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Introduction Prognosis after resuscitation from cardiac arrest (CA) remains poor, with high morbidity and mortality as a result of extensive cardiac and brain injury and lack of effective treatments. Hypertonic sodium lactate (HSL) may be beneficial after CA by buffering severe metabolic acidosis, increasing brain perfusion and cardiac performance, reducing cerebral swelling, and serving as an alternative energetic cellular substrate. The aim of this study was to test the effects of HSL infusion on brain and cardiac injury in an experimental model of CA. Methods After a 10-min electrically induced CA followed by 5 min of cardiopulmonary resuscitation maneuvers, adult swine ( n  = 35) were randomly assigned to receive either balanced crystalloid (controls, n  = 11) or HSL infusion started during cardiopulmonary resuscitation (CPR, Intra-arrest, n  = 12) or after return of spontaneous circulation (Post-ROSC, n  = 11) for the subsequent 12 h. In all animals, extensive multimodal neurological and cardiovascular monitoring was implemented. All animals were treated with targeted temperature management at 34 °C. Results Thirty-four of the 35 (97.1%) animals achieved ROSC; one animal in the Intra-arrest group died before completing the observation period. Arterial pH, lactate and sodium concentrations, and plasma osmolarity were higher in HSL-treated animals than in controls ( p  < 0.001), whereas potassium concentrations were lower ( p  = 0.004). Intra-arrest and Post-ROSC HSL infusion improved hemodynamic status compared to controls, as shown by reduced vasopressor requirements to maintain a mean arterial pressure target > 65 mmHg ( p  = 0.005 for interaction; p  = 0.01 for groups). Moreover, plasma troponin I and glial fibrillary acid protein (GFAP) concentrations were lower in HSL-treated groups at several time-points than in controls. Conclusions In this experimental CA model, HSL infusion was associated with reduced vasopressor requirements and decreased plasma concentrations of measured biomarkers of cardiac and cerebral injury.

Aims 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. Results CA was electrically induced in 20 adult swine. After 10 min, cardiopulmonary resuscitation was performed for 5 min. After return of spontaneous circulation (ROSC), the animals were randomly assigned to receive an infusion of balanced crystalloid (controls, n = 11) or SBHB (theoretical osmolarity 1189 mOsm/l, n = 8) for 12 h. Multimodal neurological and cardiovascular monitoring were implemented in all animals. Nineteen of the 20 animals achieved ROSC. Blood sodium concentrations, osmolarity and circulating KBs were higher in the treated animals than in the controls. SBHB infusion was associated with significantly lower plasma biomarkers of brain injury at 6 (glial fibrillary acid protein, GFAP and neuron specific enolase, NSE) and 12 h (neurofilament light chain, NFL, GFAP and NSE) compared to controls. The amplitude of the stereoelectroencephalograph (sEEG) increased in treated animals after ROSC compared to controls. Cerebral glucose uptake was lower in treated animals. Conclusions In this experimental model, SBHB infusion after resuscitated CA was associated with reduced circulating markers of cerebral injury and increased sEEG amplitude.

Aneurysmal subarachnoid hemorrhage (SAH) is a substantial cause of mortality and morbidity worldwide. Moreover, survivors after the initial bleeding are often subject to secondary brain injuries and delayed cerebral ischemia, further increasing the risk of a poor outcome. In recent years, the renin–angiotensin system (RAS) has been proposed as a target pathway for therapeutic interventions after brain injury. The RAS is a complex system of biochemical reactions critical for several systemic functions, namely, inflammation, vascular tone, endothelial activation, water balance, fibrosis, and apoptosis. The RAS system is classically divided into a pro-inflammatory axis, mediated by angiotensin (Ang)-II and its specific receptor AT 1 R, and a counterbalancing system, presented in humans as Ang-(1–7) and its receptor, MasR. Experimental data suggest that upregulation of the Ang-(1–7)/MasR axis might be neuroprotective in numerous pathological conditions, namely, ischemic stroke, cognitive disorders, Parkinson’s disease, and depression. In the presence of SAH, Ang-(1–7)/MasR neuroprotective and modulating properties could help reduce brain damage by acting on neuroinflammation, and through direct vascular and anti-thrombotic effects. Here we review the role of RAS in brain ischemia, with specific focus on SAH and the therapeutic potential of Ang-(1–7).

