Journal of neurotrauma
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Journal of neurotrauma · May 2010
What contributes to quality of life in adult survivors of childhood traumatic brain injury?
Adult outcome from childhood brain injury is largely unknown, and health professionals have minimal evidence available to inform families about their child's long-term prognosis. This study aimed to investigate long-term outcomes in this group, focusing on quality of life (QOL) and the injury, developmental, and environmental factors that influence this domain, using a retrospective and cross-sectional design. The sample was ascertained via medical record audit at the Royal Children's Hospital, Melbourne, Australia, and included 130 adult survivors of child traumatic brain injury (TBI) (84 men). ⋯ While most adult survivors of childhood TBI rated their QOL as intact, 17% of the sample reported poor QOL. Poor QOL was more likely with low levels of perceived independence, severe TBI, younger age at injury, failure to complete high school, and psychological problems. In conclusion, QOL in adult survivors of childhood TBI is better than expected and closely associated with both injury and noninjury factors, most consistently with the individual's perception of their level of independence.
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Journal of neurotrauma · May 2010
Diffuse brain injury elevates tonic glutamate levels and potassium-evoked glutamate release in discrete brain regions at two days post-injury: an enzyme-based microelectrode array study.
Traumatic brain injury (TBI) survivors often suffer from a wide range of post-traumatic deficits, including impairments in behavioral, cognitive, and motor function. Regulation of glutamate signaling is vital for proper neuronal excitation in the central nervous system. Without proper regulation, increases in extracellular glutamate can contribute to the pathophysiology and neurological dysfunction seen in TBI. ⋯ The amplitudes of KCl-evoked glutamate release were increased significantly only in the striatum after moderate injury, with a 249% increase seen in the dorsal striatum. Thus, with the MEAs, we measured discrete regional changes in both tonic and KCl-evoked glutamate signaling, which were dependent on injury severity. Future studies may reveal the specific mechanisms responsible for glutamate dysregulation in the post-traumatic period, and may provide novel therapeutic means to improve outcomes after TBI.
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Journal of neurotrauma · May 2010
Sensory stimulation prior to spinal cord injury induces post-injury dysesthesia in mice.
Chronic pain and dysesthesias are debilitating conditions that can arise following spinal cord injury (SCI). Research studies frequently employ rodent models of SCI to better understand the underlying mechanisms and develop better treatments for these phenomena. While evoked withdrawal tests can assess hypersensitivity in these SCI models, there is little consensus over how to evaluate spontaneous sensory abnormalities that are seen in clinical SCI subjects. ⋯ Mice subjected to either stimulus paradigm showed increased OG compared with unstimulated or uninjured mice. Histological analysis showed no difference in spinal cord lesion size due to sensory stimulation, or between mice that overgroomed or did not overgroom. The relationship between prior stimulation and contusion injury in mice that display OG indicates a critical interaction that may underlie one facet of spontaneous neuropathic symptoms after SCI.
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Journal of neurotrauma · May 2010
Blockade of acute microglial activation by minocycline promotes neuroprotection and reduces locomotor hyperactivity after closed head injury in mice: a twelve-week follow-up study.
Traumatic brain injury (TBI) causes a wide spectrum of consequences, such as microglial activation, cerebral inflammation, and focal and diffuse brain injury, as well as functional impairment. In this study we aimed to investigate the effects of acute treatment with minocycline as an inhibitor of microglial activation on cerebral focal and diffuse lesions, and on the spontaneous locomotor activity following TBI. The weight-drop model was used to induce TBI in mice. ⋯ More interestingly, minocycline significantly decreased TBI-induced locomotor hyperactivity at 48 h post-TBI, and its effect lasted for up to 8 weeks. Taken together, the results indicate that microglial activation appears to play an important role in the development of TBI-induced focal injury and the subsequent locomotor hyperactivity, and its short-term inhibition provides long-lasting functional recovery after TBI. These findings emphasize the fact that minocycline could be a promising new therapeutic strategy for head-injured patients.
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Journal of neurotrauma · May 2010
The effect of epidermal growth factor in the injured brain after trauma in rats.
Epidermal growth factor (EGF) is a known mitogen for neural stem and progenitor cells (NS/NPCs) in the central nervous system (CNS). In vitro, EGF maintains NS/NPCs in the proliferative state, whereas in the normal rodent brain it promotes their proliferation and migration in the subventricular zone (SVZ). Additionally, EGF administration can augment neuronal replacement in the ischemic-injured adult striatum. ⋯ Furthermore, we found that the EGF-induced proliferative population differentiated preferentially toward astroglial phenotype. Nevertheless, animals treated with EGF showed significant improvement in cognitive function, which was accompanied by reduced hippocampal neuronal cell loss. Collectively, the data from this study demonstrate that EGF exerts a neuroprotective rather than neurogenic effect in protecting the brain from injury.