Neuron-specific Enolase In Cerebrospinal Fluid Research Articles

Post-mortem utility of Neuron Specific Enolase (NSE) and Calcium Binding Protein B (S100B) for differentiating traumatic brain injury from other causes of death.

In forensic pathology, identifying causes of death in traumatic brain injuries (TBIs) devoid of observable signs presents a significant challenge. Post-mortem biochemistry plays a crucial role in forensic medicine, particularly in determining causes of death in TBIs that lack macroscopic or histopathological evidence. This study aimed to evaluate the utility of Neuron Specific Enolase (NSE) and S100 Calcium Binding Protein B (S100B) in post-mortem serum and cerebrospinal fluid (CSF) as markers for TBI. The relationship of these biochemical markers with survival time and post-mortem interval was also studied. The study sample consisted of 63 cases each from the TBI and the Non-TBI (NTBI) group. The NTBI group comprised of deaths due to mechanical asphyxia, myocardial infarction and isolated trunk trauma. While serum S100B and CSF NSE emerged as a promising marker for TBI, CSF S100B failed to differentiate TBI from the other causes of death. The absence of an association between the level of markers and survival time or post-mortem interval in TBIs highlights the limitations of these biomarkers in such contexts. This study underscores the potential of biochemical markers like serum S100B and CSF NSE in identifying TBI deaths, aiding forensic diagnoses where there are evidentiary limitations in traditional methods. Further research exploring additional markers and body fluids could enhance diagnostic precision in forensic neuropathology.

Cerebrospinal Fluid and Serum Biomarker Insights in Aneurysmal Subarachnoid Haemorrhage: Navigating the Brain-Heart Interrelationship for Improved Patient Outcomes.

The pathophysiological mechanisms underlying severe cardiac dysfunction after aneurysmal subarachnoid haemorrhage (aSAH) remain poorly understood. In the present study, we focused on two categories of contributing factors describing the brain-heart relationship. The first group includes brain-specific cerebrospinal fluid (CSF) and serum biomarkers, as well as cardiac-specific biomarkers. The secondary category encompasses parameters associated with cerebral autoregulation and the autonomic nervous system. A group of 15 aSAH patients were included in the analysis. Severe cardiac complications were diagnosed in seven (47%) of patients. In the whole population, a significant correlation was observed between CSF S100 calcium-binding protein B (S100B) and brain natriuretic peptide (BNP) (rS = 0.62; p = 0.040). Additionally, we identified a significant correlation between CSF neuron-specific enolase (NSE) with cardiac troponin I (rS = 0.57; p = 0.025) and BNP (rS = 0.66; p = 0.029), as well as between CSF tau protein and BNP (rS = 0.78; p = 0.039). Patients experiencing severe cardiac complications exhibited notably higher levels of serum tau protein at day 1 (0.21 ± 0.23 [ng/mL]) compared to those without severe cardiac complications (0.03 ± 0.04 [ng/mL]); p = 0.009. Impaired cerebral autoregulation was noted in patients both with and without severe cardiac complications. Elevated serum NSE at day 1 was related to impaired cerebral autoregulation (rS = 0.90; p = 0.037). On the first day, a substantial, reciprocal correlation between heart rate variability low-to-high frequency ratio (HRV LF/HF) and both GFAP (rS = -0.83; p = 0.004) and S100B (rS = -0.83; p = 0.004) was observed. Cardiac and brain-specific biomarkers hold the potential to assist clinicians in providing timely insights into cardiac complications, and therefore they contribute to the prognosis of outcomes.

Association of ultra-early diffusion-weighted magnetic resonance imaging with neurological outcomes after out-of-hospital cardiac arrest

