Effects Of Traumatic Brain Injury Research Articles

Art therapy with military families: The animal strengths and family environment directive

Military families are resilient but are impacted by service member’s deployments, combat exposure, injuries, and other stressors such as frequent moves. These factors affect the entire family, and in turn family dynamics influence injured service members’ capacity to heal. Art therapy is a regulated mental health profession that incorporates the use of visual art to address psychological and rehabilitation treatment goals provided by qualified art therapists and has been used with military families in health settings for over 70 years. Through art therapy, military families can find new ways to communicate with one another in developmentally appropriate ways. This article describes the process of the Animal Strengths and Family Environment (ASFE), an art therapy directive designed to meet the needs of families of service members recovering from effects of traumatic brain injuries (TBI) and post-traumatic stress disorder (PTSD). Case vignettes are presented illustrating the use of the ASFE, describing how two military families identified character strengths through animal metaphors, and created visual artwork to discover and express these strengths, roles, and needs. The authors contend that this process is useful in mapping family dynamics to increase communication which ultimately fosters family resiliency. Continued research is needed to better understand possible outcomes of art therapy directives with military families.

How Traumatic Brain Injury History Relates to Brain Health MRI Markers and Dementia Risk: Findings from the 3C Dijon Cohort.

The long-term effects of traumatic brain injury (TBI) with loss of consciousness (LOC) on magnetic resonance imaging (MRI) markers of brain health and on dementia risk are still debated. To investigate the associations of history of TBI with LOC with incident dementia and neuroimaging markers of brain structure and small vessel disease lesions. The analytical sample consisted in 4,144 participants aged 65 and older who were dementia-free at baseline from the Three City -Dijon study. History of TBI with LOC was self-reported at baseline. Clinical Dementia was assessed every two to three years, up to 12 years of follow-up. A subsample of 1,675 participants <80 years old underwent a brain MRI at baseline. We investigated the associations between history of TBI with LOC and 1) incident all cause and Alzheimer's disease (AD) dementia using illness-death models, and 2) neuroimaging markers at baseline. At baseline, 8.3% of the participants reported a history of TBI with LOC. In fully-adjusted models, participants with a history of TBI with LOC had no statistically significant differences in dementia risk (HR = 0.90, 95% CI = 0.60-1.36) or AD risk (HR = 1.03, 95% CI = 0.69-1.52), compared to participants without TBI history. History of TBI with LOC was associated with lower white matter volume (β= -4.58, p = 0.048), but not with other brain volumes, white matter hyperintensities volume, nor covert brain infarct. This study did not find evidence of an association between history of TBI with LOC and dementia or AD dementia risks over 12-year follow-up, brain atrophy, or markers of small vessel disease.

Adult-Born Granule Cells Contribute to Dentate Gyrus Circuit Reorganization after Traumatic Brain Injury.

Post-traumatic epilepsy (PTE) is a serious consequence of traumatic brain injury (TBI). PTE develops following a latent postinjury period during which alterations in neuronal network excitability are thought to occur, leading to the development of recurrent and unprovoked seizures. In particular,

Gene Therapy for Chronic Traumatic Brain Injury: Challenges in Resolving Long-term Consequences of Brain Damage.

The gene therapy is alluring not only for CNS disorders but also for other pathological conditions. Gene therapy employs the insertion of a healthy gene into the identified genome to replace or replenish genes responsible for pathological disorder or damage due to trauma. The last decade has seen a drastic change in the understanding of vital aspects of gene therapy. Despite the complexity of traumatic brain injury (TBI), the advent of gene therapy in various neurodegenerative disorders has reinforced the ongoing efforts of alleviating TBI-related outcomes with gene therapy. The review highlights the genes modulated in response to TBI and evaluates their impact on the severity and duration of the injury. We have reviewed strategies that pinpointed the most relevant gene targets to restrict debilitating events of brain trauma and utilize vector of choice to deliver the gene of interest at the appropriate site. We have made an attempt to summarize the long-term neurobehavioral consequences of TBI due to numerous pathometabolic perturbations associated with a plethora of genes. Herein, we shed light on the basic pathological mechanisms of brain injury, genetic polymorphism in individuals susceptible to severe outcomes, modulation of gene expression due to TBI, and identification of genes for their possible use in gene therapy. The review also provides insights on the use of vectors and challenges in translations of this gene therapy to clinical practices.

