Distal esophageal spasm is an uncommon esophageal motility disorder presenting with non-cardiac chest pain and dysphagia. The main goal of therapy is symptom relief with pharmacologic, endoscopic, and surgical therapies. Pharmacologic treatment is less invasive and is the preferred method of choice. The purpose of this study was to compare the effectiveness of diltiazem versus fluoxetine in the treatment of distal esophageal spasm.

A total of 125 patients with distal esophageal spasm diagnosed using endoscopy, barium esophagogram, and manometry were evaluated. Patients were divided into diltiazem and fluoxetine groups and received a 2-month trial of diltiazem + omeprazole or fluoxetine + omeprazole, respectively. Of 125 patients, 55 were lost to follow up and 70 were eligible for final analysis. Clinical signs and symptoms were assessed before and after therapy using four validated questionnaires: Eckardt score, short form-36, heartburn score, and the hospital anxiety and depression scale.

Both regimens significantly relieved symptoms (a decrease in mean Eckardt score of 2.57 and 3.18 for diltiazem and fluoxetine groups, respectively; and a decrease in mean heartburn score by 0.89 and 1.03 for diltiazem and fluoxetine groups, respectively). Patients' quality of life improved based on short form-36 (an increase in mean score of 2.37 and 3.95 for fluoxetine and diltiazem groups, respectively). There was no relationship between patients' improvement and severity of symptoms. Psychological findings based on the hospital anxiety and depression scale were inconsistent (a decrease in mean of 0.143 and 0.57 for fluoxetine and diltiazem groups, respectively; p > 0.05).

Fluoxetine and diltiazem were effective for clinical symptom relief in patients with distal esophageal spasm, but were not promising for improving psychological symptoms. Neither regimen was superior in terms of efficacy. Consequently, it is key to consider side effects and comorbidities when choosing a therapy.

Distal esophageal spasm (DES) is a motility disorder characterized by premature contraction of the esophageal body during single swallows. It is thought to be due to impairment of esophageal inhibitory pathways, but studies to support this are limited. The normal response to multiple rapid swallows (MRS) is deglutitive inhibition of the esophageal body during the MRS sequence. Our aim was to compare the response to MRS in DES patients and healthy control subjects. Response to MRS during HRM was evaluated in 19 DES patients (8 with and 11 without concomitant esophagogastric junction outflow obstruction [EGJOO]) and 24 asymptomatic healthy controls. Patients with prior gastroesophageal surgery, peroral endoscopic myotomy, pneumatic dilation, esophageal botulinum toxin injection within 6 months of HRM, opioid medication use, and esophageal stricture were excluded. Response to MRS was evaluated for complete versus impaired inhibition (esophageal body contractility with distal contractile integral [DCI] > 100 mmHg-sec-cm during MRS), presence of post-MRS contraction augmentation (DCI post MRS greater than single swallow mean DCI), and integrated relaxation pressure (IRP). Impaired deglutitive inhibition during MRS was significantly more frequent in DES compared to controls (89% vs. 0%, P < 0.001), and frequency was similar for DES with versus without concomitant EGJOO (100% vs. 82%, P = 0.48). The proportion of subjects with augmentation post MRS was similar for both groups (37% vs. 38%, P = 1.00), but mean DCI post MRS was higher in DES than controls (3360.0 vs. 1238.9, P = 0.009). IRP was lower during MRS compared to single swallows in all patients, and IRP during MRS was normal in 5 of 8 patients with DES and EGJOO. Our study suggests that impaired deglutitive inhibition during MRS is present in the majority of patients with DES regardless of whether they have concomitant EGJOO, and future studies should explore the usefulness of incorporating response to MRS in the diagnosis of DES.

The use of bibliometrics can help us identify the most impactful articles on a topic or scientific discipline and their influence on clinical practice. We aimed to identify the 100 most cited articles covering esophageal motility disorders and examine their key characteristics.

The Web of Science database was utilized to perform the search, using predefined search terms. The returned dataset was filtered to include full manuscripts written in the English language. After screening, we identified the 100 most cited articles and analyzed them for title, year of publication, names of authors, institution, country of the first author, number of citations and citation rate.

The initial search returned 29,521 results. The top 100 articles received a total of 20,688 citations. The most cited paper was by Inoue et al. (665 citations) who first described peroral endoscopic myotomy (POEM) for treating achalasia. The article with the highest citation rate was the third version of the Chicago Classification system, written by Kahrilas and colleagues. Gastroenterology published most papers on the list (n=32) and accrued the highest number of citations (6,675 citations). Peter Kahrilas was the most cited author (3,650 citations) and, along with Joel Richter, authored the highest number of manuscripts (n=14). Most articles were produced in the USA (n=66) between the years 1991 and 2000 (n=32).

By analyzing the most influential articles, this work is a reference on the articles that shaped our understanding of esophageal motility disorders, thus serving as a guide for future research.

Distal esophageal spasm is a rare motility disorder presenting principally with nonobstructive dysphagia and noncardiac chest pain. In symptomatic patients, the manometric diagnosis is made when >10% of the wet swallows have simultaneous and/or premature contractions intermixed with normal peristalsis. We characterize manometry and barium as complementary diagnostic approaches, and given the intermittent nature of the disorder, one should be always aware that it is almost impossible to rule out spasm. Treatment is difficult; we propose an approach beginning with the least invasive intervention.

Distal esophageal spasm (DES) is a rare motility disorder characterized by premature and rapidly propagated contractions of the distal esophagus. Treatment options are limited and often poorly effective. Peroral endoscopic myotomy (POEM) seems an effective and attractive new treatment option for DES. In this case report we describe some of the difficulties that could arise.

A 84-year old man with therapy-refractory DES and complaints of severe dysphagia and chest pain underwent a POEM procedure under general anesthesia. A longer myotomy was performed to cleave the circular muscle layer from start till end of the spastic contractions.

The length of the myotomy was 16 cm. Hyperactive spastic contractions during the procedure complicated the creation of the submucosal tunnel, extended the duration (134 vs. 60-90 min for achalasia), increased postoperative pain and prolonged hospital admission. Intravenously nitroglycerin peroperative diminished spastic contractions. Postoperative a remnant of spastic contractions was present, proximal to the myotomy, causing persistent symptoms.

Performing POEM for DES is challenging due to reactive hyperactive spastic contractions during the procedure causing technical difficulties and an extended procedure. A long myotomy, several centimeters above the proximal border of the spastic region, is essential to prevent remnants of spasticity.

