CT brain perfusion patterns and clinical outcome after successful cardiopulmonary resuscitation: A pilot study.

AIM: CT perfusion is a valuable tool for evaluating cerebrovascular diseases, but its role in patients with hypoxic ischaemic encephalopathy is unclear. This study aimed to investigate 1) the patterns of cerebral perfusion changes that may occur early on after successful resuscitation, and 2) their correlation with clinical outcome to explore their value for predicting outcome. METHODS: We conducted a retrospective analysis of perfusion maps from patients who underwent CT brain perfusion within 12 h following successful resuscitation. We classified the perfusion changes into distinct patterns. According to the cerebral performance category (CPC) score clinical outcome was categorised as favourable (CPC 1-2), or unfavourable (CPC 3-5). RESULTS: A total of 87 patients were included of whom 33 had a favourable outcome (60.6% male, mean age 60 ± 16 years), whereas 54 exhibited an unfavourable outcome (59.3% male, mean age 60 ± 19 years). Of the patients in the favourable outcome group, 30.3% showed no characteristic perfusion changes, in contrast to the unfavourable outcome group where all patients exhibit changes in perfusion. Eighteen perfusion patterns were identified. The most significant patterns for prediction of unfavourable outcome in terms of their high specificity and frequency were hypoperfusion of the brainstem as well as coexisting hypoperfusion of the brainstem and thalamus. CONCLUSION: This pilot study identified various perfusion patterns in patients after resuscitation, indicative of circulatory changes associated with post-cardiac-arrest brain injury. After validation, certain patterns could potentially be used in conjunction with other prognostic markers for stratifying patients and adjusting personalized treatment following cardiopulmonary resuscitation. Normal brain perfusion within 12 h after resuscitation is predictive of favourable outcome with high specificity.

Novel perfluorocarbon-based oxygenation therapy alleviates Post-SAH hypoxic brain injury by inhibiting HIF-1α.

In comparison to other stroke types, subarachnoid hemorrhage (SAH) is characterized by an early age of onset and often results in poor prognosis. The inadequate blood flow at the site of the lesion leads to localized oxygen deprivation, increased level of hypoxia-inducible factor-1α (HIF-1α), and triggers inflammatory responses and oxidative stress, ultimately causing hypoxic brain damage. Despite the potential benefits of oxygen (O2) administration, there is currently a lack of efficient focal site O2 delivery following SAH. Conventional clinical O2 supply methods, such as transnasal oxygenation and hyperbaric oxygen therapy, do not show the ideal therapeutic effect in severe SAH patients. The perfluorocarbon oxygen carrier (PFOC) demonstrates efficacy in transporting O2 and responding to elevated levels of CO2 at the lesion site. Through cellular experiments, we determined that PFOC oxygenation serves as an effective therapeutic approach in inhibiting hypoxia. Furthermore, our animal experiments showed that PFOC oxygenation outperforms O2 breathing, leading to microglia phenotypic switching and the suppression of inflammatory response via the inhibition of HIF-1α. Therefore, as a new type of O2 therapy after SAH, PFOC oxygenation can effectively reduce hypoxic brain injury and improve neurological function.

Multidisciplinary approach for acute MI complicated by ventricular tachycardia, stent thrombosis, and multi-organ failure: A case report.

Key Clinical Message: The case highlights the imperative requirement for multidisciplinary action in handling a myocardial infarction case, complicated by rare and severe events like ventricular tachycardia, stent thrombosis, hypoxic brain injury, and multi-organ failure. Abstract: This article presents a case of a 53-year-old male, who presented with myocardial infarction that was managed by percutaneous coronary intervention and stent placement. However, it progressed to multiple complications in sequence (ventricular tachycardia, stent thrombosis, hypoxic brain injury, and multi-organ failure). Hopefully, the condition of the patient improved after 2 months from GSC-4 to GCS-9 by a multidisciplinary approach and was discharged for home-based treatment.

Effect of Hemolysis Regarding the Characterization and Prognostic Relevance of Neuron Specific Enolase (NSE) after Cardiopulmonary Resuscitation with Extracorporeal Circulation (eCPR).

