Brain Injury Research Articles

Concussion leads to opposing sensorimotor effects of habituation deficit and fatigue in zebrafish larvae

Abstract Concussion, or mild traumatic brain injury, is caused by sudden mechanical forces impacting the brain either directly or through inertial loading. This can lead to physical, behavioural, and cognitive impairments 1. Despite concussion being a significant health issue, our understanding of the relationship between initial impact force and the subsequent neurological consequences is not well understood. Previously, we established a model of concussion in zebrafish larvae 2. Here we further investigate concussions of varying severities in zebrafish larvae using linear deceleration. Using an acoustic assay to monitor the larval sensorimotor behaviour 3, we found that different parameters of the resulting escape behaviour are modulated by the impact force of the preceding concussive insult. To investigate the relative contributions of habituation performance and fatigue on the escape response behaviour, we constructed a neurocomputational model. Our findings suggest that a concussive impact initially affects habituation performance at first and, as the impact force increases, fatigue is induced. Fatigue then alters the escape response behaviour in an opposing manner.

Cerebrovascular markers of WMH and infarcts in ADNI: A historical perspective and future directions.

White matter hyperintensities (WMH) and infarcts found on magnetic resonance imaging (MR infarcts) are common biomarkers of cerebrovascular disease. In this review, we summarize the methods, publications, and conclusions stemming from the Alzheimer's Disease Neuroimaging Initiative (ADNI) related to these measures. We combine analysis of WMH and MR infarct data from across the three main ADNI cohorts with a review of existing literature discussing new methodologies and scientific findings derived from these data. Although ADNI inclusion criteria were designed to minimize vascular risk factors and disease, data across all the ADNI cohorts found consistent trends of increasing WMH volumes associated with advancing age, female sex, and cognitive impairment. ADNI, initially proposed as a study to investigate biomarkers of AD pathology, has also helped elucidate the impact of asymptomatic cerebrovascular brain injury on cognition within a cohort relatively free of vascular disease. Future ADNI work will emphasize additional vascular biomarkers. HIGHLIGHTS: White matter hyperintensities (WMHs) are common to advancing age and likely reflect brain vascular injury among older individuals. WMH and to a lesser extent, magnetic resonance (MR) infarcts, affect risk for transition to cognitive impairment. WMHs and MR infarcts are present, even among Alzheimer's Disease Neuroimaging Initiative (ADNI) participants highly selected to have Alzheimer's disease (AD) as the primary pathology. WMH burden in ADNI is greater among individuals with cognitive impairment and has been associated with AD neurodegenerative markers and cerebral amyloidosis. The negative additive effects of cerebrovascular disease appear present, even in select populations, and future biomarker work needs to further explore this relationship.

Calcium bridges built by mitochondria-associated endoplasmic reticulum membranes: potential targets for neural repair in neurological diseases

The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions and metabolic levels. Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels between the endoplasmic reticulum membrane and the mitochondrial outer membrane, formed by various proteins and protein complexes. This microstructural domain mediates several specialized functions, including calcium (Ca2+) signaling, autophagy, mitochondrial morphology, oxidative stress response, and apoptosis. Notably, the dysregulation of Ca2+ signaling mediated by mitochondria-associated endoplasmic reticulum membranes is a critical factor in the pathogenesis of neurological diseases. Certain proteins or protein complexes within these membranes directly or indirectly regulate the distance between the endoplasmic reticulum and mitochondria, as well as the transduction of Ca2+ signaling. Conversely, Ca2+ signaling mediated by mitochondria-associated endoplasmic reticulum membranes influences other mitochondria-associated endoplasmic reticulum membrane-associated functions. These functions can vary significantly across different neurological diseases–such as ischemic stroke, traumatic brain injury, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease–and their respective stages of progression. Targeted modulation of these disease-related pathways and functional proteins can enhance neurological function and promote the regeneration and repair of damaged neurons. Therefore, mitochondria-associated endoplasmic reticulum membranes-mediated Ca2+ signaling plays a pivotal role in the pathological progression of neurological diseases and represents a significant potential therapeutic target. This review focuses on the effects of protein complexes in mitochondria-associated endoplasmic reticulum membranes and the distinct roles of mitochondria-associated endoplasmic reticulum membranes-mediated Ca2+ signaling in neurological diseases, specifically highlighting the early protective effects and neuronal damage that can result from prolonged mitochondrial Ca2+ overload or deficiency. This article provides a comprehensive analysis of the various mechanisms of Ca2+ signaling mediated by mitochondria-associated endoplasmic reticulum membranes in neurological diseases, contributing to the exploration of potential therapeutic targets for promoting neuroprotection and nerve repair.

