Relevant bibliographies by topics / Stroke/cerebral ischaemia

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Stroke/cerebral ischaemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Stroke/cerebral ischaemia"

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Khan, Sibghat Ullah, Naveed Aslam Lashari, Nadia Irum Lakho, Ambreen Faisal, and Aamir Hussain. "CEREBRAL ISCHAEMIA AND STROKE;." Professional Medical Journal 24, no. 12 (November 29, 2017): 1823–27. http://dx.doi.org/10.29309/tpmj/2017.24.12.564.

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Introduction: Colour Doppler sonography is a well-established widely available,noninvasive, cost effective and a reliable method for assessing cerebrovascular circulation.It has become a valuable completion of the sonographic workup in patients with cerebralischaemia and infarction. Its accuracy is close to angiography. Objectives: To determine thefrequency of significant carotid artery stenosis in patients of cerebral ischaemia/stroke and itscharacterized sonographic appearance of plaque. Study Design: Cross sectional study, basedon nonprobability convenience sample technique. Setting: Department of Radiology, CombinedMilitary Hospital Lahore, using Colour and Power Doppler Ultrasound machine ALOKA SSD-5500. Period: 14 October 2006 to 15 March 2007. Methodology: Total of 50 diagnosed patientsof either gender, aged 30 to 70 years with cerebral ischaemia and stroke were included in thestudy. Carotid Doppler examination was conducted in each patient and findings were recorded.Results: Among 50 patients who underwent carotid Doppler examination for diagnosis ofclinically significant carotid artery stenosis, 35 patients had carotid plaques. 08 patients werediagnosed to have more than 70 % stenosis, 07 patients with more than 50 % and 20 patientsless than 50 % carotid artery stenosis. 15 patients did not show any carotid artery disease.12 patients had bilateral stenosis while 23 had unilateral disease. Mean age of the patientswith and without carotid artery disease was 52 ± 7.87 years. Conclusion: Majority of patientswith Cerebral ischemia/stroke showed carotid artery stenosis on colour Doppler ultrasound.Common age group who developed cerebral ischemia/stroke was above 50years.
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Inoue, Isao, Mari Fukunaga, Keiko Koga, Hong-Du Wang, and Makoto Ishikawa. "Scalp Acupuncture Effects of Stroke Studied with Magnetic Resonance Imaging: Different Actions in the Two Stroke Model Rats." Acupuncture in Medicine 27, no. 4 (December 2009): 155–62. http://dx.doi.org/10.1136/aim.2009.000430.

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Background Scalp acupuncture (SA) therapy on strokes has been empirically established and widely used in clinics in China. The evidence from clinical studies suggests that SA produces significant benefits for some patients with stroke. Methods The effect of scalp acupuncture was studied using MRI for two different stroke models: spontaneously hypertensive stroke-prone (SHR-SP) rats and rats with transiently induced focal cerebral ischaemia by middle cerebral artery occlusion for 2 h (MCAO rats). Results Stroke onset in SHR-SP rats was characterised by a development of vasogenic oedema without any appearance of cytotoxic oedema. Scalp acupuncture reduced rapidly neurological dysfunction in SHR-SP rats and reduced the volume of the vasogenic oedema during the same period. In contrast, in MCAO rats, focal cerebral ischaemia caused an immediate development of cytotoxic oedema without any appearance of vasogenic oedema. Vasogenic oedema developed after reperfusion. Scalp acupuncture had no significant effects on the cytotoxic oedema, vasogenic oedema or neurological dysfunction of the MCAO rats within the time span examined. Conclusion Scalp acupuncture had a rapid and strong effect on neurological dysfunction only in the hypertensive stroke-model by reducing the vasogenic oedema. Our results suggest that, if there are similar underlying mechanisms in human strokes, scalp acupuncture may be more beneficial for patients with strokes of hypertension-caused vasogenic origin than ischaemic origin.
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Moxon, Joseph V., Alexandra F. Trollope, Brittany Dewdney, Catherine de Hollander, Domenico R. Nastasi, Jane M. Maguire, and Jonathan Golledge. "The effect of angiopoietin-1 upregulation on the outcome of acute ischaemic stroke in rodent models: A meta-analysis." Journal of Cerebral Blood Flow & Metabolism 39, no. 12 (October 4, 2019): 2343–54. http://dx.doi.org/10.1177/0271678x19876876.