Autoimmune autonomic ganglionopathy (AAG) is an immune-mediated disorder that leads to various autonomic failures associated with anti-ganglionic acetylcholine receptor antibodies (anti-gAChR-Abs). Diffuse esophageal spasm (DES) is an uncommon esophageal motility disorder. We herein report the case of a 68-year-old woman with DES as a partial symptom of AAG. She presented with chronic esophageal transit failure, constipation, and numbness of the hands and feet, Adie's pupil, thermal hypoalgesia, and decreased deep tendon reflexes. Right sural nerve biopsy showed significantly decreased numbers of small myelinated fibers. Barium swallowing X-ray showed repetitive simultaneous contractions indicating DES in the esophagus. Gastrointestinal endoscopy and CT image showed a dilated esophageal lumen and liquid effusion. Simultaneously, serum anti-gAChR-α3-Ab indicating AAG was detected. After pulse intravenous methylprednisolone (IVMP) and intravenous immunoglobulin therapy (IVIg), the bolus progression and liquid effusion improved, suggesting that DES is an important gastrointestinal symptom of AAG.

Exciting new developments-pharmacologic, endoscopic, and surgical-have arisen for the treatment of many esophageal diseases. Refractory gastroesophageal reflux disease presents a therapeutic challenge, and several new options have been proposed to overcome an insufficient effectiveness of proton pump inhibitors. In patients with distal esophageal spasm, drugs and endoscopic treatments are the current mainstays of the therapeutic approach. Treatment with proton pump inhibitors (or antireflux surgery) should be considered in patients with Barrett's esophagus, since a recent meta-analysis demonstrated a 71% reduction in risk of neoplastic progression. Endoscopic resection combined with radiofrequency ablation is the standard of care in patients with early esophageal adenocarcinoma. Mucosal squamous cancer may also be treated endoscopically, preferably with endoscopic submucosal dissection. Patients with upper esophageal cancer often refrain from surgery. Robot-assisted, thoracolaparoscopic, minimally invasive esophagectomy may be an appropriate option for these patients, as the robot facilitates a good overview of the upper mediastinum. Induction chemoradiotherapy is currently considered as standard treatment for patients with advanced squamous cell carcinoma, while the role of neoadjuvant therapy for adenocarcinoma remains controversial. A system for defining and recording perioperative complications associated with esophagectomy has been recently developed and may help to find predictors of mortality and morbidity.

According to the Chicago classification of esophageal motility disorders, distal esophageal spasm (DES) is defined as premature esophageal contractions (distal latency [DL] <4.5 s) for ≥20% of swallows, in the presence of a normal mean integral relaxation pressure (IRP). However, some patients with symptoms of DES have rapid contractions with a normal DL. The aim of this study was to characterize these patients and compare their clinical characteristics to those of patients classified as DES.

We retrospectively compared clinical characteristics and high-resolution manometry findings of patients with rapid contractions with normal latency to those meeting the Chicago classification criteria for DES.

Over a 3-year period, nine patients were diagnosed with DES and 14 showed rapid contractions in the distal esophagus with normal latency. The latter were younger than DES patients (60 ± 4 vs 72 ± 3 years, p < 0.05). Dysphagia and retrosternal pain occurred to a similar degree in both groups. Weight loss and abnormal barium esophagogram tended to be more frequent in DES patients. There was no difference in contractile front velocity (CFV) and in distal contractile integral (DCI) between patients with DES and rapid contractions with normal latency. Lower esophageal sphincter pressures were not different between groups. However, IRP was significantly higher in DES compared to rapid contractions with normal latency (11.7 ± 0.6 mmHg vs 7.6 ± 1.2 mmHg, p < 0.05), albeit still within the normal range.

These data suggest that patients with simultaneous contractions with normal latency represent a group of patients with many features similar to DES.

Distal esophageal spasm (DES) is a rare esophageal motility disorder associated with dysphagia and chest pain. In 2011, the diagnosis of DES was refined based on the occurrence of premature (rather than rapid) contractions by high-resolution manometry. New therapeutic options have also been recently proposed. Thus, a review on DES incorporating publications since 2012 is timely because of these revisions in definition and management.

DES remains a heterogeneous clinical disorder. Its pathophysiology is still debated and DES might be related to achalasia. Alternatively, it might be secondary to medications, especially opiates. Endoscopic ultrasound might be informative diagnostically by demonstrating muscularis propria hypertrophy and thickening. Botulinum toxin injection in the esophageal body has been shown superior to placebo to relieve symptoms associated with DES. Finally, per oral endoscopic myotomy is a promising therapeutic approach, but may be less effective in DES than in achalasia.

The diagnosis of DES should lead to a systematic search for medication that might promote the occurrence of esophageal dysmotility. Endoscopic treatment of DES (botulinum toxin injection or per oral endoscopic myotomy) should be further evaluated in controlled studies using current diagnostic criteria by high-resolution manometry.

Esophageal hypomotility (EH) is characterized by abnormal esophageal peristalsis, either from a reduction or absence of contractions, whereas spastic motor disorders (SMD) are characterized by an increase in the vigor and/or propagation velocity of esophageal body contractions. Their pathophysiology is not clearly known. The reduced excitation of the smooth muscle contraction mediated by cholinergic neurons and the impairment of inhibitory ganglion neuronal function mediated by nitric oxide are likely mechanisms of the peristaltic abnormalities seen in EH and SMD, respectively. Dysphagia and chest pain are the most frequent clinical manifestations for both of these dysfunctions, and gastroesophageal reflux disease (GERD) is commonly associated with these motor disorders. The introduction of high-resolution manometry (HRM) and esophageal pressure topography (EPT) has significantly enhanced the ability to diagnose EH and SMD. Novel EPT metrics in particular the development of the Chicago Classification of esophageal motor disorders has enabled improved characterization of these abnormalities. The first step in the management of EH and SMD is to treat GERD, especially when esophageal testing shows pathologic reflux. Smooth muscle relaxants (nitrates, calcium channel blockers, 5-phosphodiesterase inhibitors) and pain modulators may be useful in the management of dysphagia or pain in SMD. Endoscopic Botox injection and pneumatic dilation are the second-line therapies. Extended myotomy of the esophageal body or peroral endoscopic myotomy (POEM) may be considered in highly selected cases but lack evidence.

