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Pathophysiology

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Esophageal hypercontractility is thought to be a result of excess cholinergic secretion and/or muscular asynchrony of the esophageal wall contractions. Supporting the role of impaired cholinergic secretion, Loo et al. evaluated esophageal function in 14 patients with insulin‐dependent diabetes and peripheral and autonomic neuropathy in the absence of esophageal symptoms [150]. Diabetics with autonomic neuropathy had a higher frequency of multipeaked waves (of normal amplitude) when compared to diabetics without neuropathy or controls. Following injection of atropine, these multipeaked contractions were converted to a single‐peaked contraction [150]. Jung et al. evaluated the synchrony between muscles in the circular and longitudinal muscle layers in patients with a hypercontractile esophagus compared to healthy controls [151]. Pressure measurements were gathered from a manometry catheter, as well as imaging using high‐frequency intraluminal ultrasound at 2 and 10 cm above the LES during wet swallows. Images obtained were analyzed for the cross‐sectional area of the circular and longitudinal muscle layers. Patients with hypercontractility had temporal asynchrony between the contractions of circular and longitudinal muscle layers. [151].

The Esophagus

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