BackgroundThis study aimed to investigate the association between ultra-early (within 6 h after return of spontaneous circulation [ROSC]) brain diffusion-weighted magnetic resonance imaging (DW-MRI) and neurological outcomes in comatose survivors after out-of-hospital cardiac arrest.MethodsWe conducted a registry-based observational study from May 2018 to February 2022 at a Chungnam national university hospital in Daejeon, Korea. Presence of high-signal intensity (HSI) (PHSI) was defined as a HSI on DW-MRI with corresponding hypoattenuation on the apparent diffusion coefficient map irrespective of volume after hypoxic ischemic brain injury; absence of HSI was defined as AHSI. The primary outcome was the dichotomized cerebral performance category (CPC) at 6 months, defined as good (CPC 1–2) or poor (CPC 3–5).ResultsOf the 110 patients (30 women [27.3%]; median (interquartile range [IQR]) age, 58 [38–69] years), 48 (43.6%) had a good neurological outcome, time from ROSC to MRI scan was 2.8 h (IQR 2.0–4.0 h), and the PHSI on DW-MRI was observed in 46 (41.8%) patients. No patients in the PHSI group had a good neurological outcome compared with 48 (75%) patients in the AHSI group. In the AHSI group, cerebrospinal fluid (CSF) neuron-specific enolase (NSE) levels were significantly lower in the group with good neurological outcome compared to the group with poor neurological outcome (20.1 [14.4–30.7] ng/mL vs. 84.3 [32.4–167.0] ng/mL, P < 0.001). The area under the curve for PHSI on DW-MRI was 0.87 (95% confidence interval [CI] 0.80–0.93), and the specificity and sensitivity for predicting a poor neurological outcome were 100% (95% CI 91.2%–100%) and 74.2% (95% CI 62.0–83.5%), respectively. A higher sensitivity was observed when CSF NSE levels were combined (88.7% [95% CI 77.1–95.1%]; 100% specificity).ConclusionsIn this cohort study, PHSI findings on ultra-early DW-MRI were associated with poor neurological outcomes 6 months following the cardiac arrest. The combined CSF NSE levels showed higher sensitivity at 100% specificity than on DW-MRI alone. Prospective multicenter studies are required to confirm these results.

Adherence to hypothermia guidelines in newborns with hypoxic-ischemic encephalopathy

IntroductionWe do not have population data in Spain on the application of therapeutic hypothermia (TH). The objective was to examine adherence to management standards during TH of infants with hypoxic-ischemic encephalopathy (HIE). MethodMulticenter observational cohort study from the beginning of TH (year 2010) in 5 hospitals in a Spanish region, until year 2019. Results133 patients were recruited, 72% diagnosed with moderate HIE and the rest of them with severe HIE. In 84% of infants, passive hypothermia was started at birth. Active TH was started at a median age of 5 h of life (IQR 3.3; 6.3), although the central targeted temperature (33−34 °C) was reached at a median age of 3.5 h (IQR 1; 6). Those born extramural, initiated active TH 3.3 h on average later than those born intramural, but without differences in the age at which the targeted temperature was reached.Sedoanalgesia was used in 97%. 100% were monitored with amplitude-integrated EEG and 59% with cerebral oxymetry. MRI was performed in 94% with moderate HIE vs. 65% with severe; P < .001. Neuron-specific enolase in cerebrospinal fluid was determined in 42%. The average duration of rewarming was median 10 h (IQR 8; 12), with no differences depending on the degree of HIE (P = .57). ConclusionsThe implementation of TH successfully met the standards. However, aspects of care that could be improved were detected. Auditing newborn care with HIE is crucial to achieving programs with a high quality of care in each region

Neuron-specific enolase level is a useful biomarker for distinguishing amyotrophic lateral sclerosis from cervical spondylotic myelopathy

The current study aimed to evaluate whether cerebrospinal fluid (CSF) neuron-specific enolase (NSE) levels are elevated in amyotrophic lateral sclerosis (ALS) and are effective in distinguishing ALS from cervical spondylotic myelopathy (CSM). We retrospectively evaluated 45 patients with ALS, 23 with CSM, 28 controls, and 10 with Parkinson’s disease (PD) who underwent analysis of CSF NSE levels. The control group comprised patients aged above 45 years who underwent lumbar puncture because of suspected neurological disorders that were ruled out after extensive investigations. CSF NSE levels were evaluated using the electro-chemiluminescent immunoassay. The ALS group had significantly higher CSF NSE levels than the CSM and control groups (P < 0.001 for both comparisons). The CSM, control, and PD groups did not significantly differ in terms of CSF NSE levels. A receiver-operating characteristic curve analysis was performed to assess the diagnostic value of CSF NSE levels in distinguishing ALS from CSM. The area under the curve for CSF NSE levels was 0.86. The optimal cutoff value was 17.7 ng/mL, with a specificity of 87% and a sensitivity of 80%. Hence, CSF NSE levels are elevated in ALS and are effective in distinguishing ALS from CSM.