Primary motility disorders of the upper gastrointestinal (GI) tract result from an impairment of the motor function of the esophagus, stomach, and duodenum by malfunction of the enteric nervous system or degeneration of the gastrointestinal muscle layer. Other forms of upper GI motility disorders occur secondary to underlying systemic diseases. The exact pathophysiology of the disturbances within the enteric nervous system of the upper GI tract is not yet clearly understood. For motility disorders resulting from systemic diseases the lack of knowledge with respect to the underlying pathomechanism is even greater. The term functional dyspepsia summarizes some symptoms of the upper abdomen, suggesting a disorder of upper GI motility or perception; however, this link to disturbed physiology has never been convincingly demonstrated. This overview describes therapeutic options for motility disorders of the upper GI tract regarding medicinal, endoscopic and surgical targets. The efficacy of medicinal therapy of upper GI motility disorders is low due to the lack of understanding of the pathophysiology. Therefore, endoscopic and other interventional therapies have to be applied also in the elderly patient group. The restrictions for metoclopramide published by the European Medicines Agency (EMA) in July 2013 have limited the armentarium of medicinal therapy of chronic motility disorders of the upper GI tract.

The following on achalasia and disorders of the esophageal body includes commentaries on controversies regarding whether patients with complete lower esophageal sphincter (LES) relaxation can be considered to exhibit early achalasia; the roles of different mucle components of the LES in achalasia; sensory neural pathways impaired in achalasia; indications for peroral endoscopic myotomy and advantages of the technique over laparoscopic and thorascopic myotomy; factors contributing to the success of surgical therapy for achalasia; modifications to the classification of esophageal body primary motility disorders in the advent of high-resolution manometry (HRM); analysis of the LES in differentiating between achalasia and diffuse esophageal spasm (DES); and appropriate treatment for DES, nutcracker esophagus (NE), and hypertensive LES (HTLES).

Distal esophageal spasm (DES) is an esophageal motility disorder that presents clinically with chest pain and/or dysphagia and is defined manometrically as simultaneous contractions in the distal (smooth muscle) esophagus in ≥20% of wet swallows (and amplitude contraction of ≥30 mmHg) alternating with normal peristalsis. With the introduction of high resolution esophageal pressure topography (EPT) in 2000, the definition of DES was modified. The Chicago classification proposed that the defining criteria for DES using EPT should be the presence of at least two premature contractions (distal latency<4.5 s) in a context of normal EGJ relaxation. The etiology of DES remains insufficiently understood, but evidence links nitric oxide (NO) deficiency as a culprit resulting in a disordered neural inhibition. GERD frequently coexists in DES, and its role in the pathogenesis of symptoms needs further evaluation. There is some evidence from small series that DES can progress to achalasia. Treatment remains challenging due in part to lack of randomized placebo-controlled trials. Current treatment agents include nitrates (both short and long acting), calcium-channel blockers, anticholinergic agents, 5-phosphodiesterase inhibitors, visceral analgesics (tricyclic agents or SSRI), and esophageal dilation. Acid suppression therapy is frequently used, but clinical outcome trials to support this approach are not available. Injection of botulinum toxin in the distal esophagus may be effective, but further data regarding the development of post-injection gastroesophageal reflux need to be assessed. Heller myotomy combined with fundoplication remains an alternative for the rare refractory patient. Preliminary studies suggest that the newly developed endoscopic technique of per oral endoscopic myotomy (POEM) may also be an alternative treatment modality.

Diffuse esophageal spasm (DES) causes chest pain and/or dysphagia in adults. We reviewed charts of 278 subjects 0 to 18 years of age after esophageal manometry to describe the frequency and characteristics of DES in children. Patient diagnoses included normal motility (61%), nonspecific esophageal motility disorder (20%), DES (13%, n=36), and achalasia (4%). Of patients with DES, the most common chief complaint was food refusal in subjects younger than 5 years (14/24, 58%) and chest pain in subjects older than 5 years (4/12, 33%). Comorbid medical conditions, often multiple, existed in 33 subjects. DES should be considered when young children present with food refusal.

The concept of esophageal spastic disorders encompasses spastic achalasia, distal esophageal spasm, and jackhammer esophagus. These are conceptually distinct in that spastic achalasia and distal esophageal spasm are characterized by a loss of neural inhibition, whereas jackhammer esophagus is associated with hypercontractility. Hypercontractility may also occur as a result of esophagogastric junction outflow obstruction or inflammation. The diagnosis of jackhammer esophagus as a primary motility disorder is based on the characteristic manometric findings after ruling out mechanical obstruction and eosinophilic esophagitis. Despite the differences in pathophysiology among the esophageal spastic disorders, their management is similar.

Spastic disorders of the esophagus, associated with rapid esophageal propagation velocity, are classically associated with dysphagia and/or chest pain. The aim of this study was to characterize patients with slow esophageal propagation velocity (SPV) on high-resolution esophageal manometry (HRM).

A review of patients undergoing HRM was conducted during 1-year study period. Patients with achalasia, aperistalsis, and diffuse esophageal spasm were excluded. Patients with contractile front velocity (CFV) ≤ 2.3 cm s(-1) were defined as having SPV, whereas normal propagation velocity (NPV) was defined as ≥ 2.6 cm s(-1). A composite isobaric contour of all swallows for each patient was generated to determine composite distal contraction latency (cDL).

A total of 650 HRMs were reviewed and 552 met inclusion criteria. 173 patients had SPV and 339 had NPV. There was a greater female predominance in the SPV group compared with NPV (75.7%vs 66.4%, P = 0.03). Patients in the SPV group reported more dysphagia for solids (66.3%vs 53.3%; P = 0.004) and nausea (68.6%vs 59.0%; P = 0.04) than NPV group. Dysphagia for solids was the only symptom significantly associated with SPV group (OR = 2.21, CI = 1.21-4.02; P = .01). There was a negative correlation between CFV and cDL, r = -0.494, P < 0.001.

Patients with SPV have a higher prevalence of dysphagia for solids and nausea when compared with NPV. Dysphagia for solids was the only symptom significantly associated with SPV group. Thus, abnormal esophageal propagation velocity (both slow and rapid) is associated with dysphagia.

Distal oesophageal spasm is a rare and under-investigated motility abnormality. Recent studies indicate effective bolus transit in varying percentages of distal oesophageal spasm patients.

Explore functional aspects including contraction onset velocity and contraction amplitude cut-off values for simultaneous contractions to predict complete bolus transit.

We re-examined data from 107 impedance-manometry recordings with a diagnosis of distal oesophageal spasm. Receiver operating characteristic analysis was conducted, regarding effects of onset velocity on bolus transit taking into account distal oesophageal amplitude and correcting for intra-individual repeated measures.