This review presents a brief overview of the γ-aminobutyric acid (GABA) system in the developing and mature central nervous system (CNS) and its potential connections to pathologies of the CNS. γ-aminobutyric acid (GABA) is a major neurotransmitter expressed from the embryonic stage and throughout life. At an early developmental stage, GABA acts in an excitatory manner and is implicated in many processes of neurogenesis, including neuronal proliferation, migration, differentiation, and preliminary circuit-building, as well as the development of critical periods. In the mature CNS, GABA acts in an inhibitory manner, a switch mediated by chloride/cation transporter expression and summarized in this review. GABA also plays a role in the development of interstitial neurons of the white matter, as well as in oligodendrocyte development. Although the underlying cellular mechanisms are not yet well understood, we present current findings for the role of GABA in neurological diseases with characteristic white matter abnormalities, including anoxic-ischemic injury, periventricular leukomalacia, and schizophrenia. Development abnormalities of the GABAergic system appear particularly relevant in the etiology of schizophrenia. This review also covers the potential role of GABA in mature brain injury, namely transient ischemia, stroke, and traumatic brain injury/post-traumatic epilepsy.

Background Anoxic brain injuries represent the main determinant of poor outcome after cardiac arrest (CA). Large animal models have been described to investigate new treatments during CA and post‐resuscitation phase, but a detailed model that includes extensive neuromonitoring is lacking. Method Before an electrically‐induced 10‐minute CA and resuscitation, 46 adult pigs underwent neurosurgery for placement of a multifunctional probe (intracranial pressure or ICP, tissue oxygen tension or PbtO2 and cerebral temperature) and a bolt‐based technique for the placement and securing of a regional blood flow probe and two sEEG electrodes; two modified cerebral microdialysis (CMD) probes were also inserted in the frontal lobes and accidental misplacement was prevented using a perforated head support. Result 42 animals underwent the CA procedure and 41 achieved the return of spontaneous circulation (ROSC). In 4 cases (8.6%) an adverse event took place during preparation, but only in two cases (4.3%) this was related to the neurosurgery. In 6 animals (13.3%) the minor complications that occurred resolved after probe repositioning. Conclusion Herein we provide a detailed comprehensive neuromonitoring approach in a large animal model of CA that might help future research. The figures displays multiple neuromonitoring devices in place to allow simultaneous measurements of multiple brain‐derived parameters during cardiac arrest and post‐resuscitation period.

Background Therapeutic hypothermia (TH) improves outcomes in comatose patients resuscitated from cardiac arrest. However, nonconvulsive status epilepticus (NCSE) may cause persistent coma. The frequency and timing of NCSE after cardiac arrest is unknown. Methods Review of consecutive subjects treated with TH and receiving continuous EEG (cEEG) monitoring between 8/1/2009 and 11/16/2010. Demographic data, survival, and functional outcome were prospectively recorded. Each cEEG file was analyzed using standard definitions to define NCSE. Data were analyzed using descriptive and nonparametric statistics. Results Mean age of the 101 subjects was 57 years (SD 15) with most subjects being male ( N  = 55, 54%) and experiencing out-of-hospital cardiac arrest ( N  = 78; 77%). Ventricular fibrillation was the initial cardiac rhythm in 39 (38%). All subjects received TH. Thirty subjects (30%) awoke at a median of 41 h (IQR 30, 61) after cardiac arrest. A total of 29/30 (97%) subjects surviving to hospital discharge were awake. Median interval from arrest to placement of cEEG was 9 h (IQR 6, 12), at which time the mean temperature was 33.9°C. NCSE occurred in 12 (12%) subjects. In 3/12 (25%) subjects, NCSE was present when the cEEG recording began. In 4 subjects, NCSE occurred within 8 h of cEEG recording. One (8%) subject with NCSE survived in a vegetative state. Conclusions NCSE is common in comatose post-cardiac arrest subjects receiving TH. Most seizures occur within the first 8 h of cEEG recording and within the first 12 h after resuscitation from cardiac arrest. Outcomes are poor in those who experience NCSE.