Meta-analysis of cerebrospinal fluid neuron-specific enolase levels in Alzheimer\u2019s disease, Parkinson\u2019s disease, dementia with Lewy bodies, and multiple system atrophy

BackgroundThis study examined the usefulness of cerebrospinal fluid (CSF) neuron-specific enolase (NSE) levels as a candidate biomarker of neurodegeneration in Alzheimer’s disease (AD), Parkinson’s disease (PD), PD with dementia (PDD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA).MethodsWe performed a systematic search of PubMed, the Cochrane Library, Scopus, and Google Scholar to find studies that measured CSF NSE levels in AD, PD, DLB, and/or MSA. For each disease, we pooled all available data and performed a meta-analysis, and meta-regression analyses of age and sex were conducted if the main analysis found a significant association.ResultsTwenty studies were included (13 for AD, 8 for PD/PDD/DLB, and 4 for MSA). Significantly elevated CSF NSE levels were detected in AD (Hedges’ g = 0.822, 95% confidence interval [95% CI] 0.332 to 1.311, p = 0.0010), but the data exhibited high heterogeneity (I2 = 88.43%, p < 0.001). The meta-regression analysis of AD showed that age (p < 0.001), but not sex, had a significant effect on CSF NSE levels. A meta-analysis of the pooled data for PD/PDD/DLB did not show any significant changes in the CSF NSE level, but a sub-group analysis of PDD/DLB revealed significantly elevated CSF NSE levels (Hedges’ g = 0.507, 95% CI 0.020 to 0.993, p = 0.0412). No significant changes in CSF NSE levels were detected in MSA.ConclusionsThe CSF NSE level may be a useful biomarker of neurodegeneration in AD and PDD/DLB. Age was found to affect the CSF NSE levels of AD patients.

Adherencia a los estándares en el tratamiento con hipotermia del recién nacido con encefalopatía hipóxico-isquémica

IntroductionWe do not have population data in Spain on the application of therapeutic hypothermia (TH). The objective was to examine adherence to management standards during TH of infants with hypoxic-ischemic encephalopathy (HIE). MethodMulticenter observational cohort study from the beginning of TH (year 2010) in 5 hospitals in a Spanish region, until year 2019. Results133 patients were recruited, 72% diagnosed with moderate HIE and the rest of them with severe HIE. In 84% of infants, passive hypothermia was started at birth. Active TH was started at a median age of 5hours of life (IQR: 3.3-6.3), although the central targeted temperature (33-34°C) was reached at a median age of 3.5hours (IQR: 1-6). Those born extramural, initiated active TH 3.3hours on average later than those born intramural, but without differences in the age at which the targeted temperature was reached.Sedoanalgesia was used in 97%. The 100% were monitored with amplitude-integrated EEG and 59% with cerebral oxymetry. MRI was performed in 94% with moderate HIE vs. 65% with severe; P<.001. Neuron-specific enolase in cerebrospinal fluid was determined in 42%. The average duration of rewarming was median 10hours (IQR: 8-12), with no differences depending on the degree of HIE (P=.57). ConclusionsThe implementation of TH successfully met the standards. However, aspects of care that could be improved were detected. Auditing newborn care with HIE is crucial to achieving programs with a high quality of care in each region.

Neuron-specific enolase in cerebrospinal fluid as a biomarker of brain damage in infants with hypoxic-ischemic encephalopathy.

Neuron-specific enolase in cerebrospinal fluid as a biomarker of brain damage in infants with hypoxic-ischemic encephalopathy.