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Clinical studies report that low circulating angiopoietin-1 concentration at presentation predicts worse outcomes after ischaemic stroke. Upregulating angiopoietin-1 may therefore have therapeutic benefit for ischaemic stroke. This systematic review assessed whether upregulating angiopoietin-1 improved outcomes in rodent models of ischaemic stroke. Random-effects models quantified the effect of angiopoietin-1 upregulation on stroke severity in terms of the size of cerebral infarction and the extent of blood–brain barrier permeability. Eleven studies utilising rat and mouse models of ischaemic stroke fulfilled the inclusion criteria. Meta-analyses demonstrated that angiopoietin-1 upregulation significantly reduced cerebral infarction size (standardised mean difference: –3.02; 95% confidence intervals: –4.41, –1.63; p < 0.001; n = 171 animals) and improved blood–brain barrier integrity (standardized mean difference: –2.02; 95% confidence intervals: –3.27, –0.77; p = 0.002; n = 129 animals). Subgroup analyses demonstrated that angiopoietin-1 upregulation improved outcomes in models of transient, not permanent cerebral ischaemia. Six studies assessed the effect of angiopoietin-1 upregulation on neurological function; however, inter-study heterogeneity prevented meta-analysis. In conclusion, published rodent data suggest that angiopoietin-1 upregulation improves outcome following temporary cerebral ischaemia by reducing cerebral infarction size and improving blood–brain barrier integrity. Additional research is required to examine the effect of angiopoietin-1 upregulation on neurological function during stroke recovery and investigate the benefit and risks in patients.
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Chen, Lucia Y., Charlotte Ainscough, Mohamed Sayed, and Maneesh Bhargava. "Simultaneous treatment of ischaemic bowel and ischaemic stroke with intravenous thrombolysis therapy." BMJ Case Reports 11, no. 1 (November 2018): e227126. http://dx.doi.org/10.1136/bcr-2018-227126.

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Novel treatment of simultaneous mesenteric and cerebral ischaemia with systemic thrombolysis. A 75-year-old man presented to the acute stroke team with aphasia, right-sided weakness and distressed with a pain he was unable to localise. He was treated with intravenous thrombolysis with tissue plasminogen activator for a left middle cerebral artery stroke. Decompensation on the ward during thrombolysis with worsening abdominal distension and pain, hypotension and tachycardia prompted a CT angiogram scan, which displayed proximal inferior mesenteric artery occlusion. Thrombolysis treatment resulted in excellent improvement of both his dysphasia and weakness from the left cerebral ischaemic stroke and reperfusion of the ischaemic bowel, without surgical intervention.
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Schwaninger, M., I. Inta, and O. Herrmann. "NF-κB signalling in cerebral ischaemia." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1291–94. http://dx.doi.org/10.1042/bst0341291.

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In acute stroke, neuronal apoptosis and inflammation are considered to be important mechanisms on the road to tissue loss and neurological deficit. Both apoptosis and inflammation depend on gene transcription. We have identified a signalling pathway that regulates transcription of genes involved in apoptosis and inflammation. In a mouse model of focal cerebral ischaemia, there is an induction of the cytokine TWEAK (tumour necrosis factor-like weak inducer of apoptosis) and its membrane receptor Fn14. TWEAK promotes neuronal cell death and activates the transcription factor NF-κB (nuclear factor κB) through the upstream kinase IKK [IκB (inhibitory κB) kinase]. In vivo, IKK is activated in neurons. Neuron-specific deletion of the subunit IKK2 or inhibition of IKK activity reduced the infarct size and neuronal cell loss. A pharmacological inhibitor of IKK also showed neuroprotective properties. IKK-dependent ischaemic brain damage is likely to be mediated by NF-κB, because neuron-specific inhibition of NF-κB through transgenic expression of the NF-κB superrepressor was found to reduce the infarct size. In summary, there is evidence that IKK/NF-κB signalling contributes to ischaemic brain damage and may provide suitable drug targets for the treatment of stroke.
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Tang, LL, K. Ye, XF Yang, and JS Zheng. "Apocynin Attenuates Cerebral Infarction after Transient Focal Ischaemia in Rats." Journal of International Medical Research 35, no. 4 (July 2007): 517–22. http://dx.doi.org/10.1177/147323000703500411.

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This study investigated whether inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase attenuates cerebral infarction after transient focal ischaemia in rats. Focal ischaemia (1.5 h) was produced in male Sprague-Dawley rats (250 − 280 g) by middle cerebral artery occlusion. Some rats also received treatment with 50 mg/kg apocynin, a NADPH oxidase inhibitor, by intraperitoneal injection 30 min prior to reperfusion. Two hours after reperfusion, brains were harvested to measure NADPH oxidase activity and superoxide levels. After 24 h, the remaining brains were harvested to investigate infarct size. NADPH oxidase activity and superoxide level were all augmented 2 h after reperfusion compared with controls. Apocynin treatment significantly reduced NADPH oxidase activity and superoxide levels. Cerebral infarct size was significantly smaller in the apocynin-treated group compared with those undergoing ischaemia/reperfusion alone. These results indicate that inhibition of NADPH oxidase attenuates cerebral infarction after transient focal ischaemia in rats, suggesting that inhibition of NADPH oxidase may provide a therapeutic strategy for ischaemic stroke.
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Denorme, Frederik, and Simon F. De Meyer. "The VWF-GPIb axis in ischaemic stroke: lessons from animal models." Thrombosis and Haemostasis 116, no. 10 (2016): 597–604. http://dx.doi.org/10.1160/th16-01-0036.

