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ASKULER HAST ALIKLARDA EPiLEPSi NOBETLERi

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ASKULER HAST ALIKLARDA EPiLEPSi NOBETLERi

- 1§111a serebrovaskuler hastahk (SVH) ve epilepsi nobeti tesbit edilen 31 hastada ger9ekle~tirildi. Klinik

w...~.~r .... n.,.,falografik(EEG) ve bilgisayarll beyin tomografi(BBT) bulgulan ile kar~1la§t1nldL SVH ile epilepsi

~ incelendi. SVH'Iarda genel olarak %5 oranmda epilepsi nobeti tesbit edildi.Epilepsi nobetlerinin en s1k 1818bral kanamalar, nobetlerin buyuk 90gunlugunu da generalize tonik-klonik tip nobet te§kil etmektedir. Bu

• ...,."""" EEG ve BBT de fokal anomaliler daha s1k goruldO.

This study was performed on 31 patients with cerebrovascular diseases in whom epileptic seizures were The clinical findings were compared with the signs of electroencephalographic (EEG) and computerized scan (CT) of the brain. The relations between cereberovascular disease and epilepsy are investigated.

were detected in 5 percent of the patient with cerebrovascular diseases. Cerebral haemorrhage was

l*llnmt1n cause of the epileptic seizures, that were generalized tonic-clonic type in the majority of the patient.

fisdings it was found that focal abnormalities wer frequent on EEG and CT.

epileptik n6betlerin en onemli sebeplerinden biri SVH'Iard1r. Nobetler ateron plaklann kan ak1mln1

iilllmlllrm bloke edilerek infarkt veya odem olu§umu, kanamalarda ise s1zan kamn beyin aktivitesinde direkt olarak de§arjlar saglamas1 sonucu meydana gelir.

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Serebrovaskiiler Hastailk/arda Epi/epsi NObetleri:KARAMAN, Yahya

Ara~tmnalar intraserebral ve subaraknoid kanamalarda beyin parankim dokusu direkt etkilendiginden iskemik orijinli hastahklardan daha s1khkla epilepsi nobetlerine sebep oldugunu gostermi~tir (1,3,9,1 0,13,30,31 ). Akut serebrovaskuler olay s1rasmda ortaya 91kan nobetler odemden 90k arterterin sulama ahnmdaki infarkta ve bu bolgere yay1lan kanm irritasyonuna bagh beyin aktivitesini etkileyereke olur. Kronik vakalarda aterosklerotik degi~ikligin roiU olabildigi gibi infarkt, hematom, 6deme ilaveten atrofi de etkili olabilmektedir (1,5,6,19,21,26). Akut donemde tromboembolik hadiseler incelendiginde % 2-5, kanamalar incelendiginde % 7 hatta % 20 ye varan oranlarda epilepsi nobetleri

gozlenmi~tir (4,96,9,10,13,20,21,30). Akut donemde fokal, kronik donemde ise grand mal tipte nobetler daha s1k gorOIOr (5,6,11,16,30). Kronik donemde hastanm klinik durumun diizelmesine bagh EEG ve BBT bulgulannda da

degi~iklik olur ancak epilepsiye has EEG bulgulan klinigin diizelmesinden y1llarca sonra da devam etmektedir (8,23,27).

Materyal ve Metod

Eyi011989-Kaslm 1989 tarihleri arasmda Kayseri SSK Hastanesi Noroloji Klinigine muracaat ederek yatmlan 620 SVH tams1 alan hastadan epilepsi nobeti ge9irmi~ 31 hasta incelemeye ahnm1~t1r. Klinik bulgulan EEG ve BBT ile desteklenerek serebral hadisenin nedeni ve epilepsi nobetlerinin tipleri ay1rt edilmi~ aralanndaki ili~ki ara~!lnlml~tlr.

Ara~t1rmaya tromboembolik nedenli iskemik inmeler, intraserebral ve subaraknoid kanamalar,lateralize bulgu vermeyen iskemik ataklar, ge(jici iskemik ataklar, arteriovenoz malformasyonu olan hastalar ahnm1~tlf. Epilepsinin diger nedenleri arasmdaki serebral ve sistemik hastahklar: Beyin tOmorleri ve buna bagl1 kanamalar, kafa travmalan, enfeksiyon kaynakh hastahklar, maling hipertansiyona bagh ansefalopatiler, nedeni bilinmeyen intraserebral ve subdural hematomlar, serebral postoperatif vakalar, sekonder serebral (toksik metabolik, endokrin, konjenital, dejeneratif7 bozukluklar hari9

tutulmu~tur. Bu hastalarda klinik muayene, EEG, BBT tetkikleri yap1im1~, baz1 hastalarda EEG ve BBT kontrol maksad1yla tekrartanm1~hr.

