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Review |

Treating Achalasia:  From Whalebone to Laparoscope FREE

Anita E. Spiess, MD; Peter J. Kahrilas, MD
[+] Author Affiliations

From the Department of Medicine, Division of Gastroenterology & Hepatology, Northwestern University Medical School, Chicago, Ill.


JAMA. 1998;280(7):638-642. doi:10.1001/jama.280.7.638.
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Published online

Objective.— To review the pathophysiology and management of achalasia.

Data Sources.— Peer-reviewed publications located via MEDLINE using the search term esophageal achalasia (subheadings: complications, drug therapy, epidemiology, etiology, physiopathology, surgery, and therapy) published in English from 1966 to December 1997.

Study Selection.— Of 2632 citations identified, 4.5% were selected for inclusion by authors' blinded review of the abstracts. New developments in the understanding of achalasia or reports of therapeutic efficacy in either controlled trials or uncontrolled consecutive series involving 10 patients or more observed for a year or longer were reviewed in detail.

Data Extraction.— All 6 controlled therapeutic trials were included, and therapeutic efficacy in uncontrolled series was assessed by the authors extracting the patients with a good-to-excellent response from each study and calculating a pooled estimate of response rate with individual studies weighted proportionally to sample size.

Data Synthesis.— Achalasia results from irreversible destruction of esophageal myenteric plexus neurons causing aperistalsis and failed lower sphincter relaxation. The only therapies that adequately compensate for this dysfunction for a sustained time are pneumatic dilation and Heller myotomy. The single controlled trial comparing these treatments found surgery superior to dilation (95% vs 51% nearly complete symptom resolution, P<.01). In uncontrolled trials pneumatic dilation (weighted mean [SD]) is 72% (26%) effective vs 84% (20%) for Heller myotomy. The limitation of dilation is a 3% risk of perforation; thoracotomy morbidity has been the major limitation of myotomy. Surgical morbidity has been sharply reduced by laparoscopic techniques.

Conclusions.— Both pneumatic dilation and surgical myotomy are effective therapies for achalasia; laparoscopic Heller myotomy is emerging as the optimal surgical therapy.

ACHALASIA was first recognized more than 300 years ago. The disorder was initially labeled cardiospasm, recognizing it as a functional obstruction of the esophagus at the cardiac sphincter. The first reported treatment was to pass through the esophagus a piece of carved whalebone with a sponge affixed to the distal end.1 In 1937, Lendrum proposed our current concept of the disease as a syndrome caused by incomplete relaxation of the lower esophageal sphincter (LES) and renamed the disease achalasia ("failure to relax").2 This review summarizes the current knowledge of the pathophysiology and management of achalasia. The primary data source was a MEDLINE search of peer-reviewed articles, using the search term esophageal achalasia (subheadings: complications, drug therapy, epidemiology, etiology, physiopathology, surgery, and therapy), that were published in English from 1966 to December 1997. Reports of advances in the understanding of achalasia or of therapeutic efficacy in consecutive series of patients were reviewed in detail.

Achalasia is rare, with an estimated annual incidence of 1 per 100000 persons.35 The physiologic alterations in achalasia (impaired LES relaxation with swallowing and aperistalsis in the smooth muscle esophagus) result from damaged innervation. Neuroanatomic data suggest the esophageal myenteric plexus as the primary neurologic target. Several reports,68 including a recent study of 42 resected achalasic esophagi,9 reveal fewer ganglion cells and ganglion cells surrounded by mononuclear inflammatory cells in the smooth muscle. The ultimate cause of ganglion cell degeneration in achalasia is unknown but there is an association with the class II HLA antigen DQw1,10 and it has been hypothesized to be related to herpes zoster11 or measles virus infections.12 Support for an autoimmune pathogenesis comes from the description of antimyenteric neuron antibodies in a subset of achalasia patients.13

Physiologic studies also demonstrate myenteric plexus dysfunction in achalasia. Excitatory (cholinergic) and/or inhibitory ganglionic neurons (nitric oxide ± vasoactive intestinal polypeptide)14 are potentially affected. Physiologic and pharmacological evidence suggests partial preservation of the postganglionic cholinergic pathway in most cases.15 On the other hand, it is clear that the inhibitory ganglionic neurons must necessarily be impaired as an early manifestation of achalasia.14,16 These inhibitory neurons mediate LES relaxation and the proximal to distal sequencing of esophageal peristalsis17; their absence offers a unifying hypothesis for the key physiologic abnormalities of achalasia: impaired LES relaxation and aperistalsis.

The consequences of achalasia can be subtle early in its course, becoming more obvious with progression. The dilated esophagus with retained food and an air fluid level visible on a chest x-ray film is a late finding. Prior to the esophageal dilatation, the main symptoms are dysphagia and chest pain. In fact, the diagnosis is often delayed by the reported symptoms of chest pain and heartburn, leading the clinician to suspect reflux disease. The etiology of these symptoms is unclear, and antireflux therapy provides no relief. Experimental data show that, despite up to 47% of patients reporting the symptom of "heartburn," little reflux can be verified by pH monitoring.18,19 Furthermore, esophageal pH monitoring is deceptive in achalasia because fermentation of food retained in the esophagus produces lactic acid, which can lead to an abnormal result.20

Achalasia is best detected by functional studies, either fluoroscopy during a barium swallow or esophageal manometry. The radiographic features are aperistalsis, esophageal dilatation, and minimal LES opening with a bird-beak appearance; defining manometric features are aperistalsis and incomplete LES relaxation. Patients with spasmodic esophageal contractions define the variant known as vigorous achalasia and tend not to have esophageal dilatation, making them difficult to diagnose radiographically.21,22 Because manometry can detect the functional abnormalities of achalasia with or without esophageal dilatation, it is the most sensitive diagnostic method.23 However, both Chagas disease and pseudoachalasia can duplicate the manometric findings of achalasia. Chagas disease, caused by a parasite (Trypanosoma cruzi) and endemic in South America, tends to have multiorgan involvement and can be detected by a serum antibody.24 Tumor-related pseudoachalasia (carcinoma of the gastric cardia in >50% of cases) accounts for up to 5% of cases and can completely mimic the clinical and manometric presentation of achalasia.25 Malignant tumors produce an achalasia syndrome by infiltrating the gastroesophageal junction and creating a relative obstruction with secondary esophageal dilatation. It is this potential pitfall that mandates endoscopy as part of the diagnostic evaluation. Furthermore, the anatomic findings with pseudoachalasia can be subtle; if clinical suspicion is high, computerized tomography and endoscopic ultrasound should be considered.

Dysphagia for both solids and liquids is a major symptom of achalasia.26 The pattern of dysphagia, especially in individuals with a dilated esophagus, is unique. They often augment food passage by drinking a lot while eating or applying maneuvers such as straightening the back, raising their arms over their heads, standing, or jumping. Long-term esophageal food retention leads to progressive esophageal dilatation, in which setting regurgitation, especially nocturnal regurgitation, becomes a prominent symptom. Pulmonary complications can result from regurgitation and chronic aspiration. Theoretically, early therapy should minimize these problems by its demonstrated ability to halt and even reverse the progression of esophageal dilatation.27 Thus, therapeutic efficacy in achalasia should be assessed not only by symptom relief but also by improvement in esophageal emptying.

Another potential complication of achalasia is the development of esophageal carcinoma, first recognized by Fagge in 1872.28 Estimates of the relative risk of developing squamous cell carcinoma with achalasia range from 0- to 33-fold.2933 The only population-based study found a 16-fold risk among 1062 achalasia patients with 9864 patient-years of follow-up.34 Therapy does not eliminate the cancer risk, evident by reported cases occurring years after either medical or surgical therapy.27,35 However, despite the 16-fold relative risk, the absolute risk of cancer remains slight, and an estimated 681 annual surveillance endoscopies would detect only 1 incident cancer among achalasia patients; surveillance is not advocated by national gastroenterology societies.

