Traumatic Brain Injury (TBI)

Outpatients with an acquired brain injury (ABI) experience physical, mental, and social deficits. ABI can be classified into two subgroups based on mechanism of injury: mild traumatic brain injury (mTBI; e.g., concussion) and other ABI (e.g., stroke, brain aneurysm, encephalitis). Our understanding of habitual activity levels within ABI populations is limited because they are often collected using self-report measures. The purpose of this study was to, 1) describe the habitual activity levels of outpatients with ABI using objective and self-report monitoring, and 2) compare the activity levels of outpatients with mTBI vs. other ABI. Sixteen outpatients with other ABI (mean ​± ​standard deviation: [58 ​± ​13] years, 9 females) and 12 outpatients with mTBI ([48 ​± ​11] years, 9 females) wore a thigh-worn activPAL 24 ​h/day (h/day) for 7-days. Outpatients with ABI averaged (6.0 ​± ​2.3) h/day of upright time, (10.6 ​± ​2.2) h/day of sedentary time, (5.6 ​± ​2.7) h/day in prolonged sedentary bouts > 1 ​h, (5 960 ​± ​3 037) steps/day, and (11 ​± ​13) minutes/day (min/day) of moderate-vigorous physical activity (MVPA). There were no differences between activPAL-derived upright, sedentary, prolonged sedentary time, and physical activity between the mTBI and other ABI groups (all,  ​> ​0.31). Outpatients with ABI overestimated their MVPA levels (+138 ​min/week) and underestimated sedentary time (-4.3 ​h/day) compared to self-report (all,  ​< ​0.001). Despite self-reporting high activity levels, outpatients with ABI objectively exhibit highly inactive and sedentary lifestyles. The habitual movement behaviours of our sample did not differ by mechanism of injury (i.e., mTBI versus other ABI). Targeting reductions in objectively measured sedentary time are needed to progressively improve the habitual movement behaviours of outpatients with ABI.

Traumatic spinal cord injury (SCI), known for its limited intrinsic regeneration capacity, often results in considerable neurological impairment. Studies suggest that therapeutic techniques utilizing exosomes (Exo) to promote tissue regeneration and modulate immune responses are promising for SCI treatment. However, combining exosome therapy with biomaterials for SCI treatment is not very effective. This study developed an adhesive hydrogel using exosomes secreted by cortical neurons derived from human induced pluripotent stem cells (iPSCs) and decellularized extracellular matrix (dECM) from human umbilical cord mesenchymal stem cells (hUCMSCs) to enhance motor function recovery post-SCI. In vitro assessments demonstrated the excellent cytocompatibility of the dECM hydrogel. Additionally, the Exo-dECM hydrogel facilitated the polarization of early M2 macrophages, reduced neuronal apoptosis, and established a pro-regenerative microenvironment in a rodent SCI model. Subsequent analyses revealed significant activation of endogenous neural stem cells and promotion of axon regeneration and remyelination at eight weeks post-surgery. The Exo-dECM hydrogel also promoted the functional recovery and preservation of urinary tissue in SCI-afflicted rats. These findings highlighted that the Exo-dECM hydrogel is a promising therapeutic strategy for treating SCI.

Approximately 40% of dementia cases worldwide are attributable to 12 potentially modifiable risk factors. However, the proportion attributable to these risks in Latin America remains unknown. We aimed to determine the population attributable fraction (PAF) of 12 modifiable risk factors for dementia in seven countries in Latin America.

Language is processed incrementally, with addressees considering multiple candidate interpretations as speech unfolds, supporting the retention of these candidate interpretations in memory. For example, after interpreting the utterance, "Click on the striped bag", listeners exhibit better memory for non-mentioned items in the context that were temporarily consistent with what was said (e.g., dotted bag), vs. not consistent (e.g., dotted tie), reflecting the encoding of linguistic context in memory. Here, we examine the impact of moderate-severe traumatic brain injury (TBI) on memory for the contexts of language use. Participants with moderate-severe TBI (N=71) and non-injured comparison participants (NC, N=85) interpreted temporarily ambiguous utterances in rich contexts. A subsequent memory test demonstrated that participants with TBI exhibited impaired memory for context items and an attenuated memory advantage for mentioned items compared to NC participants. Nonetheless, participants with TBI showed similar, although attenuated, patterns in memory for temporarily-activated items as NC participants.

Exercise training (ET) is a promising rehabilitation approach for long-term negative consequences of traumatic brain injury (TBI). However, little is known regarding overall rates of attrition, adherence, and compliance to ET in TBI.

Acute internal carotid artery occlusion is a neurological emergency that can result in cerebral infarction. Superficial temporal artery to middle cerebral artery bypass is one option to treat a subset of such patients. Near-infrared spectroscopy (NIRS) is an emerging non-invasive technique that holds promise to facilitate the management of carotid occlusion patients by monitoring the oxygen saturation of specific brain areas at risk for hypoperfusion and infarction. This case report describes a man in his 50s who presented with left-sided weakness due to acute right internal carotid artery occlusion. The patient was successfully managed both medically and surgically while incorporating data from NIRS for decision-making.

Traumatic brain injury (TBI) is a critical condition associated with cognitive impairments, including dementia. This study is aimed to construct a long noncoding RNA (lncRNA)-microRNA (miRNA)-messenger RNA (mRNA) network based on bioinformatics analysis and explore molecular mechanisms underlying post-TBI dementia.

Blood biomarkers are an emerging diagnostic and prognostic tool that reflect a range of neuropathological processes following traumatic brain injury (TBI). Their effectiveness in identifying long-term neuropathological processes after TBI is unclear. Studying biomarkers in the chronic phase is vital because elevated levels in TBI might result from distinct neuropathological mechanisms during acute and chronic phases. Here, we examine plasma biomarkers in the chronic period following TBI and their association with amyloid and tau PET, white matter microarchitecture, brain age and cognition. We recruited participants ≥40 years of age who had suffered a single moderate-severe TBI ≥10 years previously between January 2018 and March 2021. We measured plasma biomarkers using single molecule array technology [ubiquitin C-terminal hydrolase L1 (UCH-L1), neurofilament light (NfL), tau, glial fibrillary acidic protein (GFAP) and phosphorylated tau (P-tau181)]; PET tracers to measure amyloid-β (18F-NAV4694) and tau neurofibrillary tangles (18F-MK6240); MRI to assess white matter microstructure and brain age; and the Rey Auditory Verbal Learning Test to measure verbal-episodic memory. A total of 90 post-TBI participants (73% male; mean = 58.2 years) were recruited on average 22 years (range = 10-33 years) post-injury, and 32 non-TBI control participants (66% male; mean = 57.9 years) were recruited. Plasma UCH-L1 levels were 67% higher {exp(b) = 1.67, P = 0.018, adjusted P = 0.044, 95% confidence interval (CI) [10% to 155%], area under the curve = 0.616} and P-tau181 were 27% higher {exp(b) = 1.24, P = 0.011, adjusted P = 0.044, 95% CI [5% to 46%], area under the curve = 0.632} in TBI participants compared with controls. Amyloid and tau PET were not elevated in TBI participants. Higher concentrations of plasma P-tau181, UCH-L1, GFAP and NfL were significantly associated with worse white matter microstructure but not brain age in TBI participants. For TBI participants, poorer verbal-episodic memory was associated with higher concentration of P-tau181 {short delay: b = -2.17, SE = 1.06, P = 0.043, 95% CI [-4.28, -0.07]; long delay: bP-tau = -2.56, SE = 1.08, P = 0.020, 95% CI [-4.71, -0.41]}, tau {immediate memory: bTau = -6.22, SE = 2.47, P = 0.014, 95% CI [-11.14, -1.30]} and UCH-L1 {immediate memory: bUCH-L1 = -2.14, SE = 1.07, P = 0.048, 95% CI [-4.26, -0.01]}, but was not associated with functional outcome. Elevated plasma markers related to neuronal damage and accumulation of phosphorylated tau suggest the presence of ongoing neuropathology in the chronic phase following a single moderate-severe TBI. Plasma biomarkers were associated with measures of microstructural brain disruption on MRI and disordered cognition, further highlighting their utility as potential objective tools to monitor evolving neuropathology post-TBI.

Although cases of neonatal opioid withdrawal syndrome (NOWS) increased 5-fold in recent years, no study has examined national hospital readmission rates for these infants.

Altered reactivity to emotional stimuli is common after traumatic brain injury (TBI), which is suggested to reflect difficulties with emotion regulation. While disinhibition is common after moderate-to-severe TBI, limited research has investigated the link between disinhibition and emotional reactivity in this clinical group. The aim of this research, therefore, was to investigate the relationship between disinhibition and TBI to anger provocation.

