Esophageal Spasm, Diffuse
Spasm
Esophageal Motility Disorders
Esophageal Achalasia
Esophagus
Spasms, Infantile
Hemifacial Spasm
Encyclopedias as Topic
Classification of oesophageal motility abnormalities. (1/19)
Manometric examination of the oesophagus frequently reveals abnormalities whose cause is unknown and whose physiological importance is not clear. A large body of literature dealing with oesophageal motility abnormalities has evolved over the past few decades but comparisons among studies have been compromised by the lack of a widely accepted system for classifying the abnormal motility patterns, and by the lack of uniform diagnostic criteria for the putative disorders. Based on an extensive review and analysis of the literature, this report suggests an operational scheme to be used for the general classification of oesophageal motility abnormalities, and proposes standardised manometric criteria for the putative oesophageal motility disorders. By applying the guidelines proposed in this report, clinicians and researchers can determine if their patients fulfil the manometric criteria for a putative motility disorder. This should facilitate and improve comparisons among patients and studies. However, it is important to emphasise that fulfilment of the proposed criteria does not establish the clinical importance of the motility abnormalities. (+info)Sustained esophageal contraction: a motor correlate of heartburn symptom. (2/19)
Heartburn occurs in the presence as well as the absence of acid reflux. We searched for a motor correlate of heartburn. Twelve subjects with heartburn were studied with 24-h synchronized pressure, pH, and high-frequency intraluminal ultrasound (HFIUS) imaging of the esophagus. The HFIUS images were analyzed every 2 s for a period of 2 min before and 30 s after the onset of heartburn during 20 acid reflux-positive and 20 acid reflux-negative heartburn episodes. The esophageal muscle thickness was measured as a marker of contraction. Esophageal pressure and HFIUS images were recorded during the Bernstein test in 15 subjects. Sustained esophageal contractions (SECs) were identified during 13 of 20 heartburn episodes associated with acid reflux and 15 of 20 heartburn episodes without acid reflux. SECs were detected during 2 of 40 matched control periods only (P < 0.05). The duration of SECs was 44.9 +/- 26.9 s. The Bernstein test reproduced heartburn symptoms in 8 of 15 subjects. SECs were identified during 6 of 8 (75%) Bernstein-positive and in 1 of 7 (14.3%) Bernstein-negative tests (P = 0.04). We conclude that a SEC precedes both spontaneous and induced heartburn symptoms and may be the cause of heartburn sensation. (+info)Relationship between esophageal muscle thickness and intraluminal pressure in patients with esophageal spasm. (3/19)
We previously showed, in normal subjects, a positive correlation between the esophageal contraction amplitude and peak muscle thickness. The goal of this study was to determine the relationship between esophageal muscle thickness and contraction amplitude in patients with high-amplitude peristaltic and simultaneous contractions. Eleven patients with high-amplitude peristaltic contractions, 8 with diffuse esophageal spasm (DES), 7 with nonspecific (NS) motor disorder of the esophagus, and 10 normal subjects were studied using simultaneous pressure and ultrasound imaging. Pressure was recorded by manometry and ultrasound imaging with a high-frequency ultrasound probe catheter. Recordings were performed in the lower esophageal sphincter (LES) and at 2, 4, 6, 8, and 10 cm above the LES during resting state and swallow-induced contractions. Baseline esophageal muscle was thicker in the distal, compared with the proximal esophagus both in normal subjects and patient groups. Patients with DES and nutcracker esophagus (NC) have a higher baseline muscle thickness compared with normal and NS patients. Correlation between the peak pressure and the peak muscle thickness was weaker in patients with NC and DES compared with normal subjects and patients with NS. Whereas normal subjects have good correlation between delta (difference between peak and baseline) muscle thickness and peak pressures, this relationship was absent in patients with NC and DES. Increase in contraction amplitude in patients with NC and DES was associated with an increase in baseline thickness of esophageal muscularis propria. Increase in baseline thickness was specific to patients with spastic motor disorders and was not seen in patients with NS. (+info)Cerebral potentials evoked by oesophageal distension in patients with non-cardiac chest pain. (4/19)
