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One in six suffers a stroke during their lifetime and stroke remains the major cause of new onset disability in adulthood. The worldwide burden of stroke is increasing due to an ageing population, however, globally haft of stroke victims are young.Stroke is the clinical diagnosis of an acute vascular incident and covers a multitude of pathophysiological causes. The clinician needs imaging to make decisions on acute treatment as well as to plan a secondary prevention strategy: a non-contrast CT and a Duplex of the carotids followed by an aspirin as a one size fits all strategy does not always provide sufficient support for those decisions.Presently, fast, generally available, and non-invasive imaging provides new possibilities of establishing a cause of stroke, provide specific information on the brain parenchyma – including possibly salvageable tissue and micro-bleeds – as well as allowing for more specific prognostication in acute stroke. This eBook covers both ischemic and haemorrhagic stroke and includes hot topics such as micro-bleeds, salvageable tissue and spot-sign, clinically challenging issues including movement artefacts in MRI as well as an overview of present options including pragmatic and feasible suggestions for an approach to state of the art acute imaging.
acute stroke --- ischemic stroke --- hemorrhagic stroke --- intracerebral hemorrage --- cerebral amyloid angiopathy --- spot-sign
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In the mid-sixties, the discovery by Altman and co-workers of neurogenesis in the adult brain changed the previous conception of the immutability of this organ during adulthood sustained among others by Cajal. This discovery was ignored up to eighty’s when Nottebohm demonstrated neurogenesis in birds. Subsequently, two main neurogenic zones were characterized: the subventricular zone of the lateral ventricle and the subgranular layer of the dentate gyrus. Half century later, the exact role of new neurons in the adult brain is not completely understand. This book is composed by a number of articles by leaders in the filed covering from an historic perspective to potential therapeutic opportunities.
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As clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. Two endogenous mechanisms have been recently characterized, ischemic preconditioning and ischemic postconditioning. In the present topic newly characterized mechanisms involved in preconditioning- and postconditioning- neuroprotection will be discussed. The understanding of the mechanisms involved in the neuroprotective pathways induced by preconditioning and postconditioning will be clinically relevant for identifying new druggable target for neurodegenerative disorder therapy. Furthermore, the importance of these neuroprotective strategies resides in that it might be easily translatable into clinical practice. Therefore, the data presented here will highlight the capacity of ischemic preconditioning and postconditioning to be of benefit to humans.
preconditioning --- postconditioning --- Neuroprotection --- NCX --- miRNA --- Stroke --- Alzheimer --- seizure
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The primary purpose of Brain Computer Interface (BCI) systems is to help patients communicate with their environment or to aid in their recovery. A common denominator for all BCI patient groups is that they suffer from a neurological deficit. As a consequence, BCI systems in clinical and research settings operate with control signals (brain waves) that could be substantially altered compared to brain waves of able-bodied individuals. Most BCI systems are built and tested on able-bodied individuals, being insufficiently robust for clinical applications. The main reason for this is a lack of systematic analysis on how different neurological problems affect the BCI performance. Neurological problems interfering with BCI performance are either a direct cause of a disability (e.g. stroke, autism, epilepsy ) or secondary consequences of a disability, often overlooked in design of BCI systems (chronic pain, spasticity and antispastic drugs, loss of cognitive functions, drowsiness, medications which are increasing/decreasing brain activity in certain frequency range) . While some of these deficits may decrease the performance of a BCI, others may potentially improve its performance compared to BCI tested on a healthy population (e.g. overactivation of motor cortex in patients with Central neuropathic pain (CNP), increased alpha activity in some patient groups). Depending on the neurological condition, a prolonged modulation of brain waves through BCI might produce both positive or detrimental effects. Thus some BCI protocols might be more suitable for a short term use (e.g. rehabilitation of movement) while the others would be more suitable for a long term use. Prolonged self-regulation of brain oscillation through BCI could potentially be used as a treatment for aberrant brain connections for conditions ranging from motor deficits to Autism Spectrum Disorders (ASD). Currently, ASD is an increasingly prevalent condition in the U.S. with core deficits in imitation learning, language, empathy, theory of mind, and self-awareness. Understanding its neuroetiology is not only critical and necessary but should provide relevant insights into the relationship between neuroanatomy, physiology and behaviour. In this Research Topic we welcome studies of the highest scientific quality highlighting how BCI systems based on different principles (SSVEP, P300, slow cortical potential, auditory potential, operant conditioning, etc) interact with the underlying neurological problems and how performance of these BCI system differ compared to similar systems tested on healthy individuals. We also welcome studies defining signatures of neurological disorders and proposing BCI based treatments. We expect to generate a body of knowledge valuable both to researchers working with clinical populations, but also to a vast majority of BCI researchers testing new algorithms on able-bodied people. This should lead towards more robust or tailor-made BCI protocols, facilitating translation of research from laboratories to the end users.
