Front Hum Neurosci
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Several studies have shown that mirrored arm or leg movements can induce altered body sensations. This includes the alleviation of chronic pain using congruent mirror feedback and the induction of abnormal sensation in healthy participants using incongruent mirror feedback. Prior research has identified neuronal and conceptual mechanisms of these phenomena. With the rising application of behavior-based methods for pain relief, a structured investigation of these reported effects seems necessary. ⋯ These results suggest that, while all mirrored hand movements induce abnormal body perceptions, the experience of an extra limb is most pronounced in the incongruent mirror movement condition. The frequent sensation of having a third arm may be related to brain processes designed to integrate input from several senses in a meaningful manner. Painful sensations are not more frequent or intense when a mirror is present.
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Patients with chronic pain often show disturbances in their body perception. Understanding the exact role played by pain is however complex, as confounding factors can contribute to the observed deficits in these clinical populations. To address this question, acute experimental pain was used to test the effect of lateralized pain on body perception in healthy subjects. ⋯ These opposite patterns suggest that the shift in SBM is likely to be specifically linked to the stimulation modality. It is concluded that acute experimental pain can induce an SBM shift toward the stimulated side, which might be functionally beneficial to protect the painful area of the body. Interestingly, it appears to be easier to bias SBM toward the right side, regardless of the modality and of the stimulated side.
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Neural mechanisms underlying nociception and pain perception are considered to serve the ultimate goal of limiting tissue damage. However, since pain usually occurs in complex environments and situations that call for elaborate control over behavior, simple avoidance is insufficient to explain a range of mammalian pain responses, especially in the presence of competing goals. In this integrative review we propose a Predictive Regulation and Action (PRA) model of acute pain processing. ⋯ The PRA model centers on neural substrates supporting the predictive nature of pain processing, as well as on finely-calibrated yet versatile regulatory processes that ultimately affect behavior. We outline several operational categories of pain behavior, from spinally-mediated reflexes to adaptive voluntary action, situated at various neural levels. An implication is that neural processes that track potential tissue damage in terms of behavioral consequences are an integral part of pain perception.
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Depending on severity, traumatic brain injury (TBI) induces immediate neuropathological effects that in the mildest form may be transient but as severity increases results in neural damage and degeneration. The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase. ⋯ Neuroimaging quantification in TBI demonstrates degenerative effects from brain injury over time. An adverse synergistic influence of TBI with aging may predispose the brain injured individual for the development of neuropsychiatric and neurodegenerative disorders long after surviving the brain injury.
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Chronic traumatic encephalopathy (CTE) is the term coined for the neurodegenerative disease often suspected in athletes with histories of repeated concussion and progressive dementia. Histologically, CTE is defined as a tauopathy with a distribution of tau-positive neurofibrillary tangles (NFTs) that is distinct from other tauopathies, and usually shows an absence of beta-amyloid deposits, in contrast to Alzheimer's disease (AD). Although the connection between repeated concussions and CTE-type neurodegeneration has been recently proposed, this causal relationship has not yet been firmly established. Also, the prevalence of CTE among athletes with multiple concussions is unknown. ⋯ Our case studies highlight that not all athletes with history of repeated concussions and neurological symptomology present neuropathological changes of CTE. These preliminary findings support the need for further research into the link between concussion and CTE as well as the need to expand the research to other possible causes of taupathy in athletes. They point to a critical need for prospective studies with good sampling methods to allow us to understand the relationship between multiple concussions and the development of CTE.