Intergenerational Perioperative Neurocognitive Disorder in Young Adult Male Rats with Traumatic Brain Injury.

The authors tested the hypothesis that the effects of traumatic brain injury, surgery, and sevoflurane interact to induce neurobehavioral abnormalities in adult male rats and in their offspring (an animal model of intergenerational perioperative neurocognitive disorder). Sprague-Dawley male rats (assigned generation F0) underwent a traumatic brain injury on postnatal day 60 that involved craniectomy (surgery) under 3% sevoflurane for 40 min followed by 2.1% sevoflurane for 3 h on postnatal days 62, 64, and 66 (injury group). The surgery group had craniectomy without traumatic brain injury, whereas the sevoflurane group had sevoflurane only. On postnatal day 90, F0 males and control females were mated to generate offspring (assigned generation F1). Acutely, F0 injury rats exhibited the greatest increases in serum corticosterone and interleukin-1β and -6, and activation of the hippocampal microglia. Long-term, compared to controls, F0 injury rats had the most exacerbated corticosterone levels at rest (mean ± SD, 2.21 ± 0.64 vs. 7.28 ± 1.95 ng/ml, n = 7 - 8; P < 0.001) and 10 min after restraint (133.12 ± 33.98 vs. 232.83 ± 40.71 ng/ml, n = 7 - 8; P < 0.001), increased interleukin-1β and -6, and reduced expression of hippocampal glucocorticoid receptor (Nr3c1; 0.53 ± 0.08 fold change relative to control, P < 0.001, n = 6) and brain-derived neurotrophic factor genes. They also exhibited greater behavioral deficiencies. Similar abnormalities were evident in their male offspring, whereas F1 females were not affected. The reduced Nr3c1 expression in F1 male, but not female, hippocampus was accompanied by corresponding Nr3c1 promoter hypermethylated CpG sites in F0 spermatozoa and F1 male, but not female, hippocampus. These findings in rats suggest that young adult males with traumatic brain injury are at an increased risk of developing perioperative neurocognitive disorder, as are their unexposed male but not female offspring.

Stakeholder views on cognitive communication assessment and intervention for a person living independently in the community with severe traumatic brain injury.

