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)

A comprehensive profile of communicative disorders in patients with Moebius syndrome was attempted. Seven patients were evaluated by the authors and the findings were added to 15 contributed case-histories. Most patients demonstrated some degree of dysarthria due to congenital paralysis of the facial nerves. Other problems such as cleft palate, hearing loss, mental retardation and delayed development of language were found in a few of the patients. As most of the older children in the sample and in reports in the literature eventually developed intelligible speech, a program of oral language stimulation and compensatory articulatory adjustments would appear to be the procedure of choice.
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PMID:Speech, language and hearing in Moebius syndrome: a study of 22 patients. 20 1

The purpose of this paper is to describe 2 siblings who had a generalized neurological disease which presented as intestinal pseudoobstruction. The siblings had 40-year histories of abdominal pain, distention, and vomiting as well as gait ataxia, small, irregular, poorly reactive pupils, dysarthria, absent deep tendon reflexes, and impaired vibratory and position senses. Compared with age-matched controls, they had inappropriate blood pressure responses to phenylephrine, the Valsalva maneuver, and upright posture, lack of sweating on warming, and pupillary denervation hypersensitivity. Radiographs revealed hyperactive, nonpropulsive contractions of a dilated esophagus and small intestine and extensive colonic diverticulosis. Esophageal manometry recorded repetitive, spontaneous, nonperistaltic waves and positive Mechyolyl tests. Postmortem examinations showed degeneration of the myenteric plexuses of the esophagus, small intestine, and colon of both patients. Myenteric plexus neurons were significantly reduced in number compared with 7 controls. About one-third of the siblings' neurons contained round, eosinophilic intranuclear inclusions, which, by histochemistry, were composed of protein by lacked RNA, DNA, carbohydrate, and fat. By electron microscopy the inclusions consisted of an irregular array of nonviral, nonmembrane-bounded filaments. Neurons and glial cells of the brain, spinal cord, dorsal root, and celiac plexus ganglia contained identical intranuclear inclusions. Intestinal smooth muscle was normal. These 2 siblings represent a unique disease in which degeneration of the myenteric plexus resulted in hyperactive but uncoordinated smooth muscle activity and the clinical syndrome of intestinal pseudoobstruction, the presenting manifestation of their neurological disease.
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PMID:A familial neuronal disease presenting as intestinal pseudoobstruction. 21 42

Paroxysmal symptoms of frequent recurrence and short duration occurring mostly unilaterally and without loss of consciousness have been described under a vast variety of headings. Brain stem origin of these symptoms was presumed. Electroencephalographic recordings usually did not show any paroxysmal discharges. 328 patients were found in the available literature including 9 patients of ours. The seizures were classified by their appearance. Tonic or dystonic, sensory, algetic, ataxic and akinetic-atonic fits were distinguished. The dystonic variety includes the "paroxysmal kinesiogenic choreoathetosis". The "paroxysmal dysarthria and ataxia" was subsumed under the ataxic type. By etiology, seizures were grouped into the cryptogenic and the symptomatic type. The symptomatic variety is frequently caused by multiple sclerosis, and rarely by tumours of the basal ganglia or by vascular disorders. Cranial computertomography showed subcortical lesions in three out of seven patients. In one case cerebral atrophy was found. All types of seizures respond very well to antiepileptic drugs. The prognosis is favourable with the cryptogenic type and unfavourable with the symptomatic variety depending on the underlying disease.
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PMID:[Brain stem seizures (author's transl)]. 25 39

The adverse effects of cerebral angiography with metrizamide and meglumine metrizoate were compared in 20 patients for each contrast medium using a double blind technic. Deterioration of the EEG and bradycardial reactions were seen more often with meglumine metrizoate than with metrizamide and these differences were statistically significant. Metrizamide also had a shorter circulation time, less influence on the blood pressure and EMG than meglumine metrizoate, but these differences were not statistically significant. The clinical examinations showed no difference in the minor adverse effects. One patient had transient hemiparesis and dysarthria after angiography with meglumine metrizoate but no serious complications were seen in the others.
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PMID:Cerebral angiography with non-ionic (metrizamide) and ionic (meglumine metrizoate) watersoluble contrast media. A comparative study with double blind technic. 33 Nov 37