BACKGROUND: Hemolysis, a common adverse event associated with veno-arterial extracorporeal membrane oxygenation (VA-ECMO), may affect neuron-specific enolase (NSE) levels and potentially confound its prognostic value in predicting neurological outcomes in resuscitated patients without return of spontaneous circulation (ROSC) that require extracorporeal cardiopulmonary resuscitation (eCPR). Therefore, a better understanding of the relationship between hemolysis and NSE levels could help to improve the accuracy of NSE as a prognostic marker in this patient population. METHODS: We retrospectively analyzed the records of patients who received a VA-ECMO for eCPR between 2004 and 2021 and were treated in the medical intensive care unit (ICU) of the University Hospital Jena. The outcome was measured clinically by using the Cerebral Performance Category Scale (CPC) four weeks after eCPR. The serum concentration of NSE (baseline until 96 h) was analyzed by enzyme-linked immunosorbent assay (ELISA). To evaluate the ability of individual NSE measurements to discriminate, receiver operating characteristic (ROC) curves were calculated. Serum-free hemoglobin (fHb, baseline until 96 h) served as a marker for identifying a confounding effect of parallel hemolysis. RESULTS: 190 patients were included in our study. A total of 86.8% died within 4 weeks after ICU admission or remained unconscious (CPC 3-5), and 13.2% survived with a residual mild to moderate neurological deficit (CPC 1-2). Starting 24h after CPR, NSE was significantly lower and continued to decrease in patients with CPC 1-2 compared to the group with an unfavorable outcome of CPC 3-5. In addition, when evaluating on the basis of receiver operating characteristic curves (ROC), relevant and stable area under the curve (AUC) values for NSE could be calculated (48 h: 0.85 // 72 h: 0.84 // 96 h: 0.80; p < 0.01), and on the basis of a binary logistic regression model, relevant odds ratios for the NSE values were found even after adjusting for fHb regarding the prediction of an unfavorable outcome of CPC 3-5. The respective adjusted AUCs of the combined predictive probabilities were significant (48 h: 0.79 // 72 h: 0.76 // 96 h: 0.72; p ≤ 0.05). CONCLUSIONS: Our study confirms NSE as a reliable prognostic marker for poor neurological outcomes in resuscitated patients receiving VA-ECMO therapy. Furthermore, our results demonstrate that potential hemolysis during VA-ECMO does not significantly impact NSE's prognostic value. These findings are crucial for clinical decision making and prognostic assessment in this patient population.

The Effect of Oxygenation on Mortality in Patients With Head Injury.

Introduction In this study, we planned to investigate the effect of hyperoxygenation on mortality and morbidity in patients with head trauma who were followed and treated in the intensive care unit (ICU). Methods Head trauma cases (n = 119) that were followed in the mixed ICU of a 50-bed tertiary care center in Istanbul between January 2018 and December 2019 were retrospectively analyzed for the negative effects of hyperoxia. Age, gender, height/weight, additional diseases, medications used, ICU indication, Glasgow Coma Scale score recorded during ICU follow-up, Acute Physiology and Chronic Health Evaluation (APACHE) II score, length of hospital/ICU stay, the presence of complications, number of reoperations, length of intubation, and the patient's discharge or death status were evaluated. The patients were divided into three groups according to the highest partial pressure of oxygen (PaO2) value (200 mmHg) in the arterial blood gas (ABG) taken on the first day of admission to the ICU, and ABGs on the day of ICU admission and discharge were compared. Results In comparison, the first arterial oxygen saturation and initial PaO2 mean values were found to be statistically significantly different. There was a statistically significant difference in mortality and reoperation rates between groups. The mortality was higher in groups 2 and 3, and the rate of reoperation was higher in group 1. Conclusion In our study, mortality was found to be high in groups 2 and 3, which we considered hyperoxic. In this study, we tried to draw attention to the negative effects of common and easily administered oxygen therapy on mortality and morbidity in ICU patients.

