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)

Amyotrophic lateral sclerosis is a progressive dengenerative neuromuscular disease of insidious onset. It involves upper and lower motor neurons and causes both spastic and atrophic muscular symptoms. More than one fourth of patients have complaints relating to the head and neck (bulbar palsy); thus, the otolaryngologist may be the first physician to see them. Predominant symptoms are slurred speech, hoarseness, dysphagia, and dyspnea. Muscular weakness, atrophy, and fasciculation are noted on examination. The course is relentless, and only 20% of patients survive five years after diagnosis.
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PMID:The otolaryngologic presentation of amyotrophic lateral sclerosis. 11 40

The mute or nearly mute patient who is alert and has good understanding of speech and a right hemiparesis could have Broca's aphasia, akinesia of speech (transcortical motor aphasia), or aphemia. The patient who has Broca's aphasia does not write well, and his speech does not improve greatly with repetition. The speech of a patient with akinesia of speech improves with repetition. The aphemic patient writes normally, but his speech does not improve with repetition. The mute patient whose eyes are open but who is poorly responsive and moves little or not at all could be an akinetic mute (with either a cingulate or a thalamomesencephalic lesion) or have a locked-in syndrome. The latter is diagnosed by asking the patient to look up and down or to open and close his eyes. If he obeys these commands, the physician questions him using a code of eye movement responses. If the patient fails to respond at all, he is an akinetic mute; intense stimulation may result in speech or movement. If the patient is drowsy and has third nerve involvement, the lesion is in the thalamomesencephalic reticular formation. If the patient appears alert and has episodes of agitation, he probably has bilateral lesions in the gyri cinguli. Patients with weakness of the bulbar musculature (facial, palatal, and tongue weakness and dysphonia) may have either upper motor neuron or lower motor neuron lesions. Only bilateral upper motor neuron lesions produce permanent dysarthria. As a typical example, a patient has a transient left hemiparesis with dysarthria and almost completely recovers. Later, however, a right hemiparesis develops and the patient experiences severe bilateral facial weakness, drooling, dysphagia, and severe dysarthria. The absence of atrophy of the bulbar musculature, a hyperactive jaw jerk and gag reflex and, sometimes, inappropriate laughing or crying episodes indicate that the lesion is located above the medulla in the corticobulbar tracts. Flaccid paralysis, absence of the jaw jerk or gag reflex, and absence of other upper motor neuron signs, such as upgoing toes, indicate a lower motor neuron or neuromuscular junction problem. Appropriate tests to rule out myasthenia gravis should be done. The other conditions discussed here are often obvious from their clinical presentation. Although the specific disorder of speech sometimes is helpful in localizing the cause, in most patients, the associated deficits on neurologic examination are of greatest value.
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PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

Myasthenia gravis is a neuromuscular disease of insidious onset, characterized by weakness and fatigability of voluntary muscles. Most patients present with symptoms relating to the head and neck and thus may be seen first by the otolaryngologist. Predominant symptoms may be ocular (ptosis or diplopia) or related to fatigue of the oropharyngeal or laryngeal musculature (dysarthria, dysphonia, or dysphagia). Alleviation of muscular weakness and fatigability after administration of anticholinesterase drugs is pathognomonic of myasthenia gravis.
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PMID:The otolaryngologic presentation of myasthenia gravis. 44 37

A patient is presented with findings of separate intracranial and extracranial meningiomas, each of a different histologic type. A calcified fibrous meningioma, with secondary psammomatous features, presented as a left neck mass associated with hoarseness, dysphagia, a unilateral facial weakness and hearing loss. A noncalcified asymptomatic intracranial syncytial meningioma was discovered in the left frontal lobe after computerized tomographic and angiographic study of the cranial contents. The origin of the extracranial meningioma producing multiple unilateralcranial nerve disturbances and serous otitis media is discussed. The noncontiguous tumors in this patients are felt to have separate origins, with the extracranial lesion most likely arising in the temporal bone.
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PMID:Extracranial meningioma. 46 34

