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This article comprehensively reviews how cerebral hypoxia impacts the physiological state of neurons and dendritic spines through a series of molecular changes, and explores the causal relationship between these changes and neuronal functional impairment. As a severe pathological condition, cerebral hypoxia can significantly alter the morphology and function of neurons and dendritic spines. Specifically, dendritic spines, being the critical structures for neurons to receive information, undergo changes such as a reduction in number and morphological abnormalities under hypoxic conditions. These alterations further affect synaptic function, leading to neurotransmission disorders. This article delves into the roles of molecular pathways like MAPK, AMPA receptors, NMDA receptors, and BDNF in the hypoxia-induced changes in neurons and dendritic spines, and outlines current treatment strategies. Neurons are particularly sensitive to cerebral hypoxia, with their apical dendrites being vulnerable to damage, thereby affecting cognitive function. Additionally, astrocytes and microglia play an indispensable role in protecting neuronal and synaptic structures, regulating their normal functions, and contributing to the repair process following injury. These studies not only contribute to understanding the pathogenesis of related neurological diseases but also provide important insights for developing novel therapeutic strategies. Future research should further focus on the dynamic changes in neurons and dendritic spines under hypoxic conditions and their intrinsic connections with cognitive function. [ABSTRACT FROM AUTHOR]

Background: Stroke, including ischemic and hemorrhagic stroke, is a severe and prevalent acute cerebrovascular disease. The development of hypoxia following stroke can trigger a cascade of pathological events, including mitochondrial dysfunction, energy deficiency, oxidative stress, neuroinflammation, and excitotoxicity, all of which are often associated with unfavorable prognosis. Nonetheless, a noninvasive intervention, referred to as normobaric hyperoxia (NBO), is known to have neuroprotective effects against stroke. Results: NBO can exert neuroprotective effects through various mechanisms, such as the rescue of hypoxic tissues, preservation of the blood–brain barrier, reduction of brain edema, alleviation of neuroinflammation, improvement of mitochondrial function, mitigation of oxidative stress, reduction of excitotoxicity, and inhibition of apoptosis. These mechanisms may help improve the prognosis of stroke patients. Conclusions: This review summarizes the mechanism by which hypoxia causes brain injury and how NBO can act as a neuroprotective therapy to treat stroke. We conclude that NBO has significant potential for treating stroke and may represent a novel therapeutic strategy. [ABSTRACT FROM AUTHOR]

Brain hypoxia is associated with a wide range of physiological and clinical conditions. Although oxygen is an essential constituent of maintaining brain functions, our understanding of how specific brain cell types globally respond and adapt to decreasing oxygen conditions is incomplete. In this study, we exposed mouse primary neurons, astrocytes, and microglia to normoxia and two hypoxic conditions and obtained genome-wide transcriptional profiles of the treated cells. Analysis of differentially expressed genes under conditions of reduced oxygen revealed a canonical hypoxic response shared among different brain cell types. In addition, we observed a higher sensitivity of neurons to oxygen decline, and dissected cell type-specific biological processes affected by hypoxia. Importantly, this study establishes novel gene modules associated with brain cells responding to oxygen deprivation and reveals a state of profound stress incurred by hypoxia. [ABSTRACT FROM AUTHOR]

Background: Cerebral hypoxia is a frequent cause of secondary brain damage in patients with acute brain injury. Although hypercapnia can increase intracranial pressure, it may have beneficial effects on tissue oxygenation. We aimed to assess the effects of hypercapnia on brain tissue oxygenation (PbtO2). Methods: This single-center retrospective study (November 2014 to June 2022) included all patients admitted to the intensive care unit after acute brain injury who required multimodal monitoring, including PbtO2 monitoring, and who underwent induced moderate hypoventilation and hypercapnia according to the decision of the treating physician. Patients with imminent brain death were excluded. Responders to hypercapnia were defined as those with an increase of at least 20% in PbtO2 values when compared to their baseline levels. Results: On a total of 163 eligible patients, we identified 23 (14%) patients who underwent moderate hypoventilation (arterial partial pressure of carbon dioxide [PaCO2] from 44 [42–45] to 50 [49–53] mm Hg; p < 0.001) during the study period at a median of 6 (4–10) days following intensive care unit admission; six patients had traumatic brain injury, and 17 had subarachnoid hemorrhage. A significant overall increase in median PbtO2 values from baseline (21 [19–26] to 24 [22–26] mm Hg; p = 0.02) was observed. Eight (35%) patients were considered as responders, with a median increase of 7 (from 4 to 11) mm Hg of PbtO2, whereas nonresponders showed no changes (from − 1 to 2 mm Hg of PbtO2). Because of the small sample size, no variable independently associated with PbtO2 response was identified. No correlation between changes in PaCO2 and in PbtO2 was observed. Conclusions: In this study, a heterogeneous response of PbtO2 to induced hypercapnia was observed but without any deleterious elevations of intracranial pressure. [ABSTRACT FROM AUTHOR]