Mental health conditions and concussion history reported by a collegiate athlete may contribute to prolonged recovery and symptom severity after concussion. This work examined the potential associations among concussion history, pre-existing conditions, and sex relative to initial symptom severity and recovery duration following sport-related concussion (SRC) in a cohort of Division 1 NCAA athletes. This prospective cohort study analyzed symptom severity, recovery and return-to-play times reported post-SRC using data collected as part of the Pac-12 CARE Affiliated Program and Health Analytics Program. Health history questionnaires which included self-reported history of pre-existing conditions were completed at baseline. When consented athletes were diagnosed with a concussion, daily post-concussion symptom scores were evaluated until an athlete was clinically determined to be asymptomatic. Generalized linear and Cox proportional hazards models were used to determine associations between pre-existing conditions and recovery and return-to-play times. 92 concussions met inclusion criteria. Notable differences in initial symptom severity existed between females and males who had mood disorders ([Cohen's d] = 0.51) and ADHD (d = 0.93). The number of previous concussions was a strong predictor of athletes reporting pre-existing mood disorders, depression, anxiety, and ADHD (p = 0.008-0.04). Females with ≥2 previous concussions required more days to return-to-play than males (d = 0.31-0.72). Weekly recovery and return-to-play probabilities substantially differed between athletes that did or did not have learning disorders (HRRecovery = 0.32, HRRTP = 0.22, d = 1.96-2.30) and ADHD (HRRecovery = 3.38, HRRTP = 2.74, d = 1.71-4.14). Although no association existed between concussion history and acute symptom severity, collegiate athletes with a history of concussion had higher probabilities of reporting depression, mood disorders, anxiety, and ADHD. Having ADHD or learning disorders likely strongly affects time to recovery and return-to-play for collegiate athletes.

Traumatic brain injury (TBI) is a common neurosurgical disease in emergency rooms with poor prognosis, imposing severe burdens on patients and their families. Evidence indicates that piracetam and compound porcine cerebroside and ganglioside injection (CPCGI) can improve cognitive levels in TBI patients to enhance functional prognosis, but there is still a research gap regarding the efficacy of CPCGI. This study aims to determine the effectiveness and safety of CPCGI in improving cognitive and functional outcomes in TBI patients.

Wu et al. (2021) investigated the neuroprotective effects of hypoxia preconditioning (HPC) in a rat model of traumatic brain injury (TBI). The study demonstrated that HPC enhances brain resilience to TBI by upregulating glucose transporters GLUT1 and GLUT3 through the HIF-1α signaling pathway. Comprehensive molecular and histological analyses confirmed increased expression of these transporters, correlating with reduced neuronal apoptosis and cerebral edema. The robust methodology, including rigorous statistical validation and time-course assessments, underscores HPC's potential therapeutic role in mitigating neuronal loss and improving glucose transport post-injury. However, the study could be strengthened by incorporating additional preconditioning controls, comparative analyses with other neuroprotective strategies, and exploring downstream metabolic effects in greater detail. Furthermore, expanding the research to include diverse animal models and examining sex-dependent responses would enhance the generalizability and translational relevance of the findings. Future studies should also integrate metabolic flux analysis and advanced imaging techniques to further elucidate HPC's mechanisms of action.

Deficits in learning and memory are some of the most commonly reported symptoms following a traumatic brain injury (TBI). We will examine whether the neural basis of these deficits stems from alterations to bidirectional synaptic plasticity within the hippocampus. Although the CA1 subregion of the hippocampus has been a focus of TBI research, the dentate gyrus should also be given attention as it exhibits a unique ability for adult neurogenesis, a process highly susceptible to TBI-induced damage. This review examines our current understanding of how TBI results in deficits in synaptic plasticity, as well as how TBI-induced changes in endocannabinoid (eCB) systems may drive these changes. Through the synthesis and amalgamation of existing data, we propose a possible mechanism for eCB-mediated recovery in synaptic plasticity deficits. This hypothesis is based on the plausible roles of CB1 receptors in regulating inhibitory tone, influencing astrocytes and microglia, and modulating glutamate release. Dysregulation of the eCBs may be responsible for deficits in synaptic plasticity and learning following TBI. Taken together, the existing evidence indicates eCBs may contribute to TBI manifestation, pathogenesis, and recovery, but it also suggests there may be a therapeutic role for the eCB system in TBI.

Neuromodulation trials for the treatment of posttraumatic stress disorder (PTSD) have yielded mixed results, and the optimal neuroanatomical target remains unclear. Here we analyzed three datasets to study brain circuitry causally linked to PTSD in military veterans. In veterans with penetrating traumatic brain injury, lesion locations that reduced probability of PTSD were preferentially connected to a circuit including the medial prefrontal cortex, amygdala and anterolateral temporal lobe. In veterans without lesions, PTSD was specifically associated with increased connectivity within this circuit. Reduced functional connectivity within this circuit after transcranial magnetic stimulation correlated with symptom reduction, even though the circuit was not directly targeted. This lesion-based 'PTSD circuit' may serve as a target for clinical trials of neuromodulation in veterans with PTSD.

Cortical contusions are common in moderate-severe traumatic brain injury (TBI). Cortical contusions often expand, potentially causing neuro-worsening several hours to days post-trauma. While contusion expansion (CE) may affect outcome, potential clinical and radiological markers that can predict CE have been insufficiently explored. In the present single-center retrospective observational cohort study, we evaluated clinical outcome by the Glasgow Outcome Scale extended (GOSE) scale and evaluated risk factor for CE.

Detecting malingered neurocognitive dysfunction is a major issue in forensic context, particularly in legal proceeding/insurance assessment after a traumatic brain injury (TBI), condition frequently associated with persistent cognitive impairments that may potentially be related to malingering. Consequently, research has devoted considerable efforts on developing tools to verify symptoms authenticity. This study compared two freestanding performance validity tests (PVTs) (Amsterdam Short-Term Memory Test-ASTM; Word Completion Memory Test-WCMT) and five embedded PVTs (Rey Complex Figure Test-RCFT-Copy and Recall trials; Reliable Digit Span-RDS; Rey Auditory Verbal Learning Test-RAVLT-Recognition and Total Learning trials) in a sample of 120 participants, including 15 patients with TBI ( = 44.40), 52 experimental simulators ( = 29.52) and 53 control ( = 29.77). Group performance was analyzed to assess tests' discriminatory power, and Receiver Operating Characteristic (ROC) curves were used to examine tools' sensitivity and specificity. Results indicated that experimental simulators performance on the ASTM, WCMT, and RAVLT differed significantly from TBI patients and controls. The RDS and RCFT did not discriminate experimental simulators from TBI group. ROC curves analysis reveals that the most accurate tests in this battery for detecting malingering were the ASTM and the RAVLT-Total Learning score. This study offers implications for identifying malingering in medico-legal settings, underscoring the importance of incorporating PVTs into clinical practice.

Converging evidence from studies of patients suffering focal brain lesions and results from animal models led to the notion of two functionally and structurally distinct memory systems, declarative-explicit-episodic and procedural-implicit-skill.

Increasing literature has affirmed that changes in the gut microbiome (GM) composition were linked to distinct brain injury (BI) through the gut-brain axis, but it is uncertain if such links reflect causality. Further, the immune cell changes mediating the impact of GM on BI are not completely understood. We made use of the summary statistics of 211 GM (MiBioGen consortium), 731 immune cells, and 2 different BIs (FinnGen consortium), namely traumatic BI (TBI) and focal BI (FBI), from the extensive genome-wide association studies to date. We executed bidirectional Mendelian randomization (MR) analyses to ascertain the causal relationships between the GM and BI, and 2-step MR to validate possible mediating immune cells. Additionally, thorough sensitivity analyses verified the heterogeneity, robustness, as well as horizontal pleiotropy of the results. Based on the results of inverse-variance weighted (IVW) and sensitivity analyses, in MR analyses, 5 specific GM taxa and 6 specific GM taxa were causally associated with FBI and TBI, respectively; 27 immunophenotypes and 39 immunophenotypes were causally associated with FBI and TBI, respectively. Remarkably, Anaerofilum, LachnospiraceaeNC2004group, RuminococcaceaeUCG004, CCR2 on myeloid dendritic cell (DC), CD123 on CD62L+ plasmacytoid DC, and CD123 on plasmacytoid DC were causally associated with TBI and FBI (all P < .040). However, our reverse MR did not indicate any influence of TBI and FBI on the specific GM. In mediation analysis, we found that the associations between Escherichia.Shigella and FBI were mediated by CD123 on CD62L + plasmacytoid DC in addition to CD123 on plasmacytoid DC, each accounting for 4.21% and 4.21%; the association between FamilyXIIIAD3011group and TBI was mediated by CCR2 on myeloid DC, with mediated proportions of 5.07%. No remarkable horizontal pleiotropy or heterogeneity of instrumental variables was detected. Our comprehensive MR analysis first provides insight into potential causal links between several specific GM taxa with FBI/TBI. Additionally, CD123 on plasmacytoid DC in conjunction with CCR2 on myeloid DC may function in gut microbiota-host crosstalk in FBI and TBI, correspondingly. Further studies are critical to unravel the underlying mechanisms of the links between GM and BI.

Despite increasing recognition of the significance of mild traumatic brain injury (mTBI), the long-term cognitive consequences of the injury remain unclear. More sensitive measures that can detect subtle cognitive changes and consideration of individual variability are needed to properly characterise cognitive outcomes following mTBI. Here, we used complex behavioural tasks, individual differences approaches, and electrophysiology to investigate the long-term cognitive effects of a history of mTBI. In Experiment 1, participants with self-reported mTBI history (n=82) showed poorer verbal working memory performance on the operation span task compared to control participants (n=88), but there were no group differences in visual working memory, multitasking, cognitive flexibility, attentional control, visuospatial ability, or information processing speed. Individual differences analyses revealed that time since injury and presence of memory loss predicted visual working memory capacity and visuospatial ability, respectively, in those with mTBI history. In Experiment 2, participants with mTBI history (n=20) again demonstrated poorer verbal working memory on the operation span task compared to control participants (n=38), but no group differences were revealed on a visuospatial complex span task or simpler visual working memory measures. We also explored the electrophysiological indices of visual working memory using EEG during a change detection task. No differences were observed in early sensory event-related potentials (P1, N1) or the later negative slow wave associated with visual working memory capacity. Together, these findings suggest that mTBI history may be associated with a lasting, isolated disruption in the subsystem underlying verbal working memory storage. The results emphasize the importance of sensitive cognitive measures and accounting for individual variability in injury characteristics when assessing mTBI outcomes.