Mean area under the receiver operating characteristic curve for saline and viscous swallows were 0.84±0.05 and 0.84±0.04, respectively. Velocity criteria of >30 cm/s when distal oesophageal amplitude>100 mmHg and 8 cm/s when distal oesophageal amplitude<100 mmHg for saline and 32cm/s when distal oesophageal amplitude>100 mmHg and >7 cm/s when distal oesophageal amplitude<100 mmHg for viscous had a sensitivity of 75% and specificity of 80% to identify complete bolus transit. Using these criteria, final diagnosis changed in 44.9% of patients. Abnormal bolus transit was observed in 50.9% of newly diagnosed distal oesophageal spasm patients versus 7.5% of patients classified as normal. Distal oesophageal spasm patients with distal oesophageal amplitude>100 mmHg suffered twice as often from chest pain than those with distal oesophageal amplitude<100 mmHg.

The proposed velocity cut-offs for diagnosing distal oesophageal spasm improve the ability to identify patients with spasm and abnormal bolus transit.

Diffuse esophageal spasm (DES) is a rare primary motility disorder of unknown cause, that can be found in patients complaining of chest pain and dysphagia and in whom ischemic heart disease and GERD have been excluded. The manometric hallmark of DES is the presence of simultaneous contractions in the distal esophagus alternating with a normal peristalsis. Even at specialized esophageal motility laboratories, DES is considered an uncommon diagnosis. In this review, the authors discuss the clinical and diagnostic aspects of this disease, as well as the possible therapeutic options (medical, endoscopic or surgical therapy). Surgery (esophageal myotomy performed through a thoracotomy or with a thoracoscopic access) seems to have a better outcome than medical or endoscopic treatment, and it is considered "the last resource" in these patients. However, satisfactory results are reported, from highly skilled centers, in only about 70% of treated cases, certainly inferior to those achieved in other esophageal disorders. The role of surgery in this disease requires therefore further study, even if controlled trials are probably difficult to perform, due to the rarity of the disease.

Diffuse esophageal spasm (DES) remains insufficiently understood. Here we aimed to summarize the demographic, clinical, radiographic, and manometric features in a large cohort of patients with DES. We identified all consecutive patients diagnosed with DES from 2000 to 2006 at Mayo Clinic Florida. The computerized records of these patients were reviewed to extract relevant information. We performed 2654 esophageal motilities during that period. There were 108 patients with esophageal spasm, and 55% were female. Median age was 71 years. The most common leading symptom was dysphagia in 55, followed by chest pain in 31. Weight loss occurred in 28 patients. The median of time from onset of symptoms to diagnosis was 48 months (range 0-480), with a median of time from the first medical consultation to diagnosis of 8 months (range 0-300). The most frequent comorbidities were hypertension and psychiatric problems. At presentation, 81 patients were taking acid-reducing medications, and 49 patients were taking psychotropic drugs. An abnormal esophagogram was noted in 46 of 76 patients with this test available, but most radiographic findings were nonspecific with the typical 'corkscrew' appearance seen in only three patients. Gastroesophageal reflux disease (GERD) was diagnosed by pH testing or endoscopy in 41 patients. We did not find any difference between the rate of simultaneous contractions or esophageal amplitude between patients with a leading symptom of dysphagia and those with chest pain. DES is an uncommon motility disorder that often goes unrecognized for years. Physicians should be aware of the clinical heterogeneity of DES and consider motility testing early in the course of unexplained esophageal symptoms. Given the high prevalence of GERD in DES, the role of GERD and the impact of acid-reducing therapy in DES deserve further study.

The evolution of nonspecific esophageal motility disorders remains unclear. The aim of this study was to investigate whether nonspecific esophageal motility disorders progress into specific motility disorders and whether such progression is predictable.

Seventy-six symptomatic patients (49 males, 27 females, mean age 57 ± 16 years) with newly diagnosed nonspecific esophageal motility disorders were prospectively registered and followed-up. Follow-up visits, with structured interviews and manometric re-evaluation, were recommended biannually and whenever symptoms exacerbated.

Forty-three patients were followed for up to 4 years, symptoms worsened in 30% of patients, resolved in 26%, improved in 14% and were unchanged in 30%. Twenty-eight patients agreed to undergo manometric re-evaluation. Fifteen (53.6%) of these patients showed a progression to achalasia. The remaining patients continued to display features of nonspecific esophageal motility disorders (32%) or had normal motility (11%). The only significant association could be determined between age and progression to achalasia reaching nearly 100% in patients' ≤46 years of age. In contrast, none of the patients' ≥68 years progressed.

More than half of the patients in our cohort with nonspecific esophageal motility disorders showed a transition into achalasia. Neither manometric nor clinical findings predicted the progression of nonspecific esophageal motility disorders. However, young patients were more likely to progress to achalasia.

The manometric diagnosis of distal esophageal spasm (DES) uses "simultaneous contractions" as a defining criterion, ignoring the concept of short latency distal contractions as an important feature. Our aim was to apply standardized metrics of contraction velocity and latency to high-resolution esophageal pressure topography (EPT) studies to refine the diagnosis of DES.

Two thousand consecutive EPT studies were analyzed for contractile front velocity (CFV) and distal latency to identify patients potentially having DES. Normal limits for CFV and distal latency were established from 75 control subjects. Clinical data of patients with reduced distal latency and/or rapid CFV were reviewed.

Of 1070 evaluable patients, 91 (8.5%) had a high CFV and/or low distal latency. Patients with only rapid contractions (n = 186 [17.4%] using conventional manometry criteria; n = 85 [7.9%] using EPT criteria) were heterogeneous in diagnosis and symptoms, with the majority ultimately categorized as weak peristalsis or normal. In contrast, 96% of patients with premature contraction had dysphagia, and all (n = 24; 2.2% overall) were ultimately managed as spastic achalasia or DES.

The current DES diagnostic paradigm focused on "simultaneous contractions" identifies a large heterogeneous set of patients, most of whom do not have a clinical syndrome suggestive of esophageal spasm. Incorporating distal latency into the diagnostic algorithm of EPT studies improves upon this by isolating disorders of homogeneous pathophysiology: DES with short latency and spastic achalasia. We hypothesize that prioritizing measurement of distal latency will refine the management of these disorders, recognizing that outcomes trials are necessary.