Relationship between YKL-40, neuron-specific enolase, tumor necrosis factor-a, interleukin-6, and clinical assessment scores in traumatic brain injury

Background and Objectives: The aim of the present study is to determine plasma and cerebrospinal levels of YKL-40, in combination with neuron-specific enolase (NSE), interleukin (IL)-6, tumor necrosis factor (TNF)-α, and the clinical scales such as Glasgow Coma Scale, Acute Physiology and Chronic Health Evaluation a III, and MARSHALL classification in traumatic brain injury (TBI). Materials and Methods: This was a prospective study conducted on patient cohort of 27 patients with isolated severe TBI. Cerebrospinal fluid (CSF) and plasma were collected on the 24th and 96th h after trauma. CSF samples were obtained also from forensic autopsies of 29 adult healthy cadavers. Results: The CSF level of YKL-40 in TBI patients was higher compared to controls, while no significant change between CSF NSE levels in patients and controls was found. We determined a strong correlation between YKL-40 and NSE levels and TBI clinical assessment scores. The analysis of the influence of independent prognostic factors on the outcome of TBI patients showed that plasma NSE concentrations are the major independent variable which is associated with the survival of TBI patients. Still, changes in IL-6 and TNF-α levels could not be considered as reliable predictors of mortality. Conclusion: We present data for correlation of YKL-40 and NSE levels with clinical scores for assessment of trauma severity and the outcome of TBI patients. Even though further large-scale investigations are required to clarify and evaluate the clinical significance of both biomarkers, our findings suggest that YKL-40 and NSE might be implicated in the pathogenesis of TBI and could indicate the degree of neuroinflammation and brain damage.

Intravenous Hydrogen Therapy With Intracisternal Magnesium Sulfate Infusion in Severe Aneurysmal Subarachnoid Hemorrhage.

Poor-grade subarachnoid hemorrhage still has a poor prognosis. This randomized controlled clinical trial evaluated intracisternal magnesium sulfate infusion combined with intravenous hydrogen therapy in patients with poor-grade subarachnoid hemorrhage. Thirty-seven patients with poor-grade subarachnoid hemorrhage were randomized to Mg+H2, Mg, and control groups. Mg and Mg+H2 groups received intracisternal magnesium sulfate infusion (2.5 mmol/L) at 20 mL/h for 14 days. Mg+H2 group also received intravenous hydrogen-rich solution infusion for 14 days. Primary outcome measures were occurrence of delayed cerebral ischemia and cerebral vasospasm. Secondary outcome measures were modified Rankin Scale and Karnofsky performance status at 3 and 12 months, Barthel index at 12 months, and serum and cerebrospinal fluid malondialdehyde and neuron-specific enolase. Serum neuron-specific enolase levels were significantly lower in the Mg+H2 group from days 3 to 14 than in the control group. Cerebrospinal fluid neuron-specific enolase levels were also significantly lower in the Mg+H2 group from days 3 to 7 than in the control group. Incidences of cerebral vasospasm and delayed cerebral ischemia were significantly higher in the control group than in other groups. Modified Rankin Scale and Karnofsky performance status did not significantly differ between the three groups at 3 months. Modified Rankin Scale scores 0 to 2 were more common in the Mg and Mg+H2 groups at 1 year. Barthel index was higher in the Mg+H2 group than in the control group. Intracisternal magnesium sulfate infusion started immediately after surgery reduces the incidence of cerebral vasospasm and delayed cerebral ischemia and improves clinical outcomes without complications in patients with poor-grade subarachnoid hemorrhage. Intracisternal magnesium sulfate infusion combined with intravenous hydrogen therapy decreases serum malondialdehyde and neuron-specific enolase and improves Barthel index, indicating hydrogen has additional effects. Registration: URL: https://www.umin.ac.jp/ctr/index.htm. Unique identifier: UMIN000014696.

Abstract 348: Impact of Low and High Partial Pressure of Carbon Dioxide on Neuron Specific Enolase Derived from Serum and Cerebrospinal Fluid in Patients Who Underwent Targeted Temperature Management After Out-of-hospital Cardiac Arrest: A Retrospective Study

