Serum neuron-specific enolase levels after subarachnoid hemorrhage

Mabe, Hideo; Suzuki, Satoru; Mase, Mitsuhito; Umemura, Atsusi; Nagai, Hirokazu

doi:10.1016/0090-3019(91)90108-l

Cited by 31 publications

(19 citation statements)

References 21 publications

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“…24 Indeed subsequent studies showed increased NSE levels in the serum of patients suffering from SAH, but studies on the prognostic value found conflicting results. [25][26][27][28][29] In this study NSE serum provided a low prognostic value which was inferior to NSE CSF . Thus, NSE does either not cross the blood-brain barrier in a relevant amount and/or extracranial factors like hemolysis and extracranial tissue damage might influence the concentration of NSE in the serum of these patients.…”

Section: Discussionmentioning

confidence: 51%

The Prognostic Value of NSE and S100B From Serum and Cerebrospinal Fluid in Patients With Spontaneous Subarachnoid Hemorrhage

Moritz¹,

Warnat

Bele

et al. 2010

Journal of Neurosurgical Anesthesiology

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Neuron-specific enolase (NSE) and S100B protein have been shown to be increased in cerebrospinal fluid (CSF) and serum of patients suffering from subarachnoid hemorrhage. This study was designed to evaluate the accuracy of NSE and S100B from CSF and serum for the prognosis of outcome and the detection of cerebral infarction, vasospasm and intracranial hypertension. In 55 patients with spontaneous subarachnoid hemorrhage and requiring external ventricular drainage the concentrations of NSE and S100B were determined daily from the serum and the CSF from admission until day 8. At ICU discharge patients' outcome was assessed by the Glasgow outcome scale and occurrence of cerebral infarction, vasospasm and intracranial hypertension were registered. Mean and peak values of each parameter for each patient were calculated. For accuracy assessment receiver operating characteristics were used. Bad outcome (Glasgow outcome scale 1 to 3) was found in 33 patients. Cerebral infarction, vasospasm, and intracranial hypertension were found in 31 (56%), 34 (62%), and 36 (65%) patients. Mean and peak values of NSE CSF (P<0.001), S100B CSF (P<0.001), and S100B serum (P<0.001) but not of NSE serum provided the ability to distinguish between patients with good and bad outcome. The accuracy of NSE CSF and S100B CSF did not differ significantly from that of S100B serum. NSE CSF (P<0.001), S100B CSF (P<0.001), and S100B serum (P<0.001) allowed the detection of cerebral infarction and intracranial hypertension. Cerebral vasospasm was detected by none of the parameters. In conclusion, NSE CSF, S100B CSF, and S100B serum provide similar prognostic values for outcome, intracranial hypertension and cerebral infarction. Significantly lower accuracy was found for NSE serum.

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Section: Discussionmentioning

confidence: 51%

The Prognostic Value of NSE and S100B From Serum and Cerebrospinal Fluid in Patients With Spontaneous Subarachnoid Hemorrhage

Moritz¹,

Warnat

Bele

et al. 2010

Journal of Neurosurgical Anesthesiology

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“…Plasma samples were collected in heparinized tubes, centrifuged within 24 hours of collection and stored at -70 ~ until analysis. Six months after the onset of symptoms, the neurological outcome of SAH was assessed using the Glasgow Outcome Scale [15] (Table 2).…”

Section: Clinical Evaluationmentioning

confidence: 99%

“…Mabe et al [15] found that patients with a poor outcome following SAH had significantly higher serum levels of NSE than patients with a favourable outcome. However, the usefulness of these markers for monitoring brain damage is limited by the fact that they are not as specific to the nervous system as previously thought: CK-BB has been found in high concentrations in several tissues other than brain [22], and serum levels of NSE have been found to be elevated in patients with tumours outside the nervous system, including small cell carcinoma of the lung.…”