No therapy for achalasia reverses the underlying neuropathology or associated impaired LES relaxation and aperistalsis. Instead, the target of treatment is to reduce the LES pressure. Gravity then facilitates esophageal emptying, reducing the symptoms associated with esophageal retention and, hopefully, preventing complications. However, there are no data on the prevention of complications, and therapeutic efficacy can only be assessed by symptomatic or functional improvement. An analysis of pneumatic dilation found that a postdilation LES pressure greater than 10 mm Hg was the best predictor of prolonged remission, while patients with values greater than 20 mm Hg had little benefit.36 Direct assessments of esophageal emptying can be performed with either fluoroscopy or scintigraphy. Radionuclide studies quantifying the esophageal retention of swallowed technetium-labeled sulfur colloid are described but rarely used. Alternatively, the height of the barium column within the esophagus 5 minutes after swallowing directly measures esophageal emptying. Although a column of less than 1 cm was initially described as indicative of inadequate emptying,37 a subsequent evaluation could not correlate this measure and symptom improvement.38 Evaluating symptom improvement is equally difficult. Although a descriptive symptom classification system has been proposed,39 most series simply report "excellent" or "good" results and emphasize relief of dysphagia. The meaning of such descriptions varies with the initial symptom severity, making comparisons difficult.

Therapeutic Modalities

Proposed treatments include drugs, mechanical dilation, or surgery. Many drugs reduce LES pressure. Although anticholinergics, amyl nitrite, sublingual nitroglycerin, theophylline, and β2 agonists have been tried,40,41 the largest reported experience has been with isosorbide dinitrate or nifedipine, administered orally or sublingually prior to eating. Isosorbide dinitrate, 5 to 10 mg sublingual, reduces the resting LES pressure by 66% for 90 minutes.42 Calcium channel blockers (diltiazem hydrochloride, nifedipine, verapamil) reduce the LES pressure by 30% to 40% for more than 1 hour.43,44 Another recently proposed achalasia treatment is intrasphincteric injection of botulinum toxin, which inhibits acetylcholine release from nerve endings,45 reducing the LES pressure by 60% in pigs and 33% in people.46,47 The site of action may be ganglionic or postganglionic. Its effect is eventually reversed by sprouting terminal axons that form new synapses.48

Forceful dilation of the LES is accomplished with a balloon dilator, designed to distend the LES to a diameter of 3 to 4 cm and reduce LES pressure by partially disrupting the sphincteric muscle.49,50 In instances of an unsatisfactory result, pneumatic dilation can be repeated once or twice. The major complication of pneumatic dilation is esophageal perforation. If perforation is suspected because of postprocedural pain or subcutaneous emphysema a Gastrografin followed by barium swallow should be obtained.51,52 Any substantial perforation requires surgical repair. Patients with perforations that are promptly recognized and treated surgically within 6 to 8 hours have outcomes comparable to patients undergoing elective thoracotomy and Heller myotomy.53

The surgical objective in the treatment of achalasia is to disrupt the LES enough to eliminate dysphagia without causing excessive reflux. Heller first described the technique in 1913, proposing anterior and posterior gastroesophageal junction incisions after accessing the area by thoracotomy.54 Subsequent modifications include eliminating the posterior myotomy, shortening the anterior myotomy, and accessing the area by laparotomy, thoracoscopy, or laparoscopy. Debate persists regarding the necessity and type of accompanying antireflux procedure. The current trend is to use a laparoscopic approach, which requires division of the phrenoesophageal ligament and partial mobilization of the esophagus.55 With this approach, at least a partial anterior fundoplication (Dohr procedure) is requisite.

Controlled Trials

Only 1 controlled trial has compared the 2 most effective therapies of achalasia. That prospective, randomized trial compared pneumatic dilation (39 patients) to Heller myotomy via thoracotomy (42 patients), reporting 95% nearly complete symptom resolution in the surgical group compared with 51% in the dilation group (P<.01) after 5 years (range, 24-156 months).27 Included among the treatment failures in the dilation group are 2 patients (5.4%) who sustained perforations and 4 (10.8%) who subsequently had a good result with a second dilation. Although that report was criticized for the method of pneumatic dilation,56 it remains the best source of comparative data. The only other controlled trials have compared pharmacological therapies either to each other or to pneumatic dilation. A controlled trial comparing botulinum toxin to pneumatic dilation found a sustained symptomatic response in 32% of botulinum toxin patients compared with 70% of the pneumatic dilation group at 12 months (P<.01).57 A trial comparing pneumatic dilatation with nifedipine found a significant decrease in LES pressure and significant symptomatic improvement in both groups after 21 months.58 In a placebo-controlled trial of 29 patients, nifedipine was significantly better than placebo, yielding good to excellent symptomatic response in 70% of achalasia patients after 6 to 18 months.59 However, subsequent placebo-controlled, crossover trials have found only minimal clinical improvement with nifedipine.60,61 In a prospective controlled trial of botulinum toxin vs placebo (saline injection), botulinum toxin provided significantly better symptomatic, manometric, and radiographic response, but 7 of the 8 patients relapsed after a mean period of 7 months.62

Uncontrolled Trials

Table 1 summarizes medical and surgical treatment data of achalasia.27,37,55,57,62108 Data in Table 1 are uncontrolled, as the few controlled trials are summarized above. All data included were consecutive series, although some were collected prospectively and others by retrospective review. These were combined in Table 1 because the results were identical. Since there was no uniformity in assessment of efficacy among trials, the proportion of patients with a good-to-excellent response were extracted from each study, regardless of criteria. The response indicated for each therapy is a pooled estimate of response rate over multiple studies with each study weighted proportionally to its sample size. Only studies including more than 10 patients and with a follow-up of at least 1 year were tabulated; since no such reports exist using smooth muscle relaxants or a thoracoscopic Heller myotomy, these treatments are not included. In calculating the response rate of each study, we extracted the number of individuals with a good-to-excellent response that was sustained until the end of the observation period without any further therapy. Thus, if a patient required a second dilation or a second injection or if a laparoscopic operation was converted to an open procedure, these were considered failures of the initial treatment. Also in Table 1 are similar calculations on the efficacy of retreatment. In the case of botulinum toxin and pneumatic dilation, the retreatment data pertain to individuals who either experienced a relapse after an initially successful therapy or had a second try after inadequate benefit from an initial treatment. Evident in Table 1, the 2 efficacious therapies are pneumatic dilation and Heller myotomy. Only 1 of 31 patients in a prospective trial of botulinum toxin had a response sustained for more than 2 years.63

Table Graphic Jump LocationPooled Estimate of Response Rate of Achalasia Treatments Across Referenced Studies*

The choice between using dilation or myotomy as the primary therapy for achalasia requires consideration of not only efficacy but also morbidity. Pneumatic dilation, an outpatient procedure, has less morbidity than any surgical approach with the caveat that the incidence of esophageal perforation is 3%. Even though these patients do well, if the perforation is recognized and operated on promptly,53 the perforation is invariably into the mediastinum, and there is no minimally invasive surgical option once that has occurred. With respect to Heller myotomy, although clearly efficacious, the greatest proportion of these cases were accomplished by thoracotomy, which has considerable morbidity. More than any other factor, it is the morbidity of thoracotomy that has led most patients to pneumatic dilation as the initial intervention. However, laparoscopic techniques have now been introduced with similar efficacy and substantially reduced morbidity. One recent series of 24 achalasia patients treated either thoracoscopically or laparoscopically had benefit similar to those of open procedures with a median hospitalization of only 3 days.109 This is compared to laparotomy and thoracotomy, which have an average hospitalization of 7 to 10 days, followed by prolonged morbidity.91,98

Although more effective in terms of relieving dysphagia, myotomy also makes reflux more likely, leading some surgeons to perform an antireflux procedure concurrently with the myotomy; others reserve this for patients with an associated hiatal hernia.110 Illustrative of reflux complications is a surgical series in which recurrent dysphagia due to insufficient myotomy or periesophageal scarring occurred in 9% of patients 3 to 30 months postoperatively, while complications due to reflux ranging from esophagitis to Barrett metaplasia occurred in 17% of patients 21 to 23 months postoperatively.94 There are also reports of adenocarcinoma developing as a late complication of postmyotomy reflux.111113 However, just as surgical techniques have evolved, so has the medical therapy of reflux esophagitis, and these reflux complications would be unlikely if individuals were treated with proton pump inhibitors.

