Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde
Düşünceler

Baykan, Betul; ATALAR, ARİFE ÇİMEN

Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler

Arife Çimen ATALAR, (Sağlık Bilimleri Üniversitesi, İstanbul Eğitim ve Araştırma Hastanesi, Nöroloji Kliniği, İstanbul, Türkiye)

Betül BAYKAN (İstanbul Üniversitesi, İstanbul Tıp Fakültesi, Nöroloji Anabilim Dalı, Klinik Nörofizyoloji Bilim Dalı, İstanbul, Türkiye)

Nöropsikiyatri Arşivi

58 15

Yıl: 2022 Cilt: 59 Sayı: 1 Sayfa Aralığı: 68 - 76 Metin Dili: Türkçe İndeks Tarihi: 17-06-2022

Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler

Öz:

Epilepsi dinamik ve heterojen yapıda bir nörolojik hastalıktır ve prognoz üzerine yapılan uzun soluklu çalışmalarda klasik olarak 5 temel seyir paterni (erken remisyonlu, geç remisyonlu, alevlenme-sönmelerle giden, kötüleşen ve remisyona hiç girmeyen) tanımlanmıştır. Bunlardan en sık görüleni alevlenme-sönmelerle giden seyir olup, genetik etyoloji varlığı, başlangıçta seyrek nöbet varlığı, psikiyatrik komorbid hastalık olmaması gibi faktörler bu seyir tipi ile ve takiplerde 5 yıllık remisyona ulaşma ile ilişkili bulunmuştur. Anti nöbet ilaç direnci (ANİ-D) ve bu direncin varlığına etki eden faktörlerin olması (semptomatik etyoloji, anormal elektroensefalografik bulgular, birden fazla nöbet tipi birlikteliği, status epileptikus ve febril nöbet öyküsü gibi) remisyon şansını azaltırken, idiyopatik/genetik etyoloji, jeneralize epilepsi olması, komorbid hastalık bulunmaması gibi özellikler uzun süreli remisyona ulaşma ile ilişkili görünmektedir. Bu temel seyir şekillerinin dışında, kötü seyirli juvenil miyoklonik epilepsi ( JME), iyi seyirli hipokampal sklerozla ilişkili meziyal temporal lob epilepsisi (HS-MTLE) ve kötü seyirli sentro-temporal dikenli çocukluk çağı epilepsisi (STDÇÇE) gibi “atipik seyir” gösteren bazı olgular bulunmakta olup, bunların altında yatan patofizyolojik mekanizmalar çeşitli hipotezlerin varlığına karşın henüz açıklığa kavuşturulamamıştır. Hormonal faktörler (katamenial epilepsilerde olduğu gibi), otoimmun süreçler, tiroid bozuklukları ve metabolik ve psikiyatrik hastalıklar gibi komorbid hastalıkların varlığı da hastalığın seyri üzerinde etkili olarak atipik seyir paternine neden olabilirler. Bu derlemede hedefimiz epilepsilerin genel seyir özelliklerinin yanısıra atipik seyir gösterebilen bazı özellikli epilepsi sendromlarını ayrıntılarıyla irdeleyerek, klinisyene epilepside prognoz özelliklerine dair güncel ve sorgulayıcı bir bakış açısı sunabilmektir.

Anahtar Kelime:

Different Prognostic Patterns in Epilepsies and Considerations About the Denotations of Atypical Patterns

Öz:

Epilepsy is a dynamic and heterogeneous neurological disease, and in long-term studies on prognosis, classically 5 basic patterns (early remission, late remission, relapsing-remitting, worsening, and nonremitting) have been identified. The most frequent pattern was relapsingremitting course, and factors such as the presence of genetic etiology, rare seizures at the beginning of epilepsy and the absence of psychiatric comorbid diseases were found to be related with this pattern as well as reaching 5 years of remission in the follow-ups. Anti-seizure drug resistance (ASD-R) and factors affecting the presence of this resistance (such as symptomatic etiology, abnormal electroencephalographic findings, having multiple seizure types together, status epilepticus and febrile seizure history) decrease the chance of remission, while idiopathic/ genetic etiology, generalized epilepsy, and absence of comorbid diseases seem to be associated with achieving long-term remission. Apart from these basic course patterns, there are some patients with an “atypical prognosis” such as drug-resistant juvenile myoclonic epilepsy ( JME), benign hippocampal sclerosis-related mesial temporal lobe epilepsy (HS-MTLE), and severe childhood epilepsy with centro-temporal spikes (CESTS), in which the pathophysiological mechanisms underlying these patterns have not been clarified despite the suggestions of various hypotheses. The presence of comorbid diseases such as hormonal factors (as in catamenial epilepsy), autoimmune processes, thyroid disorders and metabolic and psychiatric diseases may also cause an atypical prognostic pattern by affecting the course of the disease. In this review, our aim is to provide the clinician with an up-to-date and questioning perspective on the prognostic markers of epilepsy, by examining in detail some specific epilepsy syndromes that may show atypical prognosis as well as the general prognostic features of epilepsy.

