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Query: UMLS:C0014848 (achalasia)
 2,804 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

100 esophageal motility studies on 88 consecutive patients referred to the University of California Medical Center were analyzed. Diagnoses of achalasia, diffuse spasm of the esophagus, scleroderma, hiatal hernia and other conditions were made from the motility tracings. The motility tests have been found to be most helpful in differentiating various disorders of swallowing and thoracic pain of unknown cause.
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PMID:Evaluation of 100 esophageal motility studies at a university medical center. 564 Jan 87

Various swallowing disorders have been viewed to be psychogenic and an altered contractile activity of the oesophagus has been reported to occur during emotional stress. Non-propulsive activity and "cardiospasm" were suggested to represent a symbolic revulsion, referring to deep, unconscious conflict or an ambivalent attitude towards incorporation (Kronfeld, 1934; Weiss, 1944; Alexander, 1950). However, these concepts were not corroborated by subsequent research. "Globus hystericus" was shown to result from webs and folds in the hypopharynx or from gastrooesophageal reflux, whilst the term "cardiospasm" has even become obsolete: there is no spasm of the lower oesophageal sphincter but an "achalasia", i.e., a failure to relax upon swallowing, which is not induced by psychic factors, but by lesions affecting the intrinsic and extrinsic innervation. On the other hand, it has been shown that the oesophagus reacts with non-propulsive contractions not only emotional tension, but also to cold or hot food and even to stimuli not related to ingestion such as intense short sounds, and that these contractions are likely to form part of the defence reaction of the healthy organism. Despite this responsiveness of the oesophagus and the fact that strategies aimed at inducing relaxation and reassurance can help patients to cope with their swallowing disorders, the psychosomatic concept that "exaggerated" oesophageal responses can lead to organic diseases has remained purely speculative. Present knowledge of the physiology and pathophysiology of the oesophagus clearly indicates that disorders such as globus sensation, achalasia, and diffuse oesophageal spasm should not be treated by psychotherapeutic but by appropriate surgical, or medical, means.
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PMID:[Swallowing the psyche]. 663 83

Primary motor disorders of the esophagus can be managed surgically with excellent results. Between the years 1972 and 1983, 40 patients were managed by us. The patients ranged in age from 14 to 79 years (mean 36.3 years). Thirty-six patients were managed primarily by the authors and 4 patients secondarily. The distribution of the hypodynamic states were achalasia in 29 patients, vigorous achalasia in 5 patients, and diffuse spasm in 1 patient, whereas the hyperdynamic states were squeeze syndrome in 2 patients, super-squeeze syndrome in 1 patient, and hypertensive lower esophageal sphincter in 2 patients. Of the 36 patients in hypodynamic states, 27 had a modified Heller myotomy and reconstruction of the gastroesophageal junction with a Belsey fundoplication and 9 had only a modified Heller myotomy. There was only one patient with reflux esophagitis. It occurred after myotomy and Belsey fundoplication for a hypertensive lower esophageal sphincter and hiatus hernia. Four patients were managed secondarily for complicated recurrent problems, one with a Belsey fundoplication and three with a jejunal interposition graft. We recommend myotomy, with or without a Belsey fundoplication, for management of primary motor disorders and avoidance of total Nissen fundoplication and a lengthening Collis gastroplasty.
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PMID:Surgical management of primary motor disorders of the esophagus. 674 28

This study attempted to define the esophageal motor disturbances and pathogenesis of symptoms in patients with lower esophageal diverticulum. Sixty-five patients were investigated by manometry in addition to roentgenography and endoscopy. Fifty had manometric evidence of abnormal motility, most often diffuse spasm or achalasia. Of the 15 patients with normal esophageal motility, 13 had hiatal hernia, and five of these had a high grade distal esophageal stricture. Pressures in the lower esophagus and lower esophageal sphincter in patients with lower esophageal diverticulum and motor disturbance were the same as for those in matched patients with motor disturbances but no diverticulum. Dysphagia, chest pain and regurgitation were common presenting symptoms. Of 46 patients with dysphagia, only ten had mechanical obstruction to explain this symptom. Of 32 patients with chest pain, only two had ulceration in the diverticulum as a possible cause of pain. We conclude that the development of lower esophageal diverticulum and its symptoms are associated with a motor disturbance of the esophagus in the majority of patients and with an organic obstruction in the minority of patients. The diverticulum itself is usually not the sole cause of the esophageal symptoms, although diverticula can produce symptoms in the absence of other definable conditions. When surgical treatment is indicated, the diverticulum should be excised and the underlying motor or mechanical obstruction should be corrected to prevent serious postoperative complications and recurrence of the diverticulum and its symptoms.
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PMID:Physiopathology of lower esophageal diverticulum and its implications for treatment. 677 41

