colon. The increase in colonic motor activity after meals was seen only in the proximal descending colon (2.8 ± 0.8 vs. 5.8 ± 0.9,p < .03) and not in the distal descending colon (2.5 ± 0.8 vs. 3.2 ± 1.0, p = ns), or rectosigmoid. These observations may help reconcile previous findings including a significant delay of colonic transit in the rectosigmoid area and lack of postprandial increase in colonic motor activity, by demonstrating the importance of the location of the recording system with respect to the likelihood of detecting a gastrocolic response after spinal cord injury. The authors concluded that prolonged transit time in persons with spinal cord injury may be explained by decreased colonic activity, colonic contractions, and intra-luminal pressure. These findings may help to explain the difficulty with bowel evacuation after spinal cord injury, and relief from neurogenic bowel dysfunction should be directed toward modalities that increase colonic motility in general.

The imbalance between the sympathetic-parasympathetic systems resulting from spinal cord injury may lead to disturbances in normal colonic motility, but the specific pathophysio-logic mechanism has not yet been defined. The enteric nervous system and the autonomic nervous system, in general, modulate colonic function. Parasympathetic stimulation results in increased colonic contractility, motility, and tone. Thus, it may be inferred that agents or devices that enhance parasympathetic tone (such as neuroprosthetic stimulation of the sacral nerves or pharmacologic interventions) may be important adjuncts in the management of neurogenic bowel dysfunction.

The incidence and prevalence of multiple sclerosis in the United States are estimated to be 3.2 per 100,000 persons and 58.3 per 100,000 persons, respectively.50 The prevalence of gastrointestinal complaints in individuals afflicted with multiple sclerosis is high and is associated with neurogenic dysfunction of other organ systems.51 Bowel symptoms are common; at least 52% of patients in one series had constipation, fecal incontinence, or both,52 while other studies have shown that the prevalence of constipation varies from 2% to 20%.53 As in individuals with spinal cord injury, neurogenic bowel dysfunction secondary to multiple sclerosis is a source of considerable psychosocial impairment.54 Indeed, among individuals with multiple sclerosis, bladder and bowel symptoms were rated as the third most important factors, after spasticity and incoordination, associated with the limitations on their ability to work.55

Colonic transit time in individuals with multiple sclerosis was assessed by means of radiopaque markers and was found to be significantly delayed,56 suggesting either a disturbance in decreased colonic motor activity or outlet dysfunction. Colonic compliance was found to be reduced in individuals with multiple sclerosis as colonometrograms demonstrated a more rapid pressure rise in the multiple sclerosis group than in the control group; likewise, the multiple sclerosis group failed to demonstrate the postprandial increase in colonic motor and myoelectrical activity that was observed in the control group.57 The authors suggested that these findings may be features of visceral neuropathy in patients with multiple sclerosis and severe constipation.

Pelvic floor dysfunction has been demonstrated in individuals who have constipation and multiple sclerosis. Anorectal physiology testing of individuals with multiple sclerosis and constipation revealed that paradoxical puborectalis contraction is common among these individuals, and it was proposed that such is a feature of the disturbed voluntary sphincter control mechanism, analogous to detrusor sphincter dyssynergia in the bladder.58 In addition to the physiologic abnormalities of the gastrointestinal tract that are reputed to be associated with multiple sclerosis, medications such as anti-cholinergics and muscle relaxants are possible contributors to constipation.55 Bowel management in multiple sclerosis is challenging and is currently empirical, mainly because the underlying illness is progressively debilitating and is not reversible. Treatment of constipation is important, as a distended rectum may worsen bladder symptoms, and constipation may lead to increased limb spasticity.51 Empiric recommendations are the starting point of therapy, which include maintaining a high-fiber diet, high fluid intake, and physical exercise.55'59

Gastrointestinal impairment, specifically constipation, in individuals with Parkinson's disease is common and prevalent,60-64 occurring in as many as two thirds of the patients diagnosed with the disease.65,66 In a study by Siddiqui et al67 involving 68 patients diagnosed with Parkinson's disease, autonomic dysfunction was assessed by comparing gastrointestinal, urinary, sexual, cardiovascular, and thermoregulatory symptoms with a matched control group. The study found that patient's with Parkinson's disease experienced a higher frequency and severity of autonomic dysfunction, and that among the gastrointestinal symptoms that were assessed, patients reported decreased bowel movements as compared to controls (20.4% vs. 0%,p < .02).

The cause of the disturbances in gastrointestinal function after Parkinson's disease is uncertain.59 The effect of antiparkinsonian medication as a possible etiology for gastrointestinal dysfunction in Parkinson's disease is largely overestimated, although it certainly has an influence and should be adapted accordingly in patients with GI motility disorders; in particular, anti-cholinergic drugs should be avoided.68 Recent evidence suggests that the gastrointestinal symptoms seen in Parkinson's disease are related to the Parkinson's disease process itself rather than to the medications.59 The effects of the disease on skeletal muscles parallel the severity and duration of the dysfunction seen in the oropharynx, anorectum, and pelvic floor, and are thus implicated as possible etiologic factors for the morbidity.60 Evidence suggests that neuropathologic abnormalities in the enteric nervous system analogous to those anomalies regarded as pathognomonic of the parkinsonian process in the central nervous system demonstrate parallel pathologic changes in a number of disease processes previously regarded as confined to the central and somatic nervous systems.66 Depletion of dopamine-containing neurons in the central nervous system is a basic defect in Parkinson's disease.

Immunohistochemistry staining of myenteric and submucosal neurons for dopamine, tyrosine hydroxylase, and vasoactive intestinal polypep-tide (VIP) in Parkinson's disease patients revealed that the number of dopaminergic myenteric neurons is significantly decreased. When compared with controls, patients with Parkinson's disease had a mean (in percentage) of 0.4 ± 0.2 vs. 6.9 ± 2.3 in controls. The authors have suggested that the identification of this defect of dopaminergic neurons in the enteric nervous system in Parkinson's disease may offer a plausible explanation for the disturbances in gastrointestinal function in these individuals.69

Patients with tethered cord syndrome, whether secondary to myelodysplasia, presacral mass, or sacral hemivertebrae, were found to have a higher prevalence of constipation and fecal and urinary incontinence. Untethering of the cord was performed in 18 patients, and none noted improvement in their bowel symptoms.70

Constipation Prescription

Constipation Prescription

Did you ever think feeling angry and irritable could be a symptom of constipation? A horrible fullness and pressing sharp pains against the bladders can’t help but affect your mood. Sometimes you just want everyone to leave you alone and sleep to escape the pain. It is virtually impossible to be constipated and keep a sunny disposition. Follow the steps in this guide to alleviate constipation and lead a happier healthy life.

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