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1
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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Zhang, Pei-Lei, Hai-Tao Lu, Jun-Gong Zhao, and Ming-Hua Li. "Protective effect of dl-3n-butylphthalide preconditioning on focal cerebral ischaemia-reperfusion injury in rats." Acta Neuropsychiatrica 25, no. 1 (February 2013): 12–17. http://dx.doi.org/10.1111/j.1601-5215.2012.00649.x.
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ObjectiveTo investigate the effect of dl-3n-butylphthalide (NBP) on the protection of cerebral tissue and possible mechanism on ischaemia-reperfusion injury, and to find out whether NBP therapy can extend the reperfusion window in an experimental stroke model in rats.MethodsSeventy-two Sprague-Dawley rats were randomly divided into sham operation, ischaemia-reperfusion and ischaemia-reperfusion with NBP groups. Focal cerebral ischaemia was induced using the modified intraluminal thread method and maintained for 2, 3 or 4 h. The ischaemia-reperfusion group received reperfusion immediately after ischaemia-reperfusion. The NBP group received intraperitoneal injection of NBP immediately after ischaemia, followed by reperfusion. The sham operation group received only injection of physiological saline. The cerebral infarction volume and neurological deficit were analysed, and vascular endothelial growth factor (VEGF) expression in brain tissues was visualised by immunohistochemistry.ResultsNBP treatment caused a significant decrease in both infarction volume and neurological deficit compared with the ischaemia-reperfusion group at corresponding time points in each (p < 0.05). In the NBP group, the infarction volume and neurological deficit did not change with different ischaemia times. The expression of VEGF was significantly decreased in the ischaemia-reperfusion group compared with the sham group (p < 0.01), while this change was partly prevented in the NBP group (p < 0.01). The expression of VEGF in brain tissue in both the NBP and ischaemia-reperfusion groups gradually decreased when the ischaemic period was prolonged.ConclusionNBP treatment has a protective effect against cerebral ischaemia; this possible mechanism maybe related to the VEGF expression and may extend the reperfusion window for subsequent salvage of cerebral ischaemia by reperfusion.
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Ploen, Robert, Markus Zorn, Li Sun, Wei Zhou, and Roland Veltkamp. "Anticoagulation with dabigatran does not increase secondary intracerebral haemorrhage after thrombolysis in experimental cerebral ischaemia." Thrombosis and Haemostasis 110, no. 07 (2013): 153–61. http://dx.doi.org/10.1160/th12-12-0942.
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SummaryDabigatran etexilate (DE) has recently been introduced for stroke prevention in atrial fibrillation, but management of acute ischaemic stroke during therapy with DE is a challenge. Thrombolysis is contrain-dicated because of a presumed increased risk of intracerebral haemorrhagic complications. We studied in different ischaemia models whether DE increases secondary haemorrhage after thrombolysis. C57BL/6 mice were anticoagulated with high-dose DE or warfarin. After 2 hour (h) or 3 h transient filament MCAO, rt-PA was injected. At 24 h after MCAO, secondary haemorrhage was quantified using a macroscopic haemorrhage score and haemoglobin spectrophotometry. Post-ischaemic blood-brain-barrier (BBB) damage was assessed using Evans blue. To increase the validity of findings, the duration of anticoagulation was prolonged in mice (5 x DE over 2 days), and the effect of DE after thrombolysis was also examined in thromboembolic MCAO in rats. Pretreatment with warfarin resulted in significantly more secondary haemorrhage (mean haemorrhage score 2.6 ± 0.2) compared to non-anticoagulated animals (1.7 ± 0.3) and DE (9 mg/kg, 1.6 ± 0.3) in 2 h ischaemia. Also after a 3 h period of ischaemia, haemorrhage was more severe in animals anticoagulated with warfarin compared to 9 mg/kg DE and non-anticoagulated control. Prolonged or enteral dabigatran pretreatment led to identical results. Also, thrombolysis after thromboembolic MCAO in rats did not induce more severe bleeding in DE-treated animals. Mice pretreated with warfarin had higher BBB permeability and increased activation of matrix-metalloproteinase 9. In conclusion, DE does not increase the risk of secondary haemorrhage after thrombolysis in various rodent models of ischaemia and reperfusion. The implications of this finding for stroke patients have to be determined in the clinical setting.
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Nalamolu, Koteswara Rao, Bharath Chelluboina, Ian B. Magruder, Diane N. Fru, Adithya Mohandass, Ishwarya Venkatesh, Jeffrey D. Klopfenstein, David M. Pinson, Krishna M. Boini, and Krishna Kumar Veeravalli. "Post-stroke mRNA expression profile of MMPs: effect of genetic deletion of MMP-12." Stroke and Vascular Neurology 3, no. 3 (March 9, 2018): 153–59. http://dx.doi.org/10.1136/svn-2018-000142.
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Background and purposeRecent reports from our laboratory demonstrated the post-ischaemic expression profile of various matrix metalloproteinases (MMPs) in rats and the detrimental role of MMP-12 in post-stroke brain damage. We hypothesise that the post-stroke dysregulation of MMPs is similar across species and that genetic deletion of MMP-12 would not affect the post-stroke expression of other MMPs. We tested our hypothesis by determining the pre-ischaemic and post-ischaemic expression profile of MMPs in wild-type and MMP-12 knockout mice.MethodsFocal cerebral ischaemia was induced in wild-type and MMP-12 knockout mice by middle cerebral artery occlusion procedure by insertion of a monofilament suture. One hour after ischaemia, reperfusion was initiated by removing the monofilament. One day after reperfusion, ischaemic brain tissues from various groups of mice were collected, and total RNA was isolated and subjected to cDNA synthesis followed by PCR analysis.ResultsAlthough the post-stroke expression profile of MMPs in the ischaemic brain of mice is different from rats, there is a clear species similarity in the expression of MMP-12, which was found to be predominantly upregulated in both species. Further, the post-stroke induction or inhibition of various MMPs in MMP-12 knockout mice is different from their respective expression profile in wild-type mice. Moreover, the brain mRNA expression profile of various MMPs in MMP-12 knockout mice under normal conditions is also different to their expression in wild-type mice.ConclusionsIn the ischaemic brain, MMP-12 upregulates several fold higher than any other MMP. Mice derived with the genetic deletion of MMP-12 are constitutive and have altered MMP expression profile both under normal and ischaemic conditions.
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Knight, Michael J., Bryony L. McGarry, Harriet J. Rogers, Kimmo T. Jokivarsi, Olli HJ Gröhn, and Risto A. Kauppinen. "A spatiotemporal theory for MRI T2 relaxation time and apparent diffusion coefficient in the brain during acute ischaemia: Application and validation in a rat acute stroke model." Journal of Cerebral Blood Flow & Metabolism 36, no. 7 (October 14, 2015): 1232–43. http://dx.doi.org/10.1177/0271678x15608394.
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The objective of this study is to present a mathematical model which can describe the spatiotemporal progression of cerebral ischaemia and predict magnetic resonance observables including the apparent diffusion coefficient (ADC) of water and transverse relaxation time T2. This is motivated by the sensitivity of the ADC to the location of cerebral ischaemia and T2 to its time-course, and that it has thus far proven challenging to relate observations of changes in these MR parameters to stroke timing, which is of considerable importance in making treatment choices in clinics. Our mathematical model, called the cytotoxic oedema/dissociation (CED) model, is based on the transit of water from the extra- to the intra-cellular environment (cytotoxic oedema) and concomitant degradation of supramacromolecular and macromolecular structures (such as microtubules and the cytoskeleton). It explains experimental observations of ADC and T2, as well as identifying the rate of spread of effects of ischaemia through a tissue as a dominant system parameter. The model brings the direct extraction of the timing of ischaemic stroke from quantitative MRI closer to reality, as well as providing insight on ischaemia pathology by imaging in general. We anticipate that this may improve patient access to thrombolytic treatment as a future application.