Non clinical pharmacodynamic evaluation system of high-altitude hypoxic brain injury / 药学学报

The air at high altitude is thin and belongs to the environment of low temperature, low oxygen and low pressure. The human brain is the most sensitive to hypoxia. Hypoxia will cause dysfunction of the central nervous system, resulting in high-altitude hypoxic brain injury, including mild high altitude headache and more destructive high altitude cerebral edema (HACE). Recently, with more and more people work and live in high altitude areas, the development of high-altitude hypoxic brain injury drugs would produce great economic value and social significance. Non clinical pharmacodynamic evaluation is the basic of drug development, which plays a key role in improving the success rate of clinical transformation and reducing the risk of clinical research. This review summarizes the cell models and animal models, and the evaluation indicators usually used to explore the candidates of high-altitude hypoxic brain injury. We aim at establishing a standardized non clinical efficacy evaluation system for high altitude hypoxic encephalopathy, and provide a standardized reference for drug development in hypoxic encephalopathy at high altitude at nonclinical stage.

Dexmedetomidine Attenuates Apoptosis and Neurological Deficits by Modulating Neuronal NADPH Oxidase 2-Derived Oxidative Stress in Neonates Following Hypoxic Brain Injury.

Hypoxic-ischemic brain injury is an important cause of neonatal neurological deficits. Our previous study demonstrated that dexmedetomidine (Dex) provided neuroprotection against neonatal hypoxic brain injury; however, the underlying mechanisms remain incompletely elucidated. Overactivation of NADPH oxidase 2 (NOX2) can cause neuronal apoptosis and neurological deficits. Hence, we aimed to investigate the role of neuronal NOX2 in Dex-mediated neuroprotection and to explore its potential mechanisms. Hypoxic injury was modeled in neonatal rodents in vivo and in cultured hippocampal neurons in vitro. Our results showed that pre- or post-treatment with Dex improved the neurological deficits and alleviated the hippocampal neuronal damage and apoptosis caused by neonatal hypoxia. In addition, Dex treatment significantly suppressed hypoxia-induced neuronal NOX2 activation; it also reduced oxidative stress, as evidenced by decreases in intracellular reactive oxygen species (ROS) production, malondialdehyde, and 8-hydroxy-2-deoxyguanosine, as well as increases in the antioxidant enzymatic activity of superoxide dismutase and glutathione peroxidase in neonatal rat hippocampi and in hippocampal neurons. Lastly, the posthypoxicneuroprotective action of Dex was almost completely abolished in NOX2-deficient neonatal mice and NOX2-knockdown neurons. In conclusion, our data demonstrated that neuronal NOX2-mediated oxidative stress is involved in the neuroprotection that Dex provides against apoptosis and neurological deficits in neonates following hypoxia.

Regulation of Genes Related to Cognition after tDCS in an Intermittent Hypoxic Brain Injury Rat Model.

Background: Hypoxic brain injury is a condition caused by restricted oxygen supply to the brain. Several studies have reported cognitive decline, particularly in spatial memory, after exposure to intermittent hypoxia (IH). However, the effect and mechanism of action of IH exposure on cognition have not been evaluated by analyzing gene expression after transcranial direct current stimulation (tDCS). Hence, the purpose of this study was to investigate the effects of tDCS on gene regulation and cognition in a rat model of IH-induced brain injury. Methods: Twenty-four 10-week-old male Sprague−Dawley rats were divided into two groups: IH exposed rats with no stimulation and IH-exposed rats that received tDCS. All rats were exposed to a hypoxic chamber containing 10% oxygen for twelve hours a day for five days. The stimulation group received tDCS at an intensity of 200 µA over the frontal bregma areas for 30 min each day for a week. As a behavior test, the escape latency on the Morris water maze (MWM) test was measured to assess spatial memory before and after stimulation. After seven days of stimulation, gene microarray analysis was conducted with a KEGG mapper tool. Results: Although there were no significant differences between the groups before and after stimulation, there was a significant effect of time and a significant time × group interaction on escape latency. In the microarray analysis, significant fold changes in 12 genes related to neurogenesis were found in the stimulation group after tDCS (p < 0.05, fold change > 2 times, the average of the normalized read count (RC) > 6 times). The highly upregulated genes in the stimulation group after tDCS were SOS, Raf, PI3K, Rac1, IRAK, and Bax. The highly downregulated genes in the stimulation group after tDCS were CHK, Crk, Rap1, p38, Ras, and NF-kB. Conclusion: In this study, we confirmed that SOS, Raf, PI3K, Rac1, IRAK, and Bax were upregulated and that CHK, Crk, Rap1, p38, Ras, and NF-kB were downregulated in a rat model of IH-induced brain injury after application of tDCS.