In extremely advanced or refractory cases of achalasia, esophageal resection with gastric pull-up or interposition of a segment of transverse colon may be the only surgical option.91,114118 Patients with daily dysphagia and a tortuous esophagus with poor emptying, despite multiple previous procedures, are likely candidates.117 This technique is rarely if ever used as a primary intervention and, fortunately, is necessary in less than 1% of the achalasia population.

Achalasia is a rare disease consequent from esophageal myenteric neuron destruction. In the short term, this defect results in esophageal retention with dysphagia, regurgitation, and chest pain, symptoms that often provoke the misdiagnosis of reflux disease. In the long term, untreated achalasia can lead to profound dysphagia, weight loss, and chronic aspiration. Despite the minimal controlled treatment data in the literature, treatment is desirable because there is no spontaneous recovery from achalasia, and treatment that compensates for the impaired esophageal emptying is the only potential way of preventing long-term complications. Proposed treatments of achalasia can be grouped as pharmacological, dilation, or surgical with efficacy assessed in terms of symptomatic improvement, functional improvement, or both. The above considerations suggest that both sustained symptom relief and functional improvement are desirable objectives. This requirement, in essence, relegates pharmacological therapy to the role of a temporizing measure. The most intriguing data pertain to the use of botulinum toxin injection. However, the limitations of botulinum toxin injection are the following: (1) it has no proven effect in improving esophageal emptying, (2) its effect lasts for only about a year, (3) the consequences of repeated injections are unknown, and (4) it is relatively expensive.119 It would appear, therefore, that this therapeutic option should be reserved for elderly or frail individuals who are poor risks for more definitive treatments.

Definitive treatments of achalasia with the potential of satisfying long-term treatment objectives are dilation or surgical myotomy. Pneumatic dilation, a descendant of the sponge affixed to whalebone technique, results in a good response in the majority of patients, with approximately 20% of patients requiring additional dilations and 3% incurring esophageal perforation. Heller myotomy, though of more predictable efficacy than pneumatic dilation, has historically been a second-line therapy because of the morbidity associated with thoracotomy. Furthermore, even in the event of perforation from a pneumatic dilation, a successful myotomy could still be achieved by thoracotomy. However, with the recent introduction of laparoscopic myotomy, this hierarchical approach to therapy may change. Rapidly accumulating data on this new technique suggest equal efficacy of the laparoscopic procedure when compared to the open approach, but with sharply reduced morbidity. However, because laparoscopic myotomy cannot be done in the setting of esophageal perforation during pneumatic dilation, this option may be lost if not selected as the initial intervention. Given these considerations, it may be time to evolve from the whalebone to the laparoscope.

