癫痫持续状态的脑脊液和血液生物标志物_Journal of Epilepsy

Authors：

 AurélieHanin , VirginieLambrecq , JérômeAlexandre Denis , 孙威　译 , 慕洁　审

Corresponding author：

AurélieHanin, Email: vincent.navarro@aphp.fr

Keywords：

重症监护; 癫痫; 炎症; 神经元损伤; 预后

DOI：

10.7507/2096-0247.20210060

Video：

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Abstract Full text Figures/Tables Video References Cited by

癫痫持续状态（Status epilepticus，SE）是一种由于终止癫痫发作的机制失效或导致异常长时间癫痫发作的机制启动而导致的状态，需要紧急应用抗癫痫药物。难治性 SE 需用麻醉药物，并可能导致脑损伤、分子和细胞改变（如炎症、神经元和星形胶质细胞损伤），可能导致神经系统的后遗症和癫痫的进一步发展。基于人口统计学、临床和脑电图（EEG）情况的预后评分是可用的，可以预测死亡风险，但对幸存者脑损伤的严重程度的评估较差。需要新的生物标志物以更准确地预测重症监护室住院患者的预后。在此，我们总结了 SE 患者和动物模型的研究结果。在脑脊液和血液中可以检测到特异的蛋白质标记物。最早被描述的神经元死亡标志物之一是神经元特异性烯醇化酶（Neuron-specific enolase，NSE）。SE 后的炎症反应所导致的胶质增生可以通过增高的 S100-β或一些细胞因子（高迁移率族蛋白 1）被检测到。其他蛋白质，如颗粒蛋白前体（programanulin）可能反映了大脑对兴奋性毒性的适应所产生的神经保护机制。这些新的生物标志物旨在前瞻性地确定残障的严重程度和发展，以及 SE 患者随后的癫痫。我们通过评估每种生物标志物的脑特异性、在体液中的稳定性和对诸如溶血等外部干扰的敏感性来讨论其优缺点。最后，我们强调需要进一步开发和验证这些生物标志物，以便更好地评估严重的 SE 患者。

Citation： AurélieHanin, VirginieLambrecq, JérômeAlexandre Denis, 孙威　译, 慕洁　审. 癫痫持续状态的脑脊液和血液生物标志物. Journal of Epilepsy, 2021, 7(4): 367-378. doi: 10.7507/2096-0247.20210060 Copy

