what instructions should be given to a patient experiencing constipation? (select all that apply).
Can J Gastroenterol. 2011 Oct; 25(Suppl B): 16B–21B.
Language: English language | French
The pathophysiology of chronic constipation
Christopher N Andrews
1Center for Digestive Move, Sectionalisation of Gastroenterology, Department of Medicine, Academy of Calgary, Alberta;
Martin Storr
1Centre for Digestive Motility, Sectionalization of Gastroenterology, Department of Medicine, Academy of Calgary, Alberta;
twoLudwig Maximilian University, Munich, Germany
Received 2011 Jun ii; Accepted 2011 Jun 10.
Abstract
Constipation is broadly divers as an unsatisfactory defecation characterized past exceptional stools, difficult stool passage or both. The mutual approach to the pathophysiology of constipation groups the disorder into chief and secondary causes. Master causes are intrinsic bug of colonic or anorectal function, whereas secondary causes are related to organic disease, systemic disease or medications. The normal process of colonic transit and defecation is discussed, and the etiology of constipation is reviewed.
Keywords: Colonic transit, Constipation, Defecation disorders, Dyssynergia
Résumé
La constipation est largement définie comme une défécation insatisfaisante caractérisée par des selles peu fréquentes, un passage difficile des selles ou ces deux problèmes. En général, la physiopathologie de la constipation classe le problème en causes primaires et secondaires. Les causes primaires sont des problèmes intrinsèques de la fonction colique ou anorectale, tandis que les causes secondaires sont liées à une maladie organique, une maladie systémique ou des médicaments. Le processus normal de transit du côlon et de défécation est exposé, et 50'étiologie de la constipation est analysée.
Liberty of the bowels is the about precious, maybe even the most essential, of all freedoms – one without which picayune can be accomplished.
– Émile Gautier, 1909
Constipation is broadly defined as unsatisfactory defecation characterized by infrequent stools, difficult stool passage or both (i). Constipation is prevalent in North America, with most studies estimating a prevalence of 12% to 19% (2), and some Canadian national data suggesting rates up to 27% (iii). The pathophysiology of constipation is multifactorial and classification schemes can exist confusing. The common approach groups constipation into primary and secondary causes. Main causes are intrinsic problems of colonic or anorectal function, whereas secondary causes are related to organic disease, systemic illness or medications. The classification becomes confusing because secondary causes are typically ruled out outset through history, concrete examination and diagnostic testing.
The present article discusses the normal process of colonic transit and defecation, followed by a review of the etiology of constipation.
PHYSIOLOGY OF COLONIC Role
Water absorption
The colon receives approximately 1.5 L of liquid effluent daily from the small intestine, with 200 mL to 400 mL excreted in the stool. The functions of the colon are to absorb fluid and transport waste matter to the rectum, where it is expelled or stored until defecation is convenient. Removal of water from the fecal slurry is fourth dimension dependent and actively regulated, and tin can exist substantially increased in dehydration states (4). Sodium is actively reabsorbed from luminal content through several active transport channels, with water post-obit passively in response to osmotic gradients. Conversely, colonic secretion is mediated through chloride channels (eg, cystic fibrosis transmembrane conductance regulator [CFTR]), which are generally quiescent, leading to a net reabsorption of electrolytes and fluid (4). Thus, stool that remains in the colon longer will get drier, which can lead to scybalation (pebble-like stools) and impaction if the stool becomes too large and hard to pass through the anal culvert. Cholera toxin, which selectively stimulates the CFTR channel, tin produce overwhelming secretory diarrhea. In patients with cystic fibrosis, the CFTR channel is nonfunctional, which leads to overly dry stools and constipation. Lubiprostone, a selective CFTR agonist and abdominal secretagogue, is widely used in the Us for constipation, merely is not available in Canada.
Colonic motility
On a macro level, two feature movements in the colon accomplish the absorptive and send functions (5). Repetitive nonpropulsive contractions move stool in a style that aids in assimilation and mixing of content. Larger, coordinated contractions (known as high-amplitude propagated contractions [HAPCs]) bring stool forward in mass movements from the ascending colon downward to the left colon (Figure 1). HAPCs typically occur in the morning shortly after awakening, and may exist accentuated by other cues or triggers such as eating or drinking (related to the gastrocolic reflex in infants), mirroring the common experience of the urge to defecate during this time. Of note, colonic movement is strongly adulterate during slumber to avoid incontinence; thus nocturnal bowel movements or anal leakage is significantly abnormal. When stool enters the rectum, it causes distension and a conscious perception of the urge to defecate. If the fourth dimension is not appropriate, the rectum accommodates to store the stool temporarily, resulting in the dissipation of the urge and propagating contractions. Normal colonic transit in adults ranges from 20 h to 72 h (half dozen,7). The frequency of HAPCs is decreased in constipation and likely plays a significant function in its pathophysiology (7).
