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

Cricopharyngeal dysphagia, a disorder of uncertain pathogenesis, is most frequently found in patients with associated gastroesophageal reflux. Seven patients who had dominant cricopharyngeal dysphagia were evaluated. Manometry showed characteristic motor incoordination. Biochemical profiles and endoscopy were normal. Electronmicroscopic examination of the cricopharyngeal muscle biopsy specimens obtained during myotomy showed significant ultrastructural abnormalities. These included numerous and aberrant mitochondria, increased glycogen, lipid inclusions, and phagolysozomes. A striking finding was the presence of numerous nemaline rods in five of seven biopsy specimens examined. The pathologic changes in this muscle in cryopharyngeal dysphagia have not been reported previously. Structural changes are thought to be a secondary response to reflux injury. Nemaline rods form part of the structural abnormality of muscle in patients who have cricopharyngeal dysphasia with no evidence of underlying generalized disease or myopathy.
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PMID:Nemaline rods in cricopharyngeal dysphagia. 740 97

Oropharyngeal dysphagia due to iatrogenic neurological dysfunction may relate to either medication side effects or surgical complications. There are several general mechanisms by which neurological side effects of medications can cause or aggravate oropharyngeal dysphagia. These include decreased level of arousal, direct suppression of brainstem swallowing regulation, movement disorders (dyskinesias, dystonias, and parkinsonism), neuromuscular junction blockade, myopathy, oropharyngeal sensory impairment, and disturbance of salivation. Postsurgical oropharyngeal dysphagia due to neurological dysfunction has been described in association with carotid endarterectomy, esophageal cancer surgery, anterior cervical fusion, and ventral rhizotomy for spasmodic torticollis. A potential explanation for oropharyngeal dysphagia following these surgical procedures is intraoperative mechanical disruption of the innervation of the pharyngeal constrictor muscles by the pharyngeal plexus. Posterior fossa and skull base surgery can lead to dysphagia as a result of intraoperative damage to brainstem centers and/or cranial nerves involved in swallowing. Perioperative stroke is the most likely explanation for oropharyngeal dysphagia appearing acutely following surgery, especially if the type of surgery predisposes to embolism or hypoperfusion.
Dysphagia 1995
PMID:Oropharyngeal dysphagia due to iatrogenic neurological dysfunction. 749 5

Oculopharyngodistal myopathy is characterized by the adult onset of ptosis, external ophthalmoplegia, dysphagia, and distal weakness. Although dysphagia is common, other gastrointestinal involvement has not been described. We report a case with childhood onset who developed chronic intestinal pseudo-obstruction. Other myopathies associated with ophthalmoplegia and intestinal pseudo-obstruction such as mitochondrial cytopathies were excluded. Whether oculopharyngodistal myopathy is a variant of oculopharyngeal muscular dystrophy or a distinct neuromuscular disorder is unknown and requires further study.
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PMID:Childhood-onset oculopharyngodistal myopathy with chronic intestinal pseudo-obstruction. 763 Mar 44

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.
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PMID:Megaesophagus in 15 llamas: a retrospective study (1985-1993). 776 Mar 15

The potential causes of neurogenic oropharyngeal dysphagia in cases in which the underlying neurologic disorder is not readily apparent are discussed. The most common basis for unexplained neurogenic dysphagia may be cerebrovascular disease in the form of either confluent periventricular infarcts or small, discrete brainstem stroke, which may be invisible by magnetic resonance imaging. The diagnosis of occult stroke causing pharyngeal dysphagia should not be overlooked, because this diagnosis carries important treatment implications. Motor neuron disease producing bulbar palsy, pseudobulbar palsy, or a combination of the two can present as gradually progressive dysphagia and dysarthria with little if any limb involvement. Myopathies, especially polymyositis, and myasthenia gravis are potentially treatable disorders that must be considered. A variety of medications may cause or exacerbate neurogenic dysphagia. Psychiatric disorders can masquerade as swallowing apraxia. The basis for unexplained neurogenic dysphagia can best be elucidated by methodical evaluation including careful history, neurologic examination, videofluoroscopy of swallowing, blood studies (CBC, chemistry panel, creatine kinase, B12, thyroid screening, and anti-acetylcholine receptor antibodies), electromyography, and magnetic resonance imaging (MRI) of the brain, plus additional procedures such as lumbar puncture and muscle biopsy as indicated. Little is known about aging and neurogenic dysphagia, specifically the relative contributions of natural age-related changes in the oropharynx and of diseases of the elderly, including periventricular MRI abnormalities, in producing dysphagia symptoms and videofluoroscopic abnormalities in this population.
Dysphagia 1994
PMID:Neurogenic dysphagia: what is the cause when the cause is not obvious? 780 24

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.
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PMID:Endoscopic, radiographic, and manometric findings in dysphagia associated with sarcoid due to extrinsic esophageal compression from subcarinal lymphadenopathy. 787 93

