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At least 19 recordsLinked to original sources
PubMed2001

Primary esophageal motility disorders.

Esophageal motility disorders often manifest with chest pain and dysphagia. Achalasia is a disorder of the lower esophageal sphincter and the smooth musculature of the esophageal body. In achalasia the lower esophageal sphincter typically fails to relax with swallowing, and the esophageal body fails to undergo peristalsis. In contrast to spastic disorders of the esophagus, achalasia can be progressive and cause pronounced morbidity. Pseudoachalasia mimics achalasia in terms of symptoms but can be caused by infectious disorders or malignancy. Treatment for achalasia is nonstandardized and includes medical, endoscopic, and surgical options. Spastic disorders of the esophagus, such as diffuse esophageal spasm and nutcracker esophagus, and nonspecific esophageal motility disorder are benign and nonprogressive, with similar findings on esophageal manometry. Although the exact cause remains unknown, these disorders may represent a manifestation of gastroesophageal reflux disease. Treatment of spastic disorders includes medical and surgical approaches and is aimed at symptomatic relief.

Esophageal Achalasia↗
PubMed1988

Esophageal motility disorders.

Esophageal motility disorders consist of a complex array of disturbances in normal esophageal function associated with dysphagia, gastroesophageal reflux, and noncardiac chest pain. A thorough knowledge of normal esophageal anatomy and physiology is important to a full understanding of these motility derangements. Through a complicated interaction of neuromuscular and hormonal influences, the voluntary act of swallowing transforms into an automated sequence of peristaltic waves propelling food and liquids into the stomach in concert with coordinated relaxation of the sphincters. Anatomic and physiologic barriers exist within the esophagus protecting against gastroesophageal reflux and aspiration. With improvements in diagnostic tools such as barium contrast radiography, scintigraphy, pH measurements, and esophageal manometrics with provocative testing, motility disorders have become better defined and understood. Primary motility disorders consist of achalasia, diffuse esophageal spasm (DES), "nutcracker esophagus," hypertensive lower esophageal sphincter, and nonspecific esophageal motility dysfunction (NEMD). A host of secondary and miscellaneous motility disorders also affect the esophagus, including scleroderma and other connective tissue diseases, diabetes mellitus, Chagas' disease, chronic idiopathic intestinal pseudo-obstruction, and neuromuscular disorders of striated muscle. Gastroesophageal reflux disease (GERD) may also be promoted by associated motility disturbances. Treatment modalities include surgical myotomy; dilatation; and pharmacologic manipulations, including use of nitrates, calcium-channel blockers, H2-blockers, and psychotropic drugs where appropriate.

Deglutition↗
PubMed1990

Diagnosis of esophageal motility disorders.

Esophageal motility disorders are now known to be a heterogeneous group of conditions that commonly cause dysphagia and chest pain. Motor dysphagia is usually provoked by solids and liquids (in contrast to mechanical dysphagia, which is usually provoked by solids only). Chest pain with these disorders is nonspecific and can mimic angina pectoris. In many patients with diffuse esophageal spasm or nutcracker esophagus, pain appears to be caused by abnormal sensory function rather than contraction abnormalities. Barium esophagography and esophageal manometry are complementary studies in the evaluation of motility disorders.

Barium Sulfate↗
PubMed1991

Multiple swallow test for the quantitative and qualitative evaluation of esophageal motility disorders.

Esophageal motility was evaluated from the analysis of six consecutive swallows. A sum image was generated comprising the representative information of an entire study. Calculation of emptying rates and characterization of the bolus behavior was performed from the sum image and the single swallow data. In 86 patients investigated, liquid and solid-phase studies showed a remarkable variation of single swallow data in normals (relative variation coefficient for liquid: 10%, solid: 14%), which were even higher (p less than 0.001) in patients with disorders (liquid: 31%, solid: 25%). As sum images compensate for this intra-individual variation, false-positive (liquid: 16%, solid: 25%) or negative single swallow findings (liquid: 36%, solid: 27%) are reduced. Qualitative analysis of condensed sum images provided characteristic image patterns representing different pathophysiologic aspects. Since the method introduced better discriminates between normal and pathologic function, it may enhance diagnostic accuracy.

