PNIBLOG

Combating constipation associated with Parkinson’s disease.

In Part 2 of this 3-part blog series we discuss constipation related to Parkinson’s disease (PD) and the gut-brain connection.

In patients with Parkinson’s disease, the major cause of constipation is that the nervous system control of the gut slows down due to the effects of the disease, resulting in the slowing down of gut movement and leading to constipation.

The Parkinson’s disease and gut-brain connection.

Source: simplifiedwellnessforyou.com

Alpha-synuclein refers to the abnormal protein that is also seen in the brains of patients with PD. These same protein deposits have been observed in the gut prior to development of motor symptoms, up to 20 years prior to diagnosis. These abnormalities have also been found in the parasympathetic neurons of the vagus and sacral nerves that connect the brain to the visceral organs and are involved in the autonomic (i.e., automatic, subconscious) nervous system. The term parasympathetic refers to the side of the autonomic nervous system that allows the gut to move (as opposed to the sympathetic, or fight-or-flight response, which typically would inhibit gut movement). Basically as the nervous system control of the gut slows, gut function slows and constipation results.

Interestingly, patients’ self-reports of constipation may not paint the full picture of the severity of constipation. One study found that objective measurements of colon transit time (the amount of time it takes for the stool to move from one point to the next in the intestine) revealed higher rates of constipation than subjectively reported by patients. This is known as slow transit constipation.

In addition to slow transit constipation, PD patients may also experience symptoms related to impaired neurological control of the rectum and anus, which may cause straining and incomplete emptying. This is also known as outlet obstruction or dyssynergic defecation, and can occur when the rectal sphincter fails to relax.

Rates of constipation, depending on how it’s defined, vary widely, with a median 50%, ranging from 20-63%. Studies consistently show that patients with PD experience constipation significantly more frequently than control populations (in which constipation occurs in 11%). Just as constipation is a frequent non-motor symptom that predates the motor symptoms of PD, the presence of constipation increases the risk of subsequently developing PD by a factor of a little over two. Constipation risk increases as the disease progresses, which may be partially related to medication use. Constipation is increased in patients taking dopamine agonists compared to those taking levodopa.

Risks of untreated constipation include slowing gastric emptying and therefore causing a delay in absorption of levodopa (affecting how PD patients feel on an immediate basis), as well as future complications such as hemorrhoids, diverticulosis (a weakening of the colon wall which can become infected or bleed), and possibly an increased risk of colon cancer.

Evaluation of constipation may require consultation with a gastroenterologist. Differentiating between slow transit constipation and outlet obstruction may be the key for appropriate Parkinson’s disease treatment. Functional testing such as colonic transit time testing, defecography and manometry may be required.

Parkinson’s disease patients should participate in various activities.
Patients with PD should be aware of their bowel movements and remain vigilant to the development of constipation and should do the following to improve bowel regularity:

  • Stay active! A sedentary lifestyle may worsen or cause constipation
  • Go when the urge comes. Delaying defecation can worsen stretching of the colon (to the point of diverticulosis) or interfere with the natural neurologic reflex
  • Stay hydrated. Have at least a tall glass of water with each meal
  • Eat a high-fiber diet with plenty of vegetables and “roughage”
  • Minimize medications which can cause constipation (with the guidance of their physician):
    • opiates (painkillers)
    • tricyclic antidepressants such as amitriptyline
    • anticholinergic medications such as trihexyphenidyl (Artane) or benztropine (Cogentin)
    • iron supplements

For patients with constipation which does not improve with these basic measures, the following over-the-counter medications can help:

  • Caffeine (a cup of coffee, for example). This can help stimulate a bowel movement in some patients. Side effects may include insomnia, jitteriness and increased tremor.
  • Fiber (Metamucil, psyllium). However, this is not as useful with more severe cases of constipation as fiber works by bulking up the stool, which normally would trigger a bowel movement. In PD, the neurological response to bulkier stool is limited, so fiber may not be as effective.
  • Colace (docusate), stool softener. This can be taken as 100 mg once or twice a day.
  • Miralax (polyethylene glycol), osmotic laxative. This can be taken as one capful in 6-8 ounces of liquid daily or as needed. This will often produce a bowel movement within 24 hours and does not tend to cause cramps.
  • Senna (Senna-Kot), naturally derived stimulant laxative. This can be taken daily as needed but may cause cramps.
  • Dulcolax (bisacodyl), orally or as a suppository, laxative. This can be taken daily as needed but may cause cramps.

All medications for constipation can cause loose stools or diarrhea. This happens more frequently when patients get backed up for 3-4 days then take stronger and stronger medications to produce bowel movements, at which point the floodgates are open and the bowels are overstimulated. The longer patients get backed up, the more stool spends time in the small intestine, where there is minimal water absorption. This results in the loose watery stools after the initial very hard dry stool. Then patients stop taking their bowel regimen, get backed up again, and the cycle starts anew, termed “constirrhea” by one of my patients. In order to avoid this, patients should take a mild constipation medication such as colace or Miralax as frequently as necessary to produce stools every day or every other day. It’s much better to take medications daily and stay regular, preventing the pain of getting backed up and the misery of the consequent diarrhea.

For patients whose constipation does not respond to basic measures and over-the-counter medications, evaluation by a gastroenterologist is the next step. This will determine the degree to which slow transit versus obstruction are playing a role, and may also be useful to exclude other causes of constipation. A gastroenterologist can also discuss prescription-strength medications such as Linzess (linaclotide) or Trulance (plecanatide), which are guanylate cyclase-C (GC-C) agonists. These are novel agents that improve slow transit constipation by actually stimulating the movements (persistalsis) of the gut, and also can reduce pain in the gut by reducing pain-sensing nerve activity. Side effects may include of course diarrhea, as well as headache, abdominal pain and fatigue. Other advanced treatment options include Amitiza (lubiprostone) which may improve transit time but can cause nausea. There are other, non-medication treatment options which could be reviewed based on the causes of the constipation.

 

Read more about Parkinson’s disease and the gut in Part 1 and Part 3 of this 3-part blog series.

 

Melita Petrossian, MD

Dr. Melita Petrossian is Director of Pacific Movement Disorders Center and is a fellowship-trained neurologist with clinical interests and expertise in movement disorders such as Parkinson’s disease, essential tremor, dystonia, gait disorders, ataxia, myoclonus, blepharospasm, hemifacial spasm, Meige syndrome, spasticity, tics, and Tourette’s syndrome. She also specializes in Parkinson’s-related conditions such as Dementia with Lewy Bodies, progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration, primary freezing of gait, and Parkinson’s disease dementia.