Further Evidence of Neuroprotective Effects of Recombinant Human Erythropoietin and Growth Hormone in Hypoxic Brain Injury in Neonatal Mice.

Experimental in vivo data have recently shown complementary neuroprotective actions of rhEPO and growth hormone (rhGH) in a neonatal murine model of hypoxic brain injury. Here, we hypothesized that rhGH and rhEPO mediate stabilization of the blood−brain barrier (BBB) and regenerative vascular effects in hypoxic injury to the developing brain. Using an established model of neonatal hypoxia, neonatal mice (P7) were treated i.p. with rhGH (4000 µg/kg) or rhEPO (5000 IU/kg) 0/12/24 h after hypoxic exposure. After a regeneration period of 48 h or 7 d, cerebral mRNA expression of Vegf-A, its receptors and co-receptors, and selected tight junction proteins were determined using qRT-PCR and ELISA. Vessel structures were assessed by Pecam-1 and occludin (Ocln) IHC. While Vegf-A expression increased significantly with rhGH treatment (p < 0.01), expression of the Vegfr and TEK receptor tyrosine kinase (Tie-2) system remained unchanged. RhEPO increased Vegf-A (p < 0.05) and Angpt-2 (p < 0.05) expression. While hypoxia reduced the mean vessel area in the parietal cortex compared to controls (p < 0.05), rhGH and rhEPO prevented this reduction after 48 h of regeneration. Hypoxia significantly reduced the Ocln+ fraction of cortical vascular endothelial cells. Ocln signal intensity increased in the cortex in response to rhGH (p < 0.05) and in the cortex and hippocampus in response to rhEPO (p < 0.05). Our data indicate that rhGH and rhEPO have protective effects on hypoxia-induced BBB disruption and regenerative vascular effects during the post-hypoxic period in the developing brain.

Rhodiola crenulate alleviates hypobaric hypoxia-induced brain injury via adjusting NF-κB/NLRP3-mediated inflammation.

BACKGROUND: Rhodiola crenulate (R. crenulate), a famous Tibetan medicine, has been demonstrated to possess superiorly protective effects in high-altitude hypoxic brain injury (HHBI). However, its mechanisms on HHBI are still largely unknown. METHODS: Herein, the protective effects and underlying mechanisms of R. crenulate on HHBI of BABL/c mice were explored through in vivo experiments. The mice model of HHBI was established using an animal hypobaric and hypoxic chamber. R. crenulate extract (RCE) (0.5, 1.0 and 2.0 g/kg) was given by gavage for 7 days. Pathological changes and neuronal viability of mice hippocampus and cortex were evaluated using H&E and Nissl staining, respectively. The brain water content (BWC) in mice was determined by calculating the ratio of dry to wet weight of brain tissue. And serum of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH-Px) and lactate dehydrogenase (LDH) were detected via commercial biochemical kits. Synchronously, the contents of total antioxidant capacity (T-AOC), lactic acid (LA), adenosine triphosphate (ATP), succinate dehydrogenase (SDH), pyruvate kinase (PK), Ca2+-Mg2+-ATPcase, Na+-K+-ATPcase, TNF-α, IL-1ß and IL-6 in brain tissue were quantitative analysis by corresponding ELISA assay. Subsequently, NLRP3, ZO-1, claudin-5, occluding, p-p65, p65, ASC, cleaved-caspase-1, caspase-1 and IL-18 were determined by immunofluorescent and western blot analyses. RESULTS: The results demonstrated that RCE remarkably alleviated pathological damage, BWC, as well enhanced neuronal viability. Furthermore, the oxidative stress injuries were reversely abrogated after RCE treatment, evidenced by the increases of SOD, GSH-Px and T-AOC, while the decreases of MDA and LDH contents. Marvelously, the administration of RCE rectified and balanced the abnormal energy metabolism via elevating the levels of ATP, SDH, PK, Ca2+-Mg2+-ATPcase and Na+-K+-ATPcase, and lowering LA. Simultaneously, the expression of tight junction proteins (ZO-1, claudin-5 and occludin) was enhanced, illustrating RCE treatment might maintain the integrity of blood-brain barrier (BBB). Additionally, RCE treatment confined the contents of IL-6, IL-1ß and TNF-α, and attenuated fluorescent signal of NLRP3 protein. Concurrently, the results of western blot indicated that RCE treatment dramatically restrained p-p65/p65, ASC, NLRP3, cleaved-caspase-1/caspase-1 and IL-18 protein expressions in brain tissues of mice. CONCLUSION: RCE may afford a protectively intervention in HHBI of mice through suppressing the oxidative stress, improving energy metabolism and the integrity of BBB, and subsiding inflammatory responses via the NF-κB/NLRP3 signaling pathway. As a promising agent for the treatment of mice HHBI, the deep-crossing molecular mechanisms of R. crenulate still needs to be further elucidated to identify novel core hub targets.