Self-reported dizziness, balance, and multisensory impairment following mild traumatic brain injury: an exploratory study

ABSTRACT Dizziness following mild traumatic brain injury (mTBI), or concussion, is common and can encompass multiple sensations reflecting diverse aetiologies. This exploratory study investigated the types of dizzy sensations experienced, their evolution, and relationship with other post-concussion symptoms. Thirty New Zealanders (24 female) aged 49 ± 16 years who experienced dizziness or imbalance following their injury completed the Dizziness Handicap Inventory, Visual Vertigo Analogue Scale, and the Hospital Anxiety and Depression Scale. Additional custom questionnaires probed subjective experiences of dizziness and balance, headaches, and difficulties with auditory processing and vision. Just over half the participants (56.7%) experienced a single mTBI. The median time interval since the injury was 16 months (IQR = 24 months). Participants usually reported multiple dizzy symptoms which developed within a week of the injury, although delays of up to six months were reported. Most participants (70%) felt their symptoms improved over time, while lack of improvement was associated with a history of multiple mTBI (P = 0.020). Moderate to strong correlations between questionnaire scores representing dizziness handicap, visual vertigo severity, and auditory processing difficulties (P < 0.001) suggest that dizziness and sensory impairment following mTBI are multi-modal and likely to benefit from holistic, multidisciplinary treatment.

Cortical structural network characteristics in non-cognitive impairment end-stage renal disease

ObjectiveExplore alterations in topological features of gray matter volume (GMV) and structural networks in non-cognitive impairment end-stage renal disease (Non-CI ESRD).Materials and methodsUtilizing graph theory, we collected structural magnetic resonance imaging (sMRI) data from 38 Non-CI ESRD patients and 50 normal controls (NC). We compared, and extracted the GMV across subject groups, constructed corresponding structural covariance networks (SCNs), and investigated the alterations in SCNs feature parameters between groups.ResultsIn Non-CI ESRD patients, The GMV were reduced in several brain regions, predominantly on the left side (p &amp;lt; 0.05, FWE correction). The small-world network characteristics of the patient group’s brain networks showed a tendency toward regular. In a few densities, global network parameters, transitivity, (p &amp;lt; 0.05) was significantly increased in the ESRD group. Regional network measurements revealed inconsistent changes in regional efficiency across different brain areas. In the analysis of network hubs, the right temporal pole is likely a compensatory hub for Non-CI ESRD patients. The SCNs in Non-CI ESRD patients demonstrated reduced topological stability against targeted attacks.ConclusionThis study reveals that patients with renal failure exhibited subtle changes in brain network characteristics even before a decline in cognitive scores. These changes involve compensatory activation in certain brain regions, which enhances network transitivity to maintain the efficiency of whole-brain network information integration without significant loss. Additionally, the SCNs characteristics can serve as a neuroanatomical marker for brain alterations in Non-CI ESRD patients, offering new insights into the mechanisms of early brain injury in ESRD patients.