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Komiyama, M., T. Morikawa, T. Ishiguro, Y. Matsusaka, and T. Yasui. "Anterior Choroidal Artery Variant and Acute Embolic Stroke." Interventional Neuroradiology 8, no. 3 (September 2002): 313–16. http://dx.doi.org/10.1177/159101990200800312.
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The anterior choroidal artery has the cortical branches to the temporal, parietal, and occipital lobes in the early embryological stage, which later become the posterior cerebral artery distal to the posterior communicating artery (P2-4). Acute embolic stroke occurred in a 57-year-old man with an anterior choroidal artery having such a persistent embryonic branch to the temporal lobe. Recognition of this embryological form of the anterior choroidal artery is clinically important in acute cerebral ischaemia because the cerebral region between the territories supplied by the middle cerebral artery and the anterior choroidal artery is shown on carotid angiography as an avascular area, which could be misunderstood as a region of the acute ischaemia.
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Viviani, Giorgio Luciano, Franco Dallegri, Alessandra Quercioli, Edvige Veneselli, François Mach, Marisol Mirabelli-Badenier, Vincent Braunersreuther, and Fabrizio Montecucco. "CC and CXC chemokines are pivotal mediators of cerebral injury in ischaemic stroke." Thrombosis and Haemostasis 105, no. 03 (2011): 409–20. http://dx.doi.org/10.1160/th10-10-0662.
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SummaryThe definition of ischaemic stroke has been recently updated as an acute episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia in the presence of a cerebral infarction. This “tissular” definition has highlighted the importance of pathophysiological processes underlying cerebral damage. In particular, post-ischaemic inflammation in the brain and in the blood stream could influence crucial steps of the tissue injury/repair cascade. CC and CXC chemokines orchestrate the inflammatory response in atherosclerotic plaque vulnerability and cerebral infarction. These molecules exert their activities through the binding to selective transmembrane receptors. CC and CXC chemokines modulate crucial processes (such as inflammatory cell recruitment and activation, neuronal survival, neoangio-genesis). On the other hand, CXC chemokines could also modulate stem cell homing, thus favouring tissue repair. Given this evidence, both CC and CXC chemokines could represent promising therapeutic targets in primary and secondary prevention of ischaemic stroke. Only preliminary studies have been performed investigating treatments with selective chemokine agonists/antagonists. In this review, we will update evidence on the role and the potential therapeutic strategies targeting CC and CXC chemokines in the pathophysiology of ischaemic stroke.
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Yuan, Zhaohu, Zhiwu Yu, Yiyu Zhang, and Huikuan Yang. "Analysis of the Clinical Diagnostic Value of GMFB in Cerebral Infarction." Current Pharmaceutical Biotechnology 21, no. 10 (September 7, 2020): 955–63. http://dx.doi.org/10.2174/1389201021666200210102425.
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Background: Glial Maturation Factor Beta (GMFB) is a highly conserved brain-enriched protein implicated in immunoregulation, neuroplasticity and apoptosis, processes central to neural injury and repair following cerebral ischaemia. Therefore, we examined if changes in neurocellular GMFB expression and release can be used to assess brain injury following ischaemia. Methods and Results: Immunofluorescence staining, Western blotting, immunohistochemistry and ELISA were used to measure GMFB in cultured neurons and astrocytes, rat brain tissues and plasma samples from stroke model rats and stroke patients, while cell viability assays, TTC staining and micro- PET were used to assess neural cell death and infarct severity. Immunofluorescence and immunohistochemistry revealed GMFB expression mainly in astrocyte and neuronal nuclei but also in neuronal axons and dendrites. Free GMFB concentration increased progressively in the culture medium during hypoxia-hypoglycaemia treatment. Plasma GMFB concentration increased in rats subjected to middle cerebral artery occlusion (MCAO, a model of stroke-reperfusion) and in stroke patients. Plasma GMFB in MCAO model rats was strongly correlated with infarct size (R2=0.9582). Plasma GMFB concentration was also markedly elevated in stroke patients within 24 h of onset and remained elevated for more than one week. Conversely, plasma GMFB elevations were not significant in myocardial infarct patients and stroke patients without infarction. Conclusion: GMFB has the prerequisite stability, expression specificity and response dynamics to serve as a reliable indicator of ischaemic injury in animal models and stroke patients. Plasma GMFB may be a convenient non-invasive adjunct to neuroimaging for stroke diagnosis and prognosis.
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Školoudík, D., M. Král, D. Šaňák, I. Vlachová, P. Hluštík, K. Michálková, R. Herzig, and P. Kaňovský. "Thrombolytic treatment of ischaemic stroke occurring during a migrainous attack: A case report." Cephalalgia 30, no. 3 (June 1, 2009): 368–72. http://dx.doi.org/10.1111/j.1468-2982.2009.01891.x.
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Authors report a case of young female suffering from the acute ischaemic stroke with right-sided hemiplegia, hemianopsia and hemihypoaesthesia during a migrainous attack without aura. Magnetic resonance imaging detected infarction in the left occipital lobe and occlusion of branches of the posterior cerebral artery (PCA). Combined treatment with systemic thrombolysis and sonothrombolysis was used, leading to the early PCA recanalization, and to a favourable clinical outcome after 1 month. Intravenous thrombolytic treatment administered within the therapeutic window may be useful in cerebral ischaemia associated with migraine when an arterial occlusion is documented.
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Bordet, R., T. Ouk, O. Petrault, P. Gelé, S. Gautier, M. Laprais, D. Deplanque, et al. "PPAR: a new pharmacological target for neuroprotection in stroke and neurodegenerative diseases." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1341–46. http://dx.doi.org/10.1042/bst0341341.
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PPARs (peroxisome-proliferator-activated receptors) are ligand-activated transcriptional factor receptors belonging to the so-called nuclear receptor family. The three isoforms of PPAR (α, β/δ and γ) are involved in regulation of lipid or glucose metabolism. Beyond metabolic effects, PPARα and PPARγ activation also induces anti-inflammatory and antioxidant effects in different organs. These pleiotropic effects explain why PPARα or PPARγ activation has been tested as a neuroprotective agent in cerebral ischaemia. Fibrates and other non-fibrate PPARα activators as well as thiazolidinediones and other non-thiazolidinedione PPARγ agonists have been demonstrated to induce both preventive and acute neuroprotection. This neuroprotective effect involves both cerebral and vascular mechanisms. PPAR activation induces a decrease in neuronal death by prevention of oxidative or inflammatory mechanisms implicated in cerebral injury. PPARα activation induces also a vascular protection as demonstrated by prevention of post-ischaemic endothelial dysfunction. These vascular effects result from a decrease in oxidative stress and prevention of adhesion proteins, such as vascular cell adhesion molecule 1 or intercellular cell-adhesion molecule 1. Moreover, PPAR activation might be able to induce neurorepair and endothelium regeneration. Beyond neuroprotection in cerebral ischaemia, PPARs are also pertinent pharmacological targets to induce neuroprotection in chronic neurodegenerative diseases.
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Freret, Thomas, Valentine Bouet, Jérôme Toutain, Romaric Saulnier, Palma Pro-Sistiaga, Ebeline Bihel, Eric T. MacKenzie, Simon Roussel, Pascale Schumann-Bard, and Omar Touzani. "Intraluminal Thread Model of Focal Stroke in the Non-Human Primate." Journal of Cerebral Blood Flow & Metabolism 28, no. 4 (November 14, 2007): 786–96. http://dx.doi.org/10.1038/sj.jcbfm.9600575.