We tested whether the brain and kidney respond differently to cardiopulmonary bypass (CPB) and to changes in perfusion conditions during CPB. Therefore, in ovine CPB, we assessed regional cerebral oxygen saturation (rSO2) by near‐infrared spectroscopy and renal cortical and medullary tissue oxygen tension (PO2), and, in some protocols, brain tissue PO2, by phosphorescence lifetime oximetry. During CPB, rSO2 correlated with mixed venous SO2 (r = 0.78) and brain tissue PO2 (r = 0.49) when arterial PO2 was varied. During the first 30 min of CPB, brain tissue PO2, rSO2 and renal cortical tissue PO2 did not fall, but renal medullary tissue PO2 did. Nevertheless, compared with stable anaesthesia, during stable CPB, rSO2 (66.8 decreasing to 61.3%) and both renal cortical (90.8 decreasing to 43.5 mm Hg) and medullary (44.3 decreasing to 19.2 mm Hg) tissue PO2 were lower. Both rSO2 and renal PO2 increased when pump flow was increased from 60 to 100 mL kg−1 min−1 at a target arterial pressure of 70 mm Hg. They also both increased when pump flow and arterial pressure were increased simultaneously. Neither was significantly altered by partially pulsatile flow. The vasopressor, metaraminol, dose‐dependently decreased rSO2, but increased renal cortical and medullary PO2. Increasing blood haemoglobin concentration increased rSO2, but not renal PO2. We conclude that both the brain and kidney are susceptible to hypoxia during CPB, which can be alleviated by increasing pump flow, even without increasing arterial pressure. However, increasing blood haemoglobin concentration increases brain, but not kidney oxygenation, whereas vasopressor support with metaraminol increases kidney, but not brain oxygenation. [ABSTRACT FROM AUTHOR]

Changes in cerebrospinal fluid (CSF) dynamics can have adverse effects on neuronal function. We hypothesized that patients with hypoxic–ischemic brain injury (HIBI) showing poor neurological outcomes after cardiac arrest (CA) would exhibit changes in CSF dynamics, leading to abnormalities in gas diffusion within the CSF. Therefore, we investigated the prognostic value of the CSF partial pressure of carbon dioxide (PcsfCO2) in CA survivors who underwent targeted temperature management (TTM). We retrospectively analyzed the 6-month neurological outcomes, CSF, and arterial blood gas parameters of 67 CA survivors. Patients were divided into good and poor neurological outcome groups, and the predictive value of PcsfCO2 for poor neurological outcomes was assessed using receiver operating characteristic curve analysis. Among all patients, 39 (58.2%) had poor neurological outcomes. Significant differences in PcsfCO2 levels between the groups were observed, with lower PcsfCO2 levels on Day 1 showing the highest predictive value at a cutoff of 30 mmHg (area under the curve, sensitivity, and specificity were 0.823, 77.8%, and 79.0%, respectively). These results suggest that PcsfCO2 might serve not only as a unique marker for the severity of hypoxic–ischemic brain injury (HIBI), independent of extracorporeal CO2 levels, but also as an objective indicator of changes in CSF dynamics. This study highlights the potential prognostic and diagnostic utility of PcsfCO2 during TTM in CA survivors, emphasizing its importance in evaluating CSF dynamics and neurological recovery post CA. However, larger multicenter studies are warranted to address potential limitations associated with sample size and outcome assessment methods. [ABSTRACT FROM AUTHOR]

