作后血氨水平作为惊厥性癫痫发作的生物标志物：一项前瞻性研究_Journal of Epilepsy

Authors：

 AlbadareenR , GronsethG , LandazuriP , 吴梦倩 , 慕洁

Corresponding author：

AlbadareenR, Email: ralbadareen@kumc.edu; albadareenrawan@yahoo.com

Keywords：

发作后高氨血症; 血氨; 惊厥性癫痫发作; 非痫性发作; 灵敏度和特异性

DOI：

10.7507/2096-0247.20170055

Video：

Export PDF Favorites Scan Get Citation

Abstract Full text Figures/Tables Video References Cited by

有报道指出全面性惊厥性癫痫发作(Generalized convulsive seizures，GCS)后出现短暂性高血氨症(Transient hyperammonemia，THA)，没有足够的证据证实与癫痫的关系。文章的目的是确定发作后THA是否可以区分不同类型的发作，如使用视频脑电图(VEEG)监测确认脑电变化。在前瞻性队列中，筛选了所有进入癫痫监测单元并同意接受研究的成年患者(> 18岁)。血氨的基础值以及在发作(所有患者)的60 min内、发作后24 h(只要有可能)的血氨水平均被检测。根据VEEG，将患者进行分组，分别为GCS、心因性惊厥性非痫性发作(Psychogenic nonepileptic seizures with convulsions，PNES-C)或局灶性癫痫发作(Focal seizures，FS)。使用描述性统计和参数/非参数方法分析数据。纳入患者78例，13例为GCS、8例为FS、9例为PNES-C。这些组在性别(P=0.04) 和血氨基础值(P=0.02) 方面是不同的，但年龄无差异。三组之间发作后血氨水平较血氨基础值的变化差异有统计学意义(P=0.004)。区分GCS与其他组差异的发作后血氨水平ROC曲线下面积为0.88[95%CI (0.69, 0.96)]，表明检测血氨水平是一种很好的用来区分GCS与其他发作的试验。血氨水平≥80μmol/L可以准确为80%的患者分类(灵敏度53.9%，特异性100%)。VEEG监测为THA与GCS癫痫发作之间的关联提供了客观证据，并为今后关于确定发作后血氨水平作为GCS的廉价诊断试验作用的研究奠定了基础。

Citation： AlbadareenR, GronsethG, LandazuriP, 吴梦倩, 慕洁. 作后血氨水平作为惊厥性癫痫发作的生物标志物：一项前瞻性研究. Journal of Epilepsy, 2017, 3(4): 348-353. doi: 10.7507/2096-0247.20170055 Copy

1.	Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: report of the therapeutics and technology assessment subcommittee of the american academy of neurology. Neurology, 2005, 65(2): 668-675.
2.	Wyllie E, Lueders H, Pippenger C, et al. Postictal serum creatine kinase in the diagnosis of seizure disorders. Arch Neurol, 1985, 42(11): 123-126.
3.	Brigo F, Igwe SC, Erro R, et al. Postictal serum creatine kinase for the differential diagnosis of epileptic seizures and psychogenic non-epilep-tic seizures: a systematic review. J Neurol, 2015, 262(7): 251-257.
4.	Yanagawa Y, Nishi K, Sakamoto T. Hyperammonemia is associated with generalized convulsion. Intern Med, 2008, 47(6): 21-23.
5.	Liu KT, Su CS. Postictal transient hyperammonemia. Am J Emerg Med, 2008, 26(10):388.e381-382.
6.	Liu KT, Lee CW, Yang SC, et al. Postictal transient hyperammonemia as an indicator of seizure disorder. Eur Neurol, 2010, 64(4): 46-50.
7.	Hung TY, Chen CC, Wang TL, et al. Transient hyperammonemia in seizures: a prospective study. Epilepsia, 2011, 52(4): 2043-2049.
8.	Tomita K, Otani N, Omata F, et al. Clinical significance of plasma ammonia in patients with generalized convulsion. Intern Med, 2011, 50(10): 2297-2301.
9.	Berg AT, Berkovic SF, Brodie MJ, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009. Epilepsia, 2010, 51(4): 676-685.
10.	Dhiman V, Sinha S, Rawat VS, et al. Semiological characteristics of adults with psychogenic nonepileptic seizures (PNESs): an attempt towards a new classification. Epilepsy Behav, 2013, 27(2): 427-432.
11.	Banister EW, Cameron BJ. Exercise-induced hyperammonemia: peripheral and central effects. Int J Sports Med, 1990, 11(Suppl.2): 129-142.
12.	Ristic AJ, Draskovic M, Bukumiric Z, et al. Reliability of the witness descriptions of epileptic seizures and psychogenic nonepileptic attacks: a comparative analysis. Neurol Res, 2015, 37(4): 560-562.
13.	Cooper AJ. The role of glutamine synthetase and glutamate dehydrogenase in cerebral ammonia homeostasis.Neurochem Res, 2012, 37(01): 2439-2455.
14.	Albrecht J, Norenberg MD. Glutamine: a Trojan horse in ammonianeurotoxicity. Hepatology, 2006, 44(2): 788-794.
15.	During MJ, Spencer DD. Extracellular hippocampal glutamate andspontaneous seizure in the conscious human brain. Lancet, 1993, 341(4): 1607-1610.
16.	Medina-Ceja L, Pardo-Pena K, Morales-Villagran A, et al. Increase inthe extracellular glutamate level during seizures and electrical stimulation determined using a high temporal resolution technique. BMC Neu-rosci, 2015, 16(4): 11.
17.	Tsacopoulos M, Poitry-Yamate CL, Poitry S. Ammonium and glutamate released by neurons are signals regulating the nutritive function of a glial cell. J Neurosci 1997, 17(8): 2383-2390.

1. Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: report of the therapeutics and technology assessment subcommittee of the american academy of neurology. Neurology, 2005, 65(2): 668-675.
2. Wyllie E, Lueders H, Pippenger C, et al. Postictal serum creatine kinase in the diagnosis of seizure disorders. Arch Neurol, 1985, 42(11): 123-126.
3. Brigo F, Igwe SC, Erro R, et al. Postictal serum creatine kinase for the differential diagnosis of epileptic seizures and psychogenic non-epilep-tic seizures: a systematic review. J Neurol, 2015, 262(7): 251-257.
4. Yanagawa Y, Nishi K, Sakamoto T. Hyperammonemia is associated with generalized convulsion. Intern Med, 2008, 47(6): 21-23.
5. Liu KT, Su CS. Postictal transient hyperammonemia. Am J Emerg Med, 2008, 26(10):388.e381-382.
6. Liu KT, Lee CW, Yang SC, et al. Postictal transient hyperammonemia as an indicator of seizure disorder. Eur Neurol, 2010, 64(4): 46-50.
7. Hung TY, Chen CC, Wang TL, et al. Transient hyperammonemia in seizures: a prospective study. Epilepsia, 2011, 52(4): 2043-2049.
8. Tomita K, Otani N, Omata F, et al. Clinical significance of plasma ammonia in patients with generalized convulsion. Intern Med, 2011, 50(10): 2297-2301.
9. Berg AT, Berkovic SF, Brodie MJ, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009. Epilepsia, 2010, 51(4): 676-685.
10. Dhiman V, Sinha S, Rawat VS, et al. Semiological characteristics of adults with psychogenic nonepileptic seizures (PNESs): an attempt towards a new classification. Epilepsy Behav, 2013, 27(2): 427-432.
11. Banister EW, Cameron BJ. Exercise-induced hyperammonemia: peripheral and central effects. Int J Sports Med, 1990, 11(Suppl.2): 129-142.
12. Ristic AJ, Draskovic M, Bukumiric Z, et al. Reliability of the witness descriptions of epileptic seizures and psychogenic nonepileptic attacks: a comparative analysis. Neurol Res, 2015, 37(4): 560-562.
13. Cooper AJ. The role of glutamine synthetase and glutamate dehydrogenase in cerebral ammonia homeostasis.Neurochem Res, 2012, 37(01): 2439-2455.
14. Albrecht J, Norenberg MD. Glutamine: a Trojan horse in ammonianeurotoxicity. Hepatology, 2006, 44(2): 788-794.
15. During MJ, Spencer DD. Extracellular hippocampal glutamate andspontaneous seizure in the conscious human brain. Lancet, 1993, 341(4): 1607-1610.
16. Medina-Ceja L, Pardo-Pena K, Morales-Villagran A, et al. Increase inthe extracellular glutamate level during seizures and electrical stimulation determined using a high temporal resolution technique. BMC Neu-rosci, 2015, 16(4): 11.
17. Tsacopoulos M, Poitry-Yamate CL, Poitry S. Ammonium and glutamate released by neurons are signals regulating the nutritive function of a glial cell. J Neurosci 1997, 17(8): 2383-2390.

Previous Article
儿童癫痫中的神经元抗体：临床特征和未经免疫治疗的历史队列远期预后
Next Article
立体定向脑电图相关并发症的系统评价

Journal of Epilepsy

作后血氨水平作为惊厥性癫痫发作的生物标志物：一项前瞻性研究

Abstract Full text Figures/Tables Video References Cited by

Previous Article

Next Article

Format

Content