Cognitive communication disorder (CCD) following traumatic brain injury (TBI) is well documented and these communication problems impede successful re-integration into community living. While there is growing evidence for intervention to both detect and treat the impact of these deficits across the rehabilitation continuum, there are barriers to accessing services. Cognitive communication impairments may be missed because the person can talk, and this may mask the subtle but debilitating impact of a CCD. Referral to a speech and language therapist (SLT) may be overlooked or not timely, which prevents the individual accessing evidence-based interventions. Inadequate treatment provision and an under- or overestimation of communication capability can potentially undermine the effectiveness of wider team assessment and intervention. To report stakeholder views on specialist SLT input for CCD within a multidisciplinary team intervention for a community-dwelling individual with severe TBI. The investigation explored perspectives on understanding of CCD, on practice and on outcomes, in order to inform professional groups on perceived impacts of the evidence-to-practice gap. A semi-structured interview methodology was employed with 11 stakeholder participants involved in a single case. Data were evaluated using a thematic framework method. Themes were inductively derived from the stakeholder narratives. Stakeholders reported the following outcomes from specialist SLT input for CCD within a collaborative team approach: improved engagement with rehabilitation and support teams, improved health-related quality of life and well-being, and increased client participation in community activities of personal relevance. Stakeholders also reported inequities in wider service provision where limitations in professional understanding of CCD and knowledge of best practice recommendations preclude access to specialist SLT services. CCDs are under-recognised and this can have a devastating effect on people with CCD and on those around them. Stakeholder reports provide evidence for the effectiveness of SLT practice recommendations for the treatment of CCD following TBI. They also provide additional evidence of persisting barriers to accessing treatment. Future research to explore ways to close this evidence-to-practice gap is required. What is already known on this subject Cognitive communication difficulties are a well-documented consequence of TBI. There is evidence for the effectiveness of person-centred interventions for CCD across the recovery continuum. International evidence-based practice recommendations are in place for CCD assessment and management. Barriers to accessing SLT expertise for CCD have previously been reported. What this paper adds to existing knowledge This investigation explores the views of a diverse group of stakeholders involved in a single case of a community-dwelling individual with severe TBI. Stakeholders report positive real-world outcomes from SLT interventions for CCD within a coordinated multidisciplinary rehabilitation team. Stakeholder reports also indicate inequities in wider service provision and CCD knowledge gaps amongst professional groups providing rehabilitation services for people with TBI. What are the potential or actual clinical implications of this work? CCDs are under-recognised, with devastating effect for people with CCD and those around them. These findings underscore the importance of raising professional awareness of CCD and best practice recommendations, in order to improve access to SLT expertise for people with CCD following TBI.

Risk factors and consequences of traumatic brain injury in a Swiss male population cohort

Risk factors and consequences of traumatic brain injury in a Swiss male population cohort

The contribution of initial concussive forces and resulting acrolein surge to β-amyloid accumulation and functional alterations in neuronal networks using a TBI-on-a-chip model.

Trauma-induced Alzheimer's disease (AD) is rapidly emerging as a major consequence of traumatic brain injuries (TBI), with devastating social and economic impacts. Unfortunately, few treatment options are currently available due to a limited understanding of the underlying mechanisms. A clinically-relevant, in vitro experimental model that emulates in vivo scenarios with high levels of spatial and temporal resolution is critical for demystifying the pathways of post-TBI AD. Using a unique, recently established "TBI-on-a-chip" system with murine cortical networks, we demonstrate the correlative elevation of oxidative stress (acrolein), inflammation (TNF-α), and Aβ42 aggregation, with concomitant reduction of neuronal network electrical activity post-concussive impact. These findings confirm that TBI-on-a-chip could provide a novel paradigm to supplement in vivo studies of trauma, while simultaneously validating the interaction of these alleged, key-pathological factors in post-TBI AD development. Specifically, we have shown that acrolein, acting as a diffusive factor of secondary injury, is both critical and sufficient in promoting inflammation (TNF-α) and Aβ42 aggregation, two known contributors of AD pathogenesis. Furthermore, using a cell-free preparation with TBI-on-a-chip, we have confirmed that both force and acrolein can independently and directly stimulate the aggregation of purified Aβ42, highlighting the key capabilities of primary and secondary injury mechanisms towards inducing Aβ42 aggregation, independently and synergistically. In addition to morphological and biochemical assessment, we also demonstrate parallel monitoring of neuronal network activity, further validating the chief pathological role of acrolein in not only inflicting biochemical abnormalities, but also functional deficits in neuronal networks. In conclusion, through this line of investigations, we have shown that by recapitulating clinically-relevant events, the TBI-on-a-chip device is capable of quantitatively characterizing parallel force-dependent increases in oxidative stress, inflammation, protein aggregation, and network activity, offering a unique platform for mechanistic investigations of post-TBI AD, and trauma-induced neuronal injury in general. It is expected that this model could provide crucial insights into pathological mechanisms which will be critical in developing novel, effective diagnostics and treatment strategies that significantly benefit TBI victims.