The abuse of synthetic steroids, such as nandrolone decanoate (ND), is often associated with violent behavior, increasing the risk of traumatic brain injury (TBI). After a TBI, proteins like APP, β-amyloid peptide-42 (Aβ42), and phosphorylated tau (pTau) accumulate and trigger endoplasmic reticulum (ER) stress associated with an unfolded protein response (UPR). The involvement of mitochondrial bioenergetics in this context remains unexplored. We interrogate whether the abuse of ND before TBI alters the responses of ER stress and mitochondrial bioenergetics in connection with neurodegeneration and memory processing in mice. Male CF1 adult mice were administered ND (15 mg/kg) or vehicle (VEH) s.c. for 19 days, coinciding with the peak day of aggressive behavior, and then underwent cortical controlled impact (CCI) or sham surgery. Spatial memory was assessed through the Morris water maze task (MWM) post-TBI. In synaptosome preparations, i) we challenged mitochondrial complexes (I, II, and V) in a respirometry assay, employing metabolic substrates, an uncoupler, and inhibitors; and ii) assessed molecular biomarkers through Western blot. TBI significantly increased APP, Aβ42, and pTau levels, along with ER-stress proteins, GRP78, ATF6, and CHOP, implying it primed apoptotic signaling. Concurrently, TBI reduced mitochondrial Ca efflux in exchange with Na, disturbed the formation/dissipation of membrane potential, increased HO production, decreased biogenesis (PGC-1⍺ and TOM20), and ATP biosynthesis coupled with oxygen consumption. Unexpectedly, ND abuse before TBI attenuated the elevations in APP, Aβ42, and pTau, accompanied by a decrease in GRP78, ATF6, and CHOP levels, and partial normalization of mitochondrial-related endpoints. A principal component analysis revealed a key hierarchical signature featuring mitochondrial Ca efflux, CHOP, GRP78, TOM20, HO, and bioenergetic efficiency as a unique variable (PC1) able to explain the memory deficits caused by TBI, as well as the preservation of memory fitness induced by prior ND abuse.

The mitogen-activated protein kinase kinase kinase kinases (MAP4Ks) signaling pathway plays a pivotal role in axonal regrowth and neuronal degeneration following insults. Whether targeting this pathway is beneficial to brain injury remains unclear. In this study, we showed that adeno-associated virus-delivery of the Citron homology domain of MAP4Ks effectively reduces traumatic brain injury-induced reactive gliosis, tauopathy, lesion size, and behavioral deficits. Pharmacological inhibition of MAP4Ks replicated the ameliorative effects observed with expression of the Citron homology domain. Mechanistically, the Citron homology domain acted as a dominant-negative mutant, impeding MAP4K-mediated phosphorylation of the dishevelled proteins and thereby controlling the Wnt/β-catenin pathway. These findings implicate a therapeutic potential of targeting MAP4Ks to alleviate the detrimental effects of traumatic brain injury.

Palliative care is a specialized approach designed to enhance the quality of life for both patients and their families, offering patient-centered care through comprehensive assessment and care planning. However, the integration of palliative care within neuro-critical care settings has been relatively understudied. This descriptive study aims to identify the characteristics, palliative care needs, and outcomes of patients referred to palliative care services during admission to the neurosurgical intensive care unit (NS-ICU).

The involvement of the excitatory amino acids glutamate and aspartate in cerebral ischemia and excitotoxicity is well-documented. Nevertheless, the role of non-excitatory amino acids in brain damage following a stroke or brain trauma remains largely understudied. The release of amino acids by necrotic cells in the ischemic core may contribute to the expansion of the penumbra. Our findings indicated that the reversible loss of field excitatory postsynaptic potentials caused by transient hypoxia became irreversible when exposed to a mixture of just four non-excitatory amino acids (L-alanine, glycine, L-glutamine, and L-serine) at their plasma concentrations. These amino acids induce swelling in the somas of neurons and astrocytes during hypoxia, along with permanent dendritic damage mediated by N-methyl-D-aspartate receptors. Blocking N-methyl-D-aspartate receptors prevented neuronal damage in the presence of these amino acids during hypoxia. It is likely that astroglial swelling caused by the accumulation of these amino acids via the alanine-serine-cysteine transporter 2 exchanger and system N transporters activates volume-regulated anion channels, leading to the release of excitotoxins and subsequent neuronal damage through N-methyl-D-aspartate receptor activation. Thus, previously unrecognized mechanisms involving non-excitatory amino acids may contribute to the progression and expansion of brain injury in neurological emergencies such as stroke and traumatic brain injury. Understanding these pathways could highlight new therapeutic targets to mitigate brain injury.

Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury, the fundamental regulatory and functional mechanisms remain insufficiently understood. As potent anti-inflammatory agents, the use of glucocorticoids in traumatic brain injury is still controversial, and their regulatory effects on microglial polarization are not yet known. In the present study, we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action. In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization. Lipopolysaccharide, dexamethasone, RU486 (a glucocorticoid receptor antagonist), and ruxolitinib (a Janus kinase 1 antagonist) were administered. RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone. The Morris water maze, quantitative reverse transcription-polymerase chain reaction, western blotting, immunofluorescence and confocal microscopy analysis, and TUNEL, Nissl, and Golgi staining were performed to investigate our hypothesis. High-throughput sequencing results showed that arginase 1, a marker of M2 microglia, was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at 3 days post-traumatic brain injury. Thus dexamethasone inhibited M1 and M2 microglia, with a more pronounced inhibitory effect on M2 microglia in vitro and in vivo. Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury. Additionally, glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death, and also decreased the density of dendritic spines. A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway. Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia, which plays an anti-inflammatory role. In contrast, inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury. Dexamethasone may exert its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway.

Traumatic brain injury and Alzheimer's disease share pathological similarities, including neuronal loss, amyloid-β deposition, tau hyperphosphorylation, blood-brain barrier dysfunction, neuroinflammation, and cognitive deficits. Furthermore, traumatic brain injury can exacerbate Alzheimer's disease-like pathologies, potentially leading to the development of Alzheimer's disease. Nanocarriers offer a potential solution by facilitating the delivery of small interfering RNAs across the blood-brain barrier for the targeted silencing of key pathological genes implicated in traumatic brain injury and Alzheimer's disease. Unlike traditional approaches to neuroregeneration, this is a molecular-targeted strategy, thus avoiding non-specific drug actions. This review focuses on the use of nanocarrier systems for the efficient and precise delivery of siRNAs, discussing the advantages, challenges, and future directions. In principle, siRNAs have the potential to target all genes and non-targetable proteins, holding significant promise for treating various diseases. Among the various therapeutic approaches currently available for neurological diseases, siRNA gene silencing can precisely "turn off" the expression of any gene at the genetic level, thus radically inhibiting disease progression; however, a significant challenge lies in delivering siRNAs across the blood-brain barrier. Nanoparticles have received increasing attention as an innovative drug delivery tool for the treatment of brain diseases. They are considered a potential therapeutic strategy with the advantages of being able to cross the blood-brain barrier, targeted drug delivery, enhanced drug stability, and multifunctional therapy. The use of nanoparticles to deliver specific modified siRNAs to the injured brain is gradually being recognized as a feasible and effective approach. Although this strategy is still in the preclinical exploration stage, it is expected to achieve clinical translation in the future, creating a new field of molecular targeted therapy and precision medicine for the treatment of Alzheimer's disease associated with traumatic brain injury.

Participation in American-style football (ASF) has been linked to chronic traumatic encephalopathy neuropathological change (CTE-NC), a specific neuropathologic finding that can only be established at autopsy. Despite being a postmortem diagnosis, living former ASF players may perceive themselves to have CTE-NC. At present, the proportion and clinical correlates of living former professional ASF athletes with perceived CTE who report suicidality are unknown.

Chronic post-traumatic headache (CPTH) after a mild traumatic brain injury (mTBI) has been reported in up to 60% of patients and can be extremely debilitating. While pharmacological treatments are typically used for CPTH, they frequently cause side effects and have limited effectiveness, leading individuals with CPTH to be unsatisfied with current treatment options and to seek non-pharmacological options. Acupuncture has been identified as a potential treatment option; however, the evidence in this population remains limited. The overall goal of this study was to examine the effect of a once weekly (e.g., low dose) vs. twice weekly (e.g., high dose) of acupuncture treatment on CPTH in individuals with mTBI. Thirty-eight individuals were randomized to receive either 5 or 10 acupuncture treatments using a standard protocol over 5 weeks. The protocol consisted of 14 points using traditional acupuncture and 4 points using electroacupuncture. Headache outcomes, safety, treatment adherence, sleep quality, and quality of life (QOL) were assessed. The results showed that while there were no differences between dose groups for any of the outcomes assessed, acupuncture significantly reduced the number of headache days and headache pain intensity in individuals with CPTH. There were no significant changes in acute medication use or sleep quality. While there were some QOL improvements identified, these results should be interpreted with caution. Overall, acupuncture was shown to be safe and well-tolerated in people with CPTH after mTBI, and 5 acupuncture treatments using a standardized protocol shows promise in providing headache relief for this population.