Simple Summary: Brain cells require a continuous and adequate supply of oxygen for optimal functioning; however, this balance is disrupted in the presence of brain tumors. The rapid growth of these tumors exceeds the capacity of the existing blood vessels, leading to areas of hypoxia. This condition contributes to accelerated tumor growth and diminishes the effectiveness of treatments. Utilizing MRI to non-invasively map hypoxia in the brain enables doctors to tailor treatment plans more effectively and to understand the tumor's level of aggressiveness. In this study, we investigated the efficacy of a new MRI method, streamlined quantitative blood-oxygen-level-dependent (sqBOLD) MRI, in mapping hypoxia across different brain tumor types. Moreover, we utilize MRI to examine the vascular features of the tumors, aiming to elucidate the dynamics of oxygen delivery. In addition, this study includes microscopic evaluations of tumor biopsies, providing valuable insights into the hypoxic environments within the tumors. Cerebral hypoxia significantly impacts the progression of brain tumors and their resistance to radiotherapy. This study employed streamlined quantitative blood-oxygen-level-dependent (sqBOLD) MRI to assess the oxygen extraction fraction (OEF)—a measure of how much oxygen is being extracted from vessels, with higher OEF values indicating hypoxia. Simultaneously, we utilized vessel size imaging (VSI) to evaluate microvascular dimensions and blood volume. A cohort of ten patients, divided between those with glioma and those with brain metastases, underwent a 3 Tesla MRI scan. We generated OEF, cerebral blood volume (CBV), and vessel size maps, which guided 3–4 targeted biopsies per patient. Subsequent histological analyses of these biopsies used hypoxia-inducible factor 1-alpha (HIF-1α) for hypoxia and CD31 for microvasculature assessment, followed by a correlation analysis between MRI and histological data. The results showed that while the sqBOLD model was generally applicable to brain tumors, it demonstrated discrepancies in some metastatic tumors, highlighting the need for model adjustments in these cases. The OEF, CBV, and vessel size maps provided insights into the tumor's hypoxic condition, showing intertumoral and intratumoral heterogeneity. A significant relationship between MRI-derived measurements and histological data was only evident in the vessel size measurements (r = 0.68, p < 0.001). [ABSTRACT FROM AUTHOR]

Abstract Background A wide variety of movement disorders can be observed after cerebral hypoxia, including akineto-hypertonic syndrome and dystonia. Post-anoxic dystonia is a rare clinical syndrome that is not widely reported in the literatures. It is thought to be related to cerebral hypoxia leading to ischaemia of the basal ganglia. Case description We report a case of an 11-year-old girl who represented with generalized dystonia following resuscitation from a cardiac arrest after open heart surgery. Brain MRI showed basal ganglia hypersignals in T2-FLAIR (fluid attenuated inversion recovery) weighted sequence and in the diffusion sequence without restriction of ACD in favour of subacute ischemic lesions. Treated with oral baclofen, the evolution was favourable with regression of the dystonia. Conclusion It is often difficult to accurately predict the final neurological outcome of a patient who has survived cardiac arrest. Baclofen and anticholinergic can be used for the treatment for dystonia post-cerebral hypoxia.

Brain hypoxia is associated with a wide range of physiological and clinical conditions. Although oxygen is an essential constituent of maintaining brain functions, our understanding of how specific brain cell types globally respond and adapt to decreasing oxygen conditions is incomplete. In this study, we exposed mouse primary neurons, astrocytes, and microglia to normoxia and two hypoxic conditions and obtained genome-wide transcriptional profiles of the treated cells. Analysis of differentially expressed genes under conditions of reduced oxygen revealed a canonical hypoxic response shared among different brain cell types. In addition, we observed a higher sensitivity of neurons to oxygen decline, and dissected cell type-specific biological processes affected by hypoxia. Importantly, this study establishes novel gene modules associated with brain cells responding to oxygen deprivation and reveals a state of profound stress incurred by hypoxia.

Background: A wide variety of movement disorders can be observed after cerebral hypoxia, including akineto-hypertonic syndrome and dystonia. Post-anoxic dystonia is a rare clinical syndrome that is not widely reported in the literatures. It is thought to be related to cerebral hypoxia leading to ischaemia of the basal ganglia. Case description: We report a case of an 11-year-old girl who represented with generalized dystonia following resuscitation from a cardiac arrest after open heart surgery. Brain MRI showed basal ganglia hypersignals in T2-FLAIR (fluid attenuated inversion recovery) weighted sequence and in the diffusion sequence without restriction of ACD in favour of subacute ischemic lesions. Treated with oral baclofen, the evolution was favourable with regression of the dystonia. Conclusion: It is often difficult to accurately predict the final neurological outcome of a patient who has survived cardiac arrest. Baclofen and anticholinergic can be used for the treatment for dystonia post-cerebral hypoxia. [ABSTRACT FROM AUTHOR]