Twenty-four hour high-resolution colonic manometry plots in a female healthy command ( A ) and in a female patient with a defecation disorder ( B ). The plots are spatiotemporal maps of antegrade (light-green) and retrograde (red) colonic propagating contractions. In ( A ), the high amplitude propagating contractions (HAPCs) are conspicuously seen before defecation and on enkindling in the morning. In comparison, the propagated motor patterns in patients with defecation disorders ( B ) bear witness an increased frequency of low-amplitude antegrade and retrograde propagating sequences, with a reduced frequency of HAPC. Furthermore, in ( B ), no nocturnal suppression of contractile activeness nor colonic responses to a high-calorie meal are seen. Adapted with permission from reference 49
On a molecular level, gut move is a circuitous procedure that includes several layers of neural and hormonal command from the colon up to the central nervous organisation (8). On a simplified level, peristalsis, the major move theme of the gut, is mediated predominantly through the neurotransmitter serotonin (v-hydroxytryptamine [5HT]). When a food or stool bolus distends the gut wall, enterochromaffin cells release 5HT. This causes a local reflex mediated through enteric nerves, releasing stimulating neurotransmitters (such as acetylcholine, which causes muscle wrinkle) behind the bolus and inhibitory neurotransmitters (such every bit nitric oxide, which causes muscle relaxation) in front of the bolus; thus, the bolus is propelled forward along the alimentary canal. For example, disorders of 5HT overproduction, such every bit carcinoid syndrome, lead to substantial diarrhea. This complex algorithm requires intact enteroendocrine, neural and muscle mechanism to office correctly.
The gut has 7 5HT receptor subtypes, of which 5HT4 and 5HT3 are the nearly meaning. The 5HT4 receptor drives the gut'due south peristaltic response to 5HT, and 5HT4 agonists such as cisapride, tegaserod and prucalopride are, or accept been, widely used enterokinetic medications. The 5HT3 receptor, on the other hand, is more than predominantly involved in gut sensation and central processing of this information, with 5HT3 antagonist drugs such equally ondansetron being commonly used in antiemetic therapy.
Mechanism of laxatives
Using this framework of normal colonic physiology, laxatives may be broadly grouped into osmotic and stimulant types. Osmotic laxatives, such every bit 'Milk of Magnesia' (Philips, USA), lactulose and polyethylene glycol 3350, all draw water into the colonic lumen, leading to softer stool and increased defecation frequency. Lubiprostone (not available in Canada) increases colonic fluid by stimulating chloride secretion into the lumen. Stimulant laxatives include irritant substances (such as bisacodyl, senna products and cascara) that direct stimulate afferent nerves or muscle in the gut wall, and enterokinetics, which induce peristalsis (including cisapride, tegaserod and prucalopride).
PHYSIOLOGY OF DEFECATION
Normal defecation and maintenance of continence is a sophisticated process requiring rectal filling, awareness of rectal filling, and the power to propel the stool and relax the pelvic floor muscles in a coordinated way (9). Several factors human action in concert to maintain fecal continence. Anatomical factors include the anal sphincters and puborectalis muscles (ie, the pelvic floor) and rectal curvatures (ie, the rectoanal angle). Transverse rectal folds and hemorrhoidal tissue in the anal canal also serve as passive barriers.
The internal anal sphincter, which is not under witting control, is comprised of smoothen musculus and maintains 70% of the resting anal tone. The external anal sphincter (EAS) is under voluntary command, is comprised of striated muscle and accounts for the remaining xxx% of resting sphincter tone. The puborectalis maintains the rectoanal angle at remainder, and contracts farther to reduce the angle when subjects squeeze. Rectal distension from stool or gas induces reflex relaxation of the internal anal sphincter, known every bit the rectoanal inhibitory reflex (RAIR). The RAIR is mediated through the enteric nervous system and does non crave whatsoever external command from the peripheral or key nervous system. Hirschsprung'south disease, a built disorder that causes truncation of innervation of the distal colon, can exist definitively ruled out by observation of the RAIR on anorectal manometry.
