The Relationship Between Pain and Constipation in People with Parkinson Disease

Erica Vitek, MOT, OTR, BCB-PMD, PRPC has attended extensive post-graduate rehabilitation education in the area of Parkinson disease and exercise. She is certified in LSVT (Lee Silverman Voice Treatment) BIG and is a trained PWR! (Parkinson Wellness Recovery) provider, both focusing on intensive, amplitude, and neuroplasticity-based exercise programs for people with Parkinson disease. You can learn more about this topic in Erica's remote course, Parkinson Disease and Pelvic Rehabilitation scheduled for April 19-20, 2024.

Parkinson disease (PD) is the second most common neurodegenerative disorder. It is typically characterized by its cardinal motor symptoms of resting tremor, bradykinesia, and rigidity. A myriad of non-motor symptoms accompanies the motor symptoms with constipation being one of the most frequent, affecting nearly 80% of people with PD. Constipation has been labeled a prodromal symptom appearing, in some, up to 20 years pre-diagnosis. It is theorized that there are two neuropathological subtypes of PD, “brain first" and “body first."  The "brain first" subtype is characterized by central nervous system degeneration in the area of the brain that produces dopamine which results in characteristic cardinal motor system dysfunction.  In the “body first” subtype, the peripheral autonomic nervous system and enteric nervous system are said to be affected by the neurodegeneration which then spreads to the brain via the vagus nerve.

Many studies have linked greater non-motor symptom severity with the presence of constipation and irritable bowel syndrome (Tai, Y.C., et al., 2023; Yu Q.J., et al. 2018). The authors report that people with PD and Irritable bowel syndrome (IBS) have greater non-motor symptom severity than those without IBS; the severity of IBS positively correlated with non-motor symptom severity especially mood disorders and the severity of constipation correlated with the severity of motor dysfunction. In another recent study by Al-Wardat et al. 2024, the authors explored a link between constipation and pain experienced in people with PD. The prevalence of people with PD experiencing pain is 40-88%. The neuropathological mechanism is complex and multifactorial however altered pain processing due to abnormalities in neurotransmitters related to PD may impair endogenous pain modulation. Additionally, people with PD, during dopamine replacement therapy off-times, have been shown to have increased spinal nociceptive activity and decreased ascending inhibition lowering their pain thresholds. This demonstrates how neurodegeneration in the brain and enteric nervous system, which may be enhanced by constipation, contributes to non-motor symptom severity.

There appears to be a cascade of potential contributors to the relationship between constipation and pain in people with PD. First, physical inactivity, commonly seen as PD progresses, can lead to exacerbated constipation, increased muscular rigidity, and increased musculoskeletal pain sensitivity. Second, when constipated, the person with PD will have reduced dopamine replacement medication absorption which occurs in the small intestine leading to worse motor function and pain sensations. Third, opioid analgesics can contribute to slow colonic motility when they bind to receptors in the enteric nervous system consequently causing inhibition of the motor and secretory neurons. Fourth, gut microbiome dysbiosis, resulting from constipation, is hypothesized to cause maladaptive pain processing and alter the brain’s endogenous pain modulatory abilities.

Looking at the gut microbial dysbiosis further, there are three potential drivers that these alternations may be affecting the neuroplasticity of the pain processing pathways. Dysbiosis induces an immune repose, releasing proinflammatory factors which then heighten the sensory neurons of the dorsal root ganglion and dorsal horn. The gut microbiome's proper function is necessary for the gut’s serotonin production, which is one of our neurotransmitters involved in pain modulation (as well as mood and cognition). Finally, serotonin is involved in the local regulation of the movements in the gut therefore depletion will further alter motility.

Clinically, during our assessments, asking our patients with PD about any pain experiences they might have should be included. Because of this identified link between constipation, higher risk of pain, and other non-motor symptom probability, we can develop a treatment plan that will help to improve or restore motility, improve absorption of dopamine replacement medication, gut microbiome functionality, and potential reduction in pain medications with reduced sensitivity of pain. Our knowledge of behavioral and lifestyle modifications related to fiber, fluid, routine increases in physical activity, and strategies for the management of anxiety and depression can be great first steps to improving the daily lives of people with PD.

We have the tools as pelvic health clinicians to play a role in helping people with PD improve their quality of life. Knowing that improving constipation could positively affect non-motor symptom likelihood and severity and potentially slow the neurogenerative process is hope that we can offer. Let’s get together in April and explore the unique issues people with PD experience from the esophagus to the pelvic floor which will help shape your strategies for these patients in the clinic.

References:

1. Al-Wardat, M., Grillo, P., Schirinzi, T., Pavese, C., Salimei, C., Pisani, A., & Natoli, S. (2024). Constipation and pain in Parkinson’s disease: a clinical analysis. Journal of Neural Transmission, 131(2), 165-172.
2. Tai, Y. C., Liao, P. H., Leta, V., Lin, C. H., & Chaudhuri, K. R. (2023). Irritable bowel syndrome based on Rome IV diagnostic criteria associates with non-motor symptoms of Parkinson's disease. Parkinsonism & Related Disorders, 105496.
3. Yu, Q. J., Yu, S. Y., Zuo, L. J., Lian, T. H., Hu, Y., Wang, R. D., ... & Zhang, W. (2018). Parkinson disease with constipation: clinical features and relevant factors. Scientific reports, 8(1), 567.