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The common marmoset ( Callithrix jacchus), a New World monkey, has recently been used as a model of focal cerebral ischaemia. Here, we sought to develop a stroke model in this species using an intraluminal approach to occlude the middle cerebral artery (MCA). This technically simple procedure allows both transient and permanent ischaemia with minimal morbidity. Ten common marmosets underwent either transient (3 h) or permanent ischaemia by the insertion of a nylon filament through the external carotid artery up to the origin of the MCA. Cerebral blood flow (CBF) was monitored by the laser-Doppler flowmetry technique. Sensorimotor functions were regularly evaluated, and histologic, immunohistochemical, and magnetic resonance imaging analyses were performed 8 days after the occlusion. The surgical procedure was achieved straightforwardly without postoperative mortality or cerebral haemorrhage. All animals displayed a consistent decrease in CBF that remained stable over 3 h. Infarction affected both cortical and subcortical structures. Although not statistically significant, the volume of infarction was smaller in marmosets subjected to transient ischaemia compared to those permanently occluded (237±139 and 358±118 mm3, respectively). In all the behavioural tests used, reperfused marmosets exhibited fewer neurologic and functional impairments compared to permanently occluded ones. We show the feasibility of the induction of permanent or transient focal cerebral ischaemia in the marmoset using an intraluminal approach with minimal invasion. This model could be suitable as an advanced screening for potential stroke therapies in which behavioural, imaging, and histologic analyses can be compared.
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Khan, Sibghat Ullah. "CEREBRAL ISCHAEMIA AND STROKE; ROLE OF CAROTID DOPPLER." PROFESSIONAL MEDICAL JOURNAL 24, no. 12 (December 1, 2017): 1823–27. http://dx.doi.org/10.17957/tpmj/17.4001.
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Catarci, Teresa. "Occipital ischaemic stroke after visual snow phenomenon – a case report." Cephalalgia 41, no. 7 (January 12, 2021): 871–74. http://dx.doi.org/10.1177/0333102420985444.
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Background Persistent migraine with aura and neuroimaging examinations revealing ischaemia in the contralateral cortex may be associated with migrainous infarction. Despite being a neurological symptom that is distinct from migraine with aura, the visual snow phenomenon may also be associated with cerebral ischaemia. Here we describe a patient who reported short-lasting daily symptoms of visual snow that affected his entire visual field before becoming continuous and left-sided following acute occipital brain ischaemia. Case report In February 2017, a 74-year-old retired male was referred to our headache outpatient clinic with a diagnosis of recent right occipital cerebral ischaemia and migraine with aura. The patient reported visual snow symptoms that had changed from being bilateral and temporary to left-sided and permanent one day upon awakening; after being admitted to hospital a few hours later, he discovered he had had a stroke. He said he had never had any symptoms of migraine with aura. The visual snow phenomenon disappeared completely after about 1 year. Conclusions In our patient, a temporary daily visual snow phenomenon reversed to a persistent one. This phenomenon occurred in the part of his visual field that had been affected by the ischaemic occipital stroke, as typically happens in migrainous infarction. We hypothesise that the occipital lesion disrupted the inhibitory circuits, leading to a quadrantopic persistent visual snow. Since the mechanism may be the same as that observed in migrainous infarction, though with a different pathophysiology, it is possible to speculate that the aura in this case is the result, as opposed to the cause, of stroke in most patients.
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Venketasubramanian, Narayanaswamy, Pravin Mundada, Amogh Narayan Hegde, Marcus Tan, and Darren Ng. "Post-Traumatic Carotid Artery Dissection Begins at the Skull Base: A Case Report." Case Reports in Neurology 12, Suppl. 1 (December 14, 2020): 143–48. http://dx.doi.org/10.1159/000504567.
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Cervical artery dissection is a rare complication of head and neck trauma. Though it is an infrequent cause of ischaemic stroke, it is more common among the young with cerebral ischaemia. The usual location of carotid dissection is just beyond the carotid bulb. We report a case of post-traumatic internal carotid dissection that began at the base of the skull after blunt head trauma from a road traffic accident. The patient is a 25-year-old right-handed lady who, 2 days after the accident, developed dysphasia and right-sided limb weakness. She had no significant past medical history. Magnetic resonance imaging (MRI) showed acute ischaemic stroke in the internal watershed regions of the left cerebral hemisphere. MR angiogram revealed focal near-occlusion of the left internal carotid artery at the base of the skull just prior to its entry into the petrous temporal bone. There were no skull fractures. She progressed despite anticoagulation. The location of the site of dissection at the base of the skull is likely due to stresses on the carotid intima at this point during flexion-extension-rotation that occurs during head injury, as this is where the internal carotid artery is tethered to the skull. Rapid recognition of symptoms of cerebral ischaemia among patients with blunt head trauma is needed to allow prompt investigation and institution of relevant therapies.
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Rewell, Sarah SJ, Amy L. Jeffreys, Steven A. Sastra, Susan F. Cox, John A. Fernandez, Elena Aleksoska, H. Bart van der Worp, Leonid Churilov, Malcolm R. Macleod, and David W. Howells. "Hypothermia revisited: Impact of ischaemic duration and between experiment variability." Journal of Cerebral Blood Flow & Metabolism 37, no. 10 (January 13, 2017): 3380–90. http://dx.doi.org/10.1177/0271678x16688704.
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To assess the true effect of novel therapies for ischaemic stroke, a positive control that can validate the experimental model and design is vital. Hypothermia may be a good candidate for such a positive control, given the convincing body of evidence from animal models of ischaemic stroke. Taking conditions under which substantial efficacy had been seen in a meta-analysis of hypothermia for focal ischaemia in animal models, we undertook three randomised and blinded studies examining the effect of hypothermia induced immediately following the onset of middle cerebral artery occlusion on infarct volume in rats (n = 15, 23, 264). Hypothermia to a depth of 33℃ and maintained for 130 min significantly reduced infarct volume compared to normothermia treatment (by 27–63%) and depended on ischaemic duration (F(3,244) = 21.242, p < 0.05). However, the protective effect varied across experiments with differences in both the size of the infarct observed in normothermic controls and the time to reach target temperature. Our results highlight the need for sample size and power calculations to take into account variations between individual experiments requiring induction of focal ischaemia.
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Grassi, Mario, Elisabetta Del Zotto, Alessia Giossi, Irene Volonghi, Paolo Costa, Armin Grau, Mauro Magoni, Alessandro Padovani, Christoph Lichy, and Alessandro Pezzini. "Do common prothrombotic mutations influence the risk of cerebral ischaemia in patients with patent foramen ovale?" Thrombosis and Haemostasis 101, no. 05 (2009): 813–17. http://dx.doi.org/10.1160/th08-11-0747.
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SummaryConflicting results are available on the association of prothrombotic genetic abnormalities with patent foramen ovale (PFO)-related cerebral ischaemia. We comprehensively sought and identified studies of the association of both the factor V Leiden (FVG1691A mutation) and the prothrombin mutation (PTG20210A mutation) with PFO-related cerebral ischaemia and did meta-analyses to assess the evidence for such a relation. We analysed data from six eligible studies in 856 cases and 1,001 control subjects. Additional unpublished data from a new series including 463 subjects were also entered into the analysis. The PTG20210A variant was significantly associated with PFO-related stroke in comparison with both control subjects (odds ratio [OR] 3.85; 95% confidence interval [CI] 2.22 to 6.66) and non-PFO-associ ated stroke patients (OR 2.31; 95% CI 1.20 to 4.43), whereas a trend toward an association was observed for the FVG1691A mutation (OR 1.18; 95% CI 0.73 to 1.90, compared to control subjects; OR 1.14; 95% CI 0.62 to 2.09, compared to non-PFO-associated stroke patients). The status of carrier of either the FVG1691A mutation or the PTG20210A variant was associated with a risk for stroke of 1.98 (95% CI 1.38 to 2.83) and 1.62 (95% CI 1.03 to 2.57), as compared to control subjects and non-PFO-associated stroke patients, respectively. Addition of common prothrombotic genetic variants to standard initial screening may contribute to stratifying PFO-associated stroke patients at different risk of ischaemic events and targeting secondary prevention strategies.
