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中华神经创伤外科电子杂志 ›› 2023, Vol. 09 ›› Issue (06) : 367 -371. doi: 10.3877/cma.j.issn.2095-9141.2023.06.009

综述

创伤性颅脑损伤神经生理学特征
唐春雨, 李倩, 郭姗姗, 叶奇, 张丹†()   
  1. 300309　天津，武警特色医学中心烧伤冻伤及组织功能重建研究所
    100088　北京，火箭军特色医学中心中医科
    100088　北京，火箭军特色医学中心涉核人员治疗科
    100088　北京，火箭军特色医学中心护理部
    100088　北京，火箭军特色医学中心消化科
  • 收稿日期:2022-12-15 出版日期:2023-12-15
  • 通信作者: 张丹

Characteristic of neurobiology in traumatic brain injury

Chunyu Tang, Qian Li, Shanshan Guo, Qi Ye, Dan Zhang†()   

  1. Research Institute of Burn Frostbite and Tissue Functional Reconstruction, Characteristic Medical Center of the PAP, Tianjin 300309, China
    Department of Traditional Chinese Medicine, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
    Department of Treatment for Nuclear Personnel, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
    Department of Nursing, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
    Department of Gastroenterology, Characteristic Medical Center of the PLA Rocket Force, Beijing 100088, China
  • Received:2022-12-15 Published:2023-12-15
  • Corresponding author: Dan Zhang
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唐春雨, 李倩, 郭姗姗, 叶奇, 张丹. 创伤性颅脑损伤神经生理学特征[J]. 中华神经创伤外科电子杂志, 2023, 09(06): 367-371.

Chunyu Tang, Qian Li, Shanshan Guo, Qi Ye, Dan Zhang. Characteristic of neurobiology in traumatic brain injury[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2023, 09(06): 367-371.

创伤性颅脑损伤（TBI）是累及到大脑实质的结构性损害，可导致患者死亡或终生残疾。除结构性损害外，脑部意外创伤还会引起多种有害途径的激活导致继发性神经元死亡及永久性功能障碍。现有研究表明兴奋性毒性、神经炎症、水肿、氧化应激、神经元凋亡、代谢功能障碍等参与TBI主要致病过程，但相关分子机制研究仍不清楚。现有的治疗手段仅能对症处理，对控制继发性损伤仍不理想。本文通过对TBI神经生理学变化、神经化学变化以及其他病理表现作一综述，旨在为TBI相关研究提供参考，同时帮助临床制定新的治疗策略以尽可能挽救患者生命或减少并发症发生。

关键词: 创伤性颅脑损伤, 兴奋性毒性, 神经炎症, 氧化应激, 神经元凋亡

Traumatic brain injury (TBI) endangers structural damage to the brain parenchyma, which causes death or lifelong disability in patients. Besides structural damage, the accidental injuries of the brain could cause activation of various deleterious pathways, leading to subsequent neuronal death and permanent dysfunction. The present studies show excitotoxicity, neuroinflammation, edema, oxidative stress, neuronal apoptosis and cerebral metabolic dysfunction could participate in the major pathogenic process in TBI, but few was cleared about the related molecular mechanism study. The available methods could only treated patients symptomatically, and are still not ideal for controlling secondary injuries. This article provides a review of the neurophysiological changes, neurochemical changes, and other pathological manifestations of TBI, with the aim of providing reference for TBI related research and helping clinical development of new treatment strategies to rescue the patient or reduce the occurrence of complications.

