eMedicine Specialties > Gastroenterology > Esophagus

Esophageal Motility Disorders

Author: Eric A Gaumnitz, MD, Professor of Medicine, Division of Gastroenterology, University of Wisconsin School of Medicine; Program Director, Gastroenterology and Hepatology Fellowship, University of Wisconsin School of Medicine and Public Health; Director, Motility Unit, University of Wisconsin Hospitals
Coauthor(s): Abdullah Fayyad, MD, MBBS, Gastroenterology Staff, Private Practice, Digestive and Liver Disease Consultants
Contributor Information and Disclosures

Updated: Aug 29, 2009

Introduction

Background

The esophagus functions solely to deliver food from the mouth to the stomach where the process of digestion can begin. Efficient transport by the esophagus requires a coordinated, sequential motility pattern that propels food from above and clears acid and bile reflux from below. Disruption of this highly integrated muscular motion limits delivery of food and fluid, as well as causes a bothersome sense of dysphagia and chest pain. Disorders of esophageal motility are referred to as primary or secondary esophageal motility disorders and categorized according to their abnormal manometric patterns.


The typical picture of achalasia. Note the "bird-...

The typical picture of achalasia. Note the "bird-beak" appearance of the lower esophageal sphincter (LES), with a dilated, barium-filled esophagus proximal to it. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.

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The typical picture of achalasia. Note the "bird-...

The typical picture of achalasia. Note the "bird-beak" appearance of the lower esophageal sphincter (LES), with a dilated, barium-filled esophagus proximal to it. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.



The response to amyl nitrate (a smooth muscle rel...

The response to amyl nitrate (a smooth muscle relaxant), with partial relaxation of the lower esophageal sphincter (LES), allows some barium to pass through it into the stomach. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.

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The response to amyl nitrate (a smooth muscle rel...

The response to amyl nitrate (a smooth muscle relaxant), with partial relaxation of the lower esophageal sphincter (LES), allows some barium to pass through it into the stomach. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.



Esophagram of a 65-year-old man with rapid-onset ...

Esophagram of a 65-year-old man with rapid-onset dysphagia over 1 year. Although esophagram shows a typical picture of achalasia, this patient had adenocarcinoma of the gastroesophageal junction. This is an example of pseudoachalasia, which reinforces the absolute need for esophagogastroduodenoscopy (EGD) in patients with radiologic diagnosis of achalasia. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.

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Esophagram of a 65-year-old man with rapid-onset ...

Esophagram of a 65-year-old man with rapid-onset dysphagia over 1 year. Although esophagram shows a typical picture of achalasia, this patient had adenocarcinoma of the gastroesophageal junction. This is an example of pseudoachalasia, which reinforces the absolute need for esophagogastroduodenoscopy (EGD) in patients with radiologic diagnosis of achalasia. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.



An esophagram demonstrating the corkscrew esophag...

An esophagram demonstrating the corkscrew esophagus picture observed in a patient with manometry confirmed findings of diffuse esophageal spasm (DES). Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.

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An esophagram demonstrating the corkscrew esophag...

An esophagram demonstrating the corkscrew esophagus picture observed in a patient with manometry confirmed findings of diffuse esophageal spasm (DES). Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.



Response to amyl nitrate, with disappearance of t...

Response to amyl nitrate, with disappearance of the spasm on esophagram. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.

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Response to amyl nitrate, with disappearance of t...

Response to amyl nitrate, with disappearance of the spasm on esophagram. Image courtesy of Andrew Taylor, MD, Professor, Abdominal Imaging, Department of Radiology, University of Wisconsin Medical School, Madison.


Anatomy

The tubular esophagus is a muscular organ, approximately 25 cm in length, and has specialized sphincters at proximal and distal ends. The upper esophageal sphincter (UES) is comprised of several striated muscles, creating a tonically closed valve and preventing air from entering into the gastrointestinal tract. The lower esophageal sphincter (LES) is composed entirely of smooth muscle and maintains a steady baseline tone to prevent gastric reflux into the esophagus.

The body of the esophagus is similarly composed of 2 muscle types. The proximal esophagus is predominantly striated muscle, while the distal esophagus and the remainder of the GI tract contain smooth muscle. The mid esophagus contains a graded transition of striated and smooth muscle types. The muscle is oriented in 2 perpendicular opposing layers: an inner circular layer and an outer longitudinal layer, known collectively as the muscularis propria. The longitudinal muscle is responsible for shortening the esophagus, while the circular muscle forms lumen-occluding ring contractions.