Long Term Cognitive Function After Cardiac Arrest: A Mini-Review.

Out-of-hospital cardiac arrest (OHCA) is a leading cause of mortality worldwide. With better pre- and inhospital treatment, including cardiopulmonary resuscitation (CPR) as an integrated part of public education and more public-access defibrillators available, OHCA survival has increased over the last decade. There are concerns, after successful resuscitation, of cerebral hypoxia and degrees of potential acquired brain injury with resulting poor cognitive functioning. Cognitive function is not routinely assessed in OHCA survivors, and there is a lack of consensus on screening methods for cognitive changes. This narrative mini-review, explores available evidence on hypoxic brain injury and long-term cognitive function in cardiac arrest survivors and highlights remaining knowledge deficits.

Neuron-Specific Enolase and S100B: The Earliest Predictors of Poor Outcome in Cardiac Arrest.

Background: Proper prognostication is critical in clinical decision-making following out-of-hospital cardiac arrest (OHCA). However, only a few prognostic tools with reliable accuracy are available within the first 24 h after admission. Aim: To test the value of neuron-specific enolase (NSE) and S100B protein measurements at admission as early biomarkers of poor prognosis after OHCA. Methods: We enrolled 82 consecutive patients with OHCA who were unconscious when admitted. NSE and S100B levels were measured at admission, and routine blood tests were performed. Death and poor neurological status at discharge were considered as poor clinical outcomes. We evaluated the optimal cut-off levels for NSE and S100B using logistic regression and receiver operating characteristic (ROC) analyses. Results: High concentrations of both biomarkers at admission were significantly associated with an increased risk of poor clinical outcome (NSE: odds ratio [OR] 1.042 per 1 ng/dL, [1.007−1.079; p = 0.004]; S100B: OR 1.046 per 50 pg/mL [1.004−1.090; p < 0.001]). The dual-marker approach with cut-off values of ≥27.6 ng/mL and ≥696 ng/mL for NSE and S100B, respectively, identified patients with poor clinical outcomes with 100% specificity. Conclusions: The NSE and S100B-based dual-marker approach allowed for early discrimination of patients with poor clinical outcomes with 100% specificity. The proposed algorithm may shorten the time required to establish a poor prognosis and limit the volume of futile procedures performed.

Immunohistochemical Markers of Apoptotic and Hypoxic Damage Facilitate Evidence-Based Assessment in Pups with Neurological Disorders.

Seizures in puppies often present a diagnostic challenge in terms of identifying and treating the underlying cause. Dog breeds with mutations of the MDR1-gene are known to show adverse reactions to certain drugs, yet metabolic imbalance exacerbated by physiologically immature organs and other contributing pathologies require consideration before arriving at a diagnosis. This study analysed the brains of two male, 5-week-old Australian Shepherd siblings that died after displaying severe neurological symptoms upon administration of MilproVet® to treat severe intestinal helminth infection. Despite the initial symptoms being similar, their case histories varied in terms of the symptom duration, access to supportive therapy and post-mortem interval. Histopathology and immunohistochemistry were used to obtain more information about the phase of the pathological processes in the brain, employing protein markers associated with acute hypoxic damage (ß-amyloid precursor protein/APP) and apoptosis (diacylglycerolkinase-ζ/DGK-ζ, apoptotic protease activating factor 1/Apaf1, and B-cell lymphoma related protein 2/Bcl-2). The results seem to reflect the course of the animals' clinical deterioration, implicating that the hypoxic damage to the brains was incompatible with life, and suggesting the usefulness of the mentioned immunohistochemical markers in clarifying the cause of death in animals with acute neurological deficits.

