Journal of neurotrauma
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Journal of neurotrauma · Apr 2015
Transplantation of adipocyte-derived stem cells in a hydrogel scaffold for the repair of cortical contusion injury in rats.
Adipocyte-derived stem cells have emerged as a novel source of stem cell therapy for their autologous and readily accessible and pluripotent potential to differentiate into different lineages such as neural stem cells (NSCs) and endothelial progenitor cells (EPCs). Transplantation of NSCs and EPCs has been promising for the repair of brain injury. We explored using co-transplanted hydrogel scaffold to improve the survival of the transplanted cells and recovery of neurological function. ⋯ Using immunostaining, we have shown that while transplanted NSCs differentiated into both neurons and astrocytes, the EPCs were incorporated into vessel epithelia. The extent of reactive gliosis (based on glial fibrillary acidic protein immunostaining) was significantly reduced in all treatment groups (NSC-EPC-hydrogel, NSC-hydrogel, and EPC-hydrogel) when compared with the saline group, with the highest reduction in the NSC-EPC-hydrogel transplantation group. Thus, co-transplantation of hydrogel scaffold provides a more conducive environment for the survival and differentiation of NSCs and EPCs at the site of brain injury, leading to improved vascularization and better recovery of neurological function.
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Journal of neurotrauma · Apr 2015
ReviewThe manifestation of anxiety disorders after traumatic brain injury: A review.
The development of anxiety disorders after a traumatic brain injury (TBI) is a strong predictor of social, personal, and work dysfunction; nevertheless, the emergence of anxiety has been largely unexplored and poorly understood in the context of TBI. This article provides an overview of the limited published research to date on anxiety disorders that are known to develop after TBI, including post-traumatic stress disorder, generalized anxiety disorder, obsessive-compulsive disorder, panic disorder, specific phobia, and social anxiety disorder. ⋯ Putative neural correlates will be reviewed where known. A discussion of current treatment options and avenues for further research are explored.
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Journal of neurotrauma · Apr 2015
Multicenter StudyCould a traumatic epidural hematoma on early CT tell us about its future development? A multi-center retrospective study in China.
Our aim for this study was to quantitatively develop an early epidural hematoma (EDH) natural evolutionary curve and assess association of the most common radiological signs of initially nonsurgical supratentorial EDHs on early computed tomography (CT), in addition to their CT time for EDH enlargement. We retrospectively reviewed pertinent data of supratentorial EDH cases with CT ≤ 6 h postinjury (1997-2013) in three medical institutions in Shanghai. Cases involved were divided into six groups according to their initial CT time postinjury (≤ 1, 1-2, 2-3, 3-4, 4-5, and 5-6 h for groups 1 through 6, respectively). ⋯ Multi-variate analysis succeeded in determining two risk factors for EDH enlargement ≥ 30 mL and EDH enlargement requiring an operation for EDH cases with an early CT/EDH volume >10 mL on CT performed ≤ 2 h and EDH located at the temporal or temporoparietal region on CT ≤ 1 h post brain injury. Using recursive partitioning analysis, "high-risk" identification criteria were derived to predict EDH enlargement ≥ 30 mL with sensitivity of 90.5% (95% confidence interval [CI], 77.9-96.2), specificity of 60.1% (95% CI, 54.3-65.7), and EDH enlargement requiring surgery with sensitivity of 100.0% (95% CI, 89.9-100.0), and specificity of 59.9% (95% CI, 54.1-65.4). A redo-CT 5 ∼ 6 h post impact for cases at high risk is recommended.
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Journal of neurotrauma · Apr 2015
Early cortical thickness changes after mild traumatic brain injury following motor vehicle collision.
In a motor vehicle collision (MVC), survivors often receive mild traumatic brain injuries (mTBI). Although there have been some reports of early white matter changes after an mTBI, much less is known about early cortical structural changes. To investigate early cortical changes within a few days after an MVC, we compared cortical thickness of mTBI survivors with non-mTBI survivors, then reexamined cortical thickness in the same survivors 3 months later. ⋯ After 3 months, cortical thickness had decreased in left rMFG in the mTBI group but not in the non-mTBI group. The cortical thickness of the right precuneus region in the initial scans was positively correlated with acute traumatic stress symptoms for all survivors and with the number of reduced activity days for mTBI survivors who completed the follow-up. The preliminary results suggest that alterations in cortical thickness may occur at an early stage of mTBI and that frontal cortex structure may change dynamically over the initial 3 months after mTBI.
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Journal of neurotrauma · Apr 2015
Inhibition of injury-induced cell proliferation in the dentate gyrus of the hippocampus impairs spontaneous cognitive recovery following traumatic brain injury.
Neurogenesis persists throughout life in the neurogenic regions of the mature mammalian brain, and this response is enhanced after traumatic brain injury (TBI). In the hippocampus, adult neurogenesis plays an important role in hippocampal-dependent learning and memory functions and is thought to contribute to the spontaneous cognitive recovery observed after TBI. Utilizing an antimitotic agent, arabinofuranosyl cytidine (Ara-C), the current study investigated the direct association of injury-induced hippocampal neurogenesis with cognitive recovery. ⋯ We found that a 7-day infusion of Ara-C significantly reduced the total number of BrdU(+) and DCX(+) cells in the dentate gyrus (DG) in both hemispheres. Moreover, inhibition of the injury-induced cell proliferative response in the DG completely abolished the innate cognitive recovery on MWM performance at 56-60 days postinjury. These results support the causal relationship of injury-induced hippocampal neurogenesis on cognitive functional recovery and suggest the importance of this endogenous repair mechanism on restoration of hippocampal function.