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SummaryStroke is a leading cause of death and long-term disability worldwide. Ischaemic stroke is caused by a blood clot that obstructs cerebral blood flow. Current treatment mainly consists of achieving fast reperfusion, either via pharmacological thrombolysis using tissue plasminogen activator or via endovascular thrombectomy. Unfortunately, reperfusion therapy is only available to a limited group of patients and reperfusion injury can further aggravate brain damage. Hence, there is an urgent need for better understanding of ischaemic stroke pathophysiology in order to develop novel therapeutic strategies. In recent years, the pathophysiological importance of von Willebrand factor (VWF) in ischaemic stroke has become clear from both clinical and experimental studies. In particular, binding of VWF to platelet glycoprotein Ib (GPIb) has become an interesting target for ischaemic stroke therapy. Recent insights show that inhibting the VWF-GPIb interaction could result in a pro-thrombolytic activity improving cerebral reperfusion rates and concurrently reducing cerebral ischaemia/reperfusion damage. This review gives an overview of the experimental evidence that illustrates the crucial role of the VWF-GPIb axis in ischaemic stroke.
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Yamashita, T., K. Deguchi, K. Sawamoto, H. Okano, T. Kamiya, and K. Abe. "Neuroprotection and neurosupplementation in ischaemic brain." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1310–12. http://dx.doi.org/10.1042/bst0341310.

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Possible strategies for treating ischaemic stroke include: (i) neuroprotection (preventing damaged neurons from undergoing apoptosis in the acute phase of cerebral ischaemia), and (ii) neurosupplementation (the repair of broken neuronal networks with newly born neurons in the chronic phase of cerebral ischaemia). In this paper, we review our recent progress in development of these distinct new strategies for treatment of damaged brain following a stroke. Firstly, we investigated the role of endogenous IL-6 (interleukin-6), which is one of the cytokines drastically induced by ischaemic stimuli, by administering IL-6RA (anti-IL-6 receptor monoclonal antibody) to mice. We found that endogenous IL-6 plays a critical role in neuroprotection and that its role may be mediated by STAT3 (signal transducer and activator of transcription-3) activation. Secondly, we studied the endogenous sources of the newly born neurons in the ischaemic striatum by region- and cell-type-specific cell labelling techniques. The results revealed that the SVZ (subventricular zone) is the principal source of the neuronal progenitors that migrate laterally towards the infarcted regions, and differentiate into newly born neurons. Finally, we developed a restorative stroke therapy with a bio-affinitive scaffold, which is an appropriate poly-porous structure releasing bioactive substances such as neurotrophic factor. This bio-affinitive scaffold is able to give an appropriate environment for newly born neurons. In future, we will combine these strategies to develop more effective therapies for treatment of strokes.
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Segan, Louise, Fiona Permezel, Wei Ch’ng, Ian Millar, Mark Brooks, Matt Lee-Archer, and Geoffrey Cloud. "Cerebral arterial gas embolism from attempted mechanical thrombectomy: recovery following hyperbaric oxygen therapy." Practical Neurology 18, no. 2 (December 28, 2017): 134–36. http://dx.doi.org/10.1136/practneurol-2017-001828.

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Cerebral arterial gas embolism is a recognised complication of endovascular intervention with an estimated incidence of 0.08%. Its diagnosis is predominantly clinical, supported by neuroimaging. The treatment relies on alleviating mechanical obstruction and reversing the proinflammatory processes that contribute to tissue ischaemia. Hyperbaric oxygen therapy is an effective treatment and has multiple mechanisms to reverse the pathological processes involved in cerebral arterial gas embolism. Symptomatic cerebral arterial gas embolism is a rare complication of endovascular intervention for acute ischaemic stroke. Although there are no previous descriptions of its successful treatment with hyperbaric oxygen therapy following mechanical thrombectomy, this is likely to become more common as mechanical thrombectomy is increasingly used worldwide to treat acute ischaemic stroke.
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McColl, Barry W., Nicola Rose, Fiona H. Robson, Nancy J. Rothwell, and Catherine B. Lawrence. "Increased Brain Microvascular MMP-9 and Incidence of Haemorrhagic Transformation in Obese Mice after Experimental Stroke." Journal of Cerebral Blood Flow & Metabolism 30, no. 2 (October 14, 2009): 267–72. http://dx.doi.org/10.1038/jcbfm.2009.217.

