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 Seizure 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 brain MRI findings; two had focallesions with corresponding seizure foci on the EEG, one arising from temporal lobe(Hippocampal Formation atrophy) 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 Seizures 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 재단법인 인제연구 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 - 631- Journal of Korean Radi 이 ogical Society 1992 ; 28(4):631 ~638 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 epilepsy. 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 white matter gliosis( 1), communicating discharge in allleads, whereas in partial seizures hydrocephalus 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) encephalitis, 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 encephalopathy 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) . - 633- Journal of Korean Radiological Society 1992 ; 28(4):631 ~638 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 neurons in the Spmmer sector(Hl) and the end f이 ium(H3-5) with relative sparing of H2.