The demyelination that is seen in multiple sclerosis is randomly distributed and can occur at any level in the central nervous system. In addition to the somatic disruption that is similar to spinal cord injury, autonomic dysfunction frequently is present. People with dementia and other degenerative disorders that cause cognitive impairment frequently have fecal incontinence caused by overﬂow incontinence. Although sensory nerves are functioning properly, these individuals lack the cognitive awareness necessary to inhibit defecation until a socially acceptable time, and they develop overﬂow incontinence.
Lower motor neuron lesions occurring at or below the level of the defecation center in the sacral cord cause ﬂaccid bowel dysfunction. Cortical communication is disrupted, resulting in impaired cognitive control and sensory deficit. The bowel reﬂexes, including the bulbocavernosus and anal reﬂexes, are interrupted. The anal sphincter is ﬂaccid, and fecal retention with overﬂow incontinence usually occurs. Digital disimpaction and Valsalva often are required for evacuation. Digital stimulation has no effect, and medications tend to work poorly. Examples of motor neuron lesions include tumor or trauma to the cauda equina, tabes dorsalis, spina bifida, and peripheral neuropathy.
The classic example of peripheral neuropathy is congenital aganglionosis (Hirschsprung disease), which was discussed earlier. The most common peripheral neuropathy occurs with diabetes. Approximately 20% of individuals with diabetes have fecal incontinence (29). The cause tends to be multifactorial with the exact mechanism uncertain. Fecal incontinence can occur with diabetic diarrhea or years later from progressive disease. Individuals with diabetes frequently experience intestinal autonomic neuropathy, an abnormal gastrocolic reﬂex, and chronic constipation. The subsequent pelvic ﬂoor denervation causes fecal incontinence by sensory neuropathy, failure of the rectoanal inhibitory reﬂex, and sphincter dysfunction (30). Consequently, fecal incontinence from peripheral neuropathy can be the result of defective sampling, a disrupted rectoanal inhibitory reﬂex, or pudendal neuropathy with sphincter dysfunction. Patients may experience stress or urge incontinence as well as overﬂow incontinence.
Anatomic and structural causes of fecal incontinence are usually due to obstetric or surgical trauma. Damage or dysfunction of the IAS, EAS, and puborectalis can result in varying degrees
Combined Disorders of Defecation and Fecal Incontinence of fecal incontinence. Those with impaired resting tone from a defective IAS will have passive incontinence (incontinence at rest), which is worse during sleep because of decreased EAS activity (31). An inability to respond to sudden distention and to suppress defecation is often seen with external sphincter dysfunction. External and internal sphincter dysfunction often causes incontinence of liquid stool. Incontinence of solid stool is usually seen with widening of the anorectal angle from damage to the puborectalis muscles. Damage to the anal cushions usually causes minor soiling. Other anatomic and structural abnormalities associated with fecal incontinence include obstructive disorders such as pelvic organ prolapse, descending perineum syndrome, anismus, and intussusception; fistulas from diverticulitis, inﬂammatory bowel disease, cancer, or surgical trauma; and decreased rectal compliance from inﬂammatory bowel disease, cancer, and radiation. Decreased compliance results in higher intraluminal pressures with smaller volumes of stool, poor storage capacity, urgency, and incontinence (32).