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)

We present a case with an infarct limited to the right pyramidal tract in the medulla. The lesion lay approximately 1 cm below the pontomedullary junction. On the basis of this case and three previously reported cases of medullary pyramidal infarction, there is defined a syndrome of severe hemiplegia with relative sparing of the face, tongue and articulation, minimal sensory loss, and good recovery. The hemiplegia is initially flaccid and later spastic. Transient symptoms, referable to the tegmentum of the medulla, occur at the onset, and reflect ischemia in the deeper territory of a paramedian penetrating vessel.
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PMID:Pyramidal infarction in the medulla: a cause of pure motor hemiplegia sparing the face. 57 Jun 81

The clinical syndrome of "stroke" at first calls for a differentiation between the prognostic more unfavorable massive hemorrhage and the syndromes of cerebral hypoxia or ischemia. The ratio of hemorrhage to ischemia is about 1 to 5. Conclusions may already be drawn on the nature of the apoplectic insult from the clinical symptomatology. For example, the hemorrhagic insult in general begins with severe manifestations of neurological dysfunction such as hemiplegia and coma, while the symptoms of the ischemic insult frequently do not develop all of a sudden but in the course of hours, rarely from 1-2 days. Digitalisation in combination with dextran infusions is the method of choice in treating intermittent ischemias, particularly those provoked by hypertension. Rehabilitation, i.e. passive and active physical exercise, should be started as early as possible. In addition, particular importance must be attributed to prevention and especially to the early recognition of hypertension and of cardiac diseases as a socio-medical problem.
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PMID:[Clinical picture and therapy of cerebral apoplexy]. 85 97

A 6-year-old boy developed a flaccid hemiplegia and dysarthria following several transient episodes of nausea, vomiting, and ataxia. An anomly of the dens was discovered, permitting subluxation of C-1 on C-2. A segmental occlusion of the right vertebral artery and an aneurysm of the left vertebral artery were found at the C-2 level, as well as a thromboembolic occlusion of the rostral end of the basilar artery. It appeared that the repeated cervical subluxation produced occlusive, aneurysmal, and embolic vascular disease, and that clinical symptoms were the result of ischemia in the territory perfused by the vertebrobasilar arteries.
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PMID:Occlusive vertebrobasilar artery disease associated with cervical spine anomaly. 113 Mar 56

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

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

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

The cerebral protective actions of a new thyrotropin releasing hormone (TRH) analogue, YM-14673, [Na-[[(S)-4-oxo-2-azetidinyl-carbonyl]-L-histidyl-L-prolinamide] dihydrate), were compared with those of CDP-choline (cerebral metabolic enhancer) and naloxone in rats rats subjected to unilateral carotid artery ligation and anoxic exposure (Levine rats). Drugs were administered intraperitoneally or orally 20, 80, and 140 min after anoxia. YM-14673 (0.03 to 1 mg/kg i.p. and 0.3 to 10 mg/kg p.o.) decreased the incidence of neurological deficits, such as hemiplegia and convulsion followed by coma and death, for 48 h after ischemia and anoxia. Both the increase in the brain water content and the degeneration of neurons in the cerebral cortex and thalamus were prevented by YM-14673 at a dose of 0.1 mg/kg (i.p.). CDP-choline (400 mg/kg i.p.), which is currently used in the therapy of cerebral vascular diseases, and naloxone (3 mg/kg i.p.) also decreased the incidence of the neurological deficits. These results suggest that YM-14673 protects Levine rats against neurological deficits, presumably by attenuating the development of brain edema and preventing neuronal damage. This compound may be useful in the therapeutic treatment of cerebral vascular diseases.
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PMID:Pharmacological actions of a new TRH analogue, YM-14673, in rats subjected to cerebral ischemia and anoxia. 211 71

The authors report 21 cases of heparin-induced thrombocytopenia with ischemic vascular complications. The clinical presentations were peripheral arterial ischemia (16 cases), hemiplegia (1 case) and deep vein thrombosis (4 cases). The vascular surgeon confronted by these complications in an emergency situation should recognise the difficulties of clinical diagnosis (atypical forms) and biological investigations (problems of tests of platelet aggregation). Arterial occlusions are usually accessible to disobliteration with a Fogarty catheter without peroperative heparinisation. Delayed diagnosis explains the seriousness of these complications; in our series of 21 patients, there were 2 deaths, 1 paraplegia, 4 amputations due to arterial problems, 4 severe post-deep vein thrombosis conditions, two of which followed trans-metatarsal amputation. The diagnosis of heparin-induced thrombocytopenia implies immediate withdrawal of heparin therapy. A relay with a low molecular weight heparin is not without risk and should only be undertaken after a negative platelet aggregation test (with the low molecular weight heparin). These tests are rarely practicable in emergency situations and a relay using oral anti-vitamin K antagonists with a rapid onset of action is probably the safest option.
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PMID:[Ischemic vascular complications following thrombopenia induced by heparin. Diagnostic and therapeutic problems]. 212 62

To investigate the relationship between middle cerebral artery (MCA) trunk lesions and the etiology of Binswanger type (B type) infarction, which was demonstrated as a diffuse subcortical low density area/high intensity area by CT/MRI, patients with both MCA lesions and B type infarction were studied clinically. Eighteen patients with B type infarction were diagnosed among 224 patients with MCA occlusion/stenosis on angiography accounting for 8%. The incidence was as high as 25% in M2 stenosis. The mean age of B type infarction patients was 64 years and 16 of them were men. Chronologically stepwize/slowly-progressive deterioration of clinical manifestations were observed in 14. All patients had hemiplegia, though half of them were mild or moderate in severity. Furthermore, aphasia, Gerstmann syndrome and dementia were present in 10, 1 and 2 patients, respectively. Twelve had a history of hypertension, while 11 showed transient decreases with marked changes (more than 31 mmHg in mean arterial blood pressure) in arterial blood pressure during their clinical course. Out of 9 patients in whom cerebral blood flow (CBF) was measured by 133Xe injection method/inhalation method, 7 demonstrated mild to moderate decreases in mean CBF (more than 30 ml/100 g/min) with no relation to the severity of MCA lesions. These findings suggested that hemodynamic mechanisms associated with hypoperfusion due to marked fluctuations in blood pressure are accelerating factors of B type infarction and MCA lesions, even though ischemia in the subcortical area due to leptomeningeal anastomosis may be mild or moderate.
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PMID:[Clinical study on the relationship between middle cerebral artery lesions and Binswanger type infarction]. 260 75


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