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Obesity is an independent risk factor for stroke and is associated with poorer outcome after stroke. We investigated whether this poorer outcome is related to brain microvascular disruption. Focal cerebral ischaemia was induced in lean or obese ( ob/ob) mice by transient middle cerebral artery occlusion. The incidence of haemorrhagic transformation and the volume of ischaemic brain damage were significantly greater in obese mice. Blood–brain barrier permeability and brain microvascular MMP-9 expression were also markedly increased in obese mice. These effects were independent of leptin or glycaemic status, suggesting that obesity potentiates brain microvascular disruption after experimental stroke.
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Dissertations / Theses on the topic "Stroke/cerebral ischaemia"

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Bowler, John Vaughan. "Cerebral infarction and '9'9Tc'm HMPAO SPECT." Thesis, King's College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260983.

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Sibson, Nicola Ruth. "A magnetic resonance imaging study of experimental cerebral ischaemia." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360825.

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Taylor, Deanna Lesley. "Alterations in interstitial acid-base homeostasis during cerebral ischaemia." Thesis, University College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267025.

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Greenhalgh, Andrew. "Actions of interleukin-1 receptor antagonist in cerebral ischaemia." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/actions-of-interleukin1-receptor-antagonist-in-cerebral-ischaemia(50aacd97-68c1-4f91-90b5-8f8deff5d21d).html.

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Cerebral ischaemia, or stroke, is a leading cause of death and disability worldwide. Ischaemic stroke, as a result of arterial occlusion, and subarachnoid haemorrhage (SAH), as a consequence of arterial rupture in the subarachnoid space, are major subtypes of stroke. Treatment options for both are limited, and many therapeutic strategies have failed. In ischaemic stroke, lack of evidence of brain penetration of treatments has been cited as a major weakness and contributing factor to failed clinical trials. In SAH, animal models do not always mimic key pathophysiological hallmarks of the disease, hindering development of new therapeutics. Inflammation is strongly associated with brain injury after cerebral ischaemia and inhibition of the pro-inflammatory cytokine interleukin-1 (IL-1) represents apossible therapeutic target. Therefore, the key objectives of this thesis were; (1) to improve preclinical data on a promising stroke treatment, interleukin-1 receptor antagonist (IL-1Ra), by investigating its pharmacokinetic profile and brain penetration in a rat model of ischaemic stroke, (2) to investigate the endovascular perforation model of SAH in rat, as a tool for the investigation of neuroprotectants, and (3) to examine the role of the inflammatory response in the SAH model and the effects of IL-1Ra. The neuroprotective effect, pharmacokinetic profile and brain penetration of IL-1Ra were assessed after a single subcutaneous (s.c.) dose (100mg/kg) in rats, after transient (90 min) middle cerebral artery occlusion (MCAo). A single s.c. dose of IL-1Ra reduced neuronal damage, resulted in sustained, high concentrations of IL-1Ra in plasma and cerebrospinal fluid and also penetrated brain tissue exclusively in areas of blood brain-barrier (BBB) breakdown. An endovascular perforation model of SAH in rat was investigated and produced widespread multifocal infarcts. In this model, administration of IL-1Ra (s.c.) reduced BBB breakdown, which correlated with injury at 48 h. IL-1_ was expressed in the brain early after SAH in areas associated with haem oxygenase-1 (HO-1) expression, indicating the presence of free haem. Stimulation of primary mouse mixed glial cells in vitro with haem induced expression and release of IL-1 alpha but not IL-1 beta. These data, after MCAo in rat, are the first to show that a single s.c. dose of IL-1Ra rapidly reaches salvageable brain tissue and is neuroprotective. This allows confidence that IL-1Ra is able to confer its protective actions both peripherally and centrally. After experimental SAH, we suggest that haem, a breakdown product of haemoglobin, released from lysed red blood cells in the subarachnoid space, acts as a danger associated molecular pattern (DAMP) driving IL-1- dependent inflammation. These data provide new insights into inflammation after SAH-induced brain injury and suggest IL-1Ra as a candidate treatment for the disease. Overall, these findings strengthen preclinical data supporting IL-1Ra as a neuroprotective therapy for ischaemic stroke, and identify SAH as a new indication for treatment with IL-1Ra.
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Marquardt, Lars. "Large artery disease in patients with cerebral ischaemia : frequency, investigation and management." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:70b598c5-97ca-4567-ac32-ed5092972a16.