Nephropathic cystinosis is a lysosomal storage disorder leading to renal failure by age 10 years. Prolonged patient survival following renal transplantation has allowed the development of previously unknown long-term complications. Muscle involvement has been reported in a single posttransplant cystinosis patient, but the range of clinical, electrophysiologic, and histologic features has not been fully described. Thirteen of 54 post-renal-transplant patients that we examined developed weakness and wasting in the small hand muscles, with or without facial weakness and dysphagia. Tendon reflexes were preserved and sensory examinations were normal. Electrophysiologic studies in 11 affected patients showed normal nerve conduction velocities and preserved sensory action potentials. The voluntary motor units in the affected distal muscles had reduced amplitude and brief duration, confirmed with quantitative electromyography in 4 patients. Biopsy of the severely affected abductor digiti minimi or extensor carpi radialis brevis muscles in 2 patients revealed marked fiber size variability, prominent acid phosphatase-positive vacuoles, and absence of fiber type grouping or inflammatory cells. Crystals of cystine were detected in perimysial cells but not within the muscle cell vacuoles. The muscle cystine content of clinically affected muscles was markedly elevated. We conclude that a distal vacuolar myopathy is a common late complication of untreated nephropathic cystinosis. Although the cause is unclear, the general lysosomal defect in this disease may also affect the lysosomes within muscle fibers.
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PMID:Distal vacuolar myopathy in nephropathic cystinosis. 810 99

Oculopharyngeal muscular dystrophy (OPMD), a late onset autosomal dominant myopathy, is common among the French-Canadians and the Jews from Bukhara (Uzbekistan); most clinical histologic and genetic data published until now, as well as the recently suggested diagnostic criteria, are based on studies among the former. We studied 79 patients with OPMD belonging to the newly described Jewish-Bukhara cluster. The disease began between the ages of 21 and 78 yr (median 53 yr). In 11 patients (15%) it began before the age of 40. Ptosis was the first symptom in 59 patients and dysphagia in the remaining 20. Eight patients (10%) were monosymptomatic (ptosis) after more than 7 yr from the start of the disease; however, other family members had additional signs/symptoms. The patients belong to 29 families; in 26 age-dependent autosomal dominant inheritance could be documented. Among them there is certain evidence for genetic anticipation. This clinical study is the largest published concerning patients other than French-Canadians.
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PMID:Clinical features of oculopharyngeal muscular dystrophy among Bukhara Jews. 818 15

Neurogenic dysphagia results from sensorimotor impairment of the oral and pharyngeal phases of swallowing due to a neurologic disorder. The symptoms of neurogenic dysphagia include drooling, difficulty initiating swallowing, nasal regurgitation, difficulty managing secretions, choke/cough episodes while feeding, and food sticking in the throat. If unrecognized and untreated, neurogenic dysphagia can lead to dehydration, malnutrition, and respiratory complications. The symptoms of neurogenic dysphagia may be relatively inapparent on account of both compensation for swallowing impairment and diminution of the laryngeal cough reflex due to a variety of factors. Patients with symptoms of oropharyngeal dysphagia should undergo videofluoroscopy of swallowing, which in the case of neurogenic dysphagia typically reveals impairment of oropharyngeal motor performance and/or laryngeal protection. The many causes of neurogenic dysphagia include stroke, head trauma, Parkinson's disease, motor neuron disease and myopathy. Evaluation of the cause of unexplained neurogenic dysphagia should include consultation by a neurologist, magnetic resonance imaging of the brain, blood tests (routine studies plus muscle enzymes, thyroid screening, vitamin B12 and anti-acetylcholine receptor antibodies), electromyography/nerve conduction studies, and, in certain cases, muscle biopsy or cerebrospinal fluid examination. Treatment of neurogenic dysphagia involves treatment of the underlying neurologic disorder (if possible), swallowing therapy (if oral feeding is reasonably safe to attempt) and gastrostomy (if oral feeding is unsafe or inadequate).
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PMID:Dysphagia associated with neurological disorders. 820 77

Pharyngeal constrictor paresis (PHCP) is sometimes found in videoradiography of the swallowing act in patients complaining of dysphagia. Ten patients with PHCP and 10 dysphagic, age- and sex-matched controls with normal videoradiography were neurologically evaluated and examined with magnetic resonance imaging (MRI) of the brain and brainstem in order to learn the pathogenetic process behind PHCP. The study revealed 8 PHCP patients and 1 dysphagic control with abnormal clinical neurological findings such as myopathy, cerebrovascular disease, or extrapyramidal disease. The neurological examination revealed considerable information of prognostic and therapeutic value in PHCP patients. The MRI was abnormal in 7 PHCP patients and 4 dysphagic controls. However, the findings in MRI were nonspecific but the examination was found to be valuable in selected cases. It is concluded that PHCP is an indicator of neurological disease and accordingly, such patients should be examined by a neurologist to establish the cause of the disease.
Dysphagia 1993
PMID:Pharyngeal constrictor paresis: an indicator of neurologic disease? 835 45


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