Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen patients who had suffered a stroke in the previous 72 h have been studied using technetium 99m hexamethyl propylene amine oxime (HMPAO) to assess cerebral blood flow. Comparison of the scan appearances and clinical signs were made in all cases. Twelve of the patients had a repeat HMPAO scan 14 days later, together with further clinical assessment. Good correlation between the size and site of perfusion deficit and the clinical signs was found in 14 of the patients. When the results of the 12 patients who had repeat scans were examined at 14 days the correlation between the scan and the clinical signs was less accurate and it seems unlikely that the assessment of the size of cerebral infarction as demonstrated by an HMPAO scan will provide an accurate prognostic sign. Three of the patients, all of whom had suffered right hemiplegia and were dysphasic, had regions of increased uptake adjacent to the area of ischaemia and non deteriorated clinically; it is thought that this sign may represent hyperperfusion around infarction and indicates a fair prognosis. In patients suffering from transient neurological symptoms, the use of HMPAO may be useful by excluding the presence of other cerebral disease.
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PMID:The study of regional cerebral blood flow in stroke patients using technetium 99m HMPAO. 338 64

A healthy 28 year old housewife presented with sudden right hemiplegia and aphasia. No predisposing factors could be ascertained apart from posterior cusp mitral value prolapse on two dimensional echocardiography. Extensive investigations confirmed the presence of cerebral infarction and persistent occlusion of the left internal carotid artery near its origin.
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PMID:Internal carotid artery occlusion in a young female with mitral valve prolapse. 365 49

A 74-year-old, right-handed woman suffered acute aphasia and left hemiplegia secondary to a cerebral infarction in the right cerebral hemisphere. The lesion was located deep in the parietal lobe and extended to the posterior limb of the internal capsule and the head of the caudate nucleus. The patient's aphasia was characterized by severe impairment in auditory and visual comprehension and auditory retention span, as well as by anomia, agraphia, and dyscalculia. She showed rapid recovery from her aphasia, with residual deficits in writing, naming, calculation, and memory.
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PMID:Subcortical crossed aphasia: a case report. 370 65

A 36-year-old man presented with sudden onset of hemorrhagic cerebral infarction in association with polycythemia vera. On admission this patient manifested semicomatous state and left hemiplegia which were gradually progressed. X ray CT demonstrated a severe hemorrhagic infarction in right MCA territory accompanying marked shift of midline structures. Cerebral angiograms represented occlusion of right MCA showing floating emboli in the internal carotid. Hematocrit value was found to be high as 61.2 per cent. Elevated ICP levels were noted by means of epidural pressure monitoring. Deterioration of patient status was considered to be based on impairment of cerebral circulation due to hemostasis by elevated blood viscosity. In addition to administration of mannitol solution, intermittent exsanguinations, 1000 ml in total amount, were performed and hematocrit levels were corrected by hemodilution. Consciousness level was remarkably improved in accordance with reduction of ICP, which well corresponded to values of hematocrit. Level of ICP and tissue perfusion are convinced to be strongly affected by hemorheological factor in the state of raised ICP.
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PMID:[Hemodilutional therapy in raised intracranial pressure; observations in a case of cerebral infarction associated with polycythemia vera]. 370 72

Since the acute revascularization was adopted as a probable means of surgical treatment for the acute cerebral ischemia, it became essential to discuss how the initial symptom at onset can predict the subsequent development of severe or mild cerebral infarction. In the 2 past years, 207 cases of cerebral ischemic lesion were admitted non-selectively and mostly in the early stage after the attack. Excluding 40 cases of surgical treatment, 167 cases were classified into 30 cases of TIA, 13 cases of RIND, 94 cases of minor completed stroke and 30 cases of major completed stroke. In 30 cases of major completed stroke, 21 cases developed severe motor hemiplegia from the onset and the rest 9 cases initially mild hemiparesis which gradually developed to severe hemiplegia thereafter. The cases of minor completed stroke showed mild or moderate hemiparesis initially and did not worsen thereafter. In the group of TIA and RIND, no case had developed severe hemiplegia in any stage of clinical course. The disturbance of consciousness were noted in 5 cases out of 94 cases of minor completed stroke (5%) and 12 cases out of 30 cases of major completed stroke (40%) in the following time course. More than half of the cases of major completed stroke were considered to be cerebral embolism including the retrospective review.
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PMID:[Assessment of major stroke at onset in cerebral ischemia. In consideration of acute revascularization]. 399 Aug 98

A 24-year-old woman with a left-sided cerebral infarction presented with hemiplegia and aphasia. Five months earlier she had had a closed head injury. Angiography revealed bilateral extracranial post-traumatic aneurysms of the internal carotid artery at the atlanto-axial level. There was full recovery without operative treatment within a week.
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PMID:Bilateral traumatic extracranial aneurysms of the internal carotid artery with delayed brain infarction. 405 39

