Journal of neurotrauma
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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
Comparison Groups Matter in Traumatic Brain Injury Research: An Example with Dementia.
The association between traumatic brain injury (TBI) and risk for Alzheimer disease and related dementias (ADRD) has been investigated in multiple studies, yet reported effect sizes have varied widely. Large differences in comorbid and demographic characteristics between individuals with and without TBI could result in spurious associations between TBI and poor outcomes, even when control for confounding is attempted. Yet, inadvertent control for post-TBI exposures (e.g., psychological and physical trauma) could result in an underestimate of the effect of TBI. ⋯ Using data on Veterans aged ≥55 years obtained from the Veterans Health Administration (VA) for years 1999-2019, we compared risk of ADRD between Veterans with incident TBI (n = 9440) and (1) the general population of Veterans who receive care at the VA (All VA) (n = 119,003); (2) Veterans who received care at a VA emergency department (VA ED) (n = 111,342); and (3) Veterans who received care at a VA ED for non-TBI trauma (VA ED NTT) (n = 65,710). In inverse probability of treatment weighted models, TBI was associated with increased risk of ADRD compared with All VA (hazard ratio [HR] 1.94; 95% confidence interval [CI] 1.84, 2.04), VA ED (HR 1.42; 95% CI 1.35, 1.50), and VA ED NTT (HR 1.12; 95% CI 1.06, 1.18). The estimated effect of TBI on incident ADRD was strongly impacted by choice of the comparison group.
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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
Increased fear generalization and amygdala AMPA receptor proteins in chronic traumatic brain injury.
Cognitive impairments and emotional lability are common long-term consequences of traumatic brain injury (TBI). How TBI affects interactions between sensory, cognitive, and emotional systems may reveal mechanisms that underlie chronic mental health comorbidities. Previously, we reported changes in auditory-emotional network activity and enhanced fear learning early after TBI. ⋯ These findings suggest that TBI precipitates maladaptive associative fear generalization rather than non-associative sensitization. Basolateral amygdala (BLA) α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAr) subunits GluA1 and GluA2 levels were analyzed and the FPI-Noise Shock group had increased GluA1 (but not GluA2) levels that correlated with the level of tone fear generalization. This study illustrates a unique chronic TBI phenotype with both a cognitive impairment and increased fear and possibly altered synaptic transmission in the amygdala long after TBI, where stimulus generalization may underlie maladaptive fear and hyperarousal.
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Journal of neurotrauma · Nov 2022
The impact of high fat consumption on neurological functions following a traumatic brain injury in rats.
Traumatic brain injury (TBI) and obesity are two common conditions in modern society; both can impair neuronal integrity and neurological function. However, it is unclear whether the coexistence of both conditions will worsen outcomes. Therefore, in a rat model, we aimed to investigate whether the coexistence of TBI and a high-fat diet (HFD) has an additive effect, leading to more severe neurological impairments, and whether they are related to changes in brain protein markers of oxidative stress, inflammation, and synaptic plasticity. ⋯ In rats without TBI, HFD increased the pre-synaptic protein synaptophysin. In rats with TBI, HFD resulted in worsened sensory and memory function, an increase in activated macrophages, and a decrease in the endogenous antioxidant manganese superoxide dismutase (MnSOD). Our findings suggest that the additive effect of HFD and TBI worsens short term memory and sensation deficits, and may be driven by enhanced oxidative stress and inflammation.