Symptomatic Diffuse Esophageal Spasm Research Articles

Symptomatic diffuse esophageal spasm as a major ictal manifestation of post-traumatic epilepsy: a case report

Post-traumatic epilepsy (PTE) can create diagnostic confusion when typical epileptic seizures are not manifest. Abdominal symptoms as a manifestation of PTE are rare in this setting. We present a 43-year-old female with paroxysmal chest and abdominal pain, nausea, salivation, and intermittent dysphagia. Esophageal testing demonstrated diffuse esophageal spasm, but smooth muscle relaxants provided no relief. Finally, after history revealed that a motor vehicle accident temporally preceded symptom onset, video electroencephalography confirmed PTE. Therapy with anti-epileptic drug completely resolved symptoms, and the esophageal motor pattern normalized. We speculate that abnormal epileptiform discharges from the seizure focus altered cerebral input to intrinsic esophageal innervation, resulting in inhibitory dysfunction and a picture resembling diffuse esophageal spasm. This is the first report of symptomatic esophageal spasm as a major ictal manifestation of PTE.

Symptomatic Improvement of Diffuse Esophageal Spasm after Botulinum Toxin Injection

Diffuse esophageal spasm, an uncommon esophageal motility disorder, has recently been defined using high-resolution manometry. Patients with distal esophageal spasm usually complain of chest pain or dysphagia. The etiology and pathophysiology of this disorder are poorly known, and treatment options are limited. However, some options to improve symptoms are available, including endoscopic injection of botulinum toxin. Nevertheless, few reports have described the effects of endoscopic injection of botulinum toxin in patients with symptomatic diffuse esophageal spasm with clear endoscopic and high-resolution manometry images. Here, we report a case of diffuse esophageal spasm diagnosed with high-resolution manometry and treated by endoscopic injection of botulinum toxin with good results at the 7-month follow-up.

A Case of Symptomatic Diffuse Esophageal Spasm During Multiple Rapid Swallowing Test on High-Resolution Manometry

Diffuse esophageal spasm (DES) is an uncommon motility disorder of unknown etiology in which the abnormal motility has been offered as a possible cause for the patient's dysphagia or chest pain. Esophageal manometry is the gold standard for the diagnosis of DES and the diagnostic hallmark is identification of simultaneous contractions in at least 20% of wet swallows, alternating with normal peristalsis. Recently, a new diagnostic technique, high-resolution manometry has been reported to improve the accuracy and detail in describing esophageal function. We report a female patient with intermittent dysphagia and chest pain occurring only when swallowing a large amount of water. On HRM, this patient had esophageal spasms, increased pressurization front velocity attributable to rapid contractile wave front, associated with symptoms, which were provoked by a multiple rapid swallowing test, and thereby was diagnosed with DES.

Long-term treatment of symptomatic diffuse esophageal spasm by injection of botulinum toxin (BTX)

Long-term treatment of symptomatic diffuse esophageal spasm by injection of botulinum toxin (BTX)

Treatment of symptomatic diffuse esophageal spasm by endoscopic injections of botulinum toxin: A prospective study with long-term follow-up

Background: Diffuse esophageal spasm is a rare esophageal motility disorder for which there are no satisfactory pharmacologic alternatives for treatment. The aim of this study was to investigate whether botulinum toxin (BTX) injection is an effective short- and long-term treatment for patients with symptoms caused by diffuse esophageal spasm. Whether recurrence of clinical symptoms can be successfully retreated by BTX injection was also studied. Methods: Nine symptomatic patients (6 women, 3 men; 57-86 years) with manometrically proven diffuse esophageal spasm underwent BTX injection. One hundred IU BTX were diluted in l0 mL of saline solution and injected endoscopically at multiple sites along the esophageal wall beginning in the region of the lower esophageal sphincter and moving proximally in 1- to 1.5-cm intervals, and into endoscopically visible contraction rings. Symptom scores based on an analogue scale for dysphagia, regurgitation, and noncardiac chest pain were assessed before and after therapy, 1 day thereafter, and at 1 and 6 months. Results: Symptoms improved immediately in 7 (78%) patients after 1 injection session. After 4 weeks 8 (89%) patients were in remission with a decrease in total symptom score. The total symptom score decreased from a median 8.0 (interquartile range: 6.75; 9.0) before treatment to 2.0 (1.5; 3.75) after 1 day ( p < 0.01) and to 2.0 (interquartile range: 0.75; 3.0) after 1 month ( p < 0.01). After 6 months all 8 patients with a response at 1 month still had a symptom score of 3 or less without further treatment. Subsequently 4 patients required reinjection 8, 12, 15, or 24 months after the initial treatment with similarly good results. No serious adverse effects were observed. Conclusions: BTX injection at several levels of the tubular esophagus is an effective treatment for patients with symptoms caused by diffuse esophageal spasm. Symptom relapse can be effectively treated by repeated BTX injection.

Treatment of symptomatic diffuse esophageal spasm by injection of botulinum toxin (BTX)

Treatment of symptomatic diffuse esophageal spasm by injection of botulinum toxin (BTX)

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.

Pneumatic dilatation in patients with symptomatic diffuse esophageal spasm and lower esophageal sphincter dysfunction.