Esophageal peristalsis

The coordination of these simultaneously contracting muscle layers produces the motility pattern known as peristalsis. Peristalsis is a sequential, coordinated contraction wave that travels the entire length of the esophagus, propelling intraluminal contents distally to the stomach. The LES relaxes during swallows and stays opened until the peristaltic wave travels through the LES, then contracts and redevelops resting basal tone. Low peristaltic amplitudes normally occur at the transition zone between the striated and smooth muscle portions; however, the peristalsis is uninterrupted.

Primary peristalsis is the peristaltic wave triggered by the swallowing center. The peristaltic contraction wave travels at a speed of 2 cm/s and correlates with manometry-recorded contractions. The relationship of contraction and food bolus is more complex because of intrabolus pressures from above (contraction from above) and the resistance from below (outflow resistance).

The secondary peristaltic wave is induced by esophageal distension from the retained bolus, refluxed material, or swallowed air. The primary role is to clear the esophagus of retained food or any gastroesophageal refluxate.

Tertiary contractions are simultaneous, isolated, dysfunctional contractions. These contractions are nonperistaltic, have no known physiologic role, and are observed with increased frequency in elderly people. Radiographic description of this phenomenon has been called presbyesophagus.

Esophageal motility disorders

Esophageal motility disorders are not uncommon in gastroenterology. The spectrum of these disorders ranges from the well-defined primary esophageal motility disorders (PEMDs) to very nonspecific disorders that may play a more indirect role in reflux disease and otherwise be asymptomatic. Esophageal motility disorders may occur as manifestations of systemic diseases, referred to as secondary motility disorders.

Esophageal motility disorders are less common than mechanical and inflammatory diseases affecting the esophagus, such as reflux esophagitis, peptic strictures, and mucosal rings. The clinical presentation of a motility disorder is varied, but, classically, dysphagia and chest pain are reported. In 80% of patients, the cause of a patient's dysphagia can be suggested from the history, including dysmotility of the esophagus. Before entertaining a diagnosis of a motility disorder, first and foremost, the physician must evaluate for a mechanical obstructing lesion.

Esophageal motility disorders discussed in this article include the following:

  • Achalasia
  • Spastic esophageal motility disorders, including diffuse esophageal spasm (DES), nutcracker esophagus, and hypertensive LES
  • Nonspecific esophageal motility disorder (inefficient esophageal motility disorder)
  • Secondary esophageal motility disorders related to scleroderma, diabetes mellitus, alcohol consumption, psychiatric disorders, and presbyesophagus

Pathophysiology

The pathophysiology of the primary esophageal motility disorders is poorly defined, with the exception of achalasia. The underlying cause of all the primary motility disorders remains elusive. The secondary motility disorders, such as scleroderma esophagus or esophageal motility disorder of diabetes, are better understood from the standpoint of the preexisting underlying disorders.

Achalasia

Achalasia is the best defined primary motility disorder and the only one with an established pathology. The predominant neuropathologic process of achalasia involves the loss of ganglion cells from the wall of the esophagus, starting at the LES and developing proximally. The degree of ganglion cell loss parallels the disease duration such that, at 10 years, ganglion cells are likely completely absent. At the LES, the loss of inhibitory nerves is demonstrated by loss of nitric oxide synthase and vasoactive intestinal peptide (VIP) immunohistochemistry staining. Variable amounts of inflammatory cells have been described within the myenteric plexus along with the disappearing nerves. In the peristaltic esophageal body, achalasia is characterized by a loss of intrinsic acetylcholine-containing nerves. Extrinsic nerves may also be affected, characterized by Wallerian degeneration of the axoplasm and myelin sheaths within the vagus nerve and dorsal motor nucleus. Anatomically, the circular muscle layer at the

LES is thickened, but, microscopically, individual muscle cells are grossly normal.

The physiologic process of achalasia is correlated most directly to the loss of the inhibitory nerves at the sphincter, resulting in failure of the LES to completely relax and causing relative obstruction. Manometry may reveal elevated LES pressure greater than 40 mm Hg in more than 60% of patients; however, hypertensive LES is not universal or required for the manometric diagnosis. The loss of nerves along the esophageal body causes aperistalsis, leading to stasis of ingested food and subsequent dilation of the esophagus. Nonperistaltic isolated contractions or low-amplitude simultaneous contractions of the esophageal body may be observed. If high-amplitude (>60 mm Hg) simultaneous contractions occur, the entity is categorized as vigorous achalasia, which may represent an early stage of classic achalasia. Physiologic characteristics of achalasia are additionally useful in assisting with establishing the diagnosis through chemical challenge testing.

