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Query: UMLS:C0011168 (
dysphagia
)
15,644
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Abnormalities of the innervation of the oesophagus have been shown in 18 out of 20 unselected diabetics without clinical
dysphagia
or
neuropathy
. The changes appear to be in the axons of the extrinsic and intrinsic parasympathetic fibres. It is probable that, as in the peripheral nerves, the major changes are in the Schwann cells, although here the affected fibres are unmyelinated.
...
PMID:Neuropathology of the oesophagus in diabetes mellitus. 444 9
We analyzed the clinical, radiographic, esophageal manometric, and pathological features of 10 patients referred with jejunal diverticulosis. Nine patients were over age 59 yr and had symptoms of intestinal pseudoobstruction of 5-43 yr duration. Seven had surgery for mechanical obstruction, although none was found. Eight had diarrhea, steatorrhea, and weight loss. Five had Raynaud's phenomenon and heartburn, and 2 had
dysphagia
. At radiography, 9 had jejunal diverticula with or without duodenal or ileal diverticula, or both. Two each had abnormal structure or motility of the esophagus or stomach. At manometry, 3 of 7 had a nonspecific motor abnormality, and 1 other had low amplitude peristaltic waves. Light microscopy of small intestinal tissue in 7 patients showed that 4 had fibrosis and decreased numbers of normal-appearing muscle cells, findings consistent with progressive systemic sclerosis. Two others had fibrosis associated with degenerated smooth muscle cells, findings consistent with a visceral myopathy. The seventh patient had neuronal and axonal degeneration and neuronal intranuclear inclusions, findings consistent with a visceral
neuropathy
. We conclude that (a) intestinal pseudoobstruction is a major clinical manifestation of jejunal diverticulosis, (b) jejunal diverticulosis is a heterogenous disorder associated with at least three abnormalities of the smooth muscle or myenteric plexus, (c) in contrast to intestinal pseudoobstruction without diverticulosis, the esophagus, stomach, and colon are less frequently involved in jejunal diverticulosis, and (d) some patients with jejunal diverticulosis probably have clinically inapparent progressive systemic sclerosis.
...
PMID:Jejunal diverticulosis. A heterogenous disorder caused by a variety of abnormalities of smooth muscle or myenteric plexus. 640 4
A 67 years old man was admitted on July 1979 for nausea,
dysphagia
and rectal pain. At age 64 he had undergone radiotherapy on the lower lip for an epidermoid carcinoma. He remained then healthy. His medical history was negative with the exception of chronic bronchitis. He had never been exposed to toxic agents or drugs and had never left Europe. A few days after admission he suffered acute intestinal obstruction but at laparostomy no etiology was found. At the same time the patient complained of pain in all four limbs and he was found to have diffuse wasting of muscles, areflexia and distal sensory loss. No sign of dysautonomia was present. Physical examination was negative with the exception of a cervical lymphadenopathy. The lymph node biopsy showed an undifferentiated metastatic carcinoma. Negative investigations included: blood cells count; serum ionogram and immunoelectrophoresis; thyroid function tests; serological test for Chagas' disease. The following abnormalities were found: ESR: 55-105; CSF protein: 145 mg/100 ml and 1 cell mm3; whole blood folic acid: 1,7 mg/ml; Hbs antigen was present in blood; EMG showed evidence of denervation but motor conduction velocities were normal. By September the patient's weakness had increased and complete intestinal obstruction persisted. At oesophageal, gastric and duodenal fibroscopy no contraction was visible, and biopsies were negative. The patient died of peritonitis on October 5th, 1979. At necropsy peritonitis secondary to multiple perforation of the large bowel was found. No recurrence of the lip carcinoma or metastase or evidence of a primary carcinoma was found. Light microscopy showed no evidence of amyloidosis or scleroderma. Examination of the alimentary tract showed abnormalities restricted to the myenteric plexuses which varied from one level to another. In the small bowel there was hyperplasia of the smooth muscle and the myenteric plexuses were enlarged by marked proliferation of Schwann cells. Severe neuronal loss and nodules of Nageotte were also noted. Schwann cells proliferation was less marked in the stomach and large bowel. Lympho-histiocytic infiltration strictly confined to the region of the myenteric plexuses was present in oesophagus, stomach, large bowel and rectum. Mild chronic inflammatory lesions were also found in anterior and posterior spinal roots and semi-lunar ganglia. The striking feature of this case is the association of an undifferentiated carcinoma and a polyradiculoneuritis with a complete alimentary tract palsy of rapid onset, secondary to lesions restricted to the myenteric plexuses. The low folate level was insufficient to explain the
neuropathy
. Investigations showed no evidence of the usual causes of intestinal pseudo-obstruction: muscular, dysautonomic, toxic, plexic (idiopathic, familial, inflammatory), Chagas' disease). The clinical course, the pathological pictures of the alimentary tract and spinal roots and the association with a carcinoma suggest that our case may represent a paraneoplastic syndrome...
