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 case of spontaneous pontine hematoma in young boy, with remitting and relapsing clinical course of up to 11 years, suspected of having pontine glioma or multiple sclerosis is reported. Differential diagnosis of these are mentioned with reference to our cases of pontine glioma. This patient was a man aged 16. At 5 years of age he had his first episode of double vision. 20 days after first episode, gait disturbance, left facial palsy and consciousness disturbance developed. Neurological and neuroradiological examination revealed a pontine glioma and radiotherapy was administered. All signs and symptoms resolved except for bilateral abducens palsy. Four months later, he again complained of gait disturbance and facial palsy. Examination revealed bilateral conjugate ocular palsy, left facial palsy and cerebellar ataxia. These symptoms again resolved spontaneously, except for bilateral abducens palsy. At age 16 years, having been asymptomatic for 10 years, he suddenly noticed loss of taste. At that time sensory disturbance of the left side of himself, right hearing disturbance, dysarthria and retardation urinae. Neurological examination revealed bilateral optic atropy, bilateral abducens palsy, left facial palsy, right hyperacuisis, dysarthria, left hemiparesis, hypesthesia of the left side of the body and left cerebellar ataxia. The vertebral angiography was no evidences of mass lesion and vascular anomalies. The computed tomography demonstrated a pontine hematoma. Conservative therapy was performed and these symptoms cleared off except for bilateral abducens palsy.
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PMID:[A case of spontaneous pontine hematoma in patient suspected of pontine glioma and multiple sclerosis (author's transl)]. 72 72

We reported a case of bilateral cerebellar hemorrhagic infarction in the distribution of the bilateral superior cerebellar artery. A 58-year-old man suddenly developed dizziness and transient loss of consciousness. The neurological examination revealed left hearing disturbance, left sensory disturbance involving face, dysarthria and bilateral ataxia. This patient was considered to be classic clinical syndrome of right superior cerebellar artery. CT and MRI revealed hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery. The right posterior cerebral artery was filling through the right posterior communicating artery on the right carotid angiography taken 2 hours after the onset. Bilateral vertebral angiography on the 18th day demonstrated no occlusions in the basilar artery and the bilateral superior cerebellar artery. Hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery, sparing other territories as the present case, is extremely rare. In this case, cerebral embolism (top of the basilar syndrome) was suggested because of existence of atrial fibrillation and sudden onset.
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PMID:[A case of bilateral cerebellar infarction in the distribution of the bilateral superior cerebellar artery]. 181 96

A 68-year-old man without familial history developed ataxic gait and sensory disturbance in the lower extremities. At the age of 74, neurological examination revealed marked cerebellar ataxia of all limbs, dysarthria, sensory disturbance of glove and stocking type in the extremities, and slight neurogenic muscular atrophy. There were no mental deterioration and dysautonomia. He died of pneumonia at the age of 74. Neuropathological findings. The cerebellum was decreased in size. Microscopically, there were severe disappearance of Purkinje cells in the cerebellar vermis and hemispheres. The molecular layer, granular cell layer, and cerebellar white matter were preserved. Neurons of the inferior olivary nuclei were also spared. In the spinal cord, there was myelin pallor in the posterior column predominant in Goll's fascicule and moderate atrophy of neurons in the anterior horn. Degeneration of the posterior roots was greater than that of the anterior roots. No abnormal findings were found in the extrapyramidal system, cranial nerves, and cerebrum. We compared this case clinicopathologically with other diseases with cortical cerebellar atrophy; alcoholic cerebellar degeneration, phenytoin intoxication, neuroleptic malignant syndrome, and subacute paraneoplastic cerebellar degeneration. In conclusion, idiopathic late cerebellar cortical atrophy (LCCA) was different clinicopathologically from the other diseases. Especially, LCCA showed the characteristic topography of Purkinje cells loss sparing the molecular and granule cell layers.
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PMID:[An autopsied case of idiopathic late cortical cerebellar atrophy--comparison with other cortical cerebellar atrophy]. 208 23

A case of adult Moyamoya disease, with formation of a transcranial external carotid-internal carotid (EC-IC) anastomosis through burr holes which had been made previously. A 43-year-old male suffered sudden headache and vomiting. Neurological examination revealed mild consciousness disturbance and dysarthria. The computed tomography (CT) scans showed intraventricular hemorrhage, which was drained through burr holes bifrontally. The diagnosis of Moyamoya disease was subsequently made by cerebral angiography. A month later he was discharged with mild gait disturbance and mental retardation. Seven years later he suddenly complained of gait disturbance, dysarthria and sensory disturbance involving the right upper extremity. A CT scan revealed a small hemorrhage in the left putamen. Carotid angiograms disclosed transcranial EC-IC anastomosis through the burr holes which had been made previously. It is suggested that revascularization can be expected after opening burr holes and incising the dura matter for Moyamoya disease in adults as well as, possibly, in children.
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PMID:[Adult moyamoya disease with a transcranial internal carotid-external carotid (EC-IC) anastomosis through burr holes]. 237 49