Emerging science continues to establish the detrimental effects of malnutrition in acute neurological diseases such as traumatic brain injury, stroke, status epilepticus and anoxic brain injury. The primary pathological pathways responsible for secondary brain injury include neuroinflammation, catabolism, immune suppression and metabolic failure, and these are exacerbated by malnutrition. Given this, there is growing interest in novel nutritional interventions to promote neurological recovery after acute brain injury. In this review, we will describe how malnutrition impacts the biomolecular mechanisms of secondary brain injury in acute neurological disorders, and how nutritional status can be optimized in both pediatric and adult populations. We will further highlight emerging therapeutic approaches, including specialized diets that aim to resolve neuroinflammation, immunodeficiency and metabolic crisis, by providing pre-clinical and clinical evidence that their use promotes neurologic recovery. Using nutrition as a targeted treatment is appealing for several reasons that will be discussed. Given the high mortality and both short- and long-term morbidity associated with acute brain injuries, novel translational and clinical approaches are needed.

Background Although magnetic resonance imaging, particularly diffusion-weighted imaging, has increasingly been used as part of a multimodal approach to prognostication in patients who are comatose after cardiac arrest, the performance of quantitative analysis of apparent diffusion coefficient (ADC) maps, as compared to standard radiologist impression, has not been well characterized. This retrospective study evaluated quantitative ADC analysis to the identification of anoxic brain injury by diffusion abnormalities on standard clinical magnetic resonance imaging reports. Methods The cohort included 204 previously described comatose patients after cardiac arrest. Clinical outcome was assessed by (1) 3–6 month post-cardiac-arrest cerebral performance category and (2) coma recovery to following commands. Radiological evaluation was obtained from clinical reports and characterized as diffuse, cortex only, deep gray matter structures only, or no anoxic injury. Quantitative analyses of ADC maps were obtained in specific regions of interest (ROIs), whole cortex, and whole brain. A subgroup analysis of 172 was performed after eliminating images with artifacts and preexisting lesions. Results Radiological assessment outperformed quantitative assessment over all evaluated regions (area under the curve [AUC] 0.80 for radiological interpretation and 0.70 for the occipital region, the best performing ROI, p  = 0.011); agreement was substantial for all regions. Radiological assessment still outperformed quantitative analysis in the subgroup analysis, though by smaller margins and with substantial to near-perfect agreement. When assessing for coma recovery only, the difference was no longer significant (AUC 0.83 vs. 0.81 for the occipital region, p  = 0.70). Conclusions Although quantitative analysis eliminates interrater differences in the interpretation of abnormal diffusion imaging and avoids bias from other prediction modalities, clinical radiologist interpretation has a higher predictive value for outcome. Agreement between radiological and quantitative analysis improved when using high-quality scans and when assessing for coma recovery using following commands. Quantitative assessment may thus be more subject to variability in both clinical management and scan quality than radiological assessment.