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Stroke is the third leading cause of death in the developed world and is the leading neurological cause of disability with a massive impact on personal life and society. Large artery atherosclerosis is one of the main causes of ischaemic stroke. However, in several aspects of this condition there is still a significant amount of uncertainty about its prevalence, appropriate investigation and possible treatment. Reliable data on epidemiology are therefore necessary to provide clinicians and researchers with crucial information to guide diagnostic and therapeutic management as well as further research. With this thesis I aimed to provide useful information about the prevalence of large artery disease in certain groups of patients, and to contribute to investigation- and managementstrategies using data from a large population based study, the Oxford Vascular Study (OXVASC). OXVASC is a prospective, population-based incidence study of vascular disease in Oxfordshire, UK, which started in 2002 and is ongoing. The study population comprises all 91,106 individuals registered with nine general practices and uses multiple methods of case ascertainment to identify all patients with vascular events. Firstly, I have shown that the prevalence of ≥50% vertebral or basilar artery stenosis in posterior circulation TIA or minor stroke is more than twice as high as the prevalence of ≥50% carotid stenosis in patients with carotid territory events, and is associated with a very high early risk of stroke of 22% and TIA of 46%. Furthermore, severe vertebral and/or basilar artery stenosis is associated with multiple TIAs at first presentation. Secondly, I have shown that early risk of stroke was higher after posterior circulation TIA, with a 1-year risk of 16%, than after carotid territory TIA, with a 1-year risk of 9%. In addition, I was able to show for the first time, that the ABCD2 score was predictive of early stroke not only in patients with carotid circulation TIA but also in patients with vertebrobasilar TIA. Thirdly, in a pilot feasibility study about arterial spin labelling magnetic resonance imaging in patients with large artery disease in the vertebrobasilar circulation I have shown that patients with severe large artery disease have significantly impaired occipital brain perfusion. My results suggest that this new technique might be a useful tool to identify suitable patients for interventional treatment of vertebrobasilar large artery disease. Fourthly, I was able to show that the risk of ipsilateral stroke and TIA in patients with an asymptomatic carotid stenosis is very low with contemporary best medical treatment alone, suggesting that routine carotid endarterectomy for asymptomatic carotid stenosis might not longer be feasible. Finally, I have clarified that lower rates of intervention for moderate to severe symptomatic carotid stenosis in women than in men can be explained by sex-differences in the populationbased incidence of carotid large artery disease and not due to under-investigation or reluctance amongst women to undergo investigation or treatment.
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Calamante, Fernando. "Diffusion and perfusion MRI and applications in cerebral ischaemia." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314345.

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Ben-Yoseph, O. "Multinuclear magnetic resonance spectroscopy studies of perturbed cerebral metabolism in vitro." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240078.

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Thomas, David Lee. "Magnetic resonance imaging of diffusion and perfusion : techniques and applications to cerebral ischaemia." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391829.

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Smith, Stuart Ernest. "Excitatory amino acid antagonists and related agents as potential therapies in focal cerebral ischaemia in the rat." Thesis, King's College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281943.

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Milidonis, Xenios. "Multicentre evaluation of MRI variability in the quantification of infarct size in experimental focal cerebral ischaemia." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28877.

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Ischaemic stroke is a leading cause of death and disability in the developed world. Despite that considerable advances in experimental research enabled understanding of the pathophysiology of the disease and identified hundreds of potential neuroprotective drugs for treatment, no such drug has shown efficacy in humans. The failure in the translation from bench to bedside has been partially attributed to the poor quality and rigour of animal studies. Recently, it has been suggested that multicentre animal studies imitating the design of randomised clinical trials could improve the translation of experimental research. Magnetic resonance imaging (MRI) could be pivotal in such studies due to its non-invasive nature and its high sensitivity to ischaemic lesions, but its accuracy and concordance across centres has not yet been evaluated. This thesis focussed on the use of MRI for the assessment of late infarct size, the primary outcome used in stroke models. Initially, a systematic review revealed that a plethora of imaging protocols and data analysis methods are used for this purpose. Using meta-analysis techniques, it was determined that T2-weighted imaging (T2WI) was best correlated with gold standard histology for the measurement of infarctbased treatment effects. Then, geometric accuracy in six different preclinical MRI scanners was assessed using structural phantoms and automated data analysis tools developed in-house. It was found that geometric accuracy varies between scanners, particularly when centre-specific T2WI protocols are used instead of a standardised protocol, though longitudinal stability over six months is high. Finally, a simulation study suggested that the measured geometric errors and the different protocols are sufficient to render infarct volumes and related group comparisons across centres incomparable. The variability increases when both factors are taken into account and when infarct volume is expressed as a relative estimate. Data in this study were analysed using a custom-made semi-automated tool that was faster and more reliable in repeated analyses than manual analysis. Findings of this thesis support the implementation of standardised methods for the assessment and optimisation of geometric accuracy in MRI scanners, as well as image acquisition and analysis of in vivo data for the measurement of infarct size in multicentre animal studies. Tools and techniques developed as part of the thesis show great promise in the analysis of phantom and in vivo data and could be a step towards this endeavour.
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Books on the topic "Stroke/cerebral ischaemia"

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Alarcón, Gonzalo, Marian Lazaro, and Antonio Valentín. Migraine, stroke, and cerebral ischaemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0033.