Bulgular

620 SVH'h hastadan 31'inde (%5) epilepsi nobetleri gozlenmi~tir. Bunlann 20 si erkek (%64.5), 11'i kadm (%35.5) hastadlf. Hasta ya~ ortalamas1 61 (30-91 ya~)'dir. Nobetler en fazla kanamalarda (intraserebral% 7.14, suubaraknoid

% 14b28) en az tromboembolik hastalarda (%2.74) goriilmO~tiir (Tablo 1).

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Hastallldarda Epilepsi NObetleri:KARAMAN, Yahya

T oplam Hasta SaytSI

364 182 28 42 4 620

Epilepsi GorOien Hasta Saytst

10 13 4 3

31

YOzde (%)

2.74 7.14 14.28 7.14 25.00 100

l..ftNwottArintn tipleri iginde en gok genaralize tonik-klonik nobetler gozlenmi~. basil parsiel nobel sadece 6

gllnilmii~ ancak daha sonraki nobetlerin bir ktsmt basil parsiel ba§langtglt sekonder generalize nobel §ekline g6riilmii§t0r (Tablo II).

degerlendirildiginde fokal anomalilerin gogunlugu te~kil ettigi (%61 ,29) tesbit edilmi~ olup, yaptltrken unilateral bOtOn belirtiler bu Stntfa dahil edilmi~tir (Tablo Ill).

Nobetlerinin Tipleri

Hasta Saytst YOzde(%)

6 19.36

3.22

8 25.81

13 41.95

2 6.44

atipik ve kombine nobel 3.22

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Serebrovaskuler Hastal!klarda Epilepsi NObetleri:KARAMAN, Yahya

Tablo Ill. Epilepsi Nobetlerinde EEG Bulgulan

EEG Bulgulan Hasta sayiSI YOzde (%)

Normal 3 9.68

Fokal Anomali 19 61.29

Generalize Anomali 7 22.58

Fokal ve Generalize Anomali 2 6.45

Toplam 31 100

EEG de fokal anomaliler ic;inde% 6.45 fokal diken,% 3'0nde fokal yava~ dalgalar g6r010rken% 38.7 hastada hem diken hemde yava~ dalgalar bir1ikte g6rOimO~tOr. Yaygm anomali gorOime s1khg1 ise% 22.58 olup EEG lerin% 12.9'unda yayg1n yava§ dalga, % 16.12'de yaygm diken ve yava§ dalgalar tesbit edilmi§tir.

EEG bulgulan BBT ile desteklenmi§tir. BBT de 13 hastada (% 41.95) lokal serebral infarkt EEG bulgulan gibi hadiselerin c;ogunlugunu lokal bulgulann te~kil ettigini gostermektedir (Tablo IV). lskemik belirtiler gosteren 5 hasta ile subaraknoid kanama belirtisi olan bir hastamn BBT si normal degerlendirilmi~tir.

TaboiiV.Epilepsi GorOien SVH h hastalarda BBT bulgulan BBT Ozelligi

Normal

Lokal Serebral lnfarkt Multipl infarkt

Hemorajik Lezyon ve Hematom Atrofi

Toplam

Hasta Say1s1

6 13 1 10

31

YOzde(%)

19.36 41.95 3.22 32.25 3.22 100

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serebral kanamalardaki epilepsilerin ~oklugu dikkati ~ekmi~tir. Ancak klinigimize ba~vuran hastalann tromboembolik hastalar te~kil etmi~tir(% 58.7). Daha onceden ge~ici iskemik atak hikayesi bulunan ve Wlll~i;ze bulgu veren bu infarktlar tromboembolik gruba ahnm1~t1r. Arteriovenoz malformasyon bulunan bir flalloroer atrofili 3 hasta aym bir grupta incelenmi~tir.

sadeCe komplet inmeli hastalarda epilepsi nobetlerini incelemi~ ve bu oram% 5 olarak bulmu~. Hauser(16) bu oram% 1.7 kanamalarda% 16.5 bulurken Faught (10) ve arkada~lan intraserebral kanamah 123 epllepSi nobeti bulunurken bunu % 13, Sung (30)% 7, Berger (3)% 18, Cocita (5) % 7 tesbit etmi~lerdir.

cok ara~t1rmada serebral kanamalrda epilepsi diger nedenlerden daha s1khkla gozlenmi~tir(8,9, 17 ,22).

en fazla kanamah hastalarda nobetler goruldu. Epilepsi nobetlerinin ~ogunlugunu generalize tipin kanamah hastalarda fokal karakterli nobetlerin s1khg1 tesbit edildi.

