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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1976 and 1978, we examined 110 Japanese children with cerebral palsy using a CT 1000 and a CT 1010 (EMI). In 92% of all patients, there were abnormal findings. Cortical atrophy was seen in 51%, ventricular dilatation in 86%, localized low density areas in 22%, brain anomalies in 10% and asymmetry of cerebral hemisphere in 31%. In spastic hemiplegia, the characteristic CT revealed asymmetrical ventricular dilatation without cortical atrophy and localized low density areas in the cerebral hemisphere contralateral to the palsy. In spastic tetraplegia, CT revealed moderate to marked diffuse cerebral atrophy or brain anomalies. In athetosis, CT revealed normal or slight cerebral atrophy. In 60 cases where a CT 1010 was used, we calculated the volume index of CSF space by computer, Eclipse S/200, and analyzed the relationship between the clinical features of cerebral palsy and the volume index of CSF space.
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PMID:Computed tomography of cerebral palsy: evaluation of brain damage by volume index of CSF space. 55 48

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
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PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

Tactile extinction was investigated by the Quality Extinction Test (QET) of Schwartz in 39 patients, 34 of whom had congenital hemiplegia and five early-acquired hemiplegia. Extinction values were significantly higher in hemiplegia patients than in controls and usually contralateral to the side of brain damage, except for four cases with right hemiplegia. Values were also higher in males than in females. There were no significant differences between patients with left and right hemiplegia, and no correlations between extinction and IQ or the presence of epilepsy. There was a correlation between QET scores and neuroradiologically proven cerebral atrophy. The meaning of extinction in hemiplegic patients and the principal theories regarding the pathogenesis of neglect are discussed.
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PMID:Tactile extinction in childhood hemiplegia. 193 30

In 14 children with Sturge-Weber syndrome, cortical calcifications on CT scan was present in 12, localized brain atrophy in 10, enlargement of the choroid plexus in 7, and abnormal veins in 7. Cortical enhancement was present on 12 CTs performed shortly after an episode of severe seizures or hemiplegia but was absent or considerably less marked at a distance from the acute episodes. We suggest that cortical enhancement is related to seizure activity and/or blood-brain disturbances rather than to the extension of pial angioma.
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PMID:Neuroradiological findings in Sturge-Weber syndrome (SWS) and isolated pial angiomatosis. 194 17

A 10-month-old girl with mild developmental delay became hemiplegic after seizures. Cranial CT scan and magnetic resonance imaging (MRI) revealed no lesions related to vascular diseases, but brain atrophy on the right side was remarkable. Digital subtraction angiography showed slightly decreased visualization of peripheral branches of the right medial cerebral artery. Propionic acidaemia was diagnosed on the basis of high plasma levels of propionic acid and its metabolites and the elevated urinary excretion of these acids. With therapy, the levels of these acids fell, and her left hemiplegia disappeared 3 months later.
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PMID:Acute infantile hemiplegia in a patient with propionic acidaemia. 237 22

It is said that the prognosis is generally unfavorable in patients with hypertensive intracerebral hemorrhage showed extravasation on angiogram. Recently, we experienced a case whose prognosis was eventful after the removal of hematoma. So we reported this case and discussed between alcoholism and intracerebral hemorrhage accompanied with extravasation on angiogram in this paper. A 59-year-old male was transferred to our emergency center because of right hemiplegia and mild clouding of consciousness at around nine in the evening on December 12, 1983. At the time of admission, his neurological state was classified into grade II, exhibiting the right putamenal hemorrhage and pyramidal destruction type of hematoma by CT scan with 58 ml of hematoma volume. The right carotid angiography was immediately performed and confirmed the hematoma being of lateral type. At that time, extravasation proximal to the lateral lenticulostriate artery was noted. Repeated CT scan revealed the enlarged hematoma (105 ml) accompanying with ventricular hemorrhage. At the completion of these examinations, the neurological grade was III. The hematoma was surgically removed after 4 hours following the onset of cerebral hemorrhage. His postoperative course was very favorable. Although acute hydrocephalus appeared later on, it was cured by ventricular drainage. The patient become possible to walk with a helper by 1 month after operation. CT scan obtained 1 month after operation revealed a remarkable brain atrophy, which was probably derived from chronic alcoholism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case favorably progressed after operation for hypertensive intracerebral hemorrhage showed extravasation on angiogram occurred in chronic alcoholism]. 401 3

