대 한 방 사 선 의 학 회 지 1992; 28 (4) : 631~638 Journal of Korean Radiological Society, July, 1992

Brain MRI Findings of Com plex Partial in Children

Jong Deok Kim, M.D., Dong Woo Park, M.D., Tchoong Kie Eun, M.D., Duck Hwan Chung, M.D., Tae Kyu Hwang, M.D. **

Department of Diagnostic Radiology. Col1ege of Medicine, Inje University

- Abstract-

Twenty-two children(4 months to 17 years old) with a clincial diagnosis of complex partial seizure(CPS) were examined with a 0.5T MRI scanner using spin-echo sequences. Eleven patients showed abnormal MRI findings; two had focallesions with corresponding seizure foci on the EEG, one arising from temporal lobe(Hippocampal Formation ) and the other from the frontallobe. Nine patients showed diffuse le­ sions with inconsistent seizure foci on EEG. The remaining 11 patients were normal on brain MRI; two of them had normal EEG findings and the others either focal or diffuse abnorma1ities on EEG. Index Words : Brain. abnormalities Brain, MR studies 10.1214 Children, Central Nerveous System

evaluate the frequency of mesial temporal INTRODUCTION sclerosis(MTS) as the most comon cause as has been reported. and to compare the site ofbrain le- Complex partial seizures(CPS) are considered sions on MRI with seizure foci on EEG. to be the most common human seizures and the most resitant to medical management. They usuaUy begin in the temporal lobe, but may MATERIALS AND METHODS originate from the frontal. parietal. and occipital areas_ The leading causes ofthese seizures in ear­ Twenty two children with clinical diagnosis of ly childhood are defects acquired during the CPS(8 males and 13 females, 4 months to 17 years course of development, hypoxic(ischemic­ 이 d) were examined with MRI during a 7 month­ hypotensive) insult. perinatal infections, metabolic period(January 1991 to July 1991). diseases, and tuberous sclerosis. Cerebral seizures MRI studies were performed on a 0.5T super­ are late results ofthese diseases and insults, which conducting unit(Toshiba MRT-50A) with multi­ often are of quite long standing(l-3). slice spin-echo sequences in all patients. The im­ The purpose of this article is intended to aging parameters were 400115/2(TR/TE/number demonstrate the causes of CPS in children and to of excitation) for Tl-weighted images and

* 본 논문 은 1991 년도 재단법인인제연구 장학재단의 연구비 보 조 에 의한 것임 . ** 인제대학교 의과대학 소아과학교 실 ** Department of Pediatrics, College of Medicine, Inje University 이 논문은 199 2 년 l 월 9 일 접수하여 1992 년 4 월 2 0 일 에 채택되 었음. Received January 9 , Accepted April 20, 1992

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3000/30, 120/1 for proton-density and T2-weighted Table 1. Age & 5ex Distribution images and the slice thickness was 5-8mm with an interslice gap of2mm. The quisition matrix was M F Total 256x256. Pre and postcontrast axial Tl-weighted 싫℃ ---A ‘q 3 images, axial proton-density and T2-weighted im­ - 1 A 5 ‘ 1 - 5 I ages, 밍ld precontrast sagittal Tl-weighted images qι Ai 6 5 - 10 ‘ were obtained in all patients. Coronal T2-weigted q nι 5 10 - 15 니 images were obtained additionally in temporal 14 q 3 15 - 18 ‘ lobe . Used contrast media was O.lmmol/kg of Gd-DTPA. The patients under 18 Total 8 14 22 month of age were undertaken inversion-recovery sequence on occasion with 1400/30-40/400 pal Formation atrophy; the only case oftemporal (TR/TE/Tl) . lobe epilepsy of our cases) (Fig. 1) and the other lesion was frontallobe astrocytoma(Fig. 2). Of 11 patients with normal MRI findings, two disclosed RESULTS normal EEG findings and others either focal or dif­ fuse abnormalities on EEG. MRI and EEG findings of CP5 in 22 children are summarized in Table 2 and 3 , respectively. The male to female ratio was 1:1.75(Table 1). Normal DISCUSSION and abnormal MRI findings were 50%(11 patients in each), respectively. Ofthe patients with abnor­ Epileptic seizures are broadly classified into two mal MRI findings, two patien ts(9 %) showed focal groups; primary generalized seizures, in which no lesions with corresponding seizure foci on EEG epileptogenic activity arising from a local and nine patients(41 %) showed diffuse lesions anatomic region can be identified, and partial with inconsistent seizure foci on EEG. One of two seizures, in which. an epileptic focus and often focallesions was temporallobe origin(Hippocam- focal brain disease can be found. The latter is sub-