Diffuse esophageal spasm (DES) has been reported as a potential cause of dysphagia or chest pain; however, the patho-physiology of DES is unclear. The aim of this study was to examine the manometric correlates of dysphagia and chest pain in this patient population. All patients undergoing manometry at our institution are entered into a prospectively maintained database. After institutional review board approval, the database was queried to identify patients meeting criteria for DES (≥20% simultaneous waves with greater than 30 mm Hg pressure in the distal esophagus). The patient-reported symptoms and manometric data, along with the results of a 24-hour pH study (if done), were extracted for further analysis. Out of 4923 patients, 240 (4.9%) met the manometric criteria for DES. Of these, 217 patients had complete manometry data along with at least one reported symptom. Of the patients with DES, 159 (73.3%) had dysphagia or chest pain as a reported symptom. Patients reporting either dysphagia or chest pain had significantly higher lower esophageal sphincter (LES) pressure than patients without these symptoms (P= 0.007). Significant association was noted between reported dysphagia and percentage of simultaneous waves. Chest pain did not correlate with percent of simultaneous waves, mean amplitude of peristalsis, or 24-hour pH score. The origin of reported chest pain in patients with DES is not clear but may be related to higher LES pressure. Simultaneous waves were associated with reported dysphagia. Using current diagnostic criteria, the term DES has no clinical relevance.

A defining feature of peristalsis is propagation velocity, which determines the timing of the distal contraction relative to the swallow. This study aimed to exploit a coordinate-based strategy to quantify the normal latency of the distal esophageal contraction as a measure of propagation velocity optimized for high-resolution esophageal pressure topography (EPT) studies.

EPT studies for 75 healthy volunteers were merged in a computer simulation. Swallows were synchronized and analyzed as a 100 × 200 pixel grid that normalized esophageal length from the pharynx to the stomach for a 20-s period to first calculate a composite for each individual and then to establish normative values for the morphology and latency of the distal contraction among individuals.

Stereotyped landmarks in composite EPT studies were pressure troughs in the proximal and distal esophagus isolating the distal segment and the contractile deceleration point (CDP) localizing the termination of peristalsis in the distal segment. Distal contractile latency was timed to the CDP (median 6.0 s, 95% confidence interval 4.8-7.6 s) and to lower esophageal sphincter (LES) contraction (median 9.2 s, 95% confidence interval 6.5-11.5 s). Illustrative examples are shown of rapidly conducted contractions with normal or short latency, suggesting short latency to be the preferable EPT metric of rapid propagation.

The proposed scheme, utilizing the topographic coordinates of contraction relative to the swallow as an alternative to conventional measures of peristaltic velocity, lays the foundation for a physiologically grounded classification of peristaltic abnormalities in EPT. Future studies will test the clinical utility of this scheme.

 Diffuse esophageal spasm (DES) is characterized on manometry by a combination of simultaneous contractions and normal swallows. The aim of this study was to examine the manometric characteristics of simultaneous and 'normal' swallows in patients with DES patients compared with normal controls.

Manometric studies from 69 patients with DES and 20 controls were analysed to determine the proportion of normal, hypertensive, ineffective and simultaneous contractions, and the velocity of propagation along the esophagus, the duration and amplitude of contraction and the relaxation characteristics (nadir and duration) of the lower esophageal sphincter.

 The propagation velocity was the only significant difference between normal swallows and simultaneous contractions in DES patients (middle third: 49.2 VS 101.2 mm s(-1), P ≤ 0.001 lower third: 44.1 VS 88.7 mm s(-1), P ≤ 0.001). 'Normal' swallows in patients with DES had a greater velocity of propagation than those in age-matched control subjects (middle third: 49.2 VS 37.0 mm s(-1), P = 0.02, lower third: 44.1 VS 23.3 mm s(-1), P ≤ 0.001).

 As expected, simultaneous contractions of DES patients differ from 'normal' swallows in DES patients mainly regarding the velocity of propagation of contraction but are similar in amplitude, however 'normal' swallows of DES patients are also more rapidly propagated along the esophagus than normal swallows of a control group suggesting that all swallows in DES are affected to some degree by the same process.

Diffuse esophageal spasm is a primary esophageal motility disorder. The prevalence is 3-10% in patients with dysphagia and treatment options are limited. This review summarizes the treatment of diffuse esophageal spasm, including pharmacotherapy, endoscopic treatment, and surgical treatment with a special focus on botulinum toxin injection. A PubMed search was performed to identify the literature using the search items diffuse esophageal spasm and treatment. Pharmacotherapy with smooth muscle relaxants, proton pump inhibitors, and antidepressants was suggested from small case series and uncontrolled clinical trials. Endoscopic injection of botulinum toxin is a well-studied treatment option and results in good symptomatic benefit in patients with diffuse esophageal spasm. Surgical treatment was reported in patients with very severe symptoms refractory to pharmacologic treatment. This article summarizes the present knowledge on the treatment of diffuse esophageal spasm with a special emphasis on botulinum toxin injection. Endoscopic injection of botulinum toxin is presently the best studied treatment option but many questions remain unanswered.

Achalasia esophagus is characterized by loss of peristalsis and incomplete esophagogastric junction (EGJ) relaxation. We studied mechanisms of esophageal emptying in patients with achalasia using simultaneous high-resolution manometry, multiple intraluminal impedance, and high-frequency intraluminal ultrasonography image recordings.

Achalasia was categorized into 3 subtypes, based on the esophageal response to swallows: types 1 and 2 were defined by simultaneous pressure waves of <30 mm Hg and >30 mm Hg, respectively, and type 3 was defined by spastic simultaneous esophageal contractions.

Based on high-resolution manometry, the predominant achalasia pattern of type 2 was characterized by a unique motor pattern that consisted of upper esophageal sphincter contraction, simultaneous esophageal pressure (pan-esophageal pressurization), and EGJ contraction following swallows. High-frequency intraluminal ultrasonography identified longitudinal muscle contraction of the distal esophagus as the cause of pan-esophageal pressurization in type 2 achalasia. Multiple intraluminal impedance revealed that esophageal emptying occurred intermittently (36% swallows) during periods of pan-esophageal pressurization. Patients with achalasia of types 1 and 3 had no emptying or relatively normal emptying during most swallows, respectively.

In achalasia, esophageal emptying results from swallow-induced longitudinal muscle contraction of the distal esophagus, which increases esophageal pressure and allows flow across the nonrelaxed EGJ.