Aim: In a previous study, low and high-normal arterial carbon dioxide tension (PaCO 2 ) were not associated with serum neuron specific enolase (NSE) in cardiac arrest survivors. We assessed the effect of PaCO 2 on NSE in cerebrospinal fluid (CSF) and serum. Methods: This was a retrospective study. PaCO 2 for the first 24 h was analysed in four means, qualitative exposure state (qES), time-weighted average (TWA), median, and minimum-maximum (Min-Max). These subgroups were divided into low (LCO 2 ) and high PaCO 2 (HCO 2 ) groups defined as PaCO 2 ≤35.3 and PaCO 2 &gt;43.5 mmHg, respectively. NSE was measured at 24, 48, and 72 h (sNSE 24,48,72 and cNSE 24,48,72 ) from return of spontaneous circulation (ROSC). The primary outcome was the association between PaCO 2 and the NSE measured at 24 h after ROSC. Results: Forty-two subjects (male, 33; 78.6%) were included in total cohort. PaCO 2 in TWA subgroup was associated with cNSE 24,48,72 , while PaCO 2 in the other subgroup were only associated with cNSE 24 . PaCO 2 and cNSE in qES subgroup showed good correlation (r= -0.61; p&lt; 0.01), and in TWA, Median, and Min-Max subgroup showed moderate correlations (r= -0.57, r= -0.48, and r= -0.60; p&lt; 0.01). Contrastively, sNSE was not associated and correlated with PaCO 2 in all analysis. Poor neurological outcome in LCO 2 was significantly higher than HCO 2 in qES, TWA, and Median subgroups ( p&lt; 0.01, p&lt; 0.01, and p= 0.02). Conclusion: Association was found between NSE and PaCO 2 using CSF, despite including normocapnic ranges; TWA of PaCO 2 may be most strongly associated with CSF NSE levels. A prospective, multi-centre study is required to confirm our results.

Lactic acid, neuron-specific enolase, and blood–brain barrier index after a severe traumatic brain injury: a prospective study

Objective To explore the clinical significance of dynamic monitoring of cerebrospinal fluid (CSF) and serum Lactic acid（Lac), neuron-specific enolase (NSE), and the blood–brain barrier (BBB) index in evaluating the condition and prognosis after a severe traumatic brain injury (TBI). Methods A total of 52 severe TBI patients admitted to the Department of Neurosurgery within 24 hours after injury were dynamically monitored. CSF and serum samples were collected on the 1st, 3rd, and 7th day after a severe TBI to monitor the changes in Lac, NSE, and the BBB index. Intracranial pressure (ICP), Glasgow coma scale (GCS), and 6-month Glasgow outcome scale-extended (GOS-E) were tested. According to the results of GOS-E, the patients were divided into two groups (i.e. the poor prognosis group and good prognosis group). Statistical analysis was conducted to investigate the clinical significance of dynamic monitoring of CSF and serum Lac, NSE, and BBB index after a severe TBI. Results After a severe TBI, the levels of Lac, NSE, and BBB in CSF and serum were significantly higher than those in the normal range. Lac, NSE, and the BBB index did not correlate with ICP (except serum Lac) but had correlations with GCS and post-injury 6 months post-injury (except serum Lac). Moreover, the correlations between Lac, NSE, and BBB index were statistically significant (p < 0.05): CSF Lac and CSF NSE; CSF Lac and serum NSE; Lac and BBB index of CSF; Lac and BBB index of CSF; NSE and CSE of serum; CSF NSE and BBB index; and serum NSE and BBB index. Additionally, serum NSE is correlated with NSE in CSF (p < 0.05). Conclusion After a severe TBI, dynamic monitoring of CSF and serum Lac, NSE, and BBB index has the potential to assess the condition, predict the prognosis, and have clinical significance.

Detection of neuron-specific enolase in patients with subacute 1, 2-dichloroethane poisoning