We report two cases of AIDS whom we have recently experienced. One patient was a 54-year-old man who admitted our hospital due to third degree burn. In this case, we did not know whether or not he was suffered from AIDS, when he was delivered by the ambulance. In autopsy, pneumocystis carinii pneumonia and renal tuberculosis were found in addition to marked decrease of T cells in lymph nodes. The other patient was a 40-year-old man with remarkable symptoms of central nervous system. Route of infection of HIV is unknown. He had dementia, left hemiplegia, bulbar palsy, progressed to rigid decorticate posture and died of respiratory arrest due to involvement of the brain stem, despite of treatment including use of 3'-azido-2',3'-dideoxythymidine (AZT). Magnetic resonance (MR) images showed progressive cerebral atrophy and a diffuse high signal intensity area of cerebral white matter on T2-weighted MR images, suggesting the diagnosis of HIV-induced encephalopathy.
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PMID:[Two cases with acquired immunodeficiency syndrome in our hospital]. 822 67

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

Damage to the minor hemisphere or the right hemisphere of most right-handed subjects produces various neuropsychological disorders. Unilateral spatial neglect is the deficit to respond or orient to stimuli on the left side. The inferior parietal lobule is most frequently involved in the lesions of neglect patients, but lesions confined to the lobule may not cause chronic neglect. Severe and lasting neglect is frequently found in patients with an infarction in the territory of the middle cerebral artery or the anterior choroidal artery. Neglect is usually mild or moderate after frontal lesions. The most important mechanism of neglect seems to be disorders in spatial attention: rightward attentional bias, and impairment in disengagement and shift of attention from the right side. Directional hypokinesia is rarely observed in the chronic stage. Non-spatial factors, such as motivational deficit, insufficient compensation with verbal intelligence, or disuse of an appropriate spatial strategy may also contribute to the appearance of neglect. Anosognosia for hemiplegia is found in about half of patients with acute cerebrovascular accidents in the right hemisphere. Generalized attentional and intellectual deficits, diffuse brain atrophy or hypometabolism, and presence of multiple infarction may result in chronic anosognosia. Constructional disability is observed in about 30% patients with either hemisphere damage. Dressing apraxia is more frequent in right hemisphere damage. These two disorders, however, rarely appear as isolated neuropsychological deficits. Most patients show some of the accompanying disorders, such as unilateral spatial neglect, anosognosia, anosodiaphoria, and generalized attentional and intellectual impairment. By contrast, motor neglect may occur independently of the other disorders. Motor neglect follows damage to either hemisphere, although it occurs more frequently after right hemisphere damage. Neuropsychological deficits characteristic of right hemisphere damage may be unilateral spatial neglect in the acute and chronic stages and anosognosia for hemiplegia in the acute stage.
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PMID:[Neuropsychological disorders in minor hemisphere damage]. 957 65

We report the case of a 49 year-old man who presented a partial status epilepticus with left-sided clonic seizures after the occurrence of a left cerebral hematoma. The patient had left-side hemiplegia that progressively recovered in 3 months. Neuroimaging studies revealed a moderate cerebral atrophy on the right side and crossed cerebellar atrophy. Six years later, he had a partial status epilepticus with left hamiconvulsions leading to permanent left hemiplegia. The right cerebral and the left cerebellar atrophy observed one year later were significantly increased. Cerebral hemiatrophy associated with epilepsy in adulthood is exceptional. Our case suggests that the occurrence of partial status epilepticus, even during adulthood, may aggravate cerebral hemiatrophy formally silent.
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PMID:[Hemicerebral atrophy and epilepsy in an adult]. 977 25


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