Deglutition↗
PubMed2001

[Esophageal motility disorders].

Esophageal motility abnormalities are usually diagnosed when esophageal manometry is performed in patients with unexplained non-cardiac chest pain, non obstructive dysphagia or as a part of the preoperative evaluation for surgery of gastroesophageal reflux. Classification of these abnormalities has been a subject of controversy. These esophageal contraction abnormalities can be separated manometrically from the motor pattern seen in normal subjects, however, their clinical relevance is still unclear and debated. Many patients demonstrate motility abnormalities in the manometry laboratories, but may lack correlation with their presenting symptoms. Medical treatment can decrease symptoms particularly chest pain or acid reflux but there is no significant changes in the manometric patterns. Such motor abnormalities may not reflect a true disease state, but they could be markers of other abnormalities and they can modify the initial manometric findings in time.

English Abstract↗
PubMed1997

Ineffective esophageal motility (IEM): the primary finding in patients with nonspecific esophageal motility disorder.

Nonspecific esophageal motility disorder (NEMD) is a vague category used to include patients with poorly defined esophageal contraction abnormalities. The criteria include "ineffective" contraction waves, ie, peristaltic waves that are either of low amplitude or are not transmitted. The aim of this study was to identify the prevalence of ineffective esophageal motility (IEM) found during manometry testing and to evaluate esophageal acid exposure and esophageal acid clearance (EAC) in patients with IEM compared to those with other motility findings. We analyzed esophageal manometric tracings from 600 consecutive patients undergoing manometry in our laboratory following a specific protocol from April 1992 through October 1994 to identify the frequency of ineffective contractions and the percentages of other motility abnormalities present in patients meeting criteria for NEMD. Comparison of acid exposure and EAC was made with 150 patients who also had both esophageal manometry and pH-metry over the same time period. Sixty-one of 600 patients (10%) met the diagnostic criteria for NEMD. Sixty of 61 (98%) of these patients had IEM, defined by at least 30% ineffective contractions out of 10 wet swallows. Thirty-five of these patients also underwent ambulatory esophageal pH monitoring. Patients with IEM demonstrated significant increases in both recumbent median percentage of time of pH <4 (4.5%) and median distal EAC (4.2 min/episode) compared to those with normal motility (0.2%, 1 min/episode), diffuse esophageal spasm (0%, 0.6 min/episode), hypertensive LES (0%, 1.8 min/episode), and nutcracker esophagus (0.4% 1.6 min/episode). Recumbent acid exposure in IEM did not differ significantly from that in patients with systemic scleroderma (SSc) for either variable (5.4%, 4.2 min/episode). We propose that IEM is a more appropriate term and should replace NEMD, giving it a more specific manometric identity. IEM patients demonstrate a distinctive recumbent reflux pattern, similar to that seen in patients with SSc. This finding indicates that there is an association between IEM and recumbent GER. Whether IEM is the cause or the effect of increased esophageal acid exposure remains to be determined.

Adult↗
PubMed1999

Videoendoscopic diagnosis of esophageal motility disorders.

BACKGROUND: Esophageal motility disorders are usually diagnosed by manometry. We evaluated videoendoscopy as a diagnostic test. METHODS: In this study, 20 patients with achalasia, 13 with scleroderma, and 33 control subjects had a standard endoscopic examination followed by protocol videotaping of swallows to observe contractions in the esophagus and in the lower esophageal sphincter. Tapes were later reviewed by 2 blinded observers who recorded their motility findings and diagnoses. RESULTS: In the mid esophagus at 25 cm, lumen-occluding peristaltic contractions were identified in 26 of 33 control subjects versus 1 of 20 achalasia (p < 0.001) and 3 of 13 scleroderma patients (p < 0.005). As viewed in the lower esophagus, the lower esophageal sphincter opened normally in 31 of 33 control subjects versus 1 of 20 achalasia (p < 0.001). In scleroderma, the sphincter never closed in 12 of 13 patients (p < 0. 001 versus control subjects). A diagnostic sequence of sphincter opening followed by contraction in the esophageal body and subsequent sphincter closing was seen in 33 of 33 control subjects, 2 of 20 achalasia, and 1 of 13 scleroderma patients (both, p < 0. 001). The observers made the correct diagnosis in 96% of cases. CONCLUSIONS: Achalasia and esophageal scleroderma can be identified by endoscopic observation of motility. This procedure may represent an adjunctive diagnostic test to manometry.