Treatment of diseases with consequences of traumatic brain injury

Traumatic brain injury (TBI) is one of the leading causes of neurological morbidity, disability and mortality in all age groups of the population. As a result of the general increase in the number of cases of brain injuries, there is a significant increase in the consequences of TBI, the dominant part of which is asthenic, vegetative, cognitive, emotional and liquorodynamic disorders. Therapeutic measures in the long-term period of TBI should be carried out intensively as in the first 12 months. after TBI, and in the future, considering the ongoing processes of morphofunctional maturation of the CNS and high brain plasticity, especially in childhood. Syndromic treatment should be differentiated and pathogenetically substantiated. The article covers in detail the modern methods of drug therapy in patients with remote residual effects of brain injury. The high efficiency of the use of the neuroprotective drug Cortexin in the correction of the consequences of TBI was shown.

The alleged mechanisms of olfactory disorders in the new coronavirus infection

In March 2020, the World Health Organization (WHO) announced the beginning of the COVID-19 pandemic, which continues to the present. A change in the sense of smell, up to the complete disappearance of odors, is regarded as one of the early symptoms of the disease. Sometimes anosmia was the only sign of infection of the patient. As is known, a disturbance of the sense of smell indicates a serious pathology of the brain, such as the consequences of traumatic brain injuries, strokes, Alzheimer's disease, Parkinson's disease, autoimmune diseases, a side-effect of drug therapy. The review is dedicated to the pathogenesis of anosmia in COVID-19. For a better understanding of the pathogenesis, the article presents a brief anatomy and physiology of the olfactory organ as well as the probable mechanisms of anosmia: encephalitis, inflammatory edema of the olfactory cleft, olfactory epithelium damage, apoptosis of bipolar neurons, damage of olfactory cell cilia and damage of olfactory bulbs. Because of the rapid accumulation of information on this topic, there is a need to structure, periodic systematization and presentation to a wide range of specialists.

Insights into social communication following traumatic brain injury sustained in older adulthood.

There is a lack of evidence relating to cognitive-communication difficulties following traumatic brain injury (TBI) sustained in older adulthood. A prominent area in which post-TBI cognitive-communication difficulties manifest is at the level of social communication. An investigation of social communication focusing on comparison of those injured in older and younger adulthood is a practical starting point for age-related cognitive-communication outcome comparison. The overall objective of this study was to explore the social communication of individuals who sustained severe TBI in an early period of older adulthood (50-70 years) compared to younger adulthood (18-40 years), as informed by self and close other reports. This exploratory controlled group comparison study involved analysis of self-reported and close other reported La Trobe Communication Questionnaire data for 22 adults with severe TBI (11 older at injury; 11 younger at injury) and 22 control participants (11 older; 11 younger). TBI participants were matched for injury variables and participant groups were matched for sex, age and education. The close others of the older and younger adults with TBI reported them to have significantly more frequent difficulty with social communication than the close others of age-matched control groups. Older adults with TBI reported significantly more frequent difficulty with social communication than uninjured older adults. In contrast, younger adults with TBI and uninjured younger adults reported a similar frequency of difficulty with social communication. No age-based difference in the frequency of social communication difficulty was evident when comparing the self or close other reports of older and younger adults with TBI. Awareness of social communication difficulty, as indexed by comparing self and close other perceptions, showed a different pattern across the TBI groups. The older TBI group rated themselves as having significantly less frequent social communication difficulty than was perceived by their close others. In contrast, no statistically significant difference was evident between the self and close other social communication ratings of the younger TBI group. Where possible clinicians need to work with close communication partners to understand the nature and degree of social communication difficulty following severe TBI. This may be especially important when working with people who sustain TBI in older adulthood if future research shows that this population have greater difficulty with self-awareness of social communication difficulty. What is already known on the subject Cognitive-communication difficulties are a common consequence of traumatic brain injury (TBI) that can have long-term impact on everyday functioning. These challenges have primarily been investigated in individuals who sustained TBI in younger adulthood. What this paper adds to existing knowledge Individuals who sustain severe TBI in early older adulthood have a higher frequency of reported social communication difficulty to non-injured adults of a similar age, albeit they may underreport such difficulties potentially in the context of reduced self-awareness. What are the potential or actual clinical implications of this work? Social communication difficulty is an issue for people who sustain severe TBI in early older adulthood. However, a poorer overall social communication outcome in comparison to those injured in younger adulthood should not be assumed. Clinical service delivery for these challenges is most optimally delivered in a collaborative manner with the individual and their close others. Future research is required to investigate the identified trends from this study.