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Xu, Kaiyu, Xuxuan Gao, Genghong Xia, Muxuan Chen, Nianyi Zeng, Shan Wang, Chao You, et al. "Rapid gut dysbiosis induced by stroke exacerbates brain infarction in turn." Gut 70, no. 8 (February 8, 2021): 1486–94. http://dx.doi.org/10.1136/gutjnl-2020-323263.
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ObjectiveStroke is a leading cause of death and disability worldwide. Neuroprotective approaches have failed in clinical trials, thus warranting therapeutic innovations with alternative targets. The gut microbiota is an important contributor to many risk factors for stroke. However, the bidirectional interactions between stroke and gut microbiota remain largely unknown.DesignWe performed two clinical cohort studies to capture the gut dysbiosis dynamics after stroke and their relationship with stroke prognosis. Then, we used a middle cerebral artery occlusion model to explore gut dysbiosis post-stroke in mice and address the causative relationship between acute ischaemic stroke and gut dysbiosis. Finally, we tested whether aminoguanidine, superoxide dismutase and tungstate can alleviate post-stroke brain infarction by restoring gut dysbiosis.ResultsBrain ischaemia rapidly induced intestinal ischaemia and produced excessive nitrate through free radical reactions, resulting in gut dysbiosis with Enterobacteriaceae expansion. Enterobacteriaceae enrichment exacerbated brain infarction by enhancing systemic inflammation and is an independent risk factor for the primary poor outcome of patients with stroke. Administering aminoguanidine or superoxide dismutase to diminish nitrate generation or administering tungstate to inhibit nitrate respiration all resulted in suppressed Enterobacteriaceae overgrowth, reduced systemic inflammation and alleviated brain infarction. These effects were gut microbiome dependent and indicated the translational value of the brain–gut axis in stroke treatment.ConclusionsThis study reveals a reciprocal relationship between stroke and gut dysbiosis. Ischaemic stroke rapidly triggers gut microbiome dysbiosis with Enterobacteriaceae overgrowth that in turn exacerbates brain infarction.
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Seiffge, David J., Duncan Wilson, Gareth Ambler, Gargi Banerjee, Isabel Charlotte Hostettler, Henry Houlden, Clare Shakeshaft, et al. "Small vessel disease burden and intracerebral haemorrhage in patients taking oral anticoagulants." Journal of Neurology, Neurosurgery & Psychiatry 92, no. 8 (March 19, 2021): 805–14. http://dx.doi.org/10.1136/jnnp-2020-325299.
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ObjectiveWe investigated the contribution of small vessel disease (SVD) to anticoagulant-associated intracerebral haemorrhage (ICH).MethodsClinical Relevance of Microbleeds in Stroke-2 comprised two independent multicentre observation studies: first, a cross-sectional study of patients with ICH; and second, a prospective study of patients taking anticoagulants for atrial fibrillation (AF) after cerebral ischaemia. In patients with ICH, we compared SVD markers on CT and MRI according to prior anticoagulant therapy. In patients with AF and cerebral ischaemia treated with anticoagulants, we compared the rates of ICH and ischaemic stroke according to SVD burden score during 2 years follow-up.ResultsWe included 1030 patients with ICH (421 on anticoagulants), and 1447 patients with AF and cerebral ischaemia. Medium-to-high severity SVD was more prevalent in patients with anticoagulant-associated ICH (CT 56.1%, MRI 78.7%) than in those without prior anticoagulant therapy (CT 43.5%, p<0.001; MRI 64.5%, p=0.072). Leukoaraiosis and atrophy were more frequent and severe in ICH associated with prior anticoagulation. In the cerebral ischaemia cohort (779 with SVD), during 3366 patient-years of follow-up the rate of ICH was 0.56%/year (IQR 0.27–1.03) in patients with SVD, and 0.06%/year (IQR 0.00–0.35) in those without (p=0.001); ICH was independently associated with severity of SVD (HR 5.0, 95% CI 1.9 to 12.2,p=0.001), and was predicted by models including SVD (c-index 0.75, 95% CI 0.63 to 0.85).ConclusionsMedium-to-high severity SVD is associated with ICH occurring on anticoagulants, and independently predicts ICH in patients with AF taking anticoagulants; its absence identifies patients at low risk of ICH. Findings from these two complementary studies suggest that SVD is a contributory factor in ICH in patients taking anticoagulants and suggest that anticoagulation alone should no longer be regarded as a sufficient ‘cause’ of ICH.Trial registrationNCT02513316
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Thow, Lisa A., Kathleen MacDonald, William M. Holmes, Keith W. Muir, I. Mhairi Macrae, and Deborah Dewar. "Hyperglycaemia does not increase perfusion deficits after focal cerebral ischaemia in male Wistar rats." Brain and Neuroscience Advances 2 (January 2018): 239821281879482. http://dx.doi.org/10.1177/2398212818794820.
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Background: Hyperglycaemia is associated with a worse outcome in acute ischaemic stroke patients; yet the pathophysiological mechanisms of hyperglycaemia-induced damage are poorly understood. We hypothesised that hyperglycaemia at the time of stroke onset exacerbates ischaemic brain damage by increasing the severity of the blood flow deficit. Methods: Adult, male Wistar rats were randomly assigned to receive vehicle or glucose solutions prior to permanent middle cerebral artery occlusion. Cerebral blood flow was assessed semi-quantitatively either 1 h after middle cerebral artery occlusion using 99mTc-D, L-hexamethylpropyleneamine oxime (99mTc-HMPAO) autoradiography or, in a separate study, using quantitative pseudo-continuous arterial spin labelling for 4 h after middle cerebral artery occlusion. Diffusion weighted imaging was performed alongside pseudo-continuous arterial spin labelling and acute lesion volumes calculated from apparent diffusion coefficient maps. Infarct volume was measured at 24 h using rapid acquisition with refocused echoes T2-weighted magnetic resonance imaging. Results: Glucose administration had no effect on the severity of ischaemia when assessed by either 99mTc-HMPAO autoradiography or pseudo-continuous arterial spin labelling perfusion imaging. In comparison to the vehicle group, apparent diffusion coefficient–derived lesion volume 2–4 h post-middle cerebral artery occlusion and infarct volume 24 h post-middle cerebral artery occlusion were significantly greater in the glucose group. Conclusions: Hyperglycaemia increased acute lesion and infarct volumes but there was no evidence that the acute blood flow deficit was exacerbated. The data reinforce the conclusion that the detrimental effects of hyperglycaemia are rapid, and that treatment of post-stroke hyperglycaemia in the acute period is essential but the mechanisms of hyperglycaemia-induced harm remain unclear.
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Murphy, S., and C. L. Gibson. "Nitric oxide, ischaemia and brain inflammation." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1133–37. http://dx.doi.org/10.1042/bst0351133.
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Cerebral ischaemia results in the activation of three isoforms of NOS (nitric oxide synthase) that contribute to the development of and recovery from stroke pathology. This review discusses, in particular, the role of the transcriptionally activated NOS-2 (inducible NOS) isoform and summarizes the outcomes of experimental stroke studies with regard to the therapeutic utility of nitric oxide donors and NOS inhibitors.
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Liao, Boya, Leiluo Geng, Fang Zhang, Lingling Shu, Ling Wei, Patrick K. K. Yeung, Karen S. L. Lam, et al. "Adipocyte fatty acid-binding protein exacerbates cerebral ischaemia injury by disrupting the blood–brain barrier." European Heart Journal 41, no. 33 (April 29, 2020): 3169–80. http://dx.doi.org/10.1093/eurheartj/ehaa207.
