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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a new model of human ischemia encephalopathy in rabbits by means of cross-clamping the ascending aorta in combination with blood exsanguination from the right atrium. Rabbit hippocampal CAI pyramidal cells and cerebellar Purkinje cells showed only a few changes in the early period after ischemia, but 4 days after ischemia a significant decrease in cell count and marked degeneration of the remaining cells were observed. When the pathological findings 4 days after TCI in the hippocampal area and cerebellar area were compared, the rate of cytoclasis was found to be significantly higher in the latter than in the former.
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PMID:Neuropathological changes induced by total cerebral ischemia (TCI) in a new experimental model. 819 66

New insights into the pathophysiology of the hypoxic-ischemic insult have opened the possibility of pharmacologic intervention in neonatal hypoxic-ischemic encephalopathy. It is now known that many neurons survive a hypoxic-ischemic insult but remain dysfunctional for hours, with profound alterations in cell function. A cascade of biochemical alterations occurs as a consequence of cellular ionic shifts, energy depletion, degradation of cell membrane phospholipids, and increased release of neurotransmitters. In addition, there are alterations in the metabolism of arachidonic acid and prostanoids and an excessive production of oxygen free radicals. The new therapeutic modalities are aimed at preventing or arresting the biochemical changes that occur in the period after hypoxia-ischemia. This review details the biochemical alterations associated with neonatal hypoxic-ischemic encephalopathy and discusses the possible use in newborns of pharmacologic agents currently undergoing extensive investigations in experimental animals and adult humans.
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PMID:Asphyxial brain damage in the newborn: new insights into pathophysiology and possible pharmacologic interventions. 850 92

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.
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PMID:Delayed-onset progressive movement disorders after static brain lesions. 890 76

Multiple cystic lesions in brain parenchyma supplied by the anterior cerebral circulation is a recognized pattern of cerebral injury associated with hypoxic-ischemic encephalopathy in the term infant. This report presents a series of seven infants (gestational age, 39.3 +/- 2.8 weeks; range, 36 to 44 weeks) who developed multicystic encephalomalacia in the distribution of the anterior cerebral circulation after severe neonatal asphyxia. Cerebral imaging and pathologic studies demonstrate relative preservation of the cerebellum, brain stem, and cerebral structures supplied by the vertebrobasilar circulation. Compared to the vertebrobasilar vasculature, the anterior cerebral vessels in the term infant have dense sympathetic innervation. Asphyxia, a potent sympathetic stimulator, may induce vasoconstriction in the anterior circulation and differentially accentuate the effects of hypoxia/ischemia on cerebral tissue.
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PMID:Differential involvement of the brain in neonatal asphyxia: a pathogenic explanation. 857 57

Thirty newborn pigs within 3 days of life were randomly divided into different groups according to the time of hypoxic-ischemic encephalopathy. The results showed that the brain damage and pathologic changes were most obvious in the 60 min hypoxia-ischemic group. Brain edema was observed in every group, especially in the group where hypoxia-ischemic lasted for more than 30 min. Cerebromalacia and hemorrhage in ventricles of brain and in arachnoid were observed, and these were particularly noticed in the group where hypoxia-ischemia lasted for 60 min.
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PMID:[Observation on the animal model of hypoxic-ischemic encephalopathy and the change of pathology in newborn pigs]. 858 4