~ 1' j \iW;~ - ... -...a..a. r. 1 2a 2b Fig. 1. 17-year-old girl who had seizure for six years. Hippocampal Formation(HF) atrophy. Precontrast coronal Tl WI shows decrease in size of left HF without abnormal 5 I. This was the only case of TLE in our 22 cases of CP5. Mesial temporal sharp waves were appeared on EEG Fig. 2. Five-year-old boy who had seizure for two rnonths. Right frontal lobe astrocytoma. grade II . Precontrast axial Tl WI(a) shows a well-defined. lobular low 51 in right frontal lobe of mid-convexity near the midline. It was not enhanced on Gd-DTPA scan(not shown). Axial T2WI(b) reveals a high 51 lesion without surrounding edema.

- 632- Jong Deok Kim , et al : 8rain MRI Findings of Complex Partial Seizure in Children divided into simple partial seizures, where con­ In our cases, two of 11 abnormal cases were sciousness is not impaired, and complex partial astrocytoma and Hippocampal Formation atrophy seizures with impairment of consciousness either as focal causes, and the remaining nine case were at the onset of seizure or at some time during the diffuse conditions; leukodystrophy( 1), tuberous seizure. The EEG in generalized seizures reveals sc!erosis(l), stenogyria or polymicrogyria with essentially simultaneous onset of epileptic gliosis( 1), communicating discharge in allleads, whereas in partial seizures with diffuse brain atrophy( 1), and the epileptic discharge begins in only some of the localized or diffused brain atrophy(4). leads and may or may not spread to the other MTS has been studied for a long time as the regions(I-3). most common cause of CPS, but there are a small Complex partial seizures(CPS) often, but not number of reports about the individual causes of always, start with motor arrest typically follwed this seizure. by oroalimentary automatism lasting less than Mesial temporal sc!erosis(MTS), hippocampal one minute, which in turn is followed by post-ictal sc!erosis, or Ammon’ s horn sc!erosis is the most confusion and amnesia. They are the most com­ common pathological alternation in the mesial mon type ofhuman seizures, representing 25% of temporallobe, in particular, hippocampus, of pa­ all seizures, and are refractory to medical treat­ tients with intractable CPS( 10-13). The incid눔 nce ment in half of the patients with this disorder. of MTSin temporal lobe specimens of patients They are one ofthe features found in temporallobe with CPS varies from 50% to 70% in several epilepsy(TLE) and most frequently arise within a studies(2,9 , 14-15) to as high as 79% in recent in­ temporallobe, but may originate from the frontal, vcstigation using positron emission tomography parietal. or occipital areas(2-7). (PET)( 16). Hippocampal sc!erosis in temporallobe The causes of CPS are divided into focal and dif­ epilepsy probably has several causes( 1 ,4-6,15,17). fuse(3); the former commonly consist of low-grade A major association is a history of prolonged ear­ gliomas, hamartomas, and arteriovenous malfor­ ly childhood febrile convulsions, and hippocam­ mations. Among the diffuse conditions involving pal sc!erosis is a constant finding in patients such temporolimbic structures, mesial temporal a history, in which there is macroscopic shrinkage sc!erosis(MTS) is most often associated with CPS. Other area oftissue change that might be primari­ Table 2. Brain MRI Finding of CPS in Children (n = 22) ly or secondarily associated with pathophysiologic 1. Focal (2) features of CPS are areas of cortical dysplasia, focal (a) Rt. frontal astrocytoma (1) , tuberous sc!erosis, and transient (b) Hippocampal Formation atrophy (1) brain edema associated with focal ictal events(4-5, 7-9). The leading causes ofCPS in early childhood 2. Diffuse (9) are defects acquired during the course of devlelop­ (a) Leukodystrophy (1) ment, hypoxic(ischemic-hypotensive) insult, (b) Tuberous sclerosis (1) (c) Stenogyria or polymicrogyria with WM perinatal infections, metabolic diseases, and gliosis (1) tuberous sc!erosis. Cerebral seizues are late results (d) Hypoxic-ischemic with of these diseases and insults, which often are of cerebral atrophy (or spongiform quite long standing. By the time seizures occur, cerebral atrophy) (1) the only demonstrable pathologic substrate may (e) Communicating hydrocephalus with dif­ be neuronalloss and glial scarring in the anterior fuse brain atrophy (1) hippocampus of the temporal lobe(“ mesial tem­ (1) Localized or diffuse brain atrophy (4) poral sclerosis‘’) which can be difficult to in­ 3. Normal (1 1) terpret(1) .