Epigenetic regulation of the inflammatory response in stroke

Stroke is classified as ischemic or hemorrhagic, and there are few effective treatments for either type. Immunologic mechanisms play a critical role in secondary brain injury following a stroke, which manifests as cytokine release, blood–brain barrier disruption, neuronal cell death, and ultimately behavioral impairment. Suppressing the inflammatory response has been shown to mitigate this cascade of events in experimental stroke models. However, in clinical trials of anti-inflammatory agents, long-term immunosuppression has not demonstrated significant clinical benefits for patients. This may be attributable to the dichotomous roles of inflammation in both tissue injury and repair, as well as the complex pathophysiologic inflammatory processes in stroke. Inhibiting acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic strategies. Identifying agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of stroke. Furthermore, epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke management. In this review, we summarize current findings on the epigenetic regulation of the inflammatory response in stroke, focusing on key signaling pathways including nuclear factor-kappa B, Janus kinase/ signal transducer and activator of transcription, and mitogen-activated protein kinase as well as inflammasome activation. We also discuss promising molecular targets for stroke treatment. The evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke, leading to improved post-stroke outcomes.

Psychological correlates of the good old days bias in mild traumatic brain injury

ABSTRACT Non-neurological factors such as the “expectation as etiology” or the “good old days” bias (EE/GOD bias) may partially explain persistent symptoms following mild traumatic brain injury (MTBI). What is less clear from existing research is the degree to which EE/GOD bias is related to other psychological correlates of persistent post-concussive symptoms (PPCS). We examined whether the EE/GOD bias was related to illness perception beliefs, intolerance of uncertainty, suggestibility, and domain identification. Participants with MTBI history and without (controls) reported frequency and severity of current PPCS; the MTBI group additionally reported premorbid PPCS. Participants also completed measures of psychological factors potentially associated with PPCS. Consistent with previous studies of the EE/GOD bias, the MTBI group endorsed less premorbid PPCS than current PPCS and when compared to the current symptom report of the control group. The MTBI group also endorsed more current PPCS than the control group. Higher EE/GOD bias was associated with several aspects of illness identity, including belief that symptoms would be more chronic, greater illness-related psychological distress, and greater cogniphobia. Higher EE/GOD bias was also related to higher intolerance of uncertainty and stronger personal identification with memory abilities. Regression showed that perceived symptom timeline, cogniphobia, and domain identification were unique predictors of EE/GOD bias. Findings confirm that the EE/GOD bias is seen in individuals with self-reported history of MTBI and corresponds to other psychological processes that potentially explain ongoing MTBI symptoms, providing greater insight into the potential mechanisms of PPCS. Future studies should examine the EE/GOD bias and associated psychological correlates in a clinical population and also assess for potential neuropsychological correlates. Findings suggest that psychological factors and premorbid symptom report should be considered in clinical assessment and also suggest potential mechanisms of treatment of individuals with acute MTBI or prolonged MTBI symptoms.

Preterm Brain Injury: Mechanisms and Challenges.

Preterm fetuses and newborns have a high risk of neural injury and impaired neural maturation, leading to neurodevelopmental disability. Developing effective treatments is rather challenging, as preterm brain injury may occur at any time during pregnancy and postnatally, and many cases involve multiple pathogenic factors. This review examines research on how the preterm fetus responds to hypoxia-ischemia and how brain injury evolves after hypoxia-ischemia, offering windows of opportunity for treatment and insights into the mechanisms of injury during key phases. We highlight research showing that preterm fetuses can survive hypoxia-ischemia and continue development in utero with evolving brain injury. Early detection of fetal brain injury would provide an opportunity for treatments to reduce adverse neurodevelopmental outcomes, including cerebral palsy. However, this requires that we can detect injury using noninvasive methods. We discuss how circadian changes in fetal heart rate variability may offer utility as a biomarker for detecting injury and phases of injury.

The Impact of the Histone Deacetylase Inhibitor-Sodium Butyrate on Complement-Mediated Synapse Loss in a Rat Model of Neonatal Hypoxia-Ischemia.