BackgroundHypoxia can threaten the metabolic functions of different systems in immature neonates, particularly the central nervous system. The red blood cell distribution width (RDW) has recently been reported as a prognostic factor in neurologic diseases. Herein, we examined the correlation between RDW and regional cerebral tissue oxygen saturation (rcSO2).MethodsThis cross-sectional study included 110 preterm infants born at a gestational age (GA) of

Objective: Systemic hypoxia occurs in COVID-19 infection; however, it is unknown if cerebral hypoxia occurs in convalescent individuals. We have evidence from other conditions associated with central nervous system inflammation that hypoxia may occur in the brain. If so, hypoxia could reduce the quality of life and brain function. This study was undertaken to assess if brain hypoxia occurs in individuals after recovery from acute COVID-19 infection and if this hypoxia is associated with neurocognitive impairment and reduced quality of life. Methods: Using frequency-domain near-infrared spectroscopy (fdNIRS), we measured cerebral tissue oxygen saturation (StO2) (a measure of hypoxia) in participants who had contracted COVID-19 at least 8 weeks prior to the study visit and healthy controls. We also conducted neuropsychological assessments and health-related quality of life assessments, fatigue, and depression. Results: Fifty-six percent of the post-COVID-19 participants self-reported having persistent symptoms (from a list of 18), with the most reported symptom being fatigue and brain fog. There was a gradation in the decrease of oxyhemoglobin between controls, and normoxic and hypoxic post-COVID-19 groups (31.7 ± 8.3 μM, 27.8 ± 7.0 μM and 21.1 ± 7.2 μM, respectively, p = 0.028, p = 0.005, and p = 0.081). We detected that 24% of convalescent individuals' post-COVID-19 infection had reduced StO2 in the brain and that this relates to reduced neurological function and quality of life. Interpretation: We believe that the hypoxia reported here will have health consequences for these individuals, and this is reflected in the correlation of hypoxia with greater symptomology. With the fdNIRS technology, combined with neuropsychological assessment, we may be able to identify individuals at risk of hypoxia-related symptomology and target individuals that are likely to respond to treatments aimed at improving cerebral oxygenation. [ABSTRACT FROM AUTHOR]

Traumatic brain injury continues to be a leading cause of injury-related death worldwide. The immediate post-injury phase is a time of high-risk for impaired cerebral oxygen delivery and raised intracranial pressure. Initial resuscitation is therefore focused on interventions that can limit subsequent secondary brain injury. Prioritization is the main feature in this approach with rapid assessment, guided by established protocols, performed in parallel with early resuscitation. This review examines the best-practice principles involved in the initial resuscitation of traumatic brain injury in a clinically relevant systems-based approach, while recognizing the lack of strong evidence for some treatment recommendations. Patients with traumatic brain injury will often require transfer across trauma networks for definitive neurosurgical intervention and specialized neurocritical care. The precision and planning required for the transfer of brain-injured patients is also described here, alongside practical recommendations aimed at mitigating the risks involved. [ABSTRACT FROM AUTHOR]

Cerebral hypoxia significantly impacts the progression of brain tumors and their resistance to radiotherapy. This study employed streamlined quantitative blood-oxygen-level-dependent (sqBOLD) MRI to assess the oxygen extraction fraction (OEF)—a measure of how much oxygen is being extracted from vessels, with higher OEF values indicating hypoxia. Simultaneously, we utilized vessel size imaging (VSI) to evaluate microvascular dimensions and blood volume. A cohort of ten patients, divided between those with glioma and those with brain metastases, underwent a 3 Tesla MRI scan. We generated OEF, cerebral blood volume (CBV), and vessel size maps, which guided 3–4 targeted biopsies per patient. Subsequent histological analyses of these biopsies used hypoxia-inducible factor 1-alpha (HIF-1α) for hypoxia and CD31 for microvasculature assessment, followed by a correlation analysis between MRI and histological data. The results showed that while the sqBOLD model was generally applicable to brain tumors, it demonstrated discrepancies in some metastatic tumors, highlighting the need for model adjustments in these cases. The OEF, CBV, and vessel size maps provided insights into the tumor’s hypoxic condition, showing intertumoral and intratumoral heterogeneity. A significant relationship between MRI-derived measurements and histological data was only evident in the vessel size measurements (r = 0.68, p < 0.001).