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of the hippocampus sometimes associated with Table 3. EEG Finding (n = 22) more extensive temporallobe atrophy(15.23). Hip­ u Focal abnormality in temporal area pocampal sclerosis is also found in patients with 3 Focal abnormality in frontal area temporallobe epilepsy who do not have a history 2 Multifocal abnormality of prolonged convulsions. and similar MRI 3 Diffuse abnormality 2 changes are observed in such patients(l5). No abnormality Microscopically. there is severe loss of pyramidal in the Spmmer sector(Hl) and the end f이 ium(H3-5) with relative sparing of H2. Addi­ pathological abnormality is usually much smaller tionally. and infrequently emphasized. is neuronal than the region of glucose hypometabolism. Jab­ loss and gliosis in the amygdala. which is found bari et al.(2) reported that MRI demonstrated a approximately 75% of patients. moreover such significatnly higher yield than did conventional amygdaloid changes virtually never occur in the CT(43% vs 26%) in patients with CPS. His data absence of hippocampal sclerosis(l5.18). It is as well as other data from the literature. suggested estimated that about 10% to 25% of all patient the specificity of MRI for detection of common and with temporallobe seizure associated with CPS surgically treatable causes of CPS(2. 8. 10. 23. may be surgical candidates(6.19). Surgery results 26-29). Gadopentatate dimeglumine dose not ap­ in cure or significant relief from CPS in about two pear to be routinely required in the MRI workup thirds of the appropriate candidates( 10% of the of patients with chronic partial seizures and that medically intractable population)(19-20). Relative­ it should be used selectively to clarify or better Iy few series analyse the results oftemporallobec­ delineate the nature of abnormalities encountered tomy in the pediatric age groups. but overall there on unenhanced images(27). is 60% or 80% surgical success rate in children There are basically two changes associated with with medically refractory temporal lobe TLE that are accessible to evaluation by MRI; seizures(6.21-22). Correct preoperative seizure unilateral atrophy of the hippocampal formation lateralization is of paramount importance to a (HF) and to alesser extent the anterior temporal sucessful surgical outcome and this may be done 10be(ATL) ipsilateral to the electrophysiologic by means of EEG. CT. MRI or PET. focus and increased signal intensity in medial tem­ EEG study was the most widely used methods poral parenchyma in T2-weighted sequences. Cor­ oflocating a seizure focus preoperatively. but this onal images performed parallel to the long axis of requires invasive measures involving. for exam­ the brainstem as shown on the midsagittal scout ple. the surgical implantation of subdural or in­ scan is reliably found to transect the long axis of tracere bral depth electrodes and carries the hippocampus at approximately 90 degrees. corresponding risks and is subject to technical er­ Tl-weighted sequences provide the high contrast rors. These dificulties with EEG studies have pro­ between CSF and brain that is necessary for defin­ mpted evaluations by CT. PET. and MRI ing anatomic detai!s (1 3. 30-31). Normally the two modalities to locate abnormalities responsible for temporal lobes are equal in size( 1). Cascino et seizure activity(23-26). Latack et al.(23) first com­ a l.(13) reported the sensitivity of MRI-based pared CT. MRI. and PI):T findings in 50 patients volume measurements of the HF in detecting the with partial seizures. The superiority of MRI over temporallobe of seizure origin was 93% in the pa­ CT was demonstrated convincingly. Additionally. tients with MTS. with 100% specificity. MTS. the the potential contribution of PET in this disorder leading cause ofTLE. did not produce MRI signal was first estab!ished. PET has shown focal regions abnormalitïes in the majority of cases. whereas of interictal hypometabolism in 60 to 70% of pa­ PET demonstrated a hypometabolic 하ea in the af­ tients with CPS even when CT was normal. The fected lobe in approximately half of these patients.