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1. Fiest KM, Sauro KM, Wiebe S, et al. Prevalence and incidence of epilepsy: a systematic review and meta-analysis of international studies. Neurology, 2017, 88: 296-303.
2. Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus–Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia, 2015, 56(9): 1515-1523.
3. Rossetti AO, Lowenstein DH. Management of refractory status epilepticus in adults: still more questions than answers. Lancet Neurol, 2011, 10: 922-930.
4. Rossetti AO, Logroscino G, Bromfield EB. A clinical score for prognosis of status epilepticus in adults. Neurology, 2006, 66: 1736-1738.
5. Leitinger M, Trinka E, Giovannini G, et al. Epidemiology of status epilepticus in adults: a population-based study on incidence, causes, and outcomes. Epilepsia, 2019, 60(1): 53-62.
6. Meletti S, Giovannini G, d'Orsi G, et al. New-onset refractory status epilepticus with claustrum damage: definition of the clinical and neuroimaging features. Front Neurol, 2017, 8(1): 111.
7. Tschampa HJ, Greschus S, Sassen R, et al. Thalamus lesions in chronic and acute seizure disorders. Neuroradiology, 2011, 53(2): 245-254.
8. Zetterberg H, Smith DH, Blennow K. Biomarkers of mild traumatic brain injury in cerebrospinal fluid and blood. Nat Rev Neurol, 2013, 9(1): 201-210.
9. Blennow K, Hampel H, Weiner M, et al. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol, 2010, 6(1): 131-144.
10. Hall S, Surova Y, Öhrfelt A, et al. CSF biomarkers and clinical progression of Parkinson disease. Neurology, 2015, 84(1): 57-63.
11. Link H, Huang Y-M. Oligoclonal bands in multiple sclerosis cerebrospinal fluid: an update on methodology and clinical usefulness. J Neuroimmunol, 2006, 180(1): 17-28.
12. Trinka E, Kälviäinen R. 25 years of advances in the definition, classification and treatment of status epilepticus. Seizure, 2017, 44: 65-73.
13. Ciurans J, Grau-López L, Jiménez M, et al. Refractory status epilepticus: Impact of baseline comorbidity and usefulness of STESS and EMSE scoring systems in predicting mortality and functional outcome. Seizure, 2018, 56: 98-103.
14. Alvarez V, Westover MB, Drislane FW, et al. Evaluation of a clinical tool for early etiology identification in status epilepticus. Epilepsia, 2014, 55(11): 2059-2068.
15. Jun JS, Lee ST, Kim R, et al. Tocilizumab treatment for new onset refractory status epilepticus. Ann Neurol, 2018, 84(4): 940-945.
16. Meldrum BS, Horton RW. Physiology of status epilepticus in primates. Arch Neurol, 1973, 28(1): 1-9.
17. Huang CW, Cheng JT, Tsai JJ, et al. Diabetic hyperglycemia aggravates seizures and status epilepticus-induced hippocampal damage. Neurotox Res, 2009, 15(1): 71-81.
18. Sutter R, Dittrich T, Semmlack S, et al. Acute systemic complications of convulsive status epilepticus-asystematic review. Crit Care Med, 2018, 46(1): 138-145.
19. Jutila L, Immonen A, Partanen K, et al. Neurobiology of epileptogenesis in the temporal lobe. Adv Tech Stand Neurosurg, 2002, 27(1): 5-22.
20. Brandt C, Gastens AM, Mz S, et al. Treatment with valproate after status epilepticus: effect on neuronal damage, epileptogenesis, and behavioral alterations in rats. Neuropharmacology, 2006, 51: 789-804.
21. Sankar R, Shin DH, Wasterlain CG. Serum neuron-specific enolase is a marker for neuronal damage following status epilepticus in the rat. Epilepsy Res, 1997, 28(1): 129-136.
22. Parent JM, Yu TW, Leibowitz RT, et al. Dentate granule cell neurogenesis is increased by seizures and contributes to aberrant network reorganization in the adult rat hippocampus. J Neurosci Off J Soc Neurosci, 1997, 17: 3727-3738.
23. Jakubs K, Nanobashvili A, Bonde S, et al. Environment matters: synaptic properties of neurons born in the epileptic adult brain develop to reduce excitability. Neuron, 2006, 52(8): 1047-1059.
24. Huchtemann T, Körtvélyessy P, Feistner H, et al. Progranulin levels in status epilepticus as a marker of neuronal recovery and neuroprotection. Epilepsy Behav, 2015, 49(1): 170-172.
25. Ravizza T, Gagliardi B, Noé F, et al. Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy. Neurobiol Dis, 2008, 29(1): 142-160.
26. Vezzani A, Baram TZ. New roles for interleukin-1 Beta in the mechanisms of epilepsy. Epilepsy Curr, 2007, 7(1): 45-50.
27. Gorter JA, van Vliet EA, Aronica E. Status epilepticus, blood–brain barrier disruption, inflammation, and epileptogenesis. Epilepsy Behav, 2015, 49(1): 13-16.
28. Calabrese VP, Gruemer HD, James K, et al. Cerebrospinal fluid lactate levels and prognosis in status epilepticus. Epilepsia, 1991, 32(3): 816-821.