Endoscopy, Digestive System↗
PubMed2006

Esophageal motility disorders (distal esophageal spasm, nutcracker esophagus, and hypertensive lower esophageal sphincter): modern management.

The group of hypercontractile esophageal motility disorders includes distal esophageal spasm (DES), nutcracker esophagus (NE), and hypertensive lower esophageal sphincter (LES). The clinical relevance of these abnormalities identified during esophageal manometry is debated, and their management can be challenging. Hypercontractile esophageal motility abnormalities are defined through specific manometric criteria. Current pathophysiologic concepts for these abnormalities include defects in the nitronergic neural pathways and imbalances between the cholinergic and nitronergic pathway. Proposed treatments for NE, DES, and hypertensive LES include proton-pump inhibitors, nitrates, calcium channel blockers, phosphodiasterase inhibitors, and tricyclic antidepressants or serotonin reuptake inhibitors. Small case series reported benefits after botulinum toxin injections, dilatations, and myotomies. The optional management of esophageal spasm, NE, and hypertensive LES is still debated. Treatment recommendations are based on controlled studies with small numbers of patients or on case series. Medical treatment, including acid suppression, smooth muscle relaxants, and visceral analgesics, should be tried first. In nonresponding patients, botulinum toxin injections or balloon dilatations can be tried. Pneumatic dilatations or myotomies should be regarded as last-option treatments for nonresponding patients.

Journal Article↗
PubMed1994

Failing deglutitive inhibition in primary esophageal motility disorders.

BACKGROUND/AIMS: Primary esophageal motility disorders (achalasia, diffuse esophageal spasm, and intermediate forms) are suggested to be caused by different degrees of inhibitory dysfunction; however, direct evidence for this hypothesis has never been presented in humans. The aim of this study was to measure the degree of inhibition that precedes deglutitive contractions in patients with primary motility disorders. METHODS: Deglutitive inhibition was examined in patients with primary motility disorders: 9 with achalasia, 6 with symptomatic diffuse esophageal spasm, and 5 with intermediate forms. An artificial high-pressure zone was created in the esophageal body by inflating a balloon to a critical level, and pressure changes were measured at the interface between the balloon and esophageal wall. Inhibition was visualized as a relaxation of the artificial high-pressure zone. RESULTS: An inverse relationship was found between the degree of inhibition and the propagation velocity of the deglutitive contraction (r = 0.75; P < 0.001). Normally propagated contractions were preceded by an inhibition of 84.2% +/- 3.6%; fast-propagating contractions were preceded by partial inhibition of 40.6% +/- 6.2%; and, in case of simultaneous contractions, inhibition was absent, i.e., 2.6% +/- 1.6%. CONCLUSIONS: The spectrum of primary motility disorders is an expression of a progressively failing deglutitive inhibition.

Adult↗
PubMed1997

Double-blind placebo-controlled study of cisapride in patients with nonspecific esophageal motility disorder accompanied by delayed esophageal transit.

BACKGROUND: Nonspecific esophageal motility disorder (NEMD) represents a difficult therapeutic challenge because of the heterogeneous nature of the esophageal motor functions. We studied the effects of cisapride on the esophageal symptoms and esophageal motor function in a group of patients with NEMD showing delayed esophageal transit. METHODS: Seventy eligible patients were entered into a 4-week, double-blind randomized comparison of 10 mg of cisapride or placebo, four times daily. Symptom assessment, esophageal manometry after wet swallows, and esophageal scintigraphy after intake of a liquid and solid bolus were performed in each patient before and after treatment. RESULTS: After 4 weeks of treatment cisapride significantly increased the prevalence of esophageal peristaltic contractions (percentage of total contractions, P < 0.05 versus base line and placebo) and significantly improved esophageal emptying of the solid bolus (P < 0.05 versus placebo) but not of the liquid bolus. Placebo did not have any significant effects versus base line on these variables. Both placebo and cisapride improved the distal esophageal amplitude versus base line (no significant intergroup differences). Symptom scores were significantly reduced after 4 weeks of treatment versus base line in both groups (no significant intergroup differences except for heartburn and regurgitation, P < 0.05). On global evaluation of treatment, significantly more patients in the cisapride group were rated as markedly or moderately improved, when compared with placebo. CONCLUSIONS: The results of the present study showed that cisapride is effective and well tolerated in patients with NEMD accompanied by delayed esophageal transit. Symptomatic improvement may possibly be related to its beneficial action on the esophageal body by increasing the number of peristaltic contractions and esophageal emptying of solids.