The role of the microbiota-gut-brain axis in long-term neurodegenerative processes following traumatic brain injury.

Traumatic brain injury (TBI) can be a devastating and debilitating disease to endure. Due to improvements in clinical practice, declining mortality rates have led to research into the long-term consequences of TBI. For example, the incidence and severity of TBI have been associated with an increased susceptibility of developing neurodegenerative disorders, such as Parkinson's or Alzheimer's disease. However, the mechanisms linking this alarming association are yet to be fully understood. Recently, there has been a groundswell of evidence implicating the microbiota-gut-brain axis in the pathogenesis of these diseases. Interestingly, survivors of TBI often report gastrointestinal complaints and animal studies have demonstrated gastrointestinal dysfunction and dysbiosis following injury. Autonomic dysregulation and chronic inflammation appear to be the main driver of these pathologies. Consequently, this review will explore the potential role of the microbiota-gut-brain axis in the development of neurodegenerative diseases following TBI.

EPO has multiple positive effects on astrocytes in an experimental model of ischemia

Erythropoietin (EPO) has neuroprotective effects in central nervous system injury models. In clinical trials EPO has shown beneficial effects in traumatic brain injury (TBI) as well as in ischemic stroke. We have previously shown that EPO has short-term effects on astrocyte glutamatergic signaling in vitro and that administration of EPO after experimental TBI decreases early cytotoxic brain edema and preserves structural and functional properties of the blood-brain barrier. These effects have been attributed to preserved or restored astrocyte function. Here we explored the effects of EPO on astrocytes undergoing oxygen-glucose-deprivation, an in vitro model of ischemia. Measurements of glutamate uptake, intracellular pH, intrinsic NADH fluorescence, Na,K-ATPase activity, and lactate release were performed. We found that EPO within minutes caused a Na,K-ATPase-dependent increase in glutamate uptake, restored intracellular acidification caused by glutamate and increased lactate release. The effects on intracellular pH were dependent on the sodium/hydrogen exchanger NHE. In neuron-astrocyte co-cultures, EPO increased NADH production both in astrocytes and neurons, however the increase was greater in astrocytes. We suggest that EPO preserves astrocyte function under ischemic conditions and thus may contribute to neuroprotection in ischemic stroke and brain ischemia secondary to TBI.

3D printing of injury-preconditioned secretome/collagen/heparan sulfate scaffolds for neurological recovery after traumatic brain injury in rats

