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)

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.
Neurology 1978 Dec
PMID:Hereditary paroxysmal ataxia: response to acetazolamide. 36 53

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.
Prim Care 1979 Dec
PMID:Lacunar strokes. 39 51

Dysarthria due to involvement of the cerebellum represents a facultative symptom of cerebellar disease. The mechanisms by which such dysarthrias are produced are unknown but may result from pathologic involvement of the entire cerebellum. The symptoms of cerebellar dysarthria in children and in adults are described in two case histories. Characteristic speech defects or dysarthrophony occur. In addition to speech pathology, computer tomography of the skull is useful in obtaining both differential diagnosis and an estimate of prognosis. The goal of treatment should be the improvement of muscle defects of tonus and coordination needed for speech, and can employ both physio- and ergotherapy.
HNO 1977 Dec
PMID:[Cerebellar dysarthria (author's transl)]. 56 58

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.
Arch Neurol 1977 Dec
PMID:Lymphomatoid granulomatosis clinically confined to the CNS. A case report. 58 1

Eight techniques for quantifying intelligibility of dysarthric speech were compared. Eight dysarthric speakers who represented a wide range of severity were recorded producing single words and sentences. Thirty-two college students performed the following intelligibility quantification tasks: percentage estimates, rating scale estimates, work and sentence transcriptions, word and sentence completions, and word and sentence multiple-choice tasks. Intelligibility scores for transcriptions were compared to estimates and to other objective tasks with the following results: (1) all measurement techniques, except word completion, rank ordered speakers similarly to transcriptions, (2) mean estimates of intelligibility closely parallel transcription scores, but dispersion of listener estimates was large, and (3) objective tasks form a hierarchy with speakers receiving lowest scores on transcriptions, intermediate scores on completions, and highest scores on multiple-choice tasks. Mean scores for words and sentences were similar. Implications of results for clinical management of dysarthria are discussed.
J Commun Disord 1978 Dec
PMID:A comparison of techniques for measuring intelligibility of dysarthric speech. 73 65

Thirty adult aphasic subjects without apraxia of speech or dysarthria were tested for their ability to produce phonemes in single test words and in spontaneous contextual speech. Results indicated that 75% of the total phonemic errors were due to a whole-word phenomenon apparently associated with faulty processing of the word rather than faulty production of the phoneme. True phonemic errors comprised 25% of the total errors or about 2% of all responses. Phoneme substitutions were by far the most frequent error (61%). Of the 30 subjects, 28 made no phonemic errors in spontaneous contextual speech. Aphasic behavior is not characterized by significant breakdown of articulatory performance. Observed patterns of error do not clearly support a phonemic regression hypothesis.
Cortex 1976 Dec
PMID:Phonemic behavior of aphasic subjects without dysarthria or apraxia of speech. 100 73

The EEG response and drug kinetics after intravenous infusion of diazepam at 1-0 mg/min until nystagmus, dysarthria, and moderate sedation developed, has been investigated in five normal subjects and 17 patients with chronic liver disease. Diazepam induced adequate premedication with a similar clinical response in all subjects with no adverse reactions. Maximal response was during or within five minutes of infusion. The dose of diazepam required in liver chronic disease was 17-9 +/- 1-4 mg (M +/- SEM) compared with 27 +/- 5-4 mg in controls (p less than 0-01). Dose correlated significantly with serum albumin (p less than 0-05). Baseline mean dominant frequency (MDF) and slow wave index (SWI) significantly correlated with albumin (p less than 0-01). After diazepam, the MDF decreased and SWI increased. The change was greatest at the time of maximal clinical response. It was greater in liverdisease and was greatest in patients with previous hepaticencephalopathy. In spite of reduced dose requirements in liver disease, there was no significant difference in plasma concentration at the end of drug infusion...
Gut 1976 Dec
PMID:Intravenous administration of diazepam in patients with chronic liver disease. 101 18

H. I., a housewife aged 55 years, began feeling a gait disturbance at 48 years old. After this she had incoordination of arms, dysarthria and tremor of hands. Aged 54 years, she could not stand up by herself. In addition to these neurological signs she had a change of character, such as losing control of herself, unreservedness and unceremoniousness, and slight disturbance of intelligence. She died at the age of 55 years about seven years after the onset. Histopathologically, noticeable changes were observed on the medulla oblongata, pons and cerebellum; the severe neuronal loss of the pontine nuclei and the olivary nuclei with demyelination and gliosis of the cerebellopetal fibers. Especially a great deal of lipofuscin granules in the nerve cells of the frontal and temporal lobe were observed. In the substantia nigra some pigmented cells were deleted. This case was diagnosed as olivo-ponto-cerebellar atrophy clinico-histopathologically. We discussed conserning the etiology of the changes of personality and slight disturbance of intelligence in relation to histopathological changes. It is speculated that the mental disorders are due to the degeneration of the nerve cells in the frontal and temporal lobes.
No To Shinkei 1976 Dec
PMID:[Olivo-ponto-cerebellar atrophy with personality changes and slight disturbance of intelligence]. 103 31

A 48-year-old man, who took by mistake a sip of ointment containing dichloroethane, survived, and showed a course of two phases of toxic symptoms. After an initial narcosis and an interval with few pathological symptoms seizures, myoclonia and somnolence occurred. Irreversible final disturbances were lasting mental defects, cerebellar dysarthria, ataxia, and hydrocephalus. Concomitant diseases were acute liver dystrophy, nephropathy, and anemia. The clinical picture of dichoroethane posoning is outlines, the pathogenesis of this particular cerebral lesion described, and the therapy discussed.
Arch Psychiatr Nervenkr (1970) 1975 Dec 22
PMID:[Dichloroethane poisoning with myoclonic syndrome, seizures and irreversible cerebral defects (author's transl)]. 122 Jun 46

The authors report a case of acute lithium poisoning, of double interest by virtue of its accidental origin and the fact that the patient suffered from chronic uraemia treated by intermittent haemodialysis, without residual diuresis. Neurological involvement consisted of a succession of dysarthria, behaviour disturbance, extra-pyramidal hypertonia and finally coma with respiratory difficulties. A favourable outcome was obtained by daily haemodialysis which made possible the elimination of almost all the lithium introduced into the body.
Nouv Presse Med 1975 Dec 27
PMID:[Accidental lithium poisoning in a patient with chronic hemodialysis]. 124 Nov 29


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