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Abstract Aims Adipocyte fatty acid-binding protein (A-FABP) is an adipokine implicating in various metabolic diseases. Elevated circulating levels of A-FABP correlate positively with poor prognosis in ischaemic stroke (IS) patients. No information is available concerning the role of A-FABP in the pathogenesis of IS. Experiments were designed to determine whether or not A-FABP mediates blood–brain barrier (BBB) disruption, and if so, to explore the molecular mechanisms underlying this deleterious effects. Methods and results Circulating A-FABP and its cerebral expression were increased in mice after middle cerebral artery occlusion. Genetic deletion and pharmacological inhibition of A-FABP alleviated cerebral ischaemia injury with reduced infarction volume, cerebral oedema, neurological deficits, and neuronal apoptosis; BBB disruption was attenuated and accompanied by reduced degradation of tight junction proteins and induction of matrix metalloproteinases-9 (MMP-9). In patients with acute IS, elevated circulating A-FABP levels positively correlated with those of MMP-9 and cerebral infarct volume. Mechanistically, ischaemia-induced elevation of A-FABP selectively in peripheral blood monocyte-derived macrophages and cerebral resident microglia promoted MMP-9 transactivation by potentiating JNK/c-Jun signalling, enhancing degradation of tight junction proteins and BBB leakage. The detrimental effects of A-FABP were prevented by pharmacological inhibition of MMP-9. Conclusion A-FABP is a key mediator of cerebral ischaemia injury promoting MMP-9-mediated BBB disruption. Inhibition of A-FABP is a potential strategy to improve IS outcome.
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Hoffmann, Michael, and Peter Corr. "Posterior circulation positional transient ischaemic attacks due to persistent primitive hypoglossal artery with redundancy." South African Journal of Radiology 1, no. 2 (May 31, 1996): 20–23. http://dx.doi.org/10.4102/sajr.v1i2.1614.
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A persistent primitive hypoglossal artery was the sole identifiable stroke risk factor for a patient presenting with positional, posterior circulation ischaemic episodes. Diagnosis was made by magnetic resonance arteriography and verified by conventional angiography. Tortuosity and coiling of the hypoglossal artery was also present. Dynamic transcranial Doppler sonography was normal and SPECT brain scanning revealed an area of posterior hemisphere hypoperfusion. Redundancy of the primitive hypoglossal artery is the postulated mechanism of cerebral ischaemia.
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Baird, A. E. "Blood genomic profiling: novel diagnostic and therapeutic strategies for stroke?" Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1313–17. http://dx.doi.org/10.1042/bst0341313.
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Findings from gene expression profiling studies are leading to new diagnostic and therapeutic strategies that can be applied in medical practice, especially in the field of oncology. Promising results of gene expression profiling of the peripheral blood in patients with ischaemic stroke have been obtained in recent pilot studies, demonstrating a partially reproducible gene signature of acute cerebral ischaemia. However, questions remain. Given that blood is at least in part a surrogate tissue for ischaemic stroke, the specificity of these signatures needs to be evaluated. Furthermore, it needs to be determined whether standardization of this methodology is required and whether clinical signatures can be identified that are improvements over the tools currently used in clinical practice. Clinically useful signatures would include those of haemorrhagic as well as ischaemic stroke, reclassification of stroke type and prognosis, and vascular disease risk. If these conditions are met, then it should be possible to develop cost-effective and rapid assays.
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Burggraf, Dorothe, Milan Vosko, Marion Schubert, Jean-Marie Stassen, and Gerhard Hamann. "Different therapy options protecting microvasculature after experimental cerebral ischaemia and reperfusion." Thrombosis and Haemostasis 103, no. 05 (2010): 891–900. http://dx.doi.org/10.1160/th09-07-0500.
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SummaryRecombinant tissue plasminogen activator (rt-PA) is successfully used in human stroke, but often shows serious drawbacks. To find an alternative, we hypothesised that the novel thrombolytic microplasmin would have fewer adverse effects on haemoglobin extravasation and microvascular damage compared with the effects of rt-PA and tenecteplase (TNK). A constant period of ischaemia (3 hours) was induced in a rat suture model followed by reperfusion (24 hours). Mikroplasmin (10 mg/kg), TNK (5 mg/kg), rt-PA (9 mg/kg) and saline (control), were administered. The volume of the ischaemic lesion was calculated, the loss of collagen type IV and the extravasation of haemoglobin were quantified by Western blotting. The matrix-metalloproteinases 2 and 9 (MMP-2/-9) were quantified by zymography and their endogenous tissue inhibitors (TIMPs) were analysed by reverse zymography. Microplasmin treatment caused the lowest volume of the ischaemic lesion (51.0 ± 22.6 mm3) compared with control (167.3 ± 13.1 mm3; p<0.05). The content of col-lagen type IV was significantly increased and haemoglobin extravasation reduced (154 ± 24%; p<0.05) compared with control (442 ± 124%); MMP-2/-9 and the corresponding TIMPs remained unchanged. In comparison, TNK did not significantly reduce basal lamina damage and caused the highest extravasation. MMP-2/-9 were severely increased after TNK treatment (p<0.05). Thus, the balance between MMPs and TIMPs was shifted toward the inhibitory side with TNK. Microplasmin had a protective effect on the microvascular basal lamina and blood-brain barrier, whereas TNK was significantly disadvantageous from the viewpoint of ischaemic damage. Microplasmin also appears to be safer than other PAs in terms of damage to the microvasculature associated with thrombolytic therapy of ischaemic stroke.
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Ilic, Miodrag, Slobodan Tanaskovic, Nenad Ilijevski, and Djordje Radak. "Acute reversible ischaemic neurological deficit induced by internal carotid artery kinking: Case report." Srpski arhiv za celokupno lekarstvo 139, no. 1-2 (2011): 92–94. http://dx.doi.org/10.2298/sarh1102092i.
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Introduction. Internal carotid artery (ICA) kinking is a pathological malformation with angulation of the vessel?s axis of 90? or less. It is known that kinking causes the reduction of flow within the vessel that may be exacerbated by progressive head rotation up to the point that causes complete cessation of flow. In this article, we report on the case of acute reversible ischaemic deficit induced by internal carotid artery kinking and immediate neurological recovery following surgical reconstruction. Case Outline. A 64-year-old woman was admitted to Vascular Surgery Clinic due to severe dizziness, fainting and walking instability, suddenly arising a few days prior to admission. Two years before, the left ICA reconstruction was done for kinking, after which there was no cerebral ischaemia symptoms. Symptoms have been present perpetually, enhanced when resting and with head movement. CT angiography (MSCT) showed haemodynamic significant right ICA kinking. The left ICA postoperative finding was regular. Computerized tomography (CT) of the endocranium was done and no novel lessions were verified than those seen two years earlier. Resection, shortening and reimplantation of the right ICA were performed. A few hours following surgical reconstruction, there was no cerebral ischaemia symptoms, neither when resting nor with head movement. On the third postoperative day, the patient was discharged for home treatment. Conclusion. Surgical repair for symptomatic ICA kinking contributes to cerebral ischaemia symptoms reduction, improves cerebral perfusion and significantly prevents carotid thrombosis and stroke. In this paper, we have seen that in case of acute cerebral ischaemia symptoms and ICA kinking, surgical ICA treatment appears to be justified.
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Li, Ce, Tingting Zhang, Kewei Yu, Hongyu Xie, Yulong Bai, Li Zhang, Yi Wu, and Nianhong Wang. "Neuroprotective Effect of Electroacupuncture and Upregulation of Hypoxia-Inducible Factor-1α during Acute Ischaemic Stroke in Rats." Acupuncture in Medicine 35, no. 5 (October 2017): 360–65. http://dx.doi.org/10.1136/acupmed-2016-011148.
