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)

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration]. 268 32

In a 38-year-old male patient suffering from a severe postzosteric trigeminal neuralgia, intravenous application of 10 mg biperiden lactate led to a long-lasting paradoxical reaction characterized by considerable bradycardia, dysarthria, and dysphagia. The heart rate was back to normal within 12 hours upon administration of orciprenaline under cardiac monitoring in an intensive care unit. Bradycardia induced by biperiden is attributed to the speed of injection and to a dose-related dual effect of atropine-like drugs on muscarine receptors.
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PMID:Bradycardia due to biperiden. 271 Aug 9

The patient, a 31-year-old married woman, noticed spasticity on walking at the age of 19 accompanied by ataxia, dysarthria and dysphagia. Facial twitching and dystonic movement of extremities have been observed since age 27. A sister of her father showed the similar ataxia and dysarthria, and expired of pneumonia at the age of 45. On admission at the age of 29, neurological examinations revealed nystagmus, marked spasticity with pathological reflexes and clonus, cerebellar ataxia, dysarthria and dysphagia, diffuse muscle wasting, fasciculation in facial musculature, and generalized slow dystonic movement. By neuro-otological studies bilateral MLF syndrome with upward gaze limitation and decreased velocity of saccadic eye movement were detected. Surface EMG at rest showed a dystonic discharges on the extremities. Needle EMG disclosed a systemic neurogenic change with reduced interference and high amplitude potentials. Atrophy of the brainstem was remarkable on the cranial CT and MRI. These abnormal eye movements, especially bilateral MLF syndrome and generalized dystonia seem to be quite unusual in the variety of spinocerebellar degenerations. On reviewing detected clinical descriptions on Joseph disease this case can be probably included.
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PMID:[A case of spinocerebellar degeneration with bilateral MLF syndrome and dystonia]. 274 81

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

A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin was reported. The patient was a 67-year-old man. His birth and development was normal. There was no family history of neuromuscular disease. On 26th March 1987 he was admitted to a hospital because of dysarthria and dysphagia after fever and diagnosed as having viral myositis. His conditions improved spontaneously with bed rest and he left hospital on 14th April. On 23rd April he had chill and sore throat with fever. On 27th he was admitted to the same hospital because of dysarthria and muscle weakness of the proximal portion of the upper limbs. These symptoms also improved with bed rest. He had repeated these symptoms several times and then he was admitted to our hospital on 12th June. On examination he showed the skin pigmentation under the right eye and the eruption in the back of hands and the buttocks. Muscle weakness was observed in the proximal portion of the upper limbs and the neck flexor. Laboratory tests in admission were as follows: sGOT 49 mU/ml, sGPT 104 mU/ml, LDH 1064 mU/ml, CPK 565 mM/ml, aldolase 25.2 IU/1/37 degrees C. Electromyography showed the typical myogenic changes and biopsy of left biceps brachii revealed inflammatory cells in the muscle fiber which are specific to polymyositis. Immuno-histochemical study is performed to analyse the subpopulation of mononuclear cells in biopsied muscle and skin. Mononuclear cells infiltrated into perimysium, endomysium and epidermis were positive for T11 and T8, but less positive for T4, B1 and Leu11. On the basis of these findings he was diagnosed as having "polymyositis syndrome".
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PMID:[A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin]. 280 15

Patients with bulbar amyotrophic lateral sclerosis (ALS) are often referred to the otolaryngologist/head and neck surgeon and speech pathologist for evaluation and management of dysphagia and dysarthria. These patients comprise an unusual group because of the progressive and multi-system nature of their illness. The neuromuscular disabilities associated with bulbar ALS cause a myriad of related symptoms associated with swallowing, speech, and respiration. Although the rate of progression cannot be predicted, a general pattern of progression is noted. Bulbar disease accounts for the majority of the worst symptoms of ALS. The loss of the ability to swallow changes eating from a pleasurable task to a burden of survival. Loss of communication effectively imprisons the patient in a state of isolation. The progressive weakness of respiration, predominantly a spinal rather than bulbar manifestation, is the cause of death for nearly all ALS patients and is also discussed. The general patterns of progression of bulbar ALS are outlined in this paper. The development of symptoms are correlated with specific treatment recommendations to aid the clinician in devising an orderly plan of management for this progressive disease.
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PMID:Bulbar amyotrophic lateral sclerosis: patterns of progression and clinical management. 258 13

A 42-year-old man presented with right temporal headache, dysarthria, and dysphagia. On examination, he had a right hypoglossal nerve palsy. The diagnosis of right internal carotid artery dissection was suggested by magnetic resonance imaging and confirmed by carotid angiography. A dynamic computed tomogram demonstrated enlargement of the carotid artery. In carotid dissection, the hypoglossal nerve may be compromised by local factors as it passes close to the carotid artery in the neck.
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PMID:Spontaneous internal carotid artery dissection presenting as hypoglossal nerve palsy. 304 72

Magnetic resonance (MR) imaging of a case of Hallervorden-Spatz disease (HSD) using a 1.5 T system is described. The patient showed progressive spastic diplegia with equinovarus deformity of the feet, dystonic postural movements, dysarthria, dysphagia, mental deterioration, optic nerve atrophy, and peripheral neuropathy. These clinical features were compatible with HSD. Symmetrical, decreased signal intensity was seen on both proton density weighted and T2-weighted spin echo images in the globus pallidus as well as in the substantia nigra (Group I). This MR finding suggests an increased iron deposition in these subcortical nuclei, which is characteristic of HSD. The characteristic MR imaging, together with the relevant clinical features, was considered to be useful for establishing the diagnosis of HSD.
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PMID:MR imaging of a group I case of Hallervorden-Spatz disease. 317 Aug 46

Experience with liver transplantation for patients with Wilson's disease who have major neurological impairment is limited, and this report describes the results obtained in two such patients. The first was a 30-year-old man with a 14-month history of hepatic and neurological impairment. In spite of treatment with d-penicillamine, he developed increasing dysarthria, dysphagia, akinesia and rigidity of all four limbs, and required continuous nursing care. Following transplantation, liver function was almost normal from four weeks onwards, but recovery of neurological function was much slower and was not seen until two to three months after surgery. By four months he was sufficiently mobile to be discharged, and when he returned for assessment at eight months, no abnormal neurological signs were detectable. The second patient was a 27-year-old woman with worsening liver dysfunction for eight years; one year previously she had developed dysarthria, akinesia, a fine tremor and moderate rigidity of all limbs as well as marked psychological impairment. There was no improvement on treatment with d-penicillamine or trientine, but as liver function returned to normal two months after liver grafting, her neurological and psychological function began to improve so that by three months she could be discharged.
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PMID:Reversal of severe neurological manifestations of Wilson's disease following orthotopic liver transplantation. 332 13

We surveyed neurologists and chronic care facilities in and near two New Jersey counties with a combined population of 799,022, regarding cases of progressive supranuclear palsy. All suspected cases were examined personally, using rigid criteria. The prevalence ratio was 1.39/100,000. A total of 50 New Jersey cases yielded median intervals to onset of requiring gait assistance, 3.1 years; visual symptoms, 3.9 years; dysarthria, 3.4 years; dysphagia, 4.4 years; requiring wheelchair, 8.2 years; and death, 9.7 years.
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PMID:Prevalence and natural history of progressive supranuclear palsy. 338 18


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