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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nervous mechanisms that generate swallowing are still largely unknown. It has been suggested that a central pattern generator that contains a serial network of linked neurons must produce the successive excitation of motoneurons (Mns) and then the sequential activation of muscle through excitatory connections. Inhibitory connections have also been envisioned but never evidenced at the membrane level of the swallowing neurons. We investigated, by intracellular recordings, the behavior of 96 Mns in the rostral nucleus ambiguus during swallowing induced by application of superior laryngeal nerve stimulation to anesthetized sheep. The Mns were identified by antidromic activation following stimulation of glossopharyngeal, pharyngoesophageal, or cervical vagal nerves. Nine Mns showed a bell-shaped depolarization during the buccal or the early pharyngeal stage of swallowing. They probably projected to muscles of the soft palate (palatopharyngeal) and upper pharynx (stylopharyngeal, hyopharyngeal). Thirty-eight Mns exhibited a chloride-dependent hyperpolarization, indicating that they were under an active inhibition throughout the buccopharyngeal stage of swallowing. These Mns constitute a heterogeneous pool: some of them, producing spontaneous inspiratory discharges, probably innervated laryngeal or pharyngeal muscles; others might also be Mns of the esophagus, whose swallowing pattern was modified because of the anesthesia (suppression of the esophageal peristalsis). Forty-nine Mns showed a chloride-dependent hyperpolarization with a variable duration at the onset of swallowing, followed by a depolarization that could take place during either the buccopharyngeal (HD1-Mns) or the esophageal (HD2- and HD3-Mns) stage of deglutition. HD1-Mns probably projected to the median and inferior constrictors of the pharynx. HD2-Mns produced depolarizations with longer latencies and durations than those of the HD1-Mns. They probably projected to either the superior esophageal sphincter or the cervical esophagus (CE). HD3-Mns showed a buccopharyngeal hyperpolarization that was followed first by a lower-amplitude hyperpolarization accompanying the proximal CE contraction and then by a delayed depolarization. These Mns probably innervated the inferior CE or thoracic esophagus. We conclude that the initial inhibition exerted on the HD-Mns, by delaying the excitation of Mns, may play a role in the nervous mechanisms involved in temporal organization of the swallowing motor sequence. We suggest that swallowing disorders in humans such as dysphagia by failure of cricopharyngeal relaxation, diffuse esophageal spasm, and achalasia might be caused by impaired inhibitory mechanisms.
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PMID:Intracellular activity of motoneurons of the rostral nucleus ambiguus during swallowing in sheep. 906 58

Incomplete upper esophageal sphincter (UES) relaxation is not well understood. We compared clinical and manometric characteristics of patients with normal and abnormal UES relaxation. Consecutive patients (n = 208) underwent manometric evaluation of the lower esophageal sphincter (LES), esophageal body, and UES/pharynx. The patients were divided into those with abnormal UES relaxation (residual pressure > 6.7 mmHg) (n = 21) and normal relaxation (n = 187). Clinical and manometric profiles were compared. Sex, age, and presenting complaint did not correlate with UES relaxation. Normal esophageal peristaltic sequences were more frequently present in the normal UES group (73.6%) compared with the abnormal (55.8%) (p < 0.01). The UES relaxation was shorter in the group with abnormal relaxation (410.0 ms vs. 510.2 ms, p < 0.001). All other manometric parameters were not different between the two groups. When individual manometric diagnoses were analyzed, only achalasia was noted to be more common in the abnormal UES group (23.8% vs. 9.1%, p < 0.05), and a trend was noted toward diffuse esophageal spasm being more common (14.3% vs. 9.6%, not significant). We conclude that incomplete UES relaxation is a rare manometric finding, associated with achalasia and not specifically associated with any other motility disturbance. This finding may represent a secondary response to the poor esophageal emptying seen in achalasia.
Dysphagia 1997
PMID:Incomplete upper esophageal sphincter relaxation: association with achalasia but not other esophageal motility disorders. 919 Jan 1

