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Author: Alan BR Thomson, MD, MSc, PhD, Professor, Department of Medicine, Division of Gastroenterology, University of Alberta Faculty of Medicine

Alan BR Thomson is a member of the following medical societies: American Federation for Aging Research, American Federation for Clinical Research, American Gastroenterological Association, American Geriatrics Society, American Physiological Society, Canadian Association of Gastroenterology, Gastroenterology Research Group, New York Academy of Sciences, and Royal Society of Medicine

Coauthor(s): Christian Birkedal, MD, Clinical Associate Professor of Surgery, Wound Treatment Center, Florida State University College of Medicine; Medical Director, Capital Regional Medical Center and Tallahassee Memorial Hospital; J Thomas Williams, Jr, MD, Associate Program Director, Consulting Surgeon, Department of Surgery, Division of Thoracic Surgery, Baptist Health System Princeton Medical Center

Editors: John Gunn Lee, MD, Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine; Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine; 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

Author and Editor Disclosure

Synonyms and related keywords: diffuse esophageal spasm, nutcracker esophagus, DES, dysphagia, regurgitation, noncardiac chest pain, esophagectomy, achalasia, globus, gastric reflux, gastric reflux, microvascular compression of Vagus nerve

Background

Broadly, esophageal spasm can be subdivided into 2 distinct entities: (1) diffuse esophageal spasm (DES), in which contractions are uncoordinated, and (2) nutcracker esophagus, in which contractions proceed in a coordinated manner, but the amplitude is excessive.

Symptoms can include dysphagia, regurgitation, and noncardiac chest pain. Because of the vague symptoms and difficulty in diagnosis, esophageal spasm often is not diagnosed and is undertreated. Many patients with manometric and radiologic aberrations may not have any appreciable symptoms.

Currently, manometry is the best diagnostic modality. Treatment includes calcium channel blockers, botulinum toxin, nitrates, tricyclic antidepressants, dilatation, myotomy, and esophagectomy. Research is ongoing to unlock the underlying causes to improve our diagnostic capabilities and therapeutic regimens in the future.

Pathophysiology

The esophagus is comprised of 2 layers of muscle, the inner circular and the outer longitudinal layers. Arbitrarily, the esophagus can be divided into 3 zones, each with separate yet integrated anatomy and physiology.

Esophageal zones

Upper zone: Comprised entirely of striated muscle, this zone initiates the contractions that propel the food bolus down the esophagus. The upper esophageal sphincter (UES), named the cricopharyngeus muscle, is located in the upper zone.

Middle zone: Comprised of striated and smooth muscles, the inner circular muscle layer and the outer longitudinal muscle layer work in conjunction to propel the food bolus.

Lower zone: The lower segment is the lower esophageal sphincter (LES). This sphincter is a thickening of the smooth muscle that is contracted tonically to prevent reflux. At rest, the pressure in the LES is usually 15-25 mm Hg. For food to pass into the stomach, the LES relaxes.


Upper esophageal sphincter

When functioning properly, the esophagus can detect the presence of a food bolus at the UES and then coordinate progression of the food down the esophagus to the stomach. When this does not occur in a coordinated fashion, the patient can develop symptoms of esophageal spasm.

The UES is contracted tonically. Manometric evaluation of the UES reveals constant spiking activity. As food is sensed at the UES, the laryngeal muscles contract to move the cricoid cartilage anteriorly. The tonic contraction of the UES is inhibited, opening the UES to allow passage of food. The inner circular muscles and longitudinal muscles of the remainder of the upper zone then propel the food. To propel the food, the longitudinal muscles must contract, followed immediately by contraction of the circular muscles. At the end of the upper zone, the initial wave dies out as another wave starts, propelling the food down to the middle zone. The nucleus solitarius in the brainstem controls swallowing in the upper zone.

Esophageal middle zone

The middle zone propels the food bolus from the upper zone to the lower zone. This segment consists of 2 muscle layers, an inner circular and outer longitudinal layer.