Aims This study aimed to investigate the prevalence of hypoxic encephalopathy in patients with COVID-19 and its relationship with in-hospital mortality. Instruments & Methods A multicenter prospective study was conducted on 1277 patients with SARS-CoV-2 infection. All patients were evaluated based on age, severity of disease course, presence or absence of typical symptoms of COVID-19, presence of exacerbating chronic conditions, and presence of developed acute neurological complications. Patients with signs of encephalopathy were identified among patients with acute neurological complications, and a differential diagnosis was carried out to identify hypoxic encephalopathy. The data relating to severe patients with hypoxic COVID-19-associated encephalopathy was studied thoroughly for the chronology of the onset of symptoms, detection of the SARS-CoV-2, the similarity of test results, and diagnostic clinical examinations. Findings Hypoxic encephalopathy was identified as the most severe complication among patients with neurological disorders. Most often, older patients had a severe course of the disease. 20% of patients had obtained disorders of the nervous system. 92% of them were diagnosed with hypoxic encephalopathy, which led to death in 95% of cases. Conclusion SARS-CoV-2 hypoxic encephalopathy may lead to a poor prognosis for the course of the disease in the vast majority of patients with neurological complications. It means that this serious complication should be investigated more carefully for possible prevention, early diagnosis, effective treatment, and long-term rehabilitation for patients with COVID-19. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the impact of the early tracheostomy on operated patients with severe head injury. Methods: This prospective observational study was conducted at a level 1 trauma center and medical college over one-year period. The study included all surgically managed severe head injury patients without any other life-threatening major injuries. Patients who underwent tracheostomy within 7 days were classified as early tracheostomy. Results: The patient’s mean age of this cohort study was 43.4±14.5 years. Motor-vehicle accidents were being the most common cause of severe head injury. Operated patients were undergoing early tracheostomy on an average of 2.9 days. We were observed that the patients spent on a mechanical ventilation on an average 3.67±2.26 days. This was significantly lower than previous four published studies (p

The neutrophil-to-lymphocyte ratio has emerged as a predictor of functional outcome in stroke patients. However, less is known about the value of neutrophil to lymphocyte ratio in older patients. This clinical study evaluated whether the neutrophil-to-lymphocyte ratio is associated with stroke severity and early clinical outcomes in older patients with acute ischemic stroke. This observational study included acute ischemic stroke patients aged 80 years or older. The patients were divided into three groups, and information was collected, including demographic, clinical and laboratory data. The neutrophil associations to lymphocyte ratio with stroke severity and early clinical outcomes were assessed with logistic regression. Overall, 356 older patients were enrolled in this study, with a median age of 85.0 (82.0–88.0). Split by tertiles of neutrophil-to-lymphocyte ratio, 118 patients were in the bottom tertile (3.36). After multivariable analysis, patients in the highest tertile were likely to have moderate to severe stroke on admission (OR 4.87, 95% CI, 1.93–12.30, P = 0.001), higher risks of primary unfavorable outcome (OR 2.70, 95% CI, 1.09–6.69, P = 0.032) and secondary unfavorable outcome (OR 2.00, 95% CI, 1.00–4.00, P = 0.050) compared to the lowest tertile. Our finding demonstrated that the neutrophil-to-lymphocyte ratio is an independent predictor of stroke severity and early clinical outcomes in older patients with acute ischemic stroke.

Amaç: Biz bu çalışma ile bir yıl içinde konjenital kalp cerrahisi geçiren pediatrik hastalarda serebral desatürasyon oranlarını ve serebral desatürasyon ile komplikasyonlar arasındaki ilişkiyi araştırmayı amaçladık. Yöntem: Çalışma prospektif gözlemsel olarak bir üniversite hastanesinde gerçekleştirildi. Çalışmaya konjenital kalp cerrahisi geçirecek 18 yaş altındaki 115 hasta dahil edildi. Serebral desatürasyon bazal değere göre %25'lik doku oksijen satürasyonunda azalma (alt alarm limiti) olarak tanımlandı. Süre (sn), hastanın düşük alarm limitinin altında kaldığı saniye olarak, derinlik (%) hastanın serebral doku satürasyonu (rSO2) ile düşük alarm limiti altındaki rSO2 farkı arasındaki yüzdeyi ifade etmekteydi. Serebral desatürasyon skoru (eğri altında kalan alan) %*sn kullanılarak hesaplandı. Hastalar iki gruba ayrıldı: grup 1 (desatürasyon skoru >3000 %sn) ve grup 2 (desatürasyon skoru ≤% 3000 %sn). Gruplar demografik veriler, intraoperatif ve postoperatif değişkenler, postoperatif komplikasyonlar, yoğun bakım ve hastanede kalış süreleri açısından karşılaştırıldı. Bulgular: Çalışmada 59 hastayı (%51.3) erkekler oluşturmakta iken, 28 hastanın (%24.3) siyanotik kalp hastalığı mevcuttu. Ellibeş hastada (%47.8) desatürasyon skoru 3000 %sn üzerinde idi. Postoperatif komplikasyonlar Grup 1'de anlamlı olarak fazla idi (% 71 vs % 3.3; χ²=57.119, p3000 %sn (p