Seven autopsy cases of shoulder-hand syndrome following hemiplegia were studied with regard to cerebral localization. One of them showed an isolated brain lesion in the premotor area due to a metastasis from malignant melanoma. Four other cases with cerebral infarction and one with glioblastoma multiforme showed massive brain lesions involving the frontal and parietal lobe cortex in the area supplied by the middle cerebral artery. The seventh case showed a hemorrhagic cerebral lesion in the lentiform nucleus. The most common overlap area in 6 of the 7 cases was located in the premotor region including the anterior part of the motor region. The shoulder-hand syndrome following hemiplegia always develops on the side contralateral to the brain lesion which might cause a unilateral longstanding autonomic dysfunction. As corroborated in a review of the relevant literature, a lesion in the premotor area appears chiefly responsible for the primary mechanism of the shoulder-hand syndrome in post-stroke hemiplegia.
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PMID:Posthemiplegic shoulder-hand syndrome, with special reference to related cerebral localization. 615 86

A 58-year-old woman, with a past history of classic migraine since youth, suddenly experienced blurred vision and flexor spasms of her left hand, followed by a right hemicrania and photophobia, similar to previous attacks of migraine. Within a few hours a progressive left hemiplegia and paralysis of left conjugate gaze developed. Severe right hemicrania continued. CT brain scans showed a progressing large right parietotemporal infarct. Her level of consciousness declined and she died ten days after admission to hospital. The autopsy showed a large infarct in the area of supply of the right middle cerebral artery, associated with oedema and with a shift of midline structures to the left, with cingulate and right hippocampal herniation. There was secondary midbrain haemorrhage. Recent secondary haemorrhagic infarction was present in the left calcarine cortex. The carotid arteries in the neck showed only minimal atheromatous change and were patent; the cerebral arteries were remarkably free of atheroma, but the right middle cerebral artery contained red thrombus. Histologically the cerebral infarction antedated the middle cerebral artery thrombus by several days, supporting arterial spasm as the cause of infarction. The thrombosis was considered to be a secondary phenomenon.
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PMID:Fatal migraine. 656 48

Although the therapeutic effect of spinal cord stimulation (SCS) for spastic movement disorders is still controversial, its effect for multiple sclerosis has been supported by several authors. Among various clinical beneficial effects, reduction of the spasticity may be attractive for physical therapy of post-apoplectic patients. Two patients suffered from post-apoplectic spastic hemiplegia were selected for SCS. Electrodes of Medtronic's SCS system were placed at lower cervical or upper thoracic spinal cord extradura. Stimulation of 30-75 Hz in frequency and 0.3-0.5 in voltage continued for 12-14 hours during daytime every days. U.S., a 74-year-old man, suffered from cerebral infarction in the right internal capsule was treated by SCS at one year after the stroke . At the fourth day after SCS spasticity of the lower extremity reduced and his gait improved remarkably. Upper extremity also showed reduction of spasticity at the seventh day after SCS. H/M ratio before SCS was 0.85 and reduced to 0.77 at 68 th day after SCS. Recovery curve of H-wave also improved after SCS. Y.K., a 47-year-old man, suffered from pontine hemorrhage showed right spastic hemiplegia. He was treated by SCS at 13th month after the hemorrhage. Spasticity of the upper extremity reduced slightly and his gait improved obviously. H/M ratio which was 1.05 before SCS, reduced to 0.75 at 122 nd day after SCS. Recovery curve of H-wave improved remarkably after the treatment. It was obvious that the spasticity reduced after SCS and function of the extremities recovered to some extent in above patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spinal cord stimulation for post-apoplectic spastic hemiplegia]. 661 Aug 36

In order to understand the mechanism of clinical worsening in patients with cerebral infarction, attention was focused on the changes in cerebral angiograms obtained repeatedly before and after neurological deterioration. Among 212 stroke patients with minor neurological deficits, incomplete hemiparesis progressed to complete hemiplegia in 15 patients several days after the beginning of symptoms. On admission, 3 had internal carotid artery occlusion, 2 had stenosis of the internal carotid artery, 5 had occlusion of the middle cerebral arterial trunk, 2 had occlusion of the middle cerebral arterial branch, and 3 had no angiographically visible occlusion. The changes between the first and the second angiograms were of different varieties: another recurrent occlusion, progression of occlusion, new occlusion in the cerebral arteries opacified through the collateral pathway, recanalization of the initially occluded artery, and no change. Such different patterns of pathophysiological events show that the mechanism of neurological worsening in infarcted patients is not uniform. Based on the results from the present study, several problems which arose during the investigation and the somewhat vague definition of "progressing stroke" currently in use are discussed.
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PMID:Angiographical analysis of acute cerebral infarction followed by "cascade"-like deterioration of minor neurological deficits. What is progressing stroke? 665 3


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