During normal defecation, stool distends the rectum, causes reflex relaxation of the internal anal sphincter and produces the perception of the need to defecate (Figure 2). Sensory mechanisms in the anal canal, which are not well understood, enable determination of whether rectal content is gas or stool. If defecation is inconvenient, the desire to defecate prompts voluntary contraction of the EAS. The desire to defecate dissipates every bit the rectum relaxes, assuasive more stool to be accommodated. If the fourth dimension is advisable, the field of study sits or squats, holds his or her jiff, contracts the diaphragm, the abdominal and rectal muscles, and simultaneously relaxes the EAS and puborectalis musculus (10). These actions open the anus and miscarry stool. Thus, sensory perception and physiological coordination are integral components of anorectal function.
Normal anatomy and physiology of the pelvic floor in the sagittal plane at residual, during normal defecation and during dyssynergic defecation. The resting profile shows the arrangement of the internal and external anal sphincters (IAS and EAS, respectively), equally well as the puborectalis musculus. During defecation, the anal sphincters and the puborectalis relax and the abdominal and rectal contraction generate a push force to empty the rectum of stool. In patients with dyssynergia, the button effort or anal relaxation may be dumb, or the anal sphincters and puborectalis may non relax during attempted defecation, leading to incoordination (ie, dyssynergia) and stool retention. Adapted with permission from reference x
CONSTIPATION
The causes of constipation are varied and may exist multifactorial. The mutual approach groups constipation into principal and secondary causes. Primary causes are intrinsic problems of colonic or anorectal office, whereas secondary causes are related to organic disease, systemic disease or medications.
Master constipation
Primary forms of constipation ascend from intrinsic defects in colonic function or malfunction of the defecation process. These causes are typically considered later on secondary causes of constipation are ruled out, oftentimes by history (Table 1). When no obvious causes or alarm features are identified on history, empirical treatment often starts with fibre supplements and/or laxatives. If treatment is successful, no further workup is generally necessary.
TABLE one
Pathophysiology of chronic constipation
| Principal causes | Secondary causes |
|---|---|
| Normal transit (most common) | Medications |
| Slow transit | Obstacle (eg, cancer, stricture) |
| Evacuation disorder | Metabolic (eg, hypothyroid, hypercalcemia) |
| Neurological (eg, parkinsonism, multiple sclerosis) | |
| Systemic (eg, scleroderma, amyloidosis) | |
| Psychiatric (eg, depression, eating disorders) |
If further characterization of a suspected primary cause of constipation is necessary, localization of the problem – either to the colon or to the anorectum – is required. This is typically achieved with a colonic transit exam. The well-nigh common method is to use radiopaque markers (ie, Sitzmarks [Konsyl Pharmaceuticals Inc, Usa]) administered in a standardized fashion (11,12). The simplest of the methods uses a single capsule of markers that is ingested. Five days (120 h) later, a single apartment plate x-ray is taken, the markers are counted and the location described. Patients are required to discontinue all laxatives during the five-twenty-four hour period study period. The retention of more than 20% of the markers at twenty-four hours 5 is considered to be abnormal. The test provides a rough approximation of colon transit time and tin be administered in any medical imaging facility. Many other methods have been described, including multiple markers taken on subsequent days (vii). Multiple mark tests may also provide information on the etiology of the retentiveness (ie, markers grouped in the rectosigmoid suggests an outlet problem, whereas markers spread diffusely throughout the colon suggest tiresome colonic transit); yet, these methods are not equally well standardized. Scintigraphic transit tests (thirteen) and wireless move capsule studies (14) have been well characterized and are reliable, but not widely bachelor.
Normal-transit constipation
Normal-transit constipation (otherwise known equally 'functional' constipation) is the virtually common form of constipation seen by clinicians. The formal Rome 3 criteria for functional constipation are presented in Tabular array 2. In this state of affairs, patients written report symptoms they believe are consistent with constipation such equally the presence of hard stools or a perceived difficulty with evacuation (15). Withal, on testing, stool transit is not delayed and the stool frequency is ofttimes within the normal range (3,16). Patients may experience bloating and abdominal pain or discomfort, will often meet criteria for irritable bowel syndrome with constipation (IBS-C) (16) and may showroom increased psychosocial distress (17). Symptoms of functional constipation typically reply to therapy with dietary fibre solitary or with the add-on of an osmotic laxative or enterokinetic (18). Considering virtually patients are treated empirically and respond well, they typically will non require a formal transit examination, and have also been diagnosed as 'uncomplicated' or 'fibre deficiency' constipation. In general, if empirical therapy fails, further evaluation is suggested to rule out other main causes of constipation.
