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УЖМБС 2020, 5(6): 9–16
https://doi.org/10.26693/jmbs05.06.009
Medicine. Reviews

Post-Traumatic Mechanisms of Epileptogenesis

Antonenko S. A. 1, Stoyanov A. N. 2, Gryshchenko G. V. 3, Skorobrekh V. Z. 2, Kaptalan A. O. 1
Abstract

One of the most frequent and severe consequences of traumatic brain injury is post-traumatic epilepsy, which is the main identified cause of symptomatic epilepsy at a young age. Post-traumatic epilepsy develops in 11-20% of people who have had traumatic brain injury, its frequency and severity depends on the degree of damage to the central nervous system due to traumatic brain injury, the localization of the traumatic focus, the state of premorbid background, the presence of somatic and comorbid pathology, the state of the autonomic nervous system, etc. According to general population studies, severe traumatic brain injury increases the risk of post-traumatic epilepsy development by 29 times against mild, in which this indicator increases by 1.5 times. In children under 14 years old, the proportion of post-traumatic epilepsy can be up to 14%, while in people over 65 years old, this figure is 8%. The neurophysiological polymorphism of post-traumatic epilepsy is that traumatic brain injury is characterized by a predominantly focal nature of the development of the pathological process, but recently there have been many clinical and experimental confirmations of the presence of diffuse brain damage. These morphological and functional changes coexist and interact with each other with varying degrees of predominance. The work highlights the mechanisms of brain injury, including oxidative stress, leading to disruption of the functioning of all levels of the central nervous system. In the early period after traumatic brain injury, ischemic damage to the central nervous system dominates with the development of glutamate cascade, oxidative stress, etc. As a result of all pathological reactions, disintegration of the central nervous system develops with the development of basic neuropathological syndromes. In the intermediate period, with an unfavorable course of the pathological process, irritation syndromes are formed, in particular, epileptization of the brain with the possible appearance of repeated unprovoked paroxysms, as well as impairment of most neuropsychiatric functions due to excessive neuronal discharges. The formation of post-traumatic epilepsy has a delayed period of the emergence of a focus of epiactivity based on a cascade of morphofunctional "rewiring" of cortical and other networks, disorders of the functioning of the nervous system and depends on a number of "trigger" factors, incl. on the nature, localization, degree of damage, the state of the antiepileptic system and other factors stimulating the generator of hyperextension with the possible occurrence of secondary generators. At the same time, a pathological determinant is fully formed, which "epilepsizes" the brain. Conclusion. The issues of differentiation of post-traumatic epilepsy from other epileptic seizures, the dependence of post-traumatic epilepsy development on the severity of traumatic brain injury, the main risk factors for this type of epileptogenesis, as well as disorganization and damage to the antiepileptic system are considered. The existing wide range of seizures is described, incl. focal, taking into account the localization characteristic of traumatic brain injury