(1) Background: Traumatic brain injury (TBI) is caused from rapid head acceleration/deceleration, focal blows, blasts, penetrating forces, and/or shearing forces, whereas hypoxic–anoxic injury (HAI) is caused through oxygen deprivation events, including strangulation. Most service-seeking domestic violence (DV) survivors have prior mechanistic exposures that can lead to both injuries. At the time of our study, some evidence existed about the exposure to both injuries over the course of a survivor’s lifetime from abuse sources, yet little was known about their co-occurrence to the same survivor within the same episode of physical intimate partner violence (IPV). To better understand the lived experience of service-seeking DV survivors and the context in which partner-inflicted brain injury (PIBI) is sustained, we sought to understand intentional brain injury (BI) exposures that may need to be addressed and accommodated in services. Our aims were to 1. characterize the lifetime co-occurrence of strangulation and intentional head trauma exposures from all abuse sources to the same survivor and within select physical episodes of IPV and 2. establish the lifetime prevalence of PIBI. (2) Methods: Survivors seeking DV services in the state of Ohio in the United States of America (U.S.) completed interview-administered surveys in 2019 (n = 47). Community-based participatory action approaches guided all aspects of the study development, implementation, and interpretation. (3) Results: The sample was primarily women. Over 40% reported having Medicaid, the government-provided health insurance for the poor. Half had less than a postsecondary education. Over 80% of participants presented to DV services with both intentional head trauma and strangulation exposures across their lifetime from intimate partners and other abuse sources (i.e., child abuse, family violence, peer violence, sexual assault, etc.), though not always experienced at the same time. Nearly 50% reported an experience of concurrent head trauma and strangulation in either the first or last physical IPV episode. Following a partner’s attack, just over 60% reported ever having blacked out or lost consciousness—44% experienced a loss of consciousness (LOC) more than once—indicating a conservative estimate of a probable brain injury by an intimate partner. Over 80% of service-seeking DV survivors reported either a LOC or two or more alterations in consciousness (AICs) following an IPV attack and were classified as ever having a partner-inflicted brain injury. (4) Conclusions: Most service-seeking IPV survivors experience repetitive and concurrent exposures to abusive strangulation and head trauma through the life course and by intimate partners within the same violent event resulting in brain injury. We propose the use of the term partner-inflicted brain injury (PIBI) to describe the physiological disruption of normal brain functions caused by intentional, often concurrent and repeated, traumatic and hypoxic neurologic insults by an intimate partner within the context of ongoing psychological trauma, coercive control, and often past abuse exposures that could also result in chronic brain injury. We discuss CARE (Connect, Acknowledge, Respond, Evaluate), a brain-injury-aware enhancement to service delivery. CARE improved trauma-informed practices at organizations serving DV survivors because staff felt knowledgeable to address and accommodate brain injuries. Survivor behavior was then interpreted by staff as a “can’t” not a “won’t”, and social and functional supports were offered.

In brain death determination (BDD), electroencephalography (EEG) is a commonly used diagnostic method in Germany for proving irreversibility of previously clinically proven loss of brain function. Despite the comprehensive availability of EEG in intensive care units, the reliability of EEG readings is often limited by biological or technical artefacts. This study aimed to determine the detection rate of electrocerebral inactivity (ECI) with a special focus on reliability and challenges of using EEG in BDD. A retrospective monocentric analysis of all BDD EEG data acquired from January 2015 to December 2025 at our tertiary care hospital was conducted. All identified BDD EEG reports were systematically analysed for their evaluability and for technical and biological artefacts. In addition, sociodemographic and patient-specific parameters that could influence the accuracy of EEG readings (e.g., craniotomies or intracranial drainages) were recorded. A total of 47 BDD EEG reports from 42 patients (women: 38.1%, mean age: 48.4 ± 14.4 years, median age: 52 years, age range: 21-78 years) were identified. In 81.0% of the patients, BDD could be confirmed using EEG. While biological artefacts did not significantly limit the evaluability of the EEG readings (  > 0.05), technical artefacts were significantly associated with a higher risk for limited EEG readability (  = 0.0309, relative risk: 4.2, 95% confidence interval: 1.3-13.8). This finding was primarily attributable to electrode artefacts (  = 0.0030), while other artefacts such as electrocardiogram or ventilation artefacts did not significantly impair readability (  > 0.05). Neither the aetiology of brain damage nor other patient-specific or sociodemographic parameters had any influence on the usability of EEG in BDD. We conclude that EEG is a reliable diagnostic tool in BDD in most cases if technically accurately recorded. Further studies are required to optimise existing technical errors in selected patients to increase the already high level of methodological reliability.