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Background Acupuncture is a traditional method that has been widely used in various fields of medicine with therapeutic effect. However, evidence of effectiveness to support the application of electroacupuncture (EA) during the process of ischaemia is scarce. Objectives To investigate dynamic changes in hypoxia-inducible factor (HIF)-1α expression as well as its association with neurological status in rats subjected to acute ischaemic stroke and EA intervention. Methods Forty adult male rats were randomly divided into three groups that received sham surgery (Control group, n=10) or underwent middle cerebral artery occlusion and EA (MCAO+EA group, n=15) or minimal acupuncture as a control treatment (MCAO+MA group, n=15). The rats in the MCAO+EA and MCAO+MA groups received EA or acupuncture without any electrical current, respectively, during 90 min of ischaemia. Rats in the Control group received the same surgical procedure but without MCAO. EA involved electrical stimulation of needles inserted into the quadriceps at 50 Hz frequency and 3 mA current intensity. Neurological status was evaluated on postoperative day 1, and cerebral infarction volume (IV) and HIF-1α expression 24 hours later. Results Neurological scores were improved and cerebral IV was decreased in the MCAO+EA group compared to the MCAO+MA group (both p<0.05). Moreover, HIF-1α expression was higher in the MCAO+EA group versus the MCAO+MA group (p<0.05). Conclusions EA enhanced recovery of neurological function, decreased cerebral IV and increased HIF-1α expression in ischaemic rats. Further research is needed to determine whether EA is effective for stroke treatment through the stimulation of muscle contraction.
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Patabendige, Adjanie, Ayesha Singh, Stuart Jenkins, Jon Sen, and Ruoli Chen. "Astrocyte Activation in Neurovascular Damage and Repair Following Ischaemic Stroke." International Journal of Molecular Sciences 22, no. 8 (April 20, 2021): 4280. http://dx.doi.org/10.3390/ijms22084280.
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Transient or permanent loss of tissue perfusion due to ischaemic stroke can lead to damage to the neurovasculature, and disrupt brain homeostasis, causing long-term motor and cognitive deficits. Despite promising pre-clinical studies, clinically approved neuroprotective therapies are lacking. Most studies have focused on neurons while ignoring the important roles of other cells of the neurovascular unit, such as astrocytes and pericytes. Astrocytes are important for the development and maintenance of the blood–brain barrier, brain homeostasis, structural support, control of cerebral blood flow and secretion of neuroprotective factors. Emerging data suggest that astrocyte activation exerts both beneficial and detrimental effects following ischaemic stroke. Activated astrocytes provide neuroprotection and contribute to neurorestoration, but also secrete inflammatory modulators, leading to aggravation of the ischaemic lesion. Astrocytes are more resistant than other cell types to stroke pathology, and exert a regulative effect in response to ischaemia. These roles of astrocytes following ischaemic stroke remain incompletely understood, though they represent an appealing target for neurovascular protection following stroke. In this review, we summarise the astrocytic contributions to neurovascular damage and repair following ischaemic stroke, and explore mechanisms of neuroprotection that promote revascularisation and neurorestoration, which may be targeted for developing novel therapies for ischaemic stroke.
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Lu, C. Z., and B. G. Xiao. "G-CSF and neuroprotection: a therapeutic perspective in cerebral ischaemia." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1327–33. http://dx.doi.org/10.1042/bst0341327.
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In several experimental studies of cerebral ischaemia, G-CSF (granulocyte colony-stimulating factor) exerted neuroprotective effects through different mechanisms, including mobilization of haemopoietic stem cells, anti-apoptosis, neuronal differentiation, angiogenesis and anti-inflammation. Hence, G-CSF not only inhibits neuron death, but also generates ‘new’ neural tissue formation. A small pilot trial reports on the safety and feasibility of G-CSF therapy in stroke patients. According to this evidence, we can speculate that G-CSF, being used either alone or in combination with another agent, should have a dual activity beneficial both to acute neuronal protection and long-term plasticity after cerebral ischaemia, thus proposing that G-CSF is an ideal new drug for stroke and neurodegenerative diseases.
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Jia, Jia, Jie Li, and Jian Cheng. "H2S-based therapies for ischaemic stroke: opportunities and challenges." Stroke and Vascular Neurology 4, no. 2 (June 2019): 63–66. http://dx.doi.org/10.1136/svn-2018-000194.
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Stroke is a cerebrovascular disease displaying high mortality and morbidity. Despite extensive efforts, only very few therapies are available for stroke patients as yet. Hydrogen sulfide (H2S) is thought to be a signalling molecule that is endogenously produced and plays functional roles in the central nervous system. Currently, numerous studies show that H2S impacts stroke outcomes in animal and cellular models. Here, we review the recent research regarding the effects of endogenously produced H2S as well as exogenous H2S donors on stroke pathology, focusing on the potential of H2S-based therapies in treating ischaemic stroke. We also discuss the several issues that hinder the clinical translation of H2S-based therapies from the bench. Taken together, we think that H2S-based therapies are promising strategies for treating cerebral ischaemia if we successfully address these issues.
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İyigün, İ., and Y. Bakirci. "Plasma Concentrations of C-Reactive Protein and Fibrinogen in Ischaemic Stroke." Journal of International Medical Research 30, no. 6 (December 2002): 591–96. http://dx.doi.org/10.1177/147323000203000607.
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This study investigated how fibrinogen and C-reactive protein (CRP) levels change in response to neural damage occurring after ischaemia, and the relationship between the distribution of the arterial lesion, the disease prognosis and the levels of these substances. Fibrinogen and CRP levels were measured in blood samples obtained from 83 patients admitted to hospital within 72 h of a first ischaemic stroke. The patients were evaluated clinically with the Glasgow Outcome Scale (GOS), and results were compared with 43 age-matched controls. The fibrinogen and CRP levels in unconscious patients with hemiparesis or hemiplegia were higher than those in conscious hemiplegic patients. Also, the difference in GOS values between the unconscious patients with hemiparesis or hemiplegia and conscious patients with hemiparesis or hemiplegia was statistically significant. Patients with large infarcts in the median cerebral artery and anterior cerebral artery had higher fibrinogen and CRP concentrations than the control group. In conclusion, fibrinogen and CRP may be important measures for determining the prognosis and outcome in patients following ischaemic stroke.
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Faller, Kiterie M. E., Joshua Leach, Pamela Johnston, William M. Holmes, I. Mhairi Macrae, and Bruno G. Frenguelli. "Proof of concept and feasibility studies examining the influence of combination ribose, adenine and allopurinol treatment on stroke outcome in the rat." Brain and Neuroscience Advances 1 (January 1, 2017): 239821281771711. http://dx.doi.org/10.1177/2398212817717112.
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Background: Cerebral ischaemia results in a rapid and profound depletion of adenosine triphosphate (ATP), the energy currency of the cell. This depletion leads to disruption of cellular homeostasis and cell death. Early replenishment of ATP levels might therefore have a neuroprotective effect in the injured brain. We have previously shown that the ATP precursors, D-ribose and adenine (RibAde), restored the reduced ATP levels in rat brain slices to values similar to those measured in the intact rodent brain. The aim of this study was to assess whether RibAde, either alone or in combination with the xanthine oxidase inhibitor allopurinol (RibAdeAll; to further increase the availability of ATP precursors), could improve outcome in an in vivo rodent model of transient cerebral ischaemia. Methods: After 60 min occlusion of the middle cerebral artery, and upon reperfusion, rats were administered saline, RibAde, or RibAdeAll for 6 h. Baseline lesion volume was determined by diffusion-weighted MRI prior to reperfusion and final infarct volume determined by T2-weighted MRI at Day 7. Neurological function was assessed at Days 1, 3 and 7. Results: Ischaemic lesion volume decreased between Days 1 and 7: a 50% reduction was observed for the RibAdeAll group, 38% for the RibAde group and 18% in the animals that received saline. Reductions in lesion size in treatment groups were accompanied by a trend for faster functional recovery. Conclusion: These data support the potential use of ribose, adenine and allopurinol in the treatment of cerebral ischaemic injury, especially since all compounds have been used in man.
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Rothwell, Peter M., and Charles P. Warlow. "Familial frequency of ischaemic stroke and transient ischaemic attack in relation to clinical subtype and intermediate phenotypes." Stroke 32, suppl_1 (January 2001): 321. http://dx.doi.org/10.1161/str.32.suppl_1.321-a.