Willis T. Pharmaceutice Rationalis Sive Diatribe de Medicamentorum Operationibus in Human Corpore . London, England: Hagae Comitis; 1674.
Lendrum FC. Anatomic features of the cardiac orifice of the stomach with special reference to cardiospasm.  Arch Intern Med.1937;59:474-511.
Mayberry JF, Atkinson M. Studies of incidence and prevalence of achalasia in the Nottingham area.  QJM.1985;56:451-456.
Earlnam RJ, Ellis FH, Nobrega FT. Achalasia of the esophagus in a small urban community.  Mayo Clin Proc.1969;44:478-483.
Howard PJ, Maher L, Pryde A, Cameron EWJ, Heading RC. Five year prospective study of the incidence, clinical features, and diagnosis of achalasia in Edinburgh.  Gut.1992;33:1011-1015.
Cassella RR, Brown Jr AL, Sayre GP, Ellis Jr F. Achalasia of the esophagus: pathologic and etiologic considerations.  Ann Surg.1964;160:474-487.
Csendes A, Smok G, Braghetto I, Ramirez C, Velasco N, Henriquez A. Gastroesophageal sphincter pressure and histologic changes in the distal esophagus in patients with achalasia of the esophagus.  Dig Dis Sci.1985;30:941-945.
Qualman SJ, Haupt AM, Yang P, Hamilton SR. Esophageal Lewy bodies associated with ganglion cell loss in achalasia: similarity to Parkinson's disease.  Gastroenterology.1984;87:848-856.
Goldblum JR, Whyte RI, Orringer MB, Appelman HD. Achalasia, a morphologic study of 42 resected specimens.  Am J Surg Pathol.1994;18:327-337.
Wong RK, Maydonovitch CL, Metz SJ, Baker JR. Significant DQw1 association in achalasia.  Dig Dis Sci.1989;34:349-352.
Robertson CS, Martin BAB, Atkinson M. Varicella-zoster virus DNA in the oesophageal myenteric plexus in achalasia.  Gut.1993;34:299-302.
Jones DB, Mayberry JF, Rhoades J, Munro J. Preliminary report of an association between measles virus and achalasia.  J Clin Pathol.1983;36:655-657.
Verve GN, Sallustio JE, Eaker EY. Anti-myenteric neuronal antibodies in patients with achalasia: a prospective study.  Dig Dis Sci.1997;42:307-313.
Mearin F, Mourelle M, Guarner F, Papo M, Balboa A, Malagelada JR. Patients with achalasia lack nitric oxide synthase in the gastro-oesophageal junction.  Eur J Clin Invest.1993;23:724-728.
Holloway RH, Dodds WJ, Helms JF, Hogan WJ, Dent J, Arndorfer RC. Integrity of cholinergic innervation of the lower esophageal sphincter in achalasia.  Gastroenterology.1986;90:924-929.
Sifrim D, Janssens J, Vantrappen G. Failing deglutitive inhibition in primary esophageal motility disorders.  Gastroenterology.1994;106:875-882.
Murray JA, Ledlow A, Launspach J, Evans D, Loveday M, Conklin JL. The effects of recombinant human hemoglobin on esophageal motor function in humans.  Gastroenterology.1995;109:1241-1248.
Spechler SJ, Souza RF, Rosenberg SJ, Ruben RA, Goyal RK. Heartburn in patients with achalasia.  Gut.1995;37:305-308.
Smart HL, Mayberry JF, Atkinson M. Achalasia following gastroesophageal reflux.  J R Soc Med.1986;79:71-73.
Smart HL, Foster PN, Evans DF, Slevin B, Atkinson M. Twenty four hour oesophageal acidity in achalasia before and after pneumatic dilatation.  Gut.1987;28:883-887.
Goldenberg SP, Burrell M, Fette GG, Vos C, Traube M. Classic and vigorous achalasia: a comparison of manometric, radiographic, and clinical findings.  Gastroenterology.1991;101:743-748.
Todorczuk JR, Aliperti G, Staiano A, Clouse RE. Reevaluation of manometric criteria for vigorous achalasia.  Dig Dis Sci.1991;36:274-278.
Howard PJ, Maher L, Pryde A, Cameron EW, Heading RC. Five year prospective study of the incidence, clinical features, and the diagnosis of achalasia in Edinburgh.  Gut.1992;33:1011-1015.
Bettarello A, Pinotti HW. Oesophageal involvement in Chagas' disease.  Clin Gastroenterol.1976;5:103-117.
Kahrilas PJ, Kishk SM, Helm JF, Dodds WJ, Harig JM, Hogan WJ. A comparison of pseudoachalasia and achalasia.  Am J Med.1987;82:439-446.
Katz PO, Dalton CB, Richter JE, Wu WC, Castell DO. Esophageal testing of patients with noncardiac chest pain or dysphagia.  Ann Intern Med.1987;106:593-597.
Csendes A, Braghetto I, Henriquez A, Cortes C. Late results of a prospective randomised study comparing forceful dilatation and oesophagomyotomy in patients with achalasia.  Gut.1989;30:299-304.
Fagge CH. A case of simple stenosis of the oesophagus, followed by epithelioma.  Guy's Hosp Rep.1872;17:413-421.
Wychulis AR, Woolam GL, Andersen HA, Ellis Jr FH. Achalasia and carcinoma of the esophagus.  JAMA.1971;215:1638-1641.
Chuong JJ, DuBovik S, McCallum RW. Achalasia as a risk factor for esophageal carcinoma.  Dig Dis Sci.1984;29:1105-1108.
Peracchia A, Segalin A, Bardini R, Ruol A, Bonavina L, Baessato M. Esophageal carcinoma and achalasia: prevalence, incidence and results of treatment.  Hepatogastroenterology.1991;38:514-516.
Aggestrup S, Holm JC, Sorensen HR. Does achalasia predispose to cancer of the esophagus?  Chest.1992;102:1013-1016.
Meijssen MA, Tilanus HW, van Blankenstein M.  et al.  Achalasia complicated by oesophageal squamous cell carcinoma: a prospective study in 195 patients.  Gut.1992;33:155-159.
Sandler RS, Nyren O, Ekbom NO, Eisen GM, Yuen J, Josefsson S. The risk of esophageal cancer in patients with achalasia: a population-based study.  JAMA.1995;274:1359-1362.
Streitz Jr JM, Ellis Jr FH, Gibb SP, Heatley GM. Achalasia and squamous cell carcinoma of the esophagus: analysis of 241 patients.  Ann Thorac Surg.1995;58:1604-1609.
Eckardt VF, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation.  Gastroenterology.1992;103:1732-1738.
Cohen NN. An endpoint for pneumatic dilation of achalasia.  Gastrointest Endosc.1977;22:29.
Lee JD, Cecil BD, Brown PE, Wright RA. The Cohen test does not predict outcome in achalasia after pneumatic dilation.  Gastrointest Endosc.1993;39:157-160.
Vantrappen G, Hellemans J. Achalasia. In: Vantrappen G, Hellemans J, eds. Diseases of the Oesophagus . Berlin, Germany: Springer-Verlag; 1975:287-354.
Wong RK, Maydonovitch CL, Garcia JE, Johnson LF, Castell DO. The effect of terbutaline sulfate, nitroglycerin, and aminophylline on lower esophageal sphincter pressure and radionuclide esophageal emptying in patients with achalasia.  J Clin Gastroenterol.1987;9:386-389.
DiMarino AJ, Cohen S. Effect of an oral beta2-adrenergic agonist on lower esophageal sphincter pressure in normal subjects and in patients with achalasia.  Dig Dis Sci.1982;27:1063-1066.
Gelfond M, Rozen P, Keren S, Gilat T. Effect of nitrates on LOS pressure in achalasia: a potential therapeutic aid.  Gut.1981;22:312-318.
Gelfond M, Rozen P, Gilat T. Isosorbide dinitrate and nifedipine treatment of achalasia: a clinical, manometric and radionuclide evaluation.  Gastroenterology.1982;83:963-969.
Traube M, Hongo M, Magyar L, McCallum RW. Effects of nifedipine in achalasia and in patients with high-amplitude peristaltic esophageal contractions.  JAMA.1984;252:1733-1736.
Jankovic J, Brin MF. Therapeutic uses of botulinum toxin.  N Engl J Med.1991;324:1186-1194.
Pasricha PJ, Ravich WJ, Kalloo AN. Effects of intrasphincteric botulinum toxin on the lower esophageal sphincter in piglets.  Gastroenterology.1993;105:1045-1049.
Pasricha PJ, Ravich WJ, Hendrix TR, Sostre S, Jones B, Kalloo AN. Intrasphincteric botulinum toxin for the treatment of achalasia.  N Engl J Med.1995;322:774-778.
Pamphlett R. Early terminal and nodal sprouting of motor axons after botulinum toxin.  J Neurol Sci.1989;92:181-192.
Cox J, Buckton GK, Bennett JR. Balloon dilatation in achalasia: a new dilator.  Gut.1986;27:986-989.
Witzel L. Treatment of achalasia with a pneumatic dilator attached to a gastroscope.  Endoscopy.1981;13:176-177.
Olsen AM, Harrington SW, Moersch HJ, Anderson HA. The treatment of cardiospasm: analysis of a twelve year experience.  J Thorac Cardiovasc Surg.1951;22:164-187.
Vantrappen G, Janssens J. To dilate or to operate? that is the question.  Gut.1983;24:1013-1019.
Schwartz HM, Cahow CE, Traube M. Outcome after perforation sustained during pneumatic dilation for achalasia.  Dig Dis Sci.1993;38:1409-1413.
Heller E. Extramuköse Kardiaplastik beim chronischen Kardiospasmus mit dilatation des oesophagus.  Mitt Grenzgeb Med Chir.1913;27:141-149.
Hunter JG, Trus TL, Branum GD, Waring JP. Laparoscopic Heller myotomy and fundoplication for achalasia.  Ann Surg.1997;6:655-665.
Richter JE. Surgery or pneumatic dilatation for achalasia: a head-to-head comparison: now are all the questions answered?  Gastroenterology.1989;97:1340-1341.
Vaezi M, Richter J, Wilcox M, Schroeder P, Slaughter R. One year follow-up: pneumatic dilatation more effective than botulinum toxin [abstract].  Gastroenterology.1997;112:318.
Coccia G, Bortolotti M, Dodero M. Prospective clinical and manometric study comparing pneumatic dilatation and sublingual nifedipine in the treatment of oesophageal achalasia.  Gut.1991;32:604-606.
Bortolotti M, Labò G. Clinical and manometric effects of nifedipine in patients with esophageal achalasia.  Gastroenterology.1981;80:39-44.
Traube M, Dubovik S, Lange RC, McCallum RW. The role of nifedipine therapy in achalasia: results of a randomized double-blind, placebo-controlled study.  Am J Gastroenterol.1989;84:1259-1262.