- 634- Jong Deok Kim , et al : 8rain MRI Findings of Complex Partial Seizure in Children

Fig. 3. Four-year-old girl who had suffered from seizure from birth. Leukodystrophy. Axial T2WIs(a.b) show patchy high 5Is in posterior periventricuar white matter sym­ metrically. 5he has two uncles with mental retardation.

a b

Fig 4. 5even-month-old female baby who had seizure for three months. Tuberous sclerosis. Axial T2WIs(a,b) show multiple tubers scattered over the cortical surface and subepcndymaJ nodules on the walls of lateral ventricle

a b

Fig. 5. ll-year-old girl who had suffered from seizure from six month of age. Hypoxic-ischemic encephalopathy. Precontrast axial(a) and sagittal(b) T 1WIs show diffuse decrease in 51 in both cerebral hemispheres ex­ cluding left posterior parietal and ocipital region, basal ganglia, and cerebellum, and hydrocephalus. 5he was dagnoscd as Reye syn­ drome in 6 month of age at other hospitaJ and since then she has suf­ fered from epilepsy. left hemiplegia, mental retardation, a b delayed development, and visual distruance.

The high-signal areas are nonspecific, and their ex­ and Berkovic et al. (1 5) reported that the MRI act nature cannot be established (low-grade criteria of hippocampal sclerosis were an increas­ glioma. postraumatic scar. hamartomaJ, with the ed T2-weighted signal and the signal’s confine­ exception of arteriovenous malformations, which ment to a unilaterally small hippocampus. are characterized by thier effects of f1 0w and Triulzi et al. (33) reported 31 patients (1 2-69 paramagnetic substances (i.e. ‘ m ethemoglobin) on years ofage , 13 m외 es ， 18 females) with nonrefrac­ signal intensity (1 3 .27.32). But. Jackson e t a l.(1 1) tory TLE (TLE of mild to moderate severity, well

