Enolase In Cerebrospinal Fluid Research Articles

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

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.

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.

Neuron-specific enolase in cerebrospinal fluid as a neurochemical marker for brain damage in acute lymphoblastic leukemia

Background Acute lymphoblastic leukemia (ALL) is the most common form of childhood cancer with a cure rate approaching 80%. Neuron-specific enolase (NSE) is known to be a cell-specific isoenzyme of the glycolytic enzyme enolase. The expression of NSE is a late event in neural differentiation, thus making it a useful index of neural maturation. It is a highly specific marker for neurons and peripheral neuroendocrine cells. NSE in cerebrospinal fluid (CSF) is a reliable marker of neuronal damage. It is believed to signal for brain damage after hypoxic-ischemic and traumatic injury. Objective and methods This study aimed to measure CSF levels of NSE as a neurochemical marker for brain damage in response to chemotherapy at diagnosis and during induction using the enzyme-linked immunosorbent assay method. Thirty newly diagnosed ALL patients were enrolled in this study, comprising 19 male and 11 female patients. Results NSE level in the CSF samples increased from 9.3 ± 2.1 μg/l on day 0 (before the start of treatment) to 14.9 ± 1.85 μg/l on day 7 and then gradually decreased to 11.4 ± 1.46 μg/l on day 28. The increase in NSE levels in CSF on days 7 and 28 was considered highly significant when compared with those measured on day 0 (before induction therapy). Conclusion We concluded that the increase in NSE in CSF during induction therapy in children with ALL can be interpreted as an early sign of brain damage.

Limited efficacy of pentoxifylline as anti-inflammatory agent in experimental pneumococcal meningitis

SUMMARY Dexamethasone appears to show some adverse side-effects as adjunctive anti-inflammatory agent in bacterial meningitis. For this reason, we tested the anti-inflammatory and neuroprotective effect of pentoxifylline administered 15 min before starting antibiotic treatment with ceftriaxone (n = 10) versus antibiotic therapy alone (n = 9) in the rabbit model of pneumococcal meningitis. Pentoxifylline lowered the medians of leucocyte density, tumour necrosis factor-alpha (TNF-α) and lactate in the cerebrospinal fluid (CSF), but only leucocyte migration into the subarachnoid space was significantly inhibited 8 h after initiation of therapy (P = 0.01). CSF protein, brain water content, and the entry of ceftriaxone into CSF were not influenced by pentoxifylline. The density of neuronal apoptoses in the dentate gyrus was slightly lower in animals receiving pentoxifylline than in those treated with ceftriaxone only. The median concentration of neuron-specific enolase in CSF was lower in the pentoxifylline-treated group, but the difference was not significant. In conclusion, pentoxifylline showed some anti-inflammatory activity in pneumococcal meningitis, but the substance failed significantly to reduce neuronal damage.

Study on the correlation between insulin-like growth factor-I and neuron-specific enolase in cerebrospinal fluid of children with CNS infection

Objective To explore the correlation between insulin-like growth factor-I （IGF-I） and neuron-specific enolase （NSE） in cerebrospinal fluid （CSF） of children with CNS infection. Methods 90 cases were recruited in the study, among which 30 cases were patients with bacterial, meningitis （BM）, 30 cases with viral encephalitis （VM） and the rest belonged to contrast groups. CSF of all 90 cases was collected during the period from 24 to 48 hours after admission. IGF-I and NSE in CSF were measured by FJ-2008 PS γ immunocount instrument. Results Both BM and VM group had a significant difference in IGF-I and NSE as compared with control group （P 〈 0.01）, but there was no significant difference between BM and VM group （P〉0.05）. IGF-I and NSE in CSF of BM and VM group were not correlated with each other. However, IGF-I and NSE showed positive correlation in 15 patients with conscious disturbance （r = 0.94, P 〈 0.01）. Conclusion Our study showed that IGF-I and NSE in CSF of patients with CNS infection increased greatly. IGF-I and NSE in CSF of critically ill children were correlated positively. It suggests that IGF-I play a certain role in protecting and repairing central nervous system. Key words: Central nervous system; Infection; Cerebrospinal fluid; Insulin-like growth factor-I; Neuron-specific enolase

The increase of neuron-specific enolase in cerebrospinal fluid and plasma as a marker of neuronal damage in patients with acute brain infarction

Our goal was to determine the neuron-specific enolase (NSE) concentration in cerebrospinal fluid (CSF) and plasma in patients with the acute brain infarction (BI) and analyze the correlation between the measured NSE concentration and infarct volume and the degree of neurological and functional deficit. The study included 55 patients aged 56-68 with BI in the acute phase. The control group consisted of 16 patients subjected to diagnostic radiculography. The results showed a significant increase of NSE concentration within the first seven days in patients compared to the controls (2.838 +/- 0.504 ng/ml CSF and 4.479 +/- 0.893 ng/ml plasma). A significant correlation was found between NSE concentration and infarction volume and the degree of neurological and functional deficit both in the CSF (r = 0.828, r = 0.735, r = 0.796; p < 0.001) and in plasma (r = 0.810, r = 0.681, r = 0.783; p < 0.001). The results suggest that an early determination of this marker in CSF and plasma in patients with BI could be a valuable diagnostic factor.

