Colon Wall Muscles in Diverticular Disease

MUSCLE LAYERS

Between the mucus producing lining and the outer layer of the colon wall, there are two major muscle systems. The inner circular muscles surround the colon, contraction can close the colon or they can act in waves to propel contents along. Between the appendix at the beginning and the rectum at the end of the colon, longitudinal muscles are gathered into three bands known as taenia. This arrangement allows contractions to shorten the colon and propel faeces without compressing them. Coordination between the two types of muscle can produce a variety of movements. An earthworm moving along soil is a good example to observe a similar system.

MOVEMENTS ALONG THE COLON

In the caecum, repeated circular muscle contractions mix the liquid contents (chyme). These change into backwards and forwards segmenting and propulsive movements to dry and move the mushy contents along the ascending and transverse lengths of the colon. Longitudinal muscles become more involved as faeces become more solid in the second, left side, of the colon. Occasional powerful contractions sweep faeces into the descending and sigmoid areas. Faeces are stored with the sigmoid area acting as a vertical warehouse with supporting arcs of circular muscle. Strong contractions of longitudinal muscles produce a concertina effect to push out colon contents on defaecation. The first half of the colon is controlled automatically by the vagus nerve from the brain. The left side has some local nerve reflexes and a person can have some influence such as when to defaecate.

CHANGES WITH DIVERTICULAR DISEASE

Changes in the colon musculature in diverticular disease (DD) were described even before the early 20th century when DD was rare, (1) and in many reports since. Muscle abnormality and dysfunction persisted in the colon after resection of the areas with diverticula (2). Long sections of the left colon can change in appearance without any diverticula which may only occur years later. The muscular abnormalities are the primary pathogenic mechanisms of DD (3). DD is only diagnosed when diverticula are observed, changes in muscles have had little attention especially in areas without diverticula. It is doubtful if a patient or even their health care provider knows the extent of the deformity. The colon walls and/or the effect on the shape inside the colon can be observed in diagnostic scans. More detailed specific research used pathology samples (4, 5). The results in these reports suggests that increasing muscle abnormality might correlate with increased numbers of diverticula and need for surgical resection.

The colon wall is thickened with the muscles appearing in a contracted position, however this is a permanent change and they do not relax. More elastin in a contracted form is present in the muscles, and collagen has changed to a more rigid form so that the colon wall is less distendable than normal(6). In the left side colon, longitudinal muscle contraction looks like the mass peristaltic movement leading to defaecation  and with decreased internal diameter. In the caecum and ascending colon on the right side of the body, there are thickened circular muscle bands reflecting segmentation (7). Diverticula are relatively uncommon in the transverse colon so muscles there have not been examined.

CHANGES IN THE CONTROL OF MUSCLE MOVEMENTS

The nerves which control colon muscle movements are in the form of tubular networks of nerve fibres and their cells in groups (ganglia). There are specialist cells (eg. cells of Cajal) which act like pacemakers to stimulate appropriate and coordinated muscle movements needed to process the residues of digestion. This control system, often called the gut brain, is awry in DD. Fewer ganglia and Cajal cells resemble levels found in slow transit constipation and pseudo obstruction (8). There is altered response to normal neurotransmitters and to drugs which affect this nerve to nerve transmission (9, 10). There is increased sensitivity to acetylcholine – a normal part of gut function –  because receptors for this are increased (11). This favours segmentation rather than propulsive movement which can result in increased internal pressure such as after meals and also constipation.  Some of the propulsive movement was in a backwards direction (12, 13).

Early research into these changes focused on the sigmoid area of the colon but the same changes are also present in the caecum and ascending colon when diverticula are found there (14,15,16).

WHERE DIVERTICULA ARE FORMED

The colon wall changes eventually lead to uncoordinated movement, increased internal pressure and blowout producing diverticula at weak spots anywhere along the colon . Muscle abnormalities and diverticula are most obvious in areas of the most intense colon activity – the caecum and/or the sigmoid parts with appearance reflecting their functions. These have been ascribed to Eastern or Western countries but the distinction is not so clear cut. Painter (17), in England, described how wall thickening first produced diverticula in the sigmoid area but could spread until the entire colon was affected. He also, occasionally, found that the right half of the colon had diverticula when the left half was normal. In Taiwan in 1993 (18), patients were found to have diverticula equally in left and right colon. A report from Japan (19) showed that left, right or both sided DD and their changing pattern depended on age and gender, with right preceding left.