Traumatic brain injury (TBI) activates the NF-κB pathway in microglia and astrocytes, which secrete pro-inflammatory cytokines that disrupt the blood-brain barrier (BBB). Curdlan derivatives are promising carriers for the delivery of siRNA drugs. Herein, we evaluated the glial cell specificity, siRNA delivery efficiency, and the subsequent phenotypic regulation of glial cells by the Curdlan derivatives in the TBI mouse model. Our and studies confirmed that the (1) pAVC4 or CuMAN polymer encapsulating siRNA were internalized by astrocytes and microglia in a receptor-dependent manner; (2) systemic administration of the pAVC4 or CuMAN polymer encapsulating siRNA resulted in significant gene silencing efficiency, altered the phenotypic polarization of glial cells, and regulated the secretion of inflammatory cytokines; (3) this lessened neuroinflammation, ameliorated BBB destruction, and improved vascular recovery. These data suggested that pAVC4 and CuMAN polymers are promising RNA delivery vehicles that can efficiently deliver siRNA to the target cells.

Traumatic brain injury (TBI) remains a major concern for global health. Recent studies have suggested the role of NOD-like receptor pyrin domain-containing protein 3 (NLRP3), an inflammatory marker, in the cerebrospinal fluid (CSF) and serum as potential indicators of TBI prognosis. The objective of the study was to characterize NLRP3 as a clinically applicable tool for predicting the outcomes of TBI patients.

Early treatment of elevated intracranial pressure (ICP) is a cornerstone of the therapy in severe traumatic brain injury (TBI) patients. Treatment of refractory high ICP however, remain challenging as only limited and risky third-tier therapeutic interventions are available. Controlled lumbar cerebrospinal fluid (CSF) drainage has been known as an efficient method of ICP reduction after TBI for decades, but it is not recommended in international guidelines because of low evidence background and safety issues. Our centre has a long-standing experience using this intervention for more than 15 years. Here we present our data about the safety and efficacy of controlled lumbar drainage to avoid further second- and third tier ICP lowering therapies and beneficially influence functional outcome.

Traumatic brain injury (TBI) is a major cause of disability and mortality worldwide. However, existing treatments still face numerous clinical challenges. Building on our prior research showing peripheral nerve-derived stem cell (PNSC) spheroids with Schwann cell-like phenotypes can secrete neurotrophic factors to aid in neural tissue regeneration, we hypothesized that repeated intrathecal injections of PNSC spheroids would improve the delivery of neurotrophic factors, thereby facilitating the restoration of neurological function and brain tissue repair post-TBI.

Advances in trauma care have attributed to a decrease in mortality and change in cause of death. Consequently, exsanguination and traumatic brain injury (TBI) have become the most common causes of death. Exsanguination decreased by early hemorrhage control strategies, whereas TBI has become a global health problem. The aim of this study was to investigate trends in injury severity,physiology, treatment and mortality in the last decade.

Neurotrauma registries (NTR) collect data on traumatic brain injuries (TBI) to advance knowledge, shape policies, and improve outcomes. This study reviews global NTRs from High-Income (HICs) and Low- and Middle-Income countries (LMICs). A systematic review was conducted using PubMed, Google Scholar, Embase, and Web of Science following PRISMA guidelines to identify relevant NTRs. Twenty-six articles were included, revealing ten different NTRs from Europe, North America, Latin America, the Middle East, and Asia. North America had the most registries at four, followed by Europe and Asia with two each, and Latin America and the Middle East with one each. The median database size was 1,734 patients (Range: 65-25,000), with the largest registry from the United States (FITBIR DB) and the smallest from Iran (NSCIR-IR). The longest data collection period was 32 years, with a mean age of 43.1 years (Range: 9.07-60.0). Males comprised 70 % of patients. Sixty-six percent of articles emphasized outcomes such as functionality, length of stay, and mortality. Key challenges identified included issues with missing data and incomplete records (n = 4), lack of standardization in data collection procedures (n = 3), staffing shortages (n = 5), lack of IT infrastructure (n = 3), and problems with reproducibility, particularly in high-income countries (n = 4). Our review highlights the need for a large-scale global NTR, addressing LMIC barriers through private-public partnerships with organized neurosurgery members.

Demonstrate how patient-level traumatic brain injury (TBI) data from studies in the Federal Interagency Traumatic Brain Injury Research (FITBIR) Informatics System can be harmonized and pooled to examine relationships between TBI and cognitive functioning.

The aim of this study is to describe circumstances, management and short-term outcomes of neonatal head trauma, and adherence to the Paediatric Emergency Care Applied Research Network (PECARN) head trauma prediction rule for children under 2 years.

Chronic traumatic encephalopathy (CTE) has been diagnosed in 91.7% of retired United States National Football League (NFL) players at postmortem. There is no treatment or cure for CTE. Most living former NFL athletes with probable CTE suffer from obesity and its comorbidities. Our previous reviews document the improvement in cognition following metabolic/bariatric surgery (MBS) (e.g., gastric bypass, sleeve gastrectomy). These operations might reduce microglial maladaptive states, thereby attenuating neurodegeneration and CTE-like neurocognitive impairment. The study evaluated former NFL players' views on metabolic surgery in relation to reduction of obesity and CTE risk.

Cerebral complications after cardiac arrest (CA) remain a major problem worldwide. The aim was to test the effects of sodium-ß-hydroxybutyrate (SBHB) infusion on brain injury in a clinically relevant swine model of CA.

Neurological diseases, characterized by neuroinflammation and neurodegeneration, impose a significant global burden, contributing to substantial morbidity, disability and mortality. A common feature of these disorders, including stroke, traumatic brain injury and Alzheimer's disease, is the impairment of the blood-brain barrier (BBB), a critical structure for maintaining brain homeostasis. The compromised BBB in neurodegenerative conditions poses a significant challenge for effective treatment, as it allows harmful substances to accumulate in the brain. Nanomedicine offers a promising approach to overcoming this barrier, with nanoparticles (NPs) engineered to deliver therapeutic agents directly to affected brain regions. This review explores the classification and design of NPs, divided into organic and inorganic categories and further categorized based on their chemical and physical properties. These characteristics influence the ability of NPs to carry and release therapeutic agents, target specific tissues and ensure appropriate clearance from the body. The review emphasizes the potential of NPs to enhance the diagnosis and treatment of neurodegenerative diseases through targeted delivery, improved drug bioavailability and real-time therapeutic efficacy monitoring. By addressing the challenges of the compromised BBB and targeting inflammatory biomarkers, NPs represent a cutting-edge strategy in managing neurological disorders, promising better patient outcomes.

The aim of this study is to assess the effectiveness of various therapy methods in elderly individuals with traumatic brain injury (TBI), taking into account the degree of memory loss and the severity of the injury. The study was conducted in 2022 in Moscow, Russia, and Sofia, Bulgaria, involving six clinics. A total of 200 elderly patients with TBI participated in the study, with a mean age of 72 years. Patients were categorized into groups based on the degree of memory loss and severity of the injury. Standardized tests, including the Mini-Mental State Examination (MMSE), Clock Drawing Test, Digit Symbol Substitution Test, and Free, and Cued Selective Reminding Test, were used to assess cognitive functions. The Progressive Learning Test evaluated patients' ability to memorize and reproduce information over time. Groups receiving physical therapy and cognitive rehabilitation showed statistically significant improvement in cognitive functions compared to other therapy methods. Specifically, the mean score of the MMSE in these groups increased by 7 points (p < .001). Patients with more severe memory loss demonstrated more pronounced improvement in cognitive functions following the integrated therapy approach. The mean MMSE score increased by 10 points (p < .001), whereas in patients with milder memory loss, the growth was less significant (mean increase of 5 points, p < .05). Groups receiving physical therapy and cognitive rehabilitation consistently demonstrated significantly better results compared to speech therapy and psychological support throughout the study period.

The brain glymphatic system is currently being explored in the context of many neurological disorders and diseases, including traumatic brain injury, Alzheimer's disease, and ischemic stroke. However, little is known about the impact of brain tumors on glymphatic function. Mechanical forces generated during tumor development and growth may be responsible for compromised glymphatic transport pathways, reducing waste clearance and cerebrospinal fluid (CSF) transport in the brain parenchyma. One such force is solid stress, i.e., growth-induced forces from cell hyperproliferation and excess matrix deposition. Because there are no prior studies assessing the impact of tumor-derived solid stress on glymphatic system structure and performance in the brain parenchyma, this study serves to fill an important gap in the field. We adapted a previously developed Electrical Analog Model using MATLAB Simulink for glymphatic transport coupled with Finite Element Analysis for tumor mechanical stresses and strains in COMSOL. This allowed simulation of the impact of tumor mechanical force generation on fluid transport within brain parenchymal glymphatic units-which include perivascular spaces, astrocytic networks, interstitial spaces, and capillary basement membranes. We conducted a parametric analysis to compare the contributions of tumor size, tumor proximity, and ratio of glymphatic subunits to the stress and strain experienced by the glymphatic unit and corresponding reduction in flow rate of CSF. Mechanical stresses intensify with proximity to the tumor and increasing tumor size, highlighting the vulnerability of nearby glymphatic units to tumor-derived forces. Our stress and strain profiles reveal compressive deformation of these surrounding glymphatics and demonstrate that varying the relative contributions of astrocytes vs. interstitial spaces impact the resulting glymphatic structure significantly under tumor mechanical forces. Increased tumor size and proximity caused increased stress and strain across all glymphatic subunits, as does decreased astrocyte composition. Indeed, our model reveals an inverse correlation between extent of astrocyte contribution to the composition of the glymphatic unit and the resulting mechanical stress. This increased mechanical strain across the glymphatic unit decreases the venous efflux rate of CSF, dependent on the degree of strain and the specific glymphatic subunit of interest. For example, a 20% mechanical strain on capillary basement membranes does not significantly decrease venous efflux (2% decrease in flow rates), while the same magnitude of strain on astrocyte networks and interstitial spaces decreases efflux flow rates by 7% and 22%, respectively. Our simulations reveal that solid stress from growing brain tumors directly reduces glymphatic fluid transport, independently from biochemical effects from cancer cells. Understanding these pathophysiological implications is crucial for developing targeted interventions aimed at restoring effective waste clearance mechanisms in the brain. This study opens potential avenues for future experimental research in brain tumor-related glymphatic dysfunction.

