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)

To evaluate the potential for clinical application, the reputed protective action of barbiturates in cerebral ischemia was tested in a controlled study after segmental middle cerebral artery occlusion in primates. Surviving treated animals promptly recovered consciousness, locomotion, and feeding behavior despite persistent hemiplegia, while control animals ran an indolent course, with slow recovery of poor quality. Cerebral lesions in treated animals were confined to the deep hemispheric structures, while control specimens showed larger deep lesions confluent with extensive areas of cortical infarction. These results are less dramatic than those reported by others, but the protective effect observed in fields of collateral circulation deserves further exploration as an adjunct to medical and surgical management.
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PMID:Barbiturate attenuation of the clinical course and pathologic lesions in a primate stroke model. 80 60

Diazoxide given for hypertensive crises caused severe complications in two patients. Hypotension, anginal syndrome, cerebral ischemia, and right hemiplegia developed in one patient, and myocardial infarction in the other.
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PMID:Side effects of diazoxide. 94 45

We report the repeated improvement in neurological function following naloxone administration in a patient who developed acute hemiplegia after an intracranial neurological procedure. The mechanisms responsible for the neurological deficit and for its reversal by naloxone are discussed. A review of the literature suggests that the beneficial effect of naloxone can result from an improvement in haemodynamic status or from metabolic effects that could be favorable during cerebral ischaemia.
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PMID:Reversal of neurological deficit with naloxone: an additional report. 146 63

A review of the sensitivity of genetically hypertensive rats to cerebral ischemia was presented together with original data describing the systematic comparison of the effects of focal ischemia (permanent and temporary with reperfusion) performed in hypertensive and normotensive rats (i.e., blood pressures verified in conscious instrumented rats). Microsurgical techniques were used to isolate and occlude the middle cerebral artery (MCAO) of spontaneously hypertensive (SHR), Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats at the level of the inferior cerebral vein. Following permanent (24 h) MCAO, persistent and similar decreases in local microvascular perfusion (i.e., to 15.6 +/- 1.7% of pre-MCAO levels) were verified in the primary ischemic zone of the cortex for all strains using Laser-Doppler flowmetry. A contralateral hemiplegia that occurred following MCAO, evidenced by forelimb flexion and muscle weakness, was greater in SHR (neurological grade = 2.0 +/- 0.1) than SD (1.0 +/- 0.4) or WKY (0.7 +/- 0.4) rats (N = 7-9, p less than 0.05). SHR also exhibited sensory motor deficits following MCAO compared to sham-operation, with decreased normal placement response of the hindlimb (% normal = 20 vs. 83, N = 23-30, p decreased rota-rod (41 +/- 7 vs. 126 +/- 19 on rod, N = 10-15, p less than 0.05) and balance beam (25 +/- 5 vs. 116 +/- 29 s on beam, N = 5-7, p less than 0.05) performance. However, an index of general motor activity was not affected by permanent MCAO. Triphenyltetrazolium-stained forebrain tissue analyzed by planimetry revealed a significantly larger and more consistent cortical infarction in SHR (hemispheric infarction = 27.9 +/- 1.5%) compared to SD (15.4 +/- 4.1%) and WKY (4.0 +/- 2.4%) rats (N = 7-9, p less than 0.05), occupying predominantly the frontal and parietal areas. Also, a significant degree of ipsilateral hemispheric swelling (4.6 +/- 0.9%, N = 7-9, p less than 0.05) and increased brain water content (78.4 +/- 0.3% to 80.4 +/- 0.2%, N = 8-9, p less than 0.05) was identified in SHR that was not observed in SD or WKY rats. A novel model of temporary MCAO also was evaluated in the hypertensive and normotensive rat strains. Initially, the effect of increasing MCAO-time followed by 24 h reperfusion in SHR was studied. During temporary MCAO (20 to 300 min), persistent and stable decreases in local microvascular perfusion (i.e., to 15-20% of pre-MCAO levels) were verified in the primary ischemic zones of the cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetic hypertension and increased susceptibility to cerebral ischemia. 163 Jul 32

