Abnormalities of nerve fibers in the circular muscle of patients with slow transit constipation

1998 ◽  
Vol 13 (5-6) ◽  
pp. 208-216 ◽  
Author(s):  
A. J. Porter ◽  
D. A. Wattchow ◽  
A. Hunter ◽  
M. Costa
2012 ◽  
Vol 303 (9) ◽  
pp. G1004-G1016 ◽  
Author(s):  
Dante J. Heredia ◽  
Nathan Grainger ◽  
Conor J. McCann ◽  
Terence K. Smith

The mechanisms underlying slow-transit constipation (STC) are unclear. In 50% of patients with STC, some form of outlet obstruction has been reported; also an elongated colon has been linked to patients with STC. Our aims were 1) to develop a murine model of STC induced by partial outlet obstruction and 2) to determine whether this leads to colonic elongation and, consequently, activation of the inhibitory “occult reflex,” which may contribute to STC in humans. Using a purse-string suture, we physically reduced the maximal anal sphincter opening in C57BL/6 mice. After 4 days, the mice were euthanized (acutely obstructed), the suture was removed (relieved), or the suture was removed and replaced repeatedly (chronically obstructed, over 24–31 days). In partially obstructed mice, we observed increased cyclooxygenase (COX)-2 levels in muscularis and mucosa, an elongated impacted large bowel, slowed transit, nonpropagating colonic migrating motor complexes (CMMCs), a lack of mucosal reflexes, a depolarized circular muscle with slow-wave activity due to a lack of spontaneous inhibitory junction potentials, muscle hypertrophy, and CMMCs in mucosa-free preparations. Elongation of the empty obstructed colon produced a pronounced occult reflex. Removal of the obstruction or addition of a COX-2 antagonist (in vitro and in vivo) restored membrane potential, spontaneous inhibitory junction potentials, CMMC propagation, and mucosal reflexes. We conclude that partial outlet obstruction increases COX-2 leading to a hyperexcitable colon. This hyperexcitability is largely due to suppression of only descending inhibitory nerve pathways by prostaglandins. The upregulation of motility is suppressed by the occult reflex activated by colonic elongation.


2021 ◽  
Vol 23 (3) ◽  
pp. 117-124
Author(s):  
Evgenii I. Chumasov ◽  
Pavel N. Romashchenko ◽  
Nicolay A. Maistrenko ◽  
Vadim B. Samedov ◽  
Elena S. Petrova ◽  
...  

The morphological study of the resected sections of the colon obtained at the S.P. Fedorov Department of Faculty Surgery of S.M. Kirov Military Medical Academy, as a result of surgical treatment of patients with severe chronic slow-transit constipation, included an assessment of the changes in the structures of ganglion plexuses. Three cases were considered (women, aged 3740 years). Various degrees of pathological changes were detected in the ganglion plexuses (Auerbach and Meissner) of the sigmoid colon from patients with chronic slow-transit constipation using Nissls toluidine blue staining. In all cases, reactive, dystrophic, severe degenerative-necrotic changes of ganglion cells, as well as the details of their death, were described in detail. Along with pathological changes in nerve cells in the myenteric nerve plexus and gliosis, features of neuronglial relationships were described, and the death of ganglion cells in the human colon with the active participation of specialized astrocyte-like glial cells was also established for the first time. In the third case, a pattern of pronounced dysplasia and dysgangliogenesis was revealed in the myenteric ganglion plexus of the sigmoid colon, and the presence of diffuse lymphmonocytic infiltrates was noted in the circular muscle layer. Pathological changes in the enteral nervous system in chronic slow-transit constipation reflect neuropathy, which can serve as the main cause of impaired intestinal functions and of some symptoms.


2020 ◽  
Vol 58 (10) ◽  
pp. 975-981
Author(s):  
Thomas Frieling ◽  
Christian Kreysel ◽  
Michael Blank ◽  
Dorothee Müller ◽  
Ilka Melchior ◽  
...  

Abstract Background Neurological autoimmune disorders (NAD) are caused by autoimmune inflammation triggered by specific antibody subtypes. NAD may disturb the gut-brain axis at several levels including brain, spinal cord, peripheral, or enteric nervous system. Case report We present a case with antinuclear neuronal Hu (ANNA-1)- and antiglial nuclear (SOX-1) autoimmune antibody-positive limbic encephalitis and significant gastrointestinal dysmotility consisting of achalasia type II, gastroparesis, altered small intestinal interdigestive motility, and severe slow transit constipation. The autoantibodies of the patient’s serum labeled enteric neurons and interstitial cells of Cajal but no other cells in the gut wall. Achalasia was treated successfully by pneumatic cardia dilation and gastrointestinal dysmotility successfully with prucalopride. Conclusion NAD may disturb gastrointestinal motility by altering various levels of the gut-brain axis.


2021 ◽  
Vol 10 (9) ◽  
pp. 2027
Author(s):  
Samuel Tanner ◽  
Ahson Chaudhry ◽  
Navneet Goraya ◽  
Rohan Badlani ◽  
Asad Jehangir ◽  
...  

Patients with chronic constipation who do not respond to initial treatments often need further evaluation for dyssynergic defecation (DD) and slow transit constipation (STC). The aims of this study are to characterize the prevalence of DD and STC in patients referred to a motility center with chronic constipation and correlate diagnoses of DD and STC to patient demographics, medical history, and symptoms. High-resolution ARM (HR-ARM), balloon expulsion testing (BET) and whole gut transit scintigraphy (WGTS) of consecutive patients with chronic constipation were reviewed. Patients completed questionnaires describing their medical history and symptoms at the time of testing. A total of 230 patients completed HR-ARM, BET, and WGTS. Fifty (22%) patients had DD, and 127 (55%) patients had STC. Thirty patients (13%) had both DD and STC. There were no symptoms that were suggestive of STC vs. DD; however, patients with STC and DD reported more severe constipation than patients with normal transit and anorectal function. Patients with chronic constipation often need evaluation for both DD and STC to better understand their pathophysiology of symptoms and help direct treatment.


2000 ◽  
Vol 118 (4) ◽  
pp. A848 ◽  
Author(s):  
Andrew J. Malouf ◽  
Paul H. Wiesel ◽  
Tanya Nicholls ◽  
R. John Nicholls ◽  
Michael A. Kamm

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