Anahtar Kelime:

Belge Türü: Makale Makale Türü: Derleme Erişim Türü: Erişime Açık

1. Fiest KM, Sauro KM, Wiebe S, Patten SB, Kwon CS, Dykeman J ve ark. Prevalence and incidence of epilepsy: A systematic review and meta-analysis of international studies. Neurology 2017;88:296–303. [Crossref]
2. Onal AE, Tumerdem Y, Ozturk MK, Gurses C, Baykan B, Gokyigit A ve ark. Epilepsy prevalence in a rural area in Istanbul. Seizure 2002;11:397–401. [Crossref]
3. Beghi E. Addressing the burden of epilepsy: Many unmet needs. Pharmacol Res 2016;107:79–84. [Crossref]
4. Thijs RD, Surges R, O’Brien TJ, Sander JW. Epilepsy in adults. Lancet 2019;393:689–701. [Crossref]
5. Kwan P, Sander JW. The natural history of epilepsy: an epidemiological view. J Neurol Neurosurg Psychiatry 2004;75:1376–81. [Crossref]
6. Sillanpää M, Schmidt D. Natural history of treated childhood-onset epilepsy: prospective, long-term population-based study. Brain 2006;129:617–624. [Crossref]
7. Sander JWAS, Sillanpää M. Natural history prognosis. In: Engels J, Pedley TA, editors. Epilepsy. A comprehensive textbook, vol. I/III. New York: Raven Press; 1997. p.69–86.
8. Beghi E, Beretta S, Carone D, Zanchi C, Bianchi E, Pirovano M ve ark. PRO-LONG Study Group. Prognostic patterns and predictors in epilepsy: a multicentre study (PRO-LONG). J Neurol Neurosurg Psychiatry 2019;90:1276–1285. [Crossref]
9. Del Felice A, Beghi E, Boero G, La Neve A, Bogliun G, De Palo A ve ark. Early versus late remission in a cohort of patients with newly diagnosed epilepsy. Epilepsia 2010;51:37–42. [Crossref]
10. Keränen T, Riekkinen P. Remission of seizures in untreated epilepsy. BMJ 1993;307:483. [Crossref]
11. Sillanpää M, Schmidt D. Prognosis of seizure recurrence after stopping antiepileptic drugs in seizure-free patients. A long-term population-based study of childhood-onset epilepsy. Epilepsy Behav 2006;8:713–719. [Crossref]
12. Kwan P, Arzimanoglou A, Berg AT, Brodie MJ, Allen Hauser W, Mathern G ve ark. Definition of drug resistant epilepsy: consensus proposal by the ad hoc Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia 2010;51:1069–1077. [Crossref]
13. Picot MC, Baldy-Moulinier M, Daurès JP, Dujols P, Crespel A. The prevalence of epilepsy and pharmacoresistant epilepsy in adults: a population-based study in a Western European country. Epilepsia 2008;49:1230–1238. [Crossref]
14. Neligan A, Bell GS, Elsayed M, Sander JW, Shorvon SD. Treatment changes in a cohort of people with apparently drug-resistant epilepsy: an extended follow-up. J Neurol Neurosurg Psychiatry 2012;83:810–813. [Crossref]
15. Callaghan B, Schlesinger M, Rodemer W, Pollard J, Hesdorffer D, Allen Hauser W ve ark. Remission and relapse in a drug-resistant epilepsy population followed prospectively. Epilepsia 2011;52:619–626. [Crossref]
16. Schiller Y. Seizure relapse and development of drug resistance following longterm seizure remission. Arch Neurol 2009;66:1233–1239. [Crossref]
17. Berg AT, Levy SR, Testa FM, D’Souza R. Remission of epilepsy after two drug failures in children: a prospective study. Ann Neurol 2009;65:510–519. [Crossref]
18. Xue-Ping W, Hai-Jiao W, Li-Na Z, Xu D, Ling L. Risk factors for drug-resistant epilepsy: A systematic review and meta-analysis. Medicine (Baltimore) 2019;98:e16402. [Crossref]
19. Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342:314–319. [Crossref]
20. Camfield PR, Camfield CS, Gordon K, Dooley JM. If a first antiepileptic drug fails to control a child’s epilepsy, what are the chances of success with the next drug? J Pediatr 1997;131:821–824. [Crossref]
21. Choi H, Hayat MJ, Zhang R, Hirsch LJ, Bazil CW, Mendiratta A ve ark. Drug-resistant epilepsy in adults: Outcome trajectories after failure of two medications. Epilepsia 2016;57:1152–6110. [Crossref]