Neuron-specific enolase in cerebrospinal fluid and plasma of patients with acute ischemic brain disease.

The objective of this research was to determine the dynamics of change of neuron-specific enolase concentration in patients with acute ischemic brain disease in cerebrospinal fluid and plasma. The study included 103 patients, their mean age 58-66 years. The control group consisted of 16 patients, of matching age and sex, with radicular lesions of discal origin, subjected to diagnostic radiculography. Concentration of neuron-specific enolase was measured by a flouroimmunometric method. The results showed that the concentration of neuron-specific enolase in cerebrospinal fluid and plasma of patients with brain ischemic disease within first seven days significantly increased compared to the control. The highest increase of concentration was established in brain infarction, somewhat lower in reversible ischemic attack, and the lowest in transient ischemic attack. Maximal concentration was established on the 3rd-4th day upon the brain infarction. Neuron-specific enolase concentration in cerebrospinal fluid and plasma may be an indicator of pathophysiological processes in the acute phase of brain ischemia and is significant in early diagnostics and therapy of the disease.

Prolonged intrathecal release of soluble Fas following severe traumatic brain injury in humans

The mechanisms underlying cell death following traumatic brain injury (TBI) are not fully understood. Apoptosis is believed to be one mechanism contributing to a marked and prolonged neuronal cell loss following TBI. Recent data suggest a role for Fas (APO-1, CD95), a type I transmembrane receptor glycoprotein of the nerve growth factor/tumor necrosis factor superfamily, and its ligand (Fas ligand, FasL) in apoptotic events in the central nervous system. A truncated form of the Fas receptor, soluble Fas (sFas) may indicate activation of the Fas/FasL system and act as a negative feedback mechanism, thereby inhibiting Fas mediated apoptosis. Soluble Fas was measured in cerebrospinal fluid (CSF) and serum of 10 patients with severe TBI (GCS≤8) for up to 15 days post-trauma. No sFas was detected in CSF samples from patients without neurological pathologies. Conversely, after TBI 118 out of 120 CSF samples showed elevated sFas concentrations ranging from 56 to 4327 mU/ml. Paired serum samples showed above normal (8.5 U/ml) sFas concentrations in 5 of 10 patients. Serum levels of sFas were always higher than CSF levels. However, there was no correlation between concentrations measured in CSF and in serum ( r 2=0.078, p=0.02), suggesting that the concentrations in the two compartments are independently regulated. Also, no correlation was found between sFas in CSF and blood brain barrier (BBB) dysfunction as assessed by the albumin CSF/serum quotient ( Q A), and concentrations of the cytotoxic cytokine tumor necrosis factor-alpha in CSF, respectively. Furthermore, there was no correlation with two markers of immune activation (soluble interleukin-2 receptor and neopterin) in CSF. Maximal CSF levels of sFas correlated significantly ( r 2=0.8191, p<0.001) with the early peaks of neuron-specific enolase in CSF (a marker for neuronal cell destruction), indicating that activation of the Fas mediated pathway of apoptosis may be in part the direct result of the initial trauma. However, the prolonged elevation of sFas in CSF may be caused by the ongoing inflammatory response to trauma and delayed apoptotic cell death.

Increase of neuron-specific enolase in patients with Creutzfeldt-Jakob disease

Creutzfeldt-Jakob disease (CJD) is a rare neurodegenerative human disorder with an incidence of one case per 1 000 000 per year. Recently new diagnostic tests such as neuron-specific enolase (NSE), S-100, tau-protein and protein 14-3-3 have been established as markers in prion diseases. NSE is elevated in case of rapid nerve cell loss so quantitative measurement of NSE in cerebrospinal fluid (CSF) might correlate with the disease progression. To further evaluate this hypothesis we analysed longitudinal CSF samples from 16 CJD patients. The first spinal tap was taken two weeks after the first clinical signs of a neurodegenerative disorder. This showed an elevation of NSE which continued during the course of the disease. Longitudinal examination of neuron-specific enolase in cerebrospinal fluid therefore may be useful for differentiation between CJD and other dementias.

Limited efficacy of pentoxifylline as anti-inflammatory agent in experimental pneumococcal meningitis.

Dexamethasone appears to show some adverse side-effects as adjunctive anti-inflammatory agent in bacterial meningitis. For this reason, we tested the anti-inflammatory and neuroprotective effect of pentoxifylline administered 15 min before starting antibiotic treatment with ceftriaxone (n = 10) versus antibiotic therapy alone (n = 9) in the rabbit model of pneumococcal meningitis. Pentoxifylline lowered the medians of leucocyte density, tumour necrosis factor-alpha (TNF-alpha) and lactate in the cerebrospinal fluid (CSF), but only leucocyte migration into the subarachnoid space was significantly inhibited 8 h after initiation of therapy (P = 0.01). CSF protein, brain water content, and the entry of ceftriaxone into CSF were not influenced by pentoxifylline. The density of neuronal apoptoses in the dentate gyrus was slightly lower in animals receiving pentoxifylline than in those treated with ceftriaxone only. The median concentration of neuron-specific enolase in CSF was lower in the pentoxifylline-treated group, but the difference was not significant. In conclusion, pentoxifylline showed some anti-inflammatory activity in pneumococcal meningitis, but the substance failed significantly to reduce neuronal damage.

