Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Reported here are the electrodiagnostic findings in a patient with myasthenia gravis who had dysarthria, dysphagia, and dyspnea. The use of repetitive nerve stimulation and single fiber electromyography studies for the evaluation of patients suspected of myasthenia gravis is reviewed.
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PMID:AAEM case report #3: myasthenia gravis. 187 Jun 29

In myasthenia gravis and amyotrophic lateral sclerosis the ENT specialist or the phoniatrician may be consulted first, because in about 30 percent of all cases the initial symptoms are dysarthria, dysphagia or dyspnea. Three typical cases of each condition are presented. The quality of life of the patients can be improved considerably by early diagnosis and treatment. Special diagnostic and therapeutic procedures are described.
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PMID:[Dysarthria, dysphagia or dyspnea as a reason for the initial consultation in pseudoparalytic myasthenia gravis and amyotrophic lateral sclerosis]. 231 Apr 61

Dysarthria, dysphagia and repeated aspiration in a 54-year-old woman diagnosed and treated for myasthenia gravis 7 years earlier were initially thought to represent a late exacerbation of myasthenia. A cervical mass invading the jugular foramen and causing multiple lower cranial nerve palsies was biopsied and found to represent invasive ectopic thymoma.
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PMID:Late pseudo-exacerbation of myasthenia gravis due to ectopic thymoma invading lower cranial nerves. 231 Oct 16

A number of reports describe the otolaryngologic manifestations of myasthenia gravis. Symptoms such as dysphagia, dysarthria, and dysphonia are quite common to myasthenia gravis, yet the usual onset of this disorder is insidious in nature. We report a case of an 18-year-old woman, previously undiagnosed, who presented with acute dysphagia followed by the rapid onset of respiratory failure. The diagnosis and treatment of myasthenia gravis are discussed.
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PMID:Respiratory failure as the initial presentation of myasthenia gravis. 274

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.
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PMID:Neurogenic dysphagia: what is the cause when the cause is not obvious? 780 24

We report a case of myasthenia gravis in a young Melanesian woman. It is only the second case described from Papua New Guinea and the first in which antibodies to the acetylcholine receptor have been demonstrated. The patient's complaint of occasional dysarthria was initially dismissed as hysterical in nature due to her apparent normal speech on conversation. The true nature of her problem only became apparent when she was asked to read a prolonged monologue. Myasthenia gravis may present without involvement of the eye muscles and the diagnosis may only become apparent if muscle groups are specifically tested for fatiguability.
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PMID:Myasthenia gravis in a young Papuan woman. 805 51

Eight elderly men whose primary symptoms of myasthenia gravis were decreased speech and swallowing ability were seen for speech pathology evaluations and videofluoroscopic swallow studies. All patients had fatigable flaccid dysarthria and greater than expected pharyngeal phase dysphagia on videofluoroscopy; eight had decreased pharyngeal motility as demonstrated by residual material in the valleculae and pyriform sinuses bilaterally; seven had episodes of laryngeal penetration secondary to overflow of residual material; and five experienced silent aspiration despite gag reflexes and the ability to cough to command. Five patients required feeding tubes because their dysphagia responded poorly to treatment. Videofluoroscopic swallow studies revealed a common swallowing profile with pharyngeal phase dysphagia greater than expected from patient symptoms. Dysphagia did not improve at the same rate as other manifestations of myasthenia gravis.
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PMID:Dysphagia in elderly men with myasthenia gravis. 879 Dec 38

A 49-year-old man, who developed generalized symptoms of myasthenia gravis at the age of 30 and had thymomectomy, was recently admitted to our hospital for myasthenic crisis after alpha-interferon (IFN) therapy for his chronic hepatitis C. He had shown only mild ocular symptoms before the start of the IFN intramuscular injection therapy. Three months after the IFN therapy (900MU three times a week after 2 weeks of daily injection), he developed generalized weakness, dysarthria, and dysphagia. After the cessation of his IFN therapy, his conditions became worse in parallel with the increase in the titer of anti-acetylcholine receptor antibody. He required artificial ventilation for 2 weeks during myasthenic crisis and he received food and medication through nasogastric tube. He recovered from myasthenic crisis and could eat orally 4 months after the cessation of interferon therapy, but he still suffered from mild bulbar symptoms 8 months after the IFN cessation. IFN therapy should be avoided for the patients with myasthenia gravis, since it may cause myasthenic crisis, and may aggravate myasthenic symptoms for a long period.
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PMID:[A case of myasthenia gravis which developed myasthenic crisis after alpha-interferon therapy for chronic hepatitis C]. 895 52


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