...
PMID:[Paralysis of digestive tract with lesions of myenteric plexuses. A new paraneoplastic syndrome (author's transl)]. 729 42
An epidemic outbreak of peripheral neuropathy affected Cuba in 1992-93 resulting in 50,862 cases (national cumulative incidence rate (CIR) 461.4 per 100,000). Clinical forms included retrobulbar optic
neuropathy
, sensory and dysautonomic peripheral neuropathy, dorsolateral myeloneuropathy, sensorineural deafness, dysphonia and
dysphagia
, spastic paraparesis, and mixed forms. For epidemiological purposes, cases were classified as optic forms (CIR 242.39) or peripheral forms (CIR 219.25). Increased risk was found among smokers (odds ratio (OR) 4.9), those with history of missing meals (OR 4.7) resulting in lower intake of animal protein, fat, and foods that contain B-vitamins, combined drinking and smoking (OR 3.5), weight loss (OR 2.8), excessive sugar consumption (OR 2.7) and heavy drinking (OR 2.3). Optic neuropathy was characterized by decreased vision, bilateral and symmetric central or cecocentral scotomata, and loss of color vision due to selective lesion of the maculopapillary bundles. Peripheral neuropathy was a distal axonopathy lesion affecting predominantly large myelinated axons. Deafness produced selective high frequency (4-8 kHz) hearing loss. Myelopathy lesions combined dorsal column deficits and pyramidal involvement of lower limbs with spastic bladder. Clinical features were those of Strachan syndrome and beriberi. Intensive search for neurotoxic agents, in particular organophosphorus esters, chronic cyanide, and trichloroethylene intoxication, yielded negative results. Treatment of patients with B-group vitamins and folate produced rewarding results. Most patients improved significantly and less than 0.1% of them remained with sequelae; there were no fatal cases. Supplementation of multivitamins to the entire Cuban population resulted in curbing of the epidemic. Overt malnutrition was not present, but a deficit of micronutrients, in particular thiamine, cobalamine, folate and sulfur amino acids appears to have been a primary determinant of this epidemic.
...
PMID:An epidemic in Cuba of optic neuropathy, sensorineural deafness, peripheral sensory neuropathy and dorsolateral myeloneuropathy. 769 85
Megaesophagus was diagnosed in 15 llamas on the basis of survey and contrast radiography. Age of onset ranged from 13 months to 9.5 years. Clinical signs varied, with salivation being the most common; regurgitation or
dysphagia
were noted in only 33% of the cases. Duration of the disorder ranged from 1 week to 5 years. Organophosphate toxicity was the cause of megaesophagus in 1 llama. While most cases were of unknown etiology, the 3 with histological abnormalities included 1 with vagal
neuropathy
and 2 with a degenerative myopathy of esophageal muscles. The causes in most were undetermined.
...
PMID:Megaesophagus in 15 llamas: a retrospective study (1985-1993). 776 Mar 15
Esophageal dysphagia associated with sarcoid has been attributed to dysmotility from
neuropathy
, dysmotility from myopathy, mechanical obstruction from esophageal mural involvement, and mechanical obstruction from extrinsic compression by subcarinal lymphadenopathy. The relative importance of these etiologies has not been evaluated because of variable and nonstandardized analysis. In particular, manometry has not been performed to exclude esophageal dysmotility in
dysphagia
attributed solely to extrinsic compression. A 42-yr-old male with chronic sarcoid for 20 yr presented with mild
dysphagia
to solids. An upper gastrointestinal series revealed smooth narrowing of the esophageal lumen and transient hang-up of the barium column and a 1.3-cm diameter radiopaque pill at the level of the carina. Chest computerized tomography revealed esophageal narrowing at the level of the carina and splaying of the two mainstem bronchi from compression by subcarinal lymphadenopathy. Esophagogastroduodenoscopy revealed elliptical esophageal narrowing due to multiple, smooth, and nodular deformities at 29-32 cm from the incisors. Pathological examination of deep biopsies of the nodules revealed normal mucosa and submucosa without granulomas. Esophageal manometry revealed a highly localized high pressure zone of 39.8 +/- 6.1 mm Hg at 29-31 cm from the incisors (lab normal about -5 mm Hg). Esophageal muscle contractions were peristaltic and of normal amplitude above, within, and below this high pressure zone. This case report demonstrates that extrinsic compression from subcarinal lymphadenopathy is a sufficient mechanism for
dysphagia
with sarcoid, but it does not exclude a role for other mechanisms, such as nerve injury, in some cases.
...