BackgroundThe effects of traumatic brain injury (TBI) can include physical disability and even death. The development of effective therapies to promote neurological recovery is still a challenging problem. 3D-printed biomaterials are considered to have a promising future in TBI repair. The injury-preconditioned secretome derived from human umbilical cord blood mesenchymal stem cells showed better stability in neurological recovery after TBI. Therefore, it is reasonable to assume that a biological scaffold loaded with an injury-preconditioned secretome could facilitate neural network reconstruction after TBI.MethodsIn this study, we fabricated injury-preconditioned secretome/collagen/heparan sulfate scaffolds by 3D printing. The scaffold structure and porosity were examined by scanning electron microscopy and HE staining. The cytocompatibility of the scaffolds was characterized by MTT analysis, HE staining and electron microscopy. The modified Neurological Severity Score (mNSS), Morris water maze (MWM), and motor evoked potential (MEP) were used to examine the recovery of cognitive and locomotor function after TBI in rats. HE staining, silver staining, Nissl staining, immunofluorescence, and transmission electron microscopy were used to detect the reconstruction of neural structures and pathophysiological processes. The biocompatibility of the scaffolds in vivo was characterized by tolerance exposure and liver/kidney function assays.ResultsThe excellent mechanical and porosity characteristics of the composite scaffold allowed it to efficiently regulate the secretome release rate. MTT and cell adhesion assays demonstrated that the scaffold loaded with the injury-preconditioned secretome (3D-CH-IB-ST) had better cytocompatibility than that loaded with the normal secretome (3D-CH-ST). In the rat TBI model, cognitive and locomotor function including mNSS, MWM, and MEP clearly improved when the scaffold was transplanted into the damage site. There is a significant improvement in nerve tissue at the site of lesion. More abundant endogenous neurons with nerve fibers, synaptic structures, and myelin sheaths were observed in the 3D-CH-IB-ST group. Furthermore, the apoptotic response and neuroinflammation were significantly reduced and functional vessels were observed at the injury site. Good exposure tolerance in vivo demonstrated favorable biocompatibility of the scaffold.ConclusionsOur results demonstrated that injury-preconditioned secretome/collagen/heparan sulfate scaffolds fabricated by 3D printing promoted neurological recovery after TBI by reconstructing neural networks, suggesting that the implantation of the scaffolds could be a novel way to alleviate brain damage following TBI.Graphical abstract

Sex and Gender Effects in Traumatic Brain Injury: An Educational Trial For Patients and Caregivers

<h3>Research Objectives</h3> To investigate the effectiveness of a one-time educational intervention on sex (i.e., biological attributes) and gender (i.e., norms, responsibilities) influences in traumatic brain injury (TBI) for patients and caregivers. <h3>Design</h3> Pilot pre-test/post-test randomized control-group study design. <h3>Setting</h3> Zoom and the University Health Network Research Electronic Data Capture application, of the KITE Research Institute, Toronto Rehabilitation Institute UHN, Ontario, Canada. <h3>Participants</h3> Sixteen individuals with TBI and caregivers (75% persons with TBI, 63% women). <h3>Interventions</h3> Participants were randomly allocated into passive, active or control groups. The passive group received 90-minutes of lecture delivering content, and the active group received the same content in a session structured to foster interaction and dialogue. The control group did not receive any education. All participants completed a pre- and post-test questionnaire measuring knowledge, attitude, and skill towards educational content. <h3>Main Outcome Measures</h3> Individual and group learning gains, and group-average normalized gain (aNG) for knowledge, attitude, and skill were calculated. An aNG of ≥ 30% substantiated the intervention's effectiveness. <h3>Results</h3> Both educational methods led to improvements in participants' scores on knowledge, attitude, and skill. The highest aNG was observed in the passive group (i.e., 100% for knowledge, 50% for attitude, 37% for skill). The active and control groups did not demonstrate an aNG of ≥ 30%, except for the attitude domain of the control group (∼33%). Positive feedback on content, organization, and utilization of the intervention was received. <h3>Conclusions</h3> A passive educational intervention on sex and gender in TBI may be beneficial for persons with TBI and caregivers. Further research is needed to explore the effects of active engagement on knowledge, attitude, and skill acquisition. <h3>Author(s) Disclosures</h3> No conflict to disclose.

Immune modulation after traumatic brain injury.

Traumatic brain injury (TBI) induces instant activation of innate immunity in brain tissue, followed by a systematization of the inflammatory response. The subsequent response, evolved to limit an overwhelming systemic inflammatory response and to induce healing, involves the autonomic nervous system, hormonal systems, and the regulation of immune cells. This physiological response induces an immunosuppression and tolerance state that promotes to the occurrence of secondary infections. This review describes the immunological consequences of TBI and highlights potential novel therapeutic approaches using immune modulation to restore homeostasis between the nervous system and innate immunity.