Cerebral evoked potential recording was used to study the oesophagus-brain axis in 10 controls and 10 patients with non-cardiac chest pain with a manometric diagnosis of either nutcracker oesophagus or diffuse spasm and a positive edrophonium test. A series of 50 inflations (10/minute; inflation rate of 170 ml/second) of an intraoesophageal balloon (5 cm proximal to the lower oesophageal sphincter) was performed in each subject. Three different inflation volumes were used and were individually determined to cause no sensation, slight sensation, and definite sensation, respectively (volume ranges: 2-8 ml, 5-18 ml, and 8-22 ml). All signals were coded and their quality was scored on a scale from 0 (no recognisable pattern) to 5 (well defined potential of good quality) by four 'blinded' observers. The evoked potential quality scores and amplitude of the major peaks increased significantly (p less than 0.01) with increasing sensation, both in patients and in controls. In the patients, quality score and amplitude of all four peaks of the evoked potentials were lower (p less than 0.05) and latencies of two of the four peaks were longer (p less than 0.02) than in the controls. The volumes of air required to produce the various sensations were lower in the patients (p less than 0.01). When divided by the balloon volume, amplitude and quality of the evoked potential were no longer significantly different between the groups. These results suggest that the increased perception of oesophageal distension in patients with non-cardiac chest pain is caused by altered central processing rather than (functionally) abnormal receptors in the oesophageal wall. (+info)The heart and the oesophagus: intimate relations. (5/19)
The close anatomical relations of the heart and oesophagus, and the similarity of symptoms attributable to disorders of either organ, often lead to diagnostic difficulty in patients with chest pain. A definitive diagnosis of non-cardiac chest pain attributable to oesophageal reflux or spasm is hampered, both by the need for prolonged ambulatory monitoring of pH, manometry, and endoscopy, and by the common occurrence of asymptomatic reflux and spasm, and the corresponding difficulty in linking an episode of reflux or spasm with an episode of pain. Moreover, some patients with non-cardiac chest pain and normal tests of oesophageal structure and function have centrally mediated hypersensitivity, both within and without the oesophagus. Rather than proceed with investigations, in the absence of symptoms to suggest structural disease of the oesophagus, it would be reasonable to attempt symptomatic treatment with a proton pump inhibitor or an antidepressant. (+info)Coronary spasm reflects inputs from adjacent esophageal system. (6/19)
Mechanisms underlying coronary spasm are still poorly understood. The aim of the study was to assess the hypothesis that fluctuations in the development of coronary spasm might reflect inputs from the adjacent esophageal system. We enrolled patients admitted to the coronary care unit for episodes of nocturnal angina. Seven patients with variant angina and five with coronary artery disease (CAD) had concurrent ECG and esophageal manometric monitoring. ECG monitoring documented 28 episodes of ST elevation in variant angina patients and 16 episodes of ST depression in CAD patients. Manometric analysis showed that esophageal spasms resulted remarkably more frequently in variant angina patients (143 total spasms; individual range 9-31) than in CAD patients (20 total spasms; individual range 0-9; P < 0.01). Time series analysis was used to assess fluctuations in the occurrence of abnormal esophageal waves and its relationship with spontaneous episodes of ST shift. Episodes of esophageal spasm in CAD were sporadic (<1 in 30 min) and not related to ECG-recorded ischemia. In the variant angina group, esophageal spasms were time related to ischemia (>1 into 5 min before ECG-recorded ischemia) (P < 0.05). A bidirectional analysis of causal effects showed that the influence processes between esophageal and coronary spasms were mutual and reciprocal (transfer function model, P < 0.05) in variant angina. We concluded that in variant angina patients, episodes of esophageal spasms and myocardial ischemia influenced each other. Mechanisms that cause esophageal spasm can feed back to produce coronary spasm. Coronary spasm may feed forward to produce additional episodes of esophageal spasm. (+info)Review article: oesophageal spasm - diagnosis and management. (7/19)