The concept of high-resolution manometry (HRM) is to use sufficient pressure sensors such that intraluminal pressure can be monitored as a continuum along luminal length much as time is viewed as a continuum in conventional manometry. When HRM is coupled with pressure topography plots, pressure amplitude is transformed into spectral colors with isobaric conditions indicated by same-colored regions on the display. Together, these technologies are called high-resolution esophageal pressure topography (HREPT). HREPT has several advantages compared with conventional manometry, the technology that it was designed to replace. (i) The contractility of the entire esophagus can be viewed simultaneously in a uniform format, (ii) standardized objective metrics can be systematically applied for interpretation, and (iii) topographic patterns of contractility are more easily recognized and have greater reproducibility than with conventional manometry. Compared with conventional manometry, HREPT has improved sensitivity for detecting achalasia, largely due to the objectivity and accuracy with which it identifies impaired esophagogastric junction (EGJ) relaxation. In addition, it has led to the subcategorization of achalasia into three clinically relevant subtypes based on the contractile function of the esophageal body: classic achalasia, achalasia with esophageal compression, and spastic achalasia. Headway has also been made in understanding hypercontractile conditions, including diffuse esophageal spasm and a newly described entity, spastic nutcracker. Ultimately, clinical experience will be the judge, but it seems likely that HREPT data, along with its well-defined functional implications, will improve the clinical management of esophageal motility disorders.

The current available methods for diagnosis of GORD are symptom questionnaires, catheter and wireless pH-metry, impedance-pH monitoring and Bilitec(@). Osophageal pH monitoring allows both quantitative analysis of acid reflux and assessment of reflux-symptom association. Impedance-pH monitoring detects all types of reflux (acid and non-acid) and allows assessment of proximal extent of reflux, a relevant parameter for understanding symptoms perception and extraoesophageal symptoms. Bilitec provides a quantitative assessment of duodeno-gastro-oesophageal reflux. Oesophageal motor abnormalities have been associated with GORD symptoms as well as chest pain and dysphagia. High-resolution manometry contributed to re-classify oesphageal motor disorders. However, barium swallows are still essential for evaluation of oesophageal anatomy and combined oesophageal manometry-impedance can assess oesophageal motility and bolus transit simultaneously in a non-radiological way. Still in experimental phase, high-frequency ultrasound allows monitoring of the oesophageal wall thickness and exaggerated longitudinal muscle contraction that might be associated to chest pain and dysphagia. This chapter provides a critical evaluation of the clinical application of these techniques.

The purpose of this study was to determine the frequency and appearance of esophageal wall thickening on CT scans in a series of patients with findings of diffuse esophageal spasm on barium studies.

CT revealed marked esophageal wall thickening in seven (21%) of 33 patients who had findings of diffuse esophageal spasm on barium studies. CT showed significantly greater esophageal wall thickening in the lower thoracic esophagus 5 cm above the gastroesophageal junction than in the upper thoracic esophagus at the level of the aortic arch or in the midthoracic esophagus at the level of the carina (p < 0.01). This esophageal wall thickening corresponded to the presence of multiple strong nonperistaltic contractions in the lower thoracic esophagus on barium studies. Our findings suggest that diffuse esophageal spasm should be included in the differential diagnosis when CT shows smooth circumferential wall thickening in the lower half of the thoracic esophagus, particularly in elderly patients with dysphagia or chest pain.

Taking a careful history is vital for the evaluation of dysphagia. The history will yield the likely underlying pathophysiologic process and anatomic site of the problem in most patients, and is crucial for determining whether subsequently detected radiographic or endoscopic 'anomalies' are relevant or incidental. Although the symptoms of pharyngeal dysphagia can be multiple and varied, the typical features of neurogenic pharyngeal dysphagia are highly specific, and can accurately distinguish pharyngeal from esophageal disorders. The history will also dictate whether the next diagnostic procedure should be endoscopy, a barium swallow or esophageal manometry. In some difficult cases, all three diagnostic techniques may need to be performed to establish an accurate diagnosis. Stroke is the most common cause of pharyngeal dysphagia. A videoradiographic swallow study is vital in such cases to determine the extent and timing of aspiration and the severity and mechanics of dysfunction as a prelude to therapy.

Diffuse esophageal spasm is a motility disorder of undetermined cause. The optimal treatment remains controversial, and evidence-based data are lacking. Several medical treatment modalities have been proposed, but none has emerged as the treatment of choice. Patients who do not respond to medical therapy may be considered for surgical treatment. The surgical treatment of diffuse esophageal spasm is based on similar principles to the treatment of achalasia. A long esophageal myotomy is done to divide the hypertrophied circular muscle that is frequently noted in diffuse esophageal spasm. To protect against postoperative reflux, an antireflux procedure may be added. However, the surgical treatment of diffuse esophageal spasm has not been subjected to randomized clinical trials. The purpose of this article is to provide a review of the available literature regarding the surgical management of the diffuse esophageal spasm. In particular, we offer an appraisal of surgical outcomes, the effects of surgery on manometric and radiologic parameters (when available), complications, and mortality.

The purpose of this article is to review the clinical features, pathophysiology, diagnosis, and management of patients with diffuse esophageal spasm (DES). The PubMed database was searched with a focus on recent publications, using keywords "DES," plus "epidemiology," "prevalence," "diagnosis," "pathogenesis," "calcium channel blocker," "nitrates," "botulinum toxin," "antidepressants," "dilation," and "myotomy." The reference lists of papers identified in the initial PubMed search were reviewed for further relevant publications.

The role of surgery in the management of patients with diffuse oesophageal spasm (DOS) remains controversial. The aim of this study was to assess functional results after extended myotomy for DOS.

This prospective study evaluated 20 patients who had extended myotomy (14 cm on the oesophagus and 2 cm below the oesophagogastric junction) with anterior fundoplication via a laparotomy for severe DOS. Median follow-up was 50 (range 6-84) months. Functional data were assessed by means of dysphagia (range 0-3), chest pain (range 0-3) and overall clinical (range 0-12, including dysphagia, chest pain, regurgitation, gastro-oesophageal reflux) scores.

All patients had severe DOS. The median preoperative overall clinical score was 6 (range 3-8) with a dysphagia score of at least 2. Median postoperative functional scores were significantly lower than preoperative values (overall clinical score 1 versus 6, dysphagia score 0 versus 3, chest pain score 0 versus 2). At final follow-up, good or excellent results were obtained for overall clinical score in 16 patients, for dysphagia score in 18 and for chest pain score in all 20 patients. Postoperative gastro-oesophageal reflux was noted in two of the 20 patients.

Extended myotomy with anterior fundoplication is an effective treatment for severe DOS. Medium-term postoperative functional results were excellent, especially in terms of dysphagia and chest pain.