Adult↗
PubMed1997

Evaluation and treatment of primary esophageal motility disorders.

Achalasia, diffuse esophageal spasm, and nutcracker esophagus constitute the main primary esophageal motility disorders. During the past decade major progress has been made in understanding their pathophysiology and in the ability to establish a precise diagnosis. In addition, minimally invasive surgical intervention has radically changed the therapeutic approach, and thoracoscopic or laparoscopic myotomy is probably the best treatment for most patients.

Diagnosis, Differential↗
PubMed1989

Upper esophageal motility disorders.

This article begins with a summary of the anatomy and physiology of the upper esophageal region. The appropriate diagnostic tools used in the evaluation of upper esophageal motility disorders are then detailed including cineradiography, manometry, and other modalities. Specific clinical disorders associated with pharyngeal, UES, or upper esophageal dysfunction are described followed by a section on treatment.

Animals↗
PubMed1991

[Esophageal manometry as a surgical indication in primary esophageal motility disorders].

Today, esophageal manometry is the diagnostic test that enables one to establish a diagnosis of esophageal motor disorder, to make the correct diagnosis among various forms of esophageal motor dyskinesia and to guide the diagnostician, whether physician or surgeon, in making the proper choice of therapy. Achalasia and diffuse esophageal spasm are two of the better known primitive esophageal motor disorders, in which an investigation into motility makes it possible to reach a diagnosis in physiopathological terms and provides guidance in selecting the appropriate therapy. The surgical indications for these two diseases are indeed conditioned significantly by the pre-operative manometric data. The extension of the extramucous esophageal myotomy is in fact guided by the manometric tracing that precisely defines the anatomic and functional boundaries of the motor disorder. Additional support provided by esophageal manometry occurs when there are indications of repeated surgery after myotomy, whether a cardiomyotomy or a long myotomy. In these cases accurate manometry can in fact clarify the origin of the possible post-operative dysphagia and, therefore, the nature of the possible stenosis, functional or organic. It should therefore be emphasized that, as now universally recognized, it would be rather careless today to confront the chapter of functional esophageal disease without the aid of manometry.

Esophageal Achalasia↗
PubMedDate not supplied

[Primary esophageal motility disorders: medical treatment].

Primary esophageal motility disorders consist of a complex group of motor disturbances, affecting the characteristics of esophageal contractions, occurrence of peristalsis and lower esophageal sphincter function. The medical treatment is still challenging because of the absence, except for Achalasia, of generally agreed criteria for diagnosis and the still unresolved relationship between esophageal symptoms and some motor abnormalities. In Achalasia, the medical therapy does not constitute a main role and should be reserved to selected conditions. Current medical therapies for Diffuse Esophageal Spasm and Esophageal Chest Pain are often considered less than satisfactory, however, a better physiopathological knowledge of these conditions might produce a more appropriate therapeutic management of the patients with continual and disabling symptoms.

Chest Pain↗
PubMed1993

Medical treatment of esophageal motility disorders.

Swallowing is a complex mechanism that is based on the coordinated interplay of tongue, pharynx, and esophagus. Disturbances of this interplay or disorders of one or several of these components lead to dysphagia, non-cardiac chest pain, or regurgitation. The major esophageal motility disorders include achalasia, diffuse esophageal spasm, hypercontractile esophagus ("nutcracker esophagus"), and hypocontractile esophagus ("scleroderma esophagus"). Other esophageal diseases such as hypopharyngeal (Zenker's) diverticula or gastroesophageal reflux disease also may be sequelae of primary esophageal motility disorder. Finally, a substantial group of patients referred for evaluation of possible esophageal motor disorders have milder degrees of dysmotility--referred to as nonspecific esophageal motor disorder--that are of unclear clinical significance. Medical treatment of esophageal motility disorders involves the uses of agents that either reduce (anti-cholinergic agents, nitrates, calcium antagonists) or enhance (prokinetic agents) esophageal contractility. Despite the beneficial effect of the various drugs on esophageal motility parameters, the clinical benefit of medical treatment is often disappointing. From clinical and epidemiological studies there is some evidence for a "psychological" component in the pathogenesis or perception of esophageal symptoms. Further understanding of esophageal pathophysiology, as well as development of new receptor selective drugs, might increase our chances of successful treatment of esophageal motility disorders.