Tabular array 2
Rome III criteria for functional constipation
| Must include two or more than of the post-obit: |
| Straining* |
| Lumpy or difficult stools* |
| Awareness of incomplete evacuation* |
| Sensation of anorectal obstruction/blockage* |
| Manual manoeuvres to facilitate defecation (eg, digital evacuation, back up of the pelvic floor)* |
| <3 defecations/week |
| Loose stool rarely nowadays without the utilize of laxatives |
| Insufficient criteria for irritable bowel syndrome with constipation |
Irksome-transit constipation
Slow-transit constipation (STC) causes infrequent bowel movements (typically less than once per calendar week) and is nigh common in young women (nineteen). Ofttimes, patients do not feel the urge to defecate and may complain of associated bloating and abdominal discomfort. As the name suggests, colonic transit time is prolonged in these patients, and frequency of HAPCs is reduced (vii) (Figure 1).
'Colonic inertia' is a term used for a subset of patients with typically astringent dull colonic transit, and who practice not evidence an increase in motor activity after meals or later on the administration of stimulants such as bisacodyl or cholinergic agents (20). However, definitions of colonic inertia are variable, and this classification may non alter therapy significantly (20).
STC is believed to be a neuromuscular disorder of the colon. Studies have shown decreased numbers of interstitial cells of Cajal (ICC) (21) and alterations in the number of myenteric plexus neurons expressing the excitatory neurotransmitter substance P (22) in the gut wall of patients with this disorder. The recent London classification of gastrointestinal neuromuscular diseases too lists hypoganglionosis, inflammatory neuropathy and degenerative leiomyopathy equally other causes of STC (23). Because our understanding of these disorders is only emerging, no therapies take yet been directed at the underlying etiology. Treatment typically uses an aggressive laxative regimen. To complicate matters further, chronic high-dose stimulant laxative employ itself may slow colonic transit, leading to a potentially large subset of (previously) normal-transit constipation or IBS patients using laxatives who appear to have STC. Select patients with STC may answer well to subtotal colectomy and ileorectal anastomosis, provided there is no significant pelvic flooring dysfunction or dyssynergia (24).
Defecation disorders
Defecation disorders (DDs) are a group of functional and anatomical abnormalities of the anorectum that lead to symptoms of constipation. Clinically, patients with DDs nowadays with significant straining, frequently spending large amounts of time on the toilet daily. Manual rectal evacuation using a finger, position changes or frequent enema utilise is common. Frequently, laxatives are highly ineffective, and DD patients may even have difficulty evacuating liquid stools. Pelvic floor tone may exist constantly increased, which can lead to hemorrhoid formation and anal fissuring, which tin go chronic. Conversely, prolonged abstention of defecation due to pain associated with anal fissure may event in DDs. Structural abnormalities, such as rectal intussusception or prolapse, rectocele and excessive perineal descent (descending perineum syndrome), are less common causes of DDs.
Dyssynergia, probably the nigh common functional DD, is an acquired behavioural DD. In about subjects, dyssynergia is a result of poor toileting habits, painful defecation, obstetric or back injury, or brain-gut dysfunction (25,26). Some patients accept a history of sexual or physical corruption, or an eating disorder. In children, fecal retention may outcome in encopresis due to leakage of liquid stool around impacted stool (27). Patients with dyssynergia are unable to coordinate the abdominal, rectoanal and pelvic floor muscles during defecation, and may also demonstrate rectal hyposensitivity (26). Other terms have been used to describe dyssynergia, including anismus, pelvic floor dysfunction, puborectalis spasm and outlet constipation. Although each of these terms has particular nuances pertaining to the specific etiology of the dyssynergia, many clinicians apply them interchangeably.
To fulfill the formal diagnostic criteria for dyssynergic defecation (26), patients must:
-
Satisfy the symptomatic diagnostic criteria for chronic constipation (Rome Iii); and
-
Bear witness a dyssynergic design of defecation, during repeated attempts to defecate with manometry, imaging or electromyography. (Dyssynergia is defined equally a paradoxical increase in anal sphincter force per unit area [anal contraction] or less than xx% relaxation of the resting anal sphincter force per unit area or inadequate abdominorectal propulsive forces.)
-
Accept one or more than of the following:
-
an inability to expel an artificial stool (50 mL water-filled balloon) within i min;
-
prolonged colonic transit fourth dimension; or
-
an inability to evacuate, or 50% or more retention of barium during defecography.
