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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental studies of embolic cerebral ischemia using the rat are limited by variability in the location, size, and frequency of lesions produced. A technique is described herein which improves the reliability of an established model. Eight male Sprague-Dawley rats underwent injection of the cervical internal carotid artery with 0.1 ml of 1-h-old fragmented autologous blood clot through an external carotid artery cannula. The pterygopalatine artery was ligated prior to embolization. At killing 2 h after embolization, clot was observed in the proximal middle cerebral and posterior cerebral arteries in all animals. Areas of reduced blood flow at 2 h postembolization were assessed by digital image processing of iodo-[14C]antipyrine autoradiographic images. No-flow and low-flow areas were measured for each of approximately 25 serial brain sections with a computerized bit-pad. Volumes were calculated and lesions localized by anatomical reconstructions. No animal sustained a hemorrhagic lesion. One animal sustained only a very small area of ischemia in the internal capsule. Of the remaining seven, all had large regions of ischemia in the middle cerebral distribution involving cortex and basal ganglia. Posterior cerebral involvement was observed in six of the seven animals as well. The contralateral hemisphere was unaffected. Volume values could be calculated for primary vascular distributions. Most variability occurred in the pattern of posterior cerebral involvement. The technique described produces a relatively consistent region of ischemia in the middle and posterior cerebral artery distributions in the rat and is a useful model for the study of cerebral ischemia.
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PMID:A model of embolic cerebral ischemia in the rat. 356 63

We present 2 cases, one eclamptic patient and one noneclamptic patient, of headache, cortical blindness, and seizures. Both patients demonstrated findings consistent with posterior leukoencephalopathy syndrome. Posterior leukoencephalopathy syndrome is a rapidly evolving neurologic condition that is characterized by headache, nausea and vomiting, seizures, visual disturbances, altered sensorium, and occasionally focal neurologic deficits. Posterior leukoencephalopathy syndrome can be triggered by numerous conditions, including preeclampsia-eclampsia, and can be seen in the postpartum period. It is characterized predominately by white matter vasogenic edema of the occipital and posterior parietal lobes. This condition can be difficult to differentiate clinically from cerebral ischemia, and magnetic resonance imaging with diffusion-weighted imaging and apparent diffusion coefficient are needed to do so. In most cases of posterior leukoencephalopathy syndrome, the prognosis is excellent, with full resolution of symptoms.
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PMID:Postpartum blindness: two cases. 1474 15

Posterior reversible encephalopathy syndrome (PRES) is a rare neurological condition identifiable by clinical presentation and MRI appearance.1 Patients present with headache, seizures, loss of vision and altered mental function. The pathogenesis of the syndrome is poorly understood. One hypothesis is that cerebral vasospasm results in cerebral ischaemia and subsequent development of T2 hyperintensity, and the other is a temporary failure of the autoregulatory capabilities of the cerebral vessels, leading to hyperperfusion, breakdown of the blood-brain barrier, and consequent vasogenic oedema. It is believed that a rapid rise in blood pressure overcomes cerebral autoregulatory mechanisms with abrupt dilatation of cerebral arterioles. We report a patient with systemic lupus erythematosus and PRES after recurrent spontaneous abortion.
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PMID:Seizures and loss of vision in a patient with systemic lupus erythematosus. 1765 17

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V1a receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.
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PMID:Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link? 3092 75