COVID-19-induced surge in the severity of gender-based violence might increase the risk for acquired brain injuries.

While initial reports have emphasized a global rise in the frequency of intimate partner violence following COVID-19, emerging data are now showing a concerning surge in the severity of COVID-19-induced physical intimate partner violence. One of the most dangerous, frequent, yet hidden consequences of severe physical intimate partner violence is acquired brain injury, including repetitive mild traumatic brain injury and hypoxic brain injury. Although the increase in high-risk physical abuse during COVID-19 is gaining recognition, what still remains absent is the urgent discussion on intimate partner violence-related acquired brain injury during these times. The potential analogous surge in intimate partner violence-related acquired brain injury may have implications for both healthcare providers and healthcare actions/policies as repeated brain injuries have been associated with residual functional deficits and chronic disability. In addition, even in the pre-pandemic times, intimate partner violence-related acquired brain injury is likely unrecognized and/or misclassified due to overlap in symptoms with other comorbid disorders. This review aimed to raise awareness about intimate partner violence-related acquired brain injury within the context of COVID-19. Health actions and policies that should be considered as part of the pandemic response to minimize adverse outcomes associated with intimate partner violence-related acquired brain injury have also been discussed.

Grinker's myelinopathy: The rarely reported consequence of hypoxic brain injury.

A 68-year-old woman presented with chest pain and loss of consciousness following an anterior wall myocardial infarction. Magnetic resonance imaging of brain showed features of hypoxic brain injury. She subsequently developed memory deficits, drowsiness and behavioral changes. Magnetic resonance imaging of brain done 4 months after ischemic insult showed evidence of delayed posthypoxic leukoencephalopathy also known as Grinker's myelinopathy.

Delayed post-hypoxic leukoencephalopathy following alcohol consumption and cardiopulmonary arrest.

Delayed post hypoxic leukoencephalopathy (DPHL) is a rare consequence of hypoxic brain injury that occurs several days to weeks following an initial hypoxic insult. Most of the previously published cases occur in the setting of drug overdoses or carbon monoxide poisoning, where the incidence of DPHL is as high as 3%. Our case depicts a patient with delayed hypoxic brain injury following cardiac arrest with cardiopulmonary resuscitation. Initial neuroimaging was normal, and a repeat MRI scan six days later revealed DWI changes consistent with DPHL. Our patient remained comatose throughout his clinical course until his eventual death nine days after the initial incident. The autopsy confirmed hypoxic-ischemic brain injury with co-existent Wernicke's encephalopathy, a known consequence of alcohol use disorder. This case outlines the clinical course of DPHL accompanied by the unique neuroimaging features that distinguish it from conventional hypoxic-ischemic brain injury.

Neuron-specific enolase concentrations for the prediction of poor prognosis of comatose patients after out-of-hospital cardiac arrest: an observational cohort study.

BACKGROUND: Neuron-specific enolase (NSE) is a biomarker for neurological outcomes after cardiac arrest with the most evidence collected thus far; however, recommended prognostic cutoff values are lacking owing to the discrepancies in the published data. AIMS: The aim of the study was to establish NSE cutoff values for prognostication in the environment of a cardiac intensive care unit following out-of-hospital cardiac arrest (OHCA). METHODS: A consecutive series of 82 patients admitted after OHCA were enrolled. Blood samples for the measurement of NSE levels were collected at admission and after 1 hour, 3, 12, 24, 48, and 72 hours. Neurological outcomes were quantified using the cerebral performance category (CPC) index. Each patient was classified into either the good (CPC ≤2) or poor prognosis (CPC ≥3) group. RESULTS: Median NSE concentrations were higher in the poor prognosis group, and the difference reached statistical significance at 48 and 74 hours (84.4 ng/ml vs 22.9 ng/ml at 48 hours and 152.1 ng/ml vs 18.7 ng/ml at 72 hours; P <0.001, respectively). Moreover, in the poor prognosis group, NSE increased significantly between 24 and 72 hours (P <0.001). NSE cutoffs for the prediction of poor prognosis after OHCA were 39.8 ng/ml, 78.7 ng/ml, and 46.2 ng/ml for 24, 48, and 72 hours, respectively. The areas under the curve were significant at each time point, with the highest values at 48 and 72 hours after admission (0.849 and 0.964, respectively). CONCLUSIONS: Elevated NSE concentrations with a rise in levels in serial measurements may be utilized in the prognostication algorithm after OHCA.