Motor abnormalities of the oesophagus are characterised by a chronic impairment of the neuromuscular structures that co-ordinate oesophageal function. The best-defined entity is achalasia, which is discussed in a separate chapter. Other motor disorders with clinical relevance include diffuse oesophageal spasm, oesophageal dysmotility associated with scleroderma, and ineffective oesophageal motility. These non-achalasic motor disorders have variable prevalence but they could be associated with invalidating symptoms such as dysphagia, chest pain and gastro-oesophageal reflux disease. New oesophageal diagnostic techniques, including high-resolution manometry, high-frequency intraluminal ultrasound and intraluminal impedance, allow (1) better definition of peristalsis and sphincter function, (2) assessment of changes in oesophageal wall thickness, and (3) evaluation of pressure gradients within the oesophagus and across the sphincters that can produce normal or abnormal patterns of bolus transport. This chapter discusses recent advances in physiology, pathophysiology, diagnosis and treatment of non-achalasic oesophageal motor disorders.

Diffuse esophageal spasm (DES) and achalasia share both clinical and manometric characteristics. Some reports support the notion of progression of DES to achalasia. However, there are currently no prospective data in support of this theory. To assess prospectively the rate of manometric progression of DES to achalasia. Manometry tracings of DES patients diagnosed between 1992 and 2003 were independently reviewed blindly and agreed on by two esophageal experts. Patients with DES who agreed to undergo repeat esophageal manometry constituted the study cohort. Follow-up manometry tracings were evaluated blindly and independently by the same two interpreters to determine the rate of manometric progression to achalasia. Predictors of manometric progression were assessed. A total of 32 patients were diagnosed with DES between 1992-2003. Twelve patients (9M/3F; median age 62 years) agreed to participate and underwent second manometry (mean +/- SD follow-up of 4.8 +/- 3.4 years). Achalasia was diagnosed on follow-up manometry in one patient (8%), seven (58%) patients continued to have DES, three (25%) had normal motility, and one (8%) had nutcracker esophagus. There were no predictors of progression to achalasia based on the initial manometry parameters. A subgroup of DES patients with initial low esophageal body amplitude developed increase in esophageal simultaneous contractions on follow-up similar to the patient who evolved to achalasia. Following were the results. 1) Progression from DES to achalasia is uncommon. 2) DES patients with low esophageal body amplitude may develop increased simultaneous contractions over time. 3) DES remains an elusive diagnosis clinically and manometrically.

The diagnostic values of particular symptoms centred on oesophagus, among patients with suspected oesophageal motility abnormality or pathological acid exposure, are not yet fully understood. The aim of this study was to determine the predictive accuracy of these symptoms in diagnosis of oesophageal motility disorder or pathological acid exposure. PATIENTS AND METHODS.: A total of 462 patients who had undergone conventional oesophageal manometry and ambulatory 24-h pH monitoring to investigate a clinical suspicion of oesophageal motility disorder and pathological acid exposure were enrolled in this study. According to their principal complaints, the patients were divided into the dysphagia category, the non-cardiac chest pain category, the gastrooesophageal reflux disease-related symptom category and the extraoesophageal symptom category.

Two hundred and two (44%) out of 462 patients yielded abnormal findings on manometry and/or pH monitoring. Dysphagia was associated with a likelihood ratio (LR) of 2.11 [95% confidence interval (CI), 1.02-4.00)] in patients exhibiting a combination of oesophageal motility abnormality and pathological acid exposure. During oesophageal manometry, the dysphagia substantially increased the likelihood of classic achalasia (LR, 6.24; 95% CI, 3.32-8.78) and diffuse oesophageal spasm (LR, 3.58; 95% CI, 1.03-7.12). When the patients with dysphagia were divided into two groups according to the severity of their symptoms, classic achalasia was significantly frequent in patients with severe dysphagia (P = 0.016). On the other hand, non-cardiac chest pain was the clinical factor that reduced the likelihood of classic achalasia (LR, 0.22; 95% CI, 0.04-0.93). The distribution of pathological acid exposure was significantly frequent between the groups of patients with and without gastrooesophageal reflux disease-related symptom (P = 0.011).

A small number of oesophageal symptoms are helpful in predicting the likelihood of abnormal findings on oesophageal tests among patients with a clinical suspicion of oesophageal motility disorder and pathological acid exposure. The most useful finding is a severe dysphagia, which is likely to have classic achalasia.

Radiologic studies can be helpful when evaluating patients who are suspected of having esophageal motility disorders. Performing studies of the highest technical quality yields the most definitive results. The esophagus should be assessed for anatomic and functional abnormalities that may account for presenting symptoms. Motility disorders such as achalasia and scleroderma have specific radiographic findings that are described in this article; however, some motility disorders of the esophagus have nonspecific radiographic findings. In those cases, it is imperative that clinical and manometric information be combined with radiographic findings to provide accurate diagnoses. The radiographic examinations that are most commonly used include barium esophagography and nuclear medicine examinations. This article emphasizes the use of barium examinations to assess esophageal motility.

The objective of this study is to determine the prevalence of esophageal disorders (ED) associated with recurrent chest pain (RCP) and the utility of esophageal functional tests (EFT) in the study of these patients. The cross-sectional study was conducted at Hospital Clínico de La Frontera, Chile. One hundred and twenty-three patients with RCP were studied using esophageal manometry, edrophonium stimulation and 24-h pH monitoring. The performance of EFT was considered acceptable when they were capable of finding ED. To state the probability that RCP had an esophageal origin, patients were classified according to whether their pain had a probable, possible or unlikely esophageal origin. The prevalence of ED was determined according to diagnoses obtained after applying EFT and a multivariate analysis was performed to examine the association between the esophageal origin of RCP and ED. Rates of correct diagnosis of 65.9%, 56.9% and 31.7% was verified for 24-h pH monitoring, esophageal manometry and edrophonium stimulation, respectively. In 38.2% of patients with RCP, the pain was probably of esophageal origin, in 42.3% there was a possible esophageal origin and in 19.5% an unlikely esophageal origin. A 44.7% prevalence of GERD, 26.8% of GERD with secondary esophageal motor dysfunction and 8.9% of pure esophageal motor dysfunction were verified. The multivariate analysis allowed us to verify the association between the probability of esophageal origin of RCP, the variables RCP duration, esophagitis and dysphagia coexistence (P= 0.037, P= 0.030 and P= 0.024, respectively), and a statistically significant association between ED and dysphagia coexistence (P= 0.028). A high prevalence of ED was identified in patients with RCP.

We sought to reassess the function and clinical characteristics of the lower esophageal sphincter in a series of patients with radiographically defined diffuse esophageal spasm.

In reviewing records in the radiology database at our hospital, we identified 14 patients with diffuse esophageal spasm confirmed on barium studies who also underwent esophageal manometry. The radiographic findings were reviewed and correlated with the manometric findings. Medical records were also reviewed to determine the clinical presentation, treatment, and patient course.

