Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Mar 2023
Cerebral metabolic dysfunction at the acute phase of traumatic brain injury correlates with long-term tissue loss.
Following traumatic brain injury (TBI), cerebral metabolic dysfunction, characterized by an elevated cerebral microdialysis (CMD) lactate/pyruvate (LP) ratio, is associated with poor outcome. However, the exact pathophysiological mechanisms underlying this association are not entirely established. In this pre-planned analysis of the BIOmarkers of AXonal injury after Traumatic Brain Injury (BIO-AX-TBI) prospective study, we investigated any associations of LP ratio with brain structure volume change rates at 1 year. ⋯ After adjusting for age, admission Glasgow Coma Scale (GCS) score and CT Marshall score, CMD LP ratio remained strongly associated with 1-year total GM volume change rate (p < 0.001; multi-variable analysis). No relationship was found between WM volume changes and CMD metabolites. We demonstrate a strong association between acute post-traumatic cerebral metabolic dysfunction and 1-year gray matter atrophy, reinforcing the role of CMD LP ratio as an early biomarker of poor long-term recovery after TBI.
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Most patients with severe traumatic brain injury (sTBI) in low- or-middle-income countries and surprisingly many in high-income countries are managed without intracranial pressure (ICP) monitoring. The impact of the first published protocol (Imaging and Clinical Examination [ICE] protocol) is untested against nonprotocol management. ⋯ ICUs managing patients with sTBI using the ICE protocol had better functional outcome than those not using a protocol. ICUs treating patients with sTBI without ICP monitoring should consider protocolization. The ICE protocol, tested here and previously, is 1 option.
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Prehospital neuroprotective strategies aim to prevent secondary insults (SIs) in traumatic brain injury (TBI). This includes haemodynamic optimisation in addition to oxygenation and ventilation targets achieved through rapid sequence intubation (RSI).The primary aim was to report the incidence and prevalence of SIs (prolonged hypotension, prolonged hypoxia and hyperventilation) and outcomes of patients with TBI who were intubated in the prehospital setting. ⋯ SIs were common in the early phase of prehospital care. The association of prolonged hypoxia and mortality in TBI is potentially more significant than previously recognised, and if corrected early, may improve outcomes. There may be a greater role for bystander intervention in prevention of early hypoxic insult in TBI.
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Journal of neurotrauma · Mar 2023
Predictors of social participation outcome after traumatic brain injury differ according to rehabilitation pathways.
Social participation (SP) is one of many objectives in the rehabilitation of patients with traumatic brain injury (TBI). Studies on predictors of SP specific to post-acute universally accessible specialized rehabilitation pathways following TBI are scarce. Our objectives were to: 1) characterize SP, as well as a set of pre-injury, injury-related, and post-injury variables in individuals participating in inpatient-outpatient or outpatient rehabilitation pathways within a universally accessible and organized trauma continuum of care; and 2) examine the ability of pre-injury, injury-related, and post-injury variables in predicting SP outcome after TBI according to rehabilitation path. ⋯ For the outpatient sample, five variables (pre-morbid hypertension and mental health diagnosis, total indirect rehabilitation hours received, MPAI-4 Abilities and Adjustment scores at rehabilitation intake) significantly predicted SP outcome, with the regression model accounting for 47% of the variance. In conclusion, different pre-morbid and post-injury variables are involved in predicting SP, depending on the rehabilitation path followed. The predictive value of those variables could help clinicians identify patients more likely of showing poorer SP at discharge and who may require additional or different interventions.
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Traumatic brain injury (TBI) is a kind of disease with high morbidity, mortality, and disability, and its pathogenesis is still unclear. Research shows that nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) activation in neurons and astrocytes is involved in neuroinflammatory cascades after TBI. What is more, polydatin (PD) has been shown to have a protective effect on TBI-induced neuroinflammation, but the mechanisms remain unclear. ⋯ More importantly, PD could inhibit the level of SOD2 Ac-K122, NLRP3, and cleaved caspase-1 and promote the expression of SOD2 after TBI both in vivo and in vitro. Polydatin also inhibited mtROS accumulation and MMP collapse after stretching injury. These results indicated that PD inhibited SOD2 acetylation to alleviate NLRP3 inflammasome activation, thus acting a protective role against TBI neuroinflammation.