~ n6betleri Berger(3) % 68 hastada gorurken, Hauser (16)% 40, Daoniel (6) %52 nisbetinde mu~ahade

Sung (30) fokal motor nobetleri% 37, generalize nobetleri% 18 gorurken daha da degi~ik sonu~lar elde (10) basil parsiel nobetlerin Slkhgma deginmi~ ge~ donemde fokal karakterden genaralize nobel tipine

vurgulam1~t1r. Ancak Faught, Sung ve arkada~lan gibi bunu sadece kanamah hastalarda incelemi~lerdir.

en onemli husus; serebral infarkh hastalarda generalize nobeUer daha s1k gorGIOrken, kanamal1 hastalarda nobetler ag1rlik kazanmaktad1r (4,5,7,21 ,23,26,29,30).

serebral hadisenin uzerine epileptik nobetin karakteristik bulgulanmn eklenmesiyle kendini gosterir.

-.:IIVIArlt!Qri· daha ~ok olmak Ozere diken dalgalann yava~ keskin dalgalarla karakterize lezyonun !GrOne gore fokal bir bozukluk gosterir (1, 14, 18,22,23,24,28).· EEG epilepsi nobetinin tipi ile ilgili ozellik belirtir.

1'16betlerde bilateral diken ve keskin yava~ dalgalar olurken, fokal nobetlerde hadise olan yanda fokal

;tli diffOz degi~iklikler de olabilir (1 ,2, 11,12,21 ,25). Daniel (6) % 52 oramnda generalize nobel tesbit

% 70'inde diffuz yava~ dalgalar, % 30'unda fokal yava~ dalgalar i~ret etmi~tir. Faught(9, 1 0) ve - ... -~ •. hasta grubunda yapt1klan ara~t1rmada lezyonun yeri ve bOyOkiOgO ile epilepsi n6betleri arasmda s1k1 deginmi~lerdir. Faught serebrallober kanamalann s1k epileptojenik fokus olu~turduguna dikkat ~ekmi~

33'iJnde bunu tesbit ederken en fazla frontal bOige kanamalannm nobetlere sebep oldugunu bulmu~tur. ung

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Serebrovaskuler Hastaltklarda Epilepsi Nobetleri:KARAMAN, Yahya

Serebral bir lezyonun kaynag1, klinik lokalizasyonla uyumu, kesin bir te~his ve tedavide BBT den yararlamllr Daniel (6) klinik SVH ile % 84 hastada BBT bulgulann~n paralellik gosterdigini, iskemik lezyonlann daha sonraki BBT lerde

degi~tigini ve kayboldugunu gormO~!Or. Sung ve arkada~lan (3) kanamalarda epilepsiyi incelerken hastalann hepsinde BBT bozukluguna dikkat ~ekmi~. buyuk hematomlann kO~Ok ve multipl olanlardan daha ~ok epilepsiye sebep oldugunu

bulmu~lard1r. Faught (9) EEG yapmadan BBT bulgulanna gore k~uk kanamalann bilhassa Iober serebral sonra s1ras1yla bazal ganglionik ve talamik olanlarda s1k epilepsi yapabilecegini gostermi~tir. Pons ve yayg1n kanamalarda da status epileptikus ile mortalite oran1n1n Slklig~na dikkati qekmi~. Bu konudaki qall~malarda BBT bulgulan birbirine yakm ozellikler gostermektedir(B, 14,17,23,27 ,31 ).

Kaynaklar

1. Ajmone MC, Gumnit RB, Magnus 0: The Epilepsia. In Magnus 0, Haas ML (eds): Handbook of Clinical Neurology.

Vol 15, North-Holland Publishing. Amsterdam 1974, pp 486-495,720-740.