Oesophageal spasm is a common empiric diagnosis clinically applied to patients with unexplained chest pain. In contrast it is an uncommon manometric abnormality found in patients presenting with chest pain and/or dysphagia and diagnosed by >or=20% simultaneous oesophageal contractions during standardized motility testing. Using Medline we searched for diagnostic criteria and treatment options for oesophageal spasm. While the aetiology of this condition is unclear, studies suggest the culprit being a defect in the nitric oxide pathway. Well-known radiographic patterns have low sensitivities and specificities to identify intermittent simultaneous contractions. Recognizing that simultaneous contractions may result from gastro-oesophageal reflux this diagnosis should be investigated or treated first. Studies have documented improvements with proton-pump inhibitors, nitrates, calcium-channel blockers and tricyclic antidepressants or serotonin reuptake inhibitors. Small case series reported benefits after botulinium toxin injections, dilatations and myotomies. Uncertainties persist regarding the optimal management of oesophageal spasm and recommendations are based on controlled studies with small numbers of patients or on case series. Acid suppression, muscle relaxants and visceral analgetics should be tried first. Botulinium toxin injections should be reserved for patients who do not respond. Pneumatic dilatations or myotomies represent rather heroic approaches for non-responding patients. (+info)Botulinum toxin in speech rehabilitation with voice prosthesis after total laryngectomy. (8/19)
(+info)Diffuse Esophageal Spasm (DES) is a motility disorder of the esophagus, which is the muscular tube that connects the throat to the stomach. In DES, the esophagus involuntarily and uncoordinately contracts, causing difficulty swallowing (dysphagia), chest pain, and sometimes regurgitation of food or liquids.
The term "diffuse" refers to the fact that these spasms can occur throughout the entire length of the esophagus, rather than being localized to a specific area. The exact cause of diffuse esophageal spasm is not known, but it may be associated with abnormalities in the nerve cells that control muscle contractions in the esophagus.
Diagnosis of DES typically involves a combination of medical history, physical examination, and specialized tests such as esophageal manometry or ambulatory 24-hour pH monitoring. Treatment options may include medications to relax the esophageal muscles, lifestyle modifications such as avoiding trigger foods, and in some cases, surgery.
A spasm is a sudden, involuntary contraction or tightening of a muscle, group of muscles, or a hollow organ such as the ureter or bronchi. Spasms can occur as a result of various factors including muscle fatigue, injury, irritation, or abnormal nerve activity. They can cause pain and discomfort, and in some cases, interfere with normal bodily functions. For example, a spasm in the bronchi can cause difficulty breathing, while a spasm in the ureter can cause severe pain and may lead to a kidney stone blockage. The treatment for spasms depends on the underlying cause and may include medication, physical therapy, or lifestyle changes.
Esophageal motility disorders are a group of conditions that affect the normal movement (motility) of the muscles in the esophagus, which is the tube that connects the throat to the stomach. The esophageal muscles normally contract and relax in a coordinated manner to help move food from the mouth to the stomach.
In esophageal motility disorders, this muscle movement is impaired, leading to difficulty swallowing (dysphagia), chest pain, heartburn, or regurgitation of food. Some common examples of esophageal motility disorders include:
1. Achalasia: a condition in which the lower esophageal sphincter muscle fails to relax properly, preventing food from passing into the stomach.
2. Diffuse esophageal spasm: a disorder characterized by uncoordinated contractions of the esophageal muscles, leading to difficulty swallowing and chest pain.
3. Nutcracker esophagus: a condition in which the esophageal muscles contract too forcefully, causing pain and difficulty swallowing.
4. Hypertensive lower esophageal sphincter: a disorder in which the lower esophageal sphincter muscle is too tight, making it difficult to swallow and leading to symptoms such as heartburn and regurgitation.
5. Ineffective esophageal motility: a condition in which the esophageal muscles have weak or disorganized contractions, leading to difficulty swallowing and other symptoms.
Esophageal motility disorders can be diagnosed through tests such as manometry, which measures the pressure and coordination of esophageal muscle contractions, or barium swallow studies, which use X-rays to visualize the movement of food through the esophagus. Treatment may include medications, lifestyle changes, or surgery, depending on the specific disorder and its severity.