- 635 Journal of Korean Radiological Society 1992 ; 28(4):631 ""638 controlled by pharmacotherapy) with negative fin­ ding seizure foci on EEG. MTS, although the most dings at CT; MRI findings disclosed significant fin­ common cause of CPS it is, was found in only one dings in 16 patients with 9 medial temporal case of 22 chirdren with CPS. abnormalities (8: hyperintense lesion in anterior The paucity of TLE in our cases seems due to part of hippocampus without size abnormalities, small number of patients in short period of the 1 :HF atrophy), 2 basitemporal abnorrnalities, and study. We are looking forward to reporting the MRI 5 no temporal lobe abnormalities but multiple findings of TLE. hyperintense, focallesions in frontoparietal white matter without .medial temporal abnormalities. REFERENCES Correlating these focal white matter lesions with TLE appears diffcult; epilepsy may occur after 1. Huk WJ. Temporallobe epilepsy. In: Central ner­ ischemic brain damage, paticularly because of the vous system diseases. Huk WJ., Gademann G, unusual susceptibility to hypoxia ofportions ofthe Friedmann G . Berlin: Springer-Verlag, HF and th uniquely low seizure threshold of this 1990;225-228 region. 15 were normal. The nonrefractory TLE 2. Jabbari B, Gunderson CH, Wipp이 d F, et al in his patients was well controlled by phar­ Magnetic resonance imaging in partial complex macotherapy and did not require surgical therapy; epilepsy. Arch Neurol 1986;43:869-872 thus, pathologic controls were not feasible. 3. Farmer TW, Greenwood RS. Paroxysmal In one series of 100 patients with CPS studied disorders. ln: Farmer TW, ed. Pediatric with both MRI and CT. MRI was abnorrnal in 45 %, neurology. 3rd ed. Philadelphia: Harper & Row, showing focal changes in 34%(34), and in 1984:205-263 Theodore’s 36 refractory CPS patients MRI reveal­ 4. Ormson MJ, Kispert DB, Sharbrough FW. Cryp­ ed abnormal in 21 patients and normal in 15 pa­ tic sturctural1esions in refractory partial epilep­ tients( lO). sy: MR imaging and CT studies. Rad 1986; Of our 22 patients with CPS, 11 patients(50%) 160:215-219 revealed normal- and 11 patients(50%) abnormal 5. Brooks BS, King DW , Gammal TE, et a l. MR im­ MRI findings. Focallesions were showing in only aging in patients with intractable complex par­ two patients(9.1 %); one HF atrophy, the other tial epileptic seizure. AJR 1990; 154:93-99 frontallobe astrocytoma, and they had coπespon­ 6. Meyer FB, Marsh R, Laws E Jr, et a l. Temporal ding seizure foci on EEG. Remaining nine patients lobectomy in children with epilepsy. J Neurosurg showed diffuse brain lesions including 1986;64:371-37-6 leukodystrophy(Fig. 3), tuberous sclerosis(Fig. 4 ), 7. Tampier D, Moumdjian R, Melanson D, et a l. ln­ stenogyria or polymicrogyria with white matter tracerebral gangliogliomas in patients with par­ gliosis, hypoxic-ischemic encephalopathy with tial complex seizures: CT and MR imaging cerebral atrophy(Fig. 5), communicating hydro­ findings. AJR. 1991:843-849 cephalus with diffuse brain atrophy(post­ 8. Sperling MR , Wilson G , Engel J Jr, et a l. encephalitic), and only localized or diffuse brain Magnetic resonance imaging in intractable patial atrophy. These lesions did not correspond to epilepsy: Correlative studies. Ann Neurolol 1986; seizure foci on EEG. Two of 11 patients with nor­ 20:57-62 mal MRI findings had normal EEG findings and 9. Kuzneicky R. Garcia JH, Faught E, et al. Cortical remaining nine patients revealed focal or diffuse dysplasia in temporal lobe epilepsy: magnetic abnormalities on EEG. resonance imaging correlations. Ann neurol In conclusion, we observed that one half of 22 1991 ;29:293-298 patients with CPS showed normal MRI findings 10. Theodore WH , Dorwart R, Holmes M, et al. and that only focallesions revealed the correspon- Neuroimaging in refractory partial seizures: com-