All 14 patients were symptomatic, presenting with dysphagia, chest pain, or both. All the barium studies revealed intermittently absent or weakened peristalsis, with nonperistaltic contractions that were moderate in six patients (43%) and marked in eight patients (57%) (contractions nearly obliterating the lumen in six and completely obliterating the lumen in two). Nine patients (64%) had impaired opening of the lower esophageal sphincter, manifested by beaklike narrowing of the distal esophagus, and five (36%) had normal opening of the lower esophageal sphincter. Manometry revealed abnormal peristalsis in all 14 patients, with repetitive simultaneous contractions in eight (57%) and lower esophageal sphincter dysfunction in 12 (86%). All eight patients with lower esophageal sphincter dysfunction or incomplete relaxation of the lower esophageal sphincter on barium studies or manometry who were treated with the Clostridium botulinum toxin or endoscopic balloon dilatation had a positive response.

Our preliminary data show that diffuse esophageal spasm is characterized on barium studies by frequent lower esophageal sphincter dysfunction rather than a classic corkscrew appearance. Barium and manometric studies may have complementary roles in the evaluation of patients with diffuse esophageal spasm.

In chronically ill children who refuse to eat, surgery to correct anatomic problems and behavioral treatments to overcome oral aversion often succeed. A few patients fail with standard treatments. The aims of the study were to: 1) investigate motility and gastric sensory abnormalities and 2) describe treatment that was individualized based on pathophysiology in children who failed surgery and behavioral treatments.

We studied 14 patients (age 1.5-6; mean 2.5; M/F: 7/7). All had a lifelong history of food aversion and retching or vomiting persisting after feeding therapy and fundoplication. All were fed through gastrostomy or gastro-jejunostomy tubes. We studied esophageal and antroduodenal manometry, and gastric volume threshold for retching. We identified when gastric antral contractions were associated with retching and pain. A multidisciplinary treatment program included a variable combination of continuous post-pyloric feedings, drugs to decrease visceral pain, drugs for motility disorders, and behavioral, cognitive, and family therapy. We interviewed parents 2-6 months following testing to evaluate symptoms, mode of feeding and emotional health.

We found a motility disorder alone in 2, decreased threshold for retching alone in 5 and both motility and sensory abnormalities in 7. After treatment, 6 of 14 (43%) began eating orally and 80% had improved emotional health. Retching decreased from 15 episodes per day to an average of 1.4 per day (p <0.01).

Upper gastrointestinal motor and/or sensory disorders contributed to reduced quality of life for a majority of children and families with persistent feeding problems. A multidisciplinary approach improved symptoms and problems in these children

Previous studies have suggested that ineffective esophageal motility (IEM) may be a marker for gastroesophageal reflux disease (GERD), particularly supraesophageal reflux disease. We evaluated the relationship between esophageal acid exposure and esophageal body motility in patients undergoing both esophageal manometry and 24-h pH metry in the absence of antisecretory therapy.

We conducted a retrospective database review of 84 patients (mean age 47 yr, 46% male) evaluated in our GI physiology laboratory. The indication for testing was recorded and characterized as esophageal or supraesophageal. Abnormal esophageal acid exposure was defined as a distal esophageal pH <4 for more than 4.2% of the total monitoring time (>6.3% upright, >1.2% supine) or a proximal esophageal acid exposure time of greater than 1.1% total (>1.3% upright, 0% supine). IEM was defined as more than two of 10 ineffective peristaltic waves.

Seventy-two patients had esophageal-presenting symptoms, and 12 had supraesophageal symptoms. The prevalence of abnormal esophageal acid exposure was similar in patients with esophageal and supraesophageal symptoms (69% vs 92%, p = 0.17). Abnormal motility was identified in 26 patients (31%). IEM was the most common motility disturbance (77%, 20 patients). The frequency of motility disorders was similar in patients with and without abnormal esophageal acid exposure (30% vs 35%, p = 0.79), in patients with esophageal or supraesophageal symptoms (32% vs 25%, p = 0.75, for all patients; 30% vs 27%, p = 1.00, for patients with abnormal esophageal acid exposure), and among upright, supine, and combined refluxers (33%, 9%, and 35%, p = 0.26).

IEM does not stand alone as a significant marker for the presence of GERD in general or supraesophageal reflux disease in particular.

This report presents the long-term subjective and objective results of esophageal myotomy and fundoplication by thoracotomy in the treatment of esophageal spastic disorders. From 1977 to 1995, a total of 16 patients with esophageal spastic disorders were referred to our unit and underwent a myotomy with an added partial (n = 12) or total (n = 4) fundoplication. The median follow-up was 6 years. Assessments included clinical evaluation, esophagogram, radionuclide emptying, manometry, 24-hour pH studies, and endoscopy. From the global results, patients with pure spastic disorders (n = 8) were compared to patients with spastic disorders with an accompanying epiphrenic diverticulum (n = 8). There were no deaths, and morbidity was minimal. Preoperative symptoms were similar in all patients with spastic disorders. After surgery, the clinical outcome was significantly better in patients with spastic disorders in the presence of a diverticulum. Delays in esophageal emptying persisted after surgery. Patients with pure spastic disorders showed more diffuse functional abnormalities. Patients with a diverticulum had dysfunction mostly in the distal esophagus. Both groups showed signs of coordination and relaxation abnormalities in the lower esophageal sphincter. Myotomy with antireflux surgery resulted in decreased propulsion and contraction pressure. The resting pressure and relaxation at the level of the lower esophageal sphincter improved, but the coordination abnormalities remained. Failure resulted from either reflux complications (n = 1) or obstruction (n = 4). Patients with spastic disorders plus a diverticulum showed better clinical results and improved esophageal function after surgery when compared to patients with pure spastic disorders.

Oesophageal motility disorders comprise various abnormal manometric patterns which usually present with dysphagia or chest pain. Some, such as achalasia, are diseases with a well defined pathology, characteristic manometric features, and good response to treatments directed at the pathophysiological abnormalities. Other disorders, such as diffuse oesophageal spasm and hypercontracting oesophagus, have no well defined pathology and could represent a range of motility changes associated with subtle neuropathic changes, gastro-oesophageal reflux, and anxiety states. Although manometric patterns have been defined for these disorders, the relation with symptoms is poorly defined and the response to medical or surgical therapy unpredictable. Hypocontracting oesophagus is generally caused by weak musculature commonly associated with gastro-oesophageal reflux disease. Secondary oesophageal motility disorders can be caused by collagen vascular diseases, diabetes, Chagas' disease, amyloidosis, alcoholism, myxo-oedema, multiple sclerosis, idiopathic pseudo-obstruction, or the ageing process.