In the middle zone, the striated muscle transitions to smooth, or involuntary, muscle. The wave propagates down the esophagus by coordinated contractions. Again, the longitudinal muscles must contract before the circular muscle contracts. Furthermore, contraction of the muscles must proceed caudally in an organized manner. If the muscle contraction is not orderly, the food bolus cannot progress.

Two forces propel the food from cephalad to caudad. First, gravity pulls the food caudally. The organized contractions of the muscles propel the food caudally. If a myotomy is performed, the contractions will be ineffective. Only gravity forces the food caudally. Thus, patients who have had a myotomy are more likely to have dysphagia.

Lower esophageal sphincter

The lower zone is comprised of the LES. This is a condensation of the smooth muscles. Tonically, this muscle is contracted and must relax to allow food to pass. Failure of the LES to relax to allow a food bolus to pass is termed achalasia (see Achalasia).

Diffuse esophageal spasms

Simplistically, DESs occur when the propagative waves do not progress correctly. Usually, several segments of the esophagus contract simultaneously, preventing the propagation of the food bolus. The usual presentation is intermittent dysphagia with occasional chest pain. Myotomy, which is performed only in extreme cases, can relieve the uncoordinated contractions.

Nutcracker esophagus

Nutcracker esophagus occurs when the amplitude of the contractions exceeds 2 standard deviations from normal. The contractions proceed in an organized manner, propelling food down the esophagus. These patients often present with chest pain, but they present with dysphagia less often than patients with DES.

Because the progression of the contractions occurs normally, patients often do not benefit from a myotomy. Even though the increased amplitude of the contractions can be demonstrated using manometry, the symptoms often do not correlate with the manometrically documented contractions.

The symptoms of DES and nutcracker esophagus may overlap and can be distinguished only by motility study.

Frequency

United States

The true incidence of esophageal spasm cannot be determined. The symptoms range from mild to severe. Patients with mild symptoms often do not seek medical attention. Because of the similarity of symptoms of reflux disease and esophageal spasm, many patients may be misdiagnosed with reflux. Furthermore, reflux and spasm can occur concomitantly.

International

Because the symptoms are mild (or even absent) in many patients, true incidence is not known.

Mortality/Morbidity

  • Mortality is very rare, but morbidity can be significant.
  • Morbidity arises from an inability to eat, secondary to the pain, and the subsequent decline in nutritional status. The pain can be incapacitating, preventing normal activity and leading to considerable psychological challenges and impairment in the patient's quality of life.
  • The chest pain can mimic cardiac, pulmonary, or rheumatological chest pain, instigating appropriate workup.

Race

  • This condition seemingly is more common in whites.

Sex

  • This condition may be more common in women than in men.

Age

  • This condition is rare in children, and incidence increases with age.



History

  • Esophageal spasm usually presents with the following intermittent symptoms:

    • Noncardiac chest pain (Less than 10% of causes of noncardiac chest pain are due to DES.)
    • Globus (ie, the sensation that an object is trapped in the throat)
    • Dysphagia, which is more consistent and reproducible during investigative studies, may be reported by one third to two thirds of subjects.
    • Regurgitation
    • About 20% of patients will report heartburn.
    • A correlation between uncoordinated contractions and chest pain is difficult to document.

Physical

  • Physical examination is not helpful for making a diagnosis.

Causes

  • Etiology of esophageal spasm is unknown.
  • Increased release of acetylcholine appears to be a factor (sensitive to cholinergic stimulation), but the triggering event is not known.
  • Other theories include gastric reflux or a primary nerve or motor disorder.
  • Microvascular compression of the Vagus nerve in the brainstem has been demonstrated in current research as the possible triggering event. Medical therapy may focus on these blood vessels instead of on the muscles in the esophagus.



Achalasia
Angina Pectoris
Esophageal Cancer
Esophageal Diverticula
Esophageal Motility Disorders
Esophageal Stricture
Esophageal Webs and Rings
Esophagitis
Gastroesophageal Reflux Disease
Myocardial Infarction

Other Problems to Be Considered

  • Studies using catheter-based high-frequency ultrasound imaging have shown an increase in the baseline muscle thickness in patients with DES, nutcracker esophagus, and achalasia, as well as in patients with esophageal symptoms and normal static manometry.
  • Esophageal spasm can modify cardiac function and vice versa. Esophageal spasm and coronary artery disease may coexist.  Mechanisms that cause esophageal spasm can feed back to cause coronary spasm, and coronary spasm may feed forward to cause further esophageal spasm.