To examine the lived experiences of adults who have received community-based rehabilitation (CBR) services in Australia or New Zealand for cognitive-communication disorders (CCDs) following traumatic brain injury (TBI) and their support people. Participants' recommendations for future models of care were also explored to enhance rehabilitation services for people with TBI.

Cranioplasty is an elective neurosurgical procedure following decompressive craniectomy, often associated with post-operative complications such as hemorrhage, seizures, infection, hydrocephalus, and bone resorption. While seizures post-cranioplasty is not uncommon, Intractable seizures are rare but a dreadful complication following cranioplasty.

Traumatic brain injury (TBI) afflicts 69 million individuals annually, resulting in numerous neuropsychiatric sequelae. Here, we investigate the possible relation between TBI and depression.

Cognitive reserve (CR) is the brain's ability to cope with changes related to aging and/or disease. Originally introduced to explain individual differences in the clinical manifestations of dementia, CR has recently emerged as a relevant construct in stroke and traumatic brain injury (TBI). This systematic review aims to investigate whether CR could predict post-stroke and TBI clinical recovery and rehabilitation outcomes, and how different variables used to estimate CR (i.e., proxies) are related to the prognosis and effectiveness of rehabilitation in these clinical populations. A search was made in Pubmed, Embase, and PsycInfo for articles published until 12 January 2023, following the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) protocol guidelines. 31 studies were included after completing all screening stages. Overall, results show that a higher CR was associated with a better prognosis and a more effective rehabilitation in most of the clinical aspects considered: cognitive functioning, functional, occupational, and socio-emotional abilities, as well as psychiatric and neurological scales. A higher CR seems to be associated with a more favorable prognosis and a better rehabilitation outcome after stroke and TBI. Results suggest that CR should be taken into account in clinical practice to make more accurate predictions about recovery and effectiveness of rehabilitation. However, some inconsistencies suggest the need for further investigations, possibly using multiple proxies for CR.

Cross-sectional study.

The Rey-Osterrieth Complex Figure Test (ROCFT) and the Clock Drawing Test (CDT) are commonly used in clinical practice. The ROCFT measures constructional praxis, visual perception, and visuospatial learning and memory, and the CDT assesses for visuospatial, constructional, and executive difficulties. Several neurological disorders are associated with visuospatial and visuo-constructional impairments, yet reliable normative data accounting for sociodemographic and acculturative variables are scarce for Hispanics living in the U.S.

Guidelines for the management of pediatric severe traumatic brain injury (TBI) recommend external ventricular drainage for CSF drainage as a first-tier treatment in the intracranial pressure (ICP) pathway. However, ventriculostomy in children can sometimes be challenging because of the small size of the lateral ventricles. External lumbar drainage (ELD) may be a useful alternative; therefore, the authors analyzed the outcome of a cohort of pediatric patients who underwent ELD to manage intracranial hypertension (ICH).

Traumatic brain injury (TBI) often results in persistent learning and memory deficits, likely due to disrupted hippocampal circuitry underlying these processes. Precise temporal control of hippocampal neuronal activity is important for memory encoding and retrieval and is supported by oscillations that dynamically organize single unit firing. Using high-density laminar electrophysiology, we discovered a loss of oscillatory power across CA1 lamina, with a profound, layer-specific reduction in theta-gamma phase amplitude coupling in injured rats. Interneurons from injured animals were less strongly entrained to theta and gamma oscillations, suggesting a mechanism for the loss of coupling, while pyramidal cells were entrained to a later phase of theta. During quiet immobility, we report decreased ripple amplitudes from injured animals during sharp-wave ripple events. These results reveal deficits in information encoding and retrieval schemes essential to cognition that likely underlie TBI-associated learning and memory impairments, and elucidate potential targets for future neuromodulation therapies.

Traumatic brain injuries (TBIs) pose significant challenges to public health, medicine, and society due to their substantial impact on victims, caregivers, and the community. While indicators like life expectancy or death rates provide insights into mortality and long-term outcomes, they fail to address how TBIs affect aging, neurological sequelae, cognitive impairment, and psychological or psychiatric disorders. Moreover, most studies are limited to North America, limiting the generalizability of findings across different social welfare systems. As a result, clinicians face difficulties in providing optimal care and prognosis, hindering the improvement of life quality for victims and caregivers and efficient public health service planning. This study aims to address these limitations by examining life expectancy, mortality rates, and long-term outcomes in severely injured individuals.

Trauma to the brain can induce a contusion characterized by a discrete intracerebral or diffuse interstitial hemorrhage. In humans, "computed tomography (CT)-positive", i.e., hemorrhagic, temporal lobe contusions (tlCont) have unique sequelae. tlCont confers significantly increased odds for moderate or worse disability and the inability to return to baseline work capacity compared to intra-axial injuries in other locations. Patients with tlCont are at elevated risks of memory dysfunction, anxiety and post-traumatic epilepsy due to involvement of neuroanatomical structures unique to the temporal lobe including the amygdala, hippocampus and ento-/perirhinal cortex. Because of the relative inaccessibility of the temporal lobe in rodents, no preclinical model of tlCont has been described, impeding progress in elucidating the specific pathophysiology unique to tlCont. Here, we present a minimally invasive mouse model of tlCont with the contusion characterized by a traumatic interstitial hemorrhage. Mortality was low and sensorimotor deficits (beam walk, accelerating rotarod) resolved completely within 3-5 days. However, significant deficits in memory (novel object recognition, Morris water maze) and anxiety (elevated plus maze) persisted at 14-35 days, and non-convulsive electroencephalographic seizures and spiking were significantly increased in the hippocampus at 7-21 days. Immunohistochemistry showed widespread astrogliosis and microgliosis, bilateral hippocampal sclerosis, bilateral loss of hippocampal and cortical inhibitory parvalbumin neurons, and evidence of interhemispheric connectional diaschisis involving the fiber bundle in the ventral corpus callosum that connects temporal lobe structures. This model may be useful to advance our understanding of the unique features of tlCont in humans.

Post-traumatic Parkinsonism (PTP) is a complex neurological disorder that is often associated with the occurrence of a traumatic brain injury (TBI). PTP can occur either in the acute or chronic phase of TBI. There is still uncertainty about the mechanisms provoking PTP, which can be the result of the acute blast itself or secondary neurodegenerative process occurring months to years post the acute trauma. Currently there is an underestimation of the clinical importance of PTP and lack of specific and proven therapeutic interventions, both in the pharmacological and the neurorehabilitation field. This narrative review aims to summarize the actual knowledge about PTP in terms of its pathophysiology, clinical aspects, treatments and perspective of care in the neurorehabilitative setting.

Traumatic brain injury (TBI) is a prevalent problem with survivors suffering from chronic cognitive impairments. Following TBI there is a series of neuropathological changes including neurogenesis. It is well established that neurogenesis in the dentate gyrus (DG) of the hippocampus is important for hippocampal dependent learning and memory functions. Following TBI, injury-enhanced hippocampal neurogenesis is believed to contribute to post-injury cognitive recovery. Behavioral function is connected to synaptic plasticity and neuronal dendritic branching is critical for successful synapse formation. To ascertain the functional contribution of injury-induced DG new neurons in post-TBI cognitive recovery, it is necessary to study their dendritic morphological development and the molecular mechanisms controlling this process. Utilizing transgenic mice with tamoxifen-induced GFP expression and Notch1 knock-out in nestin+ neural stem cells, this study examined dendritic morphology, the role of Notch1 in regulating dendritic complexity of injury-induced DG new neurons, and their association to post-TBI cognitive recovery. We found that at 8 weeks after a moderate TBI, injury-induced DG new neurons in the injured control mice displayed a similar dendritic morphology as the cells in non-injured mice accompanied with cognitive recovery. In comparison, in Notch1 conditional knock-out mice, DG new neurons in the injured mice had a significant reduction in dendritic morphological development including dendritic arbors, volume span, and number of branches in comparison to the cells in non-injured mice concomitant with persistent cognitive dysfunction. The results of this study confirm the importance of post-injury generated new neurons in cognitive recovery following TBI and the role of Notch1 in regulating their maturation process.

Neurons are the primary cells responsible for information processing in the central nervous system (CNS). However, they are vulnerable to damage and insult in a variety of neurological disorders. As the most abundant glial cells in the brain, astrocytes provide crucial support to neurons and participate in synapse formation, synaptic transmission, neurotransmitter recycling, regulation of metabolic processes, and the maintenance of the blood-brain barrier integrity. Though astrocytes play a significant role in the manifestation of injury and disease, they do not work in isolation. Cellular interactions between astrocytes and neurons are essential for maintaining the homeostasis of the CNS under both physiological and pathological conditions. In this review, we explore the diverse interactions between astrocytes and neurons under physiological conditions, including the exchange of neurotrophic factors, gliotransmitters, and energy substrates, and different CNS diseases such as Alzheimer's disease, Parkinson's disease, stroke, traumatic brain injury, and multiple sclerosis. This review sheds light on the contribution of astrocyte-neuron crosstalk to the progression of neurological diseases to provide potential therapeutic targets for the treatment of neurological diseases.

