Journal of neurotrauma
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Journal of neurotrauma · Nov 2009
Randomized Controlled TrialProtective effect of moderate hypothermia on severe traumatic brain injury in children.
This study investigated the safety and neuroprotective effect of moderate hypothermia in children with severe traumatic brain injury (TBI). Twenty-two children suffering from TBI were randomly divided into groups treated with moderate hypothermia (intracranial temperature of 34.5 +/- 0.2 degrees C, maintained for 72 h, n = 12) or normothermia (intracranial temperature of 38.0 +/- 0.5, n = 10). The cerebrospinal fluid levels of neuron-specific enolase (NSE), S-100, brain-specific creatine kinase (CK-BB), and intracranial pressure (ICP) levels were used to assess the protective effects. ⋯ In the moderate hypothermia group, the pH and electrolyte balance at the end of the monitoring period were normal, but the heart rates were lower (p < 0.05). There were a total of three deaths (13.6%) in this study: one in the moderate hypothermia group (8.3%) and two in the normothermia group (20%). In conclusion, moderate hypothermia provided neuronal protection for children with severe TBI, and maintaining the intracranial temperature at 34.5 degrees C for 72 h was safe in this clinical setting.
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Journal of neurotrauma · Nov 2009
A panel of neuron-enriched proteins as markers for traumatic brain injury in humans.
Surrogate markers have enormous potential for contributing to the diagnosis, prognosis, and therapeutic evaluation of acute brain damage, but extensive prior study of individual candidates has not yielded a biomarker in widespread clinical practice. We hypothesize that a panel of neuron-enriched proteins measurable in cerebrospinal fluid (CSF) and blood should vastly improve clinical evaluation and therapeutic management of acute brain injuries. Previously, we developed such a panel based initially on the study of protein release from degenerating cultured neurons, and subsequently on rodent models of traumatic brain injury (TBI) and ischemia, consisting of 14-3-3beta, 14-3-3zeta, three distinct phosphoforms of neurofilament H, ubiquitin hydrolase L1, neuron-specific enolase, alpha-spectrin, and three calpain- and caspase-derived fragments of alpha-spectrin. ⋯ Whereas different markers peaked coordinately, the time to peak varied across TBI cases from 24-96 h post-injury. In serum, TBI increased all four members of the marker panel for which sandwich immunoassays are currently available: a calpain-derived NH(2)-terminal alpha-spectrin fragment and the three neurofilament H phosphoforms. Our results identify neuron-enriched proteins that may serve as a panel of CSF and blood surrogate markers for the minimally invasive detection, management, mechanistic, and therapeutic evaluation of human TBI.
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Journal of neurotrauma · Nov 2009
Conversion in ASIA impairment scale during the first year after traumatic spinal cord injury.
The neurological severity of a spinal cord injury (SCI) is commonly classified according to the American Spinal Injury Association (ASIA) Impairment Scale (AIS). The aim of this study was to assess the course of the AIS following SCI, and to discern the nature of any changes in the classification that occur. Assessments were performed in a European cohort of SCI patients within 2 weeks and at 1, 3, 6, and 12 months after the initial injury. ⋯ When the AIS remained unchanged between successive assessment points, there was no change in the number of muscles graded three or more (NMG3(+)) in 73% of the transitions. An improvement in AIS was associated with a gain in NMG3(+) in 49% of the transitions, while an aggravation in AIS was accompanied by a loss in NMG3(+) in 10% of the transitions. These results, documenting a substantial amount of spontaneous AIS conversions, should be taken into consideration when designing clinical trials to assess the effects of potential new treatments for SCI.
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Journal of neurotrauma · Nov 2009
Difficulty of elderly SCI subjects to translate motor recovery--"body function"--into daily living activities.
The objective of this retrospective analysis was to determine whether outcome of body functions and activities as well as length of stay of inpatient rehabilitation is related to age in patients with traumatic spinal cord injury (SCI). Data were collected from a European network of 17 SCI rehabilitation centers (EM-SCI); a total of 237 traumatic SCI subjects were included. Assessments were performed at 1, 6, and 12 months after SCI. ⋯ Length of stay was not associated with age. It was concluded that age is an important determining factor for functional outcome after SCI and that elderly patients have difficulties in translating an improvement in neurological outcome into functional changes. Therefore, rehabilitation approaches in elderly subjects should focus on functional training.
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Journal of neurotrauma · Nov 2009
Human amnion-derived multipotent progenitor cell treatment alleviates traumatic brain injury-induced axonal degeneration.
To identify a viable cell source with potential neuroprotective effects, we studied amnion-derived multipotent progenitor (AMP) cells in a rat model of penetrating ballistic-like brain injury (PBBI). AMP cells were labeled with fluorescent dye PKH26 and injected in rats immediately following right hemispheric PBBI or sham PBBI surgery by ipsilateral i.c.v. administration. At 2 weeks post-injury, severe necrosis developed along the PBBI tract and axonal degeneration was prominent along the corpus callosum (cc) and in the ipsilateral thalamus. ⋯ None of the labeled AMP cells appeared to express neural differentiation, as evidenced by the lack of double labeling with nestin, S-100, GFAP, and MAP-2 immunostaining. In conclusion, AMP cell migration was specifically induced by PBBI and requires SVZ homing, yet the neuroprotective effect of intracerebral ventrical treatment using AMP cells was not limited to the area where the cells were present. This suggests that the attenuation of the secondary brain injury following PBBI was likely to be mediated by mechanisms other than cell replacement, possibly through delivery or sustained secretion of neurotrophic factors.