Achalasia of the esophagus is one of very common diseases of the esophagus, even thoughits etiology remains obscure yet.
Although many hypotheses about its cause have been proposed since last century, therehas been no hypothesis which has been generally accepted except one that a feature of achalasiamight be neuromuscular disturbance.
This study was undertaken to define the neuropathological changes of the esophagus inachalasia.
The specimens of the esophagus taken from twenty six patients of achalasia at the time ofoperation and total esophagus which was taken from three necropsy caseswere studied.The eso phagus, the stomach and the intestine of normal three adults were also investigated as acontrol.
The specimens obtained from operative cases were cut at 5mm intervals and the esophagusof necropsy cases was also cut in same fashion from the cardia to the pharynx. All sectionswere stained with hematoxylin-eosin solution.
Results were summarized as follows:
1. Thirty five per cent of ganglion cells of Auerbach's plexus in normal gastrointestinal tract was observed to be morphologically abnormal and these cells could not be differentiatedfrom degenerated ganglion cells in achalasia. Therefore, quantitative analysis of ganglion cellswas very important.
2. Degeneration or complete absence of myenteric ganglion cells was observed in theesophagus, especially in the middle and lower esophagus. In the upper part of the esophagusa few ganglion cells remained in normal or various degenerative forms.
3. Small round cells were observed infiltrating into the myeteric plexus which ganglioncells almost disappeared or were degenerated.
This finding was seen in 27 out of 28 cases, especially in early cases. This phenomenonmight be postulated due to specific inflammatory changes of the Auerbach's plexus of the esophagus, because in surrounding tissue of Auerbach's ple, cus there was no small cell infiltration.
4. There was no morphological or quantitative difference of myenteric ganglion cells ofthe stomach and the intestine between in achalasia and controls
5. The hypertrophy of the inner circular muscle layer of the esophagus, which was possiblydue to compensatory hypertrophy, was observed especially in the middle part of the esophagus.
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