Keywords: post-traumatic epilepsy, epileptogenesis, risk factors

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References
  1. Stoyanov OM, Muratova TM, Kolesnyk OO, Oliynyk SM. Neyrovehetatyvni rozlady v klinitsi posttravmatychnoi epilepsiyi [Neurovegetative disorders in the clinic of post-traumatic epilepsy]. Ukr visnyk psykhonevrolohiyi. 2017; 25(1): 108. [Ukrainian]
  2. Stoyanov OM, Kolesnik OO, Mashchenko SS, Antonenko SA. Participation of the vegetative system on paroxismality and formation of posttraummatic epilepsy. Journal of Education, Health and Sport. 2016; 6(11): 889-904.
  3. Mamalyga ML. Vozmozhnosti autoregulyaczii czerebral`nogo krovotoka pri khronicheskoj serdechnoj nedostatochnosti i ikh svyaz s proyavleniemyai sudorozhnoj gotovnosti [Possibilities of autoregulation of cerebral blood flow in chronic heart failure and their relationship with the manifestation of I and convulsive readiness]. Materialy 2 nats kongressa "Kardionevrologiya". M; 2012. s. 401. [Russian]
  4. Mamalyga ML. Fiziologicheskie osnovy vzaimoobuslovlennykh proczessov v mozge i serdcze [Physiological bases of interdependent processes in the brain and heart]. Nauchno-prakticheskie i uchebno-metodicheskie rekomendaczii. M: MPGU; 2014. 124 s. [Russian]
  5. Matyash MM, Khudenko LI. Travmatichna enczefalopatiya – osoblivosti reabilitatsiyi z vikoristannyam suchasnikh metodiv refleksoterapiyi [Traumatic encephalopathy - features of rehabilitation using modern methods of reflexology]. Fitoterapiya. 2014; 2: 30-33. [Ukrainian]
  6. Iliev RT, Dostaeva BS. Posttravmaticheskaya epilepsiya [Post-traumatic epilepsy]. Vestnik KazNMU. 2015; 2: 385-386. [Russian]
  7. Grinenko OG, Zajczev OS, Oknina LB, Urakov SV, Golovteev AL, Potapov AA. Diagnostika i lechenie posttravmaticheskoj epilepsii [Diagnostics and treatment of post-traumatic epilepsy]. Nevrologiya, nejropsikhiatriya, psikhosomatika. 2011; 3: 13-17. [Russian]
  8. Isaeva RKh, Avtonyuk IA, Gridyakina AV, Evstafeva AE. Immunologicheskie izmeneniya pri cherepno-mozgovoj travme [Immunological changes in traumatic brain injury]. Mezhdunarodnyj zhurnal prikladnykh i fundamentalnykh issledovanij. 2014; 8(2): 41-47. [Russian]
  9. Seo W, Oh H. Comparisons of acute physiological parameters influencing outcome in patients with traumatic brain injury and hemorrhagic stroke. Worldviews Evid Based Nurs. 2009; 6(1): 36-43.
  10. Niizuma K, Endo H, Chan PH. Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival. J Neurochem. 2009; 109(1): 133-138.
  11. Wu L, Xiong X, Wu X, Ye Y, Jian Z, Zhi Z, et al. Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury. Front Mol Neurosci. 2020; 13: 28. https://doi.org/10.3389/fnmol.2020.00028
  12. Dizregulyaczionnaya patologiya nervnoj sistemy [Dysregulatory pathology of the nervous system]. Pod red EI Guseva, GN Kryzhanovskogo. M: OOO «Med informaczionnoe agentstvo»; 2009. 512 s. [Russian]
  13. Kurbanova SA. Kliniko-nejrofiziologicheskie osobennosti simptomaticheskoj posttravmaticheskoj epilepsii [Clinical and neurophysiological features of symptomatic post-traumatic epilepsy]. Abstr. PhDr. (Med.). M; 2007. 18 s. [Russian]
  14. Likhterman LB. Klassifikacziya ChMT. Chast 3. Slagaemye diagnoza ChMT i princzipy ego postroeniya [TBI classification. Part 3. Terms of TBI diagnosis and principles of its construction]. Sudebnaya mediczina. 2015; 1(4): 34-40. [Russian]
  15. Ritter AC, Wagner AK, Fabio A, Pugh MJ, Walker WC, Szaflarski JP, et al. Incidence and risk factors of posttraumatic seizures following traumatic brain injury: A Traumatic Brain Injury Model Systems Study. Epilepsia. 2016; 57: 1968-1977. https://doi.org/10.1111/epi.13582
  16. Zajczev OS, Grinenko OA, Shaginyan GG. Rannie sudorozhnye pristupy i posttravmaticheskaya epilepsiya [Early seizures and post-traumatic epilepsy]. Nejrokhirurgiya i nevrologiya Kazakhstana. 2010; 4(21): 20-24. [Russian]
  17. Saviczkij IV, Mironov AA, Myastkovskaya IV. Endotelialnaya disfunkcziya pri posttravmaticheskoj epilepsii [Endothelial dysfunction in post-traumatic epilepsy]. Jornal of Education, Health and Sport. 2016; 6(6): 245-252. [Russian]
  18. Alekseenko YuV. Posttravmaticheskaya e`pilepsiya: problemy` diagnostiki, lecheniya i profilaktiki [Post-traumatic epilepsy: problems of diagnosis, treatment and prevention]. Mediczinskie novosti. 2006; 11: 25-28. [Russian]
  19. Bramlett HM, Dirtrich WD. Patofiziologiya ishemicheskogo i travmaticheskogo porazheniya mozga: skhodstvo i razlichiya [Pathophysiology of ischemic and traumatic brain injury: similarities and differences]. Meditsina neotlozhnykh sostoyaniy. 2006; 5: 36-43. [Russian]
  20. Volokhova GA, Stoyanov AN, Vastyanov RS. Intensifikacziya proczessov lipoperoksidaczii i ugneteniya aktivnosti antiradikalnykh mekhanizmov kak odnonapravlennye mekhanizmy povrezhdeniya mozga [Intensification of lipid peroxidation processes and inhibition of the activity of antiradical mechanisms as unidirectional mechanisms of brain damage]. Liky Ukrayini. 2009; 5(131): 92-97. [Russian]