The aim of this paper is to describe and discuss, on the basis of the available literature, the case of an old female patient, admitted to our university hospital because of a severe dysphagia for solid foods, in whom laboratory data showed a marked hypomagnesemia. She reported a long history (20 years) of allergic bronchial asthma treated with theophylline. Esophagography evidenced a disorder of esophagus motility with diffuse multiple spasm, reminiscent of the 'corkscrew esophagus'. A link with the severe hypomagnesemia (Mg 1.1 mEq/l, normal range 1.6-2.1) was suspected, and a therapy with oral pidolate of Mg (1.5 g/twice a day) was started and continued for 4 months. This was associated with a slow progressive normalization of the Mg plasma level and reverted radiographic esophageal findings with disappearance of dysphagia. Mg is an important element for health and disease, and today Mg deficiency in man has become an accepted medical problem which might complicate many diseases. Neuromuscular disorders, as laryngeal spasm, are recognized complications of hypomagnesemia, but until now only 1 case of motor esophageal disorder associated with a low Mg plasma level was briefly reported in the literature, even if dysphagia is generally included in the symptomatological pattern of hypomagnesemia. Our observation of a severe form of esophageal spasm, associated with hypomagnesemia, in an aged female patient underlines the pathophysiological meaning of the plasma Mg level and suggests the need for routine Mg determination in the clinical setting.
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PMID:Hypomagnesemia and smooth muscle contractility: diffuse esophageal spasm in an old female patient. 970 72

A 52-year-old man with idiopathic diffuse esophageal spasm and hypertensive lower esophageal sphincter presented with dysphagia for several years. After unsuccessful therapy with forceful pneumatic dilation of the cardia, a myotomy of the cardia and distal esophagus was performed. The patient became asymptomatic, lower esophageal sphincter pressure diminished to less than 10 mm Hg, and esophageal body motor activity was normalized. This situation remains unchanged 6 years after the operation.
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PMID:Normal esophageal function after myotomy in a patient with idiopathic diffuse esophageal spasm. 1040 39

Swallowing is a complex mechanism based on the coordinated collaboration of tongue, pharynx and esophagus. Disturbances of this interplay or disorders of one or several of these components lead to dysphagia, non-cardiac chest pain or regurgitation. The major primary esophageal motility disorders--achalasia, diffuse esophageal spasm, hypercontractile esophagus ('nutcracker esophagus') and non-specific motility disorder--are of unknown etiology. Other esophageal diseases, such as cervical diverticula or gastroesophageal reflux disease, might also be caused by a primary esophageal motility disorder. Medical treatment of esophageal disorders with esophageal hyper- or dysmotility requires agents that reduce esophageal contractile force (anticholinergic agents, nitrates, calcium antagonists). Despite the beneficial effect of the various drugs on esophageal motility parameters, the clinical benefit of medical treatment of esophageal motility disorders is rather disappointing. Calcium channel antagonist, alone or in combination with anticholinergics or nitrates, can be used as a medical trial, especially in mild achalasia. However, medical therapy is clearly inferior to pneumatic balloon dilation therapy. Recently, botulinum toxin injection was suggested as a therapeutic option in achalasia patients with good results on lower esophageal sphincter pressure (LESP) and symptom scores that were similar to the results achieved by pneumatic balloon dilation. Hypercontractile esophagus shows a good manometric response to calcium channel antagonists, but only little clinical effect in terms of improvement of symptoms. Diffuse esophageal spasm is a relatively rare disease and few clinical studies are available. The use of calcium channel antagonists can be beneficial, at least in some patients with diffuse esophageal spasm. From clinical and epidemiological studies, there is some evidence of a 'psychological' component in the pathogenesis or perception of esophageal symptoms. There is some clinical benefit from centrally acting drugs such as benzodiazepines or antidepressants. With the exception of botulinum toxin for achalasia, medical therapy of primary esophageal motility disorders is rather limited and the clinical results are poor. Further understanding of esophageal pathophysiology as well as development of new receptor-selective drugs might increase our chances of a successful treatment of primary esophageal motility disorders.
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PMID:Esophageal pharmacology and treatment of primary motility disorders. 1077 Mar 58

Cardiac and musculoskeletal disease should be excluded before considering an esophageal etiology for chest pain. Acid reflux is a common cause of chest pain and should be identified and treated. A therapeutic trial should consist of a proton pump inhibitor (omeprazole 20 mg or lanzoprazole 30 mg) given one or two times per day for at least 6 to 8 weeks. An alternative is to use an ambulatory pH study to confirm reflux. Also, if the patient fails the initial treatment, reflux should be confirmed with pH testing before increasing the dose of proton pump inhibitor or considering combination or surgical therapy. Esophageal manometry should be considered in patients with chest pain and dysphagia. It is also reasonable to perform manometry before a pH study since manometric localization of the lower esophageal sphincter (LES) is needed to ensure accurate pH probe placement. Only after manometric confirmation of a spastic esophageal motility disorder should patients be treated for esophageal spasm. In these patients, it is reasonable to try a long-acting formulation of a calcium-channel blocker or nitrate. Patients with chest pain who have a negative cardiac evaluation and who do not have reflux may have an abnormality in esophageal or cardiac sensation. These patients should be treated with a trial of an antidepressant and considered for referral to a mental health practitioner. All medication trials should continue at least 6 to 8 weeks to avoid a placebo effect and to allow adequate time for a therapeutic response.
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PMID:Noncardiac Chest Pain of Esophageal Origin. 1109 64