WHAT MIGHT CAUSE DD

Much research is carried out on people who have DD to help with symptoms, treatments and in the hope of preventing complications. Dietary changes, probiotics etc. which produce relief from problems in some people are welcome. However, the cause of symptoms leading to diagnosis of DD are not the cause of DD. Along the length of the colon there is different overall brain control, different available personal control, different local nerve control, difference in content from liquid to solid and differences in functional movement in specific parts of the colon. Any theory on the cause of DD must accommodate such differences and their effects.

The changes in the colon wall muscles and nerves cannot be sudden and may start years earlier in life. These changes precede the formation of diverticula even if both are only discovered in examinations later in life for investigation of symptoms or screening purposes. Opinions diverge on the importance of colon wall thickening. This itself was not considered a pathology meriting colonoscopy by some researchers, even though 26% of those affected had diverticula (20). Colon wall thickening has been reported in other diseases for example IBS (21). However the appearance of the thickening caused by muscle changes in DD is unique. Research into the gut brain and motility of the colon continues. Hopefully this will lead to a better understanding of the cause of DD and it’s prevention.

© Mary Griffiths 2012

REFERENCES

1   Spriggs EI.  Lantern demonstration. Multiple colic diverticulosis. Brit Med J. 1925, 5th Dec, 1061.

2   Parks TG.  Rectal and colonic studies after resection of the sigmoid for diverticular disease. Gut, 1970, 11, 121.

3    Ludeman L et al. The pathology of diverticular disease. Best Practice and Research Clinical Gastroenterology. 2002,16, 543.

4    Park TG.  The pathogenesis of large bowel diverticula. Ulster Med J. 1971, 41, 45.

5    Hughes LE.  Postmortem survey of diverticular diseaseof the colon 11. The muscular abnormality of the sigmoid colon. Gut. 1969, 10, 344.

6    Stollman N & Raskin JB.  Diverticular disease of the colon. Lancet. 2004, 363, 631.

7    Chou YH et al. Sonography of acute right side colonic diverticulitis. Am J Surg. 2001, 181, 122.

8    Bassotti G et al. Interstitial cells of Cajal, enteric nerves and glial cells in colonic diverticular disease. J Clin Pathol. 2005, 58, 973.

9    Guagnini F et al. Neural contractions in colonic strips from patients with diverticular disease: role of endocannabinoids and substance P. Gut. 2006, 55, 946.

10  Liu L et al. Roles of substance P receptors in human colon circular muscles: alterations in diverticular disease. J Pharmacol Exp Ther. 2002, 302, 627.

11  Golder M et al. Smooth muscle cholinergic denervation hypersensitivity in diverticular disease. Lancet 2003, 361,1945.

12  Huizinga JD et al. Abnormal response to cholinergic stimulation in the circular muscle layer of the human colon in diverticular disease. Scand J Gastroenterol. 1999, 34, 683.

13  Bassotti G et al. Twenty-four hour recordings of colonic motility in patients with diverticular disease: evidence of abnormal motility and propulsive activity. Dis Colon Rectum. 2001, 44, 1814.

14  Cobben LP et al. Right colonic diverticulitis: MR appearance. Abdom Imaging, 2003, 28, 794.

15  Hildebrand P et al. Surgical therapy in right- sided diverticulitis. Zentralbl Chir. 2005, 130, 123.

16   Tomita R et al. Physiological studies on nitric oxide in the right-sided colon of patients with diverticular disease. Hepatogastroenterology. 1999, 46, 2839.

17  Painter NS. Diverticular disease of the colon. Brit med J. 1968, 3, 475.

18  Chen SC et al. Distributional pattern of diverticular disease of the colon in Taiwan. J Formos Med Assoc. 1993, 92, 662.

19  Sugihara K et al. Diverticular disease of the colon in Japan. A review of 615 cases. Dis Colon Rectum. 1984, 27, 531.

20  Stermer E et al. Incidental colorectal computed tomography abnormalities: would you send every patient for a colonoscopy? Can J Gastroenterol. 2008, 22, 759.

21  Crade M & Pham V. Ultrasound examination of the sigmoid colon: possible new diagnostic tool for irritable bowel syndrome. Ultrasound Obstet Gynecol. 2006, 27, 206.

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