Objective: To investigate the changes of neuron-specific enolase (NSE) in serum and cerebrospinal fluid of patients with subacute 1, 2-dichloroethane (DCE) poisoning. Methods: Ten patients with subacute 1, 2-DCE poisoning hospitalized in Guangzhou 12th Municipal People's Hospital from December 2014 to March 2019 were taken as the subacute 1, 2-DCE poisoning group, 34 typical acute toxic encephalopathy patients hospitalized at the same time as typical acute toxic encephalopathy group, 40 healthy physical examinees as normal control group. The levels of serum NSE in patients of subacute 1, 2-DCE poisoning and typical acute toxic encephalopathy group during onset and improvement were detected by chemiluminescence method, and the results were analyzed statistically. The level of NSE in cerebrospinal fluid of subacute 1, 2-DCE poisoning group was detected and analyzed its correlation with the level of NSE in serum. Using receiver operator characteristic (ROC) curve to analyze the diagnostic efficacy of NSE in subacute 1, 2-DCE poisoning and typical acute toxic encephalopathy (area under curve, AUC) . Results: There was no significant difference between the serum NSE level of the patients with subacute 1, 2-DCE poisoning in the onset group and the normal control group and the improvement group (P>0.05) . The serum NSE level of subacute 1, 2-DCE poisoning in the improvement group was lower than those in the normal control group (P<0.01) . The serum NSE level of the subacute 1, 2-DCE poisoning in the onset group was lower than those in the typical acute toxic encephalopathy in the onset group (P<0.01) . There was no linear correlation between cerebrospinal fluid NSE and serum NSE in patients with subacute 1, 2-DCE poisoning (r=-0.183, P=0.52) . ROC curve showed that the AUC of serum NSE in diagnosing subacute 1, 2-DCE poisoning and typical acute toxic encephalopathy were 0.661 and 0.726, respectively. Conclusion: There is no significant change in serum NSE in patients with subacute 1, 2-DCE poisoning.

Impact of low and high partial pressure of carbon dioxide on neuron-specific enolase derived from serum and cerebrospinal fluid in patients who underwent targeted temperature management after out-of-hospital cardiac arrest: A retrospective study

AimIn a previous study, low and high-normal arterial carbon dioxide tension (PaCO2) were not associated with serum neuron-specific enolase (NSE) in cardiac arrest survivors. We assessed the effect of PaCO2 on NSE in cerebrospinal fluid (CSF) and serum. MethodsThis was a retrospective study. PaCO2 for the first 24 h was analysed in four means, qualitative exposure state (qES), time-weighted average (TWA), median, and minimum–maximum (Min–Max). These subgroups were divided into low (LCO2) and high PaCO2 (HCO2) groups defined as PaCO2 ≤ 35.3 and PaCO2 > 43.5 mmHg, respectively. NSE was measured at 24, 48, and 72 h (sNSE24,48,72 and cNSE24,48,72) from return of spontaneous circulation (ROSC). The primary outcome was the association between PaCO2 and the NSE measured at 24 h after ROSC. ResultsForty-two subjects (male, 33; 78.6%) were included in total cohort. PaCO2 in TWA subgroup was associated with cNSE24,48,72, while PaCO2 in the other subgroup were only associated with cNSE24. PaCO2 and cNSE in qES subgroup showed good correlation (r = −0.61; p < 0.01), and in TWA, median, and Min–Max subgroup showed moderate correlations (r = −0.57, r = −0.48, and r = −0.60; p < 0.01). Contrastively, sNSE was not associated and correlated with PaCO2 in all analysis. Poor neurological outcome in LCO2 was significantly higher than HCO2 in qES, TWA, and median subgroups (p < 0.01, p < 0.01, and p = 0.02). ConclusionAssociation was found between NSE and PaCO2 using CSF, despite including normocapnic ranges; TWA of PaCO2 may be most strongly associated with CSF NSE levels. A prospective, multi-centre study is required to confirm our results.

Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model.

Specific neuroprotective strategies to minimize cerebral damage caused by severe hypoxia or hypovolemia are lacking. Based on previous studies showing that relaxin-2/serelaxin increases cortical cerebral blood flow, we postulated that serelaxin might provide a neuroprotective effect. Therefore, we tested serelaxin in two emergency models: hypoxia was induced via inhalation of 5% oxygen and 95% nitrogen for 12 min; thereafter, the animals were reoxygenated. Hypovolemia was induced and maintained for 20 min by removal of 50% of the total blood volume; thereafter, the animals were retransfused. In each damage model, the serelaxin group received an intravenous injection of 30 µg/kg of serelaxin in saline, while control animals received saline only. Blood gases, shock index values, heart frequency, blood pressure, and renal blood flow showed almost no significant differences between control and treatment groups in both settings. However, serelaxin significantly blunted the increase of lactate during hypovolemia. Serelaxin treatment resulted in significantly elevated cortical cerebral blood flow (CBF) in both damage models, compared with the respective control groups. Measurements of the neuroproteins S100B and neuron-specific enolase in cerebrospinal fluid revealed a neuroprotective effect of serelaxin treatment in both hypoxic and hypovolemic animals, whereas in control animals, neuroproteins increased during the experiment. Western blotting showed the expression of relaxin receptors and indicated region-specific differences in relaxin receptor-mediated signaling in cortical and subcortical brain arterioles, respectively. Our findings support the hypothesis that serelaxin is a potential neuroprotectant during hypoxia and hypovolemia. Due to its preferential improvement of cortical CBF, serelaxin might reduce cognitive impairments associated with these emergencies.