Somatosensory evoked potential amplitudes correlate with long-term consciousness recovery in patients with unresponsive wakefulness syndrome.

OBJECTIVE: To prospectively investigate relationships of cortical somatosensory evoked potential (SEP) amplitudes with consciousness recovery and disability in the year following brain injury in patients with vegetative state/unresponsive wakefulness syndrome (VS/UWS). METHODS: SEPs of 42 patients with VS/UWS were recorded 51.7 ± 23.3 days post-injury. N20-P25 amplitudes were compared between patients with and without consciousness recovery at 6 months and 1 year post-injury. RESULTS: SEPs were present in 21 patients and bilaterally absent in 21 patients. N20-P25 amplitudes were significantly higher in patients who recovered consciousness than in those who died or did not recover consciousness at 6 months (median, 4.6 vs. 1.9 µV; P = 0.004) and 1 year (median, 4.6 vs. 2.1 µV; P = 0.02) after injury. The lowest N20-P25 amplitude in a patient who recovered consciousness was 2.15 µV. N20-P25 amplitudes correlated significantly with Coma Recovery Scale-Revised and Disability Rating Scale scores at 6 months and 1 year post-injury (both P < 0.05). CONCLUSIONS: In patients with VS/UWS, SEP amplitudes are related to consciousness recovery and disability at 6 months and 1 year post-injury. SIGNIFICANCE: The evaluation of SEP amplitudes can help to refine prognoses for patients with VS/UWS.

LncRNA SNHG1 protects SH-SY5Y cells from hypoxic injury through miR-140-5p/Bcl-XL axis.

Background: Hypoxic brain injury is one of the major causes of neurodevelopmental impairment and cardiovascular disability. LncRNA SNHG1 works as a critical factor in hypoxic induced injury, however, the potential mechanism is still not known well.Methods: The expression level of small nucleolar RNA host gene 1 (SNHG1) and miR-140-5p was detected by qRT-PCR. The western blot assay was performed to measure the level of Bcl-XL and apoptosis-related proteins. The target relationship between lncRNA SNHG1 and miR-140-5p, as well as miR-140-5p and Bcl-XL was detected by dual luciferase reporter gene assay. Cell apoptosis was assessed using Annexin V/PI staining by flow cytometry. Cell viability was analyzed by MTT assay.Results: Oxygen glucose deprivation (OGD) treatment inhibited SNHG1 and Bcl-XL expression and enhanced miR-140-5p expression. OGD treatment-induced cell viability inhibition, cell apoptosis promotion were partially abrogated when SH-SY5Y cells were transfected with pcDNA3.1-SNHG1 or miR-140-5p inhibitor. Moreover, luciferase reporter assay revealed that lncRNA SNHG1 bound directly to miR-140-5p, and miR-140-5p directly targeted Bcl-XL. The protective effect of SNHG1 overexpressing on cell apoptosis induced by OGD was attenuated after transfected with miR-140-5p mimic or sh-Bcl-XL in SH-SY5Y cells.Conclusion: LncRNA SNHG1-modulated miR-140-5p inhibition regulates Bcl-XL expression, thereby reducing cell apoptosis and recovering cell viability of SH-SY5Y cells. The results in this study provide novel insight into the mechanism of SNHG1 mediated signaling pathway during hypoxic brain injury.

Lesson of the month: Oxycodone-induced leukoencephalopathy: a rare diagnosis.

Oxycodone-induced leukoencephalopathy is a rare diagnosis that should be considered in unconscious patients with appropriate history. We describe a case of a 57-year-old unconscious woman who required intubation and did not respond to naloxone infusion. The unconsciousness was initially thought to be due to hypoxic brain injury. However, a further review of brain imaging showed characteristic features of oxycodone-induced leukoencephalopathy. We describe the pathological and radiological features of this condition, and provide a concise review of the limited literature on this condition. Accurate diagnosis of this condition will be valuable to clinicians and patients in terms of their medium-term and long-term prognosis, and potential for rehabilitation.