Cerebrovascular disease is one of the most common causes of epilepsy in the elderly. Most of the studies published relate to cortical infarction, subarachnoid, and intracranial hemorrhage, whereas the incidence of epilepsy from subcortical ischemia, i.e. deep lacunar infarctions and diffuse white matter lesions, is obscure. Therefore, we prospectively examined 18 patients with the precisely defined diagnosis of subcortical vascular encephalopathy (SVE), who were admitted to our hospital due to epileptic seizures (group A), and compared them to a similarly selected group matched for age, sex, risk factors, and neurological deficits with an equivalent severity of SVE but without seizures (group B). Subcortical lacunar infarctions were significantly more frequent in group A than group B (15/18 versus 4/18, p < 0.001), whereas neither the extension, degree, distribution of periventricular white matter changes, nor the presence of internal hydrocephalus, focal or diffuse cortical atrophy showed any statistical significance. However, a temporal constant theta or delta EEG focus was present in 10/18 patients in group A but only in 1/18 patients from group B (p < 0.005). 10/18 patients developed epilepsy with further seizures during follow-up. The association of SVE, multiple subcortical lacunas, and temporal EEG abnormalities are suggestive for an increased risk for epileptic seizures, which is particularly important for the treatment of patients with SVE if uncertain paroxysmal episodes occur, e.g. transient ischemic attacks, seizures, or cardiac syncope.
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PMID:Epileptic seizures in subcortical vascular encephalopathy. 858 82

Both the period of total circulatory arrest to the brain and postischemic-anoxic encephalopathy (cerebral postresuscitation syndrome or disease), after normothermic cardiac arrests of between 5 and 20 mins (no-flow), contribute to complex physiologic and chemical derangements. The best documented derangements include the delayed protracted inhomogeneous cerebral hypoperfusion (despite controlled normotension), excitotoxicity as an explanation for selectively vulnerable brain regions and neurons, and free radical-triggered chemical cascades to lipid peroxidation of membranes. Protracted hypoxemia without cardiac arrest (e.g., very high altitude) can cause angiogenesis; the trigger of it, which lyses basement membranes, might be a factor in post-cardiac arrest encephalopathy. Questions to be explored include: What are the changes and effects on outcome of neurotransmitters (other than glutamate), of catecholamines, of vascular changes (microinfarcts seen after asphyxia), osmotic gradients, free-radical reactions, DNA cleavage, and transient extracerebral organ malfunction? For future mechanism-oriented studies of the brain after cardiac arrest and innovative cardiopulmonary-cerebral resuscitation, increasingly reproducible outcome models of temporary global brain ischemia in rats and dogs are now available. Disagreements exist between experienced investigative groups on the most informative method for quantitative evaluation of morphologic brain damage. There is agreement on the desirability of using not only functional deficit and chemical changes, but also morphologic damage as end points.
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PMID:Cerebral resuscitation from cardiac arrest: pathophysiologic mechanisms. 860 7

In 1961, in Pittsburgh, PA, "cerebral" was added to the cardiopulmonary resuscitation system (CPR --> CPCR). Cerebral recovery is dependent on arrest and cardiopulmonary resuscitation times, and numerous factors related to basic, advanced, and prolonged life support. Postischemic-anoxic encephalopathy (the cerebral postresuscitation disease or syndrome) is complex and multifactorial. The prevention or mitigation of this syndrome requires that there be development and trials of special, multifaceted, combination treatments. The selection of therapies to mitigate the postresuscitation syndrome should continue to be based on mechanistic rationale. Therapy based on a single mechanism, however, is unlikely to be maximally effective. For logistic reasons, the limit for neurologic recovery after 5 mins of arrest must be extended to achieve functionally and histologically normal human brains after 10 to 20 mins of circulatory arrest. This goal has been approached, but not quite reached. Treatment effects on process variables give clues, but long-term outcome evaluation is needed for documentation of efficacy and to improve clinical results. Goals have crystallized for clinically relevant cardiac arrest-intensive care outcome models in large animals. These studies are expensive, but essential, because positive treatment effects cannot always be confirmed in the rat forebrain ischemia model. Except for a still-elusive breakthrough effect, randomized clinical trials of CPCR are limited in their ability to statistically document the effectiveness of treatments found to be beneficial in controlled outcome models in large animals. Clinical studies of feasibility, side effects, and acceptability are essential. Hypertensive reperfusion overcomes multifocal no-reflow and improves outcome. Physical combination treatments, such as mild resuscitative (early postarrest) hypothermia (34 degrees C) plus cerebral blood flow promotion (e.g., with hypertension, hemodilution, and normocapnia), each having multiple beneficial effects, achieved complete functional and near-complete histologic recovery of the dog brain after 11 mins of normothermic, ventricular fibrillation cardiac arrest. Calcium entry blockers appear promising as a treatment for postischemic-anoxic encephalopathy. However, the majority of single or multiple drug treatments explored so far have failed to improve neurologic outcome. Assembling and evaluating combination treatments in further animal studies and determining clinical feasibility inside and outside hospitals are challenges for the near future. Treatments without permanent beneficial effects may at least extend the therapeutic window. All of these investigations will require coordinated efforts by multiple research groups, pursuing systematic, multilevel research--from cell cultures to rats, to large animals, and to clinical trials. There are still many gaps in our knowledge about optimizing extracerebral life support for cerebral outcome.
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PMID:Cerebral resuscitation from cardiac arrest: treatment potentials. 860 8