Amyotrophic lateral sclerosis (ALS) is a degenerative neurologic disease having both upper and lower motor neuron signs and symptoms. When the speech musculature is involved, a mixed dysarthria and dysphagia usually result. In a 49-year-old man with ALS, dysarthria and dysphagia progressed from mild to severe forms over 17 months. Eleven months after the patient first experienced symptoms, neurologic examination showed fasciculations of the extremities and tongue, limb weakness, and hyperreflexia of the limbs and velopharyngeal mechanism. Tongue strength was one-fourth that of normal. Lingual alternate motions rates for consonant-vowel syllables were also reduced. To enhance lingual strength and swallowing, a tongue-strengthening program was developed for use with articulation training; to augment velopharyngeal function, a palatal lift was fitted; and to increase extremity strength, physical therapy was initiated. Six months after the initial neurologic examination, medical and speech reevaluation showed progressive weakness of the body parts affected initially; continued decline in tongue strength and lingual alternate motion rate; hypoactive reflex activity, indicative of progressive involvement of the lower motor neuron system; and continued deterioration of articulation and phonation owing to the progressive nature of the disease.
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PMID:Progressive speech deterioration and dysphagia in amyotrophic lateral sclerosis: case report. 49 10

A 64-year-old hypertensive man presented with the dysarthria--clumsy hand syndrome, manifested by dysarthria, dysphagia, central facial weakness, deviation of the tongue on protrusion, incoordination of the affected hand, and mild imbalance on walking. A computed tomograpphic scan demonstrated a resolving acute infarction in the vicinity of the genu of the internal capsule.
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PMID:Dysarthria--clumsy hand syndrome produced by capsular infarct. 53 26

A family is described in which five males have late-onset facial weakness, dysarthria, dysphagia, and slowly progressive proximal weakness. Electrodiagnostic studies and muscle biopsy were compatible with spinal muscular atrophy. This family appears quite similar to several previously reported families with late-onset X-linked recessive spinal and bulbar muscular atrophy. Because of the relative homogeneity of this particular phenotype of spinal muscular atrophy, a single metabolic derangement was sought. Three obligate carriers were studied, and no abnormality was detected. A further family with this condition is briefly discussed.
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PMID:Late-onset X-linked recessive spinal and bulbar muscular atrophy. 57 30

A 38-year-old man developed pain and peripheral-type weakness on the right side of his face and was discovered to have decreased hearing bilaterally, as well as optic nerve swelling on the right. The pain and optic nerve swelling subsided over a period of six weeks, but hearing loss and facial weakness persisted. Thirty months later, he developed dysphagia, ataxia, dysarthria, nystagmus, and progressive spastic quadriparesis. He died approximately four years after the onset of the illness. Although no evidence of disease was found other than in the central nervous system during life, two nodules in the right lower lung were found on autopsy. The examination of these nodules, as well as the brain stem, showed an angiocentric and angionecrotic process with lymphoreticular and plasmacytoid invasion.
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PMID:Lymphomatoid granulomatosis clinically confined to the CNS. A case report. 58 1

Systemic lupus erythematosus with polymyositis and polyarthritis was diagnosed in a 7-year-old female Standard Poodle. Pertinent clinical signs included extreme muscular weakness, muscle wasting, atrial fibrillation, and dysphagia due to megaesophagus. Aspiration pneumonia secondary to the megaesophagus contributed to the death of the dog. Serum muscle enzyme activities were increased. Electromyographic findings included fibrillation potentials, positive sharp waves, increased insertional activity, and bizarre high-frequency repetitive potentials. Histopathologic findings in skeletal muscle included myofiber necrosis and phagocytosis; regeneration of myofibers; perivascular and interstitial infiltrations of macrophages, lymphocytes, and plasma cells; and type I and II myofiber degeneration and vacuolation.
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PMID:Polymyositis and polyarthritis associated with systemic lupus erythematosus in a dog. 83 Jun 33

Thirty-one polymyositis patients treated with low-dose corticosteroid were age and sex matched with 31 polymyositis patients treated with high-dose corticosteroid. Although disease severity at onset of the study was similar in the groups, no statistically significant difference in survival was found. The death rate in each group was greater than normal. The presence of dysphagia or severe muscle weakness lessened the chances of survival. Controlled trials with other drugs should be carried out.
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PMID:Survival in polymyositis: corticosteroids and risk factors. 88 99


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