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 clinical and pathological findings of a 41-year-old male patient with atypical Charcot-Marie-Tooth disease were reported. There were 3 cases of subarachnoid haemorrhage, 2 nerve deafness and 2 hereditary motor and sensory neuropathy (HMSN) in his family. He had suffered from progressive nerve deafness since 5 years old and gait disturbance since 37 years old. He had been admitted to the psychiatric hospital 3 times because of hallucinatory-delusional state and behavior abnormalities. Neurological examinations at 39 years old revealed that he had mental deterioration (IQ 66), nerve deafness, diffuse muscle atrophy, most marked distally, sensory disturbance, areflexia, positive Romberg's sign, orthostatic hypotension, dysphagia and slurred speech. MCV of median nerve was 27.8 m/sec, and SCV was not evoked. EEG revealed nonspecific dysfunction of the brain. He died of ileus-like condition at 41 years old. General autopsy showed haemorrhagic infarction of the jejunum and ileum due to compression of the superior mesenteric artery and vein by an adhesion band of connective tissue formed after previous appendectomy. Neuropathological examinations revealed axonal degeneration and loss of myelinated fibers with schwannosis of anterior and posterior spinal nerve roots as well as peripheral nerves. The posterior roots were more severely affected than the anterior ones. Ganglion cells of the posterior root ganglia showed remarkable degeneration and loss. There was severe degeneration of the posterior columns, especially in the gracilis, of the spinal cord. Nerve cells in the anterior horns and Clarke's columns also displayed conspicuous atrophy or central chromatolysis followed by gliosis. There was slight degeneration of the posterior spinocerebellar tracts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of neuronal type Charcot-Marie-Tooth disease (HMSN type II) with nerve deafness and psychiatric symptoms]. 138 65

Eleven patients with dysphagia caused by severe esophageal stricture (length 2 to 10 cm) resulting from reflux esophagitis were treated with fibroendoscopic dilation (Eder-Puestow) and Roux-en-Y partial gastrectomy with vagotomy during 10 years (1979 to 1988). There was no operative mortality, but complications developed in three patients: One patient had a mediastinal abscess demanding thoracotomy as a result of esophageal perforation after dilatation; one had postoperative pneumonia; and one patient had ileus. After a mean follow-up of 4 years (range 1 to 10 years) esophagitis healed in all cases, as judged by endoscopy. Eight patients were asymptomatic, but three had slight transient dysphagia. Postoperatively one to eight dilations (average three to four) were needed to relieve dysphagia in the first postoperative year, but later the stricture healed in every case. Postoperative pH measurement was performed in six latest patients and showed complete absence of reflux in all cases. It is concluded that Roux-en-Y partial gastrectomy with vagotomy and endoscopic dilation is an effective, simple, and safe procedure in the management of severe peptic esophageal (acid or alkaline esophagitis) stricture. However, occasional postoperative dilations at the outpatient clinic are often needed in severe cases in the first postoperative year.
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PMID:Treatment of severe peptic esophageal stricture with Roux-en-Y partial gastrectomy, vagotomy, and endoscopic dilation. A follow-up study. 200 14

Endoscopic neodymium-YAG laser therapy for the gastrointestinal tract has been proved since 1975. Mortality and time of convalescence of patients treated with laser for acute or potential bleeding lesions have been markedly reduced in contrast to surgery. Sessile neoplastic polyps can be removed endoscopically by laser. Laser recanalization of obstructed carcinoma or scars in the upper and lower gastrointestinal tract to relieve dysphagia or ileus improves the patient's quality of life and has benefits for subsequent operations.
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PMID:[Endoscopic use of the neodymium YAG laser in the upper and lower gastrointestinal tract]. 257 63

Application of clinical endoscopic Nd:YAG laser (lambda = 1.06 micron) therapy has been introduced in 1975. It is suitable to stop all kinds of gastrointestinal bleeding with a primary success rate of 94% (1144/1212). Compared to surgical results a reduction in mortality rate has been achieved. These results have been confirmed worldwide in routine clinical application and in controlled trials with selected patients. Potential bleeding lesions such as Osler haemangiomas and angiodysplasias can be sealed. Recanalization of inoperable obstructed oesophageal and gastric carcinoma by laser vaporization to relieve dysphagia and subsequently endoscopic iridium after loading irradiation show a medium survival time of 7.4 months. Preoperative recanalization of obstructed colorectal carcinoma to relieve ileus or subileus allows preoperative peroral bowel lavage and total colonoscopy to find synchronous cancers and polyps and to perform primary resections without intraoperative colon lavage. Sessile benign neoplastic polyps can be resected curatively by Nd:YAG laser vaporization. Recanalization of peptic stenosis and anastomotic scar stenosis can be performed.
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PMID:Indications for endoscopic neodymium-YAG laser treatment in the gastrointestinal tract. Twelve years' experience. 332