22. Mbuba CK, Ngugi AK, Newton CR, Carter JA. The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia 2008;49:1491–1503. [Crossref]
23. Diop AG, Hesdorffer DC, Logroscino G, Hauser WA. Epilepsy and mortality in Africa: a review of the literature. Epilepsia 2005;46:33–35. [Crossref]
24. Singh G, Sander JW. The global burden of epilepsy report: Implications for low- and middle-income countries. Epilepsy Behav 2020;105:106949. [Crossref]
25. Placencia M, Sander JW, Roman M, Madera A, Crespo F, Cascante S ve ark. The characteristics of epilepsy in a largely untreated population in rural Ecuador. J Neurol Neurosurg Psychiatry 1994;57:320–325. [Crossref]
26. Nicoletti A, Sofia V, Vitale G, Bonelli SI, Bejarano V, Bartalesi F ve ark. Natural history and mortality of chronic epilepsy in an untreated population of rural Bolivia: a follow-up after 10 years. Epilepsia 2009;50:2199–2206. [Crossref]
27. Seneviratne U, Cook M, D’Souza W. The prognosis of idiopathic generalized epilepsy. Epilepsia 2012;53:2079–2090. [Crossref]
28. Mohanraj R, Brodie MJ. Outcomes of newly diagnosed idiopathic generalized epilepsy syndromes in a non-pediatric setting. Acta Neurol Scand 2007;115:204–208. [Crossref]
29. Callenbach PM, Bouma PA, Geerts AT, Arts WF, Stroink H, Peeters EA ve ark. Long-term outcome of childhood absence epilepsy: Dutch Study of Epilepsy in Childhood. Epilepsy Res 2009;83:249–256. [Crossref]
30. Wirrell EC, Camfield CS, Camfield PR, Gordon KE, Dooley JM. Long-term prognosis of typical childhood absence epilepsy: remission or progression to juvenile myoclonic epilepsy. Neurology 1996;47:912—918. [Crossref]
31. Trinka E, Baumgartner S, Unterberger I, Unterrainer J, Luef G, Haberlandt E ve ark. Long-term prognosis for childhood and juvenile absence epilepsy. J Neurol 2004;251:1235–1241. [Crossref]
32. Baykan B, Matur Z, Gürses C, Aykutlu E, Gökyiğit A. Typical absence seizures triggered by photosensitivity. Epilepsia 2005;46:159–163. [Crossref]
33. Healy L, Moran M, Singhal S, O’Donoghue MF, Alzoubidi R, Whitehouse WP. Relapse after treatment withdrawal of antiepileptic drugs for Juvenile Absence Epilepsy and Juvenile Myoclonic Epilepsy. Seizure 2018;59:116– 122. [Crossref]
34. Martinez-Juarez IE, Alonso ME, Medina MT, Duron RM, Bailey JN, LopezRuiz M ve ark. Juvenile myoclonic epilepsy subsyndromes: Family studies and longterm follow-up. Brain 2006;129:1269–1280. [Crossref]
35. Baykan B, Wolf P. Juvenile myoclonic epilepsy as a spectrum disorder: A focused review. Seizure 2017;49:36–41. [Crossref]
36. Geithner J, Schneider F, Wang Z, Berneiser J, Herzer R, Kessler C ve ark. Predictors for long-term seizure outcome in juvenile myoclonic epilepsy:25–63 years of follow-up. Epilepsia 2012;53:1379–1386. [Crossref]
37. Senf P, Schmitz B, Holtkamp M, Janz D. Prognosis of juvenile myoclonic epilepsy 45 years after onset: seizure outcome and predictors. Neurology 2013;81:2128–2233. [Crossref]
38. Baykan B, Altindag EA, Bebek N, Ozturk AY, Aslantas B, Gurses C ve ark. Myoclonic seizures subside in the fourth decade in juvenile myoclonic epilepsy. Neurology 2008;70:2123–2129. [Crossref]
39. Guaranha MSB, de Araujo Filho GM, Lin K, Guilhoto LMFF, Caboclo LOSF, Yacubian EMT. Prognosis of juvenile myoclonic epilepsy is related to endophenotypes. Seizure 2011;20:42–48. [Crossref]
40. Baykan B, Martínez-Juárez IE, Altindag EA, Camfield CS, Camfield PR. Lifetime prognosis of juvenile myoclonic epilepsy. Epilepsy Behav 2013;28:S18–524. [Crossref]
41. Stevelink R, Koeleman BPC, Sander JW, Jansen FE, Braun KPJ. Refractory juvenile myoclonic epilepsy: a meta-analysis of prevalence and risk factors. Eur J Neurol 2019;26:856–864. [Crossref]
