Neuroscience
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Injury to the adult nervous system promotes the expression and secretion of brain-derived neurotrophic factor (BDNF). Because it promotes neuronal growth, survival and neurogenesis, BDNF may initiate compensatory processes that mitigate the deleterious effects of injury, disease or stress. Despite this, BDNF has been implicated in several injury-induced maladaptive processes including pain, spasticity and convulsive activity. ⋯ BDNF effects are confined to changes in synaptic transmission as there is little change in the passive or active properties of neurons in the superficial dorsal horn. Actions of BDNF in the brain stem and periphery also contribute to the onset and persistence of chronic pain. In spite of its role in compensatory processes that facilitate the recovery of the nervous system from injury, the widespread maladaptive actions of BDNF mean that there is literally "no gain without pain".
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Loudness is the primary perceptual correlate of sound intensity. The relationship between sound intensity and loudness is not fixed, and can be modified by short-term sound deprivation or stimulation. ⋯ Although there is sufficient evidence to conclude that loudness can be modulated in normal hearing listeners by temporary sound deprivation and stimulation, evidence is scanter for the hearing-impaired listeners. In addition, cortical effects of sound deprivation and stimulation in humans, which may correlate with loudness coding, are still largely unknown and should be the target of future research.
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Multiple sclerosis (MS) is a chronic neurological disease characterized by inflammation and degeneration within the CNS. Over the course of the disease, most MS patients successively accumulate inflammatory lesions, axonal damage, and a rather diffuse CNS pathology, along with an increasing degree of disability. Pharmacological treatment options which are currently approved for MS aim at limiting inflammation and decreasing the relapse rate, or at simply relieving symptoms. ⋯ In addition, and probably closest to rehabilitative approaches, practice-induced plasticity has been probed in a few studies. Altogether, there is growing evidence for a preservation of rapid-onset motor plasticity and for functionally relevant chronic reorganization processes, which might be limited by high CNS injury in advanced stages of the disease. Clinical implications of these findings with regard to the development and optimization of rehabilitative treatments in MS are discussed, as well as open questions which need to be addressed by future studies.
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Brain-derived neurotrophic factor, BDNF, is one of the most important neurotrophic factors acting in the peripheral and central nervous system. In the auditory system its function was initially defined by using constitutive knockout mouse mutants and shown to be essential for survival of neurons and afferent innervation of hair cells in the peripheral auditory system. Further examination of BDNF null mutants also revealed a more complex requirement during re-innervation processes involving the efferent system of the cochlea. ⋯ Additionally, BDNF is required for maintenance of voltage-gated potassium channels (KV) in cochlear neurons, which may form part of a maturation step within the ascending auditory pathway with onset of hearing and might be essential for cortical acuity of sound-processing and experience-dependent plasticity. A presumptive harmful role of BDNF during acoustic trauma and consequences of a loss of cochlear BDNF during aging are discussed in the context of a partial reversion of this maturation step. We compare the potentially beneficial and harmful roles of BDNF for the mature auditory system with those BDNF functions known in other sensory circuits, such as the vestibular, visual, olfactory, or somatosensory system.
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Hyperglycemia is a common phenomenon in the early phase of brain injury (BI). The management of blood glucose levels after BI, however, is subject of a growing debate. ⋯ Intensive glucose-lowering therapy, on the other hand, inevitably results in an increased rate of hypoglycemic episodes with detrimental effects on the injured brain. In this review, we give an overview on the current knowledge about causes and pathophysiological consequences of dysglycemia in patients with BI and offer some suggestions for clinical glucose management.