12 cases of food-borne botulism were registered in Sion, Switzerland, between 31 December, 1993 and 12 January, 1994. A type B toxin was isolated from the serum of one patient and from the incriminated ham. Clinical data of 10 male patients aged 21 to 54 years and some epidemiologic data are reported. The clinical course was mild to moderate with predominant autonomic and gastro-intestinal symptoms and signs: blurred vision (10 patients of 10), dry mouth with dysphagia (9/10), asthenia (7/10), diarrhea and/or constipation (7/10), nausea and vomiting (6/10), abdominal cramps (5/10), impaired sexual function (5/10), dilated pupils (4/10). Some discomfort (mainly blurred vision, asthenia and impaired sexual function) persisted for several months in most patients. Neuromuscular involvement was never the reason for seeking medical assistance and had often disappeared at the time of the first visit. Two patients were hospitalized, one for transient ileus of unknown origin and the second (first suspected case) for monitoring and infusion of trivalent equine botulinum antitoxin. This treatment was administered on day eight after intoxication and had no effect on this patient's outcome when compared with others. No patient died. Epidemiology, diagnosis, treatment and prognosis of botulism are discussed.
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PMID:[Epidemic of type B botulism: Sion, December 1993-January 1994]. 748 37

In an effort to explore the utility of classic Nissen fundoplication performed laparoscopically, 16 adult patients with well documented gastroesophageal reflux underwent laparoscopic Nissen fundoplication. A full gastric fundal dissection was performed, with division of at least 2 short gastric vessels. The crura were approximated with 1-3 sutures, and a loose fundoplication was performed over an esophageal dilator (minimum 46 F) with three stitches, encompassing the esophageal wall (2.5 cm in length). All patients had symptoms of reflux refractory to medical therapy, and four had an esophageal stricture requiring preoperative dilatation. Fifteen of 16 procedures were completed laparoscopically; one patient required conversion to an open procedure to control bleeding from a posterior gastric vein. There were no other operative complications. The average operative time was 180 minutes (range 120-285). Clear liquids were begun at the passage of flatus (average 2.7 days postop), and patients were discharged an average of 4.1 days postoperatively. Postoperative complications included ileus (1 patient for 6 days), severe subcutaneous emphysema (1 patient), and dysphagia requiring dilatation (5 patients). In short follow-up (mean 4.43 mo., range 1-12 mo.) 14 of 15 patients had complete abolition of reflux symptoms, but one patient with persistent heartburn had reflux demonstrated on a postoperative upper GI series. Thirteen of 16 patients returned to full function within 14 days of surgery. We conclude that standard Nissen fundoplication is possible laparoscopically, and allows a rapid recovery from surgery. However, it is difficult, time consuming, and associated with a significant rate of recurrence in the short term (6%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Initial experience with laparoscopic Nissen fundoplication. 783 76

We report a case of oesophageal disease as the first manifestation in a patient with CREST syndrome. A 46-year-old man with achalasia-like syndrome developed CREST syndrome 4 years later. A pneumatic dilatation of the cardia was performed. After pneumatic dilatation the dysphagia and regurgitation disappeared but the patient developed reflux oesophagitis. Four years after diagnosis of oesophageal disease he presented with a clinical picture of CREST syndrome. An acute ileus and constipation developed later. After receiving medical therapy with omeprazole and cisapride the patient is free of oesophageal symptoms and bowel movements are normal. Oesophageal disease is common in patients with limited and diffuse scleroderma, but to our knowledge achalasia-like syndrome has not been previously described as the first manifestation of the systemic disease.
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PMID:Achalasia-like syndrome as the first manifestation in a patient with CREST syndrome. 872 33

Myotonic dystrophy is an autosomal dominant inherited disease of the skeletal and cardiac musculature that involves the pharyngeal and gastrointestinal smooth and striated muscles, resulting in velopharyngeal insufficiency, Swallowing difficulties, gastrointestinal motility disorders and anal incontinence. Gastrointestinal symptoms are found in a large proportion of patients suffering from this disease and may herald the onset of muscular disorders, in rare cases they are even the predominant feature of the disorder. We report on a 31-years-old patient with formerly undiagnosed myotonic dystrophy in combination with a non-rotation of the intestinal tract, an association of disorders that to our knowledge never has been reported before. Our patient was admitted as an emergency with signs of an acute abdomen with ileus, associated with acute aspiration pneumonia. Surgical intervention was avoided once the diagnosis of myotonic dystrophy had been confirmed and the patient was treated successfully by conservative therapy. A review of the literature indicates that conservative treatment of motility disorders of the bowel in patients with myotonic dystrophy is to be recommended.
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PMID:Intestinal non-rotation and pseudoobstruction in myotonic dystrophy: case report and review of the literature. 891 34