Two different techniques were utilized to identify the infiltration of polymorphonuclear leukocytes (PMN) into cerebral tissue following focal ischemia: histologic analysis and a modified myeloperoxidase (MPO) activity assay. Twenty-four hours after producing permanent cortical ischemia by occluding and severing the middle cerebral artery of male spontaneously hypertensive rats, contralateral hemiparalysis and sensory-motor deficits were observed due to cerebral infarction of the frontal and parietal cortex. In hematoxylin-and-eosin-stained histologic sections, PMN, predominantly neutrophils, were identified at various stages of diapedesis from deep cerebral and meningeal vessels at the periphery of the infarct, into brain parenchyma. When MPO activity in normal brain tissue was studied initially, it could not be demonstrated in normal tissues extracted from non-washed homogenates. However, if tissue was homogenized in phosphate buffer (i.e., washed), MPO activity was expressed upon extraction. Utilizing this modified assay, MPO activity was significantly increased only in the infarcted cortex compared to other normal areas of the brain. This was observed in non-perfused animals and after perfusion with isotonic saline to remove blood constituents from the vasculature prior to brain removal. The increased PMN infiltration and MPO activity were not observed in forebrain tissue of sham-operated control rats. Also, MPO activity was not increased in the ischemic cortex of MCAO rats perfused immediately after middle cerebral artery occlusion, indicating that blood was not trapped in the ischemic area. By using a leukocyte histochemical staining assay, activity of peroxidases was identified within vascular-adhering/infiltrating PMN in the infarcted cortex 24 hr after focal ischemia. An evaluation of several blood components indicated that increased MPO activity was selective for PMN. The observed increase of approximately 0.3 U MPO/g wet weight ischemic tissue vs. nonischemic cerebral tissues probably reflects the increased vascular adherance/infiltration of approximately 600,000 PMN/g wet weight infarcted cortex 24 hr after focal ischemia. This combined biochemical and histological study strongly suggests that PMN adhere within blood vessels and infiltrate into brain tissue injured by focal ischemia and that the associated inflammatory response might contribute to delayed progressive tissue damage in focal stroke. This modified MPO assay is a useful, quantitative index of PMN that can be utilized to elucidate the potential deleterious consequences of neutrophils infiltrating into the central nervous system after cerebral ischemia, trauma, or other pro-inflammatory stimuli.
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PMID:Polymorphonuclear leukocyte infiltration into cerebral focal ischemic tissue: myeloperoxidase activity assay and histologic verification. 165 59

Moyamoya disease is a chronic occlusive cerebrovascular disorder characterized by stenosis of the intracranial internal carotid artery often accompanied by stenosis of the anterior and/or middle cerebral arteries. This results in cerebral ischemia, which manifests clinically as transient, repetitive episodes of hemiplegia, dysarthria, and involuntary movements. This case report documents a patient in whom an initial extracranial-intracranial bypass (superficial temporal-middle cerebral artery) failed to alleviate the ischemic symptoms. In a subsequent procedure, a pedicle graft of omentum was created and through a subcutaneous tunnel was placed on the right cerebral cortex. Over a 2 1/2-year period, this has resulted in a dramatic resolution of the patient's symptomatology. The report delineates the condition and reviews other therapeutic options.
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PMID:Encephalo-omental synangiosis in the management of moyamoya disease. 173 85