Key words: Traumatic brain injury, Excitotoxicity, Neuroinflammation, Oxidative stress, Neuronal apoptosis
[1]
Gorman KM, Dumire RD. Knowledge retention of the traumatic brain injury guidelines at a level 1 trauma center[J]. J Emerg Crit Care Med, 2019, 3: 17. DOI: 10.21037/jeccm.2019.02.06.
[2]
Young JT, Hughes N. Traumatic brain injury and homelessness: from prevalence to prevention[J]. Lancet Public Health, 2020, 5(1): e4-e5. DOI: 10.1016/s2468-2667(19)30225-7.
[3]
邹隽风,黄贤键,吴楚伟,等.中国颅脑创伤流行病学中存在的部分问题探讨[J].中华神经创伤外科电子杂志, 2021, 7(1): 59-62. DOI: 10.3877/cma.j.issn.2095-9141.2021.01.014.
[4]
Zetterberg H, Winblad B, Bernick C, et al. Head trauma in sports-clinical characteristics, epidemiology and biomarkers[J]. J Intern Med, 2019, 285(6): 624-634. DOI: 10.1111/joim.12863.
[5]
Prasetyo E. The primary, secondary, and tertiary brain injury[J]. Crit Care Shock, 2020, 23(2020): 4-13.
[6]
Thapa K, Khan H, Singh TG, et al. Traumatic brain injury: mechanistic insight on pathophysiology and potential therapeutic targets[J]. J Mol Neurosci, 2021, 71(9): 1725-1742. DOI: 10.1007/s12031-021-01841-7.
[7]
Alexandris AS, Lee Y, Lehar M, et al. Traumatic axonopathy in spinal tracts after impact acceleration head injury: ultrastructural observations and evidence of SARM1 - dependent axonal degeneration[J]. Exp Neurol, 2023, 359: 114252. DOI: 10.1016/j.expneurol.2022.114252.
[8]
Albert WC, Sirén A. Experimental traumatic brain injury[J]. Exp Transl Stroke Med, 2010, 2(1): 16. DOI: 10.1186/2040-7378-2-16.
[9]
Chelly H, Chaari A, Daoud E, et al. Diffuse axonal injury in patients with head injuries: an epidemiologic and prognosis study of 124 cases[J]. J Trauma, 2011, 71(4): 838-846. DOI: 10.1097/TA.0b013e3182127baa.
[10]
Dewan MC, Rattani A, Gupta S, et al. Estimating the global incidence of traumatic brain injury[J]. J Neurosurg, 2018, 130(4): 1080-1097. DOI: 10.3171/2017.10.Jns17352.
[11]
Dikranian K. Modeling traumatic brain injury: mechanisms of early neuronal and axon degeneration in the infant rodent brain[J]. Biomedical Reviews, 2019, 30: 25-36. DOI: 10.14748/BMR.V30.6385.
[12]
Sowers JL, Sowers ML, Shavkunov AS, et al. Traumatic brain injury induces region-specific glutamate metabolism changes as measured by multiple mass spectrometry methods[J]. iScience, 2021, 24(10): 103108. DOI: 10.1016/j.isci.2021.103108.
[13]
Sibarov DA, Antonov SM. Calcium-dependent desensitization of nmda receptors[J]. Biochemistry (Mosc), 2018, 83(10): 1173-1183. DOI: 10.1134/s0006297918100036.
[14]
Cheng G, Kong RH, Zhang LM, et al. Mitochondria in traumatic brain injury and mitochondrial-targeted multipotential therapeutic strategies[J]. Br J Pharmacol, 2012, 167(4): 699-719. DOI: 10.1111/j.1476-5381.2012.02025.x.
[15]
Kaur D, Pahwa P, Goel RK. Protective effect of nerolidol against pentylenetetrazol-induced kindling, oxidative stress and associated behavioral comorbidities in mice[J]. Neurochem Res, 2016, 41(11): 2859-2867. DOI: 10.1007/s11064-016-2001-2.
[16]
崔大勇,王新,张博.小胶质细胞在颅脑损伤中免疫调控及对神经元的作用机制[J].中华神经创伤外科电子杂志, 2022, 8(1): 56-58. DOI: 10.3877/cma.j.issn.2095-9141.2022.01.012.
[17]
Xu H, Wang Z, Li J, et al. The polarization states of microglia in tbi: a new paradigm for pharmacological intervention[J]. Neural Plast, 2017, 2017: 5405104. DOI: 10.1155/2017/5405104.
[18]
Kaur D, Sharma V, Deshmukh R. Activation of microglia and astrocytes: a roadway to neuroinflammation and Alzheimer's disease[J]. Inflammopharmacology, 2019, 27(4): 663-677. DOI: 10.1007/s10787-019-00580-x.
[19]
Shetty AK, Mishra V, Kodali M, et al. Corrigendum: blood brain barrier dysfunction and delayed neurological deficits in mild traumatic brain injury induced by blast shock waves[J]. Front Cell Neurosci, 2014, 8: 404. DOI: 10.3389/fncel.2014.00404.
[20]
Loane DJ, Stoica BA, Tchantchou F, et al. Novel mGluR5 positive allosteric modulator improves functional recovery, attenuates neurodege-neration, and alters microglial polarization after experimental traumatic brain injury[J]. Neurotherapeutics, 2014, 11(4): 857-869. DOI: 10.1007/s13311-014-0298-6.
[21]
Loane DJ, Kumar A. Microglia in the TBI brain: the good, the bad, and the dysregulated[J]. Exp Neurol, 2016, 275(3): 316-327. DOI: 10.1016/j.expneurol.2015.08.018.
[22]
Cherry JD, Olschowka JA, O'Banion MK. Neuroinflammation and M2 microglia: the good, the bad, and the inflamed[J]. J Neuroinflammation, 2014, 11(1): 98. DOI: 10.1186/1742-2094-11-98.
[23]
Ponomarev ED, Maresz K, Tan Y, et al. CNS-derived interleukin-4 is essential for the regulation of autoimmune inflammation and induces a state of alternative activation in microglial cells[J]. J Neurosci, 2007, 27(40): 10714-10721. DOI: 10.1523/JNEUROSCI.1922-07.2007.