Objectives: To test if the early kinetics of neurofilament light (NFL) in blood adds to the absolute values of NFL in the prediction of outcome, and to evaluate if NFL can discriminate individuals with severe hypoxic–ischemic brain injury (sHIBI) from those with other causes of poor outcome after out-of-hospital cardiac arrest (OHCA). Design and setting: Monocentric retrospective study involving individuals following non-traumatic OHCA between April 2014 and April 2016. NFL concentrations were determined on a SiMoA HD-1 device using NF-Light Advantage Kits. Participants: Of 73 patients screened, 53 had serum samples available for NFL measurement at three timepoints (after 3, 24, and 48 h of admission). Of these 53 individuals, 43.4% had poor neurologic outcome at discharge as assessed by Glasgow–Pittsburgh cerebral performance categories, and, according to a current prognostication algorithm, poor outcome due to sHIBI in 20.7%. Main outcome measure: Blood NFL and its early kinetics for prognostication of outcome and prediction of sHIBI after OHCA. Results: An absolute NFL > 508.6 pg/ml 48 h after admission, or a change in NFL > 494 pg/ml compared with an early baseline value predicted outcome, and discriminated severe sHIBI from other causes of unfavorable outcome after OHCA with high sensitivity (100%, 95%CI 70.0–100%) and specificity (91.7%, 95%CI 62.5–100%). Conclusions: Not only absolute values of NFL, but also early changes in NFL predict the outcome following OHCA, and may differentiate sHIBI from other causes of poor outcome after OHCA with high sensitivity and specificity. Our study adds to published data, overall corroborating that NFL measured in blood should be implemented in prognostication algorithms used in clinical routine. [ABSTRACT FROM AUTHOR]

Correlation between individual typological features like sex-related characteristics and low initial level of stress resistance and unfavorable prognosis of ischemic brain damage is shown. At the same time, the astrocytes’ participation in neuroplasticity in this disease represents the purpose of the study. The goal was to study the cerebral cortex astrocytes’ morphometric characteristics during the cerebral hypoxia in rats of different sexes with different stress tolerance levels. We performed the study with 72 Wistar rats. According to the Open Field test results all the animals were divided into two subgroups: with high and low level of stress tolerance. Both carotid arteries of the experimental group animals (48 animals) were bandaged. Animals were removed from the experiment at 21, 60 and 90 days after surgery. Glial fibrillary acidic protein (GFAP), a marker of mature astrocytes, was detected on histological sections of the central brain gyrus using primary polyclonal rabbit antibodies. Progressive decrease of the astrocytes’ numerical density and the number of first order processes were obtained during the study. It was less pronounced in animals with high stress tolerance and females. Increase of the processes’ distribution area was reliably detected. Area decreased after 90th day of the experiment. It is concluded that the astrocytes’ alteration develops earlier in animals with high stress tolerance and males, later in females (60 days) and animals with low stress tolerance (90 days).

