Serum neuron-specific enolase predicts outcome in post-anoxic coma: a prospective cohort study

Meynaar, Iwan A.; Straaten, Heleen M. Oudemans–van; Wetering, Jacobus van der; Verlooy, P.; Slaats, Ed H.; Bosman, Rob J.; Spoel, J. I. van der; Zandstra, D. F.

doi:10.1007/s00134-002-1573-2

Cited by 111 publications

(50 citation statements)

References 13 publications

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“…Serum NSE above 33 g/L proved to be equally accurate, with a prevalence of 60%. An important additional finding, confirming earlier reports, 14,15 was the incomplete overlap of the results of SSEP and NSE. The prevalence of at least one abnormal test result derived from patients in whom both tests were performed was 66%.…”

Section: Neurophysiologic Variablessupporting

confidence: 89%

“…[1][2][3][4][5] With our study, we could make such a comparison, and it is evident that the predictive value of some laboratory tests (SSEP and serum NSE) is superior to that of clinical tests in terms of low false positive rates and high prevalence of abnormal test results. Based on all available evidence, [1][2][3][4][5][14][15][16] confirmed and extended by the current results, we therefore propose the following strategy: Patients who are still unconscious at least 24 hours after an anoxic-ischemic insult undergo SSEP recordings and determination of serum NSE. When N20 is bilaterally absent or serum NSE is Ͼ33 g/L, further treatment will be withheld.…”

Section: 15supporting

confidence: 59%

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Cavernoma of cavernous sinus

Surendrababu

Rao²

2006

Neurology

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Abstract-Objective:To determine the optimal timing of somatosensory evoked potential (SSEP) recordings and the additional value of clinical and biochemical variables for the prediction of poor outcome in patients who remain comatose after cardiopulmonary resuscitation (CPR). Methods: A prospective cohort study was conducted in 32 intensive care units including adult patients still unconscious 24 hours after CPR. Clinical, neurophysiologic, and biochemical variables were recorded 24, 48, and 72 hours after CPR and related to death or persisting unconsciousness after 1 month. Results: Of 407 included patients, 356 (87%) had a poor outcome. In 301 of 305 patients unconscious at 72 hours, at least one SSEP was recorded, and in 136 (45%), at least one recording showed bilateral absence of N20. All these patients had a poor outcome (95% CI of false positive rate 0 to 3%), irrespective of the timing of SSEP. In the same 305 patients, neuron-specific enolase (NSE) was determined at least once in 231, and all 138 (60%) with a value Ͼ33 g/L at any time had a poor outcome (95% CI of false positive rate 0 to 3%). The test results of SSEP and NSE overlapped only partially. The performance of all clinical tests was inferior to SSEP and NSE testing, with lower prevalences of abnormal test results and wider 95% CI of false positive rates. Conclusion: Poor outcome in postanoxic coma can be reliably predicted with somatosensory evoked potentials and neuron-specific enolase as early as 24 hours after cardiopulmonary resuscitation in a substantial number of patients.

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Section: Neurophysiologic Variablessupporting

confidence: 89%

Section: 15supporting

confidence: 59%

Cavernoma of cavernous sinus

Surendrababu

Rao²

2006

Neurology

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“…Numerous prior studies have evaluated other proteins as potential surrogate markers for ischemic brain damage, including the astrocyte-enriched S100b as well as the neuronal proteins NSE and a cleavage fragment of tau of indeterminate origin. Serum and CSF levels of these proteins have a prognostic relationship with neurologic outcome, morbidity, and mortality (Wunderlich et al, 1999;Zemlan et al, 2002;Meynaar et al, 2003). Unfortunately, high serum concentrations of S100b can arise from extracranial sources (Snyder-Ramos et al, 2004;Hasselblatt et al, 2004), and result indirectly from the reactive astrogliosis and increased S100b expression that accompany neuronal injury (Miyake et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Novel Surrogate Markers for Acute Brain Damage: Cerebrospinal Fluid Levels Corrrelate with Severity of Ischemic Neurodegeneration in the Rat

Siman

Zhang

Roberts

et al. 2005

J Cereb Blood Flow Metab

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Previously, we identified proteins released from degenerating cultured cortical neurons as novel cerebrospinal fluid (CSF) markers for acute brain injury in the rat. Here, we investigate relationships between CSF changes in these novel markers and the severity of acute ischemic brain injury. Rats underwent sham surgery or 3,6,8, or 10 mins of transient global forebrain ischemia. At 48 h after insult, CSF levels of 14-3-3b, 14-3-3f, and calpain cleavage products of a-spectrin and tau were quantified. Regional acute neurodegeneration was assessed by Fluoro-Jade and silver impregnation staining, and confirmed by immunohistochemical detection of the activation of calpain and caspase, cysteine proteases involved in neurodegenerative signaling. Ischemic neurodegeneration and activation of at least one cysteine protease were observed in the hippocampal CA1 sector, dentate hilus, caudate nucleus, parietal cortex, thalamus, and inferior colliculus. As expected, the total number of degenerating cells increased as a function of ischemia duration. Cerebrospinal fluid levels of the four marker proteins increased markedly after ischemia, and rose in proportion with its duration. Irrespective of the length of ischemia, CSF levels of the neuron-enriched proteins 14-3-3b and calpain-cleaved tau correlated significantly with the magnitude of acute ischemic neurodegeneration. Additionally, CSF levels of the two proteins correlated with one another. These results show that certain proteins released from degenerating neurons are CSF markers for brain injury in the rat whose levels reflect the severity of acute ischemic neurodegeneration. Measurement of 14-3-3b and calpain-cleaved tau may be useful for the minimally invasive diagnosis, prognosis, and therapeutic evaluation of acute brain damage.

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“…(28) Increased levels of NSE were found in blood and liquor of patients with stroke, intracerebral hemorrhage and after cardiopulmonary resuscitation. (30) NSE also increases and associates with brain injury in patients with severe sepsis and septic shock. (31) Tumor cells in APUDomas, neuroblastomas and small cell lung carcinomas are able to produce NSE and increase serum levels of this protein, That is why, serum dosage of NSE has been considered as a diagnostic and prognostic serum marker in the clinical management of these neoplasms.…”

Section: S100bmentioning

confidence: 96%