42. Lamberink HJ, Otte WM, Geerts AT, Pavlovic M, Ramos-Lizana J, Marson AG ve ark. Individualised prediction model of seizure recurrence and longterm outcomes after withdrawal of antiepileptic drugs in seizure-free patients: a systematic review and individual participant data meta-analysis. Lancet Neurol 2017;16:523–531. [Crossref]
43. Panayiotopoulos CP, Michael M, Sanders S, Valeta T, Koutroumanidis M. Benign childhood focal epilepsies: assessment of established and newly recognized syndromes. Brain 2008;131:2264–2286. [Crossref]
44. Koutroumanidis M, Aggelakis K, Panayiotopoulos CP. Idiopathic epilepsy with generalized tonic-clonic seizures only vs. idiopathic epilepsy with phantom absences and generalized tonic-clonic seizures: one or two syndromes? Epilepsia 2008;49:2050–2062. [Crossref]
45. Fejerman N, Caraballo R, Tenembaum SN. Atypical evolutions of benign localization-related epilepsies in children: are they predictable? Epilepsia 2000;41:380–390. [Crossref]
46. Cerulli Irelli E, Cocchi E, Morano A, Casciato S, Fanella M, Albini M ve ark. Valproate impact and sex-dependent seizure remission in patients with idiopathic generalized epilepsy. J Neurol Sci 2020;415:116940. [Crossref]
47. Parisi P, Paolino MC, Raucci U, Ferretti A, Villa MP, Trenite DK-N. “Atypical forms” of benign epilepsy with centrotemporal spikes (BECTS): How to diagnose and guide these children. A practical/scientific approach. Epilepsy Behav 2017;75:165–169. [Crossref]
48. Garcia-Ramos C, Jackson DC, Lin JJ, Dabbs K, Jones JE, Hsu DA ve ark. Cognition and brain development in children with benign epilepsy with centrotemporal spikes. Epilepsia 2015;56:1615–1622. [Crossref]
49. Cherian A, Baheti NN, Menon RN, Iyer RS, Rathore C, Radhakrishnan A. Atonic variant of benign childhood epilepsy with centrotemporal spikes (atonic-BECTS): a distinct electro-clinical syndrome. Brain Dev 2012;34:511– 519. [Crossref]
50. Park JI, Kim SJ, Kim HG. Acoustic effects of carbamazepine in benign rolandic epilepsy. Epilepsy Behav 2005;7:468–471. [Crossref]
51. Prats JM, Garaizar C, García-Nieto ML, Madoz P. Antiepileptic drugs and atypical evolution of idiopathic partial epilepsy. Pediatr Neurol 1998;18:402– 406. [Crossref]
52. Semah F, Lamy C, Demeret S. Hippocampal sclerosis and other hippocampal abnormalities in the early identification of candidates for epilepsy surgery. Arch. Neurol 2002;59:1042—1043. [Crossref]
53. Stephen LJ, Kwan P, Brodie MJ. Does the cause of localization related epilepsy influence the response to antiepileptic drug treatment? Epilepsia 2011;43:357—362. [Crossref]
54. Varoglu AO, Saygi S, Acemoglu H, Ciger A. Prognosis of patients with mesial temporal lobe epilepsy due to hippocampal sclerosis. Epilepsy Res 2009;85:206–211. [Crossref]
55. Leong ECS, Seneviratne U. “Benign” temporal lobe epilepsy with hippocampal sclerosis: A forgotten entity? Epilepsy Behav Rep 2020;14:100407. [Crossref]
56. Kobayashi E, D’Agostino MD, Lopes-Cendes I, Berkovic SF, Li ML, Andermann E ve ark. Hippocampal atrophy and T2-weighted signal changes in familial mesial temporal lobe epilepsy. Neurology 2003;60:405–409. [Crossref]
57. Gambardella A, Labate A, Giallonardo AT, Aguglia U. Familial mesial temporal lobe epilepsies: clinical and genetic features. Epilepsia 2009;50:55– 57. [Crossref]
58. Cvetkovska E, Kuzmanovski I, Babunovska M, Boshkovski B, Cangovska TC, Trencevska GK. Phenotypic spectrum in families with mesial temporal lobe epilepsy probands. Seizure 2018;58:13–16. [Crossref]
59. Striano P, Gambardella A, Coppola A, Di Bonaventura C, Bovo G, Diani E ve ark. Familial mesial temporal lobe epilepsy (FMTLE): a clinical and genetic study of 15 Italian families. J Neurol 2008;255:16–23. [Crossref]
