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Congratulations to our authors, reviewers and editors for accelerating new knowledge and solutions — and for helping everyone to live great lives on a healthy planet. Stroke has been among the most rapidly evolving field of medicine in the last three decades. From an area filled with nihilism and unproven dogmas, an incredible research momentum has led to major breakthroughs in understanding for instance i the mechanisms leading to ischemic and hemorrhagic stroke, including vascular, hematological and genetic factors, and those underlying the outcome of acutely ischemic tissue, namely infarction or survival, and the benefits of early reperfusion ; ii the events that take place in peri-lesional tissue, including inflammation, selective neuronal death and plasticity; iii the processes underlying brain reorganization and functional recovery; and iv the contribution of incipient vascular brain damage in the cognitive deterioration including dementia of the elderly.
These advances have led to clinical revolutions for instance in the secondary prevention of stroke, acute stroke therapy, management of transient ischemic attacks and subarachnoid hemorrhage, and neurorehabilitative interventions, that have had major impact on both mortality and functional outcome. However, the incidence of stroke remains extremely high due to aging populations worldwide, the fraction of patients who benefit from these advances remains limited and overall stroke outcome remains unsatisfactory.
Hemorrhagic stroke remains a major challenge in terms of both lack of evidence-based acute therapy and risk related to antithrombotic therapies in the elderly. Likewise, the mechanisms underlying cerebral small vessel disease cSVD , including hypertension-related cSVD and cerebral amyloid angiopathy, remain largely unknown, yet their incidence and impact increase dramatically with aging of the populations. There is therefore an urgent need to further improve stroke therapy and outcome through basic, translational and clinical research.
All manuscripts must be submitted directly to the section Stroke, where they are peer-reviewed by the Associate and Review Editors of the specialty section. Articles published in the section Stroke will benefit from the Frontiers impact and tiering system after online publication. Authors of published original research with the highest impact, as judged democratically by the readers, will be invited by the Chief Editor to write a Frontiers Focused Review - a tier-climbing article.
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Focused Reviews are centered on the original discovery, place it into a broader context, and aim to address the wider community across all of Neurology. For all queries regarding manuscripts in Review and potential conflicts of interest, please contact neurology. View all copies of this ISBN edition:. Synopsis Stroke is the most common neurologic disease and the leading cause of adult disability in Western countries. Buy New Learn more about this copy. Customers who bought this item also bought.
Stock Image. Karger New Hardcover Quantity Available: 2. Seller Rating:. Manifestations Of Stroke Caso, V. New Quantity Available: 2. Manifestations of Stroke M Paciaroni. Published by Karger , Basel New Quantity Available: 1. Chiron Media Wallingford, United Kingdom. Manifestations of Stroke M. Published by Karger Verlag Apr Rheinberg-Buch Bergisch Gladbach, Germany. BuchWeltWeit Inh. Ludwig Meier e. Bergisch Gladbach, Germany. CSD elicits changes in vascular tone, resulting in areas of transient hyperperfusion in healthy tissue haemodynamic physiological response through the mechanism of vascular dilation.
Alternatively, it causes areas of hypoperfusion in tissues at risk for a progressive lesion inverse haemodynamic response by provoking severe microvascular spasm. Experimental studies have shown that oxyhaemoglobin, increased extracellular potassium, and decreased levels of NO, glutamate, and ET-1 are all involved in the development of CSD after SAH.
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Hyponatraemia is regarded as an independent risk factor for unfavourable prognosis.. Low magnesium levels are related to vascular dilation and the inhibition of platelet aggregation and ET-1 synthesis, meaning that low magnesium exacerbates EBI.
These deficits also contribute to increased intracellular levels of calcium, which is regarded as the main mediator of neuronal death. Researchers have observed that both glutamate and glutamate transporters GT play an important role in the pathogenesis of ischaemic neurological lesions. Their levels seem to be associated with the intensity of the initial injury. However, induced SAH in a rat model seems to produce an excessive and prolonged increase in extracellular GT levels and downregulation of GT.
These processes are accompanied by increased basilar artery wall thickness and neuronal degeneration in the hippocampus. The initial phenomenon occurring immediately after rupture of the aneurysm is acute CBF arrest, resulting in a state of transient global brain ischaemia which can itself be lethal. The targets of these apoptotic pathways are essentially neurons, glial cells, and cerebral vascular cells smooth muscle and endothelium.. It is obvious that many of the current diagnostic techniques for SAH are only able to identify physiological changes once neuronal damage is so well-established that it is probably irreversible.