A clinical case of presumed cerebellar medulloblastoma in a Japanese Black calf with increased neuron-specific enolase in cerebrospinal fluid.

A 2-day-old Japanese Black male calf that presented with opisthotonos with spastic extension of all four limbs and nystagmus was presented. Evaluation of cranial neurology revealed a horizontal slow nystagmus and absence of menace response in the left eye. Necropsy revealed a mass located between the posterior margin of the cerebrum and anterior margin of the cerebellum, and continuously with the cerebellar lesion. The brainstem was severely compressed by those lesions. Original structures of the cerebellum were mostly replaced by grayish-white and brownish tissues. Those lesions were diagnosed as presumed cerebellar medulloblastoma by histopathological and immunohistochemical examination. As neuron-specific enolase in the cerebrospinal fluid which is a biomarker for neuronal damage was increased compared with healthy calves.

Abstract 23: The Usefulness of Neuron-Specific Enolase in Cerebrospinal Fluid to Predict Neurological Prognosis in Cardiac Arrest Survivors Who Underwent Target Temperature Management: A Prospective Observational Study

Aim: We aimed to investigate the prognostic performance between serum NSE and cerebrospinal fluid (CSF) NSE for 6-month neurologic outcome in OHCA survivors underwent target temperature management (TTM). Hypothesis: We hypothesized that the NSE levels measured in the CSF would affect the change, earlier and more sensitively than serum, according to severity of hypoxic brain damage. Methods: This single-centre prospective observational study included out-of-hospital cardiac arrest (OHCA) patients underwent TTM. NSE levels were assessed in blood and CSF samples obtained immediately (Day 0), and 24 h (Day 1), 48 h (Day 2), and 72 h (Day 3) after return of spontaneous circulation (ROSC). The primary outcome was the 6-month neurological outcome. Results: We enrolled 34 patients (males, 24; 70.6%), 16 (47.1%) had a poor neurologic outcome. CSF NSE and serum NSE values were significantly higher in the poor outcome group compared to the good outcome group at each time point, except for serum Day 0. CSF NSE and serum NSE had area under curve (AUC) of 0.819-0.972 and 0.648-0.920, respectively. CSF NSE prognostic performances were significant higher than serum NSE at Day 1 and showed excellent AUC values (0.969; 95% Confidential Interval [CI] 0.844-0.999) and high sensitivity (93.8%; 95% CI 69.8-99.8) at 100% specificity. Conclusion: We found CSF NSE values were highly predictive and sensitive markers of 6-month poor neurological outcome in OHCA survivors treated with TTM at Day 1 after ROSC. Thus, CSF NSE level at day 1 after ROSC can be a useful early prognosticator in OHCA survivors.

The usefulness of neuron-specific enolase in cerebrospinal fluid to predict neurological prognosis in cardiac arrest survivors who underwent target temperature management: A prospective observational study

AimCerebrospinal fluid (CSF) neuron-specific enolase (NSE) levels increase ahead of serum NSE levels in patients with severe brain injury. We examined the prognostic performance between CSF NSE and serum NSE levels in out-of-cardiac arrest (OHCA) survivors who had undergone target temperature management (TTM). MethodsThis single-centre prospective observational study included OHCA patients who had undergone TTM. NSE levels were assessed in blood and CSF samples obtained immediately (Day 0), and at 24 h (Day 1), 48 h (Day 2), and 72 h (Day 3) after return of spontaneous circulation (ROSC). The primary outcome was the 6-month neurological outcome. ResultsWe enrolled 34 patients (males, 24; 70.6%), and 16 (47.1%) had a poor neurologic outcome. CSF NSE and serum NSE values were significantly higher in the poor outcome group compared to the good outcome group at each time point, except for serum Day 0. CSF NSE and serum NSE had an area under curve (AUC) of 0.819–0.972 and 0.648–0.920, respectively. CSF NSE prognostic performances were significantly higher than serum NSE levels at Day 1 and showed excellent AUC values (0.969; 95% confidence interval [CI] 0.844–0.999) and high sensitivity (93.8%; 95% CI 69.8–99.8) at 100% specificity. ConclusionWe found CSF NSE values were highly predictive and sensitive markers of 6-month poor neurological outcome in OHCA survivors treated with TTM at Day 1 after ROSC. Therefore, CSF NSE levels at day 1 after ROSC can be a useful early prognosticator in OHCA survivors.

