Neuroscience
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This review covers the main principles of the Lund concept for treatment of severe traumatic brain injury. This is followed by a description of results of clinical studies in which this therapy or a modified version of the therapy has been used. ⋯ The non-randomized studies indicated that the Lund concept is beneficial for outcome. The two randomized studies were small but showed better outcome in the groups of patients treated according to the modified principles of the Lund concept than in the groups given a more conventional treatment.
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Plasticity constitutes the basis of behavioral changes as a result of experience. It refers to neural network shaping and re-shaping at the global level and to synaptic contacts remodeling at the local level, either during learning or memory encoding, or as a result of acute or chronic pathological conditions. 'Plastic' brain reorganization after central nervous system lesions has a pivotal role in the recovery and rehabilitation of sensory and motor dysfunction, but can also be "maladaptive". Moreover, it is clear that brain reorganization is not a "static" phenomenon but rather a very dynamic process. ⋯ We will briefly discuss these dependencies, trying to highlight their translational value. Overall, it is not only necessary to better understand how the brain can reorganize after injury with or without therapy, it is also necessary to clarify when and why brain reorganization can be either "good" or "bad" in terms of its clinical consequences. This information is critical in order to develop and optimize cost-effective therapies to maximize functional recovery while minimizing maladaptive states after spinal cord injury.
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Stress is an adaptive response to demands of the environment and thus essential for survival. Exposure to stress triggers hypothalamic-pituitary-adrenocortical (HPA) axis activation and associated neurochemical reactions, following glucocorticoid release from the adrenal glands, accompanied by rapid physiological responses. Stimulation of this pathway results in the activation of specific brain regions, including the hippocampus, amygdala and prefrontal cortex which are enriched with glucocorticoid receptors (GRs). ⋯ Whereas an optimal stress level leads to enhancement of memory performance, the exposure to extreme, traumatic or chronic stressors is a risk factor for psychopathologies which are associated with memory impairment and cognitive deficits such as posttraumatic stress disorder (PTSD). In this review article, we will outline the implications of stress exposure on memory formation involving the role of glucocorticoids and BDNF. Within this context, potential adverse effects of neuroplastic alterations will be discussed using the example of PTSD.
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Brain injuries such as focal stroke initiate a myriad of neural events leading to local and remote alterations in cerebral networks. The neurochemical and neurophysiological mechanisms underlying these postlesion changes raise the question of their beneficial or adverse effects on functional recovery. In this review, we aim to reconcile findings from animal and patients studies using a "from cellular-to network-levels" perspective to gain further insights into the neuroplasticity mechanisms underlying recovery of sensorimotor functions. Ultimately, an integrative view of the multiple facets of poststroke changes should give an impetus to novel neurorehabilitation strategies by providing evidence of how neuroscience findings can be translated and operationalized within the context of restorative stroke.
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Nogo-A interaction with its different receptors (Nogo receptor 1 (NgR1), S1P receptor 2 (S1PR2), paired immunoglobulin-like receptor B (PirB)) restricts plasticity and growth-dependent processes leading, via the activation of different signaling pathway to the stabilization of the neuronal networks (either developmentally or during processes of memory consolation in the mature nervous system). Taking away these molecular brakes might allow for the induction of extensive structural and functional rearrangements and might promote compensatory growth processes after an injury of the CNS, in cortical structures as well as in the spinal cord. However, it is important to keep in mind that this could as well be a dangerous endeavor, since it might facilitate unwanted and unnecessary (and probably even maladaptive) neuronal connections.