Perinatal asphyxia is one of the most important causes of morbidity and mortality in newborns. One of the key pathogenic factors in hypoxic-ischemic (HI) brain injury is the inflammatory reaction including complement system activation. Over-activated complement stimulates cells to release inflammatory molecules and is involved in the post-ischemic degradation of synaptic connections. On the other hand, complement is also involved in regenerative processes. The histone deacetylase inhibitor (HDACi)-sodium butyrate (SB)-provides reduction of inflammation by decreasing the expression of the proinflammatory factors. The main purpose of this study was to examine the effect of SB treatment on complement activation and synapse elimination after HI. Neonatal HI was induced in Wistar rats pups by unilateral ligation of the common carotid artery followed by 60-min hypoxia (7.6% O2). SB (300mg/kg) was administered on a 5-day regimen. Our study has shown decreased levels of synapsin I, synaptophysin, and PSD-95 in the hypoxic-ischemic hemisphere, indicating synaptic loss after neonatal HI. Transmission electron microscopy revealed injury of the synaptic structures in the brain after HI. SB treatment increased the level of the synaptic proteins, improved tissue ultrastructure, and reduced degradation of the synapses. Neonatal HI induced mRNA expression of the complement C1q, C3, C5, and C9, and their receptors C3aR and C5aR. The effect of SB was different depending on the time after induction of hypoxic-ischemic damage. Our study demonstrated that neuroprotective effect of SB may be related to the modulation of complement activity after HI brain injury.

Raloxifene Protects Oxygen-Glucose-Deprived Astrocyte Cells Used to Mimic Hypoxic-Ischemic Brain Injury

Perinatal asphyxia (PA) is a clinical condition characterized by oxygen supply suspension before, during, or immediately after birth, and it is an important risk factor for neurodevelopmental damage. Its estimated 1/1000 live births incidence in developed countries rises to 5–10-fold in developing countries. Schizophrenia, cerebral palsy, mental retardation, epilepsy, blindness, and others are among the highly disabling chronic pathologies associated with PA. However, so far, there is no effective therapy to neutralize or reduce PA-induced harm. Selective regulators of estrogen activity in tissues and selective estrogen receptor modulators like raloxifene have shown neuroprotective activity in different pathological scenarios. Their effect on PA is yet unknown. The purpose of this paper is to examine whether raloxifene showed neuroprotection in an oxygen–glucose deprivation/reoxygenation astrocyte cell model. To study this issue, T98G cells in culture were treated with a glucose-free DMEM medium and incubated at 37 °C in a hypoxia chamber with 1% O2 for 3, 6, 12, and 24 h. Cultures were supplemented with raloxifene 10, and 100 nM during both glucose and oxygen deprivation and reoxygenation periods. Raloxifene 100 nM and 10 nM improved cell survival—65.34% and 70.56%, respectively, compared with the control cell groups. Mitochondrial membrane potential was preserved by 58.9% 10 nM raloxifene and 81.57% 100 nM raloxifene cotreatment. Raloxifene co-treatment reduced superoxide production by 72.72% and peroxide production by 57%. Mitochondrial mass was preserved by 47.4%, 75.5%, and 89% in T98G cells exposed to 6-h oxygen–glucose deprivation followed by 3, 6, and 9 h of reoxygenation, respectively. Therefore, raloxifene improved cell survival and mitochondrial membrane potential and reduced lipid peroxidation and reactive oxygen species (ROS) production, suggesting a direct effect on mitochondria. In this study, raloxifene protected oxygen–glucose-deprived astrocyte cells, used to mimic hypoxic–ischemic brain injury. Two examiners performed the qualitative assessment in a double-blind fashion.

Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0

The brain is composed of different cells, such as neurons, glia, endothelial cells, etc [...]

EEG Infrastructure Within the Veterans Administration: A Survey.

EEG is a vital tool in the diagnosis and management of neurologic conditions prevalent among veterans such as seizures, epilepsy, and brain injuries. This cross-sectional study aimed to assess the state of EEG infrastructure within the Veterans Administration (VA), focusing on availability, utilization, and the potential avenues to addressing gaps in infrastructure. This survey was distributed to 123 VA hospitals using the Research Electronic Data Capture (REDCap) platform, gathering data on EEG equipment, staffing, and service provision from June to December 2023. Of the 123 VA hospitals surveyed, 70 responded (56.9% response rate). Most respondents (88.6%) reported having EEG services, although only 38.7% offering continuous EEG (cEEG). Respondents reported having less EEG technologists, machines, and faculty readers than what they thought would be ideal. Significant correlations were found between the availability of resources (e.g., number of EEG machines) and service capabilities, including remote access and cEEG. The use of alternative EEG technologies such as rapid or quantitative EEG varied greatly. Interest in participating in the VA Tele-EEG program was reported by 59.4% of respondents. There is large variability in EEG infrastructure across the VA. Tele-EEG has the potential to maintain continuity of operations through challenges affecting staffing and to improve EEG service access, especially in resource-limited settings. Expanding access to quantitative, rapid, and tele-EEG services may enhance patient management and may be a potential avenue to explore as the VA continues to invest in and grow its capacity for treating neurologic conditions.

