Abstract
The symptoms and signs of achalasia are due to the loss of ganglion cells in the body of the oesophagus, leading to dilatation and loss of peristaltic activity. The data pertaining to the lower oesophageal sphincter are still somewhat conflicting. The ganglion cells may be absent, but pharmacological evidence suggests denervation to be pre-ganglionic. The classical view of a normotensive, non-relaxing achalasic sphincter has been challenged by recent observations which suggest the presence of a hypertensive, partially relaxing sphincter, which is supersensitive to gastrin and acetylcholine.
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Selected References
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