PMID:Endoscopic, radiographic, and manometric findings in dysphagia associated with sarcoid due to extrinsic esophageal compression from subcarinal lymphadenopathy. 787 93
We report a 65-year-old woman with progressive multiple cranial
neuropathy
. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side;
dysphagia
was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85
Percutaneous gastrostomy is reported to be an effective alternative to total parenteral feeding or long-term nasogastric tube in the treatment of mechanical or functional
dysphagia
. The authors report their personal experience with 137 percutaneous gastrostomies performed on 98 men and 39 women from January 1986 through December 1993. All the maneuvers were performed under fluoroscopic guidance in the patients with head or neck cancer, neoplastic, vascular or post-traumatic
neuropathy
and upper GI tract cancer. To avoid left hepatic lobe trauma, percutaneous gastrostomy needs to be performed under US guidance. A 7F nasogastric tube is used to fill the stomach with air. After distending the gastric cavity, with the Seldinger technique under local anesthesia, fascial dilators of progressively increasing caliber are introduced into the gastric cavity and the final 12F gastrostomy catheter is positioned under fluoroscopic guidance. No major complications, such as hemorrhage or peritonitis, occurred. In one case, during the maneuver, the patient complained of severe epigastric pain which regressed with no further problems two hours later. In three cases the gastrostomy catheter fell out of place and was replaced by running the fistolous tract with a venous cannula and then a guidewire for gastrostomy repositioning. With this type of treatment, the patient can be given enteral feeding the following day. The maneuver requires approximately 10 minutes to perform and is well tolerated by the patient as it requires no general anesthesia. Percutaneous gastrostomy is more cost-effective than surgery or endoscopy and hospitalization is shorter. The only contraindications to this maneuver are hepatomegaly (because of the risk of liver trauma during percutaneous maneuvers), ascites (because of the risk of infection) and finally the complications resulting from gastric resection.
...
PMID:[Percutaneous gastrostomy. Personal experience in 137 cases]. 787 38
The EORTC Study Group on Quality of Life has developed a modular system for assessing the quality of life of cancer patients in clinical trials composed of two basic elements: (1) a core quality of life questionnaire, the EORTC QLQ-C30, covering general aspects of health-related quality of life, and (2) additional disease- or treatment-specific questionnaire modules. Two international field studies were carried out to evaluate the practicality, reliability and validity of the core questionnaire, supplemented by a 13-item lung cancer-specific questionnaire module, the EORTC QLQ-LC13. In this paper, the results of an evaluation of the QLQ-LC13 are reported. The lung cancer questionnaire module comprises both multi-item and single-item measures of lung cancer-associated symptoms (i.e. coughing, haemoptysis, dyspnoea and pain) and side-effects from conventional chemo- and radiotherapy (i.e. hair loss,
neuropathy
, sore mouth and
dysphagia
). It was administered to patients with non-resectable lung cancer recruited from 17 countries. In total, 883 and 735 patients, respectively, completed the questionnaire prior to and once during treatment. The symptom measures discriminated clearly between patients differing in performance status. All item scores changed significantly in the expected direction (i.e. lung cancer symptoms decreased and treatment toxicities increased) during treatment. With one exception (problems with a sore mouth), the change of toxicity measures over time was related specifically to either chemo- or radiotherapy. However, the single item on
neuropathy
did not measure adequately the full range of symptoms. The hypothesised scale structure of the questionnaire was partially supported by the data. The multi-item dyspnoea scale met the minimal standards for reliability (Cronbach alpha coefficient > 0.70), while the pain items did not form a scale with reliability estimates acceptable for group comparisons. In conclusion, the results form international field testing lend support to the EORTC QLQ-LC13 as a clinically valid and useful tool for assessing disease- and treatment-specific symptoms in lung cancer patients participating in clinical trials, when combined with the EORTC core quality of life questionnaire. In a few areas, however, the questionnaire module could benefit from further refinements. In addition, its performance over a longer period of time still needs to be investigated.
...
PMID:The EORTC QLQ-LC13: a modular supplement to the EORTC Core Quality of Life Questionnaire (QLQ-C30) for use in lung cancer clinical trials. EORTC Study Group on Quality of Life. 808 Jun 79
A 43-year-old male was referred by a veterinarian who evaluated his dog for a seizure and suspected a toxic lead exposure for both. He refurbished houses, removing old paint, and complained of decreased cognition, fatigue, and muscle cramps. He had a depressed affect, postural tremor, right arm weakness with partial denervation on EMG, and borderline-low sensory nerve action potential (SNAP) amplitudes. A mild anemia and elevated serum and urine lead levels supported a diagnosis of lead
neuropathy
. Chelation therapy increased urine lead excretion without symptomatic improvement. His brother worked part-time with him and developed similar findings, but also had difficulty chewing,
dysphagia
, perioral twitching, gynecomastia, and multifocal denervation of extremity and facial muscles. His lead levels were not elevated, but an androgen receptor mutation identified on the X chromosome for both brothers confirmed the diagnosis of X-linked bulbospinomuscular atrophy (Kennedy's disease).
...
PMID:X-linked bulbospinomuscular atrophy (Kennedy's disease) masquerading as lead neuropathy. 817 Apr 88
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