Journal of neurotrauma
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Journal of neurotrauma · Nov 2010
Diffusion tensor imaging and fiber tractography of patients with cervical spinal cord injury.
To verify the usefulness of diffusion tensor imaging (DTI) and fiber tractography (FT) compared with routine magnetic resonance imaging (MRI) in patients with cervical spinal cord injury, and to clarify the relationship between motor and sensory impairments and DTI and FT parameters, we performed routine MRI and DTI on 10 patients with chronic cervical spinal cord injury and on 10 controls. Quantitative parameters of DTI, such as fractional anisotropy (FA) and apparent diffusion coefficient (ADC), were calculated for each cervical cord level. FT parameters of imaginary crossing fiber numbers were also determined at the C3 level, from C3-C6, and from C3-C7, as well as each connection rate. ⋯ In patients with cervical cord injury, abnormal cervical levels detected on routine MRI were not correlated with clinical findings and DTI parameters, but FA of DTI was correlated with motor function, as were imaginary crossing fiber numbers and connection rates of FT. Quantitative DTI and FT analyses were useful in the evaluation of patients with cervical spinal cord injury. The injured cervical spinal cord can be evaluated in more detail and more precisely using DTI and FT, for which findings are correlated with clinical findings such as neurological impairments.
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Journal of neurotrauma · Nov 2010
Prognostic influence and magnetic resonance imaging findings in paroxysmal sympathetic hyperactivity after severe traumatic brain injury.
Paroxysmal sympathetic hyperactivity (PSH) is a clinical syndrome affecting a subgroup of survivors of severe brain injury. In this study, the prevalence, magnetic resonance imaging (MRI) presentation, influence on the clinical course in the intensive care unit (ICU), and effect on neurological recovery of PSH were prospectively surveyed in 87 patients with severe traumatic brain injury (TBI). Cranial MRI was performed during the first 30 days after injury. ⋯ Patients with PSH had more deep lesions as shown on cranial MRI, significantly longer ICU stays, and worse outcomes. PSH was shown to be common among patients with severe TBI who also had deep intraparenchymal lesions. The mechanism by which PSH influences patient outcomes has yet to be defined, but we believe that it may be mediated by diencephalic-mesencephalic dysfunction or disconnection.
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Journal of neurotrauma · Nov 2010
Post-traumatic hypoxia exacerbates brain tissue damage: analysis of axonal injury and glial responses.
Traumatic brain injury (TBI) resulting in poor neurological outcome is predominantly associated with diffuse brain damage and secondary hypoxic insults. Post-traumatic hypoxia is known to exacerbate primary brain injury; however, the underlying pathological mechanisms require further elucidation. Using a rat model of diffuse traumatic axonal injury (TAI) followed by a post-traumatic hypoxic insult, we characterized axonal pathology, macrophage/microglia accumulation, and astrocyte responses over 14 days. ⋯ Extensive microglia/macrophage accumulation detected with the CD68 antibody was maximal at 14 days post-injury in the corpus callosum (macrophages 157.5 ± 55.48; microglia 72.71 ± 20.75), and coincided with regions of axonal damage. Astrocytosis assessed with glial fibrillary acidic protein (GFAP) antibody was also abundant in the corpus callosum and maximal at 14 days, with a trend toward an increase in TAI + Hx animals (18.99 ± 2.45 versus 13.56 ± 0.81; p = 0.0617). This study demonstrates for the first time that a hypoxic insult following TAI perpetuates axonal pathology and cellular inflammation, which may account for the poor neurological outcomes seen in TBI patients who experience post-traumatic hypoxia.
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Journal of neurotrauma · Nov 2010
Nogo receptor deletion and multimodal exercise improve distinct aspects of recovery in cervical spinal cord injury.
We tested the ability of two plasticity-promoting approaches to enhance recovery in a mouse model of incomplete spinal cord injury (SCI). Genetically, we reduced myelin-mediated inhibition of neural plasticity through Nogo66-receptor (NgR) gene deletion. Behaviorally, we utilized a novel multimodal exercise training paradigm. ⋯ Thus either NgR gene deletion or exercise training benefits mice with mild cervical spinal injury. In this lesion model, the effects of NgR deletion and training were not synergistic for the tasks assessed. Further work is required to optimize the interaction between pharmacological and physical interventions for SCI.
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Journal of neurotrauma · Nov 2010
Chondroitinase ABC enhances pericontusion axonal sprouting but does not confer robust improvements in behavioral recovery.
Traumatic brain injury (TBI) results in enduring functional deficits. Strategies aimed at promoting plasticity within the injured brain may aid in enhancing functional outcome. We have previously shown that spontaneous pericontusional axon sprouting occurs within 7-14 days after controlled cortical impact injury in the adult rat, but ultimately fails due to an increasingly growth-inhibitory environment. ⋯ There was no overall benefit on forelimb function during the time of maximal sprouting or at any subsequent times in three of four behavioral outcome measures. However, there was a chondroitinase-induced improvement in recovery from unskilled limb use deficits on the staircase forelimb reaching test toward sham-injured values at 28 days, which was not achieved by the vehicle-treated rats, indicating that there is some minor functional benefit of the increased sprouting induced by chondroitinase treatment. The current results, together with data from spinal cord injury models after chondroitinase intervention, suggest that a combinatorial approach with the addition of neurotrophins and rehabilitation would result in more robust axon sprouting and consequently improve behavioral outcome.