Lab Studies

  • Laboratory evaluation usually does not aid in the diagnosis if patients' history and physical examination are unremarkable for other diseases mentioned in the differential diagnosis. All differentials mentioned can present with esophageal dysmotility.
  • The diagnostic modalities of choice are barium swallow and esophageal manometry.
  • Blood sugar and hemoglobin A1C should be checked to rule out diabetes. However, patients can have esophageal spasm and diabetes concomitantly.
  • The findings discovered by monitoring a patient's pH can demonstrate reflux, which can present with somewhat similar symptoms. In fact, gastroesophageal reflux is thought by some to trigger esophageal spasm.

Imaging Studies

  • Barium swallow

    • Barium swallow is the best imaging study to aid in the diagnosis of esophageal spasm.
    • Upon barium swallow, DES has a characteristic appearance of multiple simultaneous contractions. This is often referred to as a corkscrew appearance (see Media file 1).
    • Unlike in DES, the barium swallow findings for nutcracker esophagus are not specific.
  • CT scan

    • Nino-Murcia and colleagues demonstrated thickening of the esophagus with CT scan studies in patients with esophageal spasm.22
    • Muscular hypertrophy has been documented in some patients with DES and nutcracker esophagus.
    • The hypertrophy of the muscle wall is the cause of the increased thickness that is observed on CT scan images. The normal thickness of the esophagus is less than 3 mm.
    • Many other disease processes, including malignancy, cause thickening of the esophagus that can be seen radiographically. Thus, thickening of the esophagus seen on CT scan images should prompt further workup.
    • Even in patients with symptoms consistent with esophageal spasm, thickening seen on CT scan images should not be dismissed as muscular hypertrophy secondary to the esophageal spasms without further investigation.
  • Ultrasound

    • Catheter-based high-frequency intraluminal ultrasound imaging assesses both the sensory function and the motor function of the esophagus.
    • This imaging modality may be useful to distinguish between DES, nutcracker esophagus, and achalasia.

 

Other Tests

  • Manometry

    • Manometry is the best modality to help diagnose DES. The classic definition is more than 2 uncoordinated contractions during 10 consecutive wet swallows (≥20% simultaneous esophageal contractions during standardized stationary motility testing). At least one peristaltic contraction must be present. Artificial neural networks may be useful in the recognition and objective classification of primary esophageal motor disorders investigated with stationary esophageal manometry recordings.
    • Contraction amplitude is normal.
    • Media file 2 is a normal manometric tracing, and Media file 3 is an example of DES.
    • Manometry in patients with nutcracker esophagus demonstrates contractions that progress in an orderly manner, but the amplitude of the contraction is excessive. Amplitude greater than 2 standard deviations above the normal value is considered diagnostic for nutcracker esophagus (see Media file 4).
    • There may be a disassociation between symptoms and manometric findings.
    • Esophageal electrical impedance recordings show abnormal transit in DES.
    • Esophageal manometry may be combined with multichannel intraluminal impedance to obtain pressure and bolus transit information. About one half of patients with DES have normal transit for liquids and fluids, one fourth have abnormal transit for one substance, and one fourth have abnormal transit for both.
    • Esophageal pH recording and 24-hour ambulatory manometry may improve the detection of esophageal muscle dysfunction. This method shows that, in persons presenting with noncardiac chest pain, gastroesophageal reflux symptoms are common and DES is rare.
  • Endoscopy: This test is not useful to help diagnose dysmotility, but it may be helpful to exclude erosive esophagitis or stricture.



Medical Care

Medical and surgical options are available for the treatment of DES and nutcracker esophagus and have been used with moderate success. Each treatment has a high failure rate, which drives the constant search for a better treatment. Medical treatment consists of calcium channel blockers, tricyclic antidepressants, nitrates, botulinum toxin, and dilatation. These conditions are usually not progressive but may interfere with the patient's quality of life.

