An esophageal motility disorder (EMD) is any medical disorder that causes difficulty in swallowing, regurgitation of food and a spasm-type pain.
Dysphasia, heartburn, regurgitation are symptoms of an aberrant esophageal motility and reflex disease.
Symptoms of EMD can include chest pain, and intermittent dysphagia for solids, liquids, or both, and regurgitation.
There are contractions along the lower esophagus, and these contractions prevent the passage of food.
Gastroesophageal reflux disease (GERD) is the second most common G.I. diagnosis in an ambulatory setting, with the most common being abdominal pain.
GERD is present in 18-28% of patients.
GERD complications include: stricture, Barrett’s esophagus, and esophageal adenocarcinoma.
The esophagogastric junction mechanism consist of a lower esophageal sphincter made up of smooth muscle, and the crural diaphragm made up of skeletal muscle.
The above sphincters are referred to as an internal and external lower esophageal sphincter, respectively.
The lower esophageal sphincter has circular muscles which cross each other and continue into the stomach as sling fibers.
The right crus of the diaphragm has muscle fascicles which cross and encircle the esophagus.
The lower esophageal sphincter and crural diaphragm are superimposed on each other and are anchored by the phrenoesophageal ligament.
The lower esophageal sphincter is elevated by the vagus parasympathetic or inhibitory nerves and the spinal, sympathetic or excitatory nerves by neurons of the myenteric plexus.
The crural diaphragm is innervated by two phrenic nerves.
The tone of the lower esophageal sphincter is mostly myogenic and the excitatory and inhibitory neurons of the myenteric plexus and neurohormonal factors modulate this tone.
The crural diaphragm provides an extrinsic squeeze and increases the esophagitis gastric junction pressure during inspiration, coughing, sneezing, or bending and guards against increases in pressure gradient between the chest and the abdomen.
Swallowing relaxes the upper and lower esophageal sphincter and any ongoing esophageal contractions.
Swallowing that is repeated at short intervals of less than four seconds induces prolonged inhibition of the esophagus and lower esophageal sphincter.
The neural control of the skeletal and smooth muscle of the esophagus occurs through the nucleus ambiguus and dorsomotor nucleus of the vagus nerve, in the brain stem, respectively.
The esophageal myenteric plexus contains excitatory neurons that release acetylcholine and substance P, and inhibitory neurons that release nitro oxide and vasoactive intestinal polypeptide.
The myenteric plexus is located between the circular and longitudinal muscles of the esophagus and provides for its local control mechanism.
During peristalsis, circular and longitudinal esophageal muscles contract and relax in a synchronous fashion, and a liquid bolus travels through the esophagus.
Similar to contraction, relaxation of the esophagus move sequentially along the length of the esophagus.
The longitudinal muscle contraction results in the shortening and sliding between the circular and longitudinal muscle layers in the distended segment.
Esophageal distention is a stimulus for esophageal peristalsis, as is a change in posture from supine to upright and the Trendelenburg position affect the amplitude of esophageal contraction and relaxation.
The esophagus shortens during peristalsis and lifts the lower esophageal sphincter by 2-3 cm, which is critical for relaxation of the lower esophageal sphincter: The lower esophageal sphincter goes from an intrathoracic to a intra-abdominal location.
Esophageal motility disorders are characterized and secondary and primary.
Secondary esophageal motility disorders include: myasthenia gravis, dermatomyositis, scleroderma, connective tissue disorders, diabetes, secondary achalasia esophagus.
Esophageal motility disorder may be a result of CREST syndrome (calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly and telangiectasia).
Dysphagia could be for solids only, or for solids and liquids both.
Solid dysphagia is due to obstructions such as esophageal cancer, esophageal webs, or stricture.
Solid-and-liquid dysphagia is due to an esophageal motility disorder of either the upper esophagus, or the lower esophagus.
Upper motility disorders: myasthenia gravis, stroke, or dermatomyositis.
Lower esophagus motility disorders include systemic sclerosis, CREST syndrome, or achalasia.
The most common form of dysphagia is achalasia.
Achalasia is caused by degeneration of the nerves in the esophagus, causing the muscles to stop working and prevents the valve at the bottom of the esophagus from being able to open properly.
Testing to diagnose an EMD include: barium esophagography, upper endoscopy, and esophageal manometry.
There is no cure for EMD.
Symptom management includes eating slower and taking smaller bites.
Medications that can be useful: proton pump inhibitor to ease gastroesophageal reflux or a smooth muscle relaxant for issues with the muscles.