The authors used between October 1993 and January 1997 in 131 patients with inoperable malignant or benign stenosis of the oesophagus an expansible metal stent. In 25 patients the stenosis was in the upper third of the oesophagus, in 44 in the medium part, in 53 in the lower third of the oesophagus and in 9 patients in the area of the anastomosis. All patients suffered at the time when the stent was introduced from marked dysphagia (stage 3-4 according to the international classification). In 45 patients the authors introduced more than one stent. 112 patients suffered from malignant stenosis (67 squamous cell carcinoma, 27 adenocarcinoma, 9 pulmonary or bronchogenic carcinoma, in two instances lymphoma, in two instances leiomyosarcoma and in five patients another type of tumour). Seventeen patients suffered from benign stenosis (8 complications of reflux oesophagitis, 3 stenosis in the anastomosis, in two instances corrosion by acid, 2 cases of epidermolysis bullosa oesophagi and one post-radiation stenosis). In these patients repeatedly before introduction of the stent dilatation of the stenosis by means of a balloon dilatation catheter was attempted. In two instances the etiology of the stenosis was obscure. Complications related to the procedure proper or after insertion of the stent were recorded in 49 patients-dislocation of the stent 23x, occlusion of the stent 17x, development of a fistula 6x, ulceration 16x, haemorrhage 4x, hyperplasia of the mucosa 21x, ileus 2x, inadequate expansion of the stent 8x.
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PMID:[Metal stents in patients with malignant and benign esophageal stenoses]. 944 43

Autonomic dysfunction constitutes a prominent clinical feature of equine grass sickness (EGS). Significant injury to the nervous control of the alimentary system is life threatening, partly because of dysphagia but also because of the failure of the unique regulatory mechanisms in equine digestion involving water and electrolyte balance. The neuropathology also indicates the presence of a somatic polyneuropathy. The morphological features of EGS are similar to those of excitotoxic neuronal degeneration, which resembles neuronal apoptosis. It is difficult to ascertain from published accounts the degree of damage to central neurones: the distribution is well documented and selective but the proportion of damage is poorly quantified. If lesions involve a significant number of regulatory neurones they should produce functional deficits. Any clinical assessment of horses, especially those with chronic EGS, should include a thorough neurological examination. Although this will not necessarily improve the outcome of the case, it may enable the rational selection of animals with a reasonable prognosis for recovery which is partly determined by the extent of CNS lesions. The evidence supports the following pathogenesis. There is an initial lesion in the enteric nervous system of susceptible horses. In the acute form of EGS, massive enteric neuronal damage occurs first functionally, then structurally leading to generalized alimentary smooth muscle atony, enhanced secretions and altered fluid fluxes. Severe distension of the stomach and small intestines rapidly develops, which augments the intestinal ileus by intersegmental inhibitory reflexes and causes colic and dehydration. In subacute cases, failure of intestinal bicarbonate buffer together with alimentary stasis rapidly reduces caecal-colonic fermentation. Thus the osmolality of large intestinal digesta reduces and water travels out of the bowel along osmotic gradients. Water returns to the circulation, but is eventually lost in the gastric and small intestinal secretions. The observation that pathological lesions may not be seen in the prevertebral ganglia within the first few days of acute cases supports the view that a functional deficit precedes structural lesions which may be secondary to a retrograde degeneration. It is therefore possible to resolve the observations that less damage may be seen in prevertebral ganglia and elsewhere in peracute and acute cases with the more common finding that greater neuronal damage is present in acute than in chronic cases. These different observations are probably time dependent. Chronic EGS occurs when there is less initial enteric nerve damage which may lead to less secondary prevertebral ganglionic pathology, and more time for functional and structural compensatory mechanisms to develop. Denervation hypersensitivity develops at target sites both in the gut and in peripheral somatic nerves which may account, in part, for the clinical signs of patchy sweating and muscle tremors. Raised circulating adrenaline levels may also account for generalized sweating, may contribute to gastrointestinal atony and may affect pacemakers at the pelvic flexure. Many of the features of EGS make worthwhile the re-investigation of Clostridium botulinum Group III toxins, which are known to prevent vesicular exocytosis, stimulate neurosecretion, produce neuronal chromatolysis and inhibit neutrophil migration. Also, evidence from other species suggests that increased nitrergic neuronal activity can account for many of the clinical signs of EGS, namely dysphagia, generalized ileus, gastric dilatation, sweating, peripheral vasodilatation, tachycardia, salivary hypersecretion, muscle wastage and cachexia.
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PMID:The neurology and enterology of equine grass sickness: a review of basic mechanisms. 1032 May 95


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