Figure 10 - Pathophysiology of idiopathic achalasia.


From the following article

Pathophysiology of achalasia and diffuse esophageal spasm

Ikuo Hirano

GI Motility online (2006)

doi:10.1038/gimo22

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Left: The normal condition where excitatory, cholinergic (Ach) motor neurons innervate the smooth muscle cells of the LES and contribute to the genesis of basal pressure of the LES (LESP). Inhibitory, nitric oxide (NO) motor neurons also act on the LES to produce the relaxation that accompanies a swallow. Middle: Achalasia resulting from the loss of inhibitory neurons. In this situation, the absence of NO motor neurons results in an elevation in the basal LESP and absence of swallow induced relaxation of the LES. Esophageal aperistalsis is defined by simultaneous esophageal body contractions. Right: Achalasia with complete loss of myenteric neurons. Here the basal LESP is below normal owing to the absent excitatory neurons, and swallow-induced relaxation is absent owing to the lack of inhibitory neurons. Esophageal aperistalsis is defined by the absence of esophageal body contractions. (Source: Hiranoand Kahrilas112 with permission from Blackwell Publishing.)

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