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parison of PET. CT. and MRI. Neurology 1986; epilepsy during childhood. Br Med J 1972;2: 20:57-62 631-635 1 1. Jackson GD. Berkovic SF. Tress BM. et a l. Hip­ 23. Latack JT. Abou-Khalil BW. Siegel GJ. et a l. Pa­ pocampal sclerosis can be reliably detected by tients with partial seizures: evaluation by MR. magnetic resonance imaging. Neurology 1990; CT. and PET imaging. Rad 1986;159:159-163 40:1869-1875 24. Blom RJ. Vinuela F. Fox AJ. et a l. Computed 12. Kuzneicky R. Sayette Vdl, Ethier R. et al. tomography in temporallobe epilepsy. J Com­ Magnetic resonance imaging in temporal lobe put Assit Tomogra 1984;8:401-405 epilepsy;pathological correlations. Ann Neurol 25. Spencer SS. Spencer DD. Williamson PD. et a l. 1987;22:341-347 The localizing value of depth elec­ 13. Cascino GD. Jack CR. Parisi JE. et a l. Magnetic troencephalography in 32 patients with refrac­ resonance imaging-based volume studies in tem­ tory epilepsy. Ann Neurol 1982; 12:248-253 porallobe epilepsy: pathologic correlations. Ann 26. Laster DW. Penry JK. Moody DM. et al. Chronic Neurol 1991:30:31-36 seizure disorder: contribution of MR imaging 14. Mathieson G. Pathology oftemporallobe foci. ln: when CT is normal. AJNR 1985; 6:177-180 Penry JK. Dalay DD. eds. Complex partial 27. Elster AD. Mirsa W. MR imaging in chronic par­ seizures and their treatment. New York: Raven tial epilepsy: role of contrast enhancement. AJR press. 1975:165-183 1991; 156:605-610 15. Berkovic SF. Andermann F. Olivier A. et a l. Hip­ 28. Sperling MR. Wilson C. Engel J Jr. et a l. pocampal sclerosis in temporal lobe epilepsy Magnetic resonance imaging in intractable par­ demonstrated by MRI. Ann Neurol 1991:29: tial epilepsy: correlative studies. Ann Neurol 175-182 1986: 20:57-62 16. Engel J. Brown WJ. Kuhi DE. et a l. Pathological 29. Brooks BS. King DW. El Gammal T. et a l. MR findings underlying focal temporal lobe imaging in patinets with intractable complex metabolism in partial epilepsy. Ann Neuro11982: partial epileptic seizures. AJNR 1990; 11:93-99 12:518-528 30. Jack CR J R. Sharbrough F.W. Twomey CK. et 17. Sagar HJ. Oxbury JM. Hippocampal loss al. Temporal lobe seizures: lateralization with in temporallobe epilepsy: correlation with ear­ MR volume measurements of the hippocampal Iy childhood convulsions. Ann Neurol 1987;22: formation. Rad 1990; 175:423-429 334-340 3 1. Jack CR Jr. Gehring DG. Sharbrough FW. et al. 18. Bruton CJ. The neuropathology oftemporallobe Temporal lobe volume measurement from MR epilepsy. Oxford: Oxford university press. images: accuracy and left-right asymmetry in 1988;1-158 normal person. J Comput Assit Tomogra 1988; 19. Glaser GH. Treatment of intractable temporal 12:21-29 lobe-limbic epilepsy(complex partial seizures) 32. Cascino GD. Hirschorn KA. Jack CJ. et a l. by temporal lobectomy. Ann Neurol 1980; Gadolinium-DTPA-enhanced magnetic 8 :455-459 resonance imaging in intractable partial epilep­

20. Crandal PM. Cahan LD. Sutherling W ‘ et a l. sy. Neurology 1989; 39:1115-1118 Surgery or intractable partial complex epilepsy. 33. Triulzi F. Franceschi M. Fazio F. Nonrefractory In: Porter RJ. Morselli PL. eds. The . temporallobe epilepsy: 1. 5-T MR imaging. Rad Stoneham: Butterworth. 1985:307-321 1988; 166;181-185 2 1. Davidson S. Falconer MA . Outcome of surgery 34. Riela AV. Penry J K. Laster DW. et a l. Magnetic in 40 children in temporallobe epilepsy. Lancet resonance imaging versus computerized cranial 1975; 1: 1260-1263 tomography in complex partial seizures. Epilep­ 22. Falconrer MA. Place of surgery for temporallobe sia 1984; 25:650

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〈국문 요약〉 소아 복잡성(초점성) 부분간질의 뇌자기공명영상소견

인제대학교 의과대학 진단방사선과학교실， 소아과학교실*

김종덕 • 박동우 • 은충기 • 정덕환 • 황태규*

복잡성 혹은 초점성 부분간질은 모든 간질의 25%를 차지하는 가장 흔한 간질의 형태로 반수 정도에서 약물로 치료되지 않으며 ， 뇌측두엽에서 발생하는 경우가 많다. 약물로 치료되지 않는 간질환자에서 과거에는 뇌파검사에 의존하여 간질의 초점을 수술로 제거했으나， 뇌자기공명영상상 나타나는 국소성명변은 수술전 간질초점의 확인과 아울러 술자에게 큰 도움을 주며 ， 술후의 효과도 훨씬 좋음이 발표되고 있다. 소아에서 이 간질의 원인으로는 발달과정에서 발생하는 후천적 결함， 저산소증 혹은 괴사성 -저혈압성 손상， 분만시 의 감염， 대사성 질환， 결절성뇌경화증 등이 있다. 우리나라 소아에서 복잡성 부분간질 때에 나타날 수 있는 뇌자기공명영상의 소견을 알아보고1 또 뇌파소견상의 간질의 초점과 뇌자기공명영상소견을 비교해 보고자 하였다.

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