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The present E-book consists of original articles and reviews published in our Research Topic on injuries to the spinal cord and peripheral nerves and presents a wide array of novel findings and in depth discussions on topics within the field of nerve injury and repair. Our aim with this Research Topic is to bring together knowledge spanning from basic laboratory studies to clinical findings and strategies within the field of spinal cord and nerve injury and repair. We hope this publication will provide a basis for accelerated knowledge exchange within the field and hopefully a subsequent increase in research efforts and collaborations.

dorsal root --- glial scar --- nerve injury --- brachial plexus --- ventral root --- plasticity --- nerve regeneration --- Spinal cord injury

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The brainstem is a conduit connecting higher brain centers, cerebellum and spinal cord and provides the main sensory and motor innervation to the face, head and neck via the cranial nerves. It plays a pivotal role in the regulation of respiration, locomotion, posture, balance, arousal (alertness, awareness and consciousness), sensory information processing (nociception, etc.), autonomic functions (including control of bowel, bladder, blood pressure and heart rate) and is responsible for the regulation of numerous reflexes including swallowing, coughing and vomiting. It is controlled by higher brain centers originating from cortical and subcortical regions including the basal ganglia and diencephalon as well as feedback loops from the cerebellum and spinal cord. A modulatory control of brainstem output can be accomplished by affecting individual neurons and consequently, the operation of neural microcircuits and behavior. This is achieved by altering cellular excitability, synaptic transmission (release probability, postsynaptic receptor responsiveness, thus altering synaptic strength and efficacy) and network properties. Such dynamic control provides flexibility of the nervous system to adapt neural output according to the functional requirements and/or demands of the individual to achieve the desired behavioral state in a changing environment. Neuromodulation can be achieved by the “classical” neurotransmitters glutamate and GABA (gamma-amino butyric acid) by primary excitation and inhibition of the “anatomical network”, but can also be achieved through the use of transmitters acting on G- protein coupled receptors. Such neuromodulators include the monoamines (serotonin, noradrenaline and dopamine), acetylcholine, but also glutamate and GABA. In addition, neuropeptides and purines act as neuromodulators. Other chemical mediators such as nitric oxide and growth factors may also have similar actions. The aim of this Research Topic is to highlight recent advances in our understanding of the intrinsic and extrinsic neuromodulatory systems affecting brainstem function from the anatomical, physiological and pharmacological perspective and to emphasize how these advances strengthen, modify or challenge existing conceptual models of sensorimotor and autonomic control.

Science: general issues --- Neurosciences --- brainstem --- neuromodulation --- locomotion --- neurotransmitters and motor control --- autonomic function --- spinal cord injury --- movement-related disorders --- pain --- brainstem --- neuromodulation --- locomotion --- neurotransmitters and motor control --- autonomic function --- spinal cord injury --- movement-related disorders --- pain

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Traumatic injury of the spinal cord affects the entire organism directly and indirectly. Primary injury destroys neurons and severs axons which participate in neural circuits. Secondary injuries and pathologies arise from numerous sources including systemic inflammation, consequential damage of cutaneous, muscular, and visceral tissues, and dysregulation of autonomic, endocrine and sensory-motor functions. Evidence is mounting that spinal cord injury (SCI) affects regions of the nervous system spatially remote from the injury site, as well as peripheral tissues, and alters some basic characteristics of primary afferent cell biology and physiology (cell number, size/frequency, electrophysiology, other). The degree of afferent input and processing above the lesion is generally intact, while that in the peri-lesion area is highly variable, though pathologies emerge in both regions, including a variety of pain syndromes. Primary afferent input to spinal regions below the injury and the processing of this information becomes even more important in the face of complete or partial loss of descending input because such spared sensory processing can lead to both adaptive and pathological outcomes. This issue hosts review and research articles considering mechanisms of plasticity of primary afferent neurons and sensory processing after SCI, and how such plasticity contributes to sparing and/or recovery of functions, as well as exacerbation of existing and/or emergent pathologies. A critical issue for the majority of the SCI community is chronic above-, peri-, and below-level neuropathic pain, much of which may arise, at least in part, from plasticity of afferent fibers and nociceptive circuitry. For example, autonomic dysreflexia is common hypertensive syndrome that often develops after SCI that is highly reliant on maladaptive nociceptive sensory input and processing below the lesion. Moreover, the loss of descending input leaves the reflexive components of bladder/bowel/sexual function uncoordinated and susceptible to a variety of effects through afferent fiber plasticity. Finally, proper afferent feedback is vital for the effectiveness of activity-dependent rehabilitative therapies, but aberrant nociceptive input may interfere with these approaches since they are often unchecked due to loss of descending modulation.

Spinal cord. --- Sensory neurons. --- Neurons --- Central nervous system --- sensory systems --- sensory neurons --- sensory plasticity --- spinal cord injury (SCI) --- sensory perceptions

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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.We are looking for the original work, data supported findings, as well as comprehensive review articles that map out what is and is not possible in this filed in the near and far future.

Brain-computer interfaces. --- BCIs (Brain-computer interfaces) --- Brain-machine interfaces --- Computer-brain interfaces --- Direct neural interfaces --- User interfaces (Computer systems) --- spinal cord injury --- Stroke --- Brain Computer Interface --- amyothopic lateral sclerosis --- Rehabilitation --- Cerebral Palsy --- Patients --- autism

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Spinal cord injury (SCI) leads to paralysis, sensory, and autonomic nervous system dysfunctions. However, the pathophysiology of SCI is complex, and not limited to the nervous system. Indeed, several other organs and tissue are also affected by the injury, directly or not, acutely or chronically, which induces numerous health complications. Although a lot of research has been performed to repair motor and sensory functions, SCI-induced health issues are less studied, although they represent a major concern among patients. There is a gap of knowledge in pre-clinical models studying these SCI-induced health complications that limits translational applications in humans. This reprint describes several aspects of the pathophysiology of spinal cord injuries. This includes, but is not limited to, the impact of SCI on cardiovascular and respiratory functions, bladder and bowel function, autonomic dysreflexia, liver pathology, metabolic syndrome, bones and muscles loss, and cognitive functions.

Medicine --- Neurosciences --- micturition --- external urethral sphincter --- spinal cord injury --- serotonin --- electromyogram --- fecal microbiota transplant --- inflammation --- anxiety --- rehabilitation --- autonomic dysreflexia --- immune dysfunction --- SCI-IDS --- primary afferents --- nociceptor --- reach-to-grasp --- forelimb function --- upper extremity function --- cardiovascular --- contusion --- neuroplasticity --- osteopenia --- bone loss --- recovery of function --- monoamines --- GABA --- neuromodulation --- pain --- spasticity --- ionic plasticity --- repetitive transcranial magnetic stimulation --- phrenic motor network --- motoneuron excitability --- diaphragm muscle --- spinal cord injury severity --- cardiometabolic disease --- liver and cardiac dysfunctions --- fibrosis --- pathophysiology --- oxidative stress --- contusion model --- respiratory function --- diaphragmatic activity --- phrenic motoneurons --- neuroinflammation --- cytokines --- tumor necrosis factor --- immune cells --- microglia