Untreated Achalasia Research Articles

Effect of Transcutaneous Nerve Stimulation on Esophageal Motility in Patients with Achalasia and Scleroderma

It has been suggested that low-frequency transcutaneous electric nerve stimulation (TENS) alleviates the dysphagia produced by achalasia and scleroderma of the esophagus. The present study was conducted to elucidate whether TENS treatment improves dysphagia because of changes it induces on esophageal motility. We studied nine achalasia patients before forceful dilatation of the cardias, nine achalasia patients after dilatation, and nine patients with scleroderma. High-frequency TENS was applied to the hand for 30 min while esophageal motility was monitored by manometry. In none of the groups did TENS produce any change in the basal tone of the lower esophageal sphincter, lower esophageal sphincter relaxation, or esophageal body wave amplitude. Low-frequency TENS, used in another seven untreated achalasia patients, also did not improve esophageal motility. Our data indicate that high- or low-frequency TENS does not induce detectable changes in esophageal motility in patients with achalasia or scleroderma.

Mucosal Response to Esophageal Motor Disorders

The mucosa of the esophagus is involved in only one disorder of motor function, lower esophageal sphincter (LES) incompetence. Although long-standing megaesophagus in untreated achalasia used to be associated with inflammation, leukoplakia, and carcinomatous degeneration,1,2modern treatment has made such mucosal changes distinctly more uncommon. This communication, therefore, discusses changes in the esophageal mucosa brought about by reflux of gastrointestinal contents into the esophagus through an incompetent LES. METHODS OF MUCOSAL EVALUATION Several different methods of studying the esophageal mucosa are available, both clinically and experimentally. Roentgenographic contrast study of the mucosa during a barium swallow certainly is the most common form of investigation employed clinically, but unfortunately it is one of the least sensitive. Unless mucosal damage has progressed to deep ulceration or stricture formation, the barium examination of the esophageal mucosa will usually be reported as normal.3This is not surprising, since primary mucosal diseases in

Mucosal response to esophageal motor disorders

The mucosa of the esophagus is involved in only one disorder of motor function, lower esophageal sphincter (LES) incompetence. Although long-standing megaesophagus in untreated achalasia used to be associated with inflammation, leukoplakia, and carcinomatous degeneration,^1,2modern treatment has made such mucosal changes distinctly more uncommon. This communication, therefore, discusses changes in the esophageal mucosa brought about by reflux of gastrointestinal contents into the esophagus through an incompetent LES. <h3>METHODS OF MUCOSAL EVALUATION</h3> Several different methods of studying the esophageal mucosa are available, both clinically and experimentally. Roentgenographic contrast study of the mucosa during a barium swallow certainly is the most common form of investigation employed clinically, but unfortunately it is one of the least sensitive. Unless mucosal damage has progressed to deep ulceration or stricture formation, the barium examination of the esophageal mucosa will usually be reported as normal.³This is not surprising, since primary mucosal diseases in

The Immediate Effect of Successful Pneumatic Dilatation on Esophageal Function in Achalasia

In 10 patients with achalasia, successful pneumatic dilatation induced a predictable and significant reduction of elevated resting lower esophageal sphincter (LES) pressure. This weakened LES was still able to maintain an effective barrier against reflux after dilatation. In untreated achalasia, incomplete relaxation left a residual pressure at the LES indicating obstruction at this level during swallowing. After dilatation, this residual pressure was equal to normal, independently of resting LES pressure, and complete relaxation became an all or none response to swallowing. Elevated resting pressure in the body of the esophagus reverted to normal, but characteristic abnormal swallowing responses of this segment were not modified by pneumatic dilatation.

Role of gastrin supersensitivity in the pathogenesis of lower esophageal sphincter hypertension in achalasia.

Intraluminal manometric studies were carried out in 19 patients with untreated achalasia and in 20 normals. Lower esophageal sphincter (LES) pressure was 50.5 +/-4.6 mm Hg in patients with achalasia as compared with 19.4 +/-1.3 mm Hg in the normal group. In both groups, the LES pressure was lowered when exogenous 0.1 N HCl was placed into the stomach. Although the nadir of pressure attained with acid suppression was the same, the per cent inhibition was significantly greater in patients with achalasia. Serum gastrin levels were the same in the two groups studied. The patients with achalasia, pre- and postpneumatic dilatation, showed a supersensitivity to exogenous intravenous gastrin I, as compared with normals. These data suggest that high, acid-suppressible levels of LES pressure, in patients with achalasia, are due to supersensitivity to endogenous gastrin.