Brain Computer Interface --- Patients --- Rehabilitation --- Stroke --- spinal cord injury --- autism --- amyothopic lateral sclerosis --- Cerebral Palsy
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Hemispatial neglect is the failure to report, respond to, or orient to novel or meaningful stimuli presented in the contralesional visual field. It constitutes one of the most invalidating neurological disorders that can occur after stroke. It is therefore important to treat neglect as adequate as possible and much of the research dedicated to neglect therefore focuses on rehabilitation. In this special topic, you will find 29 articles on the rehabilitation of neglect. This Research Topic has opened new perspectives, and has given us an indication of where the field is going. Although some of the current rehabilitation techniques have proven to be beneficial, there is limited agreement on the most valuable technique or the mechanisms underlying the ameliorating effects.
neglect --- Rehabilitation --- Stroke --- Prism adaptation --- brain damage --- Neuropsychology --- computer-based testing --- visual scan training --- Brain Stimulation
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Non-coding RNAs (ncRNAs), and in particular microRNAs are rapidly becoming the focus of research interest in numerous basic and translational fields, including brain research; and their importance for many aspects in brain functioning merits special discussion. The wide-scope, multi-targeted and highly efficient manner of ncRNA regulatory activities draws attention to this topic by many, but the available research and analysis tools and experimental protocols are still at their infancy, and calls for special discussion given their importance for many aspects in brain functioning. This eBook is correspondingly focused on the search for, identification and exploration of those non-coding RNAs whose activities modulate the multi-leveled functions of the eukaryotic brain. The different articles strive to cover novel approaches for identifying and establishing ncRNA-target relationships, provide state of the art reports of the affected neurotransmission pathways, describe inherited and acquired changes in ncRNA functioning and cover the use of ncRNA mimics and blockade tools for interference with their functions in health and disease of the brain. Non-coding RNAs are here to stay, and this exciting eBook provides a glimpse into their impact on our brain’s functioning at the physiology, cell biology, behavior and immune levels.
MicroRNAs --- long non-coding RNAs --- Central Nervous System --- cholinergic signaling --- Schizophrenia --- Epilepsy --- ischemic stroke --- Alzheimer
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Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory ‘collateral damage’ in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms.
Neuroinflammation --- Stroke --- Immunity --- intracerebral hemorrhage --- Leukocytes --- Cytokines --- neurodegeneration --- Traumatic Brain Injury
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Stroke remains one of the most devastating diseases in industrialized countries. Recanalization of the occluded arterial vessel using thrombolysis is the only causal therapy available. However, thrombolysis is limited due to severe side effects and a limited time window. As such, only a minority of patients receives this kind of therapy, showing a need for new and innovative treatment strategies. Although neuroprotective drugs have been shown to be beneficial in a variety of experimental stroke models, they ultimately failed in clinical trials. Consequently, recent scientific focus has been put on modulation of post-ischemic neuroregeneration, either via stimulation of endogenous neurogenesis or via application of exogenous stem cells or progenitor cells. Neurogenesis persists within the adult brain of both rodents and primates. As such, neural progenitor cells (NPCs) are found within distinct niches like the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone of the dentate gyrus. Cerebral ischemia stimulates these astrocyte-like progenitor cells, upon which NPCs proliferate and migrate towards the site of lesion. There, NPCs partly differentiate into mature neurons, without significantly being integrated into the residing neural network. Rather, the majority of new-born cells dies within the first weeks post-stroke, leaving post-ischemic neurogenesis a phenomenon of unknown biological significance. Since NPCs do not replace lost brain tissue, beneficial effects observed in some studies after either stimulated or protected neurogenesis are generally contributed to indirect effects of these new-born cells. The precise identification of appropriated cellular mediators, however, is still elusive. How do these mediators work? Are they soluble factors or maybe even vesicular structures emanating from NPCs? What are the cues that guide NPCs towards the ischemic lesion site? How can post-ischemic neurogenesis be stimulated? How can the poor survival of NPCs be increased? In order to support post-ischemic neurogenesis, a variety of research groups have focused on application of exogenous stem/progenitor cells from various tissue sources. Among these, cultivated NPCs from the SVZ and mesenchymal stem cells (MSCs) from the bone marrow are frequently administered after induction of stroke. Although neuroprotection after delivery of stem/progenitor cells has been shown in various experimental stroke models, transplanted cells are usually not integrated in the neural network. Again, the vast amount of grafted cells dies or does not reach its target despite profound neuroprotection, also suggesting indirect paracrine effects as the cause of neuroprotection. Yet, the factors being responsible for these observations are under debate and still have to be addressed. Is there any “optimal” cell type for transplantation? How can the resistance of grafted cells against a non-favorable extracellular milieu be increased? What are the molecules that are vital for interaction between grafted cells and endogenous NPCs? The present research topic seeks to answer - at least in part - some of the aforementioned questions. Although the research topic predominantly focuses on experimental studies (and reviews alike), a current outlook towards clinical relevance is given as well.
cerebral ischemia --- mesenchymal stem cells (MSCs) --- Neural progenitor cells (NPCs) --- Neurogenesis --- Neuroregeneration --- Stroke --- Transplantation
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This ebook contains a series of original publications, reviews and mini-reviews by leaders in the field that address the growing importance of the plasminogen activating system in neurobiology. The articles included cover the role of the plasminogen activating system as a key modulator of blood brain barrier permeability, and the implications of this in traumatic brain injury and in ischemic stroke. State-of-the-Art manuscripts are also included that address the regulatory mechanisms that control this important process.This ebook contains a series of original publications, reviews and mini-reviews by leaders in the field that address the growing importance of the plasminogen activating system in neurobiology. The articles included cover the role of the plasminogen activating system as a key modulator of blood brain barrier permeability, and the implications of this in traumatic brain injury and in ischemic stroke. State-of-the-Art manuscripts are also included that address the regulatory mechanisms that control this important process.
plasminogen activation --- tissue-type plasminogen activator --- Neurobiology --- blood brain barrier --- ischaemic stroke --- Traumatic Brain Injury --- Neuroserpin
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This book focuses on the investigation, development, and modernization of acupuncture in basic research settings as well as in clinical applications. The book contains 13 chapters reporting the latest evidence-based results of acupuncture research and exploring acupuncture in general. Altogether, 44 authors from all over the world contributed to this book.
acupuncture --- moxibustion --- myopia --- post-stroke --- depression --- pulse diagnosis --- low back pain (LBP) --- osteoarthritis --- uterine cancer --- sciatica
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