-
Information technology should be noted that prolonged colonic transit time can exist seen in patients with DD and in patients with STC. With low specificity, it is clear that diagnosis of principal constipation subtypes oft relies on more than a single functional examination; detailed history is crucial. Furthermore, anorectal manometry and defecography (defecating proctography) may just be bachelor in specialized centres. As the name suggests, anorectal manometry incorporates a manometric evaluation of the pressures of the anal culvert during rest, squeeze and bearing downward. Testing also typically includes assessments of rectal awareness using a balloon in the rectum. A final evaluation consists of a airship expulsion test, in which the patient attempts to expel a rectal balloon filled with a standardized volume of water into a commode. This provides an objective assessment of the patient's ability to defecate because near normal patients should be able to expel the balloon. Anorectal manometry and balloon expulsion are generally considered to be the aureate-standard exam for the diagnosis of functional DDs (28).
Defecography involves placing a barium paste simulating stool into the rectum. The patient then attempts to defecate in a commode while undergoing fluoroscopy. Defecography provides useful information regarding the anatomical and, to a bottom degree, functional changes of the anorectum. It can reveal abnormalities that may not be clinically or endoscopically apparent, such as rectocele, mucosal intussusception, rectal prolapse or excessive perineal descent. Functional issues may be revealed as poor activation of the levator muscles, prolonged retention or disability to expel the barium. Defecography is specially useful when a structural outlet trouble is suspected.
If anorectal functional testing for DD is non available, it may be reasonable to go on to physiotherapy (and biofeedback, if available) in which symptoms and other testing suggest a functional DD. Pelvic flooring physiotherapy, with a focus on education and recoordination of the defecation manoeuvre, is available at most centres. There is no risk involved and the results are positive (26–29).
Secondary constipation
Drugs causing constipation:
Constipation is a common side issue of many drugs, and a detailed medication history should be taken during the initial workup (30,31).
Antihypertensive drugs such equally clonidine, calcium antagonists, and ganglionic blockers reduce smooth muscle contractility and tin can crusade constipation. In patients with constipation, these should be preferably replaced by beta-blockers, angiotensin-converting enzyme inhibitors, or angiotensin II receptor antagonists (32). Another group of drugs oft associated with constipation are antidepressants, especially tricyclic antidepressants. Selective 5HT reuptake inhibitors and 5HT norepinephrine reuptake inhibitors are alternatives that are less associated with constipation and may exist preferred in these patients (33).
Oral iron supplementation frequently causes constipation and, in patients in whom iron supplementation is necessary, intravenous supplementation of iron or the improver of a laxative may be options. Aluminum-containing drugs such as sucralfate and antacids can cause constipation, and these drugs may be replaced by proton pump inhibitors (34). Analgesics, such as opiates and cannabinoids, are especially notorious for causing constipation. Switching to a different class of analgesic drugs or using an opiate in combination with a peripherally agile opiate receptor antagonist, such equally naloxone or methylnaltrexone, may exist considered (35).
Furthermore anti-Parkinson, antiepileptic and antipsychotic drugs are associated with constipation due to their anticholinergic and dopaminergic deportment, and should be avoided or combined with the regular use of laxatives. Antihistamines, antispasmodics and vinca alkaloids are associated with constipation as a side effect and should be replaced (xxx,31).
NEUROLOGICAL DISORDERS AND CONSTIPATION
Diseases that involve the nervous arrangement may crusade chronic constipation. These diseases include autonomic neuropathy, diabetes mellitus, and other endocrine diseases too as rare causes such every bit Chagas disease and Hirschsprung's illness.
Amid these conditions, diabetes tin can cause multiple gastrointestinal symptoms, especially gastroparesis and abdominal enteropathy. Abdominal enteropathy can cause diarrhea, constipation and fecal incontinence, alternation of symptoms or a combination of these. Although some studies have indicated that diabetic autonomic neuropathy that causes abdominal enteropathy may be the principal underlying machinery, the exact causes of constipation in patients with diabetes are poorly defined. Constipation tin be found in patients with type 1 and type 2 diabetes and is clearly more frequent compared with healthy individuals, although definite statistics regarding frequency are non bachelor (36). Presently, it remains unclear why constipation is more frequent in female person patients with diabetes than in males.