  • Calcium channel blockers can reduce the amplitude of the contractions.

    • In patients with nutcracker esophagus, calcium channel blockers effectively reduce the amplitude of the contractions, but the chest pain may not always be reduced.
    • Traditionally, calcium channel blockers were thought to decrease the contractions. 
  • Nitrates also have been used with some success.

    • The mechanism of action is unknown but may be related to decreasing vasospasm in the brainstem, similar to calcium channel blockers.
    • Some patients benefit from sublingual nitroglycerin for acute symptoms of esophageal spasm. 
  • Tricyclic antidepressants, specifically imipramine, have been shown to decrease chest pain with no apparent cause on angiogram. Studies specifically evaluating nutcracker esophagus are not yet available.
  • Botulinum toxin binds receptors in the nerve endings, thereby decreasing the release of acetylcholine.
    • By endoscopically injecting botulinum toxin above the LES, symptoms may improve.
    • The effect is temporary, and the response decreases with repeated injections.
  • Balloon dilatation is commonly used for achalasia, but it has been used to treat DES and nutcracker esophagus.

    • The studies are small, the relief is not uniform, and symptoms recur.
    • Dilation with mercury-filled bougies has been used in the past.
  • Proton pump inhibitors effectively reduce or alleviate the symptoms of gastroesophageal reflux disease, which may mimic DES. A trial of acid lowering therapy may be undertaken prior to instigating other treatments. Although treatment is often ineffective, the symptoms from DES and nutcracker esophagus usually improve over time.

Surgical Care

For extreme cases, operative treatment usually involves a myotomy. Myotomy relieves symptoms by eliminating the effectiveness of the contractions. Traditionally, a thoracotomy was required to obtain access to the esophagus, but now, a thoracoscopic approach can be used. In rare, recalcitrant cases, esophagectomy can relieve symptoms.

  • Myotomy is effective for treating DES.
    • The myotomy should extend the entire length of the involved segment, which should be determined preoperatively with manometry.

    • Furthermore, the myotomy should extend through the LES to help prevent dysphagia postoperatively by preventing outlet obstruction.

    • Finally, an antireflux procedure should be performed concomitantly, by either a partial wrap or a floppy Nissen.
  • Myotomy should be used with caution in patients with nutcracker esophagus because it may worsen the symptoms.
    • Myotomy reduces the amplitude of the contractions, but this does not consistently improve symptoms, especially if the primary complaint is pain.

    • Furthermore, dysphagia can develop or worsen after myotomy because the effectiveness of the propagative waves is eliminated, leaving gravity to propel food caudally.
  • As a last resort, esophagectomy can be used to relieve symptoms.
    • The esophagus is resected, and the stomach, small intestine, or colon is used to restore the continuity of the GI tract.

    • Morbidity and mortality of esophagectomy are substantial; therefore, this should be performed only after other treatments have been exhausted.

Diet

  • Diet-induced symptoms are patient-specific.
  • Dietary restriction, even to pureed foods, can decrease symptoms temporarily.



Medical therapy is the first line of treatment for esophageal spasm. Because the etiology is unknown, all medical therapies are directed at symptoms, not etiology. Proton pump inhibitors may be useful if there is associated gastroesophageal reflux disease. Calcium channel blockers and nitrates may decrease pain associated with esophageal spasms. Botulinum toxin decreases acetylcholine available at nerve endings. Imipramine improves pain by an unknown mechanism of action.

Drug Category: Calcium channel blockers

Reduce amplitude of contractions. In nutcracker esophagus, calcium channel blockers effectively reduce amplitude of contractions, but chest pain often is not reduced. Whether calcium channel blockers decrease force of contraction of muscle or decrease underlying stimulus is unknown.