Triadafilopoulos G, Aaronson M, Sackel S, Burakoff R. Medical treatment of esophageal achalasia: double-blind crossover study with oral nifedipine, verapamil, and placebo.  Dig Dis Sci.1991;36:260-267.
Annese V, Basciani M, Perri F.  et al.  Controlled trial of botulinum toxin injection versus placebo and pneumatic dilation in achalasia.  Gastroenterology.1996;111:1418-1424.
Pasricha P, Rai R, Ravich W, Hendrix T, Kalloo A. Botulinum toxin for achalasia: long-term outcome and predictors of response.  Gastroenterology.1996;110:1410-1415.
Cuilliere C, Ducrotte P, Zerbib F.  et al.  Achalasia: outcome of patients treated with intrasphincteric injection of botulinum toxin.  Gut.1997;41:87-92.
Fishman VM, Parkman HP, Schiano TD.  et al.  Symptomatic improvement in achalasia after botulinum toxin injection of the lower esophageal sphincter.  Gastroenterology.1996;91:1724-1730.
Wehrmann T, Jacobi V, Jung M, Lembcke B, Caspary WF. Pneumatic dilation in achalasia with a low-compliance balloon: results of a 5-year prospective evaluation.  Gastrointest Endosc.1995;42:31-36.
Mearin F, Armengol JR, Chicharro L.  et al.  Forceful dilatation under endoscopic control in the treatment of achalasia: a randomised trial of pneumatic versus metallic dilator.  Gut.1994;35:1360-1362.
Barnett J, Eisenman R, Nostrant TT, Elta GH. Witzel pneumatic dilation for achalasia: safety and long-term efficacy.  Gastrointest Endosc.1990;36:482-484.
Barkin J, Guelrud M, Reiner D, Goldberg R, Phillips R. Forceful balloon dilation: an outpatient procedure for achalasia.  Gastrointest Endosc.1990;36:123-126.
Kadakia S, Wong R. Graded pneumatic dilation using rigiflex achalasia dilators in patients with primary esophageal achalasia.  Am J Gastroenterol.1993;88:34-38.
Eckardt VF, Kanzler G, Westermeier T. Complications and their impact after pneumatic dilation for achalasia: prospective long-term follow-up study.  Gastrointest Endosc.1997;45:349-353.
Fellows IW, Oglivie AL, Atkinson M. Pneumatic dilatation in achalasia.  Gut.1983;24:1020-1023.
Heimlich JJ, O'Connor TW, Flores DC. Case for pneumatic dilatation in achalasia.  Ann Otolaryngol.1978;87:519-522.
Jacobs JB, Cohen NL, Mattel S. Pneumatic dilatation as the primary treatment for achalasia.  Ann Otol Rhinol Laryngol.1983;92:353-356.
Levine MJ, Moskowitz G, Dorf B, Bank S. Pneumatic dilation in patients with achalasia with a modified gruntzig dilator (Levine) under direct endoscopic control: results after 5 years.  Am J Gastroenterol.1991;86:1581-1584.
Yon J, Christensen J. An uncontrolled comparison of treatments for achalasia.  Ann Surg.1975;182:672-676.
Robertson CS, Fellows IW, Mayberry JF, Atkinson M. Choice of therapy for achalasia in relation to age.  Digestion.1988;40:244-250.
Sauer L, Pellegrini C, Way L. The treatment of achalasia.  Arch Surg.1989;124:929-932.
Parkman H, Reynolds J, Ouyang A, Rosato EF, Eisenberg JM, Cohen S. Pneumatic dilatation or esophagomyotomy treatment for idiopathic achalasia: clinical outcomes and cost analysis.  Dig Dis Sci.1993;38:75-85.
Lambroza A, Schuman R. Pneumatic dilation for achalasia without fluoroscopic guidance: safety and efficacy.  Am J Gastroenterol.1995;90:1226-1229.
Vantrappen G, Hellemans J, Deloof W, Valembois P, Vandenbroucke J. Treatment of achalasia with pneumatic dilatation.  Gut.1971;12:268-275.
Abid S, Champion G, Richter JE, McElvein R, Slaughter RL, Koehler RE. Treatment of achalasia: the best of both worlds.  Am J Gastroenterol.1994;89:979-985.
Ferguson M, Reeder L, Olak J. Results of myotomy and partial fundoplication after pneumatic dilation for achalasia.  Ann Thorac Surg.1996;62:327-330.
Duranceau AC, LaFontaine ER, Vallieres B. Effects of total fundoplication on function of the esophagus after myotomy for achalasia.  Am J Surg.1982;143:22-27.
Donahue PE, Schlesinger PK, Sluss KF.  et al.  Esophagocardiomyotomy: floppy Nissen fundoplication effectively treats achalasia without causing esophageal obstruction.  Surgery.1994;116:719-725.
Sariyannis C, Mullard KS. Oesophagomyotomy for achalasia of the cardia.  Thorax.1975;30:539-542.
Stipa S, Fegiz G, Iascone C.  et al.  Heller-Belsey and Heller-Nissen operations for achalasia of the esophagus.  Surg Gynecol Obstet.1990;170:212-215.
Castrini G, Pappalarado G, Mobarhan S. New approach to esophagocardiomyotomy.  J Thorac Cardiovasc Surg.1982;84:575-578.
Okike N, Payne WS, Neufeld DM.  et al.  Esophagomyotomy versus forceful dilation for achalasia of the esophagus: results in 899 patients.  Ann Thorac Surg.1979;28:119-124.
Pai G, Ellison R, Rubin J, Moore H. Two decades of experience with modified Heller's myotomy for achalasia.  Ann Thorac Surg.1984;38:201-206.
Ellis Jr FH. Oesophagomyotomy for achalasia: a 22-year experience.  Br J Surg.1993;80:882-885.
Jara M, Toledo-Pereyra LH, Lewis JW, Magilligan DJ. Long-term results of esophagomyotomy for achalasia of esophagus.  Arch Surg.1979;114:935-936.
Menzies-Gow N, Gummer JWP, Edwards DAW. Results of Heller's operation for achalasia of the cardia.  Br J Surg.1978;65:483-485.
Mattioli S, Di Simone MP, Bassi F.  et al.  Surgery for esophageal achalasia: long-term results with three different techniques.  Hepatogastroenterology.1996;43:492-500.
Ellis Jr FH, Watkins Jr E, Gibb SP, Heatley GJ. Ten- to 20-year clinical results after short esophagomyotomy without an antireflux procedure (modified Heller operation) for esophageal achalasia.  Eur J Cardiothorac Surg.1992;6:86-90.
Di Simone M, Felice V, D'Errico A.  et al.  Onset timing of delayed complications and criteria of follow-up after operation for esophageal achalasia.  Ann Thorac Surg.1996;61:1106-1111.
Gallone L, Peri G, Galliera M. Proximal gastric vagotomy and anterior fundoplication as complementary procedures to Heller's operation for achalasia.  Surg Gynecol Obstet.1982;155:337-341.
Malthaner R, Todd T, Miller L, Pearson FG. Long-term results in surgically managed esophageal achalasia.  Ann Thorac Surg.1994;58:1343-1347.
Bonavina L, Rosati R, Segalin A, Peracchia A. Laparoscopic Heller-Dor operation for the treatment of oesophageal achalasia: technique and early results.  Ann Chir Gynaecol.1995;84:165-168.
Picciocchi A, Cardillo G, D'Ugo D, Castrucci G, Mascellari L, Granone P. Surgical treatment of achalasia: a retrospective comparative study.  Jpn J Surg.1993;23:855-859.
Murray G, Battaglini J, Keagy B, Starek P, Wilcox B. Selective application of fundoplication in achalasia.  Ann Thorac Surg.1984;37:185-188.
Cosentini E, Berlakovich G, Zacherl J.  et al.  Achalasia: results of myotomy and antireflux operation after failed dilatations.  Arch Surg.1997;132:143-147.
Pandolfo N, Bortolotti M, Spigno L, Bozzano PL, Mattioli FP. Manometric assessment of Heller-Dor operation for esophageal achalasia.  Hepatogastroenterology.1996;43:160-166.
Robertson GSM, Lloyd DM, Wicks ACB, DeCeastecker J, Veitch PS. Laparoscopic Heller's cardiomyotomy without an antireflux procedure.  Br J Surg.1995;82:957-959.
Mitchell P, Watson D, Devitt PG.  et al.  Laparoscopic cardiomyotomy with a Dor patch for achalasia.  Can J Surg.1995;38:445-448.
Raiser F, Perdikis G, Hinder R.  et al.  Heller myotomy via minimal-access surgery.  Arch Surg.1996;131:593-598.
Morino M, Rebecchi F, Festa V, Garrone C. Laparoscopic Heller cardiomyotomy with intraoperative manometry in the management of oesophageal achalasia.  Int Surg.1995;80:332-335.
Rosati R, Fumagalli U, Bonavina L, Segalin A, Montorsi M, Bona S. Laparoscopic approach to esophageal achalasia.  Am J Surg.1995;169:424-427.
Foley R, Brough W. Thoracoscopic cardiomyotomy for achalasia of the cardia: early results.  Ann R Coll Surg Engl.1995;77:60-62.
Cushieri A. Endoscopic oesophageal myotomy for specific motility disorders and non-cardiac chest pain.  Endosc Surg Allied Technol.1993;1:280-287.
Gallez JF, Berger F, Moulinier B, Partensky C. Esophageal adenocarcinoma after Heller myotomy for achalasia.  Endoscopy.1987;19:76-78.
Goodman P, Scott L, Verani R, Berggreen C. Esophageal adenocarcinoma in a patient with surgically treated achalasia.  Dig Dis Sci.1990;35:1549-1552.
Shah AN, Gunby TC. Adenocarcinoma and Barrett's esophagus following surgically treated achalasia.  Gastroenterol Endosc.1994;30:294-296.
Orringer MB, Stirling MC. Esophageal resection for achalasia: indications and results.  Ann Thorac Surg.1989;47:340-345.
Pinotti HW, Cecconello I, Mariano da Rocha J, Zilberstein B. Resection for achalasia of the esophagus.  Hepatogastroenterology.1991;38:470-473.
Feketé F, Breil P, Tossen JC. Reoperation after Heller's operation for achalasia and other motility disorders of the esophagus: a study of eighty-one reoperations.  Int Surg.1982;67:103-110.
Peters JH, Kauer WK, Crookes PF, Ireland AP, Bremner CG, DeMeester TR. Esophageal resection with colon interposition for end-stage achalasia.  Arch Surg.1995;130:632-637.
Miller D, Allen M, Trastek V, Deschamps C, Pairolero P. Esophageal resection for recurrent achalasia.  Ann Thorac Surg.1995;60:922-926.
Panaccione R, Gregor JR, Reynolds RPE, Preiksaitis HG. A cost minimization analysis of intrasphincteric botulinum toxin versus pneumatic dilatation in patients with achalasia [abstract].  Gastroenterology.1997;112:318.