For patients with type ane and type 2 diabetes, no single risk factor for the development of gastrointestinal complications has been identified; still, there are multiple studies investigating potential underlying mechanisms. The possible etiology of constipation in patients with diabetes is probably multifactorial, and includes both reversible and irreversible, and astute and chronic processes. There is potent testify that despite being oft linked to autonomic neuropathy, most of the gastrointestinal complications, including constipation, can be linked to poor glycemic command and less to the duration of the disease (37). Interestingly, constipation in diabetic patients does non correlate with autonomic neuropathy, indicating that neuropathy is not the principal mechanism causing constipation in these patients.
Both hyperglycemia and hypoglycemia were shown in acute and chronic studies to impair functioning of enteric neuronal regulation and to cause constipation (38). This suggests that in patients with diabetes and constipation, optimizing glycemic control should exist the first priority.
The exact mechanisms involved in the development of constipation in patients with diabetes are poorly understood; however, one principal mechanism seems to be the loss of functional ICC (39,40). ICC are the pacemaker cells in the gastrointestinal tract, and are crucially involved in the initiation and coordination of phasic and propagating contractions. Another office of the ICC is the command of neuronal input from nerves to smooth muscle cells for both excitatory and inhibitory neuronal input. More descriptive studies (41) found that in patients with diabetes, numerical changes in the number of ICC, and of excitatory and inhibitory neurons exist; however, the functional consequences of these numerical changes have yet to be determined.
Another mechanism discussed in the pathophysiology of diabetic constipation is smooth musculus myopathy caused by diabetes that impairs gastrointestinal motility and results in delayed gastrointestinal transit. Additionally, neuroendocrine imbalances tin can cause delayed gastrointestinal transit and contribute to the evolution of constipation in patients with diabetes. It remains speculative as to what extent additional mechanisms, including autoimmune harm, alterations of neuronal and shine muscular trophic factors and apoptosis, contribute to the development of constipation; these potential mechanisms are subject area to ongoing studies (42). All of the above-mentioned mechanisms are involved to some extent in gastrointestinal dysfunction in patients with diabetes, and result in impaired motor function including changes in complex motor functions such as the peristaltic reflex, sphincter tone and intestinal sectionalisation (42,43).
Neurogenic bowel dysfunction in patients with spinal cord injury, multiple sclerosis and Parkinson's disease
Spinal cord injury, multiple sclerosis and Parkinson's disease are frequently associated with constipation. The origin of constipation in patients with these conditions is complex and include disease-related autonomic and pelvic nerve dysfunction as well as generalized systemic factors. The systemic factors include a broad variety ranging from contradistinct solid and liquid diet and behaviour, impaired mobility and psychological disturbances. Furthermore, drugs used in the treatment of these atmospheric condition may too cause constipation; regular utilise of laxatives in these patients is appropriate.
In patients with multiple sclerosis, bowel dysfunction including fecal incontinence and constipation is mutual. These symptoms frequently coexist, with bowel dysfunction occurring in upwardly to 70% of patients with the illness (44,45).
Little is known about the pathophysiology of bowel dysfunction in patients with multiple sclerosis. Small studies identified that colonic activity is reduced and transit time may be delayed, indicating that it is largely dumb colonic motility that causes the constipation (46). Treatment of constipation in these patients follows a purely symptomatic approach. When treating constipation in patients with multiple sclerosis, spastic disorders of the pelvic flooring should exist ruled out considering these patients will probably non respond to treatment with laxatives.
Some other neurological disorder ofttimes associated with gastrointestinal dysfunction is Parkinson's disease. Gastrointestinal symptoms are common and include dysphagia, esophageal dysmotility and, well-nigh normally, constipation. Whereas dysphagia and esophageal dysmotility occur with advanced illness, constipation may occur early in the class of Parkinson's affliction and sometimes even precedes the motor manifestations (47). The pathophysiology of constipation in Parkinson'southward disease includes central and peripheral mechanisms. Cardinal mechanisms include changes in dorsal vagal nucleus function, although there is no clear correlation between the degree of cell loss or Lewy body counts in the dorsal vagal nucleus and the severity of constipation in patients with Parkinson's disease (48). At a peripheral site, the loss of dopaminergic neurons contributes to constipation; however, consequent dopaminergic treatment rarely alleviates constipation in patients with Parkinson's illness.
Footnotes
CONFLICTS OF INTEREST: Dr C Andrews has acted as a consultant, advisory board fellow member and has received honoraria from Janssen, Inc. Dr Martin Storr has no financial disclosures or conflicts of interest to declare.
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