[Etiopathogenetic hypothesis on the course of esophageal dyskinesias regarding particularly the transitional forms between esophageal spasm, vigorous achalasia and decompensated achalasia].

The aetiology of oesophageal motor disturbances (OMD) including achalasia is unknown. Many causes have been hypothesised including: autoimmune inflammatory lesions, mechanical obstruction, degeneration of the dorsal nucleus of the vagus etc. to explain the anatomopathological lesions of Auerbach's plexus. On the basis of the manometric studies carried out so far on motor disturbances of the oesophagus, it is considered that dyskinesia develop into decompensated achalasia. The disturbance would appear to begin as an oesophageal spasm, turn into vigorous achalasia and finally reach the point of decompensated achalasia characterised by hypotonic, synchronous waves and the absence of relaxation of the lower oesophageal sphincter. A personal series of 76 cases of OMD chosen from among 420 monometries carried out from 1980 to 1987 showed that the duration of the wave, namely the length of time the abnormal pressure is maintained is as important as the pressure of the peristaltic wave and the lower oesophageal sphincter. In fact, wave pressure is generally greater than the systolic pressure of the patient and hence, during contraction, the oesophageal walls are ischaemic and this ischaemia might be the cause of the anatomopathological lesions of Auerbach's plexus observed in decompensated achalasia.