Neuroprotective Effects of Ethanol Extract Polyscias guilfoylei (EEPG) Against Glutamate Induced Neurotoxicity in HT22 Cells

Oxidative stress induced by glutamate is a significant contributor to neuronal cell damage and can lead to neurodegenerative diseases such as Alzheimer’s, Huntington’s, and ischemic brain injury. At the cellular level, oxidative stress increases Ca2+ ion influx and reactive oxygen species (ROS), which activate the MAPK signaling pathway. Additionally, the generation of ROS causes mitochondrial dysfunction, triggering apoptosis by promoting the translocation of AIF to the nucleus from the mitochondria. The neuroprotective potential of Polyscias guilfoylei has not yet been reported. Therefore, in this study, the ethanol extract of Polyscias guilfoylei (EEPG) was examined for its protective effect against oxidative cell damage caused by glutamate in neuronal cells. EEPG treatment increased the viability of HT22 cells exposed to high concentrations of glutamate. Cellular Ca2+ ion influx and ROS generation decreased with EEPG treatment in glutamate-treated HT22 cells. EEPG treatment inhibited MAPK activation and AIF nuclear translocation. In an in vivo study, EEPG attenuated brain cell death in an ischemic brain injury rat model. This study demonstrates the potential therapeutic effects of Polyscias guilfoylei in the treatment of ischemic brain injury.

Abstract 4122507: Fetal Socioeconomic and Environmental Exposures Influence Fetal Brain Growth and Risk of Neonatal Brain Injury in Congenital Heart Disease

Introduction: Fetuses with CHD have smaller total brain volume (TBV) and are at risk for acquired brain white matter injury (WMI), both of which are linked to neurodevelopmental impairments. Social determinants of health (SDOH) and other fetal environmental factors have been linked to fetal brain health in other populations. Our aim was to test our hypothesis that these exposures influence fetal brain growth and postnatal WMI risk in severe CHD. Methods: Our prospective longitudinal cohort study enrolled fetuses with severe CHD to undergo fetal brain MRI and postnatal pre-operative brain MRI. Participants completed home environment surveys on individual SDOH and exposures. Community SDOH metrics were determined using Child Opportunity Index (COI) based on home address. An ‘at risk’ fetus composite was created if there was exposure to: personal/household smoking, welfare/food stamps, or poverty. TBV was calculated at both time points. Presence/degree of WMI was determined on postnatal MRI. Repeated measures analysis and logistic regression were performed to determine association between individual and community SDOH metrics with rate of TBV growth and risk of WMI. Results: 55 participants enrolled (54 fetal scans: mean GA 33.9 wks, 95%CI: 33.7,34.1; 47 neonatal scans: mean GA 39.3 wks 95%CI: 38.9,39.6). Fetal sex, smoking exposure, and several individual SDOH were associated with TBV growth. Adjusting for fetal sex and GA at scan, rate of TBV growth was slower with smoking exposure (coeff: -5.2, 95%CI: -10.3, -0.2, p= 0.04) and trended towards significance for those with welfare/food stamps or poverty. ‘At risk’ fetuses had slower rate of TBV growth than those without risk (coeff: -2.5, 95%CI: -5.0, -0.07, p= 0.04) (Figure 1). There were lower odds of pre-operative WMI with high COI compared to low after adjusting for GA at scan (OR= 0.16, 95%CI: 0.03, 0.9, p= 0.04). Conclusion: Smoking exposure and individual-level SDOH influence brain growth, while community COI is associated with risk of postnatal pre-op WMI in CHD. Our findings identify targets for intervention to optimize brain growth and outcomes in the CHD population, including smoking cessation programs, and nutritional and needs assessment during pregnancy.

