Articles: traumatic-brain-injuries.
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Review
Group-based delivery of interventions in traumatic brain injury rehabilitation: a scoping review.
Whilst there are potential advantages of group-based interventions in rehabilitation, facilitation of groups for patients following traumatic brain injury (TBI) has challenges due to the complexity of impairments experienced. This paper aims to review the literature concerning therapy groups within TBI rehabilitation. ⋯ Studies of the effectiveness of interventions targeting 'real-world' activities and participation-based goals are under-represented in the TBI rehabilitation literature. Further research investigating the effectiveness of group processes and the perceptions of patients and clinicians is warranted to guide clinical practice. Implications for Rehabilitation Group-based interventions are common in TBI rehabilitation, usually targeting cognitive skills and impairments. The majority of studies demonstrated positive changes pre-post group interventions on some outcome measures. Few studies directly compare the outcome of an intervention delivered in a group setting to the same intervention delivered in an individual setting. Patients perceive group interventions to be beneficial for sharing experiences and reducing isolation, receiving help and feedback and, assisting with adjustment and adaptation to life after TBI, however, this research is limited. Greater emphasis on group-delivered interventions that target 'real world' activities, or participation may be beneficial with this population. Further research regarding consumer experiences and processes that facilitate effective group interventions in TBI rehabilitation is recommended.
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Meta Analysis
Is APOE ε4 associated with poorer cognitive outcome following traumatic brain injury? A meta-analysis.
Cognitive impairment is a common sequelae of traumatic brain injury (TBI); however, predicting who will experience poorer outcomes remains challenging. A potential risk factor that has gained attention is the APOE gene, with the ε4 allele hypothesized to have a detrimental effect on post-TBI cognitive outcome. The aim of this meta-analysis was to evaluate the effect of APOE ε4 both in terms of general cognitive function and within specific domains known to be prone to impairment following TBI (executive function, working memory, verbal memory and visual memory). ⋯ This meta-analysis indicates that APOE ε4 does not have a detrimental effect on cognitive performance following TBI. We propose that the relationship between APOE and cognitive function following TBI is complex, and a more-nuanced exploration of APOE genotypes is needed. (PsycINFO Database Record
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Neurosurg. Clin. N. Am. · Oct 2016
ReviewThe Role of Multimodal Invasive Monitoring in Acute Traumatic Brain Injury.
This article reviews the role of modalities that directly monitor brain parenchyma in patients with severe traumatic brain injury. The physiology monitored involves compartmental and perfusion pressures, tissue oxygenation and metabolism, quantitative blood flow, pressure autoregulation, and electrophysiology. There are several proposed roles for this multimodality monitoring, such as to track, prevent, and treat the cascade of secondary brain injury; monitor the neurologically injured patient; integrate various data into a composite, patient-specific, and dynamic picture; apply protocolized, pathophysiology-driven intensive care; use as a prognostic marker; and understand pathophysiologic mechanisms involved in secondary brain injury to develop preventive and abortive therapies, and to inform future clinical trials.
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Meta Analysis
A meta-analysis of working memory impairments in survivors of moderate-to-severe traumatic brain injury.
To establish the magnitude of deficits in working memory (WM) and short-term memory (STM) in those with moderate-to-severe traumatic brain injury (TBI) relative to age-matched, healthy controls and to explore the moderating effects of time since injury and age at injury on these impairments. ⋯ Evidence for WM impairments following TBI is consistent with previous research. Larger verbal STM and verbal WM deficits were related to a longer time postinjury, suggesting that these aspects of memory do not "recover" over time and instead, individuals might show increased rates of cognitive decline. Age at injury was associated with the severity of verbal WM impairments, with larger deficits evident for injuries that occurred later in life. Further research needs to chart the long-term effects of TBI on WM and to compare the effects of injury on verbal relative to visuospatial memory. (PsycINFO Database Record
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Journal of neurotrauma · Oct 2016
Microglial/macrophage polarization dynamics following traumatic brain injury.
Activated microglia and macrophages exert dual beneficial and detrimental roles after central nervous system injury, which are thought to be due to their polarization along a continuum from a classical pro-inflammatory M1-like state to an alternative anti-inflammatory M2-like state. The goal of the present study was to analyze the temporal dynamics of microglia/macrophage polarization within the lesion micro-environment following traumatic brain injury (TBI) using a moderate-level controlled cortical impact (CCI) model in mice. We performed a detailed phenotypic analysis of M1- and M2-like polarized microglia/macrophages, as well as nicotinamide adenine dinucleotide phosphate oxidase (NOX2) expression, through 7 days post-injury using real-time polymerase chain reaction (qPCR), flow cytometry and image analyses. ⋯ In a follow up study, we administered a selective NOX2 inhibitor, gp91ds-tat, to CCI mice starting at 24 h post-injury to investigate the relationship between NOX2 and M1-like/Mtran phenotypes. Delayed gp91ds-tat treatment altered M1-/M2-like balance in favor of the anti-inflammatory M2-like phenotype, and significantly reduced oxidative damage in neurons at 7 days post-injury. Therefore, our data suggest that despite M1-like and M2-like polarized microglia/macrophages being activated after TBI, the early M2-like response becomes dysfunctional over time, resulting in development of pathological M1-like and Mtran phenotypes driven by increased NOX2 activity.