Traumatic Brain Injury during the SARS-CoV-2 Pandemics in Slovenia: A Single Center Study.

(1) Background: The SARS-CoV-2 pandemic had a significant impact on the management of traumatic brain injury (TBI). We aimed to compare the clinical characteristics and outcomes of TBI patients before and during the SARS-CoV-2 pandemic.; (2) Methods: We analyzed depicted data from existing medical records on sex, age, mechanism of injury, clinical performance at admission and discharge, neuroimaging, laboratory values at admission, mortality, duration of hospitalization, and referrals after discharge from the traumatology department for all adult patients during the SARS-CoV-2 pandemic and a year before. Variables were compared using the Chi-square or t-test between both groups.; (3) Results: Most patients had mild (n = 477), followed by moderate (11) and severe (11) TBI. Mild TBI was less frequent during the SARS-CoV-2 period (n = 174 vs. n = 303). The incidence of high falls increased during the SARS-CoV-2 period (14.5% vs. 24.7%; p < 0.05) in the group with mild TBI. Patients had similar mean Glasgow Coma Scales (GCS), Glasgow Outcome Scales-Extended (GOSE), and glucose levels at admission before and during the pandemic. Serum ethanol levels were significantly lower during the SARS-CoV-2 period (1.3 ± 0.7 mmol/L vs. 0.7 ± 1.2 mmol/L; p < 0.001). At discharge, the mean GCS was significantly lower (14.7 ± 1.8 vs. 14.1 ± 0.5; p < 0.05) for patients treated during the SARS-CoV-2 period than before the SARS-CoV-2 period. There were no differences in GOSE; (4) Conclusions: our results demonstrated a significant impact of SARS-CoV-2 pandemic on the frequency, mechanism, and consequences of TBI, and may help improve care for our patients.

Abrocitinib Attenuates Microglia-Mediated Neuroinflammation after Traumatic Brain Injury via Inhibiting the JAK1/STAT1/NF-κB Pathway.

Neuroinflammation has been shown to play a critical role in secondary craniocerebral injury, leading to poor outcomes for TBI patients. Abrocitinib, a Janus kinase1 (JAK1) selective inhibitor approved to treat atopic dermatitis (AD) by the Food and Drug Administration (FDA), possesses a novel anti-inflammatory effect. In this study, we investigated whether abrocitinib could ameliorate neuroinflammation and exert a neuroprotective effect in traumatic brain injury (TBI) models. First, next-generation sequencing (NGS) was used to select genes closely related to neuroinflammation after TBI. Then, magnetic resonance imaging (MRI) was used to dynamically observe the changes in traumatic focus on the 1st, 3rd, and 7th days after the induction of fluid percussion injury (FPI). Moreover, abrocitinib's effects on neurobehaviors were evaluated. A routine peripheral blood test was carried out and Evans blue dye extravasation, cerebral cortical blood flow, the levels of inflammatory cytokines, and changes in the numbers of inflammatory cells were evaluated to investigate the function of abrocitinib on the 1st day post-injury. Furthermore, the JAK1/signal transducer and activator of transcription1 (STAT1)/nuclear factor kappa (NF-κB) pathway was assessed. In vivo, abrocitinib treatment was found to shrink the trauma lesions. Compared to the TBI group, the abrocitinib treatment group showed better neurological function, less blood-brain barrier (BBB) leakage, improved intracranial blood flow, relieved inflammatory cell infiltration, and reduced levels of inflammatory cytokines. In vitro, abrocitinib treatment was shown to reduce the pro-inflammatory M1 microglia phenotype and shift microglial polarization toward the anti-inflammatory M2 phenotype. The WB and IHC results showed that abrocitinib played a neuroprotective role by restraining JAK1/STAT1/NF-κB levels after TBI. Collectively, abrocitinib treatment after TBI is accompanied by improvements in neurological function consistent with radiological, histopathological, and biochemical changes. Therefore, abrocitinib can indeed reduce excessive neuroinflammation by restraining the JAK1/STAT1/NF-κB pathway.