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This chapter reviews the electroencephalographic changes associated with migraine, stroke and cerebral ischaemia, and their interpretation to aid in their differential diagnosis. The incidence of stroke and cerebral ischaemia is increasing with population aging. They are some of the most common problems faced in emergency medicine, and their diagnosis can be puzzling. This chapter describes and illustrates the patterns seen in such conditions, such as slowing, frontal intermittent delta activity (FIRDA), periodic lateralized epileptiform discharge (PLED), generalized periodic lateralized epileptiform discharge (GPED), and bilateral periodic lateralized epileptiform discharge (BiPED). The chapter reviews their prognostic value in critical care medicine and their differential diagnosis with status epilepticus.
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Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_002.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, mechanical thrombectomy in case of proximal occlusion (middle cerebral artery, intracranial internal carotid artery, basilar artery), on top of thrombolysis in the absence of contraindication or alone otherwise, aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, while surgery does not seem effective to reduce death and disability.
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Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0067.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, otherwise aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, but surgery does not seem effective to reduce death and disability.
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Leys, Didier, Charlotte Cordonnier, and Valeria Caso. Stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0067_update_001.

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Stroke is a major public health issue. Many are treatable in the acute stage, provided patients are admitted soon enough. The overall incidence of stroke in Western countries is approximately 2400 per year per million inhabitants, and 80% are due to cerebral ischaemia. The prevalence is approximately 12 000 per million inhabitants. Stroke is associated with increased long-term mortality, handicap, cognitive and behavioural impairments, recurrence, and an increased risk of other types of vascular events. It is of major interest to take the heterogeneity of stroke into account, because of differences in the acute management, secondary prevention, and outcomes, according to the subtype and cause of stroke. In all types of stroke, early epileptic seizures, delirium, increased intracranial pressure, and non-specific complications are frequent. In ischaemic strokes, specific complications, such as malignant infarcts, spontaneous haemorrhagic transformation, early recurrence, and a new ischaemic event in another vascular territory, are frequent. In haemorrhagic strokes, the major complication is the subsequent increased volume of bleeding. There is strong evidence that stroke patients should be treated in dedicated stroke units; each time 24 patients are treated in a stroke unit, instead of a conventional ward, one death and one dependence are prevented. This effect does not depend on age, severity, and the stroke subtype. For this reason, stroke unit care is the cornerstone of the treatment of stroke, aiming at the detection and management of life-threatening emergencies, stabilization of most physiological parameters, and prevention of early complications. In ischaemic strokes, besides this general management, specific therapies include intravenous recombinant tissue plasminogen activator, given as soon as possible and before 4.5 hours, otherwise aspirin 300 mg, immediately or after 24 hours in case of thrombolysis, and, in a few patients, decompressive surgery. In intracerebral haemorrhages, blood pressure lowering and haemostatic therapy, when needed, are the two targets, but surgery does not seem effective to reduce death and disability.
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Rothwell, Peter. Cerebrovascular diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0767.

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This chapter is concerned with those diseases of the cerebral and ocular circulation that cause ischaemia or infarction of the brain and eye or spontaneous haemorrhage into or around the brain. The main clinical manifestations of these diseases are transient ischaemic attack and stroke.
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Patarroyo, Sully Xiomara Fuentes, and Craig Anderson. Management of ischaemic stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0236.

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Ischaemic stroke is the most common cause of stroke around the world. It is a complex disease with a range of causes, manifestations, outcomes, and treatments. As the therapeutic time window to rescue or ‘protect’ the brain from ischaemic damage is extremely short, effective treatment requires coordinated systems of care, which commence in the prehospital paramedical setting and continue through the emergency department into the critical care environment, neurology ward, rehabilitation, and re-settlement back home. Successful outcomes from ischaemic stroke can be achieved through the effective use of thrombolytic therapy to re-canalize an occluded vessel and re-perfuse the ‘at risk’ area of the brain. Other aspects of management include the prevention of complications of the neurological (cerebral) disability, timely introduction of rehabilitation, realistic goal-setting towards satisfactory recovery, and secondary prevention measures to reduce the high risk of recurrent stroke and other serious vascular events.
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Markus, Hugh, Anthony Pereira, and Geoffrey Cloud. Cerebral haemorrhage. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198737889.003.0013.

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This chapter covers the several types of cerebral haemorrhage: extradural, subdural, subarachnoid, and intracerebral. Subarachnoid haemorrhage (SAH) is an important cause of neurological disability and mortality, although only occasionally present with focal stroke symptoms. Intracerebral haemorrhage usually presents with a stroke, which can only be reliably distinguished from ischaemic stroke by brain imaging. The chapter discusses the diagnosis, investigation, and management of both SAH and intracerebral haemorrhage.
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Haunton, Victoria, Aung Sett, Amit Mistri, and Martin Fotherby. Stroke. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0227.