Drug NameDiltiazem (Cardizem)
DescriptionFDA-approved for hypertension, vasospastic angina, and chronic stable angina. Decreases calcium ion flux across cell membranes in smooth muscle, thereby relaxing vascular smooth muscle.
Adult DoseInitial: 120 mg PO qd; titrate to effect without significant adverse effects; optimal dose not known
Pediatric DoseNot recommended
ContraindicationsDocumented hypersensitivity; severe CHF; sick sinus syndrome; acute MI; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
InteractionsBeta-blockers are usually well tolerated but can result in hypotension or CH; cimetidine may increase levels by inhibiting P-450 metabolism of diltiazem; may increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and a decrease in cardiac output
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsHypotension, dizziness, flushing, nausea, and bradycardia/conduction delays; caution in impaired renal or hepatic function; may increase LFT levels; hepatic injury may occur

Drug Category: Nitrates

Like calcium channel blockers, nitrates may decrease the pain associated with esophageal spasm. The mechanism of action is unknown but may be related to decreasing vasospasm in the brainstem, similar to calcium channel blockers, or it may be a direct effect on the myocytes.

Drug NameIsosorbide dinitrate (Dilatate SR, Isordil)
DescriptionApproved indication is for angina pectoris. Relaxes vascular smooth muscle by stimulating intracellular cyclic GMP. By decreasing left ventricular pressure and dilating arteries, reduces cardiac oxygen demand.
Adult Dose5 mg PO ac or 2.5 mg SL pc
Pediatric DoseNot established
ContraindicationsDocumented hypersensitivity; severe anemia; closed-angle glaucoma; postural hypotension; head trauma; cerebral hemorrhage
InteractionsCoadministration with alcohol may cause severe hypotension and cardiovascular collapse; aspirin may increase serum concentrations of isosorbide and actions; coadministration with channel blockers may increase symptomatic orthostatic hypotension (adjust dose of either agent); isosorbide may decrease effects of heparin
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsThe most common adverse reactions are hypotension and headache; methemoglobinemia rarely occurs; safety not known with CHF, with acute myocardial infarction, or in mothers who are breastfeeding; tolerance to vascular and antianginal effects of nitrates may develop; minimize tolerance by using smallest effective dose, pulse therapy (intermittent dosing), or by alternating with other coronary vasodilators (take last daily dose of short-acting agent no later than 7 pm); caution with glaucoma

Drug Category: Tricyclic antidepressants

These agents, specifically imipramine, have been shown to decrease chest pain with no apparent cause on angiogram. Studies specifically evaluating nutcracker esophagus are not yet available. The mechanism of action of imipramine is not known.

Drug NameImipramine (Tofranil)
DescriptionDecreases pain in patients with chest pain with no apparent cause on angiogram, which may be esophageal spasm. This is not an FDA-approved use. Mechanism of action is not known. Primary use of imipramine is in the treatment of depression.
Adult Dose25 mg PO qhs; titrate to effect as tolerated
Pediatric DoseNot recommended
ContraindicationsDocumented hypersensitivity; secreted in breast milk, therefore, should not be used in mothers who are breastfeeding; narrow-angle glaucoma; in acute recovery phase following myocardial infarction; MAOIs or fluoxetine or took them in previous 2 wk
InteractionsMetabolized by P450, therefore, caution with other medications metabolized by this system; potentiates effects of alcohol; additive with CNS depressants; may potentiate effect of sympathomimetics, such as nasal decongestants; increases toxicity of sympathomimetic agents, such as isoproterenol and epinephrine by potentiating effects and inhibiting antihypertensive effects of clonidine
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in cardiovascular disease, increased intraocular pressure, narrow-angle glaucoma, hyperthyroidism, and history of seizure disorder; decrease dose in elderly patients because of increased adverse effects, such as CV arrhythmias, hypotension, hypertension, or CHF; psychiatric confusion; neurologic paresthesias, extrapyramidal symptoms, lower seizure threshold, allergic reactions, hematologic bone marrow suppression, nausea, vomiting, diarrhea, gynecomastia, galactorrhea, and CVA may occur; adverse anticholinergic effects are a concern

Drug Category: Toxins (botulinum toxin)

Binds receptors in nerve endings, decreasing release of acetylcholine. Injecting botulinum toxin endoscopically above the LES improves symptoms of patients with esophageal spasms. However, effect is temporary and response decreases with repeated injections.