Twenty-two patients with a history of between one and four (average of two) unsuccessful prior esophageal operations for neuromotor dysfunction were treated with esophageal resection and replacement. Eleven (50%) had recurred reflux esophagitis in association with various disorders of motility: esophageal spasm in 4, achalasia in 3, scleroderma in 2, and esophageal atresia in 2. Eight (36%) had primary esophageal spasm and 3 (14%) had achalasia. Esophageal obstruction, regurgitation, and severe spasm were the most common manifestations of the inability to swallow normally. Transthoracic or transhiatal (blunt) esophagectomies were performed in 5 and 17 patients, respectively. The stomach, with a cervical esophagogastric anastomosis, was used for esophageal substitution in 15 patients. Six patients underwent a long-segment colonic interposition, and 1 patient with achalasia underwent a distal esophagectomy and short-segment colonic interposition. One patient undergoing transthoracic esophagectomy for achalasia died from unrecognized intraoperative bleeding into the opposite chest. There were no other operative deaths. Additional complications included transient hoarseness in 8 patients, chylothorax in 1, and anastomotic leak in 1. After an average follow-up of 25 months for the 21 surviving patients, ability to eat is regarded as good in 18 (85%), fair in 1 (5%), and poor in 2 (10%). In patients with incapacitating esophageal neuromotor disease, a more radical operative approach-esophagectomy--may be safer and more reliable than attempting another procedure and risking another failure. Esophagectomy ensures definitive elimination of the esophageal problem and as optimal an ability to eat as possible. Our experience suggests that the stomach, with a cervical esophagogastric anastomosis, offers a better functional esophageal substitute than does a colonic interposition.
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PMID:Esophagectomy: definitive treatment for esophageal neuromotor dysfunction. 711 44

In 15 patients suspected to have achalasia or diffuse spasm of the oesophagus we were unable to make the final diagnosis of their motility disorder in spite of radiologic, endoscopic, and manometric examinations. In 5 patients the radiologic and manometric results showed a discrepancy. In 4 patients only the lower oesophageal sphincter exhibited failure fo complete relaxations typical of achalasia; however, the motility of the body of the oesophagus was peristaltic in nature. In 6 patients the initial diagnosis had to be changed during follow-up. In conclusion, motility disorders occur in the oesophagus which cannot be classified according to existent definitions. It is possible therefore that achalasia and oesophageal spasm are different and not always fixed expressions of one nosologic entity.
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PMID:[Diagnostic problems in the differentiation of achalasia and spasm of the oesophagus (author's transl)]. 742 76

In reflux disease the authors emphasize the following diagnostic procedures: a satisfactory case-history, endoscopy, aimed biopsy, radiographic evidence of reflux, radionuclide reflux scintigraphy and pH-metry. As to subsidiary examinations, they recommend Bernstein's perfusion test. In 50% of the patients with non-coronary chest pain the complaints are caused by diseases of the oesophagus. The latter include achalasia, dysphagia, idiopathic diffuse spasm, hyperdynamic oesophagus and irritable oesophagus. In the treatment of reflux disease the stage of the disease is decisive. Treatment is prolonged and the doses of drugs are higher than in duodenal ulcers. The basis are H2 blockers. In severe forms treatment with omeprazole is indicated. Surgery is indicated only in severe mucosal complications. In achalasia of the oesophagus this is disruption of the sphincter by the method of pneumatic dilatation or surgical myotomy. Idiopathic diffuse spasm and other disorders of oesophageal motility respond in different ways to treatment with calcium autagonists and nitrate treatment.
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PMID:[Diagnosis and therapy of esophageal diseases]. 850 59