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The World Health Organization defines stroke as ‘a clinical syndrome consisting of rapidly developing clinical signs of focal (at times global) disturbance of cerebral function lasting greater than 24 hours (or leading to death) with no apparent cause other than that of vascular origin’. Transient ischaemic attack (TIA) is defined as a rapid presentation of neurological deficit with complete recovery within 24 hours of the onset of symptoms. However, the 24-hour cut-off is arbitrary, has no biological basis, and is of limited use clinically. A shorter duration is now regarded as more appropriate, although it has yet to be universally accepted. In clinical practice, stroke and TIA are best thought of as comprising a continuum, as they have similar pathological mechanisms, etiologies, and management strategies. While subarachnoid haemorrhage is a type of stroke based on the above definition, it is not covered in this chapter, as its pathophysiology, clinical manifestations, and management are distinct from those for ischaemic stroke and haemorrhagic stroke.
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Henzi, Bettina, and Maja Steinlin. Stroke in children. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0013.

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Stroke in children is a rare, but terrifying disease and its lifelong sequelae weigh heavy on patients and families. It is also increasingly recognized as a socioeconomic burden, ongoing for many years after the acute manifestation. There is a significant delay in diagnosis of childhood stroke. This is caused by several factors: lack of awareness among the public and professionals, childhood-specific manifestations, numerous stroke mimics, and last but not least, limited access to emergency neuroimaging for children. Fast stroke recognition tools need adaption to the special needs in children. Childhood arterial ischaemic stroke differs in aetiology from adult stroke with cerebral vasculopathies being the leading cause and cardioembolic aetiology ranking second. However, treatment guidelines are largely based on adult guidelines and expert consensus. Future research has to put emphasis on understanding pathophysiology, defining specific treatment options, and providing evidence for treatment guidelines in paediatric stroke.
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Morrison, Karen. Prevention of cerebrovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0348.

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Stroke is the main cause of neurological morbidity in adults and the third most common cause of death worldwide after ischaemic heart disease and cancer (all forms combined). It is more common in older people, with three-quarters of strokes occurring in people over 65 years of age, and estimates are that overall stroke morbidity will double by the early 2020s. The worldwide figure of increasing incidence of stroke detection masks the fact that mortality from stroke has actually been falling in developed countries since the latter half of the twentieth century while the mortality has continued to rise in China, Asia, and eastern Europe. This chapter discusses prevention of cerebrovascular disease, and includes strategies to reduce the risk of thromboembolic stroke and cerebral haemorrhage.
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Book chapters on the topic "Stroke/cerebral ischaemia"

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Kalaria, R. N., W. C. Low, A. E. Oakley, J. Y. Slade, P. G. Ince, C. M. Morris, and T. Mizuno. "CADASIL and genetics of cerebral ischaemia." In Stroke-Vascular Diseases, 75–90. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-6137-1_5.

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Bousser, M. G., J. C. Baron, and J. Chiras. "Ischemic strokes and migraine." In Cerebral Ischaemia, 133–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_16.

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Godon-Hardy, S., J. F. Meder, A. Dilouya, V. Monsaingeon, and D. Fredy. "Ischemic strokes and oral contraception." In Cerebral Ischaemia, 138–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_17.

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Chiras, J., J. Bories, M. O. Barth, A. Aymard, and B. Poirier. "Cerebral angiography in ischemic strokes." In Cerebral Ischaemia, 71–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_9.

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Raybaud, C. A., Marie-Odile Livet, M. Jiddane, and Nicole Pinsard. "Radiology of ischemic strokes in children." In Cerebral Ischaemia, 117–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70943-2_14.

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Saraswat, Komal, Raushan Kumar, Syed Ibrahim Rizvi, and Abhishek Kumar Singh. "The Role of Autophagy in Ischaemic Stroke: Friend or Foe?" In Advancement in the Pathophysiology of Cerebral Stroke, 59–71. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-1453-7_5.

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Agostoni, Elio Clemente, and Marco Longoni. "Cerebrovascular Interactions in Cerebral Disorders (Stroke, Transient Ischaemic Attacks, Microvascular Disease, Migraine)." In Arterial Disorders, 333–45. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14556-3_23.

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Bruno, Askiel, Subhashini Ramesh, and Jeffrey L. Saver. "Supportive Care during Acute Cerebral Ischaemia." In Stroke Prevention and Treatment, 77–97. Cambridge University Press, 2020. http://dx.doi.org/10.1017/9781316286234.006.

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Sweeney, Kieron, A. O’Hare, and Mohsen Javadpour. "Carotid artery disease and cerebral ischaemia." In Oxford Textbook of Neurological Surgery, edited by Ramez W. Kirollos, Adel Helmy, Simon Thomson, and Peter J. A. Hutchinson, 615–26. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198746706.003.0051.