Creatine kinase BB and neuron-specific enolase in cerebrospinal fluid in the diagnosis of brain insult.

Cerebrospinal fluid (CSF) markers provide useful information about the extent of brain damage. These biochemical indices may also be used when postmortem histopathological examination does not confirm antemortem brain insult. Seven biochemical parameters--creatine kinase (CK), creatine kinase BB isoenzyme (CK-BB), lactate dehydrogenase (LDH), gamma-glutamyltransferase, aldolase, leucine aminopeptidase (LAP), and neuron-specific enolase (NSE)--were analyzed in CSF from 82 cadavers. Case studies were categorized into one of four diagnostic groups. There were 15 cases of head trauma, 23 of hypoxia (hangings, carbon monoxide, and drug poisonings), 23 sudden cardiac death, and 21 miscellaneous cases. The degree of craniocerebral trauma was graded. In CSF there was a statistically significant correlation between the severity of craniocerebral trauma and levels of CK, CK-BB, aldolase, LDH, and LAP. CSF CK-BB [median U/L (range)] for the groupings of head trauma, hypoxia, sudden cardiac death, and miscellaneous were, respectively, 873 (1-12,100), 26 (2-2,780), 16 (1-42), and 18 (0-2,780). Corresponding CSF CK levels were 9,370 (28-67,842), 101 (18-36,840), 180 (10-29,622), and 264 (17-26,556). There were no statistical significant differences among the NSE concentrations in the four diagnostic groups. The testing of biochemical markers could be a reliable indicator of the degree of brain insult in support of morphological studies.

Neuron specific enolase in cerebrospinal fluid: a biochemical marker for neuronal degeneration in dementia disorders?

Alzheimer's disease (AD) is the most common disease causing dementia. Today the clinical diagnosis of AD is made by way of exclusion, and no biochemical markers are available to assist the clinical diagnosis. We examined the potential of neuron-specific enolase (NSE) in cerebrospinal fluid (CSF) as a diagnostic marker for AD. NSE was determined with a monoclonal antibody two-site immunoradiometric assay (IRMA) in serum (S) and cerebrospinal fluid (CSF) samples from 45 patients with "probable Alzheimer's disease (AD)", 19 patients with vascular dementia (VAD) and 33 age-matched healthy individuals. There was no significant correlation between S-NSE and CSF-NSE, or between CSF/S albumin ratio and CSF-NSE, findings suggesting that the major portion of CSF-NSE is intrathecally produced and that analysis of CSF-NSE alone (without accompanying analysis of serum) is sufficient. CSF-NSE was significantly higher in the AD group (4.7 +/- 2.7 ng/mL; p < 0.0001) and in VAD group (4.5 +/- 2.5 ng/mL; p < 0.001) as compared with the control group (2.2 +/- 1.0 ng/mL), while it did not differ significantly between the AD and the VAD group. These findings suggest that CSF-NSE have a potential as a non-disease specific marker for the neuronal degeneration in dementia disorders.

Neuron-specific enolase as a marker of in vitro neuronal damage. Part I: Assessment of neuron-specific enolase as a quantitative and specific marker of neuronal damage.

Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia. We assessed neuron-specific enolase (NSE) as a quantitative and specific biochemical marker of neuronal damage in an experimental model of kainate neurotoxicity. Rat hippocampal cultures were treated with various concentrations of kainate. NSE release into the culture medium was compared with neuronal death estimated either by direct cell counting or by lactate dehydrogenase (LDH) release, largely used to quantify neuronal injury. A dose-response relationship was observed between kainate concentration and the amount of NSE released (r = -0.69; p < 0.05) as well as a significant correlation between NSE release and neuronal death (r = 0.64; p < 0.05). Likewise, a significant correlation was found between LDH and NSE release (r = 0.85; p < 0.05). The specificity of NSE as an indicator of neuronal death was demonstrated using immunocyto-chemistry labeling and measurement of NSE release by pure astrocyte cultures. We concluded that NSE is a reliable, quantitative, and specific marker of neuronal injury.

Neuron-specific enolase in cerebrospinal fluid of patients with metastatic and non-metastatic neurological disease

Neuron-specific enolase (NSE) activities were measured in cerebrospinal fluid (CSF) in 361 patients with various neurological diseases. CSF was collected as part of the diagnostic procedure both in the control group, which consisted of 189 subjects with low back pain, and in the patient group (172 patients). The mean CSF NSE level in 189 control subjects was 7.14 ± 1.94 μg/l. Slight elevations of CSF NSE (≥ 11.0 μg/l) were observed in 9 patients with non-malignant diseases and in 2 patients with malignant diseases. The findings of this study indicate that measurement of NSE in CSF cannot be used an adjunctive diagnostic test for CNS metastases.