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)

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 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

The first autopsy of a case of multiple sclerosis from the District of Hokuriku was reported. The patient, a 50-year-old house-wife, born in Toyama Prefecture, had noticed a paresthesia of her face, fatigue, numbness and weakness in the right limbs, dimness of vision and gait disturbance at ave 44. Furthermore, in the course of the disease, she had suffered from visual disorder, tetraplegia, hyperreflexia, pyramidal signs and cerebellar syndroms such as dysarthria, nystagmus, intention tremor and ataxia. She also showed symptoms of euphoria and dementia. After a course of six years she died of bronchopneumonia. Remissions and exacerbations were noted four times during her clinical history. Histopathologically, there were many recent and old demyelinating lesions of varying sizes and shapes in all parts of the central nervous system, namely the cerebrum, brainstem, spinal cord and optic nerve. In contrast to the clinical symptoms, the cerebellum itself revealed less plaques than the other areas of the brain. According to the observed distributions of the lesions, our case can be classified as belonging to the optico-cerebro-spinal type in the Ikuta and Zimmerman classification. The demyelinated lesions were characterized by a perivenular distribution of the plaques, lack of tissue necrosis, paucity of inflammatory reaction and marked fibrous gliosis of varying degrees.
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PMID:First autopsy report of a multiple sclerosis case in Hokuriku District of Japan. 53 38

An account is given of a form of hereditary, cerebellar ataxia and photomyoclonus. Eight cases from 5 generations were affected. The disease seemed to be transmitted as an autosomal dominant trait. The age at onset usually varied between 35 to 40 years. The symptoms and signs consisted of a cerebellar ataxia, dysarthria and intention tremor. There was no nystagmus. All patients exhibited photomyoclonus and were extremely sensitive to photic stimuli. Other signs were dementia, kyphosis, pes cavus and lipoma localized in the nape of the neck, shoulders and back. Two patients had a partial syndrome with photonyoclonus and skeletal deformities. None of the patients suffered from epilepsy, In one case, histopathological examination revealed atrophy within the cerebellar cortex, dentate nucleus and the posterior columns of the spinal cord. It is concluded that this syndrome belongs to a groups of hereditary ataxias and myoclonus, and differs from myoclonic cerebellar dyssynergia (Ramsay Hunt) and alos from a variety of familial myoclonus and ataxia (Gilbert et al. 1963);
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PMID:Hereditary ataxia, photomyoclonus, skeletal deformities and lipoma. 113 Jan 71

Cerebral dyspraxia associated with hemodialysis is a progressive, fatal syndrome. Patients suffer from a combination of psychiatric and neurological signs and symptoms. Psychiatric manifestations include anxiety, depression, paranoid ideation, and a progressive dementia with impaired concentration, decreased memory, personality changes, and hallucinations. Neurological findings include deliberate speech, stuttering, dysarthria, dyspraxia of speech and movement, tremulousness, myoclonic activity, asterixis, and seizures. These symptoms are aggravated during and immediately following dialysis. Patients usually die within 6 months of its onset. The etiology is unknown. Treatment efforts have failed to reverse its course. Recognition of this syndrome is highlighted so that informed, critical decisions can be made as to whether to continue dialysis therapy.
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PMID:Clinical and psychological test findings in cerebral dyspraxia associated with hemodialysis. 125 51

A 68-year-old right-handed woman was admitted to Tokyo Metropolitan Geriatric Hospital because of slowly progressive dysarthria and writing disability over 2-year period. On admission, severe dysarthria was observed, but no dysphagia. The dysarthria mostly resembled a type of pseudobulbar palsy, although it was associated with effortful speech production. An oro-facial apraxia was also found. She could name objects, and could understand spoken words correctly. Examination using the Western Aphasia Battery showed diminution of word fluency, impaired repetition and perseveration and writing errors. On the Wechsler Adult Intelligence Scale-R verbal IQ was 100 and performance IQ was 87. These scores did not suggest any significant degree of general intellectual deterioration. Wisconsin card sorting test disclosed mild frontal dysfunction. Magnetic resonance imaging showed cortical atrophy in the bilateral frontal and temporal lobes. Measurements of regional cerebral metabolic rate by 18F-FDG-PET demonstrated decreased uptake in the latero-dorso-inferior area of the bilateral frontal lobes, especially on the left side. The present case showed slowly progressive dysarthria and progressive aphasia without generalized dementia, and without typical aphasia. These symptoms are speculated to be related to the atrophy in the bilateral frontal and temporal lobes shown by MRI and the decreased metabolic rate in the left dominant bilateral frontal lobes on PET study. The pathologic process responsible for these lesions remains obscure.
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PMID:[Slowly progressive dysarthria and impaired language function--a case report]. 128 97