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Due to the high incidence carotid artery disease and cerebral ischaemia, accurate and timely diagnosis and treatment is required to reduce the significant morbidity and mortality associated with these conditions. This chapter discusses the epidemiology, pathophysiology, clinical presentation, investigation, and treatment of these conditions. Cerebral ischaemia and stroke can occur due to a heterogeneous number of pathological processes. These pathological processes can affect either large or small vessels and can be broadly classified into thrombotic, embolic, or occlusive causes. The most common cause of thrombotic ischaemic is atherosclerosis. The most common cause of embolic ischaemia is cardiogenic due to atrial fibrillation followed by extracranial atherosclerosis of the aorta or carotids. Both of these causes can affect both the large and small vessels. This chapter explores the current evidence for medical, interventional, and surgical treatment options.
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Mattle, Heinrich P., Simon Jung, Jan Gralla, Marcel Arnold, and Urs Fischer. "Treatment of acute stroke." In ESC CardioMed, edited by Hans-Christoph Diener, 960–64. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0229.

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Stroke is caused by a clot blocking a cerebral artery and leading to ischaemic damage or by haemorrhage destroying cerebral tissue. The goal of stroke treatment is recanalization of the blocked cerebral artery and reperfusion in order to salvage the tissue jeopardized by ischaemia. Clots blocking the internal carotid T or the main stem of the middle cerebral artery are large and usually cause moderate to severe neurological deficits. They can be removed quickly and safely with mechanical thrombectomy, with or without prior thrombolytics. Clots blocking peripheral branches are smaller, usually associated with minor or moderate neurological deficits, and can be dissolved with recombinant tissue plasminogen activator. Clots blocking the basilar artery can be treated with recombinant tissue plasminogen activator or removed mechanically, but there is equipoise regarding what approach results in better clinical outcomes. Treatment of acute cerebral haemorrhage is limited to blood pressure lowering when elevated, normalization of coagulation when abnormal, and surgery in selected patients. Stroke treatment is time critical. Time is brain, and therefore stroke is an emergency. Stroke treatment requires teamwork in stroke units or centres and should best be organized in regional stroke networks.
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Conference papers on the topic "Stroke/cerebral ischaemia"

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Alessandri, C., F. Violi, M. Rasura, C. Caliendo, and P. Pelaia. "BEHAVIOUR OF ADREN0CHR0ME PATHWAY IN PATIENTS WITH CEREBROVASCULAR DISEASES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643169.

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Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a neutrophil oxidase able to convert,in vitro, adrenaline to adrenochrome.Aim of present study was to evaluate if neutrophil activation can be observed in patients with brain hemor ragie (BH) also.Six patients (females 1,males 5;age 68-79 years) suffering from BH and 15 patients (females 5, Males 10;age 58-86 years) affected by brain infarction (BI) were studied within 20-48 hours from acute episode.Diagnosis of stroke was made by computerized tomography.Neutrophil activation was studied in plasma evaluating the oxidation of adrenaline to adrenochrome according to Matthews and Campbell method.20 matched for age and sex healthy subjects were studied as control.A significant rise of plasma adrenaline oxidase activity was observed in patients with BI.This preliminary investigation suggests that neutrophil activation could be restricted to patients with BI.In fact,patients with BH had plasma oxidase activity similar to controls.Clinical data should be necessary to evaluate if a relation between leucocyte activation and the natural course of cerebral ischemia does exist.
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Prins, M. H., G. J. H. den Ottolander, R. Gelsema, T. C. M. van Woerkom, A. K. Sing, and I. Heller. "DEEP VENOUS THROMBOSIS PR0FYLAXIS WITH A LMW HEPARIN (KABI 2165) IN STROKE PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643217.

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In a group of 60 patients entering our hospital for completed stroke, within 72 hours after onset of symptoms, treatment with Kabi 2165 2x 2500 anti-Xa U s.c. was compared to placebo 2x s.c. in a double blind trial to test the assumption that Kabi 2165 could prevent DVT, without causing cerebral bleeding in the ischaemic area. The diagnosis of stroke was made on clinical grounds. A.CT-scan of the head was performed before entering the trial to exclude cerebral bleeding or tumor. Follow-up during a trial period of 14 days included a Fibrinogen scan - if positive followed by flebografy. After the trial period or when clinical deterioration occurred a CT-scan of the head was repeated. Before and during the trial period haematologic and coagulation data were obtained and will be reported. Obduction was obtained whenever possible.The patient groups were comparable, except for a slight preponderance of disturbed consciousness and atrial fibrillation in the Kabi 2165-treated group. This difference did not reach statistic significance. In the Kabi 2165 group there were 6 cases of DVT compared to 15 in the placebo group (p=0,05). In the Kabi 2165-treated group there were slightly more cases of cerebral bleeding and death during trial, respectively 4 versus 2 and 9 versus 4 (both NS). Cerebral bleeding occurred only in patients with a bloodpressure above 150/90 mmHg on entering.Although the patient group is still small, we like to conclude that in normotensive stroke patients Kabi 2165 2x 2500 anti-Xa U s.c. per 24 hours, is a safe method of DVT profylaxis.
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