Journal of neurotrauma
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Journal of neurotrauma · Nov 2022
Females Exhibit Better Cerebral Pressure Autoregulation, Less Mitochondrial Dysfunction, and Reduced Excitotoxicity following Severe Traumatic Brain Injury.
The aim of the study was to investigate sex-related differences in intracranial pressure (ICP) dynamics, cerebral pressure autoregulation (PRx55-15), cerebral energy metabolism, and clinical outcome after severe traumatic brain injury (TBI). One-hundred sixty-nine adult patients with TBI, treated at the Neurointensive Care (NIC) Unit at Uppsala University Hospital between 2008 and 2020 with ICP and cerebral microdialysis (MD) monitoring were included. Of the 169 patients with TBI, 131 (78%) were male and 38 (22%) female. ⋯ There was no difference in mortality or the degree of favorable outcome between the sexes. Altogether, females exhibited more favorable cerebral physiology post-TBI, particularly better mitochondrial function and reduced excitotoxicity, but this did not translate into better clinical outcome compared with males. Future studies are needed to further explore potential sex differences in secondary injury mechanisms in TBI.
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Journal of neurotrauma · Nov 2022
Effects of isolated and combined exposure of the brain and lungs to a laser-induced shock wave(s) on physiological and neurological responses in rats.
Blast-induced traumatic brain injury (bTBI) has been suggested to be caused by direct head exposure and by torso exposure to a shock wave (thoracic hypotheses). It is unclear, however, how torso exposure affects the brain in real time. This study applied a mild-impulse laser-induced shock wave(s) (LISW[s]) only to the brain (Group 1), lungs (Group 2), or to the brain and lungs (Group 3) in rats. ⋯ Alternatively, two groups of rats with lung exposure (Group 2 and Group 3) exhibited continuously aggravated motor functions for up to seven days post-exposure, suggesting different mechanisms for motor dysfunction caused by brain exposure and that caused by lung exposure. As for the reported thoracic hypotheses, our observations seem to support the volumetric blood surge and vagovagal reflex. Overall, the results of this study indicate the importance of the torso guard to protect the brain and its function.
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Journal of neurotrauma · Nov 2022
ReviewCerebral Autoregulation Monitoring in Traumatic Brain Injury: An Overview of Recent Advances in Personalized Medicine.
Impaired cerebral autoregulation (CA) in moderate/severe traumatic brain injury (TBI) has been identified as a strong associate with poor long-term outcomes, with recent data highlighting its dominance over cerebral physiological dysfunction seen in the acute phase post-injury. With advances in bedside continuous cerebral physiological signal processing, continuously derived metrics of CA capacity have been described over the past two decades, leading to improvements in cerebral physiological insult detection and development of novel personalized approaches to TBI care in the intensive care unit (ICU). ⋯ The CA-based personalized targets, such as optimal cerebral perfusion pressure (CPPopt), lower/upper limit of regulation (LLR/ULR), and individualized intracranial pressure (iICP) are positioned to change the way we care for patients with TBI in the ICU, moving away from the "one treatment fits all" paradigm of current guideline-based therapeutic approaches toward a true personalized medicine approach tailored to the individual patient. Future perspectives regarding research needs in this field are also discussed.
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Journal of neurotrauma · Nov 2022
Understanding primary blast injury: High frequency pressure acutely disrupts neuronal network dynamics in cerebral organoids.
Blast exposure represents a common occupational risk capable of generating mild to severe traumatic brain injuries (TBI). During blast exposure, a pressure shockwave passes through the skull and exposes brain tissue to complex pressure waveforms. The primary neurophysiological response to blast-induced pressure waveforms remains poorly understood. ⋯ Conversely, organoids exposed to higher amplitude pressure (350k Pa) displayed drastic neurophysiological differences that failed to recover within 24 h. Further, lower amplitude "blast" (250 kPa) did not induce cellular damage whereas the higher amplitude "blast" (350 kPa) generated greater apoptosis throughout each organoid. Our data indicate that specific features of pressure waves found intracranially during blast TBI have varied effects on neurophysiological activity that can occur even without cellular damage.