Forty-five patients taking bismuth subnitrate orally for therapeutic reasons were admitted to hospital with a myoclonic encephalopathy of acute onset. The clinical features were similar, mostly with mental confusion, disorder of walking and standing, dysarthria, and myoclonic jerks. In 31 cases the EEG showed a characteristic pattern, not previously recognised, which assisted differential diagnosis.
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PMID:Toxic encephalopathy due to ingestion of bismuth salts: clinical and EEG studies of 45 patients. 33 49

From early childhood, eight patients in a kindred had paroxysmal bouts of ataxia, dysarthria, and nystagmus. The disorder was inherited as an autosomal dominant. Attacks occurred weekly and lasted 1 to 6 hours; there were slight cerebellar signs between attacks. Although the etiology was not determined, a serendipitous trial of acetazolamide completely abolished attacks, and all patients have remained free of attacks for as long as 5 years.
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PMID:Hereditary paroxysmal ataxia: response to acetazolamide. 36 53

A patient is reported whose ailment meets the criteria of CPM. The illness was complicated by pneumonitis, most likely of the aspiration type. Of particular interest was the reversibility of a clinical picture of marked deterioration when attention was paid to fluid and electrolyte balance and maintenance of respiration. This patient's illness appears to meet the criteria of CPM, namely impairment of the facial muscles and tongue with dysphagia and dysarthria, flaccid quadriparesis or quadriplegia, and frequently, lack of response to painful stimuli followed by respiratory paralysis. The presence of peripheral neuropathy has been previously noted in a patient with CPM, but it is not an integral part of the disease.
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PMID:Central pontine myelinolysis. 37 56

Arterial hypertension causes the formation of small lacunes, or ischemic brain infarcts, which may result in transient ischemic attacks, hemiparesis, sensory loss, ataxic hemiparesis, or dysarthria. Usually these effects are reversible with physical therapy, but multiple lesions may lead to dementia. Prevention of lacunar disease is possible with vigorous control of hypertension.
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PMID:Lacunar strokes. 39 51

A patient with symptomatic epilepsy receiving only phenytoin developed choreoathetosis and orofacial dyskinesias. These movement disorders disappeared when the drug was stopped and reappeared when the patient was challenged. Throughout the period of treatment, concentrations of phenytoin in serum were consistently low within the therapeutic range. Interfering symptoms from the cardiovascular system and the absence of some classic symptoms of phenytoin intoxication (nystagmus and dysarthria) contributed to delay the diagnosis. The patient died in hospital and autopsy of the brain showed rather localized encephalomalacies of corpus striatum. The pathogenic action of phenytoin and the role of preexisting brain lesions are discussed. Phenytoin must be suspected as the cause, when patients on this drug present with uncontrolllable epilepsy or neurological or mental deterioration.
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PMID:Choreoathetosis during phenytoin treatment. 40 43

A 35-year-old patient with terminal renal failure who had received 30 mg piperazine hexahydrate/kg body weight daily for 10 days for oxyuriasis was subsequently admitted to hospital in precoma with severe clinical symptoms not unlike those observed in so-called dialysis dementia: loss of consciousness, dysarthria, apraxia, clonic spasms, tremor, muscular weakness, dropping of objects, inability to think clearly and/or hallucinations. The EEG showed disturbances with diffuse, multifocal delta waves. Under maintenance hemodialysis the patient became asymptomatic one week after discontinuation of the piperazine therapy. Piperazine is contraindicated in patients with renal failure.
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PMID:[Piperazine intoxication in long-term hemodialysis]. 41 54


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