For more than 2 centuries, the nature and pathophysiology of pharyngoesophageal (Zenker's) diverticulum has been a matter of argument. The intrinsic or extrinsic forces and structures that might play a role in the development of this disorder have been repeatedly scrutinized, and still today the different theories of muscular incoordination and/or spasm, cricopharyngeal achalasia, gastroesophageal reflux, or neuromuscular abnormalities try to find their way as the final word regarding etiology remains to be told. Options for treatment follow a similar pattern although myotomy and diverticulopexy seem to have yielded the best results. In this review, historical and current data gathered from the world literature are compiled in an attempt to give a clear overview of the pathophysiology surrounding the genesis of Zenker's diverticulum and the clinical manifestations, diagnosis, and different alternatives for definite treatment of this disorder.
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PMID:Zenker's diverticulum: reappraisal. 912 43

Primary esophageal motility disorders (i.e. achalasia, diffuse spasm and related conditions) but also gastroesophageal reflux disease are characterised by a more or less pronounced dysfunction of esophageal body peristalsis and gastroesophageal sphincter relaxation. A normal interplay between inhibitory and excitatory peripheral nerves in the smooth muscle part of the esophagus is essential for the generation of esophageal peristalsis. The inhibitory nerve pathway determines the timing of the contraction; its neurotransmitter is NO. The excitatory pathway mainly determines the strength of the contraction; the neurotransmitter is acetylcholine. We have recently developed a technique to visualize the effect of the inhibitory nerves in the human tubular esophagus as a manometric relaxation of an artificial high pressure zone. We used this technique in patients with achalasia, diffuse spasm and related conditions and found an inverse relationship between percent inhibition and progression velocity of the contractions. We have examined with the same technique patients with reflux disease and found in these patients that the occurrence of acid reflux during TLESR's is accompanied by inhibition of the esophagus, whereas in normal controls it is accompanied by excitation. From a pathogenetic viewpoint we conclude as follows. Disorders of the inhibitory nerve pathway result in achalasia, diffuse spasm or related condition. We do not know exactly what happens when the excitatory pathway is diseased; there are arguments that these patients may have reflux disease.
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PMID:New insights in the pathophysiology of primary motility disorders of the esophagus. 949 Sep 18

The esophageal primary motor disorders like achalasia, diffuse esophageal spasm or the nutcracker can involve the upper esophageal sphincter, the esophageal body, the lower esophageal sphincter or a combination of them. This article will focus on the esophageal body and abnormal peristalsis. A normal esophageal peristaltic contraction occurs after a latency period following a swallow and requires a minimum amplitude to be propulsive. Abnormal latencies may generate simultaneous contractions whereas low amplitude contractions may be inefficient i.e. GERD and high amplitude contractions my provoke chest pain or dysfagia i.e. diffuse spasm. The latency period between deglutition and contraction is due to a muscle inhibition immediately after the swallow. This inhibition is due to release of NO by an inhibitory neurone located in the myenteric plexus. At the end of the inhibition, the contraction occurs due to release of acetyl choline by an excitatory cholinergic neurone. The exact interplay between these two neurones will determine the <<timing>> or propagation velocity and the amplitude of esophageal contractions. Patients with achalasia have a predominant loss of inhibitory neurones (VIP and NOS) with a relative preservation of excitatory cholinergic neurones. The histophatologic and immunohistochemical status in patients with esophageal primary motor disorders other than achalasia is poorly characterised Examples of deglutitive inhibition in the esophagus can be observed during the relaxation of the lower esophageal sphincter or when a subject swallows very frequently. In order to quantify deglutitive inhibition we developed a method that induces an artificial high pressure zone in the mid esophageal body. During the latency period after a swallow, the high pressure zone relaxes (is inhibited). With this method, we could measure the magnitude and duration of the inhibitory phenomenon. There is a very good correlation between the degree of deglutitive inhibition and propagation velocity of esophageal contractions. The less inhibition, the faster the propagation velocity of contractions. Simultaneous contractions are the consequence of absent inhibition. Patients with esophageal primary motor disorders may have very fast propagating contractions and a small percentage of simultaneous contractions or up to 100% of simultaneous contractions. The correlation between the degree of inhibition and propagation velocity of contractions suggests that the different primary motor disorders are the expression of a progressive failure in esophageal inhibition.
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PMID:[Role of deglutitive inhibition in the pathophysiology of esophageal primary motor disorders]. 1060 60


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