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28 Susceptibility to cerebral ischaemia is influenced by genetic factors. However, although a number of rare Mendelian syndromes have been characterised, there have been few studies of the genetic epidemiology of the common forms of ischaemic stroke and TIA. Previous studies have not reported familial frequency in the specific clinical subtypes of ischaemic stroke, and have not assessed the extent to which familial susceptibility is related to intermediate phenotypes such as hypertension, diabetes and hyperlipidaemia. We studied family history of stroke in 544 ischaemic strokes (Oxfordshire Community Stroke Project: OCSP) and 469 TIAs (hospital-referred case series in Oxford). Information on history of stroke in first degree relatives (FDR) was obtained in 535 stokes and 467 TIAs. Stroke had occurred in a FDR of 40 (8%, 95% CI = 6 - 10) stroke cases. Positive family history was unrelated to clinical subtype (OCSP classification). In particular, it was no more common in lacunar than non-lacunar stroke. In the TIAs, there was a history of stroke in at least one FDR in 98 (21%, 95% CI = 17 - 25) cases: 80 (17%) with one FDR, 16 (3.4%) with two FDRs and 2 (0.4%) with 3+ FDRs. The frequency of hypertension increased with the number of FDRs affected (P=0.003): nil - 105/373 (28%), one - 32/78 (41%); two or more - 12/18 (67%). Mean (SD) systolic blood pressure (mmHg) also increased across these groups (P=0.02): 157 (31), 162 (30) and 177 (36). In the strokes, a history of hypertension was also more frequent in those with a family history of stroke (P=0.02), and this was also shown by differences in measured blood pressure. In both cohorts, cases without hypertension, diabetes or hyperlipidaemia were least likely to have a family history of stroke. A history of stroke in a FDR was relatively infrequent, and was not related to the clinical subtype of stroke. However, in both the strokes and TIAs, family history of stroke was strongly related to intermediate phenotypes, particularly hypertension. These data suggest that genetic susceptibility to hypertension might account for a substantial proportion of the familial clustering of ischaemic stroke and TIA.
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Bahor, Zsanett, Jing Liao, Malcolm R. Macleod, Alexandra Bannach-Brown, Sarah K. McCann, Kimberley E. Wever, James Thomas, et al. "Risk of bias reporting in the recent animal focal cerebral ischaemia literature." Clinical Science 131, no. 20 (October 13, 2017): 2525–32. http://dx.doi.org/10.1042/cs20160722.
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Background: Findings from in vivo research may be less reliable where studies do not report measures to reduce risks of bias. The experimental stroke community has been at the forefront of implementing changes to improve reporting, but it is not known whether these efforts are associated with continuous improvements. Our aims here were firstly to validate an automated tool to assess risks of bias in published works, and secondly to assess the reporting of measures taken to reduce the risk of bias within recent literature for two experimental models of stroke. Methods: We developed and used text analytic approaches to automatically ascertain reporting of measures to reduce risk of bias from full-text articles describing animal experiments inducing middle cerebral artery occlusion (MCAO) or modelling lacunar stroke. Results: Compared with previous assessments, there were improvements in the reporting of measures taken to reduce risks of bias in the MCAO literature but not in the lacunar stroke literature. Accuracy of automated annotation of risk of bias in the MCAO literature was 86% (randomization), 94% (blinding) and 100% (sample size calculation); and in the lacunar stroke literature accuracy was 67% (randomization), 91% (blinding) and 96% (sample size calculation). Discussion: There remains substantial opportunity for improvement in the reporting of animal research modelling stroke, particularly in the lacunar stroke literature. Further, automated tools perform sufficiently well to identify whether studies report blinded assessment of outcome, but improvements are required in the tools to ascertain whether randomization and a sample size calculation were reported.
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Hebel, Kazimiera, Przemysław Kowiański, and Katarzyna Rogoza. "Assessment of the Functional Status of Patients with Ischaemic Stroke Receiving Thrombolytic Treatment." Journal of Neurological and Neurosurgical Nursing 9, no. 1 (March 2020): 12–19. http://dx.doi.org/10.15225/pnn.2020.9.1.2.
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Introduction. Intravenous thrombolysis is a gold standard in the treatment of acute ischaemic stroke. It causes reperfusion in the region of ischaemia and as a result it has a positive effect on functional outcomes of patients. The sooner this treatment is introduced the higher efficacy can be expected. Aim. The study objective was to assess the functional status of patients with ischaemic stroke, undergoing thrombolytic treatment and the incidence of thrombolysis complications. Material and Methods. Retrospective studies were conducted on a group of 109 patients hospitalised due to ischaemic cerebral stroke and qualified for thrombolytic treatment. The functional status was assessed with the use of the modified Rankin Scale and National Institutes of Health Stroke Scales on admission and discharge day. The study group included 55 males and 54 females (respectively: 50.5% and 49.5% of the total study population). The subject age was between 32 and 96 years, with the mean age of 69.8. Results. The average time between the onset of symptoms and initiation of thrombolytic treatment was 182 minutes. The National Institutes of Health Stroke Scale at the moment of qualification for treatment was 10.11 points, and the Rankin Scale was 2.88 points. On the day of discharge, the values were 5.81 and 2.05, respectively. A statistically significant (p < 0.0001) improvement in the functional status was observed in the group of patients who had no intra cerebral haemorrhage after thrombolysis. The most common complication of thrombolytic treatment was haemorrhagic transformation of the ischaemic stroke focus — 27 cases (24.77%). Death occurred in 9 subjects (8.26% of total), including 6 cases in males (10.91% of males) and was related to haemorrhagic transformation of the ischaemic stroke focus (p = 0.000). Conclusions. The implemented treatment of stroke resulted in improvement of the functional status. The most frequent complication was haemorrhagic conversion of stroke. (JNNN 2020;9(1):12–19) Key Words: stroke, thrombolysis, functional status
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Sablot, Denis, Faouzi Belahsen, Fabrice Vuillier, Jean-François Cassarini, Pierre Decavel, Laurent Tatu, Thierry Moulin, and Elisabeth Medeiros de Bustos. "Predicting Acute Ischaemic Stroke Outcome Using Clinical and Temporal Thresholds." ISRN Neurology 2011 (September 6, 2011): 1–9. http://dx.doi.org/10.5402/2011/354642.
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Background. Few studies have analysed the natural course of cerebral ischaemia for predicting outcome. We aimed to determine the early clinical findings and the thresholds for deficit severity and symptom duration that make it possible to stratify outcome. Methods. We included 154 patients with transient ischaemic attack or ischaemic stroke. Stroke profiles and neurological status were assessed from onset to 24 hrs, on admission, at 48 hrs, and at discharge. Outcomes were evaluated using the modified Rankin Scale. Positive and negative predictive values were calculated for the different thresholds. The model was subsequently evaluated on a new prospective cohort of 157 patients. Results. Initial National Institute of Health Stroke Scale (NIHSS) score <5 and symptoms regressing within 135 min were predictive of good outcome. Initial NIHSS score >22 and symptom stability after 1,230 min were predictive of physical dependency or death. Conclusions. Low and high NIHSS cut-off points are effective positive predictive values for good and poor outcomes. Thresholds for symptom duration are less conclusive.
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Krishna, Smriti Murali, Alexandra Fay Trollope, and Jonathan Golledge. "The relevance of epigenetics to occlusive cerebral and peripheral arterial disease." Clinical Science 128, no. 9 (January 27, 2015): 537–58. http://dx.doi.org/10.1042/cs20140491.