Figures

Tables

Table Graphic Jump LocationPooled Estimate of Response Rate of Achalasia Treatments Across Referenced Studies*

References

Willis T. Pharmaceutice Rationalis Sive Diatribe de Medicamentorum Operationibus in Human Corpore . London, England: Hagae Comitis; 1674.
Lendrum FC. Anatomic features of the cardiac orifice of the stomach with special reference to cardiospasm.  Arch Intern Med.1937;59:474-511.
Mayberry JF, Atkinson M. Studies of incidence and prevalence of achalasia in the Nottingham area.  QJM.1985;56:451-456.
Earlnam RJ, Ellis FH, Nobrega FT. Achalasia of the esophagus in a small urban community.  Mayo Clin Proc.1969;44:478-483.
Howard PJ, Maher L, Pryde A, Cameron EWJ, Heading RC. Five year prospective study of the incidence, clinical features, and diagnosis of achalasia in Edinburgh.  Gut.1992;33:1011-1015.
Cassella RR, Brown Jr AL, Sayre GP, Ellis Jr F. Achalasia of the esophagus: pathologic and etiologic considerations.  Ann Surg.1964;160:474-487.
Csendes A, Smok G, Braghetto I, Ramirez C, Velasco N, Henriquez A. Gastroesophageal sphincter pressure and histologic changes in the distal esophagus in patients with achalasia of the esophagus.  Dig Dis Sci.1985;30:941-945.
Qualman SJ, Haupt AM, Yang P, Hamilton SR. Esophageal Lewy bodies associated with ganglion cell loss in achalasia: similarity to Parkinson's disease.  Gastroenterology.1984;87:848-856.
Goldblum JR, Whyte RI, Orringer MB, Appelman HD. Achalasia, a morphologic study of 42 resected specimens.  Am J Surg Pathol.1994;18:327-337.
Wong RK, Maydonovitch CL, Metz SJ, Baker JR. Significant DQw1 association in achalasia.  Dig Dis Sci.1989;34:349-352.
Robertson CS, Martin BAB, Atkinson M. Varicella-zoster virus DNA in the oesophageal myenteric plexus in achalasia.  Gut.1993;34:299-302.
Jones DB, Mayberry JF, Rhoades J, Munro J. Preliminary report of an association between measles virus and achalasia.  J Clin Pathol.1983;36:655-657.
Verve GN, Sallustio JE, Eaker EY. Anti-myenteric neuronal antibodies in patients with achalasia: a prospective study.  Dig Dis Sci.1997;42:307-313.
Mearin F, Mourelle M, Guarner F, Papo M, Balboa A, Malagelada JR. Patients with achalasia lack nitric oxide synthase in the gastro-oesophageal junction.  Eur J Clin Invest.1993;23:724-728.
Holloway RH, Dodds WJ, Helms JF, Hogan WJ, Dent J, Arndorfer RC. Integrity of cholinergic innervation of the lower esophageal sphincter in achalasia.  Gastroenterology.1986;90:924-929.
Sifrim D, Janssens J, Vantrappen G. Failing deglutitive inhibition in primary esophageal motility disorders.  Gastroenterology.1994;106:875-882.
Murray JA, Ledlow A, Launspach J, Evans D, Loveday M, Conklin JL. The effects of recombinant human hemoglobin on esophageal motor function in humans.  Gastroenterology.1995;109:1241-1248.
Spechler SJ, Souza RF, Rosenberg SJ, Ruben RA, Goyal RK. Heartburn in patients with achalasia.  Gut.1995;37:305-308.
Smart HL, Mayberry JF, Atkinson M. Achalasia following gastroesophageal reflux.  J R Soc Med.1986;79:71-73.
Smart HL, Foster PN, Evans DF, Slevin B, Atkinson M. Twenty four hour oesophageal acidity in achalasia before and after pneumatic dilatation.  Gut.1987;28:883-887.
Goldenberg SP, Burrell M, Fette GG, Vos C, Traube M. Classic and vigorous achalasia: a comparison of manometric, radiographic, and clinical findings.  Gastroenterology.1991;101:743-748.
Todorczuk JR, Aliperti G, Staiano A, Clouse RE. Reevaluation of manometric criteria for vigorous achalasia.  Dig Dis Sci.1991;36:274-278.
Howard PJ, Maher L, Pryde A, Cameron EW, Heading RC. Five year prospective study of the incidence, clinical features, and the diagnosis of achalasia in Edinburgh.  Gut.1992;33:1011-1015.
Bettarello A, Pinotti HW. Oesophageal involvement in Chagas' disease.  Clin Gastroenterol.1976;5:103-117.
Kahrilas PJ, Kishk SM, Helm JF, Dodds WJ, Harig JM, Hogan WJ. A comparison of pseudoachalasia and achalasia.  Am J Med.1987;82:439-446.
Katz PO, Dalton CB, Richter JE, Wu WC, Castell DO. Esophageal testing of patients with noncardiac chest pain or dysphagia.  Ann Intern Med.1987;106:593-597.
Csendes A, Braghetto I, Henriquez A, Cortes C. Late results of a prospective randomised study comparing forceful dilatation and oesophagomyotomy in patients with achalasia.  Gut.1989;30:299-304.
Fagge CH. A case of simple stenosis of the oesophagus, followed by epithelioma.  Guy's Hosp Rep.1872;17:413-421.
Wychulis AR, Woolam GL, Andersen HA, Ellis Jr FH. Achalasia and carcinoma of the esophagus.  JAMA.1971;215:1638-1641.
Chuong JJ, DuBovik S, McCallum RW. Achalasia as a risk factor for esophageal carcinoma.  Dig Dis Sci.1984;29:1105-1108.
Peracchia A, Segalin A, Bardini R, Ruol A, Bonavina L, Baessato M. Esophageal carcinoma and achalasia: prevalence, incidence and results of treatment.  Hepatogastroenterology.1991;38:514-516.
Aggestrup S, Holm JC, Sorensen HR. Does achalasia predispose to cancer of the esophagus?  Chest.1992;102:1013-1016.
Meijssen MA, Tilanus HW, van Blankenstein M.  et al.  Achalasia complicated by oesophageal squamous cell carcinoma: a prospective study in 195 patients.  Gut.1992;33:155-159.
Sandler RS, Nyren O, Ekbom NO, Eisen GM, Yuen J, Josefsson S. The risk of esophageal cancer in patients with achalasia: a population-based study.  JAMA.1995;274:1359-1362.
Streitz Jr JM, Ellis Jr FH, Gibb SP, Heatley GM. Achalasia and squamous cell carcinoma of the esophagus: analysis of 241 patients.  Ann Thorac Surg.1995;58:1604-1609.
Eckardt VF, Aignherr C, Bernhard G. Predictors of outcome in patients with achalasia treated by pneumatic dilation.  Gastroenterology.1992;103:1732-1738.
Cohen NN. An endpoint for pneumatic dilation of achalasia.  Gastrointest Endosc.1977;22:29.
Lee JD, Cecil BD, Brown PE, Wright RA. The Cohen test does not predict outcome in achalasia after pneumatic dilation.  Gastrointest Endosc.1993;39:157-160.
Vantrappen G, Hellemans J. Achalasia. In: Vantrappen G, Hellemans J, eds. Diseases of the Oesophagus . Berlin, Germany: Springer-Verlag; 1975:287-354.
Wong RK, Maydonovitch CL, Garcia JE, Johnson LF, Castell DO. The effect of terbutaline sulfate, nitroglycerin, and aminophylline on lower esophageal sphincter pressure and radionuclide esophageal emptying in patients with achalasia.  J Clin Gastroenterol.1987;9:386-389.
