Bladder and bowel dysfunction in multiple sclerosis (MS) arise primarily from the damage MS causes to the nervous system pathways that control these functions. MS is an autoimmune disease where the immune system mistakenly attacks the protective myelin sheath around nerve fibers in the central nervous system, including the brain, spinal cord, and optic nerves. This demyelination disrupts the normal transmission of nerve signals, leading to various neurological symptoms, including problems with bladder and bowel control.
The mechanisms behind bladder dysfunction in MS involve lesions in areas of the central nervous system responsible for coordinating bladder storage and emptying. Normally, the brain and spinal cord work together to regulate when the bladder fills and when it empties. The brain sends inhibitory signals to prevent involuntary bladder contractions during filling, allowing urine to be stored until voluntary voiding is appropriate. In MS, demyelination can occur in the spinal cord or brain regions such as the pontine micturition center, disrupting these inhibitory pathways. This leads to overactive bladder symptoms like urgency, frequency, and urge incontinence, where the bladder contracts involuntarily. Alternatively, lesions can impair the bladder’s ability to contract properly, causing urinary retention or incomplete emptying. The bladder wall may become thickened and less compliant due to chronic dysfunction, further complicating voiding.
Bowel dysfunction in MS shares similar underlying causes. The nervous system controls bowel movements through complex coordination between the brain, spinal cord, and enteric nervous system. MS lesions can impair the sensory and motor pathways that regulate bowel motility and sphincter control. This can result in constipation due to slowed colonic transit or difficulty with stool evacuation because of impaired coordination of the pelvic floor muscles and anal sphincters. Conversely, some patients experience fecal incontinence due to loss of sphincter control or impaired sensation. Autonomic nervous system involvement in MS also affects bowel function by altering the reflexes that regulate bowel emptying.
In both bladder and bowel dysfunction, the location and extent of demyelinating lesions determine the specific symptoms. Lesions in the spinal cord, especially in the thoracic and sacral segments, are particularly important because these areas contain nerve fibers that directly control pelvic organs. Damage here can disrupt both sensory input from the bladder and bowel and motor output to the muscles involved in storage and elimination. Additionally, lesions in the brain can impair higher-level control and coordination, exacerbating dysfunction.
The immune-mediated inflammation in MS not only damages myelin but also causes axonal injury and neuronal loss, which can lead to permanent impairment of bladder and bowel control. Over time, chronic dysfunction may cause secondary changes such as bladder wall thickening, reduced bladder compliance, and increased risk of urinary tract infections due to incomplete emptying. Similarly, chronic constipation can lead to complications like hemorrhoids or fecal impaction.
In summary, bladder and bowel dysfunction in MS result from the disruption of neural pathways controlling these functions due to demyelination and neurodegeneration. This leads to a spectrum of symptoms ranging from urgency and incontinence to retention and constipation, depending on the pattern of nervous system involvement. The complex interplay between sensory, motor, and autonomic pathways explains the variability and severity of these dysfunctions in individuals with MS.