[24]
Kumar A, Loane DJ. Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention[J]. Brain Behav Immun, 2012, 26(8): 1191-1201. DOI: 10.1016/j.bbi.2012.06.008.
[25]
Gyoneva S, Ransohoff RM. Inflammatory reaction after traumatic brain injury: therapeutic potential of targeting cell-cell communication by chemokines[J]. Trends Pharmacol Sci, 2015, 36(7): 471-480. DOI: 10.1016/j.tips.2015.04.003.
[26]
Shlosberg D, Benifla M, Kaufer D, et al. Blood-brain barrier breakdown as a therapeutic target in traumatic brain injury[J]. Nat Rev Neurol, 2010, 6(7): 393-403. DOI: 10.1038/nrneurol.2010.74.
[27]
Gilbert M, Snyder C, Corcoran C, et al. The association of traumatic brain injury with rate of progression of cognitive and functional impairment in a population-based cohort of Alzheimer's disease: the Cache county dementia progression study[J]. Int Psychogeriatrics, 2014, 26(10): 1593-1601. DOI: 10.1017/S1041610214001689.
[28]
张建宁.颅脑创伤后脑水肿机制的研究进展[J].中华神经创伤外科电子杂志, 2020, 6(5): 257-258. DOI: 10.3877/cma.j.issn.2095-9141.2020.05.001.
[29]
DeWitt DS, Prough DS. Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature[J]. J Neurotrauma, 2003, 20(9): 795-825. DOI: 10.1089/089771503322385755.
[30]
Unterberg AW, Stover J, Kress B, et al. Edema and brain trauma[J]. Neuroscience, 2004, 129(4): 1019-1027. DOI: 10.1016/j.neuroscience.2004.06.046.
[31]
Donkin JJ, Vink R. Mechanisms of cerebral edema in traumatic brain injury: therapeutic developments[J]. Curr Opin Neurol, 2010, 23(3): 293-299. DOI: 10.1097/WCO.0b013e328337f451.
[32]
Konar SK, Shukla D, Agrawal A. Posttraumatic brain edema: Pathophysiology, management, and current concept[J]. Apollo, 2019, 16(1): 2-7. DOI: 10.4103/am.am_82_18.
[33]
Winkler EA, Minter D, Yue JK, et al. Cerebral edema in traumatic brain injury: pathophysiology and prospective therapeutic targets[J]. Neurosurg Clin N Am, 2016, 27(4): 473-488. DOI: 10.1016/j.nec.2016.05.008.
[34]
Prins M, Greco T, Alexander D, et al. The pathophysiology of traumatic brain injury at a glance[J]. Dis Model Mech, 2013, 6(6): 1307-1315. DOI: 10.1242/dmm.011585.
[35]
Islam MT. Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders[J]. Neurol Res, 2017, 39(1): 73-82. DOI: 10.1080/01616412.2016.1251711.
[36]
Huang Y, Long X, Tang J, et al. The attenuation of traumatic brain injury via inhibition of oxidative stress and apoptosis by tanshinone IIA[J]. Oxid Med Cell Longev, 2020, 2020: 4170156. DOI: 10.1155/2020/4170156.
[37]
Daglas M, Truong PH, Miles LQ, et al. Deferiprone attenuates neuropathology and improves outcome following traumatic brain injury[J]. Br J Pharmacol, 2023, 180(2): 214-234. DOI: 10.1111/bph.15950.
[38]
de Lores AG, Bersier M. Relationship between Na+, K+-ATPase and NMDA receptor at central synapses[J]. Curr Protein Pept Sci, 2014, 15(8): 761-777. DOI: 10.2174/1389203715666140903145608.
[39]
Hiebert JB, Shen Q, Thimmesch AR, et al. Traumatic brain injury and mitochondrial dysfunction[J]. Am J Med Sci, 2015, 350(2): 132-138. DOI: 10.1097/MAJ.0000000000000506.
[40]
Kasahara A, Scorrano L. Mitochondria: from cell death executioners to regulators of cell differentiation[J]. Trends Cell Biol, 2014, 24(12): 761-770. DOI: 10.1016/j.tcb.2014.08.005.
[41]
McGuire JL, Ngwenya LB, McCullumsmith RE. Neurotransmitter changes after traumatic brain injury: an update for new treatment strategies[J]. Mol Psychiatry, 2019, 24(7): 995-1012. DOI: 10.1038/s41380-018-0239-6.
[42]
Kawa L, Arborelius UP, Yoshitake T, et al. Neurotransmitter systems in a mild blast traumatic brain injury model: catecholamines and serotonin[J]. J Neurotrauma, 2015, 32(16): 1190-1199. DOI: 10.1089/neu.2014.3669.
[43]
Hameed MQ, Hsieh TH, Morales QL, et al. Ceftriaxone treatment preserves cortical inhibitory interneuron function via transient salvage of GLT-1 in a rat traumatic brain injury model[J]. Cereb Cortex, 2019, 29(11): 4506-4518. DOI: 10.1093/cercor/bhy328.
[44]
Jenkins PO, Mehta MA, Sharp DJ. Catecholamines and cognition after traumatic brain injury[J]. Brain, 2016, 139(Pt 9): 2345-2371. DOI: 10.1093/brain/aww128.
[45]
Kgosidialwa O, Hakami O, Hussnain HM, et al. Growth hormone deficiency following traumatic brain injury[J]. Int J Mol Sci, 2019, 20(13): 3323. DOI: 10.3390/ijms20133323.
[46]
Kajal B, Puneet K, Rahul D. Neurobiology of traumatic brain injury[J]. Brain Injury, 2021, 35(10): 1113-1120. DOI: 10.1080/02699052.2021.1972152.
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