Section: Specificity Of Nse and Ck-bbmentioning

confidence: 99%

S-100 protein plasma levels after aneurysmal subarachnoid haemorrhage

et al. 1997

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We investigated the level of S-100 protein in blood as an indicator of brain damage in 71 patients suffering from subarachnoid haemorrhage (SAH) due to ruptured aneurysms. Concentrations of S-100 protein were determined by micro-titre based immunofluorometic assay detecting predominantly S-100b on blood samples obtained 24 hours, 3 days and 7 days after onset of symptoms in patients with SAH and from 120 healthy control subjects. Neurological status was assessed using the Hunt and Hess (HH) scale on admission and by the Glasgow Outcome Scale (GOS) 6 months later. Mean concentrations of S-100 protein in blood were significantly (p < 0.0001) higher in patients 24 hours (0.263 +/- 0.387 microgram/l), 3 days (0.192 +/- 0.288 microgram/l) and 7 days (0.256 +/- 0.442 microgram/l) after onset of SAH symptoms compared to controls (0.050 +/- 0.081 microgram/l). More severe neurological symptoms (higher HH scale scores) on admission correlated with higher S-100 levels on admission (R = 0.70) and Day 3 (R = 0.66) (p < 0.0001). Worse outcome (lower GOS score) 6 months after SAH was also associated with higher plasma concentration of S-100 in the first week after SAH. In summary, this study showed that in patients with SAH due to ruptured aneurysm, S-100 protein levels correlate with early neurological deficit and are as sensitive as HH scores in predicting neurological outcome (GOS scores). Measurement of S-100 protein in blood is a reliable non-invasive method and may be clinically useful to screen for and monitor progression of central nervous system diseases of various origins.

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“…Increased serum levels are proportionally related to the extent of cellular brain injury (Martens et al, 1998). So serum NSE and S-100B are sensitive and quantitative markers of parenchymal brain injury due to ischemia stroke, intracerebral hemorrhage, trauma and cardiopulmonary surgery (Mabe et al, 1991;Skogseid et al, 1992;Schaarschmidt et al, 1994;Isgro et al, 1997;Missler et al, 1997;Elting et al, 2000;Jonsson et al, 2001). Cardiac arrest leads to a period of temporary systemic and global cerebral ischemia, while the following cardiopulmonary resuscitation causes reperfusion injury, mediated by a series of inflammatory responses (Jean et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Basic fibroblast growth factor alleviates brain injury following global ischemia reperfusion in rabbits

Zhang

Gan

et al. 2005

J. Zhejiang Univ. Sci.

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Abstract:The aim of this study was to explore the protective effect of basic fibroblast growth factor (bFGF) on brain injury following global ischemia reperfusion and its mechanisms. Brain injury following global ischemia was induced by four vessels occlusion and systemic hypotension. Twenty-four rabbits were randomized into three groups: group A, only dissection of vessels; group B, intravenous infusion of normal saline after reperfusion for 6 h; group C, 30 µg/kg bFGF injected intravenously at the onset of reperfusion, then infused with 10 µg/(kg⋅h) for 6 h. Serum neuron specific enolase (NSE), S-100B, tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-8 (IL-8) were measured before ischemia, 30 min after ischemia, 0.5, 1, 3, 6 h after reperfusion. Brain water content was determined and cerebral histopathological damages were compared. NSE and S-100B were increased 1 h after reperfusion and reached their peaks 6 h after reperfusion, but were much higher in group B than those in group C 3, 6 h after reperfusion. In groups B and C, TNF-α was increased after ischemia and IL-1 and IL-8 were increased significantly 0.5 h after reperfusion, then reached their peaks 6 h, 3 h, 6 h after reperfusion respectively. TNF-α and IL-8 at the time points of 1 h and 3 h and IL-1 at 3 h and 6 h in group C were correspondingly lower than those in group B. These indices in group A were nearly unchanged. There were less severe cerebral histopathological damages in group C compared with group B, but no difference in brain water content. It could be concluded that bFGF alleviates brain injury following global ischemia and reperfusion by down-regulating expression of inflammatory factors and inhibiting their activities.

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Serum neuron-specific enolase levels after subarachnoid hemorrhage

Cited by 31 publications

References 21 publications

The Prognostic Value of NSE and S100B From Serum and Cerebrospinal Fluid in Patients With Spontaneous Subarachnoid Hemorrhage

The Prognostic Value of NSE and S100B From Serum and Cerebrospinal Fluid in Patients With Spontaneous Subarachnoid Hemorrhage

S-100 protein plasma levels after aneurysmal subarachnoid haemorrhage

Basic fibroblast growth factor alleviates brain injury following global ischemia reperfusion in rabbits

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