With the partial ganglion cell loss in patients with achalasia, edrophonium (acetylcholine esterase inhibitor) increases LES pressure while atropine (muscarinic antagonist) decreases LES pressure. This characteristic likely explains why the botulinum toxin (acetylcholine release inhibitor) may have therapeutic benefit in patients with achalasia.

Spastic motility disorders of the esophageal body

No documented abnormalities exist regarding the distribution of myenteric neurons in patients diagnosed with spastic motility disorders of the esophageal body, but diffuse fragmentation of vagal filaments, increased endoneural collagen, and mitochondrial fragmentation are described. There appears to be a functional imbalance between excitatory and inhibitory postganglionic pathways, disrupting the coordinated components of peristalsis. In DES, muscular hypertrophy or hyperplasia has been described in the distal two thirds of the esophagus. Muscle wall thickening has been described in patients who are asymptomatic and, conversely, has been absent in some patients with typical symptoms and manometric findings. This controversial finding causes difficulty in attributing symptoms or manometric abnormalities to muscle structure changes. In addition, anxiety states may also play a role in some patients.

Scleroderma esophagus

In scleroderma, the primary defect in this systemic process is related to smooth muscle atrophy and fibrosis. Esophageal dysmotility develops as the smooth muscle of the esophagus is replaced by scar tissue, gradually leading to progressive loss of peristalsis and a weakening of LES. Motility is preserved at the proximal striated muscle portion of the esophagus.

Frequency

United States

Esophageal motility disorders, excluding achalasia, lack population-based studies. The 2 best-characterized motility disorders, achalasia and DES, represent only a small percentage of diagnosed motility disorders. The incidence of achalasia is 1-3 case per 100,000 population per year.1 As with any other chronic illness, prevalence exceeds incidence significantly. Familial clustering is observed, but a genetic relationship is not established. Nutcracker esophagus is the most common motility disorder (>40% of all motility disorders diagnosed), but it is the most controversial in significance.

International

In Europe, the incidence of achalasia is similar to that of the United States.

Mortality/Morbidity

  • Achalasia is associated with significant and progressive symptomatic discomfort. When advanced, this condition can lead to such severe dysphagia that malnutrition, weight loss, and dehydration can develop. Increased incidence of both esophageal squamous cell and adenocarcinoma is observed in patients with long-standing achalasia. Therapeutic procedures and operations are associated with a small but significant risk of mortality and morbidity.
  • Spastic esophageal motility disorders are associated with symptomatic discomfort but do not lead to the severity of dysphagia observed in patients with achalasia. Chest pain is, in fact, a more common complaint that may precipitate emergency room visits and cardiologic evaluations.
  • Scleroderma esophagus is associated with severe and progressive acid reflux symptoms and complications. Associated complications, including strictures, Barrett esophagus, and adenocarcinoma of the esophagus, are the concern.

Race

Racial and environmental differences in the incidence of achalasia and other esophageal motility disorders might be present; however, because of the low incidence of disease and underdiagnosis in developing countries, these differences have not been demonstrated. Racial differences in the incidence of achalasia and other esophageal motility disorders have not been established.

Sex

Achalasia affects both sexes in equal numbers. No reliable information for other motility disorders exists.

Age

Achalasia commonly presents in the fifth decade but rarely may develop in children as well as in elderly persons.