Thirty-six parkinsonian patients were selected by age of onset of over 70 and a minimum of five years duration of illness. The mean age of onset was 73.5 years and 30 patients were still alive after a mean of 7.2 years. We found that late onset Parkinson's disease has a relatively benign course with more "axial symptoms" especially dysarthria, freezing and postural instability. Dyskinesias and fluctuations are rare and dementia occurs in few patients in spite of their old age.
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PMID:Some clinical aspects of late onset parkinsonism. 132 Apr 90

Three cases of later onset metachromatic leukodystrophy in one family were reported. The brother is 32 years old, younger sister is 35 years old and the elder sister is 39 years old, who were normal as child without any family history of neurological disease. The three cases began their illness at about the age of 30 years old with dysarthria, progressive dementia, motor disturbance and numbness in the extremities. CT scan showed low density in the white matter of frontal, parietal lobes and around the ventricle. The written reports of CT scan were lacunar infarction in brother, multiple lacunar infarction in younger sister and Binswanger's disease in elder sister. Nerve biopsy showed myelinated fibers were decreased in number. Metachromatical materials were seen in and around the Schwann cell cytoplasm. Metachromatical materials were lamillar inclusions in granular matrix by electromicroscopic examination. So nerve biopsy is easy, safe and effective method to diagnose the uncertain pathogenic leukoence-phalopathy.
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PMID:[Later onset metachromatic leukodystrophy diagnosed by nerve biopsy]. 133 86

We examined six patients with an abrupt change in behavior after infarction involving the inferior genu of the internal capsule. The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation, suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia occurred in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients showed a focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. We infer that the capsular genu infarct interrupted the inferior and anterior thalamic peduncles, resulting in functional deactivation of the ipsilateral frontal cortex. These observations suggest that one mechanism for cognitive deterioration from a lacunar infarct is thalamocortical disconnection of white-matter tracts, in some instances leading to "strategic-infarct dementia."
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PMID:Confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome? 841 58

Neuropathological study of the visual pathway from the retina to the occipital cortex in Creutzfeldt-Jakob disease (CJD) has been scarcely performed. In the present study, pathological involvement of the visual pathway was observed in a 54-year-old man with CJD. The patient had the onset of visual disturbances in December 1985. He subsequently developed progressive dementia, right hemiparesis, ataxia and dysarthria, and rapidly fell into decerebrate posture in February 1986. In March 1986, myoclonus appeared on the whole body and EEG revealed periodic synchronous discharges, while brain CT and CSF findings showed no abnormalities. Myoclonus was observed most frequently from May to October 1986, and then reduced gradually. Brain atrophy on CT started from April 1986, and was progressive till the end stage of the disease. He died in January 1988, and the total clinical course was about 24 months. Neuropathological examination revealed severe degeneration of the cerebral cortex and the white matter. In the cerebral cortex, marked loss of neurons, astrogliosis, and spongiform changes were observed. In the cerebral white matter, the destruction of myelin sheaths and axons were evident. The cerebellum showed prominent loss of granule cells. These findings are consistent with those of the panencephalopathic type of CJD. In the visual pathway, loss of ganglion cells and bipolar cells in the retina, mild demyelination of the optic nerve, neuronal loss in the lateral geniculate body, and severe degeneration in the visual cortex were observed. The present case suggests that the neuropathological investigation in the visual pathway from the retina to the occipital cortex is important for clarifying the pathological processes in the visual system in CJD.
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PMID:[A case of the panencephalopathic type of Creutzfeldt-Jakob disease with retinal involvement]. 142 8


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