Manometry is a medical test that measures pressure inside various parts of the gastrointestinal tract. It is often used to help diagnose digestive disorders such as achalasia, gastroparesis, and irritable bowel syndrome. During the test, a thin, flexible tube called a manometer is inserted through the mouth or rectum and into the area being tested. The tube is connected to a machine that measures and records pressure readings. These readings can help doctors identify any abnormalities in muscle function or nerve reflexes within the digestive tract.
Esophageal achalasia is a rare disorder of the esophagus, the tube that carries food from the mouth to the stomach. In this condition, the muscles at the lower end of the esophagus fail to relax properly during swallowing, making it difficult for food and liquids to pass into the stomach. This results in symptoms such as difficulty swallowing (dysphagia), regurgitation of food, chest pain, and weight loss. The cause of esophageal achalasia is not fully understood, but it is believed to be related to damage to the nerves that control the muscles of the esophagus. Treatment options include medications to relax the lower esophageal sphincter, botulinum toxin injections, and surgical procedures such as laparoscopic Heller myotomy or peroral endoscopic myotomy (POEM).
The esophagus is the muscular tube that connects the throat (pharynx) to the stomach. It is located in the midline of the neck and chest, passing through the diaphragm to enter the abdomen and join the stomach. The main function of the esophagus is to transport food and liquids from the mouth to the stomach for digestion.
The esophagus has a few distinct parts: the upper esophageal sphincter (a ring of muscle that separates the esophagus from the throat), the middle esophagus, and the lower esophageal sphincter (another ring of muscle that separates the esophagus from the stomach). The lower esophageal sphincter relaxes to allow food and liquids to enter the stomach and then contracts to prevent stomach contents from flowing back into the esophagus.
The walls of the esophagus are made up of several layers, including mucosa (a moist tissue that lines the inside of the tube), submucosa (a layer of connective tissue), muscle (both voluntary and involuntary types), and adventitia (an outer layer of connective tissue).
Common conditions affecting the esophagus include gastroesophageal reflux disease (GERD), Barrett's esophagus, esophageal cancer, esophageal strictures, and eosinophilic esophagitis.
Infantile spasms, also known as West syndrome, is a rare but serious type of epilepsy that affects infants typically between 4-8 months of age. The spasms are characterized by sudden, brief, and frequent muscle jerks or contractions, often involving the neck, trunk, and arms. These spasms usually occur in clusters and may cause the infant to bend forward or stretch out. Infantile spasms can be a symptom of various underlying neurological conditions and are often associated with developmental delays and regression. Early recognition and treatment are crucial for improving outcomes.
Hemifacial spasm is a neuromuscular disorder characterized by involuntary, irregular contractions or twitching of the muscles on one side of the face. These spasms typically begin around the eye and may progress to involve the muscles of the lower face, including those around the mouth.
The primary cause of hemifacial spasm is pressure on or irritation of the facial nerve (cranial nerve VII) as it exits the brainstem, often due to a blood vessel or tumor. This pressure can lead to abnormal electrical signals in the facial nerve, resulting in uncontrolled muscle contractions.
In some cases, hemifacial spasm may be associated with other conditions such as multiple sclerosis or Bell's palsy. Treatment options for hemifacial spasm include medications to help relax the muscles, botulinum toxin (Botox) injections to paralyze the affected muscles temporarily, and, in rare cases, surgical intervention to relieve pressure on the facial nerve.
Coronary vasospasm refers to a sudden constriction (narrowing) of the coronary arteries, which supply oxygenated blood to the heart muscle. This constriction can reduce or block blood flow, leading to symptoms such as chest pain (angina) or, in severe cases, a heart attack (myocardial infarction). Coronary vasospasm can occur spontaneously or be triggered by various factors, including stress, smoking, and certain medications. It is also associated with conditions such as coronary artery disease and variant angina. Prolonged or recurrent vasospasms can cause damage to the heart muscle and increase the risk of cardiovascular events.
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