29. Chatzikonstantinou A, Ebert AD, Hennerici MG. Cerebrospinal fluid findings after epileptic seizures. Epileptic Disord, 2015, 17: 453-459.
30. Sokrab TE, Kalimo H, Johansson BB. Endogenous serum albumin content in brain after short-lasting epileptic seizures. Brain Res, 1989, 489: 231-236.
31. Royds JA, Davies-Jones GA, Lewtas NA, et al. Enolase isoenzymes in the cerebrospinal fluid of patients with diseases of the nervous system. J Neurol Neurosurg Psychiatry, 1983, 46: 1031-1036.
32. Rabinowicz AL, Correale J, Boutros RB, et al. Neuron-specific enolase is increased after single seizures during inpatient video/EEG monitoring. Epilepsia, 1996, 37(1): 122-125.
33. Suzuki Y, Toribe Y, Goto M, et al. Serum and CSF neuron-specific enolase in patients with West syndrome. Neurology, 1999, 53(7): 1761-1764.
34. Tanabe T, Suzuki S, Hara K, et al. Cerebrospinal fluid and serum neuron-specific enolase levels after febrile seizures. Epilepsia, 2001, 42(3): 504-507.
35. Correale J, Rabinowicz AL, Heck CN, et al. Status epilepticus increases CSF levels of neuron-specific enolase and alters the blood-brain barrier. Neurology, 1995, 50(5): 1388-1391.
36. DeGiorgio CM, Correale JD, Gott PS, et al. Serum neuron-specific enolase in human status epilepticus. Neurology, 1995, 45(4): 1134-1137.
37. DeGiorgio CM, Heck CN, Rabinowicz AL, et al. Serum neuron-specific enolase in the major subtypes of status epilepticus. Neurology, 1999, 52(3): 746-749.
38. Maiti R, Mishra BR, Sanyal S, et al. Effect of carbamazepine and oxcarbazepine on serum neuron-specific enolase in focal seizures: A randomized controlled trial. Epilepsy Res, 2017, 138(1): 5-10.
39. Ramont L, Thoannes H, Volondat A, et al. Effects of hemolysis and storage condition on neuron-specific enolase (NSE) in cerebrospinal fluid and serum: implications in clinical practice. Clin Chem Lab Med, 2005, 43(5): 1215-1217.
40. van Vliet EA, da Costa AS, Redeker S, et al. Blood-brain barrier leakage may lead to progression of temporal lobe epilepsy. Brain J Neurol, 2007, 130(3): 521-534.
41. Tibbling G, Link H, Ohman S. Principles of albumin and IgG analyses in neurological disorders. I. Establishment of reference values. Scand J Clin Lab Invest, 1977, 37(2): 385-390.
42. Li YJ, Wang ZH, Zhang B, et al. Disruption of the blood-brain barrier after generalized tonic-clonic seizures correlates with cerebrospinal fluid MMP-9 levels. J Neuroinflammation, 2013, 10(1): 80.
43. Donato R. S100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles. Int J Biochem Cell Biol, 2001, 33(3): 637-668.
44. Sen J, Belli A. S100B in neuropathologic states: the CRP of the brain? J Neurosci Res, 2007, 85(5): 1373-1380.
45. Beaudeux J-L, Laribi S. S100B protein serum level as a biomarker of minor head injury. Ann Biol Clin (Paris), 2013, 71(1): 71-78.
46. Rezaei O, Pakdaman H, Gharehgozli K, et al. S100 B: A new concept in neurocritical care. Iran J Neurol, 2017, 16(1): 83-89.
47. Freund Y, Bloom B, Bokobza J, et al. Predictive value of S100-B and copeptin for outcomes following seizure: the BISTRO International Cohort Study. PLoS One, 2015, 10: e0122405.
48. Vizuete AFK, Hennemann MM, Gonçalves CA, et al. Phase-dependent astroglial alterations in Li-Pilocarpineinduced status epilepticus in young rats. Neurochem Res, 2017, 42(11): 2730-2742.
49. Gurnett CA, Landt M, Wong M. Analysis of cerebrospinal fluid glial fibrillary acidic protein after seizures in children. Epilepsia, 2003, 44(8): 1455-1458.
50. Chali F, Djelti F, Eugene E, et al. Inhibiting cholesterol degradation induces neuronal sclerosis and epileptic activity in mouse hippocampus. Eur J Neurosci, 2015, 41(5): 1345-1355.
51. Maroso M, Balosso S, Ravizza T, et al. Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures. Nat Med, 2010, 16(2): 413-419.
52. Lehtimäki KA, Keränen T, Palmio J, et al. Levels of IL- 1-beta, and IL-1ra in cerebrospinal fluid of human patients after single and prolonged seizures. Neuro Immuno Modulation, 2010, 17(1): 19-22.
53. Lehtimäki KA, Keränen T, Palmio J, et al. Increased plasma levels of cytokines after seizures in localization-related epilepsy. Acta Neurol Scand, 2007, 116(2): 226-230.
54. Alapirtti T, Rinta S, Hulkkonen J, et al. Interleukin-6, interleukin-1 receptor antagonist and interleukin-1beta production in patients with focal epilepsy: a video-EEG study. J Neurol Sci, 2009, 280(1): 94-97.
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56. Lehtimäki KA, Peltola J, Koskikallio E, et al. Expression of cytokines and cytokine receptors in the rat brain after kainic acid-induced seizures. Brain Res Mol Brain Res, 2003, 110(2): 253-260.
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