Fifty-three patients with infarction of the corona radiata adjacent to the body of the lateral ventricle were clinically evaluated in order to determine the clinical characteristics of this infarction and localization of the pyramidal tract in this area, as well as its somatotopy and etiology. Clinical characteristics included the following: (1) this type of infarction was observed in 9.1% of all patients with cerebral infarction; (2) although 81.1% of the patients of this type had clear consciousness and neuropsychological symptoms in some patients; (3) motor paralysis usually occurred in the upper limbs; (4) monoplegia occurred in 13.2% of patients, with monoplegia of upper and lower limbs being associated with infarction of the anterior and posterior portion, respectively, of the corona radiata adjacent to the body of the lateral ventricle; (5) pure motor hemiplegia was observed in 45.3% of patients; (6) facial paralysis and dysarthria were observed in 54.7% and 58.5% of patients, respectively, and the incidence of these symptoms was the highest in the infarction of the anterior portion of the corona radiata; (7) sensory disturbance, which was usually recognized as a mild subjective feeling of abnormality and localized to the limbs, was reported by 47.2% of patients; (8) risk factors included hypertension, diabetes and high hematocrit and triglyceride levels; (9) arteriosclerosis was often noted in areas between the siphon of the internal carotid artery and the main stem of the anterior and middle cerebral arteries; (10) 64.2% of patients were able to conduct independent activities of daily life (ADL) 1 month after the onset of the disease and more marked paralysis remained in the infarction of the middle portion than in the anterior or posterior portion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical characteristics of infarction of the corona radiata adjacent to the body of the lateral ventricle]. 275 54

The patient, a man aged 57, was admitted to our clinic on May 1, 1987, because of severe vertigo and unsteadiness in standing. Since the age of 55 he had been suffered from hypertension and atrial fibrillation. In September, 1986, he experienced vertigo but recovered soon without therapy. On April 25, 1987, while working, he noticed severe vertigo, nausea and vomiting. He was admitted to a hospital, and then transferred to our clinic. On admission, he was alert and the mentality was normal. Slight ptosis abducent nerve paresis, hypalgesia on the forehead, nose and cheek, facial paresis of peripheral type and hypacusis were detected on the left side. No anisocoria was observed. Sweating was impaired over the left side of the face. Elevation of the soft palate was limited on the left side and the tongue deviated to the left on protrusion. Dysarthria was detected. Though there was no muscular weakness in the extremities, incoordination and dysmetria were noted in the left arm and leg. He could not stand up because of vertigo and unsteadiness. There was no sensory disturbance in the trunk and extremities. Deep tendon reflexes were well elicited and no pathological reflex was observed. These clinical manifestations, except for the ipsilateral palatal and lingual disturbances, were typical of the lateral inferior pontine syndrome caused by occlusion of anterior inferior cerebellar artery, and the lesion was clearly demonstrated by horizontal and coronal MRI. The palatal and lingual disturbances might be due to the involvements of the corticobulbar tracts of the 10th and 12th nerves after the fibers had decussated.
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PMID:[Lateral inferior pontine syndrome: a case report]. 280 19

Symptomatic common carotid artery occlusion (CCAO) is rare. We studied 17 patients with ischemic cerebrovascular symptoms and unilateral CCAO on angiography to help clarify clinical and radiologic features. Mean age was 62 years; 65% were women. Predominant symptoms and signs included visual-ipsilateral monocular or retrochiasmal symptoms (88%), motor weakness (88%), sensory disturbance (59%), dizziness/lightheadedness (53%), and syncope (24%). Dysarthria, headache, or involuntary limb shaking occurred less frequently. Positionally related symptoms occurred in approximately two-thirds of the patients. TIAs were often multiple and preceded a stroke or occurred without subsequent stroke in 82%. Hemispheric TIAs contralateral to the CCAO occurred in 41%. Ten patients (59%) suffered stroke, seven (70%) of which were ipsilateral to the CCAO. Vascular risk factors included cigarette use (76%), hypertension (71%), diabetes mellitus (41%), and hyperlipidemia (41%); 82% had two or more risk factors. Known cardiac disease was present in 59%. CCAO was present at the origin of the vessel in most patients. Most had atherosclerotic narrowing of multiple extracranial large vessels. During follow-up, none of the patients had a spontaneous second infarct; five had TIAs, including two with amaurosis fugax, all in the CCAO territory. More restricted external carotid collaterals may, in part, explain the higher frequency of ipsilateral stroke and contralateral TIAs than reported for internal carotid occlusion.
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PMID:Common carotid artery occlusion. 279 68