Primary clinical manifestations in patients with Takayasu arteritis are mostly unspecific signs of inflammation. First involved are the main brachiocephalic arteries and the aorta. Later the disease becomes symptomatic through organ ischemia. Often a renal hypertension appears due to an arteritic stenosis of the renal artery. Here we present a patient suffering from Takayasu arteritis. The disease first appeared with renal hypertension and an encephalopathy. The hypertension was induced by compression of the right renal artery which in turn was caused by an aortic aneurysm. The aneurysm had been resected and the aorta was reconstructed by aorto-aortal prosthetic interposition and implantation of the renal arteries. The postoperative course was uneventful.
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PMID:[Atypical initial manifestation of Takayasu arteritis]. 867 2

Phospholipase C (PLC) and related enzymes in signal transduction system are closely linked to cellular damage in ischemic encephalopathy. This study was undertaken to elucidate the time sequential changes of PLC isoenzymes (beta and gamma) in vulnerable areas of hippocampus in global ischemia and infarcted area in focal infarction. Mongolian gerbils were used because of their susceptibility to ischemic encephalopathy and divided into the following groups: the bilateral ischemia with various reperfusion periods group, unilateral progressive ischemia group, and focal ischemia group induced by infusion of iron particles through the femoral artery. The changes of PLC isoenzymes were observed immunohistochemically and matched with morphological changes. In the global ischemia with reperfusion group, the changes were most significant in hippocampus. Sequential changes of neurons such as red neurons at an early stage progressed to pknotic neurons at a later stage were noted with typical delayed neuronal damage in the corns ammonis (CA) 1 subfield of hippocampus. Red neurons and pyknotic neurons as well as intracytoplasmic inclusion in 3 to 24 hours of reperfusion showed loss of PLC isoenzymes as well as tubulin. The changes of PLC expression were corresponding to the degeneration of neurons with no discernible time sequential changes in remaining neurons. In the unilateral hemispheric progressive ischemia group, ischemic damage was far more marked and extensive with no selective injury pattern according to time and location. At 1 day, there was diffuse vacuolization and necrosis of neuropil with a loss of neuron. Admixed surviving neurons and vacuolated neuropil showed increased reaction to anti-PLC antibodies, which could be either an evidence of protein synthesis responding to ischemic insult or an artifactual change. Focal ischemia group showed time sequential changes of blood vessels and white blood cells with necrosis of surrounding tissue. Degenerating hippocampal neurons in infarction also showed a strong positive reaction to anti-PLC antibody, which was most likely due to condensation of cytoplasm rather than increased synthesis. This study showed different changes of PLC expression in global ischemic encephalopathy with reperfusion, progressive ischemia, and focal infarction, which suggested different pathophysiologic mechanism between these conditions.
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PMID:Immunohistochemical expression of phospholipase C in global and focal ischemic encephalopathy in gerbil: relationship with morphological changes. 870 70


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