Esophageal motility disorders often manifest with chest pain and dysphagia. Achalasia is a disorder of the lower esophageal sphincter and the smooth musculature of the esophageal body. In achalasia the lower esophageal sphincter typically fails to relax with swallowing, and the esophageal body fails to undergo peristalsis. In contrast to spastic disorders of the esophagus, achalasia can be progressive and cause pronounced morbidity. Pseudoachalasia mimics achalasia in terms of symptoms but can be caused by infectious disorders or malignancy. Treatment for achalasia is nonstandardized and includes medical, endoscopic, and surgical options. Spastic disorders of the esophagus, such as diffuse esophageal spasm and nutcracker esophagus, and nonspecific esophageal motility disorder are benign and nonprogressive, with similar findings on esophageal manometry. Although the exact cause remains unknown, these disorders may represent a manifestation of gastroesophageal reflux disease. Treatment of spastic disorders includes medical and surgical approaches and is aimed at symptomatic relief.
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PMID:Primary esophageal motility disorders. 1149 31

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.
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PMID:Oesophageal motility disorders. 1180 95

Dysphagia in Parkinson's disease (PD) is known to correlate with abnormalities of oropharyngeal function. Oesophageal abnormalities have not been previously demonstrated to correlate with dysphagia. The aim of the study was to determine if motor dysfunction of the oesophageal body correlates with dysphagia or disease severity in PD. Twenty-two patients with PD were assessed for the severity of their dysphagia (scale of 1-7) and severity of PD (Hoehn and Yahr scale 1-4). All underwent oesophageal manometry. Dysphagia was present daily in 10 patients (45%). Parkinson's disease was graded as severe (Hoehn and Yahr > or =3) in eight (36%) patients. Oesophageal manometry was abnormal in 16 (73%) patients. Thirteen patients had either complete aperistalsis or multiple simultaneous contractions (diffuse oesophageal spasm). These findings were significantly more common in patients with daily dysphagia (90% vs. 33%; P < 0.005), and were not related to duration or severity of PD. We conclude that the presence of aperistalsis or multiple simultaneous contractions in the oesophagus does correlate with dysphagia and is independent of PD severity or duration. This may reflect selective involvement of either the dorsal motor nucleus of the vagus or the oesophageal myenteric plexus.
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PMID:Manometric abnormalities of the oesophagus in patients with Parkinson's disease. 1157 95

Although several modalities are available to investigate oesophageal motility disorders, manometry is the gold standard. The procedure is increasingly available in district general hospitals but the clinical utility of this investigation in this setting remains unclear. The aim in this study was to evaluate the use and outcome of oesophageal manometry in a district general hospital. Data on 100 consecutive oesophageal manometry procedures were analysed, taking into account the referral pattern, indications, and results. The indications were gastro-oesophageal reflux disease (preoperative assessment before fundoplication) (58), dysphagia (28), chest pain (12), and epigastric pain (2). Diagnoses were made using predefined standard criteria and were as follows: normal (41), non-specific motility disorder (NSMD) (38), achalasia (15), diffuse oesophageal spasm (4), and scleroderma (2). Of the 58 patients who had undergone manometry as a preoperative assessment of oesophageal motility, 27 (47%) were abnormal. Twenty five (43%) had NSMD and two (3%) had achalasia. Forty eight of these preoperative cases were combined with 24 hour pH recording, which confirmed acid reflux in 35 (73%). The experience reported here reflects the published evidence that the use of manometry is changing. It is now more commonly used for assessment before antireflux surgery and for dysphagia, and the use in the assessment of chest pain is declining. The findings confirm the importance of eliminating achalasia before inappropriate antireflux surgery.
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PMID:A review of oesophageal manometry testing in a district general hospital. 1179 70


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