DiMarino AJ, Cohen S. Effect of an oral beta2-adrenergic agonist on lower esophageal sphincter pressure in normal subjects and in patients with achalasia.  Dig Dis Sci.1982;27:1063-1066.
Gelfond M, Rozen P, Keren S, Gilat T. Effect of nitrates on LOS pressure in achalasia: a potential therapeutic aid.  Gut.1981;22:312-318.
Gelfond M, Rozen P, Gilat T. Isosorbide dinitrate and nifedipine treatment of achalasia: a clinical, manometric and radionuclide evaluation.  Gastroenterology.1982;83:963-969.
Traube M, Hongo M, Magyar L, McCallum RW. Effects of nifedipine in achalasia and in patients with high-amplitude peristaltic esophageal contractions.  JAMA.1984;252:1733-1736.
Jankovic J, Brin MF. Therapeutic uses of botulinum toxin.  N Engl J Med.1991;324:1186-1194.
Pasricha PJ, Ravich WJ, Kalloo AN. Effects of intrasphincteric botulinum toxin on the lower esophageal sphincter in piglets.  Gastroenterology.1993;105:1045-1049.
Pasricha PJ, Ravich WJ, Hendrix TR, Sostre S, Jones B, Kalloo AN. Intrasphincteric botulinum toxin for the treatment of achalasia.  N Engl J Med.1995;322:774-778.
Pamphlett R. Early terminal and nodal sprouting of motor axons after botulinum toxin.  J Neurol Sci.1989;92:181-192.
Cox J, Buckton GK, Bennett JR. Balloon dilatation in achalasia: a new dilator.  Gut.1986;27:986-989.
Witzel L. Treatment of achalasia with a pneumatic dilator attached to a gastroscope.  Endoscopy.1981;13:176-177.
Olsen AM, Harrington SW, Moersch HJ, Anderson HA. The treatment of cardiospasm: analysis of a twelve year experience.  J Thorac Cardiovasc Surg.1951;22:164-187.
Vantrappen G, Janssens J. To dilate or to operate? that is the question.  Gut.1983;24:1013-1019.
Schwartz HM, Cahow CE, Traube M. Outcome after perforation sustained during pneumatic dilation for achalasia.  Dig Dis Sci.1993;38:1409-1413.
Heller E. Extramuköse Kardiaplastik beim chronischen Kardiospasmus mit dilatation des oesophagus.  Mitt Grenzgeb Med Chir.1913;27:141-149.
Hunter JG, Trus TL, Branum GD, Waring JP. Laparoscopic Heller myotomy and fundoplication for achalasia.  Ann Surg.1997;6:655-665.
Richter JE. Surgery or pneumatic dilatation for achalasia: a head-to-head comparison: now are all the questions answered?  Gastroenterology.1989;97:1340-1341.
Vaezi M, Richter J, Wilcox M, Schroeder P, Slaughter R. One year follow-up: pneumatic dilatation more effective than botulinum toxin [abstract].  Gastroenterology.1997;112:318.
Coccia G, Bortolotti M, Dodero M. Prospective clinical and manometric study comparing pneumatic dilatation and sublingual nifedipine in the treatment of oesophageal achalasia.  Gut.1991;32:604-606.
Bortolotti M, Labò G. Clinical and manometric effects of nifedipine in patients with esophageal achalasia.  Gastroenterology.1981;80:39-44.
Traube M, Dubovik S, Lange RC, McCallum RW. The role of nifedipine therapy in achalasia: results of a randomized double-blind, placebo-controlled study.  Am J Gastroenterol.1989;84:1259-1262.
Triadafilopoulos G, Aaronson M, Sackel S, Burakoff R. Medical treatment of esophageal achalasia: double-blind crossover study with oral nifedipine, verapamil, and placebo.  Dig Dis Sci.1991;36:260-267.
Annese V, Basciani M, Perri F.  et al.  Controlled trial of botulinum toxin injection versus placebo and pneumatic dilation in achalasia.  Gastroenterology.1996;111:1418-1424.
Pasricha P, Rai R, Ravich W, Hendrix T, Kalloo A. Botulinum toxin for achalasia: long-term outcome and predictors of response.  Gastroenterology.1996;110:1410-1415.
Cuilliere C, Ducrotte P, Zerbib F.  et al.  Achalasia: outcome of patients treated with intrasphincteric injection of botulinum toxin.  Gut.1997;41:87-92.
Fishman VM, Parkman HP, Schiano TD.  et al.  Symptomatic improvement in achalasia after botulinum toxin injection of the lower esophageal sphincter.  Gastroenterology.1996;91:1724-1730.
Wehrmann T, Jacobi V, Jung M, Lembcke B, Caspary WF. Pneumatic dilation in achalasia with a low-compliance balloon: results of a 5-year prospective evaluation.  Gastrointest Endosc.1995;42:31-36.
Mearin F, Armengol JR, Chicharro L.  et al.  Forceful dilatation under endoscopic control in the treatment of achalasia: a randomised trial of pneumatic versus metallic dilator.  Gut.1994;35:1360-1362.
Barnett J, Eisenman R, Nostrant TT, Elta GH. Witzel pneumatic dilation for achalasia: safety and long-term efficacy.  Gastrointest Endosc.1990;36:482-484.
Barkin J, Guelrud M, Reiner D, Goldberg R, Phillips R. Forceful balloon dilation: an outpatient procedure for achalasia.  Gastrointest Endosc.1990;36:123-126.
Kadakia S, Wong R. Graded pneumatic dilation using rigiflex achalasia dilators in patients with primary esophageal achalasia.  Am J Gastroenterol.1993;88:34-38.
Eckardt VF, Kanzler G, Westermeier T. Complications and their impact after pneumatic dilation for achalasia: prospective long-term follow-up study.  Gastrointest Endosc.1997;45:349-353.
Fellows IW, Oglivie AL, Atkinson M. Pneumatic dilatation in achalasia.  Gut.1983;24:1020-1023.
Heimlich JJ, O'Connor TW, Flores DC. Case for pneumatic dilatation in achalasia.  Ann Otolaryngol.1978;87:519-522.
Jacobs JB, Cohen NL, Mattel S. Pneumatic dilatation as the primary treatment for achalasia.  Ann Otol Rhinol Laryngol.1983;92:353-356.
Levine MJ, Moskowitz G, Dorf B, Bank S. Pneumatic dilation in patients with achalasia with a modified gruntzig dilator (Levine) under direct endoscopic control: results after 5 years.  Am J Gastroenterol.1991;86:1581-1584.
Yon J, Christensen J. An uncontrolled comparison of treatments for achalasia.  Ann Surg.1975;182:672-676.
Robertson CS, Fellows IW, Mayberry JF, Atkinson M. Choice of therapy for achalasia in relation to age.  Digestion.1988;40:244-250.
Sauer L, Pellegrini C, Way L. The treatment of achalasia.  Arch Surg.1989;124:929-932.
Parkman H, Reynolds J, Ouyang A, Rosato EF, Eisenberg JM, Cohen S. Pneumatic dilatation or esophagomyotomy treatment for idiopathic achalasia: clinical outcomes and cost analysis.  Dig Dis Sci.1993;38:75-85.
