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本文引用的文献

1
Zinc deficiency and anencephaly in Turkey.
Teratology. 1980 Aug;22(1):141. doi: 10.1002/tera.1420220116.
2
Commentary kindling as a model for limbic epilepsy.作为边缘叶癫痫模型的点燃效应述评
Neuroscience. 1981;6(9):1695-1706. doi: 10.1016/0306-4522(81)90205-0.
3
The selective inhibition of hippocampal glutamic acid decarboxylase in zinc-induced epileptic seizures.锌诱导癫痫发作时海马谷氨酸脱羧酶的选择性抑制作用
Neurochem Res. 1982 Oct;7(10):1287-98. doi: 10.1007/BF00965899.
4
Zinc and copper metabolism in phenytoin therapy.苯妥英治疗中的锌和铜代谢
Epilepsia. 1982 Oct;23(5):453-61. doi: 10.1111/j.1528-1157.1982.tb05433.x.
5
Relationship between GABA concentrations in cerebrospinal fluid and seizure excitability.脑脊液中γ-氨基丁酸浓度与癫痫易感性之间的关系。
J Neurochem. 1982 Jan;38(1):293-5. doi: 10.1111/j.1471-4159.1982.tb10886.x.
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Zinc-induced seizures: a new experimental model of epilepsy.锌诱导的癫痫发作:一种新的癫痫实验模型。
Epilepsia. 1983 Apr;24(2):169-76. doi: 10.1111/j.1528-1157.1983.tb04876.x.
8
Levels of gamma-aminobutyric acid in cerebrospinal fluid in various neurologic disorders.各种神经系统疾病患者脑脊液中γ-氨基丁酸的水平
Arch Neurol. 1980 Jun;37(6):352-5. doi: 10.1001/archneur.1980.00500550054006.
9
Mechanisms of action of antiepileptic drugs.抗癫痫药物的作用机制。
Res Publ Assoc Res Nerv Ment Dis. 1983;61:179-223.
10
The role of zinc and zinc-binding proteins in regulation of glutamic acid decarboxylase in brain.锌及锌结合蛋白在大脑中对谷氨酸脱羧酶的调节作用。
Prog Clin Biol Res. 1984;144A:255-75.

热性惊厥时脑脊液锌浓度

Cerebrospinal fluid zinc concentrations in febrile convulsions.

作者信息

Garty B Z, Olomucki R, Lerman-Sagie T, Nitzan M

机构信息

Department of Pediatrics A, Schneider Children's Medical Center of Israel, Sackler Faculty of Medicine, Tel Aviv University, Israel.

出版信息

Arch Dis Child. 1995 Oct;73(4):338-41. doi: 10.1136/adc.73.4.338.

DOI:10.1136/adc.73.4.338
PMID:7492199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1511328/
Abstract

Zinc modulates the activity of glutamic acid decarboxylase, the rate limiting enzyme in the synthesis of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter. Low cerebrospinal fluid GABA values have been reported in association with several seizure disorders, including febrile convulsions. It is also known that fever and/or infections may cause a reduction in serum zinc concentrations. In this study the hypothesis that febrile convulsions are related to low cerebrospinal fluid zinc was tested. Cerebrospinal fluid zinc concentrations were measured in 66 febrile children: 32 with febrile convulsions, 18 with fever but without convulsions, and 16 with aseptic (viral) meningitis. There was no statistically significant difference in the cerebrospinal fluid zinc between the three groups of children, and the mean concentration was 26.2 micrograms/l. No significant relationship was found between either age, gender, maximal temperature, type of infection, or time of performance of the lumbar puncture and cerebrospinal fluid zinc concentration. These results do not support the hypothesis that febrile convulsions are related to reduced cerebrospinal fluid zinc concentrations.

摘要

锌可调节谷氨酸脱羧酶的活性,谷氨酸脱羧酶是γ-氨基丁酸(GABA,一种主要的抑制性神经递质)合成过程中的限速酶。据报道,脑脊液中GABA值较低与多种癫痫疾病有关,包括高热惊厥。还已知发热和/或感染可能导致血清锌浓度降低。在本研究中,对高热惊厥与脑脊液低锌有关这一假说进行了检验。对66名发热儿童的脑脊液锌浓度进行了测量:32名患有高热惊厥,18名发热但无惊厥,16名患有无菌性(病毒性)脑膜炎。三组儿童的脑脊液锌含量无统计学显著差异,平均浓度为26.2微克/升。在年龄、性别、最高体温、感染类型或腰椎穿刺时间与脑脊液锌浓度之间均未发现显著关系。这些结果不支持高热惊厥与脑脊液锌浓度降低有关这一假说。