60. Nilo A, Gelisse P, Crespel A. Genetic/idiopathic generalized epilepsies: Not so good as that! Rev Neurol (Paris) 2020;176:427–438. [Crossref]
61. Gesche J, Christensen J, Hjalgrim H, Rubboli G, Beier CP. Epidemiology and outcome of idiopathic generalized epilepsy in adults. Eur J Neurol 2020;27:676–684. [Crossref]
62. Cerulli Irelli E, Morano A, Barone FA, Fisco G, Fanella M, Orlando B ve ark. Persistent treatment resistance in genetic generalized epilepsy: A long-term outcome study in a tertiary epilepsy center. Epilepsia 2020;61:2452–2460. [Crossref]
63. Aydin-Özemir Z, Matur Z, Bebek N, Gürses C, Gökyiğit A, Baykan B. Longterm follow-up of adult patients with genetic generalized epilepsy with typical absence seizures and generalized paroxysmal fast activity in their EEG. Seizure 2014;23:607–615. [Crossref]
64. Bansal L, Vargas Collado L, Pawar K, Nagesh D, Ilyas M, Hall A ve ark. Electroclinical Features of Generalized Paroxysmal Fast Activity in Typical Absence Seizures. J Clin Neurophysiol 2019;36:36–44. [Crossref]
65. Gesche J, Khanevski M, Solberg C, Beier CP. Resistance to valproic acid as predictor of treatment resistance in genetic generalized epilepsies. Epilepsia 2017;58:e64–e69. [Crossref]
66. Löscher W, Potschka H, Sisodiya SM, Vezzani A. Drug Resistance in Epilepsy: Clinical Impact, Potential Mechanisms, and New Innovative Treatment Options. Pharmacol Rev 2020;72:606–638. [Crossref]
67. Weston MC. A tRNA Variant Translates Into Seizure Resistance. Epilepsy Curr 2021;21:126–128. [Crossref]
68. Löscher W. Animal models of drug-resistant epilepsy. Novartis Found Symp 2002;243:149–59;discussion 159–66, 180–5. https://pubmed.ncbi.nlm.nih. gov/11990774/
69. Fang M, Xi ZQ, Wu Y, Wang XF. A new hypothesis of drug refractory epilepsy: neural network hypothesis. Med Hypotheses 2011;76:871–876. [Crossref]
70. Shimada T, Takemiya T, Sugiura H, Yamagata K. Role of inflammatory mediators in the pathogenesis of epilepsy. Mediators Inflamm 2014;2014:901902. [Crossref]
71. Liimatainen S, Lehtimäki K, Palmio J, Alapirtti T, Peltola J. Immunological perspectives of temporal lobe seizures. J Neuroimmunol 2013;263:1–7. [Crossref]
72. Atmaca MM, Tuzun E, Erdag E, Bebek N, Baykan B, Gurses C. Investigation of anti-neuronal antibodies in status epilepticus of unknown etiology: a prospective study. Acta Neurol Belg 2017;117:841–848. [Crossref]
73. Wang M, Backstrom T, Sundstrom I, Wahlström G, Olsson T, Zhu D ve ark. Neuroactive steroids and central nervous system disorders. Int Rev Neurobiol 2001;46:421–459. [Crossref]
74. Reddy DS. The role of neurosteroids in the pathophysiology and treatment of catamenial epilepsy. Epilepsy Res 2009;85:1–30. [Crossref]
75. Herzog AG, Frye CA. Seizure exacerbation associated with inhibition of progesterone metabolism. Ann Neurol 2003;53:390–391. [Crossref]
76. Grover S, Talwar P, Gourie-Devi M, Gupta M, Bala K, Sharma S ve ark. Genetic polymorphisms in sex hormone metabolizing genes and drug response in women with epilepsy. Pharmacogenomics 2010;11:1525–1534. [Crossref]
77. Verrotti A, Laus M, Coppola G, Parisi P, Mohn A, Chiarelli F. Catamenial epilepsy: hormonal aspects. Gynecol Endocrinol 2010;26:783–790. [Crossref]
78. Choi H, Detyniecki K, Bazil C, Thornton S, Crosta P, Tolba H ve ark. EPIGEN Consortium. Development and validation of a predictive model of drugresistant genetic generalized epilepsy. Neurology 2020;95:e2150–e2160. [Crossref]
79. Reddy DS, Rogawski MA. Neurosteroid replacement therapy for catamenial epilepsy. Neurotherapeutics 2009;6:392–401. [Crossref]
80. Schroeder AC, Privalsky ML. Thyroid hormones, t3 and t4, in the brain. Front Endocrinol (Lausanne) 2014;5:40. [Crossref]