Clinical

History

  • Achalasia
    • Progressive dysphagia for both solids and liquids is the hallmark of achalasia. Dysphagia for solids is more common than for liquids.
    • Retrospectively, symptoms are present on average as long as 6 years prior to presentation.
    • Regurgitation of food retained in the proximal dilated esophagus is a common occurrence, especially at night, requiring patients to sleep using multiple pillows or upright in a chair. This symptom worsens as the esophagus dilates with time.
    • Chest pain may be another early symptom, characterized by a squeezing retrosternal pain radiating to the neck, jaw, arms, or back. The chest pain may worsen with food and can awaken patients from sleep.
    • A sensation of heartburn may be reported by 30% of patients and is assumed to be related to retained food fermentation and lactic acid.
    • Emotional stress or rapid eating may worsen all of the symptoms described above.
    • Weight loss is common with achalasia; however, the loss is usually slight.
  • Spastic esophageal motility disorders
    • Chest pain is the hallmark of spastic esophageal motility disorders, although patients with spastic esophageal motility disorders also may report dysphagia. Similar to the chest pain of achalasia, it may mimic angina. The mechanism is not clear but may be related to transient esophageal muscle ischemia, luminal distension, or altered visceral sensation.
    • Dysphagia is not necessarily related to chest pain. Dysphagia for solids and liquids is a common symptom and especially seen in DES. Dysphagia may be intermittent and nonprogressive in nature, typically not prolonging mealtime or causing weight loss.
    • Patients also commonly report heartburn, regurgitation, or other esophageal complaints of reflux disease due to ineffective acid clearance from the esophagus.
    • Weight loss is common with achalasia; however, the loss is usually slight.
  • Scleroderma esophagus
    • Scleroderma involves the esophagus in more than 75% of patients, regardless of clinical type. Two forms of this disease exist–(1) progressive systemic sclerosis (PSS), characterized by diffuse scleroderma, and a more fulminant form with early involvement of internal organs or (2) CREST syndrome, characterized by calcinosis, Raynaud phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia. The severity of esophageal involvement does not correlate necessarily with severity of involvement of other organs. In fact, dysphagia may be the presenting clinical symptom in some patients.
    • The esophageal symptoms of scleroderma usually reflect the severity of acid reflux disease, including heartburn, regurgitation, and dysphagia.
    • Erosive esophagitis is observed in as many as 60% of patients, and the incidence of Barrett esophagus and adenocarcinoma of the esophagus is increased.
    • Dysphagia usually is due to diminishing peristalsis, peptic strictures, or a combination of both.

Physical

In patients with primary motility disorders, results of a physical examination often are unrevealing.

  • Clinical signs of scleroderma in the proper clinical setting must be noted, especially skin changes.
  • A bedside swallowing challenge may be performed with a glass of water.
  • Check general nutrition and hydration if significant dysphagia is reported.

Causes

Primary esophageal motility disorders are idiopathic in nature, but postviral, infectious, environmental, and genetic factors have been hypothesized. See Pathophysiology.

More on Esophageal Motility Disorders

Overview: Esophageal Motility Disorders
Differential Diagnoses & Workup: Esophageal Motility Disorders
Treatment & Medication: Esophageal Motility Disorders
Follow-up: Esophageal Motility Disorders
Multimedia: Esophageal Motility Disorders
References
Further Reading
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References

  1. Sonnenberg A. Hospitalization for achalasia in the United States 1997-2006. Dig Dis Sci. Aug 2009;54(8):1680-5. [Medline].

  2. Salvador R, Dubecz A, Polomsky M, et al. A new era in esophageal diagnostics: the image-based paradigm of high-resolution manometry. J Am Coll Surg. Jun 2009;208(6):1035-44. [Medline].

  3. Pandolfino JE, Fox MR, Bredenoord AJ, Kahrilas PJ. High-resolution manometry in clinical practice: utilizing pressure topography to classify oesophageal motility abnormalities. Neurogastroenterol Motil. Aug 2009;21(8):796-806. [Medline].

  4. Gravesen FH, Gregersen H, Arendt-Nielsen L, Drewes AM. Reproducibility of axial force and manometric recordings in the oesophagus during wet and dry swallows. Neurogastroenterol Motil. Aug 24 2009;[Medline].

  5. Eckardt AJ, Eckardt VF. Current clinical approach to achalasia. World J Gastroenterol. Aug 28 2009;15(32):3969-75. [Medline]. [Full Text].

  6. Leonard DS, Broe P. Oesophageal achalasia: an argument for primary surgical management. Surgeon. Apr 2009;7(2):101-13. [Medline].

  7. Abid S, Champion G, Richter JE, et al. Treatment of achalasia: the best of both worlds. Am J Gastroenterol. Jul 1994;89(7):979-85. [Medline].

  8. Achem SR, Crittenden J, Kolts B, Burton L. Long-term clinical and manometric follow-up of patients with nonspecific esophageal motor disorders. Am J Gastroenterol. Jul 1992;87(7):825-30. [Medline].

  9. Achem SR, Kolts BE, Wears R, et al. Chest pain associated with nutcracker esophagus: a preliminary study of the role of gastroesophageal reflux. Am J Gastroenterol. Feb 1993;88(2):187-92. [Medline].

  10. Annese V, Basciani M, Perri F, et al. Controlled trial of botulinum toxin injection versus placebo and pneumatic dilation in achalasia. Gastroenterology. Dec 1996;111(6):1418-24. [Medline].