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Athero-thrombosis of the arteries supplying the brain and lower limb are the main causes of stroke and limb loss. New therapies are needed to improve the outcomes of athero-thrombosis. Recent evidence suggests a role for epigenetic changes in the development and progression of ischaemic injury due to atherosclerotic occlusion of peripheral arteries. DNA hypermethylation have been associated with cardiovascular diseases. Histone post-translational modifications have also been implicated in atherosclerosis. Oxidized low-density lipoprotein regulated pro-inflammatory gene expression within endothelial cells is controlled by phosphorylation/acetylation of histone H3 and acetylation of histone H4 for example. There are a number of challenges in translating the growing evidence implicating epigenetics in atherosclerosis to improved therapies for patients. These include the small therapeutic window in conditions such as acute stroke and critical limb ischaemia, since interventions introduced in such patients need to act rapidly and be safe in elderly patients with many co-morbidities. Pre-clinical animal experiments have also reported conflicting effects of some novel epigenetic drugs, which suggest that further in-depth studies are required to better understand their efficacy in resolving ischaemic injury. Effective ways of dealing with these challenges are needed before epigenetic approaches to therapy can be introduced into practice.
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Clarkson, Andrew N., Lily Boothman-Burrell, Zita Dósa, Raghavendra Y. Nagaraja, Liang Jin, Kim Parker, Petra S. van Nieuwenhuijzen, et al. "The flavonoid, 2′-methoxy-6-methylflavone, affords neuroprotection following focal cerebral ischaemia." Journal of Cerebral Blood Flow & Metabolism 39, no. 7 (January 29, 2018): 1266–82. http://dx.doi.org/10.1177/0271678x18755628.
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Tonic inhibitory currents, mediated by extrasynaptic GABAA receptors, are elevated at a delay following stroke. Flavonoids minimise the extent of cellular damage following stroke, but little is known about their mode of action. We demonstrate that the flavonoid, 2′-methoxy-6-methylflavone (0.1–10 µM; 2′MeO6MF), increases GABAA receptor tonic currents presumably via δ-containing GABAA receptors. Treatment with 2′MeO6MF 1–6 h post focal ischaemia dose dependently decreases infarct volume and improves functional recovery. The effect of 2′MeO6MF was attenuated in δ−/− mice, indicating that the effects of the flavonoid were mediated via δ-containing GABAA receptors. Further, as flavonoids have been shown to have multiple modes of action, we investigated the anti-inflammatory effects of 2′MeO6MF. Using a macrophage cell line, we show that 2′MeO6MF can dampen an LPS-induced elevation in NFkB activity. Assessment of vehicle-treated stroke animals revealed a significant increase in circulating IL1β, TNFα and IFγ levels. Treatment with 2′MeO6MF dampened the stroke-induced increase in circulating cytokines, which was blocked in the presence of the pan-AKT inhibitor, GSK690693. These studies support the hypothesis that compounds that potentiate tonic inhibition via δ-containing GABAA receptors soon after stroke can afford neuroprotection.
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Hayon, Yael, Olga Dashevsky, Ela Shai, David Varon, and Ronen Leker. "Platelet lysates stimulate angiogenesis, neurogenesis and neuroprotection after stroke." Thrombosis and Haemostasis 110, no. 08 (2013): 323–30. http://dx.doi.org/10.1160/th12-11-0875.
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SummaryPlatelets contain chemo-attractants and mitogens that have a major role in tissue repair. Therefore we hypothesised that tissue regeneration secondary to activation of endogenous neural stem cells (eNSC) can be enhanced by delivering platelets to the ischaemic brain. To examine these potential therapeutic effects we injected platelet-poor plasma (PPP), fibroblast growth factor (FGF2) and platelet lysate (PLT) to the lateral ventricles after permanent middle cerebral artery occlusion (PMCAO) in rats. The animals were tested with the neurological severity score, and infarct volumes were measured at 90 days post–PMCAO. Immunohistochemistry was used to determine the fate of newborn cells and to count blood vessels in the ischaemic brain. Platelets significantly increased eNSC proliferation and angiogenesis in the subventricular zone (SVZ) and in the peri-lesion cortex. Functional outcome was significantly improved and injury size was significantly reduced in rats treated with PLT suggesting additional neuroprotective effects. In conclusion, local delivery of PLT to the lateral ventricles induces angiogenesis, neurogenesis and neuroprotection and reduces behavioural deficits after brain ischaemia.
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Akhmedov, Alexander, Nicole R. Bonetti, Martin F. Reiner, Remo D. Spescha, Heidi Amstalden, Mario Merlini, Daniel S. Gaul, et al. "Deleterious role of endothelial lectin-like oxidized low-density lipoprotein receptor-1 in ischaemia/reperfusion cerebral injury." Journal of Cerebral Blood Flow & Metabolism 39, no. 11 (August 3, 2018): 2233–45. http://dx.doi.org/10.1177/0271678x18793266.
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Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is implicated in cardiovascular disease by modulating apoptosis and oxidative stress. We hypothesized that LOX-1 may be involved in pathophysiology of stroke by mediating ischaemia/reperfusion (I/R)-dependent cell death. Transient middle cerebral artery occlusion (tMCAO) was performed in wild-type (WT) mice, endothelial-specific LOX-1 transgenic mice (eLOX-1TG) and WT animals treated with LOX-1 silencing RNA (siRNA). In WT mice exposed to tMCAO, LOX-1 expression and function were increased in the MCA. Compared to WT animals, eLOX-1TG mice displayed increased stroke volumes and worsened outcome after I/R. Conversely, LOX-1-silencing decreased both stroke volume and neurological impairment. Similarly, in HBMVECs, hypoxia/reoxygenation increased LOX-1 expression, while LOX-1 overexpressing cells showed increased death following hypoxia reoxygenation. Increased caspase-3 activation was observed following LOX-1 overexpression both in vivo and in vitro, thus representing a likely mediator. Finally, monocytes from ischaemic stroke patients exhibited increased LOX-1 expression which also correlated with disease severity. Our data unequivocally demonstrate a key role for LOX-1 in determining outcome following I/R brain damage. Our findings could be corroborated in human brain endothelial cells and monocytes from patients, underscoring their translational relevance and suggesting siRNA-mediated LOX-1 knockdown as a novel therapeutic strategy for stroke patients.
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Lucaci, Paul, Marius Neculaes, and Danisia Haba. "The Contribution of Imaging and Functional Diagnosis to the Rehabilitation of Patients with Stroke." Revista de Chimie 70, no. 8 (September 15, 2019): 2847–50. http://dx.doi.org/10.37358/rc.19.8.7440.
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The research conducted is based on the clinical evaluation through magnetic resonance and on functional testing using the stabilometric platform, of a sample of 23 subjects with a stroke ischemic localised in the area of the middle cerebral artery. With the help of magnetic resonance, the structural changes of the ischaemic focus were determined. At the same time, the evolution in time of the ischaemia and the alteration at the level of the ischaemic area were monitored. By using the stabilometric platform GPS 400, the distribution of the load at the level of the lower limbs was analysed, as well as barycentre variations. The results obtained after conducting the study highlight the high possibility of the functional re-education of the subjects when brain lesions do not extend and no complications arise, elements underlined by imaging exploration using magnetic resonance.
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Percie du Sert, Nathalie, Alessio Alfieri, Stuart M. Allan, Hilary VO Carswell, Graeme A. Deuchar, Tracy D. Farr, Paul Flecknell, et al. "The IMPROVE Guidelines (Ischaemia Models: Procedural Refinements Of in Vivo Experiments)." Journal of Cerebral Blood Flow & Metabolism 37, no. 11 (August 11, 2017): 3488–517. http://dx.doi.org/10.1177/0271678x17709185.
Full textAbstract:
Most in vivo models of ischaemic stroke target the middle cerebral artery and a spectrum of stroke severities, from mild to substantial, can be achieved. This review describes opportunities to improve the in vivo modelling of ischaemic stroke and animal welfare. It provides a number of recommendations to minimise the level of severity in the most common rodent models of middle cerebral artery occlusion, while sustaining or improving the scientific outcomes. The recommendations cover basic requirements pre-surgery, selecting the most appropriate anaesthetic and analgesic regimen, as well as intraoperative and post-operative care. The aim is to provide support for researchers and animal care staff to refine their procedures and practices, and implement small incremental changes to improve the welfare of the animals used and to answer the scientific question under investigation. All recommendations are recapitulated in a summary poster (see supplementary information).