81. Tamijani SM, Karimi B, Amini E, Golpich M, Dargahi L, Ali RA ve ark. Thyroid hormones: Possible roles in epilepsy pathology. Seizure 2015;31:155–164. [Crossref]
82. Wallis K, Sjögren M, van Hogerlinden M, Silberberg G, Fisahn A, Nordström K ve ark. Locomotor deficiencies and aberrant development of subtypespecific GABAergic interneurons caused by an unliganded thyroid hormone receptor alpha1. J Neurosci 2008;28:1904–1915. [Crossref]
83. Han JY, Lee IG, Shin S, Park J. Seizure duration may increase thyroidstimulating hormone levels in children experiencing a seizure. J Int Med Res 2020;48:300060519888401. [Crossref]
84. Aydin-Ozemir Z, Tüzün E, Baykan B, Akman-Demir G, Ozbey N, Gürses C ve ark. Autoimmune thyroid encephalopathy presenting with epilepsia partialis continua. Clin EEG Neurosci 2006;37:204–209. [Crossref]
85. Hamed SA. The effect of antiepileptic drugs on thyroid hormonal function: causes and implications. Expert Rev Clin Pharmacol 2015;8(6):741–750. [Crossref]
86. Vezzani A, Balosso S, Ravizza T. Neuroinflammatory pathways as treatment targets and biomarkers in epilepsy. Nat Rev Neurol 2019;15:459–472. [Crossref]
87. Bauer J, Bien CG. Neuropathology of autoimmune encephalitides. Handb Clin Neurol 2016;133:107–20. [Crossref]
88. Ekizoglu E, Tuzun E, Woodhall M, Lang B, Jacobson L, Icoz S ve ark. Investigation of neuronal autoantibodies in two different focal epilepsy syndromes. Epilepsia 2014;55:414–422. [Crossref]
89. Vanli-Yavuz EN, Erdag E, Tuzun E, Ekizoglu E, Baysal-Kirac L, Ulusoy C ve ark. Neuronal autoantibodies in mesial temporal lobe epilepsy with hippocampal sclerosis. J Neurol Neurosurg Psychiatry 2016;87:684–692. [Crossref]
90. Karaaslan Z, Ekizoğlu E, Tektürk P, Erdağ E, Tüzün E, Bebek N ve ark. Investigation of neuronal auto-antibodies in systemic lupus erythematosus patients with epilepsy. Epilepsy Res 2017;129:132–137. [Crossref]
91. Steriade C, Titulaer MJ, Vezzani A, Sander JW, Thijs RD. The association between systemic autoimmune disorders and epilepsy and its clinical implications. Brain 2021;144:372–390. [Crossref]
92. Keezer MR, Sisodiya SM, Sander JW. Comorbidities of epilepsy: current concepts and future perspectives. Lancet Neurol 2016;15:106–115. [Crossref]
93. Cameron FJ, Scratch SE, Nadebaum C, Northam EA, Koves I, Jennings J ve ark. DKA Brain Injury Study Group. Neurological consequences of diabetic ketoacidosis at initial presentation of type 1 diabetes in a prospective cohort study of children. Diabetes Care 2014;37:1554–1562. [Crossref]
94. Mastrangelo M, Tromba V, Silvestri F, Costantino F. Epilepsy in children with type 1 diabetes mellitus: Pathophysiological basis and clinical hallmarks. Eur J Paediatr Neurol 2019;23:240–247. [Crossref]
95. Verrotti A, Scaparrotta A, Olivieri C, Chiarelli F. Seizures and type 1 diabetes mellitus: current state of knowledge. Eur J Endocrinol 2012;167:749e58. [Crossref]
96. Leen WG, Taher M, Verbeek MM, Kamsteeg EJ, van de Warrenburg BP, Willemsen MA. GLUT1 deficiency syndrome into adulthood: a follow-up study. J Neurol 2014;261:589–599. [Crossref]
97. Sharma S, Prasad AN. Inborn Errors of Metabolism and Epilepsy: Current Understanding, Diagnosis, and Treatment Approaches. Int J Mol Sci 2017;18:1384. [Crossref]
98. Lu E, Pyatka N, Burant CJ, Sajatovic M. Systematic Literature Review of Psychiatric Comorbidities in Adults with Epilepsy. J Clin Neurol 2021;17:176– 186. [Crossref]
99. Hitiris N, Mohanraj R, Norrie J, Sills GJ, Brodie MJ. Predictors of pharmacoresistant epilepsy. Epilepsy Res 2007;75:192–196. [Crossref]
100. Kanner AM. Can neurobiological pathogenic mechanisms of depression facilitate the development of seizure disorders? Lancet Neurol 2012;11:1093– 1102. [Crossref]