  11. Champion JK, Delisle N, Hunt T. Laparoscopic esophagomyotomy with posterior partial fundoplication for primary esophageal motility disorders. Surg Endosc. Aug 2000;14(8):746-9. [Medline].

  12. Clouse RE. Spastic disorders of the esophagus. Gastroenterologist. Jun 1997;5(2):112-27. [Medline].

  13. Clouse RE, Staiano A. Manometric patterns using esophageal body and lower sphincter characteristics. Findings in 1013 patients. Dig Dis Sci. Feb 1992;37(2):289-96.

  14. Ferguson MK, Reeder LB, Olak J. Results of myotomy and partial fundoplication after pneumatic dilation for achalasia. Ann Thorac Surg. Aug 1996;62(2):327-30. [Medline].

  15. Goldblum JR, Whyte RI, Orringer MB. Achalasia. A morphologic study of 42 resected specimens. Am J Surg Pathol. Apr 1994;18(4):327-37.

  16. Goldenberg SP, Burrell M, Fette GG, et al. Classic and vigorous achalasia: a comparison of manometric, radiographic, and clinical findings. Gastroenterology. Sep 1991;101(3):743-8. [Medline].

  17. Grande L, Monforte R, Ros E, et al. High amplitude contractions in the middle third of the oesophagus: a manometric marker of chronic alcoholism?. Gut. May 1996;38(5):655-62. [Medline].

  18. Holloway RH, Tippett MD, Horowitz M, et al. Relationship between esophageal motility and transit in patients with type I diabetes mellitus. Am J Gastroenterol. Nov 1999;94(11):3150-7. [Medline].

  19. Katada N, Hinder RA, Hinder PR, et al. The hypertensive lower esophageal sphincter. Am J Surg. Nov 1996;172(5):439-42; discussion 442-3. [Medline].

  20. Katz PO, Richter JE, Cowan R. Apparent complete lower esophageal sphincter relaxation in achalasia. Gastroenterology. Apr 1986;90(4):978-83.

  21. Lock G, Straub RH, Zeuner M, et al. Association of autonomic nervous dysfunction and esophageal dysmotility in systemic sclerosis. J Rheumatol. Jul 1998;25(7):1330-5. [Medline].

  22. Lock G, Zeuner M, Straub RH, et al. Esophageal manometry in systemic sclerosis: screening procedure or confined to symptomatic patients?. Rheumatol Int. 1997;17(2):61-6. [Medline].

  23. Malagelada JR, Distrutti E. Management of gastrointestinal motility disorders. A practical guide to drug selection and appropriate ancillary measures. Drugs. Oct 1996;52(4):494-506. [Medline].

  24. Malthaner RA, Tood TR, Miller L, Pearson FG. Long-term results in surgically managed esophageal achalasia. Ann Thorac Surg. Nov 1994;58(5):1343-6; discussion 1346-7. [Medline].

  25. McBride PJ, Hinder RA, Filipi C, et al. Surgical treatment of spastic conditions of the esophagus. Int Surg. Apr-Jun 1997;82(2):113-8. [Medline].

  26. Meijssen MA, Tilanus HW, van Blankenstein M, et al. Achalasia complicated by oesophageal squamous cell carcinoma: a prospective study in 195 patients. Gut. Feb 1992;33(2):155-8. [Medline].

  27. Melzer E, Ron Y, Tiomni E, et al. Assessment of the esophageal wall by endoscopic ultrasonography in patients with nutcracker esophagus. Gastrointest Endosc. Sep 1997;46(3):223-5. [Medline].

  28. Micromedex Healthcare Series. MICROMEDEX, Inc. Englewood, Co;[Full Text].

  29. Miller DL, Allen MS, Trastek VF, et al. Esophageal resection for recurrent achalasia. Ann Thorac Surg. Oct 1995;60(4):922-5; discussion 925-6. [Medline].

  30. Miller LS, Parkman HP, Schiano TD, et al. Treatment of symptomatic nonachalasia esophageal motor disorders with botulinum toxin injection at the lower esophageal sphincter. Dig Dis Sci. Oct 1996;41(10):2025-31. [Medline].

  31. Pellegrini CA, Leichter R, Patti M, et al. Thoracoscopic esophageal myotomy in the treatment of achalasia. Ann Thorac Surg. Sep 1993;56(3):680-2. [Medline].