Thirty out of 287 patients (10.4%) admitted to hospital for infective endocarditis between December 1970 and January 1990 had neurological complications. Twenty-three patients had native valve infectious endocarditis and 7 had prosthetic valve endocarditis. The clinical features were characterized by the frequency of aortic valve involvement (23 out of 30) and other complications, especially cardiac failure (16 cases) and peripheral vascular manifestations (7 cases). The commonest organism was the staphylococcus (53% of identified organisms) but the number of negative blood cultures was high (50% of cases). The neurological complication was often the presenting symptom of the endocarditis (19 cases) but it occurred after bacteriological cure in 4 cases. The complications observed were cerebral ischemia (16 cases), cerebral haemorrhage (11 cases), coma (2 cases), and one peripheral neuropathy causing a Claude Bernard Horner syndrome. These complications presented with hemiplegia in 17 cases, a meningeal syndrome in 8 cases, a convulsion in 1 case, a Von Wallenberg syndrome in 1 case, and a Claude Bernard Horner syndrome in 1 case. Twelve patients had a transient or permanent neurological coma. Cerebral CT scan showed ischemic lesions in 7 cases and haemorrhagic lesions in 10 cases. Carotid angiography demonstrated mycotic aneurysms in 6 patients. Twelve patients died: the cause of death was neurological coma (7 cases), low cardiac output (4 cases) and haemorrhagic shock (1 case). Four patients underwent neurosurgery: 3 for clipping a mycotic aneurysm and 1 for drainage of an intracerebral haematoma. Poor prognostic factors were: coma, cardiac failure, cardiac valve prosthesis and, above all, the extent and multiplicity of the neurological lesions. The authors propose the following measures to improve the prognosis: early surgery in cases of large and/or mobile vegetations especially when the infecting organism is a staphylococcus and when a systemic embolism has occurred; routine CT scanning and/or digitised cerebral angiography in all patients with infective endocarditis to detect surgically accessible mycotic aneurysms.
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PMID:[Neurologic manifestations of infectious endocarditis]. 201 89

Oculomotor palsy is a well-known complication of herpes zoster ophthalmicus (HZO). Combination with homolateral cerebral media infarction and contralateral hemiplegia is very rare. Since the first paper on HZO and cerebral ischemia was published, in 1919, about 70 cases have been described. Zoster infection is thought to encroach from the fifth cranial nerve on to a cerebral artery at the base of the brain. The authors describe a case of HZO seen by them, with oculomotor palsy and ipsilateral media infarction with contralateral hemiplegia and aphasia. A review of the literature is given and etiologic and therapeutic aspects are discussed.
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PMID:[Herpes zoster ophthalmicus with subsequent oculomotor paralysis and homolateral media infarct]. 247 Sep 51

We observed the effects of a new thyrotropin-releasing hormone derivative, YM-14673 (N alpha-[[(S)-4-oxo-2-azetidinyl]carbonyl]-L-histidyl-L-prolinamide dihydrate), on behavioral changes in rats for 3 weeks after focal cerebral ischemia. Under halothane anesthesia, the left middle cerebral artery was occluded via a transretro-orbital approach. YM-14673 was administered just after the operation and once a day for 3 weeks. Neurologic deficits, including hemiplegia and abnormal posture, and disturbance of passive avoidance learning were present in solvent-treated control rats for the entire 3 weeks. YM-14673 at 0.1 or 0.3 mg/kg i.p. or 1 mg/kg p.o. significantly accelerated the recovery of neurologic deficits and ameliorated cognitive disturbance compared with the solvent-treated controls although the drug at 0.1 and 0.3 mg/kg i.p. did not influence the size of the ischemic infarct. YM-14673 mitigated the behavioral disturbances in this model of chronic focal cerebral ischemia. We also discuss the suitability of this model for the evaluation of drugs.
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PMID:Effects of a new thyrotropin-releasing hormone derivative on behavioral changes after focal cerebral ischemia in rats. 249 90

A modified method of occluding the middle cerebral artery (MCA) by inserting a tiny copper wire into the lumen of the vessel to make a model for cerebral ischemia in the cat is described. Of 22 rats, 4 were controls and the remaining 18 were divided into two groups. Bipolar electrocoagulation was used in 9 cats and copper wire insertion was used in the other 9 to occlude the MCA through a transorbital approach. Two cats died after surgery and were excluded from this study. Of the 16 cats in two experimental groups, 13 of 14 showed hemiplegia and the other 2 were killed under anesthesia. Typical ischemic changes can be seen in the territory of the occluded MCA. Increased water content and decreased amplitude of somatosensory evoked potentials can be found in the ischemic hemisphere. Histochemical fluorescence study demonstrated that the sympathetic nerve fibers normally existing on the MCA can be completely destroyed by electrocoagulation but may remain intact with the copper wire method. This new method may have less influence on the vascular regulative function of the autonomic nervous system and be more similar to the pathological changes of cerebral infarction in man. We think our method can be useful for further research in cerebral ischemic disease and the regulative effects of the nervous system on brain vessels.
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PMID:Modification of a model for cerebral ischemia in the cat: a new method to occlude the middle cerebral artery. 275 79


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