Background: Vascular access, including arteriovenous fistula (AVF), is essential in patients undergoing hemodialysis (HD). However, the presence of AVF is non-physiological in humans and could pose a burden to the systemic circulation or tissue microcirculation, potentially affecting tissue oxygenation, including in the brain. Recently, near-infrared spectroscopy has been used to measure regional oxygen saturation (rSO 2 ) as a marker of cerebral oxygenation in various settings, including in patients undergoing HD. Thus far, no studies have reported changes in cerebral rSO 2 before and after AVF creation. This study aimed to monitor the differences in cerebral oxygenation before and after AVF creation and to clarify the clinical factors affecting the changes in cerebral rSO 2 ., Methods: Forty-eight patients (34 men, 14 women) with chronic kidney disease (CKD) who were not undergoing dialysis and newly created AVF were recruited. Cerebral rSO 2 values before and after AVF creation were evaluated using near-infrared spectroscopy (INVOS 5100c)., Results: Cerebral rSO 2 values were significantly changed from 60.3% ± 7.5% to 58.4% ± 6.8% before and after AVF creation in all patients ( p  < 0.001). Cerebral rSO 2 were also lower in patients with diabetes mellitus (DM) than in those without DM (57.5 ± 7.1 vs 63.7 ± 6.5, p  = 0.003) before surgery; however, no differences of changes in cerebral rSO 2 were observed between the two groups after AVF creation. Additionally, multivariate regression analysis identified changes in HR (standardized coefficient: 0.436) as independent factors associated with changes in cerebral rSO 2 ., Conclusion: Surgically created AVF was associated with the deterioration of cerebral rSO 2 in patients with CKD not undergoing dialysis. Notably, AVF could cause cerebral hypoxia, and thus further studies are needed to clarify the clinical factors influencing changes in cerebral oxygenation after AVF creation., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background: Neuropsychological recovery is important for survivors' quality of life after cardiac arrest. However, most studies on cognitive symptoms after cardiac arrest examined cognitive functions within one year after onset. Aim: To investigate long‐term changes in cognitive functions in individuals with hypoxic encephalopathy after cardiac arrest. Methods: We retrospectively recruited survivors of cardiac arrest who demonstrated cognitive dysfunction at the chronic stage. The inclusion criteria were follow‐up period of more than 3 years with multiple neuropsychological examinations and brain MRI/CT within 1 year after onset. Results: Five patients showed various cognitive dysfunctions 1 year after onset, and the follow‐up periods were 3 to 13 years. Four patients showed temporal recovery of cognitive functions over a period of a few years followed by gradual deterioration afterward. The youngest patient, 48 years of age at the final assessment, demonstrated gradual improvement without clear evidence of deterioration for 4 years. Brain magnetic resonance imaging (MRI) revealed hyperintense areas at the acute stage in 2 patients, and mild cortical atrophy and cerebral hypoperfusion were observed in 3 patients. Delayed cognitive decline in our cases differs in length of the course from that in previously reported "delayed" postanoxic encephalopathy, which appears several days to weeks after onset. Conclusions: Cognitive functions in survivors of cardiac arrest recovered for a few years and then gradually deteriorated, which suggests hypoxic changes induce long‐term impact on cerebral functions. [ABSTRACT FROM AUTHOR]

Abstract Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1‐weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3‐year‐old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three‐Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2‐weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W‐hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion‐weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia‐related brain hypoxia. Three‐Tesla MRI enabled identification of the laminar pattern of the cortical lesions.

Introduction Covid-19 causes neuro/psychiatric problems by cerebral hypoxia. Objectives My therapy could allow us to cross Covid-19 infection by minimizing both immediate and chronic lung damage and would avoid many deaths and neuro/psychiatric problems from cerebral hypoxia. Methods In the case of a Covid-19 lung infection, the virus infects type II alveolar cells which consequently reduce the production of pulmonary surfactant. The surfactant has the function of reducing the surface tension of the alveoli. The less pulmonary surfactant there is, the more the alveoli tend to collapse due to the increased surface tension of their surface. Consequently, the lung would tend to collapse, that is, to reduce its volume, but collapse is prevented by the muscular movement of inspiration, which instead increases its volume. This means that a “low-pressure area” is created in the interstitial space which attracts liquid and substances which are often inflammatory and which organize over time, giving rise to interstitial pneumonia. Results I propose to administer the pulmonary surfactant to the patient Covid-19 in the presence of dyspnea and certainly during assisted ventilation. This technique is routinely used in preterm infants suffering from lack of pulmonary surfactant production due to the immaturity of type II alveolar cells, pending that once matured these cells produce it autonomously. Conclusions Similarly, the administration of surfactant during Covid-19 lung infection would allow the correct amount of surfactant to be maintained during the acute phase of the infection and would give time for type II alveolar cells to heal and independently resume surfactant production. Disclosure No significant relationships.

