Constipation is a very common complaint among patients with PD and is probably multifactorial in origin. Frequency estimates vary, but in one study of 94 patients, 71% were constipated as defined by less than one bowel movement in three days (44). Although the neuropathology of PD itself is a major causative factor, these authors pointed out in addition that PD patients have a significantly reduced water intake per day when compared with controls. Further questioning of these constipated PD patients revealed that, in most, decreased water drinking preceded the onset of constipation.
Braak et al. (45) observed that the neuropathology of PD begins in the glos-sopharyngeal and vagal nerves and then spreads caudally into the brainstem where the substantia nigra becomes affected. In accordance with this finding, Singaram et al. (46) counted neurons in the myenteric plexus of the colon and found that 9 of 11 PD patients had fewer intact dopaminergic neurons in the colon compared with controls. Since this is an early finding, one would expect constipation to precede the onset of motor symptoms of PD and, in fact, several careful studies have affirmed this supposition. Abbott et al. (47,48) reporting on the long-term follow-up of 6790 men in the Honolulu Heart Program observed that the incidence of PD was higher in those with constipation than in those without (18.9/10,000 person-years vs. 3.8/10,000 person-years). Patients whose constipation was resistant to treatment had the highest incidence of developing PD during the follow-up period (51.6/10,000 person-years). The main strength of this study was the elimination of recall bias through the study design, which asked patients about bowel habits an average of 12 years before they developed PD.
In addition to slowed colonic motility due to dopaminergic denervation of the GI tract, anal sphincter dysfunction has been reported in PD patients, which may contribute to constipation. Mathers (49) described paradoxical anal sphincter muscle contraction during simulated defecation straining in five of six patients with PD studied with anal electromyography (EMG), and they suggested, based on this finding, that functional anal outlet obstruction may contribute to constipation. In four of these patients, they noted improvement in the defecatory mechanism following apo-morphine, suggesting that this anal dyscoordination may occur on the basis of dopaminergic deficiency. Stocchi et al. (50) confirmed the finding of impaired anal relaxation during straining in PD and added that anal sphincter EMG was normal in PD patients; by comparison, sphincter EMG in MSA patients showed denervation and chronic neurogenic signs.
Antiparkinsonian medication has been implicated as another factor contributing to constipation in PD. The literature is conflicting on whether drugs have a significant effect on colonic motility, and perhaps the most reasonable answer is that drug therapy is not the primary cause of constipation, but in some cases may aggravate the condition. This is probably most important for anticholinergic agents, which are known to reduce intestinal motility (51).
As the cause of constipation in PD is multifactorial, its management requires a multimodality approach. All patients should be advised to increase daily water consumption and add bulking agents to the diet, such as psyllium preparations and high-fiber foods; however, rarely is this sufficient therapy. Cisapride, a prokinetic agent that directly stimulates acetylcholine release in the gut, has been shown to improve constipation and shorten colonic transit time in PD (52). However, this drug was withdrawn from the market in most countries due to QT prolongation and its proarrhythmic effect in some patients. Mosapride citrate is a newly synthesized agent with a similar mechanism of action as cisapride but without known cardiac toxicity. It was recently studied using an open-label design in 14 patients with PD and MSA, where it was well tolerated and effective in producing subjective improvement in bowel frequency and difficult defecation (53). The value of this agent remains to be validated by placebo-controlled trials. Of agents that are currently available for the treatment of constipation, the osmotic laxative polyethylene glycol (Miralax) has been shown to be safe and effective in randomized clinical trials, though none of these have been conducted specifically in PD patient populations (54-56). Although a 17- or 34-gm daily dose has been shown to improve bowel movement frequency within two weeks, a 68-gm dose has been more recently recommended to produce a bowel movement in most constipated patients within 24 hours. For the minority of constipated PD patients in whom anal outlet obstruction is the suspected cause (presumably due to paradoxical contraction of the puborectalis muscle during straining), botulinum toxin type-A injections of 100 U into this muscle under transrectal ultrasonographic guidance has been shown to be effective in a small open-label trial (57). The duration of benefit was not measured and this finding needs to be confirmed using controlled trials before it can be recommended.
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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.