Survivor Health Connection Project: Understanding Experiences of Accessing Health Care Among Those Affected by Intimate Partner Violence During the COVID-19 Pandemic.

Intimate partner violence (IPV) has short- and long-term health effects, including physical injuries and traumatic brain injury, as well as sexual, reproductive, and mental health issues. However, accessing necessary health care is often challenging for IPV survivors and became even more difficult during the COVID-19 pandemic. We examined access to health care among those affected by IPV during the COVID-19 pandemic to better connect survivors to health and social support services. The Health Resources and Services Administration's Office of Women's Health partnered with its Bureau of Primary Health Care, the Administration for Children and Families' Office of Family Violence Prevention and Services, and the National Domestic Violence Hotline (Hotline) on the 2-year Survivor Health Connection Project. The Hotline administered 2 surveys to its contacts: a 2-question postinteraction survey from March 29, 2021, through September 30, 2022, and a longer focused survey in 2021 and 2022 that measured barriers and restrictions to accessing health care, telehealth safety, and interactions with health care providers. Of 9918 respondents to the postinteraction survey, 6173 (62.2%) reported current health needs related to their abusive experience. Nearly half of 242 respondents to the 2021 survey (n = 106, 43.8%) indicated that the frequency or intensity of abuse increased during the COVID-19 pandemic, and 157 of 338 respondents to the 2022 survey (46.4%) reported that their partner had controlled and/or restricted their access to health care. Participants described barriers to accessing health care, including finances, health insurance coverage, and transportation. Findings illuminate opportunities to further support the health and social needs of those experiencing IPV, including continued coordination of efforts across health care and social service delivery partners.

Physiotherapists knowledge, attitudes, and practices about therapeutic interventions for cognitive and motor impairments in adult patients with traumatic brain injury

Abstract Background and aim Traumatic brain injury (TBI) affects brain functions, often leading to a range of cognitive and motor impairments, necessitating effective rehabilitation. It is expedient for physiotherapists to have adequate knowledge, an appropriate attitude, and practice towards managing cognitive and motor impairments in adults with TBI. This study assessed physiotherapists’ knowledge, attitudes, and practices of cognitive and motor impairments in adult patients with TBI. Methods This cross-sectional study involved 75 physiotherapists recruited from 8 hospitals in South-West Nigeria via purposive sampling. A self-developed questionnaire administered via Google Forms® was used to assess the knowledge, attitude, and practice (KAP) of physiotherapists towards cognitive and motor impairments in adult patients with TBI. Descriptive statistics of mean, median, range, percentages, and frequency distribution tables were used in summarizing the KAP, while the association/correlation between KAP scores and selected demographic/profession-related characteristics was also investigated using inferential statistics of the Man-Whitney U, Kruskal Wallis, and Spearman ranked correlation. The level of significance was set at p &lt; 0.05. Results The mean age of the participants was 28.73 ± 7.093 years, predominantly female (53.3%), with a bachelor’s degree in physiotherapy (78.7%), and specializing in neuro-physiotherapy. Most respondents demonstrated knowledge of cognitive 45 (60%) and motor 42 (56%) impairments in adult TBI patients. There was a (rho = 0.259) positive significant correlation (p = 0.025) between the age of the physiotherapist and their knowledge of the management of cognitive and motor impairment in adult patients with TBI. Conclusion Many physiotherapists in South-West Nigeria demonstrate good knowledge of TBI, with this knowledge increasing with age. This study underscores the importance of continuous educational training for physiotherapists, a consequence of which should be better rehabilitation and functional outcomes for people with TBI.

Lack of additional benefit from slow rewarming after therapeutic hypothermia for ischaemic brain injury in near-term fetal sheep.