2. Barolin GS: The cerebrovascular epilepsia. J Clln Neurophysiology (Suppl) 35:287-295,1982.

3. Berger AR, Lipton RB, Lesser ML, Lantos G: Early seizures following intracerebral haemorrhage. Implication for theraphy. J Neurology 38:1363-1365,1988.

4. Cocito L, Favale E, Renni L: Epileptic seizures in cerebral arterila occlusive disease. J Stroke 14:305-306,1986.

5. Cocito L, Favale E, Renni L:The frequency, characteristic and prognosis of epileptic seizures at the onset of stroke. J Neural Neusurg Psychiatry 4:292,1989.

6. Daniele E, Tassinari CA, Mattaliona A, Natale E: Epileptic seizures and cerebrovascular disease. J Acta Neural Scand 80:17-22,1989.

7. De Carolis P, D'Aiessandro R, Ferrera A, Andredi A: Late seizures in patients with internal carotid and middle cerebral occlusive disease following ischeamic events. J Neural Neurosurg Psychiatry 47:1345-1347,1984.

8. Durury L, Whisnot JP, Garraway WD:Primary intracerebral haemorrhage; 1mpact of CT on incidence.J Neurology 34:653-657,1984.

9. Faught E, Peters D:Seizures in intracerebral haemorrhage. J Epllepsia 25:66,1984.

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Hastaflk/arda Epi/epsi Nobetleri:KARAMAN, Yahya

E. Peters

o ,

Bartolucci A, Muore L, Miller PC: Seizures after primery intracerebral haemorrhage. J 39:1089-1093,1989.

E: cerebral ischemia as a cause of epileptic seizures. In Loeb C (ed): Studies In Cerebrovascular -IWIIIQI"/1981 pp 121-140.

CM: Lacuner strokes and infarct; A rewiev.J Neurology 32:871-875,1982.

s .

Herishano YO: Frequency of epilepsy preceding stroke Lancet ii:393, 1987.

Stettner O, Luderwold A: Electroencephalography and computerized tomography in epilepsy diagnosis.

Eleetroencep 9:159-169,1978.

WK, Goldensohn ES: Clinical and electroencephalographic consideration in the diagnosis of carotid artery J Neuro/9:574,1979.

WA, Ramirez M: Risk for seizures and epileps following cerebrovascular insults. J Epilepsla 1985.

CS, Williams JP, Wyott PA, Mohr JP: Lobar intracerebra haematomas; Clinicad and CT analysis of 22 J Neurology 32:1146-1150,1982 .

Comas AJ, Osselton JW: Clinical Electroencephalography. Butterworths, London 1981, pp 149-161.

LP, Luders H, Dinner D$, Morris HH: Epileptic seizures due to trombotic and embolic cerebrovascular in older patients. J Epilepsia 26:622-630,1985.

S, Dowel F: Epileptic seizures in non embolic cerebral infarction. J Arc Neurol17:4184-4188, 1967.

K, Jenson LK, Plesner AM: Etiology of seizures in the erderly. J Epllepsia 27:454-463,1986.

JH, Binnie CD, Caul iD: Electroencephalographic signs employed in the location of ruptured

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Serebrovaskiiler Hastaliklarda Epilepsi NObetleri:KARAMAN, Y ahya

24. Niedermeyer E: The electroencephalography and vertebrobasiler artery insufficiency. J Neura/13:412, 1983.

25. Olsen TS, Hogenhavar H, Thage 0: Epilepsy after stroke. J Neural37:1209-1211, 1987.

26. Shinton RA, Gill JS, Melnick SC, Gunner KT: The frequency, characteristics and prognosis of epileptic seizures at the onset of stroke. J Neural Neurasurg Psychiatry 51:274-276,1988.

27. Shorvon SO, Gilliatt RW, Cox TC, Yu UYL: Evidence of vascular disease from CT scanning in late onset epilepsy. J Neural Neurasurgy Psychiatry 47:225-230,1984.

28. SolomonS: Evaluation of carotid artery compression in cerebrovascular disease an electroencephalographic clinical correlation J Arch Neural14:165-168, 1986.

29. Starkey LR: Epilepsy preceding stroke. Lancet i: 742-743,1987.

30. Sung CY, Chu NS: Epileptic seizures in intracerebral haemorrhage J Neural Neurasurg Psychiatry 52:1273-1276,1989.

31. Weisberg LA: Subcortical lobar intracerebral haemorrhage; Clinical computed tomographic correlation. J Neural Neurasurg Psychiatry 48:1078-1084,1985.

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