Therefore, a sizeable percentage of current research on this topic focuses on identifying markers that enable early detection of the lesions produced by SAH. The two main lines of research in pursuit of this objective explore neuroimaging techniques and biomarkers in bodily fluids.. Numerous methods of measuring cerebral perfusion have been used in recent years. Of the methods listed above, TCD is the most widely used due to being a non-invasive process that yields good results.
However, we must be aware of its limitations: the method is operator-dependent, unable to measure CBF, and offers non-specific information regarding the treatment to be used. On the other hand, images obtained by computed tomography are an emerging topic in this field. CT perfusion imaging is able to provide several quantitative parameters for brain haemodynamics, including mean transit time MTT , cerebral blood volume, and CBF. In practice, visual inspection of CTP maps may be used as a reliable method for assessing cerebral hypoperfusion.
These maps may show decreased perfusion in areas with minimal or no VSP according to the angiography. This fact lets us identify ischaemic risk which would otherwise go unnoticed. In fact, findings from different studies employing CTP seem to have a better predictive value than those from studies using CT angiography 51 or TCD 54 to diagnose late-onset cerebral ischaemic lesions in patients with signs of clinical impairment..
Of all the measurements taken by CTP, mean transit time MTT has been identified not only as the most sensitive perfusion parameter for detecting cerebral VSP, but also as an independent predictor of early mortality following SAH. Large volumes of literature are available on biomarker analysis within the context of different human biological samples and SAH. Distinct techniques and theoretical perspectives have been used to study biomarkers at different historical moments. Each approach evolved from the theoretical understanding of data such as the underlying pathophysiological mechanisms in the development of VSP or in existing EBI..
Although CMD has delivered contradictory results, it is regarded as a promising method for monitoring patients who have experienced SAH. Proteomics delivers a large-scale analysis of all the proteins in a biological sample simultaneously. Authors such as Lad et al. According to their system, biomarkers fall into 3 categories according to their predictive value: a markers with auspicious value; b candidate markers; c noncandidate markers.
Increasing numbers of authors state that combining data collected using different techniques can provide doctors with better information, given that each method provides a distinct perspective on cerebral physiology and metabolism. This concept, known as multimodal neuromonitoring, has emerged as an auspicious approach in specific studies of patients with SAH.
This new research opportunity should foster cooperative efforts among doctors representing basic neurosciences, neurosurgery, neurology, and neurocritical care with a view to achieving better prevention of secondary ischaemic lesions resulting from EBI..
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EBI is probably caused by a series of interrelated pathophysiological mechanisms that all yield the same outcome: cell death. We have yet to determine the principal factor or factors in this process. What is clear is that research is delivering spectacular advances; furthermore, since reverting VSP does not seem to improve clinical outcomes, anti-EBI treatments may be a viable treatment option for patients with SAH in the future..
The authors have no conflicts of interest to declare.. ISSN: Previous article Next article. Issue 5. Pages June From vasospasm to early brain injury: New frontiers in subarachnoid haemorrhage research. Download PDF. Corresponding author. This item has received. Article information.
Introduction Delayed vasospasm has traditionally been considered the most important determinant of poor outcome after subarachnoid haemorrhage SAH. It has also changed the idea of VSP's role in brain damage, and suggests the need for re-evaluating the pathophysiological process of SAH. Development This review examines the current state of knowledge on the pathophysiological mechanisms associated with EBI and summarises the diagnostic options currently available.
Conclusion It seems that the research approach needs to be changed, so that investigators will focus on prevention of EBI, reduction of secondary brain complications and ultimately, the optimisation neurological outcome. Palabras clave:. Hemorragia subaracnoidea. This review analyses the current state of knowledge about pathophysiological mechanisms associated with EBI and offers a summary of currently available diagnostic options.
Development Early brain injury and its pathophysiological mechanisms One of the most important advances made in recent years was learning to recognise EBI after SAH, along with the consequences resulting from the initial haemorrhage, and the harmful effects of both processes on the patient's outcome. This evidence indirectly suggests that multiple pathways and mechanisms participate in EBI pathophysiology and urges us to undertake more in-depth research on EBI. Figure 1.
Related Manifestations of Stroke (Frontiers of Neurology and Neuroscience, Volume 30)
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