Diffuse esophageal spasm pathophysiology
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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 inhibitory 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.[1] These neurons use nitric oxide (NO) as neurotransmitter.[2] Hence, these patients may also have dysregulation of endogenous NO synthesis or/and degradation. Inhibitory neurotransmitters are nitric oxide (NO), vaso-active intestinal peptide (VIP) and ATP whereas excitatory neurotransmitter are acetyl choline (ACh), glutamate and substance P.[3] Anti-ganglionic acetylcholine receptor antibodies (anti-gAChR-Abs) are reported in some cases.[4] 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.[5] 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.[6]
Gross Pathology
On gross pathology, gross thickening of muscularis propria layer and LES than normal subjects are characteristic findings of DES.[7] This gross thickening is due to hyperplasia (not hypertrophy).
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 on microscopic pathology of DES are limited due to rarity of disease and even less common need of surgery as a treatment.
References
- ↑ Roman S, Kahrilas PJ (2012). "Distal esophageal spasm". Dysphagia. 27 (1): 115–23. doi:10.1007/s00455-011-9388-3. PMID 22215281.
- ↑ Yamato S, Spechler SJ, Goyal RK (1992). "Role of nitric oxide in esophageal peristalsis in the opossum". Gastroenterology. 103 (1): 197–204. PMID 1612326.
- ↑ Jiang Y, Bhargava V, Mittal RK (2009). "Mechanism of stretch-activated excitatory and inhibitory responses in the lower esophageal sphincter". Am J Physiol Gastrointest Liver Physiol. 297 (2): G397–405. doi:10.1152/ajpgi.00108.2009. PMC 2724084. PMID 19520741.
- ↑ 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.