Lambroza A, Schuman R. Pneumatic dilation for achalasia without fluoroscopic guidance: safety and efficacy.  Am J Gastroenterol.1995;90:1226-1229.
Vantrappen G, Hellemans J, Deloof W, Valembois P, Vandenbroucke J. Treatment of achalasia with pneumatic dilatation.  Gut.1971;12:268-275.
Abid S, Champion G, Richter JE, McElvein R, Slaughter RL, Koehler RE. Treatment of achalasia: the best of both worlds.  Am J Gastroenterol.1994;89:979-985.
Ferguson M, Reeder L, Olak J. Results of myotomy and partial fundoplication after pneumatic dilation for achalasia.  Ann Thorac Surg.1996;62:327-330.
Duranceau AC, LaFontaine ER, Vallieres B. Effects of total fundoplication on function of the esophagus after myotomy for achalasia.  Am J Surg.1982;143:22-27.
Donahue PE, Schlesinger PK, Sluss KF.  et al.  Esophagocardiomyotomy: floppy Nissen fundoplication effectively treats achalasia without causing esophageal obstruction.  Surgery.1994;116:719-725.
Sariyannis C, Mullard KS. Oesophagomyotomy for achalasia of the cardia.  Thorax.1975;30:539-542.
Stipa S, Fegiz G, Iascone C.  et al.  Heller-Belsey and Heller-Nissen operations for achalasia of the esophagus.  Surg Gynecol Obstet.1990;170:212-215.
Castrini G, Pappalarado G, Mobarhan S. New approach to esophagocardiomyotomy.  J Thorac Cardiovasc Surg.1982;84:575-578.
Okike N, Payne WS, Neufeld DM.  et al.  Esophagomyotomy versus forceful dilation for achalasia of the esophagus: results in 899 patients.  Ann Thorac Surg.1979;28:119-124.
Pai G, Ellison R, Rubin J, Moore H. Two decades of experience with modified Heller's myotomy for achalasia.  Ann Thorac Surg.1984;38:201-206.
Ellis Jr FH. Oesophagomyotomy for achalasia: a 22-year experience.  Br J Surg.1993;80:882-885.
Jara M, Toledo-Pereyra LH, Lewis JW, Magilligan DJ. Long-term results of esophagomyotomy for achalasia of esophagus.  Arch Surg.1979;114:935-936.
Menzies-Gow N, Gummer JWP, Edwards DAW. Results of Heller's operation for achalasia of the cardia.  Br J Surg.1978;65:483-485.
Mattioli S, Di Simone MP, Bassi F.  et al.  Surgery for esophageal achalasia: long-term results with three different techniques.  Hepatogastroenterology.1996;43:492-500.
Ellis Jr FH, Watkins Jr E, Gibb SP, Heatley GJ. Ten- to 20-year clinical results after short esophagomyotomy without an antireflux procedure (modified Heller operation) for esophageal achalasia.  Eur J Cardiothorac Surg.1992;6:86-90.
Di Simone M, Felice V, D'Errico A.  et al.  Onset timing of delayed complications and criteria of follow-up after operation for esophageal achalasia.  Ann Thorac Surg.1996;61:1106-1111.
Gallone L, Peri G, Galliera M. Proximal gastric vagotomy and anterior fundoplication as complementary procedures to Heller's operation for achalasia.  Surg Gynecol Obstet.1982;155:337-341.
Malthaner R, Todd T, Miller L, Pearson FG. Long-term results in surgically managed esophageal achalasia.  Ann Thorac Surg.1994;58:1343-1347.
Bonavina L, Rosati R, Segalin A, Peracchia A. Laparoscopic Heller-Dor operation for the treatment of oesophageal achalasia: technique and early results.  Ann Chir Gynaecol.1995;84:165-168.
Picciocchi A, Cardillo G, D'Ugo D, Castrucci G, Mascellari L, Granone P. Surgical treatment of achalasia: a retrospective comparative study.  Jpn J Surg.1993;23:855-859.
Murray G, Battaglini J, Keagy B, Starek P, Wilcox B. Selective application of fundoplication in achalasia.  Ann Thorac Surg.1984;37:185-188.
Cosentini E, Berlakovich G, Zacherl J.  et al.  Achalasia: results of myotomy and antireflux operation after failed dilatations.  Arch Surg.1997;132:143-147.
Pandolfo N, Bortolotti M, Spigno L, Bozzano PL, Mattioli FP. Manometric assessment of Heller-Dor operation for esophageal achalasia.  Hepatogastroenterology.1996;43:160-166.
Robertson GSM, Lloyd DM, Wicks ACB, DeCeastecker J, Veitch PS. Laparoscopic Heller's cardiomyotomy without an antireflux procedure.  Br J Surg.1995;82:957-959.
Mitchell P, Watson D, Devitt PG.  et al.  Laparoscopic cardiomyotomy with a Dor patch for achalasia.  Can J Surg.1995;38:445-448.
Raiser F, Perdikis G, Hinder R.  et al.  Heller myotomy via minimal-access surgery.  Arch Surg.1996;131:593-598.
Morino M, Rebecchi F, Festa V, Garrone C. Laparoscopic Heller cardiomyotomy with intraoperative manometry in the management of oesophageal achalasia.  Int Surg.1995;80:332-335.
Rosati R, Fumagalli U, Bonavina L, Segalin A, Montorsi M, Bona S. Laparoscopic approach to esophageal achalasia.  Am J Surg.1995;169:424-427.
Foley R, Brough W. Thoracoscopic cardiomyotomy for achalasia of the cardia: early results.  Ann R Coll Surg Engl.1995;77:60-62.
Cushieri A. Endoscopic oesophageal myotomy for specific motility disorders and non-cardiac chest pain.  Endosc Surg Allied Technol.1993;1:280-287.
Gallez JF, Berger F, Moulinier B, Partensky C. Esophageal adenocarcinoma after Heller myotomy for achalasia.  Endoscopy.1987;19:76-78.
Goodman P, Scott L, Verani R, Berggreen C. Esophageal adenocarcinoma in a patient with surgically treated achalasia.  Dig Dis Sci.1990;35:1549-1552.
Shah AN, Gunby TC. Adenocarcinoma and Barrett's esophagus following surgically treated achalasia.  Gastroenterol Endosc.1994;30:294-296.
Orringer MB, Stirling MC. Esophageal resection for achalasia: indications and results.  Ann Thorac Surg.1989;47:340-345.
Pinotti HW, Cecconello I, Mariano da Rocha J, Zilberstein B. Resection for achalasia of the esophagus.  Hepatogastroenterology.1991;38:470-473.
Feketé F, Breil P, Tossen JC. Reoperation after Heller's operation for achalasia and other motility disorders of the esophagus: a study of eighty-one reoperations.  Int Surg.1982;67:103-110.
Peters JH, Kauer WK, Crookes PF, Ireland AP, Bremner CG, DeMeester TR. Esophageal resection with colon interposition for end-stage achalasia.  Arch Surg.1995;130:632-637.
Miller D, Allen M, Trastek V, Deschamps C, Pairolero P. Esophageal resection for recurrent achalasia.  Ann Thorac Surg.1995;60:922-926.
Panaccione R, Gregor JR, Reynolds RPE, Preiksaitis HG. A cost minimization analysis of intrasphincteric botulinum toxin versus pneumatic dilatation in patients with achalasia [abstract].  Gastroenterology.1997;112:318.

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