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Neurogenic bowel dysfunction
Human disease involving inability to control defecation
Medical condition
Neurogenic bowel dysfunction
Other names
Neurogenic bowel
The image shows the 4 parts of the colon (ascending, transverse, descending and sigmoid) and the rectum. Feces are transported along and stored in the rectum before excretion.
The gastrointestinal tract (GI tract) has a complex control mechanism that relies on coordinated interaction between muscular contractions and neuronal impulses (nerve signals).[3] Fecal incontinence or constipation occurs when there is a problem with normal bowel functioning. This could be for a variety of reasons. The normal defecation pathway involves contractions of the colon which helps mix the contents, absorb water and propel the contents along. This results in feces moving along the colon to the rectum.[4] The presence of stool in the rectum causes reflexive relaxation of the internal anal sphincter (rectoanal inhibitory reflex), so the contents of the rectum can move into the anal canal. This causes the conscious feeling of the need to defecate. At a suitable time the brain can send signals causing the external anal sphincter and puborectalis muscle to relax as these are under voluntary control and this allows defecation to take place.[4][5]
Spinal cord injury and other neurological problems mostly affect the lower GI tract (i.e., jejunum, ileum, and colon) leading to symptoms of incontinence or constipation. However, the upper GI tract (i.e., esophagus, stomach, and duodenum) may also be affected and patients with NBD often present with multiple symptoms.[6][7] Research shows there is a high prevalence of upper abdominal complaints, for example a study showed that approximately 22% of SCI patients reported feeling bloated,[6][8] and about 31% experienced abdominal distension.[6][9]
^Brookes, SJ; Dinning, PG; Gladman, MA (December 2009). "Neuroanatomy and physiology of colorectal function and defaecation: from basic science to human clinical studies". Neurogastroenterol Motil. 21: 9–19. doi:10.1111/j.1365-2982.2009.01400.x. PMID19824934. S2CID33885542.