Neuron-Specific Enolase in Cerebrospinal Fluid Predicts Brain Injury After Sudden Unexpected Postnatal Collapse

BackgroundBiomarkers of brain injury with high predictive value in newborns in critical neurological status are increasingly required. Neuron-specific enolase in cerebrospinal fluid has been shown to be highly predictive in newborns with perinatal hypoxic-ischemic encephalopathy, but its utility has not been examined in sudden unexpected postnatal collapse. PurposeWe analyzed whether the levels of neuron-specific enolase in cerebrospinal fluid can be a useful biomarker to estimate the severity of brain injury in neonates after a sudden unexpected postnatal collapse. MethodsThis is a prospective observational study of near-term infants who were consecutively admitted with sudden unexpected postnatal collapse in two neonatal intensive care units during a nine-year period. Variables were collected and analyzed regarding the perinatal period, clinical course, severity of encephalopathy, amplitude-integrated encephalography, magnetic resonance imaging findings, and outcome. Neuron-specific enolase in cerebrospinal fluid samples were obtained in 18 infants with sudden unexpected postnatal collapse between 12 and 72 hours after the collapse and compared with those of 29 controls. ResultsThe levels of neuron-specific enolase in cerebrospinal fluid were higher in patients than in controls (P < 0.001). Levels of neuron-specific enolase in cerebrospinal fluid in infants with sudden unexpected postnatal collapse were significantly higher in patients who presented severe encephalopathy, seizures, abnormal amplitude-integrated encephalography background, or brain injury on magnetic resonance imaging. Receiver operator characteristic curve analysis revealed a neuron-specific enolase in cerebrospinal fluid cutoff value of maximum predictive accuracy of 61 ng/mL (area under the curve, 1.0; sensitivity, specificity, positive predictive value, and negative predictive value, 100%) for identifying infants who died or had adverse outcomes. ConclusionsLevels of neuron-specific enolase in cerebrospinal fluid obtained between 12 and 72 hours after a sudden unexpected postnatal collapse event seem to be a useful biomarker for identifying newborns with severe brain injury and for predicting outcome.

Elevated neuron-specific enolase and S100 calcium-binding protein B concentrations in cerebrospinal fluid of patients with anti-N-methyl-d-aspartate receptor encephalitis

BackgroundAnti‑N‑methyl‑d‑aspartate receptor (NMDAR) encephalitis is a relatively common autoimmune neurological disease of the central nervous system (CNS). Neuron-specific enolase (NSE) and S100 calcium-binding protein B (S100B) are structural proteins of the central nervous system (CNS). In patients with CNS injury accompanied by nervous tissue and cellular damage, these structural proteins are released from cells; their extracellular concentrations, including those in cerebrospinal fluid (CSF) and blood, subsequently increase. MethodsThirty-six patients with anti-NMDAR encephalitis were prospectively recruited. The CSF NSE and S100B concentrations were measured in 19 and 17 patients, respectively. The CSF NSE and S100B concentrations were measured in 21 patients with noninflammatory neurological disease as controls. All measurements were performed using enzyme-linked immunosorbent assays. ResultsThe CSF NSE and S100B concentrations were remarkably higher in the patients with anti-NMDAR encephalitis than in the controls. The early NSE or S100B concentrations in CSF were associated with the mRS. ConclusionCSF NSE and S100B concentration in patients with anti-NMDAR encephalitis is higher than in patients with non-inflammatory neurological disease. The early NSE or S100B concentrations in CSF were associated with the mRS and we can use it to determine the prognosis of the disease.