Nine patients with severe symptoms of diffuse esophageal spasm and lower esophageal sphincter dysfunction who were unresponsive to medical therapy and bougienage dilatation were treated by forceful pneumatic dilatation. Treatment with pneumatic dilatation in eight of the nine patients produced a marked improvement in dysphagia and regurgitation (average follow-up of 37.4 months). Esophageal motility performed up to three years (average 12.4 months) after clinically successful pneumatic dilatation revealed a decrease in lower esophageal sphincter pressure from 34.0 +/- 4.0 mm Hg (mean +/- standard error) to 19.2 +/- 2.7 mm Hg (P less than 0.01). There were no significant changes in either the percentage of lower esophageal sphincter relaxation or the type of esophageal motor pattern. We conclude from this study that pneumatic dilatation is an effective form of therapy for a select group of patients with severe symptomatic diffuse esophageal spasm with lower esophageal sphincter dysfunction who are unresponsive to conventional medical therapy.

Spike-associated and spike-independent esophageal contractions in patients with symptomatic diffuse esophageal spasm

We report the electrical correlates of esophageal and lower esophageal sphincter contraction in humans using a bipolar ring electrode assembly mounted on a catheter. No spike activity was seen in the resting state in the esophagus or lower esophageal sphincter. Swallowing induced both electrical spike activity and contractile activity in both areas. The delay in the proximal and distal esophagus from swallowing to the onset of electrical activity was 0.3 ± 0.1 s and 3.3 ± 0.2 s, respectively, and from swallowing to the onset of contractile activity the time was 1.9 ±0.1 s and 5.2 ± 0.2 s, respectively. The rate of propagation of electrical activity was constant throughout the esophageal body while contractile activity was propagated more rapidly in the middle third of the esophagus. Spike activity preceded the peak of esophageal contractions in 100% of swallows. Lower esophageal sphincter relaxation was initiated without spike activity, but the postswallow lower esophageal sphincter contraction was preceded by spike activity in 100% of cases. Basal lower esophageal sphincter pressure was maintained in the absence of spike activity. Spontaneous esophageal contractions, seen in patients with symptomatic diffuse esophageal spasm, were spike-independent in 70% of cases. Prolonged repetitive contractions, once initiated, were also spike-independent. Thus, with the use of intraluminal ring electrodes, we suggest that the human esophagus and lower esophageal sphincter are capable of generating both spike-dependent and spike-independent contractions. The latter may be prominent in patients with esophageal motor disorders.

Sensitivity of esophageal peristalsis to pentagastrin (PG) in patients with symptomatic diffuse esophageal spasm (SDES)

Sensitivity of esophageal peristalsis to pentagastrin (PG) in patients with symptomatic diffuse esophageal spasm (SDES)

Symptomatic Diffuse Esophageal Spasm: Manometric follow-up and response to cholinergic stimulation and cholinesterase inhibition

Uniform criteria for defining symptomatic diffuse esophageal spasm (SDES) are lacking. Records of patients undergoing esophageal motility studies over a 3-year period were reviewed. Those patients who fulfilled a predefined set of arbitrary criteria for SDES returned for repeat motility study. Manometric abnormalities seen on initial examination remained unchanged on follow-up evaluation. In addition, response in SDES to two pharmacological agents--a cholinergic agonist and cholinesterase inhibitor--was evaluated and compared to that seen in normal subjects and in subjects with heartburn. Patients with SDES responded similarly to both agents, and their responses were significantly greater than those seen in controls or in subjects with heartburn. The results suggest that SDES is a relatively homogenous entity, with respect to both maintaining stability of manometric abnormalities and response to two different pharmacological agents. The future evaluation of similarly defined patients may lead to ascertaining more clearly the underlying pathophysiology of this "syndrome".

Editorial: symptomatic diffuse esophageal spasm and its relation to gastrin supersensitivity.

Editorial Notes1 May 1975Symptomatic Diffuse Esophageal Spasm and Its Relation to Gastrin SupersensitivitySIDNEY COHEN, M.D.SIDNEY COHEN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-82-5-714_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe gastrointestinal hormones, a group of peptides released at different portions of the gastrointestinal tract, have diverse effects on the motor activity of each luminal and sphincteric portion of the gut. The effects of these hormones are summarized in Table 1. Although these hormonal actions have been confirmed in multiple laboratories, the physiological significance of their effects has been challenged (1). Is each motor response to a hormone a meaningful physiological action occurring in the normal digestive state? Unfortunately the answer to this question is not known. To date, there are no proved, valid criteria upon which to base an...

Characteristics of Lower Esophageal Sphincter Function in Symptomatic Diffuse Esophageal Spasm

The purpose of this study was to determine the characteristics of lower esophageal sphincter (LES) function in patients with symptomatic diffuse esophageal spasm (SDES) as compared with agematched control subjects. All patients with SDES were diagnosed by: (1) a history of substernal chest pain and dysphagia; and (2) characteristic manometric abnormalities in peristalsis. In patients with SDES, LES pressure was 28.2 ± 2.5 mm Hg (mean ± SEM) as compared with 19.2 ± 1.3 mm Hg in control subjects (P