The development of an optical interface to directly distinguish the brain tissue's biochemistry is the next step in understanding traumatic brain injury (TBI) pathophysiology and the best and most appropriate treatment in cases where in-hospital intracranial access is required. Despite TBI being a globally leading cause of morbidity and mortality in patients under 40, there is still a lack of objective diagnostical tools. Further, given its pathophysiological complexity the majority of treatments provided are purely symptomatic without standardized therapeutic targets. Our tailor-engineered prototype of the intracranial Raman spectroscopy probe (Intra-RSP) is designed to bridge the gap and provide real-time spectroscopic insights to monitor TBI and its evolution as well as identify patient-specific molecular targets for timely intervention. Raman spectroscopy being rapid, label-free and non-destructive, renders it an ideal portable diagnostics tool. In combination with our in-house developed software, using machine learning algorithms for multivariate analysis, the Intra-RSP is shown to accurately differentiate simulated TBI conditions in rat brains from the healthy controls, directly from the brain surface as well as through the rat's skull. Using clinically pre-established methods of cranial entry, the Intra-RSP can be inserted into a 2-piece optimised cranial bolt with integrated focussing and correctly identify a sample in real-life conditions with an accuracy >80 %. To further validate the Intra-RSP's efficiency as a TBI monitoring device, rat brains mildly damaged from inflicted spinal cord injury were found to be correctly classified with 94.5 % accuracy. Through optimization and rigorous in-vivo validation, the Intra-RSP prototype is envisioned to seamlessly integrate into existing standards of neurological care, serving as a minimally invasive, in-situ neuromonitoring tool. This transformative approach has the potential to revolutionize the landscape of neurological care by providing clinicians with unprecedented insights into the nature of brain injuries and fostering targeted, timely and effective therapeutic interventions.

Military personnel exposed to blasts receive repeated subconcussive head impacts. Although these events typically do not cause immediate symptoms and do not lead to medical evaluation, the cumulative effects of subconcussive impacts can be significant and can include postconcussive symptoms, changes in brain structure and function, long-term cognitive dysfunction, depression, and chronic traumatic encephalopathy. Retinal measures such as thickness of retinal neural layers, density of retinal microvasculature, and strength of retinal neuronal firing are associated with cognitive function and brain structure and function in healthy populations and in neurodegenerative disease cohorts, and changes over time in retinal indices predict cognitive decline and brain atrophy in longitudinal studies in a range of medical populations. This commentary highlights the potential benefits of using retinal biomarkers in the routine screening and monitoring of brain health in warfighters and veterans. Retinal measures can be rapidly acquired (often in a matter of seconds) using methods that are inexpensive and noninvasive, and they can be collected with movable and often portable equipment that uses automated scoring routines that can be used for prediction and decision-making at the individual level. To date, however, retinal biomarkers have not been included in studies of blast overpressure exposures in military personnel. Despite this, preclinical and human evidence suggests that they could be among the most effective methods for tracking central nervous system damage in people exposed to repeated blasts. Retinal biomarkers could also contribute to brief test batteries to determine who is most at risk for long-term negative effects of future exposures. In addition, the sensitivity of retinal indices to blast exposure and mild traumatic brain injury suggests that they should be incorporated into research on strategies to minimize or prevent blast-related short- and long-term central nervous system changes in blast-exposed military personnel.

The neuroinflammatory response promotes secondary brain injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 1 (TREM1) is a key regulator of inflammation. However, the role of TREM1 in TBI is poorly studied. The purpose of this study was to investigate the role of TREM1 in TBI and the possible underlying mechanism. We found that the protein expression of TREM1 significantly increased after TBI in rats, and the TREM1 protein localized to microglia. Inhibition of the TREM1 protein with LP17 significantly blocked ERK phosphorylation and reduced cytoplasmic phospholipase A2 (cPLA2) protein expression and phosphorylation. In addition, LP17-mediated TREM1 inhibition significantly reduced the protein expression of iNOS and increased the protein expression of Arg1 . Moreover, after TREM1 was inhibited, the secretion of the proinflammatory factors TNF-α and IL-1β was significantly reduced, while the secretion of the anti-inflammatory factors IL-4 and IL-10 was significantly increased. Additionally, inhibition of TREM1 by LP17 significantly reduced neuronal apoptosis and ameliorated nerve dysfunction in TBI model rats. In conclusion, our findings suggest that TREM1 enhances neuroinflammation and promotes neuronal apoptosis after TBI, and these effects may be partly mediated via the ERK/cPLA2 signalling pathway.

Deep brain stimulation (DBS) results in improvements in motor function and quality of life in patients with Parkinson disease (PD), which might impact a patient's perception of valued personal characteristics. Prior studies investigating whether DBS causes unwanted changes to oneself or one's personality have methodological limitations that should be addressed.

(1) Introduction: Since electric scooters were launched in 2017, they have become increasingly popular worldwide and a cause of childhood trauma. (2) Case reports: This paper has a double-fold purpose: it reports two cases of epidural hematomas and compares them with electric scooter-related head trauma in the literature. An overview of the literature on this topic was performed to make such a comparison. Our cases are one of almost 52 cm and one of 129 cm both in two eight-year-olds. (3) Discussion: Although usually mild, traumatic brain injuries following e-scooter falls can also be moderate and severe. Reduced helmet use, high speed, and a lack of experience are the perfect set-up for potential severe injuries. Intracranial bleeds are not frequent, and epidural hematomas are rare in such cases, but they can significantly impact the individual, community, and healthcare system. No other medium- or large-sized epidural hematomas were reported in children sustaining electric scooter-related head trauma. (4) Conclusions: Our review parallels the literature and our hospital's experience. Although there are both similarities and discrepancies between our cases and the literature, mild trauma should not be disregarded, for it may hide serious complications requiring immediate surgery.

Retraction: M. C. Liu, V. Akle, W. Zheng, J. Kitlen, B. O'Steen, S. F. Larner, J. R. Dave, F. C. Tortella, R. L. Hayes, and K. K. W. Wang, "Extensive Degradation of Myelin Basic Protein Isoforms by Calpain Following Traumatic Brain Injury," Journal of Neurochemistry 98, no. 3 (2006): 700-712. https://doi.org/10.1111/j.1471-4159.2006.03882.x. The above article, published online on 19 June 2006, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Andrew Lawrence; the International Society for Neurochemistry; and John Wiley and Sons Ltd. A third party reported that they had detected evidence of image manipulation and duplication throughout the published article. An investigation by the publisher and the editors concluded that there was evidence of splicing in Figures 2a, 2b, 3a, 5a, 6a, and 8a. The investigation also found duplications of lanes in Figures 3a, 3d, and 4a. Lastly, the investigation found that the same actin blots in Figure 3 have been used in two other articles by many of the same authors, despite representing different experimental conditions. The authors did not respond to an inquiry by the publisher. The retraction has been agreed to because the results presented in the article can no longer be considered reliable. The authors did not respond to the notice of retraction.

Post-traumatic epilepsy (PTE) is a recurrent and often drug-refractory seizure disorder caused by traumatic brain injury (TBI). No single drug treatment prevents PTE, but preventive drug combinations that may prophylax against PTE have not been studied. Based on a systematic evaluation of rationally chosen drug combinations in the intrahippocampal kainate (IHK) mouse model of acquired epilepsy, we identified two multi-targeted drug cocktails that exert strong antiepileptogenic effects. The first, a combination of levetiracetam (LEV) and topiramate, only partially prevented spontaneous recurrent seizures in the model. We therefore added atorvastatin (ATV) to the therapeutic cocktail (TC) to increase efficacy, forming "TC-001". The second cocktail - a combination of LEV, ATV, and ceftriaxone, termed "TC-002" - completely prevented epilepsy in the mouse IHK model. In the present proof-of-concept study, we tested whether the two drug cocktails prevent epilepsy in a rat PTE model in which recurrent electrographic seizures develop after severe rostral parasagittal fluid percussion injury (FPI). Following FPI, rats were either treated over 3-4 weeks with vehicle or drug cocktails, starting either 1 or 4-6 h after the injury. Using mouse doses of TC-001 and TC-002, no significant antiepileptogenic effect was obtained in the rat PTE model. However, when using allometric scaling of drug doses to consider the differences in body surface area between mice and rats, PTE was prevented by TC-002. Furthermore, the latter drug cocktail partially prevented the loss of perilesional cortical parvalbumin-positive GABAergic interneurons. Plasma and brain drug analysis showed that these effects of TC-002 occurred at clinically relevant levels of the individual TC-002 drug components. In silico analysis of drug-drug brain protein interactions by the STITCH database indicated that TC-002 impacts a larger functional network of epilepsy-relevant brain proteins than each drug alone, providing a potential network pharmacology explanation for the observed antiepileptogenic and neuroprotective effects observed with this combination.

Traumatic brain injury (TBI) is among the leading causes of death and disability globally. Identifying and assessing the risk of in-hospital mortality in traumatic brain injury patients at an early stage is challenging. This study aimed to develop a model for predicting in-hospital mortality in TBI patients using prehospital data from China.