Does Vitamin D Administration Increase the Neuroprotective Effect of Estrogen in Male Rats with Traumatic Brain Injury?

Background: In our previous studies, the effect of sex hormones on brain edema reduction after traumatic brain injury (TBI) was demonstrated. In the current study, alone and combined effects of 17-β estradiol (E2) and vitamin D (Vit D) on TBI in male rats were investigated.Methods: Male rats were divided into six groups, including sham, TBI, vehicle, E2, Vit D, and E2+Vit D. In all groups except sham, moderate-intensity diffuse TBI was induced by the Marmarou’s method. Vehicle, E2, Vit D and their combination were intramusculary injected one and 12 hours after the TBI. The brain water content, permeability of blood brain barrier (BBB) and histopathological outcome were assessed 24h after TBI. The neurological outcome score was determined using the veterinary coma scale (VCS).Results: Significant reductions in brain water content (P<0.001, P<0.05 and P<0.01, respectively) and BBB permeability (P<0.001) appeared in the treated groups with E2, Vit D, and E2+Vit D compared to the vehicle group. Twenty-four hours after the injury, the neurological scores in the E2, Vit D, and E2+Vit D groups increased significantly compared to the vehicle group (P<0.05). Dramatic improvement in histopathological outcome was also observed in the treated groups compared to the vehicle group.Conclusion: Alone and combined consumption of estrogen and vitamin D may similarly decrease the development of brain edema and improve the neurological and histopathological consequences of TBI. Therefore, consumption of vitamin D did not enhance the neuroprotective effect of estrogen in TBI.

Blood Pressure Control in Traumatic Subdural Hematomas

Background There is debate over optimal systolic blood pressure (SBP) after traumatic subdural hematoma. Increased SBP has the benefit of increasing cerebral perfusion pressure and limiting the detrimental secondary effects of traumatic brain injurybut poses a risk of hematoma expansion. While prior studies have shown that SBP<90mmHg is associated with worsened morbidity and mortality in subdural hematoma patients, clinical guidelines and expert opinion have differing initial SBP goals. The aim of this study is to leverage a large database to determine the effects of two such goals, namely SBP 100-150mmHg versus SBP<180mmHg in this patient population. Methods A de-identified database network (TriNetX Research Network) was used to retrospectively query all patients with a first instance diagnosis of acute traumatic SDH, who also had a recorded GCS, with maintenance of SBP 100-150 within the first 24 hours (cohort 1) versus patients with an SBP<180 (cohort 2). Data came from 68 health care organizations (HCOs) with a total of 105,897,964 patients on 9/1/2022. The primary outcome of interest was mortality within 30 days. Secondary outcomes include gastrostomy tube placement, craniotomy/craniectomy/burr hole drainage, venous thromboembolism, ischemic stroke, myocardial infarction, seizure, falls, cardiac arrest, and acute kidney injury within 30 days. Cohorts were propensity-score matched for confounders. Results After propensity score matching, 1,243 patients were identified in each cohort. Age at index was 57.97+/-23.21 years and 58.28+/-22.35 years for cohorts 1 and 2, respectively.Mortality was seen in 243 patients (19.756%) vs. 209 (16.992%) (OR 1.203, 95% CI (0.98,1.476), p=0.0767) in cohorts 1 and 2, respectively. There was no statistical difference in secondary outcomes. Conclusion The results of this study demonstrate that the primary outcome of mortality at 30 days is not statistically different in acute traumatic SDH patients, whether their SBP is kept at 100-150 or below 180. Likewise, it shows no statistical difference in the subsequent incidence of gastrostomy tube placement, craniotomy/craniectomy/burr holes, venous thromboembolism, ischemic stroke, myocardial infarction, seizure, falls, or acute kidney injury.