Diffuse esophageal spasm pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The exact pathogenesis of DES is not fully understood. Current high-resolution manometric studies suggests impairment of inhibitory neurons. These neurons use NO as neurotransmitter. | The exact pathogenesis of DES is not fully understood. Current high-resolution manometric studies suggests impairment of inhibitory neurons. These neurons use nitric oxide (NO) as neurotransmitter. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 17:19, 21 November 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]
Overview
The exact pathogenesis of DES is not fully understood. Current high-resolution manometric studies suggests impairment of inhibitory neurons. These neurons use nitric oxide (NO) as neurotransmitter.
Pathophysiology
Pathogenesis
- The exact pathogenesis of DES is not fully understood. However, current high-resolution manometric studies suggest impairment of inhibitory myenteric plexus neurons in DES. These neurons use nitric oxide (NO) as neurotransmitter[1]. Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. Anti-ganglionic acetylcholine receptor antibodies (anti-gAChR-Abs) are reported in some cases[2]. The final result is premature and rapidly propagated or simultaneous contraction of smooth muscles of distal esophagus.
Genetics
There are reports of families with achalasia and esophageal spasm which supports the hypothesis that genetic traits may play role in pathogenesis of DES as well as association between the two disorders.[3] However, genetic inheritance is not fully established.
Associated Conditions
DES occurs in association with other motility disorders of esophagus like achalasia. Esophageal epiphrenic diverticulum is also commonly associated with DES[4].
Gross Pathology
- On gross pathology, gross thickening of muscularis propria layer and LES which is due to hyperplasia (not hypertrophy) than normal subjects are characteristic findings of DES[5].
Microscopic Pathology
- On microscopic histopathological analysis, degeneration of vagal fibres, inflammatory infiltration of myenteric plexus, and hyperplasia of smooth muscles are characteristic findings of DES. Data are limited due to rarity of disease and even less common need of surgery as a treatment.
References
- ↑ Yamato S, Spechler SJ, Goyal RK (1992). "Role of nitric oxide in esophageal peristalsis in the opossum". Gastroenterology. 103 (1): 197–204. PMID 1612326.
- ↑ Morimoto N, Takahashi S, Inaba T, Takamiya M, Kageyama Y, Morimoto M; et al. (2017). "A case of seropositive autoimmune autonomic ganglionopathy with diffuse esophageal spasm". J Clin Neurosci. 39: 90–92. doi:10.1016/j.jocn.2017.01.027. PMID 28214088.
- ↑ Frieling T, Berges W, Borchard F, Lübke HJ, Enck P, Wienbeck M (1988). "Family occurrence of achalasia and diffuse spasm of the oesophagus". Gut. 29 (11): 1595–602. PMC 1433819. PMID 3061886.
- ↑ Taniguchi Y, Takahashi T, Nakajima K, Higashi S, Tanaka K, Miyazaki Y; et al. (2017). "Multiple huge epiphrenic esophageal diverticula with motility disease treated with video-assisted thoracoscopic and hand-assisted laparoscopic esophagectomy: a case report". Surg Case Rep. 3 (1): 63. doi:10.1186/s40792-017-0339-6. PMC 5422214. PMID 28485002.
- ↑ Champion JK, Delise N, Hunt T (2001). "Myenteric plexus in spastic motility disorders". J Gastrointest Surg. 5 (5): 514–6. PMID 11986002.