S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system.

Persson, Lennart; Hårdemark, Hans‐Göran; Gustafsson, J; Rundström, Gerd; Mendel‐Hartvig, I.; Esscher, T; Påhlman, Sven

doi:10.1161/01.str.18.5.911

Cited by 454 publications

(288 citation statements)

References 33 publications

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“…The ENC group was characterized by heterogeneous neurological disorders that had in common lower scores on the Glasgow Coma Scale. These results indicate that cNSE provides a good indicator of brain injury, as suggested by previous studies (10)(11)(12)14).…”

Section: Discussionsupporting

confidence: 87%

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Lima

Takayanagui

Garcia

et al. 2004

Braz J Med Biol Res

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Neuron-specific enolase (NSE) is a glycolytic enzyme present almost exclusively in neurons and neuroendocrine cells. NSE levels in cerebrospinal fluid (CSF) are assumed to be useful to estimate neuronal injury and clinical outcome of patients with serious clinical manifestations such as those observed in stroke, head injury, anoxic encephalopathy, encephalitis, brain metastasis, and status epilepticus. We compared levels of NSE in serum (sNSE) and in CSF (cNSE) among four groups: patients with meningitis (N = 11), patients with encephalic injuries associated with impairment of consciousness (ENC, N = 7), patients with neurocysticercosis (N = 25), and normal subjects (N = 8). Albumin was determined in serum and CSF samples, and the albumin quotient was used to estimate blood-brain barrier permeability. The Glasgow Coma Scale score was calculated at the time of lumbar puncture and the Glasgow Outcome Scale (GOS) score was calculated at the time of patient discharge or death. The ENC group had significantly higher cNSE (P = 0.01) and albumin quotient (P = 0.005), but not sNSE (P = 0.14), levels than the other groups (KruskalWallis test). Patients with lower GOS scores had higher cNSE levels (P = 0.035) than patients with favorable outcomes. Our findings indicate that sNSE is not sensitive enough to detect neuronal damage, but cNSE seems to be reliable for assessing patients with considerable neurological insult and cases with adverse outcome. However, one should be cautious about estimating the severity of neurological status as well as outcome based exclusively on cNSE in a single patient.

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Section: Discussionsupporting

confidence: 87%

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Lima

Takayanagui

Garcia

et al. 2004

Braz J Med Biol Res

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“…[7-9] Marked expression of serum S100 proteins was found in patients with serious brain injury and showed the predictive value for minor brain injury to some extent. [10] Belonging to this family, S100A8 has been implicated in the pathobiology of inflammatory and tumor disorders in recent studies. [11-13]…”

Section: Discussionmentioning

confidence: 99%

Upregulated expression of S100A8 in mice brain after focal cerebral ischemia reperfusion

Sun

Zhang

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND:Recent studies have showed that S100A8 has been implicated in the pathobiology of inflammatory disorders, and that cerebral ischemia reperfusion (I/R) rapidly activates inflammation responses via Toll-like receptor 4 (TLR4). This study aimed to explore the expression of S100A8 and the relationship between S100A8 and TLR4 in focal cerebral ischemia reperfusion injury.METHODS:C3H/HeJ mice (n=30) and C3H/HeN mice (n=30) were divided randomly into a C3H/HeJ model group (n=18), a C3H/HeJ control group (n=12), a C3H/HeN model group (n=18), and a C3H/HeN control group (n=12). Middle cerebral artery I/R model in mice was produced using a thread embolism method. The brains of the mice were collected after ischemia for 1 hour and reperfusion for 12 hours. Stroke outcome was evaluated by determination of infarct volume and assessment of neurological impairment scores. Brain injury after cerebral I/R was observed by an optical microscope after TTC and HE dyeing. The immunofluorescence technique and real time PCR were used to test the expression level of S100A8 in brain damage.RESULTS:Compared with C3H/HeN mice, TLR4-deficient mice (C3H/HeJ) had lower infarct volumes and better outcomes in neurological tests. The levels of S100A8 increased sharply in the brains of mice after I/R injury. In addition, mice that lacked TLR4 (C3H/HeJ) had lower expression of I/R-induced S100A8 than C3H/HeN mice in the model group, indicating that a close relationship might exist between the levels of S100A8 and TLR4.CONCLUSION:S100A8 interaction with TLR4 might be involved in brain damage and in inflammation triggered by I/R injury.

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“…Normal CSF levels of NTP S-100 are 1.9 mg.l 21 [7], and increased CSF NTP S-100 has been found after stroke [8], head injury [9] and insertion of a ventricular catheter [10]. During thoracic aortic surgery, CSF NTP ) from serum (n 10) (circles, thin line) and thoracic CSF (n 6) (squares, thick line); error bars are SD.…”

Section: Discussionmentioning

confidence: 99%

“…The patient who developed a stroke had an intra-operative increase in serum NSE, but this returned to normal by 4 h later even though serum NTP S-100 was increasing. This suggests that NSE changes were nonspecific because the response of NTP S-100 is faster than NSE [8].…”

Section: Discussionmentioning

confidence: 99%

Nerve tissue protein S‐100 and neurone‐specific enolase concentrations in cerebrospinal fluid and blood during carotid endarterectomy

Gao¹,

Harris

Sapsed-Byrne³

et al. 2000

Anaesthesia

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Nerve tissue protein S‐100 and neurone‐specific enolase levels in serum were studied in 10 patients before, during and for 2 days after elective carotid endarterectomy performed under general anaesthesia and using a Javid Shunt. In six patients, simultaneous cerebrospinal fluid samples were also obtained. Serum nerve tissue protein S‐100 was normal throughout the operation, but in one patient with severe hypertension, levels increased to 1.38 µg.l−1 at 1 h postoperatively. Two patients showed an increase in cerebrospinal fluid nerve tissue protein S‐100 during clamping: these patients also had neurological deficits at 6 months. Serum neurone‐specific enolase increased from 5.8 to 9.3 µg.l−1 during shunting while cerebrospinal fluid neurone‐specific enolase did not change. Uncomplicated carotid endarterectomy does not produce cerebral damage as measured by serum nerve tissue protein S‐100; cerebrospinal fluid nerve tissue protein S‐100 may be more sensitive for minor cerebral damage. Neurone‐specific enolase appeared to be nonspecific. The lack of correlation between the neuroproteins may need to be explained before relying on these simple assays as diagnostic indicators of cerebral ischaemia.

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S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system.

Cited by 454 publications

References 33 publications

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Use of neuron-specific enolase for assessing the severity and outcome of neurological disorders in patients

Upregulated expression of S100A8 in mice brain after focal cerebral ischemia reperfusion

Nerve tissue protein S‐100 and neurone‐specific enolase concentrations in cerebrospinal fluid and blood during carotid endarterectomy

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