Journal of neurotrauma
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Journal of neurotrauma · Jun 2019
Earlier Decompression (< 8 hours) Results in Better Neurological and Functional Outcome After Traumatic Thoracolumbar Spinal Cord Injury.
The optimal timing of surgical intervention following spinal cord injury (SCI) remains under debate. Recent studies indicate a potential neurological and functional benefit of early surgery (< 8 h) after cervical SCI. For thoracolumbar SCI syndromes, fewer studies exist. ⋯ Here, we observed improved bladder outcome (i.e., SCIM-6 sub-item; p < 0.021) and a trend towards better functional bowel management (i.e., SCIM-7; p < 0.090). Linear regression models showed that early surgery was an independent predictor for higher AIS shifts and improved total SCIM difference. Our data suggests that prompt surgical management after thoracolumbar SCI might have a positive impact on the functional and neurological outcome.
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Spinal cord injury (SCI) interrupts the brain-body input-output exchange and modifies the mental representation of disconnected body parts, with decreased reliance on sensorimotor aspects of body representation and increased weighting of visuospatial ones. We hypothesized that physiotherapy-related benefits might extend to the re-establishment of the typical interplay between these two types of strategies. ⋯ Results showed that only after physiotherapy the individuals with SCI showed the sensorimotor biomechanical effect (orientation-dependent modulation of response times) for the mental rotation of foot images (absent in pre-physiotherapy). This highlights that body representation is adaptable to contingent conditions, in that the reliance on sensorimotor or visuospatial strategies can be altered and, at least partially, restored as a function of physiotherapy.
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Journal of neurotrauma · Jun 2019
Altered amniotic fluid levels of hyaluronic acid in fetal rats with myelomeningocele: understanding spinal cord injury.
Myelomeningocele (MMC) is a devastating congenital neural tube defect that results in the exposure of spinal cord to the intrauterine environment, leading to secondary spinal cord injury and severe impairment. Although the mechanisms underlying the secondary pathogenesis are clinically relevant, the exact cause of in utero-acquired spinal cord damage remains unclear. The objective of this study was to determine whether the hyaluronic acid (HA) concentration in amniotic fluid (AF) in the retinoic acid-induced model of MMC is different from that in normal controls and whether these differences could have an impact on the viscosity of AF. ⋯ No HA-degrading activity was detected in MMC-AF. In summary, we identified a deficiency in the AF level of HA and the viscosity of AF in fetal rats with MMC. These data are discussed in relation to a potential role the reduction in the AF viscosity due to the low level of HA may play in the exacerbating effects of mechanical trauma on spinal cord damage at the MMC lesion site.
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Journal of neurotrauma · Jun 2019
Peripheral inflammation accelerates the onset of mechanical hypersensitivity after spinal cord injury and engages TNFα signaling mechanisms.
Previously, we showed that noxious stimulation of the tail produces numerous detrimental effects after spinal cord injury (SCI), including an earlier onset and increased magnitude of mechanical hypersensitivity. Expanding on these observations, this study sought to determine whether localized peripheral inflammation similarly impacts the expression of mechanical hypersensitivity after SCI. Adult rats received a moderate contusion injury at the thoracic level (Tl0) or sham surgery, and were administered complete Freund's adjuvant (CFA) or vehicle in one hindpaw 24 hours later. ⋯ Expression levels of c-fos, tumor necrosis factor α (TNFα), TNF receptors, and members of the TNFα signaling pathway such as caspase 8 and phosphorylated extracellular related kinase (pERK) were preferentially upregulated in the lumbar spinal cord of SCI-CFA rats. Meanwhile, c-jun was significantly increased in both CFA-treated groups. Overall, these results together with our previous reports, suggest that peripheral noxious input after SCI facilitates the development of pain by mechanisms that may require TNFα signaling.
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Journal of neurotrauma · Jun 2019
Plasticity induced recovery of breathing occurs at chronic stages after cervical contusion.
Severe midcervical contusion injury causes profound deficits throughout the respiratory motor system that last from acute to chronic time points post-injury. We use chondroitinase ABC (ChABC) to digest chondroitin sulphate proteoglycans within the extracellular matrix (ECM) surrounding the respiratory system at both acute and chronic time points post-injury to explore whether augmentation of plasticity can recover normal motor function. We demonstrate that, regardless of time post-injury or treatment application, the lesion cavity remains consistent, showing little regeneration or neuroprotection within our model. ⋯ To further understand this effect, we assessed the anatomical mechanism of this recovery. Increased EMG activity in previously paralyzed muscles was brought about by activation of spared bulbospinal pathways through the site of injury and/or sprouting of spared serotonergic fibers from the contralateral side of the cord. Accordingly, we demonstrate that alterations to the ECM and augmentation of plasticity at chronic time points post-cervical contusion can cause functional recovery of the respiratory motor system and reveal mechanistic evidence of the pathways that govern this effect.