Articles: traumatic-brain-injuries.
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Adiponectin plays an important role in the regulation of tissue inflammation. There is a paucity of data on circulating plasma adiponectin concentrations in human traumatic brain injury. This study is designed to investigate the potential associations between plasma adiponectin levels and clinical outcomes after traumatic brain injury. ⋯ Plasma adiponectin level may represent a novel biomarker for predicting clinical outcomes of traumatic brain injury.
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This study investigates coping strategies after traumatic brain injury (TBI) and their associations with health-related quality of life (HRQoL). ⋯ This study highlights the relationship of coping strategies and HRQoL after TBI. For the assessment of HRQoL a novel disease-specific instrument was applied, that provides in detail TBI-relevant aspects of well-being and HRQoL. Individuals after TBI use two main sets of coping strategies that are differentially associated with HRQoL (and clinical variables). One is adaptive and the other maladaptive for HRQoL after TBI. Maladaptive and adaptive coping strategies used by the individual should be identified and considered in rehabilitation efforts to improve HRQoL after TBI.
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J Clin Exp Neuropsychol · Jan 2014
Development of a novel task for investigating decision making in a social context following traumatic brain injury.
Examination of social cognition as a target for assessment and intervention is beginning to gain momentum in a number of illnesses and acquired disorders. One facet of social cognition is decision making within interpersonal situations. This skill forms an important part of our everyday lives and is commonly impaired in those with neurological and mental health conditions. A novel task was developed to allow the assessment of decision making specifically within a social context and was examined within a group known to experience this difficulty. ⋯ The SDMT offers a novel way of examining decision making within a social context following TBI and may also be useful in other populations known to have specific social cognition impairment. Future research should aim to provide further clarification of the mechanisms of action and neuroanatomical correlates of poor performance on this task.
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Traumatic subarachnoid hemorrhage (SAH) is a common intracranial lesion after traumatic brain injury (TBI). As in aneurysmal SAH, cerebral vasospasm is a common cause of secondary brain injury and is associated with the thickness of traumatic SAH. Unfortunately, there is limited literature on an effective treatment of this entity. The vasodilatory and inotropic agent, Milrinone, has been shown to be effective in treating vasospasm following aneurysmal SAH. The authors hypothesized that this agent could be useful and safe in treating vasospasm following tSAH. ⋯ This is the first report of the use of intravenous Milrinone to treat cerebral vasospasm following traumatic SAH. This treatment option appeared to be safe and potentially useful at treating post-traumatic vasospasm. Prospective studies are necessary to establish Milrinone's clinical effectiveness in treating this type of cerebral vasospasm.
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Dysregulation of autophagy contributes to neuronal cell death in several neurodegenerative and lysosomal storage diseases. Markers of autophagy are also increased after traumatic brain injury (TBI), but its mechanisms and function are not known. Following controlled cortical impact (CCI) brain injury in GFP-Lc3 (green fluorescent protein-LC3) transgenic mice, we observed accumulation of autophagosomes in ipsilateral cortex and hippocampus between 1 and 7 d. ⋯ This was accompanied by appearance of SQSTM1 and ubiquitin-positive puncta in the affected cells, suggesting that, similar to the situation observed in neurodegenerative diseases, impaired autophagy may contribute to neuronal injury. Consistently, GFP-LC3 and SQSTM1 colocalized with markers of both caspase-dependent and caspase-independent cell death in neuronal cells proximal to the injury site. Taken together, our data indicated for the first time that autophagic clearance is impaired early after TBI due to lysosomal dysfunction, and correlates with neuronal cell death.