Linear fractures through the occipital bone are common, whereas depressed fractures in the posterior cranial fossa are rare because the occipital bone is protected by the surrounding thick muscles. The authors describe an unusual case of depressed fracture localized in the posterior cranial fossa associated with the syndrome of acute central cervical spinal cord injury. A 50-year-old female struck her face against the table and fell backward, while drunk, resulting in the bruise over the occipital region. Three days after injury she was transferred to our hospital because of progressive disturbance of consciousness, brain stem dysfunction and tetraplegia. Neurological examination on admission showed that she was drowsy, had tetraplegia and could not speak. However, she could obey commands only by moving her eyes and the ocular movements were normal in all directions except for horizontal nystagmus. Plain skull x-ray revealed a conspicuously depressed fracture in the posterior cranial fossa, but cervical spine x-ray showed neither fracture nor dislocation. Immediately suboccipital craniectomy was done and there were a thin subdural hematoma on the cerebellar surface, cerebellar contusion, and subarachnoid hemorrhage around the cisterna magna. Soon after operation impaired consciousness and paraplegia were improved, but recovery of both arms was delayed. Five months after injury, she still had left IX, X and XI nerve paresis, bilateral arm weakness, dysarthria, swallowing disturbance and bilateral sensory disturbance below C4 level. These findings indicated that she had sustained brain stem and cerebellar compression by the depressed fracture and also had suffered an acute central cervical spinal cord injury.
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PMID:[Unusual case of depressed fracture of the posterior cranial fossa associated with the syndrome of acute central cervical spinal cord injury]. 374 92

An autopsy case of hereditary spastic ataxia is reported. There are four family members with similar symptomatology through three generations. A 36-year-old man developed atactic gait at the age of 22 years, with following dysarthria, scanning speech, pyramidal signs, dysmetria, dysdiadochokinesia, nystagmus and mild sensory disturbance. The clinical course was steadily progressive and terminated about 14 years after the onset. The gross examination showed smallness of the brain stem and spinal cord with marked symmetrical atrophy of the anterior and lateral columns, especially at thoracic level. Histologically, pronounced degeneration was found in the anterior and posterior spino-cerebellar tracts, spino-thalamic tracts, and spinal ganglia. The olivary nuclei, pons and cerebellum were spared. The dentate nuclei showed considerable loss of neurons with degeneration, however there were no clinical signs related to this pathology. This case is considered to fall in the group of hereditary spastic ataxia according to Greenfield's classification, however, there was no report on degeneration of the dentate nucleus in this disease for the present. Hereditary spastic ataxia is very rare disease and only four cases have well been documented in our country to the best of our knowledge. The presence of nystagmus and superficial sensory disturbance, and sparing of the posterior column of the spinal cord seems to be common clinico-pathology in Japanese cases, differing from those of foreign cases. The fact that reactive astrogliosis was immunohistochemistry demonstrated in the degenerative regions of the spinal cord and where is no discrepancy between degenerative and reparative processes as reported before is stressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of hereditary ataxia (hereditary spastic ataxia)]. 404 Dec 92

A 46-year-old man developed sudden dysarthria and atactic gait and was noted to be unable to get up even on the bed about one year prior to his death. By following several days, he started to have scanning speech, nausea, trancal ataxia and dysmetria in succession. The cerebro-spinal fluid yielded moderate pleocytosis. There were no sensory disturbance, pathological reflexes and Romberg's sign. Half a year later, submandibular tumor was noted. The biopsy showed metastatic small cell undifferentiated carcinoma, presumably of pulmonary origin, and paraneoplastic cerebellar degeneration was suspected. He died of bronchopneumonia, superimposed on lung cancer on February 25 in 1979. The necropsy showed a large tumor in the right lung which was histologically verified small cell undifferentiated carcinoma (so-called oat-cell carcinoma). The cerebellum disclosed diffuse cortical atrophy, chiefly of Purkinje cell type. Moderate demyelination with reparative gliosis and foamy macrophages was seen in the white matter, which was considered secondary to cortical devastation. The morphometric study on Purkinje cell loss showed interesting distribution of the lesions. The severely affected portions were the central lobe and culmen in the vermis, and the ala lobuli centralis and quadrangular lobe in the hemisphere, respectively. The lingula was strikingly spared. The finding was compared with that of other cerebellar disease in reviewing the literature.
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PMID:[An autopsy case of carcinomatous subacute cerebellar degeneration--on distribution of cerebellar cortical lesions]. 609 6


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