Journal of neurotrauma
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Journal of neurotrauma · Dec 2009
Both hypoxemia and extreme hyperoxemia may be detrimental in patients with severe traumatic brain injury.
An association between hypoxemia and poor outcomes from traumatic brain injury (TBI) is well documented. However, it is unclear whether hyperoxygenation is beneficial. This registry-based analysis explores the relationship between early hypoxemia and hyperoxemia on outcome from moderate-to-severe TBI. ⋯ Logistic regression revealed an optimal Po(2) range (110-487 mm Hg), with an independent association observed between decreased survival and both hypoxemia (OR 0.54; 95% CI 0.42, 0.69; p < 0.001) and extreme hyperoxemia (OR 0.50; 95% CI 0.36, 0.71; p < 0.001). The association between hypoxemia and extreme hyperoxemia and worse outcomes was also present with use of "good outcomes" as the outcome variable (discharge to home, rehabilitation, jail, or psychiatric facility, or leaving against medical advice). We conclude that both hypoxemia and extreme hyperoxemia are associated with increased mortality and a decrease in good outcomes among TBI patients.
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Journal of neurotrauma · Dec 2009
Lack of axonal sprouting of spared propriospinal fibers caudal to spinal contusion injury is attributed to chronic axonopathy.
We have previously shown that a small percentage of long descending propriospinal tract (LDPT) axons are spared, whereas few short thoracic propriospinal (TPS) fibers survive 2 weeks following severe (50 mm weight drop) low thoracic spinal cord contusion injury (SCI). Here, we extended those findings to a moderate (25 mm weight drop) T9 SCI and assessed the effects of this lesion severity on propriospinal tract fibers at different time periods after injury. We anterogradely labeled fibers with fluororuby (FR) or WGA-HRP to determine their location and number 2, 4, 6, and 16 weeks post-SCI. ⋯ One striking difference in the WGA-HRP experimental operates was the increased density of labeling of spared axons within the white matter caudal to the injury compared to controls. This labeling pattern was reminiscent of the labeling found after axotomy in studies by others, and raises a question as to contusion injury-induced impaired axonal transport. We hypothesize that axonal sprouting of axons after partial spinal cord injury seen in previous investigations was not found in the present investigation because of the additional pathological effects of contusion injury, similar to what is observed after traumatic brain injury.
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Journal of neurotrauma · Dec 2009
Blast-related brain injury: imaging for clinical and research applications: report of the 2008 st. Louis workshop.
Blast-related traumatic brain injury (bTBI) and post-traumatic stress disorder (PTSD) have been of particular relevance to the military and civilian health care sectors since the onset of the Global War on Terror, and TBI has been called the "signature injury" of this war. Currently there are many questions about the fundamental nature, diagnosis, and long-term consequences of bTBI and its relationship to PTSD. This workshop was organized to consider these questions and focus on how brain imaging techniques may be used to enhance current diagnosis, research, and treatment of bTBI. ⋯ Foremost among our recommendations is that human autopsy and pathoanatomical data from bTBI patients need to be obtained and disseminated to the military and civilian research communities, and advanced neuroimaging used in studies of acute, subacute, and chronic cases, to determine whether there is a distinct pathoanatomical signature that correlates with long-term functional impairment, including PTSD. These data are also critical for the development of animal models to illuminate fundamental mechanisms of bTBI and provide leads for new treatment approaches. Brain imaging will need to play an increasingly important role as gaps in the scientific knowledge of bTBI and PTSD are addressed through increased coordination, cooperation, and data sharing among the academic and military biomedical research communities.
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Journal of neurotrauma · Nov 2009
ReviewReorganization and preservation of motor control of the brain in spinal cord injury: a systematic review.
Reorganization of brain function in people with CNS damage has been identified as one of the fundamental mechanisms involved in the recovery of sensorimotor function. Spinal cord injury (SCI) brain mapping studies during motor tasks aim for assessing the reorganization and preservation of brain networks involved in motor control. Revealing the activation of cortical and subcortical brain areas in people with SCI can indicate principal patterns of brain reorganization when the neurotrauma is distal to the brain. ⋯ In addition, several aspects of reorganization of brain function following SCI resembled those reported in stroke. This review demonstrates that brain networks involved in different demands of motor control remain responsive even in chronic paralysis. These findings imply that therapeutic strategies aimed at restoring spinal cord function, even in people with chronic SCI, can build on preserved competent brain control.
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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.