Esophageal Motility Disorders↗
PubMed1982

Effect of isosorbide and hydralazine in painful primary esophageal motility disorders.

Five patients with painful primary esophageal motility disorders underwent pharmacologic testing with isosorbide and hydralazine. While neither agent affected baseline amplitude or duration of distal esophageal contractions, pretreatment with hydralazine significantly blunted the response to bethanechol (mean esophageal contraction duration, 31.4 +/- 4.8 s after bethanechol alone vs. 12.7 +/- 1.8 s after bethanechol and hydralazine p less than 0.005). Premedication with isosorbide was significantly less effective. In addition, while all 5 patients experienced chest pain in response to bethanechol alone, only 1 of 5 experienced chest pain in response to bethanechol after previous hydralazine administration; 3 patients had chest pain after previous administration of isosorbide. Patients who were placed on long-term oral hydralazine therapy experienced improvement in chest pain and dysphagia with concomitant decrease in amplitude and duration of esophageal contractions on repeat motility study (176.5 +/- 23.8 mmHg to 97.3 +/- 27.0 mmHg, p less than 0.05, 7.5 +/- 0.8 s to 5.2 +/- 0.5 s, p less than 0.005). Hydralazine appears to be of value in the treatment of diffuse esophageal spasm and other painful primary esophageal motility disorders.

Adult↗
PubMed2003

Fundoplication improves disordered esophageal motility.

Patients with gastroesophageal reflux disease (GERD) and disordered esophageal motility are at risk for postoperative dysphagia, and are often treated with partial (270-degree) fundoplication as a strategy to minimize postoperative swallowing difficulties. Complete (360-degree) fundoplication, however, may provide more effective and durable reflux protection over time. Recently we reported that postfundoplication dysphagia is uncommon, regardless of preoperative manometric status and type of fundoplication. To determine whether esophageal function improves after fundoplication, we measured postoperative motility in patients in whom disordered esophageal motility had been documented before fundoplication. Forty-eight of 262 patients who underwent laparoscopic fundoplication between 1995 and 2000 satisfied preoperative manometric criteria for disordered esophageal motility (distal esophageal peristaltic amplitude < or =30 mm Hg and/or peristaltic frequency < or =80%). Of these, 19 had preoperative manometric assessment at our facility and consented to repeat study. Fifteen (79%) of these patients had a complete fundoplication and four (21%) had a partial fundoplication. Each patient underwent repeat four-channel esophageal manometry 29.5 +/- 18.4 months (mean +/- SD) after fundoplication. Distal esophageal peristaltic amplitude and peristaltic frequency were compared to preoperative data by paired t test. After fundoplication, mean peristaltic amplitude in the distal esophagus increased by 47% (56.8 +/- 30.9 mm Hg to 83.5 +/- 36.5 mm Hg; P < 0.001) and peristaltic frequency improved by 33% (66.4 +/- 28.7% to 87.6 +/- 16.3%; P < 0.01). Normal esophageal motor function was present in 14 patients (74%) after fundoplication, whereas in five patients the esophageal motor function remained abnormal (2 improved, 1 worsened, and 2 remained unchanged). Three patients with preoperative peristaltic frequencies of 0%, 10%, and 20% improved to 84%, 88%, and 50%, respectively, after fundoplication. In most GERD patients with esophageal dysmotility, fundoplication improves the amplitude and frequency of esophageal peristalsis, suggesting refluxate has an etiologic role in motor dysfunction. These data, along with prior data showing that postoperative dysphagia is not common, imply that surgeons should apply complete fundoplication liberally in patients with disordered preoperative esophageal motility.

Adult↗