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Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Cerebral edema occurs as a consequence of cerebral infarction and usually peaks around 3–5 days after stroke. In patients with large areas of brain infarction, such as large middle ± anterior cerebral artery infarction, it may cause mass effect sufficient to raise intracranial pressure (Figures 12.206—12.208) and lead to subsequent brainstem herniation and death without intervention.
The cases
Published in Chris Schelvan, Annabel Copeman, Jacky Davis, Annmarie Jeanes, Jane Young, Paediatric Radiology for MRCPCH and FRCR, 2020
Chris Schelvan, Annabel Copeman, Jacky Davis, Annmarie Jeanes, Jane Young
Brain infarction may result from occlusion of one (focal) or more (multifocal) vascular territories. The specific vascular distribution distinguishes vascular occlusive disease from the more generalized changes seen with hypoxic ischaemic encephalopathy (HIE) due to circulatory arrest.
Death from natural causes
Published in Jason Payne-James, Richard Jones, Simpson's Forensic Medicine, 2019
Jason Payne-James, Richard Jones
Sudden bleeding into brain tissue is common, usually in old age and in those with significant hypertension and, together with cerebral thrombosis and resulting brain infarction, is the commonest cause of the well-recognised cluster of neurological signs colloquially termed a ‘stroke’.
Therapeutic impact of thymoquninone to alleviate ischemic brain injury via Nrf2/HO-1 pathway
Published in Expert Opinion on Therapeutic Targets, 2021
Nashwa Amin, Xiaoxue Du, Shijia Chen, Qiannan Ren, Azhar B. Hussien, Benson O.A. Botchway, Zhiying Hu, Marong Fang
Motor dysfunction is oftentimes seen in ischemic stroke patients [31]. Therefore, an improvement in this dysfunction could indicate an individual responding favorably to treatment. In our study, we observed extensive brain infarction in diseased animals and was concomitant with significant motor dysfunction. As expected, these observations negatively correlated with neuronal cell numbers. In the TQ-treated group, these effects were reversed, thus, evidencing remarkable improvement. In a recent study, the instigation of the Nrf2/HO-1 signaling pathway mediated the oxidative stress, inflammatory, and apoptotic factors in rats’ model of lung fibrosis. This was attained through the employment of TQ. For example, in the oxidative stress evaluation, TQ significantly augmented the antioxidant levels, glutathione, and catalase [27,32].
Sepsis-associated encephalopathy and septic encephalitis: an update
Published in Expert Review of Anti-infective Therapy, 2021
Simone C. Tauber, Marija Djukic, Johannes Gossner, Helmut Eiffert, Wolfgang Brück, Roland Nau
Brain CT scans are relatively easy to perform even in ICU patients and are therefore often used to rule out intracranial bleeding and other conditions requiring surgery, larger brain infarction, or abscesses. However, cCT is often unremarkable since its sensitivity to detect small infarcts or small abscesses or (focal) brain edema is low. cMRI is much more sensitive to detect lesions in the brains of septic patients, but is afflicted with considerably higher efforts in critically ill patients. Multiple small ischemic lesions, posterior reversible encephalopathy, diffuse white matter hyperintensities, small intraparenchymal hemorrhage, and direct or indirect signs of infective intracranial aneurysms can be seen [23–26]. For the proof of these aneurysms, digital subtraction angiography is the method of choice [24]. White matter hyperintense lesions are seen in the majority of patients with SE [27], but are also frequent in normal elderly subjects. MRI detected diffuse axonal injury in nine and small ischemic lesions in 3 of 13 patients with SAE [28]. Fluid attenuated inversion recovery (FLAIR) sequences and diffusion-weighted imaging (DWI) can be used to differentiate new and older lesions in SEE (Figure 2).
Prolactin attenuates global cerebral ischemic injury in rat model by conferring neuroprotection
Published in Brain Injury, 2020
Bhawna Vermani, Sumedha Mukherjee, Gaurav Kumar, Ranjana Patnaik
Brain infarction is the hallmark of ischemic reperfusion injury and neuroprotection strategies aim at reducing the infarct volume (2). This study revealed that though all three doses of PRL significantly reduced infarction volume in brain (p < .001) in comparison to infarct volumes observed in vehicle groups, Treated-A group had most successful effect on cerebral infarction reduction. Another characteristic of cerebral ischemia is increased brain water content (2) resulting due to BBB damage [44]. Compared to the vehicle group animals, where an increased brain edema by 23.8% was observed (compared to sham group), cerebral edema was significantly reduced in Treated-A and Treated-B group of animals (p < .001), but Treated-C group did not show any significant restoration. Decrease in cerebral infarct volume and cerebral edema by PRL treatment highlights the ability of PRL in ameliorating the ischemic damage incurred by brain tissues.