Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We report a case of myasthenia gravis presenting to the department of otolaryngology with acute dysphagia on two separate occasions over a one-year period. Diagnosis of myasthenia gravis was made when the patient developed ventilatory failure after his second general anaesthetic for rigid oesophagoscopy. Our patient required emergency transfer to the intensive therapy unit for ventilation. He improved after treatment with corticosteroids, anticholinesterase and immunosuppressive medications. Our case was unusual in that cricopharyngeal spasm causing dysphagia and significant aspiration was demonstrated by a barium swallow and this was completely resolved after treatment of the myasthenia gravis.
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PMID:Myasthenia gravis presenting with dysphagia and postoperative ventilatory failure. 1020 22

A 36-year-old woman presented an inability to ingestion and mild hemiparesis with superficial and deep sensory disturbances on the left side for two months after a stroke. Dysphagia was originated from bilateral cricopharyngeal spasm, which was disclosed by videofluorography, manometry at the pharyngo-esophageal segment, and needle electromyography. Although no focal lesion of the brain was detected even with MRI, neurological and electrophysiological findings suggested that the lesion was localized to the lower pontine and mudullary tegmentum on the right side. Two months after the onset, botulinum toxin (10 units) was administered into the bilateral cricopharyngeal muscles, which resulted in restoration of the normal swallowing function in 5 days, and the normal function is lasting 5 years. Botulinum toxin therapy is non-invasive and effective for cricopharyngeal spasm. This non-invasive method will be the first choice for cricopharyngeal spasm replacing surgical intervention.
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PMID:[Botulinum toxin therapy for cricopharyngeal spasm]. 1039 Oct 83

We described a 47-year-old man with ischemic stroke who developed a brainstem syndrome with persistent dysphagia. He was fed by the nasogastric tube placed intermittently by himself for almost 7 months after the stroke. Elective feeding via percutaneous endoscopic gastrostomy (PEG) was not accepted by the patient. All treatment attempts with benzodiazepines, antidepressants and spasmolytic agents were unsuccessful. Videofluoroscopic investigation revealed excessive and long-lasting spasm of the upper esophageal sphincter which was associated with the massive aspiration of the contrast. The patient dramatically improved after treatment with nitroglycerin and long-acting nitrates with almost complete recovery of normal swallowing. A strikingly good effect of nitrates in the treatment of oropharyngeal dysphagia is emphasized by the authors.
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PMID:[A case of neurogenic dysphagia responding to nitrates]. 1079 Oct 45

Patients with thoracic outlet syndrome (TOS) who improve temporarily after anesthetic blockade of the anterior scalene muscles have been shown to improve after ultimate surgical decompressions at the interscalene triangle. Anesthetic blockade of the scalene muscles, even with the addition of steroids, however, rarely produces any prolonged relief as patients are awaiting definitive surgery. The present study was undertaken to determine if more effective and prolonged relief might be obtained with electrophysiologically and fluoroscopically guided selective injection of the scalene muscles with botulinum toxin, which has been used in the past for treating conditions associated with spasm of cervical muscles. In 14 of 22 patients (64%) with a clinical diagnosis of TOS, there was more than a 50% reduction of symptoms measured by a 101-point scale for at least 1 month after botulinum chemodenervation of the scalene muscles. Only 4 of the 22 patients (18%) had a 50% reduction of symptoms for at least 1 month after injection with lidocaine and steroids. In no patient were the results of lidocaine and steroid injection superior to botulinum chemodenervation. Chemodenervation had a mean duration of effect of 88 days. No significant side effects were encountered with botulinum chemodenervation except for mild transient dysphagia in two cases. These results appear to demonstrate that botulinum chemodenervation of the scalene muscles may be helpful in alleviating symptoms in patients with TOS awaiting definitive surgical decompression.
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PMID:Selective botulinum chemodenervation of the scalene muscles for treatment of neurogenic thoracic outlet syndrome. 1094 89

Dysphagia is a common symptom in various neurological disorders affecting pharyngeal functions. Cricopharyngeal dysfunction is one of the major findings in these patients. The most effective treatment for restoring normal swallowing function in persistent cricopharyngeal dysfunction is cricopharyngeal myotomy, especially when mechanical obstruction or a well-localized neuromuscular dysfunction, such as a cricopharyngeal muscle spasm, is present. However, when there is a more diffuse neurological disorder present the results of surgery are more disappointing. In unclear cases, or in patients with temporary problems, no good method other than swallowing training, bougienage, and tube feeding are available. During the past decade, botulinum toxin has been found to be of therapeutic value in the treatment of a variety of neurological disorders associated with inappropriate muscular contractions such as torticollis and spasmodic dysphonia. Recently, injections of botulinum toxin in patients with cricopharyngeal muscle dysfunction have been reported to result in marked relief of dysphagia. In this article we describe our experiences with botulinum toxin injections to treat four patients suffering from deglutition problems and cricopharyngeal dysphagia of different origins. Botulinum toxin was injected into the cricopharyngeus muscle that was identified by endoscopy under general anesthesia. In this study, no major side effects were observed. Three patients obtained a significant improvement of esophageal symptoms after the first injection. The treatment had limited effect in one patient who had reflux disease and only slight cricopharyngeus dysfunction.
Dysphagia 2001
PMID:Botulinum toxin in the treatment of cricopharyngeal dysphagia. 1145 61