  32. Peters JH, Kauer WK, Crookes PF, et al. Esophageal resection with colon interposition for end-stage achalasia. Arch Surg. Jun 1995;130(6):632-6; discussion 636-7. [Medline].

  33. Pouderoux P, Lin S, Kahrilas PJ. Timing, propagation, coordination, and effect of esophageal shortening during peristalsis. Gastroenterology. Apr 1997;112(4):1147-54. [Medline].

  34. Richter JE. Practical approach to the diagnosis and treatment of esophageal dysphagia. Compr Ther. Sep 1998;24(9):446-53. [Medline].

  35. Richter JE, Wu WC, Johns DN. Esophageal manometry in 95 healthy adult volunteers. Variability of pressures with age and frequency of "abnormal" contractions. Dig Dis Sci. Jun 1987;32(6):583-92.

  36. Roland J, Dhaenen H, Ham HR. Oesophageal motility disorders in patients with psychiatric disease. Eur J Nucl Med. Dec 1996;23(12):1583-7. [Medline].

  37. Ros E, Armengol X, Grande L, et al. Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder?. Dig Dis Sci. Jul 1997;42(7):1344-53. [Medline].

  38. Rosati R, Fumagalli U, Bonavina L, et al. Laparoscopic approach to esophageal achalasia. Am J Surg. Apr 1995;169(4):424-7. [Medline].

  39. Siddiqui MA, Castell DO. Gastrointestinal disorders in the elderly. Compr Ther. May 1997;23(5):349-59. [Medline].

  40. Sifrim D, Janssens J, Vantrappen G. Failing deglutitive inhibition in primary esophageal motility disorders. Gastroenterology. Apr 1994;106(4):875-82. [Medline].

  41. Sobin J, Nathanson A, Engstrom CF. Endoluminal ultrasonography: a new method to evaluate dysphagia. ORL J Otorhinolaryngol Relat Spec. Mar-Apr 1996;58(2):105-9. [Medline].

  42. Storr M, Allescher HD. Esophageal pharmacology and treatment of primary motility disorders. Dis Esophagus. 1999;12(4):241-57. [Medline].

  43. Taub W, Achkar E. Hiatal hernia in patients with achalasia. Am J Gastroenterol. Dec 1987;82(12):1256-8. [Medline].

  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. Oct 1989;84(10):1259-62. [Medline].

  45. Vaezi MF, Richter JE. Current therapies for achalasia: comparison and efficacy. J Clin Gastroenterol. Jul 1998;27(1):21-35.

  46. Verne GN, Sninsky CA. Diabetes and the gastrointestinal tract. Gastroenterol Clin North Am. Dec 1998;27(4):861-74, vi-vii. [Medline].

  47. Wehrmann T, Jacobi V, Jung M, et al. Pneumatic dilation in achalasia with a low-compliance balloon: results of a 5-year prospective evaluation. Gastrointest Endosc. Jul 1995;42(1):31-6. [Medline].

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Further Reading

Related eMedicine Topics

Clinical Trials
 National Guideline Clearinghouse

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Keywords

esophageal motility disorders, esophageal motility dysfunction, esophagus dysfunction, esophageal peristalsis dysfunction, esophageal peristalsis, achalasia, dysphagia, gastrointestinal motility, primary spastic esophageal motility disorders, diffuse esophageal spasm, DES, nutcracker esophagus, hypertensive lower esophageal sphincter, hypertensive LES, presbyesophagus, lower esophageal sphincter dysfunction, scleroderma esophagus, spastic motility disorder of the esophageal body, Heller myotomy, esophagectomy

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Contributor Information and Disclosures

Author

Eric A Gaumnitz, MD, Professor of Medicine, Division of Gastroenterology, University of Wisconsin School of Medicine; Program Director, Gastroenterology and Hepatology Fellowship, University of Wisconsin School of Medicine and Public Health; Director, Motility Unit, University of Wisconsin Hospitals
Eric A Gaumnitz, MD is a member of the following medical societies: American Gastroenterological Association, American Motility Society, and American Society of Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Coauthor(s)

Abdullah Fayyad, MD, MBBS, Gastroenterology Staff, Private Practice, Digestive and Liver Disease Consultants
Abdullah Fayyad, MD, MBBS is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

Medical Editor

Ronnie Fass, MD, Director of GI Motility Laboratory, Tucson VA Medical Center, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of Arizona School of Medicine
Ronnie Fass, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Motility Society, American Society for Gastrointestinal Endoscopy, and Israel Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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