Neuron-specific enolase increases in cerebral and systemic circulation following focal ischemia

Barone, Frank C.; Clark, Robert K.; Price, William J.; White, R. F.; Feuerstein, Giora; Storer, Barbara; Ohlstein, Eliot H.

doi:10.1016/0006-8993(93)90012-c

Cited by 106 publications

(67 citation statements)

References 29 publications

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“…NSE is located in cytoplasm of nerve cells or neuroendocrine cells, and it is released into blood and cerebrospinal fluid (CSF) when brain tissue is damaged (Isgrò, Bottoni, & Scatena, 2015). Animal experiments have verified that plasma NSE begins rising within 2 hr of ischemia, and continues for 2.5 days (Barone et al., 1993). Stevens, Jakobs, de Jager, Cunningham, and Korf (1999) observed that in 19 patients with acute cerebral embolism, serum NSE levels increased within 4 hr of the attack.…”

Section: Discussionmentioning

confidence: 99%

Clinical and laboratory factors related to acute isolated vertigo or dizziness and cerebral infarction

et al. 2018

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ObjectiveTo clarify the relationship of clinical factors with isolated vertigo or dizziness of cerebrovascular origin.MethodsClinical data of patients admitted in East Hospital from Jan. 2015 to Apr. 2016, whose complaint were acute vertigo or dizziness were retrospectively collected. All patients arrived at the emergency department within 24 hr of symptom onset, had no acute ischemic lesion first CT and NIHSS score of 0. Patients were divided into cerebral infarction group and noncerebral infarction group according to subsequent cerebral imaging results and clinical and laboratory factors related to cerebral infarction were analyzed.Result51.6% of patients were female (n = 141). 46 patients (16.8%) were diagnosed with acute cerebral infarction. Baseline demographic data of the two groups was not significantly different. Univariate analysis found that history of smoking (p = 0.009), headache (p = 0.028), unsteadiness (p = 0.009), neuron specific enolase (p = 0.001), and vertebral artery abnormalities found on imaging (p = 0.009) were the significant difference between two groups. Increased neuron specific enolase (p = 0.005) and an abnormal vertebral artery (p = 0.044) were significant on multivariate analysis.Conclusions16.8% of acute isolated vertigo or dizziness presentations were diagnosed with acute cerebral infarction. Increased serum neuron specific enolase and vertebral artery abnormalities were the strongest indicators of acute cerebral infarction.

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Section: Discussionmentioning

confidence: 99%

Clinical and laboratory factors related to acute isolated vertigo or dizziness and cerebral infarction

et al. 2018

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“…NSE is considered to be specific for neuronal, rather than glial, damage and its concentration is correlated with the extent of neuronal loss [11]. It is increased in CSF 24 h after cardiopulmonary bypass [12] and levels tend to be higher in patients showing neurological dysfunction.…”

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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“…The serum neuron-specific enolase (NSE) level is one of these markers. NSE, a dimeric isoenzyme of the glycolytic enzyme enolase, is found in the cytoplasm of neurons and cells with neuroendocrine differentiation [1,2]. The ac and cc (more common) isoforms are known as NSE because they initially were found in neurons and neuroendocrine cells.…”

Section: Introductionmentioning

confidence: 99%

Correlation of Brain Biomarker Neuron Specific Enolase (NSE) with Degree of Disability and Neurological Worsening in Cerebrovascular Stroke

Bharosay

Varma

et al. 2011

Ind J Clin Biochem

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Stroke is the third major cause of death and foremost cause of disability worldwide. Cerebrovascular stroke remains largely a clinical diagnosis. The use of biomarkers in diagnosing stroke and assessing prognosis is an emerging and rapidly evolving field. The study aimed to investigate the predictive value of neurobiochemical marker of brain damage (neuron-specific enolase [NSE]) with respect to degree of disability at the time of admission and neurological worsening in acute ischemic stroke patients. We investigated 150 patients with cerebrovascular stroke who were admitted within 72 h of onset of stroke in the Department of Neurology at SAIMS. Venous blood samples were taken after admission and NSE was analyzed by solid enzyme linked immunosorbent assay using Analyzer and microplate reader from Biored: Code 680. In all patients, the neurological status was evaluated by a standardized neurological examination and the National Institutes of Health Stroke Scale on admission and on day 7. Serum NSE concentration was found to significantly correlate with both degree of disability and neurological worsening in acute ischemic stroke cases in the present study. The maximum serum NSE level within 72 h of admission was significantly higher in patients with greater degree of disability at the time of admission. Serum NSE levels were also found to be significantly elevated in patients with bad neurological outcome. Our study showed that serum NSE has high predictive value for determining severity and early neurobehavioral outcome after acute stroke.

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Neuron-specific enolase increases in cerebral and systemic circulation following focal ischemia

Cited by 106 publications

References 29 publications

Clinical and laboratory factors related to acute isolated vertigo or dizziness and cerebral infarction

Clinical and laboratory factors related to acute isolated vertigo or dizziness and cerebral infarction

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

Correlation of Brain Biomarker Neuron Specific Enolase (NSE) with Degree of Disability and Neurological Worsening in Cerebrovascular Stroke

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