Neuroscience
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The gate control theory proposed that the nociceptive sensory information transmitted to the brain relies on an interplay between the inputs from nociceptive and non-nociceptive primary afferent fibers. Both inputs are normally under strong inhibitory control in the spinal cord. ⋯ However, under pathological conditions, this spinal inhibition may be altered and lead to chronic pain. This review summarizes our knowledge of presynaptic inhibition in pain control, with particular focus on how its alteration after nerve or tissue injury contributes to neuropathic or inflammatory pain syndromes, respectively.
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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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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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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.