Drug NameBotulinum toxin (BOTOX®)
DescriptionTreats excessive abnormal contractions associated with blepharospasm. Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which, in turn, inhibits transmission of impulses in neuromuscular tissue.
Adult DoseInitial dose: 20 U have been used; reexamine patients at 7-14 d to assess for response; increase dose 2-fold over previous dose for patients experiencing incomplete paralysis of target muscle; not to exceed 25 U when administering as single injection or 200 U as cumulative dose in 30-d period; approved for strabismus and blepharospasm
Pediatric Dose<12 years: Not established
>12 years: Administer as in adults
ContraindicationsDocumented hypersensitivity
InteractionsAminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsMost adverse reactions are local irritation; systemic reactions are rare; do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy



Further Inpatient Care

  • Usually, the workup and treatment are performed in an outpatient setting.
  • Patients in whom medical management fails and who require operative intervention should have routine postoperative care based on the procedure performed.

Further Outpatient Care

  • Patients need close follow-up care upon the initiation of therapy or with a change in therapy.
  • Patients should be monitored for improvements in symptoms and for adverse effects of the medications.
  • Patients in whom medical management fails should be referred to a thoracic surgeon for possible operative intervention.

In/Out Patient Meds

  • Calcium channel blockers and nitrates are first-line therapy.

Complications

  • Potential problems are based on the therapy. All medications have possible adverse effects, and patients should be monitored.
  • Esophageal perforation can occur with esophageal dilatation, leading to admission to the hospital, time lost from work, and possible surgery.
  • Operative complications are the same as for any operation on the esophagus.
    • Esophageal perforation can occur during the myotomy. If a perforation of the mucosa occurs, the defect should be closed and the patient should have a contrast swallowing test prior to resuming a diet.
    • Vagal injury can occur during the dissection.
    • Other postoperative complications include wound infection, atelectasis, pneumonia, and persistent air leak.
    • Any complication of a thoracic operation or an esophageal operation can occur.

Prognosis

  • Prognosis is moderate. Symptom scores improve over time (3 y or longer) from DES and nutcracker esophagus.
  • The mortality rate is minuscule, but the morbidity rate is high.
  • No treatment is effective in all patients. Some patients do not respond to any treatment.
  • In most patients, symptoms are controllable with a combination of treatment modalities.

Patient Education

  • Patients should be educated about the symptoms and treatment options for the disease.
  • Patient involvement and education are crucial to the success of any treatment modality.
  • For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article BOTOX® Injections.



Medical/Legal Pitfalls

  • As with any medical problem, a thorough systematic workup should be performed in patients with symptoms consistent with esophageal spasm. Manometry is the criterion standard, with a high sensitivity and high specificity. Chest pain deserves consideration of cardiac, pulmonary, and rheumatologic etiologies.
  • Failure to exclude serious causes of chest pain (eg, coronary artery disease) and inappropriate treatment of DES without excluding another primary or associated etiology may lead to mortality or further morbidity.
  • CT scan images can demonstrate thickening of the esophagus in patients with esophageal spasm or patients with other diseases of the esophagus, such as carcinoma. Therefore, abnormal findings on a CT scan should be followed by endoscopy and manometry if esophageal spasm is a concern.
  • Specific diagnosis should be made prior to operative intervention. Performing a myotomy in a patient with nutcracker esophagus worsens the dysphagia without improving the pain.
  • Reflux can mimic esophageal spasm; therefore, this should be ruled out or treated prior to instigating other treatments.



Media file 1:  Barium swallow demonstrates diffuse uncoordinated contractions of the esophagus in a patient with diffuse esophageal spasm.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  X-RAY

Media file 2:  This is normal esophageal manometry tracing with normal amplitude of the contractions. The contractions are coordinated because the contractions in the proximal esophagus (top of image) occur before the contractions further distal in the esophagus.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Graph

Media file 3:  Esophageal manometry tracing demonstrates diffuse esophageal spasm. Note the multiple uncoordinated contractions in the third tracing from the distal esophagus.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Graph

Media file 4:  Esophageal manometry tracing demonstrates nutcracker esophagus. Note the excessive amplitude of the contractions.
Click to see larger pictureClick to see detailView Full Size Image
Media type:  Graph



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Esophageal Spasm excerpt

Article Last Updated: Jul 10, 2007