  21. Hertsev VN, Stoyanov AN, Bocherova TI. Applied clinical and pathogenetic aspects of interdisciplinary cooperation in the diagnosis and treatment of concussion of brain. Journal of Education, Health and Sport. 2017; 7(5): 913-927.
  22. Ding K, Gupta PK, Diaz-Arrastia R. Laskowitz D, Grant G, Eds. Translational Research in Traumatic Brain Injury. Boca Raton (FL): CRC Press/Taylor and Francis Group; 2016. Chapter 14.
  23. Len TK, Neary JP. Cerebrovascular pathophysiology following mild traumatic brain injury. Clin Physiol Funct Imaging. 2011; 31: 85-93.
  24. Grimajlo VN, Litovchenko TA, Yakubenko YuV, Markova TV. Osobennosti sindroma vegetativnoj distonii u paczientov s posttravmaticheskoj epilepsiej [Features of vegetative dystonia syndrome in patients with post-traumatic epilepsy]. Mezhdunarodnyj mediczinskij zhurnal. 2015; 3: 32-35. [Russian]
  25. Barkhatov MV, Nosyrev AV, Dekhtyar AV, Galaktionova MYu. Primenenie preparata Meksidol v kompleksnom lechenii detej s posttravmaticheskoj epilepsiej [Application of the drug Mexidol in the complex treatment of children with post-traumatic epilepsy]. Byulleten eksperimentalnoj biologii i medicziny. 2006; 1: 9-13. [Russian]
  26. Hervan ST. Epilepsy after brain insult: targeting rpileptogenesis. Neurology. 2002; 59(Suppl 5): S21-6. https://doi.org/10.1212/wnl.59.9_suppl_5.s21
  27. Benjamins JA, Nedelkoska L, Bealmear B, Lisak RP. ACTH protects mature oligodendroglia from excitotoxic and inflammation-related damage in vitro. Glia. 2013; 61: 1206-17. https://doi.org/10.1002/glia.22504
  28. Gusev EI, Konovalov AN, Skvorczova VI, Gekht AB. Nevrologiya. Naczionalnoe rukovodstvo [Neurology. National leadership]. M: GEOTAR-Media; 2013. 1040 s. [Russian]
  29. Gardner G. Struktura razuma: teoriya mnozhestvennogo intellekta [The structure of the mind: the theory of multiple intelligences]. Per s angl. M: OOO "ID Vilyams"; 2007. 512 s. [Russian]
  30. Magniczkaya KB. Epileptogenez i patogeneticheskaya terapiya [Epileptogenesis and pathogenetic therapy]. In: Epilepsiya u detej: problem i resheniya. Materialy mezhd konf. Volgograd; 2007. s. 6-13. [Russian]
  31. Patofiziologiya: rukovodstvo k prakt. zanyatiyam [Pathophysiology: a guide to practice]. Uchebnoe posobie. Pod red VV Noviczkogo, OI Urazovoj. M; 2011. 336 s. [Russian]
  32. Vastyanov RS, Shandra OA. Funkczionalna perebudova ta zmina lokalizacziyi korkovikh motornikh nejroni`v v umovakh khronichnoyi epileptichnoyi aktivnosti [Functional overdrive and change of localization of cortical motor neurons in the minds of chronic epileptic activity]. Tavricheskij mediko-biologicheskij vestnik. 2012; 15(3): 51-53. [Ukrainian]
  33. Bushnik T, Englander J, Wright J, Kolakowsky-Hayner SA. Traumatic brain injury with and without late posttraumatic seizures: what are the impacts in the post‐acute phase: a NIDRR Traumatic Brain Injury Model Systems study. J Head Trauma Rehabil. 2012; 27: E36–E44. https://doi.org/10.1097/HTR.0b013e318273375c
  34. Guzeva VI. Epilepsiya i neepilepticheskie paroksizmalnye sostoyaniya u detej [Epilepsy and non-epileptic paroxysmal states in children]. M: OOO «Mediczinskoe informaczionnoe agentstvo»; 2007. 568 s. [Russian]
  35. Generalov VO. Epilepsiya i strukturnye povrezhdeniya mozga [Epilepsy and structural damage to the brain]. Abstr. Dr. Sci. (Med.). M; 2010. 35 s. [Russian]
  36. Generalov VO, Mishnyakova LP, Fedin AI. Vliyanie lokalizaczii ochaga epilepticheskoj aktivnosti na sroki razvitiya posttravmaticheskoj epilepsii [Influence of localization of the focus of epileptic activity on the timing of the development of post-traumatic epilepsy]. Materialy X Vserossijskogo sjezda nevrologov. Yaroslavl; 2006. s. 535. [Russian]
  37. Fazel S, Wolf A, Långström N, Newton CR, Lichtenstein P. Premature mortality in epilepsy and the role of psychiatric comorbidity: a total population study. Lancet. 2013; 382(9905): 1646-1654. https://doi.org/10.1016/S0140-6736(13)60899-5
  38. Feeney DM, Walker AE. The prediction of posttraumatic epilepsy. A mathematical approach. Arch Neurol. 1979 Jan; 36(1): 8-12. https://doi.org/10.1001/archneur.1979.00500370038005
  39. De Carolis P, D’Alessandro R, Ferrara R, Andreoli A, Sacquegna T, Lugaresi E. Late seizures in patients with internal carotid and middle cerebral artery occlusive disease following ischaemic events. J Neurol Neurosurg Psychiatry. 1984; 47(12): 1345-1347. https://doi.org/10.1136/jnnp.47.12.1345
  40. Faught E, Peters D, Bartolucci A, Moore L, Miller PC. Seizures after primary intracerebral hemorrhage. Neurology. 1989; 39(8): 1089-1093. https://doi.org/10.1212/wnl.39.8.1089
  41. Golden N, Darmadipura S, Bagiada NA. The difference in seizure incidences between young and adult rats related to lipid peroxidation after intracortical injection of ferric chloride. Singapore Med J. 2010; 51(2): 105-109.
  42. Ganz T. Systemic iron homeostasis. Physiol Rev. 2013; 93(4): 1721-1741. https://doi.org/10.1152/physrev.00008.2013