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)

The known risk factors for atherosclerosis do not possess the same significance in young people as in the elderly. Hypercholesterolemia, diabetes and cigarette smoking appear to have a greater bearing below the age of 50 than later, particularly in myocardial infarction but also in apoplexy. On the other hand, hypertension is an important factor in the young and, especially in the case of apoplexy, even more so in advanced age. There is marked difference with regard to preexisting heart disease, which scarcely plays a role in myocardial infarction of the younger patient but is a factor in some 50% of hemiplegia cases. Only one fifth of elderly patients with this disease have no preexisting carcdiopathy. The similarity of the risk factors in elderly patients either with or without apoplexy is due to the fact that arteriosclerosis is already established in both groups and the risk factors which give rise to ischemia, thrombosis or embolism assume prominence. The therapeutic implications are briefly discussed.
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PMID:[Risk factors and age]. 113 58

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

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.
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PMID:Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly. 709 54

A case of severe epistaxis with hypertension and arteriosclerosis was treated by embolizing the ipsilateral internal maxillary artery after routine methods of hemostasis had failed. Although epistaxis stopped after embolization, cerebral infarction, hemiplegia and deep coma developed, and the patient died on the ninth postoperative day. We conclude that superselective embolization of the branches of external carotid artery for treating severe epistaxis should be used with great caution or not be used in patients with arteriosclerosis.
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PMID:[Arterial embolization leading to fatal cerebral infarction (a case report)]. 780 19

We report a case of Prader-Willi syndrome (PWS) complicated with juvenile stroke. The patient is a 19-year-old man with right hemiplegia, who has had a history of non-insulin-dependent diabetes mellitus (NIDDM) for ten years. The diagnosis of PWS was confirmed genetically by the method of fluorescence in situ hybridization which showed the deletion of chromosome 15. His brain MRI revealed abnormal signal intensities in the left basal ganglia and around the right trigone of the lateral ventricle. Angiographic examination showed occlusions of bilateral proximal middle cerebral arteries with basal moyamoya vessels. The left vertebral artery was also occluded at its origin. Only a few cases of PWS complicated with stroke have been reported before and, to date, there has been no case with arterial occlusion similar to our case. Though the cause of these arterial occlusions is unknown, it may be related to arteriosclerosis following NIDDM.
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PMID:[A case of Prader-Willi syndrome with bilateral middle cerebral artery occlusion and moyamoya phenomenon]. 893 99

Clinical features of the anterior inferior cerebellar artery (AICA) territory infarcts were investigated in ten patients, ranging in age from 38 to 76 years. In all patients, there were MR images of infarction located in the area supplied by the AICA. The lesion was on the left side in 6 patients and right side in 4. The lesion of brain stem including the middle cerebellar peduncle was found in 7 patients and that extended to the cerebellum was in 3 patients. The main ipsilateral neurological signs were the VII and VIII cranial nerves palsy and cerebellar ataxia. The V and VI cranial nerves palsy. Horner's syndrome, and dysphagia were also present. The main contralateral sign was superficial sensory disturbance, but no hemiplegia. The underlying pathology included chiefly hyperlipidemia, hypertension, and diabetes mellitus. Cerebral angiography was performed in 8 patients, most of which was observed severe arteriosclerosis suggesting poor hemodynamics in the vertebral and basilar arteries. The prognosis was relatively good, but the VII, VIII, and V cranial nerves palsy and contralateral superficial sensory disturbance remained as the sequelae. As mentioned above, there were various neurological findings and MR images in AICA territory infarcts. Especially there were some patients whose lesion extended to the upper medulla and neurological findings were similar to the Wallenberg syndrome. It is important that one investigates not only axial slices but also coronal slices of MR image to estimate the extension of AICA territory infarct.
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PMID:[Clinical features of anterior inferior cerebellar artery territory infarcts--a study of ten patients]. 904 27

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
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PMID:[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset]. 1006 67

Cerebral haemorrhage without hypertension, arteriosclerosis or clotting defect has not been reported in patients with Turner's syndrome before. In a 51 year old female patient with non-mosaic Turner's syndrome, acute aphasia and right-sided hemiplegia occurred, due to left-sided basal ganglia haemorrhage. The history for hypertension was negative, blood pressure was normal throughout hospitalisation as well as during 24 h monitoring, and all tests for secondary hypertension were negative. There was no indication of arteriosclerosis or a clotting defect. Since there were hypermobile joints, hyperextensible skin and ectatic ascending aorta and brachiocephalic trunk on angiography, a general connective tissue defect was assumed, making arteries more vulnerable to physiologically increased blood pressure and rupture of intracerebral arteries with consecutive bleeding.
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PMID:Spontaneous cerebral haemorrhage without hypertension in non-mosaic 45X Turner's syndrome. 1093 18

A 77-year-old male pedestrian was hit by a car. On admission, he had disturbance of consciousness and left hemiplegia. Computed tomography (CT) indicated only left frontal subcutaneous hematoma and minor hemorrhage in the left frontal lobe, suggesting axonal injury. CT on hospital day 2 revealed a low density area in the right paramedian pons, but CT angiography showed no dissection or occlusion of the vertebrobasilar artery. The diagnosis was pontine infarction resulting from shearing force injury to the paramedian branch of the basilar artery. He was transferred to another hospital for rehabilitation without improvement of symptoms on hospital day 51. Paramedian pontine infarction tends to occur in patients with risk factors for arteriosclerosis, including hypertension, diabetes mellitus, hyperlipidemia, or smoking. The present elderly patient had hypertension and hyperlipidemia, so arteriosclerosis in the paramedian branch may have contributed to his susceptibility to such injury.
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PMID:Pontine infarction induced by injury of the perforating branch of the basilar artery after blunt head impact: case report. 1871 23

Posterior circulation stroke, which includes basilar artery occlusion (BAO), accounts for approximately 20% of all ischemic strokes. Much is unclear concerning the early historical descriptions of basilar artery occlusion, and some modern authors cite the historical sources incorrectly and incompletely. The case described by the Scottish physician John Abercrombie in 1828 is probably the first description of this form of stroke. The progressive bulbar signs that Abercrombie described in his case were striking, i.e., dysphagia and speech difficulties. Many authors in the 19th century described a waxing and waning clinical course for several days before profound coma and death. They also noticed signs and symptoms such as hemiplegia without loss of sensitivity and bulbar symptoms such as swallowing and speech impairment, vertigo, and altered consciousness. After Virchow's epoch-making work on embolism and thrombosis, all authors correctly described BAO as resulting from emboli and thrombosis based on arteriosclerosis instead of ossification of the arterial walls or inflammation. Around 1880, the clinical symptoms of BAO were obviously well-known to the experienced clinician. In this article we offer a chronological description of historical sources.
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PMID:Historical sources of basilar artery occlusion. 2151 3


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