Achalasia is an idiopathic neuromuscular disorder of the esophagus which is associated with absence of esophageal peristalsis and incomplete relaxation of a normal or raised lower esophageal sphincter (LES). Dysphagia is the most commonly associated symptom. Conventional therapeutic approaches are directed to reducing LES pressure and include orally-administered smooth muscle relaxants, forceful sphincter dilation with balloon dilators, and open or laparoscopic-assisted myotomy of the LES. Pharmacologic therapies have a low success rate. Forceful dilation has a perforation complication rate of 2% to 5%, and myotomies may precipitate significant gastroesophageal reflux, a complication minimized when a partial fundal wrap is employed simultaneously. In recent years, botulinum toxin, utilized widely as a striated muscle relaxant in managing blepharospasm, anal sphincter spasm, and muscle spasm complicating CVAs, and in smoothening facial wrinkles, has been extended to the management of achalasia on the basis that it impairs smooth muscle responsiveness to acetylcholine. Eighty units of Botox (botulinum toxin) are injected directly into the endoscopically (endoscopic ultrasound techniques may facilitate localization) located LES region (20 units into each of 4 quadrants). Symptom relief lasting 6 months on average is experienced in more than 65% of treated patients, and the complication rate is negligible. This therapeutic option is reserved for patients too ill to undergo any surgical procedure and is most effective when the lower esophageal region is hypertonic.
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PMID:Treatment of achalasia with botulinum A toxin. 1189 30

1. This complex of symptoms appears to be congenital, familial, and hereditary. It is apparently transmitted by a dominant gene, probably on chromosome 5. 2. Hypertonicity with rigidity of all voluntary muscles usually presents at birth. 3. Feeding problems are due to dysphagia or laryngospasm associated with aspiration and dyspnea. 4. Respiratory problems are characterized by apneic episodes due to muscle spasm. 5. Prolonged episodes of muscular rigidity secondary to sudden stimuli result in frequent falls, characteristically en bloc, like a statue. 6. Continuous electromyographic activity even at rest (with absence of fasciculations) improves after intravenous diazepam.
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PMID:Congenital familial hypertonia. 1236 18

Twelve patients underwent 17 endoscopic injections of botulinum toxin type A in the cricopharyngeus muscle for the treatment of dysphagia and cricopharyngeal spasm over a 3-year period. The patient's charts were reviewed. Preoperative and postoperative symptoms, examination, and swallowing studies were reviewed. Eleven of the 12 patients had improvement in their symptoms, which lasted for a mean of 3.8 months. Two patients elected cricopharyngeal myotomy for permanent correction of their dysphagia. There was 1 case of postoperative neck cellulitis in an immunocompromised patient undergoing simultaneous excision of a thyroglossal duct cyst. We conclude that endoscopic injection of botulinum toxin is a relatively safe and viable technique for the treatment of dysphagia associated with cricopharyngeal spasm. It requires simple tools readily available to otolaryngologists. Larger, prospective controlled studies are necessary to establish its effectiveness and role in the management of this condition.
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PMID:Endoscopic botulinum toxin injection for cricopharyngeal dysphagia. 1238 53

Botulinum toxin is a dreaded biological toxin elaborated by Clostridium botulinum. The action of this toxin is to cause paralysis of both voluntary and involuntary muscles. The unique property of paralysing capability of muscles has been used for the benefit of human beings. Dr Allan Scot, an ophthalmologist, first used the toxin in a patient with squint in 1981 and since then the botulinum toxin is being used in various disorders characterised by muscle overactivity such as spasticity in both children and adult, dystonic conditions such as blepharospasm, cervical dystonia, spasmodic dysphonia, writer's cramp, etc, hemifacial spasm and headache. Its main action is at the terminal nerve endings of myoneural junction and it prevents release of acetylcholine from vesicles thus causing chemical denervation. Its action persists for 3 to 4 months on an average. Its side effects such as drooping, diplopia, dysphagia, depending on the sites of injection, are few and usually transient. Generalised anaphylaxis is almost unknown. Now botulinum toxin is being used in non-neurological conditions where muscles are under spasmodic state such as achalasia cardia, anal fissure, spasm of urethral sphincter, etc. Because of wider safety range and fewer complications, botulinum toxin has been an important therapeutic armamentarium in different branches of medicine and surgery.
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PMID:Botulinum toxin: a dreaded toxin for use in human being. 1245 15


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