Hyperventilation in Severe Traumatic Brain Injury Has Something Changed in the Last Decade or Uncertainty Continues? Keywords: hyperventilation; intracranial hypertension; intracranial pressure; hypocapnia; cerebral ischemia; cerebral hypoxia; severe traumatic brain injury EN hyperventilation intracranial hypertension intracranial pressure hypocapnia cerebral ischemia cerebral hypoxia severe traumatic brain injury N.PAG N.PAG 5 03/12/21 20210311 NES 210311 Graph: Graphical Abstract Diagram about the mechanisms in which hyperventilation affects the brain pathophysiology. Hyperventilation, intracranial hypertension, intracranial pressure, hypocapnia, cerebral ischemia, cerebral hypoxia, severe traumatic brain injury Is There New Evidence About the Role of Hyperventilation in the Management of Severe Traumati... Recently, two manuscripts were published regarding the use of hyperventilation in TBI ([27], [28]). [Extracted from the article]

Objective: In this study, we aimed to investigate the incidence of cerebral desaturation and the possible relationship between intraoperative cerebral desaturation and postoperative complications. Methods: A prospective, observational study was performed 115 patients under 18 years of age who required open heart surgery in a university hospital. Cerebral desaturation was defined as a 25% decrease in cerebral saturation (low alarm limit) when compared with the basal value. Duration (second) was referred to the amount of time the patient stays below low alarm limit. Depth (%) was referred to gap between the patient's cerebral regional oxygen saturation (rSO2) level and the rSO2 low alarm limit. The cerebral desaturation score was calculated using the %*seconds. The patients were divided into two groups: group 1 (desaturation score >3000 %sec) and group 2 (desaturation score = 3000 %sec). The groups were compared in terms of demographic data, intraoperative and postoperative variables, postoperative complications, and duration of intensive care and hospital stays. Results: In the study, 59 patients (51.3%) were male and 28 patients (24.3%) had cyanotic heart disease. A total of 55 patients (47.8%) experienced over 3000 %sec desaturation. Postoperative complications were found to be increased in group 1 (71% vs 3.3%; X²=57.119, p<0.001). In the multiple logistic regression analysis, desaturation score>3000 %sec (p<0.001), low body surface area (p=0.001) and prolonged cardiopulmonary bypass (p=0.006) were found to be associated with postoperative complications. Conclusion: In patients undergoing congenital heart surgery, cerebral desaturation score >3000 %sec is associated with a negative effect on patient prognosis. [ABSTRACT FROM AUTHOR]

Background: Cerebral hypoxia may occur during surgery but currently used cerebral oxygenation saturation (rSO2) monitors remain controversial with respect to improving clinical outcome. Novel neuroprotein biomarkers are potentially released into systemic circulation and combined with near‐infrared spectroscopy (NIRS) could clarify the presence of per‐operative cerebral hypoxia. We investigated changes to serum‐neuroprotein concentrations post‐surgically, paired with NIRS and cognitive outcome, in patients operated in the beach chair position (BCP). Methods: A prospective cohort in 28 shoulder surgery patients placed in the BCP. Blood samples were collected before induction of anaesthesia, and 2 hours and 3‐5 days post‐operatively. We analysed blood levels of biomarkers including tau and neurofilament light (NFL). We post hoc assessed the cross‐wise relationship between biomarker levels and post‐surgical changes in cognitive function and intraoperatively monitored rSO2 from NIRS. Results: Serum‐NFL decreased from 24.2 pg/mL to 21.5 (P =.02) 2 hours post‐operatively, then increased to 27.7 pg/mL on day 3‐5 (P =.03). Conversely, s‐tau increased from 0.77 pg/mL to 0.98 (2 h), then decreased to 0.81 on day 3‐5 (P =.08). In 14/28 patients, episodic rSO2 below 55% occurred, and the duration < 55% was correlated to change in s‐tau (P <.05). The cognitive function z‐score at 1 week and 3 mo. correlated to the change in tau (P =.01), but not to NFL. Conclusion: Some biomarkers were significantly changed with surgery in the beach chair position. The change was at some points associated to post‐operative cognitive decline, and to intraoperative low rSO2. (237). [ABSTRACT FROM AUTHOR]

Posterior Reversible Encephalopathy Syndrome (PRES), also known as Reversible Posterior Leukoencephalopathy Syndrome, presents with rapid onset symptoms, including headache, seizures, altered consciousness, and visual disturbance. It is seen most frequently in settings of acute hypertension and is usually related to eclampsia. Only a few cases in the literature described PRES syndrome following benzodiazepines. We present a young male with benzodiazepine poisoning brought to the hospital in a deep coma, hypoxia, acidosis, and shock. Diagnosis of PRES was made on history, clinical examination, and radiologic findings of symmetric bilateral hyperintensities on T2 weighted Magnetic Resonance Imaging (MRIs) representing vasogenic edema.