The optimal rate of rewarming after therapeutic hypothermia is unclear. Slow rewarming may reduce cardiovascular instability and rebound seizures, but there is little controlled evidence to support this. The present study aimed to determine whether slow rewarming can improve neuroprotection after 72h of hypothermia. Fetal sheep (0.85 gestation) received sham occlusion (n=8) or 30min of global cerebral ischaemia followed by normothermia (n=7), or hypothermia from 3 to 72h with either fast, spontaneous rewarming within 1h (n=8) or slow rewarming at 0.5°Ch-1 over 10h (n=8). Hypothermia improved EEG and spectral edge recovery, with no significant difference between fast and slow rewarming. Hypothermia reduced the number of seizures, with no significant difference in seizure activity between fast and slow rewarming. Hypothermia improved neuronal survival in the cortex, CA1, CA3, CA4 and dentate gyrus regions of the hippocampus, with no significant difference between fast and slow rewarming. Hypothermia attenuated microglia counts in the cortex, with no significant difference between fast and slow rewarming. The rate of rewarming after a clinically relevant duration of hypothermia did not affect neurophysiological recovery, neuronal survival or attenuation of microglia after global cerebral ischaemia in term-equivalent fetal sheep. KEY POINTS: The rate of rewarming after 72h of hypothermia did not affect recovery of EEG or spectral edge. There was no difference in the occurrence of seizures as a result of the rate of rewarming after hypothermia. The rate of rewarming after 72h of hypothermia did not affect neuronal survival in the cortex or hippocampus.

Prevalence of epilepsy: a population-based cohort study in Denmark with comparison to Global Burden of Disease (GBD) prevalence estimates

BackgroundThe Global Burden of Disease Study (GBD) produces prevalence estimates for ‘idiopathic epilepsy’ (ie, of unknown aetiology) and ‘secondary epilepsy’ (ie, with known aetiology) but does not report prevalence by...

Exploring multimodal biomarker candidates of post-traumatic epilepsy following moderate to severe traumatic brain injury: A systematic review and meta-analysis.

This review systematically analyzes potential biomarker candidates for post-traumatic epilepsy (PTE) in humans who have experienced moderate to severe traumatic brain injury (TBI). Focusing on biomarkers across biofluid-based protein, genetic, neuroimaging, and neurophysiological categories, this review distinguishes between TBI patients who develop PTE and those who do not. The review adheres to established methodologies outlined in the Cochrane Handbook for Systematic Reviews of Interventions. Data presentation follows the Meta-analyses of Observational Studies (MOOSE) and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Medline, Embase, and Web of Science were systematically searched and yielded 7538 records, of which 18 met inclusion criteria (moderate-severe TBI in humans, follow-up of at least 6 months, and no prior history of epilepsy). The review aggregates data from 15 cohort and 3 case-control studies (risk of bias was assessed using the Newcastle-Ottawa Scale). Statistically significant biomarkers were identified, with neurophysiological biomarkers showing the strongest effect size in a two-study meta-analysis. PTE, a severe long-term outcome of TBI affecting 2% to 53% of individuals with TBI, lacks validated biomarkers for forecasting development, crucial for designing preventive clinical trials. A multimodal approach, integrating biofluid-based protein, genetic, neuroimaging, and neurophysiological data, offers a promising strategy to enhance the predictability of PTE development and, potentially, its treatment. The study's protocol is registered in the International Prospective Register of Systematic Reviews PROSPERO (Registration ID: CRD42023470245).

Seizures and Epilepsy in Association With Neurocysticercosis: A Nosologic Proposal.

Neurocysticercosis is one of the main risk factors of seizures and epilepsy in many regions of the world, which are Taenia solium-endemic but resource-constrained to control the parasite. The nosology of seizures and the classification of epilepsy in the context of neurocysticercosis are somewhat uncertain. Many seizures associated with the infection are customarily referred to as "acute symptomatic seizures." The term, however, seems unsuitable. Neither is the condition acute nor does it allow the avoidance of long-term antiseizure medications, as is the case with acute symptomatic seizures, for instance, associated with traumatic brain injury. We propose that seizures be classified according to the evolutionary stage of parenchymal cysticercosis in addition to the conventional classification of seizures and epilepsy and identification of the epileptogenic zone. An often-ignored aspect is the identification of comorbidities, many of which are specific to neurocysticercosis.