APA	ATALAR A, Baykan B (2022). Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. , 68 - 76.
Chicago	ATALAR ARİFE ÇİMEN,Baykan Betul Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. (2022): 68 - 76.
MLA	ATALAR ARİFE ÇİMEN,Baykan Betul Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. , 2022, ss.68 - 76.
AMA	ATALAR A,Baykan B Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. . 2022; 68 - 76.
Vancouver	ATALAR A,Baykan B Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. . 2022; 68 - 76.
IEEE	ATALAR A,Baykan B "Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler." , ss.68 - 76, 2022.
ISNAD	ATALAR, ARİFE ÇİMEN - Baykan, Betul. "Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler". (2022), 68-76.

APA	ATALAR A, Baykan B (2022). Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. Nöropsikiyatri Arşivi, 59(1), 68 - 76.
Chicago	ATALAR ARİFE ÇİMEN,Baykan Betul Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. Nöropsikiyatri Arşivi 59, no.1 (2022): 68 - 76.
MLA	ATALAR ARİFE ÇİMEN,Baykan Betul Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. Nöropsikiyatri Arşivi, vol.59, no.1, 2022, ss.68 - 76.
AMA	ATALAR A,Baykan B Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. Nöropsikiyatri Arşivi. 2022; 59(1): 68 - 76.
Vancouver	ATALAR A,Baykan B Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler. Nöropsikiyatri Arşivi. 2022; 59(1): 68 - 76.
IEEE	ATALAR A,Baykan B "Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler." Nöropsikiyatri Arşivi, 59, ss.68 - 76, 2022.
ISNAD	ATALAR, ARİFE ÇİMEN - Baykan, Betul. "Epilepsilerde Farklı Seyir Tipleri ve Sıradışı Seyirlerin Anlamı Üzerinde Düşünceler". Nöropsikiyatri Arşivi 59/1 (2022), 68-76.