Journal of neurotrauma
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Journal of neurotrauma · Apr 2022
Randomized Controlled TrialCervicovestibular Rehabilitation in Adults with Mild Traumatic Brain Injury: A Randomised Clinical Trial.
The objective of this study was to compare the effects of a cervicovestibular rehabilitation program combined with symptom-limited aerobic exercise (SLAE) program to a SLAE program alone in adults with persistent symptoms after mild traumatic brain injury (mTBI) on severity of symptoms and other indicators of clinical recovery. In this single-blind, parallel-group randomized controlled trial, 60 adults with persistent symptoms after mTBI were randomly assigned to: (1) a 6-week SLAE program or (2) a 6-week cervicovestibular rehabilitation program combined with a SLAE program. All participants took part in four evaluation sessions (baseline, week 6, 12, and 26) performed by a blinded evaluator. ⋯ For PCSS, NPRS, NDI, HDI, DHI, and return to function, there were no group-by-time interactions at any time points follow-up (p > 0.05); clinically significant time effects were, however, observed (p < 0.05). There were group-by-time interactions at weeks 6 and 12 for vestibulo-ocular reflex (p < 0.003) and the craniovertebral mobility (p < 0.001) measures in favor of the cervicovestibular rehabilitation group. The study indicates that a cervicovestibular rehabilitation program combined with SLAE was not superior to a SLAE program alone in term of symptoms and functional level improvement but resulted in improved physical cervical and vestibular function.
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Journal of neurotrauma · Apr 2022
Dysfunctional ER-mitochondrion coupling is associated with ER stress-induced apoptosis and neurological deficits in a rodent model of severe head injury.
Cellular homeostasis requires critical communications between the endoplasmic reticulum (ER) and mitochondria to maintain the viability of cells. This communication is mediated and maintained by the mitochondria-associated membranes and may be disrupted during acute traumatic brain injury (TBI), leading to structural and functional damage of neurons and supporting cells. To test this hypothesis, we subjected male C57BL/6 mice to severe TBI (sTBI) using a controlled cortical impact device. ⋯ This enhanced coupling correlated closely with increases in the expression of the Ca2+ regulatory proteins (inositol 1,4,5-trisphosphate receptor type 1 [IP3R1], voltage-dependent anion channel 1 [VDAC1], glucose-regulated protein 75 [GRP75], Sigma 1 receptor [Sigma-1R]), production of ROS, degree of ER stress, levels of UPR, and release of proinflammatory cytokines. Further, the neurological function of sTBI mice was significantly improved by silencing the gene for the ER-mitochondrion tethering factor PACS2, restoring the IP3R1-GRP75-VDAC1 axis of Ca2+ regulation, alleviating mitochondria-derived oxidative stress, suppressing inflammatory response through the PERK/eIF2α/ATF4/CHOP pathway, and inhibiting ER stress and associated apoptosis. These results indicate that dysfunctional ER-mitochondrion coupling might be primarily involved in the neuronal apoptosis and neurological deficits, and modulating the ER-mitochondrion crosstalk might be a novel therapeutic strategy for sTBI.