Prolonged changes to functional network connectivity as a result of a traumatic brain injury (TBI) may relate to long-term cognitive complaints reported by TBI survivors. No interventions have proven to be effective at treating long-term cognitive complaints after TBI but physical activity has been shown to promote cognitive function and modulate functional network connectivity in non-injured adults. Therefore, the objective of this study was to test if physical activity engagement was associated with functional connectivity of the cognitively relevant frontoparietal control network (FPCN) in adults with a TBI history.

Mild traumatic brain injury (mTBI), i.e. a TBI with an admission Glasgow Coma Scale (GCS) of 13-15, is a common cause of emergency department visits. Only a small fraction of these patients will develop a traumatic intracranial hemorrhage (tICH) with an even smaller subgroup suffering from severe outcomes. Limitations in existing management guidelines lead to overuse of computed tomography (CT) for emergency department (ED) diagnosis of tICH which may result in patient harm and higher healthcare costs.

Repetitive Transcranial Magnetic Stimulation (rTMS) is emerging as a promising treatment for persons with disorder of consciousness (DoC) following traumatic brain injury (TBI). Clinically, however, there are concerns about rTMS exacerbating baseline seizure risk. To advance understanding of risks, this article reports evidence of DoC-TBI rTMS-related seizure risk.

Stroke and traumatic intracranial hemorrhage (tICH) are major causes of disability worldwide, with stroke exerting significant negative effects on the brain, potentially elevating tICH risk. In this study, we investigated tICH risk in stroke survivors.

(1) To determine the proportion of participants admitted to supported community living (SCL) programs over the course of 5 years who improve, decline, or maintain functioning and community integration and (2) to examine the associations of time since injury, time in program, and age to their functional trajectory.

Understanding the extent to which neighborhood impacts recovery following traumatic brain injury (TBI) among older adults could spur targeting of rehabilitation and other services to those living in more disadvantaged areas. The objective of the present study was to determine the extent to which neighborhood disadvantage influences recovery following TBI among older adults.

Neuroinflammation is an important feature of traumatic brain injury (TBI) that remains poorly understood in the 3- to 12-month period post-TBI.

Changes in health behavior are key to maintaining health, safety, and independence of older adults. The purpose of this study was to explore factors impacting training in self-management and behavior change in older adults with and without traumatic brain injury (TBI), informing efforts to improve safety and independent function.

The inflammatory response in patients with traumatic brain injury (TBI) offers opportunities for stratification and intervention. Previous unselected approaches to immunomodulation in patients with TBI have not improved patient outcomes.

Identifying the origins and contributions of peripheral-derived immune cell populations following brain injury is crucial for understanding their roles in neuroinflammation and tissue repair. This study investigated the infiltration and phenotypic characteristics of skull bone marrow-derived immune cells in the murine brain after traumatic brain injury (TBI). We performed calvarium transplantation from GFP donor mice and subjected the recipients to controlled cortical impact (CCI) injury 14 days post-transplant. Confocal imaging at 3 days post-CCI revealed GFP+ calvarium-derived cells were present in the ipsilateral injured cortex, expressing CD45 and CD11b immune markers. These cells included Ly6G-positive neutrophil or Ccr2-positive monocyte identities. Calvarium-derived GFP+/Iba1+ monocyte/macrophages expressed the efferocytosis receptor MERTK and displayed engulfment of NeuN+ and cleaved caspase 3+ apoptotic cells. Phenotypic analysis showed that greater calvarium-derived monocytes/macrophages disproportionately express the anti-inflammatory arginase-1 marker than pro-inflammatory CD86. To differentiate the responses of blood- and calvarium-derived macrophages, we transplanted GFP calvarium skull bone into tdTomato bone marrow chimeric mice, then performed CCI injury 14 days post-transplant. Calvarium-derived GFP+cells predominantly infiltrated the lesion boundary, while blood-derived tdTomato+ cells dispersed throughout the lesion and peri-lesion. Compared to calvarium-derived cells, more blood-derived cells expressed pro-inflammatory CD86 and displayed altered 3D morphologic traits. These findings uniquely demonstrate that skull bone marrow-derived immune cells infiltrate the brain after injury and contribute to the neuroinflammatory milieu, representing a novel immune cell source that may be further investigated for their causal role in functional outcomes.

The literature on health shocks finds that minor injuries have only short-term labor market impacts. However, mild traumatic brain injuries (mTBIs, commonly referred to as concussions) may be different as the medical literature highlights that they can have longer-term health and cognitive effects. Moreover, TBIs are one of the most common causes of disability globally, with the vast majority being mild. Thus, it is important to understand the impact of mTBIs on labor market outcomes. We use administrative data on all medically-diagnosed mild traumatic brain injuries (mTBIs) in New Zealand linked to monthly tax records to examine the labor market effects of a mTBI. We use a comparison group of those who suffer a mTBI at a later date to overcome potential endogeneity issues, and employ a doubly-robust difference-in-differences method. We find that suffering a mTBI has negative labor market effects. Rather than dissipating over time, these negative effects grow, representing a decrease in employment of 20 percentage points and earning losses of about a third after 48 months. Our results highlight the need for timely diagnosis and treatment to mitigate the effect of mTBIs to reduce economic and social costs.

Hispanics are a significant demographic in the U.S., with diverse cultures and languages. Assessing cognition in this group is complex as cultural and linguistic factors have been found to affect test performance.

Soccer-related concussions (SRC) have increased despite an overall reduction of concussions across all sports activities. Few papers have studied the mechanism of injury, and have been mostly done in high-income countries or focused on small populations, preventing generalization. Our goal was to analyze the available data published about SRC over the past 10 years, independent of the country's income level. A narrative review was performed. The definition of sport-related concussion from the American Academy of Neurology and studies published between 2013 and 2023 were used. Of 1210 articles, 45 met the inclusion criteria. The results showed that SRC was more frequent in females (57.6%) than males (44.3%). Player-to-player interaction was the most common mechanism of injury, with midfielders being the most affected position. The first providers to diagnose were certified athletic trainers, within the first 24 hours. Neurological evaluations, including SCAT (Sport Assessment Concussion Tool) and ImPact (Immediate Post-concussion Assessment and Cognitive Testing), were included in 42.2% of the studies, with SCAT and ImPact specifically used in 15.5% and 11% of cases, respectively. Need for hospitalization was found in 8.9% of participants and one player required surgical intervention. At the time of the concussion, confusion, dizziness, and amnesia were reported frequently. However, after the concussion, headaches and dizziness were prevalent. Follow-up data were included in 35.5% of the studies. On average, children missed 15 practice days and returned to school after 8 days. In conclusion, future research should focus on the circumstances around head-to-head injuries by age, sex, and level of professionalism as well as the importance of early diagnosis and careful follow-up, to protect the players and improve their outcomes.

Epidural haematoma (EDH) is a common finding in many traumatic brain injury scenarios, which necessitates surgical evacuation if the volume equals 30 cm3. The Tada formula, despite its convenience, have been observed to inaccurately depict haemorrhage volume, which can lead to inappropriate decision-making. Objective: (I) to determine if there are statistical differences between EDH volumes as calculated using three-dimensional (3D) software versus Tada's formula; and (II) whether this difference leads to differences in treatment options.

Concussions are increasingly recognized as a public health concern. This paper evaluates Canadian concussion care guidelines, advocating for the inclusion of a broader range of healthcare professionals (HCPs) in concussion assessment, diagnosis, and management. It emphasizes the role of chiropractors, in addition to medical doctors (MDs) and nurse practitioners (NPs), highlighting their extensive training in musculoskeletal and neurological disorders. Chiropractors are adept at managing symptoms like headache, neck pain, and dizziness, and employing evidence-based, comprehensive interventions including patient education, exercise therapy, manual therapy, cervicovestibular rehabilitation, and return-to-sport (RTS) protocols. The paper also addresses regional variations in chiropractors' roles, focusing on Ontario's "Rowan's Law," and argues that limiting aspects of concussion care (assessment, diagnosis, RTS clearance) to MDs and NPs may result in healthcare inefficiencies and inequities. The findings are significant for policymakers and healthcare leaders, indicating a need for updated concussion care guidelines that integrate and utilize diverse HCPs. This could lead to improved patient outcomes, healthcare efficiency, and equity in concussion management across Canada.

Introduction Traumatic brain injuries (TBI) in recent years have proved to be a significant public health problem, with potentially life-changing consequences for the individual and their family. Alcohol consumption is a regular, well-documented problem among persons sustaining TBI due to road traffic accidents and accidental falls. The primary objective of this study was to find out the correlation between the Glasgow Coma Scale (GCS) score and CT brain findings among mild TBI patients under acute alcohol intoxication and determine if early CT-brain is indicated in this group. Methods A prospective observational study was conducted involving 111 alcohol-intoxicated patients with mild head injuries admitted to the surgical wards of Thanjavur Medical College Hospital over a period of three months. The Glasgow Coma Scale was used to assess the patient's neurological status and determine the severity of the brain injury. A semi-structured CT-brain findings chart and a severity of alcohol intoxication objective-based scoring system were developed and validated by experts. Descriptive statistics tools such as frequency, percentage, and mean were used, along with inferential statistics tools like the Chi-squared test, Fisher exact test, and Pearson's correlation coefficient test. Results The study findings showed that the comparison of GCS with early CT-brain was significant at a p-value of 0.012, and a negative correlation (r=-0.253) was found between GCS and CT-brain findings. A comparison of CT-brain findings with the severity of alcohol intoxication was non-significant at a p-value of 0.433. Conclusions Early CT-brain in intoxicated mild TBI patients may have a positive impact on early diagnosis and management, even in centers with limited resources catering to low-income population groups. The results of our short-term study show that early CT-Brain picks up lesions and helps initiate early management while it is up to the attending physician to keep in mind an adverse cost-benefit ratio in overuse of hospital resources and misdiagnosis leading to undertreatment causing long-term sequelae and morbidity before prescribing early CT-brain in this cohort of patients.

Electrolyte disturbances are common in patients with traumatic brain injury (TBI), particularly affecting sodium, potassium, chloride, and calcium levels. This study aims to provide insights into these disturbances within the first 24 h post-injury.

Traumatic brain injury has been a leading cause of morbidity, mortality, and disability. Patients may experience cognitive and functional decline, depending on the severity. In this case report, a patient presents with a closed-head traumatic brain injury that was sustained after a motor vehicle accident. Through a comprehensive inpatient rehabilitation plan with physical therapy, speech therapy, occupational therapy, and neuropsychological assessments, this patient was able to gain functionality, as shown by his Ranchos Los Amigos Revised Scale. This scale is used to describe the cognitive and behavioral patterns found in recovering patients following a traumatic brain injury. With this case report, we hope to raise awareness within the medical community of the benefits of inpatient rehabilitation so that patients suffering from traumatic brain injury can receive better functional and cognitive recovery.

Brain health has been a growing concern across a wide range of contact sports in the last three decades. While most of the early brain health research was focused on identifying and preventing concussions, newer research has found that an accumulation of repetitive head impacts (RHI) are more predictive of long-term brain health than the number of concussions sustained. Consequently, being able to assess RHI in sports despite the lack of outward symptoms has become paramount in promoting the long-term health of athletes. The sport of rodeo has long been regarded as one of the most dangerous contact sports. While some epidemiological research has been done on injury rates in rodeo that has largely backed up its dangerous reputation, no research has been done into RHI in rodeo athletes.

Vanishing white matter disease (VWMD), also known as childhood ataxia with central hypoventilation, is a rare leukodystrophy that is inherited in an autosomal recessive manner. It is triggered by either traumatic brain injury or a febrile episode. The patient was a three-year-old male child who presented with complaints of fever and diarrhea for three days, along with a paucity of movements of both upper and lower limbs, with decreased tone and diminished reflexes. Previously the child had normal developmental milestones. MRI done showed T2 hyperintensities involving bilateral peri-ventricular white matter, deep white matter, and bilateral sub-cortical U-fibres in bilateral fronto-parietal region and bilateral cerebellar hemispheres. The bilateral external capsule and posterior limb of the internal capsule were also involved. All these findings were likely suggestive of leukodystrophy. Whole exome sequencing was done and a homozygous mutation of the eIF2B5 was noted, which confirmed the diagnosis of VWMD. The physician must keep in mind this diagnosis in cases of sudden motor abnormalities following any event and proceed for early management such as controlling febrile episodes with liberal use of antibiotics and antipyretics, along with prevention of traumatic brain injury or any stressful event. There is no definitive treatment. Management of these patients includes symptomatic and supportive care. Patients with this disease (VMND) have a poor quality of life as the disease progresses and eventually, death occurs.

A huge number of new cases - around a few million of traumatic brain injury (TBI) - are recorded globally each year, making it a major public health risk. A significant portion of all accident-related deaths are attributable to TBI, a notable mortality rate. There are TBI deaths in every age range. Long-term neurobehavioral impacts, such as altered emotions and personalities, cognitive and mental deficits, and so on, are experienced by the majority of survivors. Our main objective is to understand the possible mechanism of the NLRP3 inflammasome in retinal neurons and enhance precision regarding reducing the burden of retinal neurodegeneration in TBI-induced AD. Both primary and secondary insults initiate the intricate pathophysiology of traumatic brain injury. Primary injuries are caused by mechanical force and occur right after the collision. Long-lasting and delayed secondary injuries follow. Studies demonstrating the continuous nature of research on the relationship between retinal neurons and TBI-induced Alzheimer's disease (AD) include neurodegeneration, retinal changes, and inflammatory response biomarkers. TBI can cause changes that resemble those seen in AD. This includes the accumulation of tau tangles and amyloid-beta plaques, which are also observed in the retina and imply a potential relationship between AD, traumatic brain injury, and retinal health. The linkage between TBI and AD, the effect of the innate immune system in post-TBI AD, the function of immunological moderators, the activation and assembly of inflammasomes in TBI, the pathophysiology of TBI, and the connection between TBI and inflammasome activity were the main topics of discussion in the following discussions. Of particular interest was the potential mechanism by which the NLRP3 inflammasome, in conjunction with SREBP2 and SCAP inflammasome, in retinal neurons in TBI-induced AD. The thinning of RNFL, poor lipid metabolism, and new developments such as drug delivery technologies, lipid metabolism modulation in retinal neurons, and drug-targeting lipid pathways and their mechanisms are then covered in this article.

Cranioplasty performed after a decompressive craniectomy (DC) for traumatic brain injury (TBI), stroke, or aneurysmal bleed has a role of restoring cerebral protection and craniofacial cosmesis as well as improving neuromotor function. There has been no consensus with regards to the ideal timing of cranioplasty (CP) after DC. A retrospective cohort study was carried out at a tertiary care hospital on patients who had undergone early (less than or equal to 12 weeks) and late (greater than 12 weeks) cranioplasty using autologous cranial bone after DC. Functional independence measure (FIM) tools were used to compare neuromotor and cognitive function outcome between the two groups. Appropriate statistical tools were used to compare neuromotor and cognitive function improvement as well as complication rates between early and late cranioplasty. A total of 31 adult patients of cranioplasty (21 male and 10 female) were evaluated. Sixteen had undergone early and 15 late cranioplasty. Comparison for neuromotor and cognitive function using FIM tools revealed statistically significant neuromotor and cognitive advantages in the early cranioplasty group. Overall complication rates between the two groups varied but were statistically insignificant. Performing an early cranioplasty provides advantages of improvement of neuromotor and cognitive function through early restoration of cerebrospinal fluid and intracerebral haemo-dynamics. It further avoids the potential problems of developing the 'Syndrome of the Trephined' (otherwise known as sinking skin flap syndrome) and resorption of the autologous bone.

Critically ill patients, including those with brain injuries (BI), are frequently hospitalized in an intensive care unit (ICU). As with other critical states, an adequate stress response is essential for survival. Research on the hypothalamic-pituitary-adrenal gland (HPA) axis function in BI has primarily focused on assessing ACTH and cortisol levels. However, the immunological, metabolic, and hemodynamic effects of glucocorticoids (GCs) are mediated through the glucocorticoid receptor (GCR), a ubiquitously distributed intracellular receptor protein. Data on expression and its signaling in acute BI injury are lacking.

Hyperbaric oxygen (HBO) therapy can attenuate neurological impairment after traumatic brain injury (TBI) and alleviate intestinal dysfunction. However, the role and mechanism of HBO therapy in intestinal dysfunction following TBI remain unclear. Herein, by establishing a mouse model of controlled cortical impact (CCI), we found that HBO therapy reduced histopathological lesions and decreased the levels of inflammatory and oedema proteins in the intestinal tissues of mice 10 days after TBI. We also showed that HBO therapy improved microbiome abundance and probiotic (particularly ) colonisation in mice post-CCI. Then, we identified that the mA level imcreased notably in injured cortical tissue of CCI+HBO group compared with the CCI group following CCI. Thus, our results suggested that HBO therapy could alleviate TBI-induced intestinal dysfunction and mA might participate in this regulation process, which provides new insights for exploring the specific mechanism and targets of HBO in the treatment of intestinal dysfunction after TBI, thereby improving the therapeutic effect of HBO.

Research indicates young individuals with traumatic brain injuries (TBI) in juvenile justice settings lack essential support, mainly due to staff members' insufficient knowledge and skills in TBI-related areas stemming from a lack of relevant professional development. This study aimed to improve services for justice-involved youths with TBI in juvenile correction facilities by establishing empirically validated core competencies tailored to their needs. Through a Delphi study involving experts in juvenile services, juvenile corrections, TBI, transition services, and professional development, we identified and refined a set of 44 competencies distributed across six domains: knowledge (12 competencies), screening (6 competencies), eligibility (3 competencies), assessment (4 competencies), intervention (10 competencies), and community reentry (9 competencies).

Carotid-cavernous fistulas (CCFs) are abnormal connections between the carotid arteries and the cavernous sinus, posing significant neuro-ophthalmologic risks. This report presents a rare case of bilateral post-traumatic CCFs, focusing on clinical presentation, diagnosis, and management. Symptoms mimic conjunctivitis, causing diplopia, exophthalmos, and ophthalmoplegia. Diagnosis relied on computed tomography, magnetic resonance angiography, and digital subtraction angiography. Management involved transarterial embolization with coils, achieving successful outcomes. This highlights the importance of timely intervention and comprehensive imaging to prevent complications. This case report details a rare instance of bilateral post-traumatic carotid-cavernous fistulas, emphasizing clinical presentation, diagnostic evaluation, and management.

Coagulopathy is associated with poor prognosis of traumatic brain injury (TBI) patients. This study is performed to explore the association between serum magnesium level and the risk of coagulopathy in TBI.

As the population of U.S. service members (SMs) who have sustained concussions and more severe traumatic brain injuries (TBIs) during military service ages, understanding the long-term outcomes associated with such injuries will provide critical information that may promote long-term assessment, support, and rehabilitation following military service. The objective of this research was to examine whether concussion and more severe TBIs are associated with greater risk of precursors to dementia (i.e., mild cognitive impairment, memory loss), early-onset dementia, and any dementia.