- Email: [email protected]
MRI lesions masked by brain development: a case of infant-onset focal epilepsy
MRI Lesions Masked by Brain Development: A Case of Infant-Onset Focal Epilepsy Junichi Furusho, MD, PhD*†, Toshinori Kato, MD, PhD†‡, Izumi Tazaki, MD, PhD*†, Yoji Iikura, MD, PhD†, and Seiji Takita, MD, PhD† A 3-month-old male presented with right-side– dominant focal seizures. Focal spikes were observed on the left side of an electroencephalogram obtained at the time of onset. The immature development in the left middle temporal lobe was observed by initial magnetic resonance imaging (MRI). The hypoperfusion in the left temporal lobe observed with single-photon computed tomography was consistent with MRI findings. These MRI findings were not observed in a second MRI at 11 months of age. This observation may explain one of the causes of infant-onset focal epilepsy. © 1998 by Elsevier Science Inc. All rights reserved.
reported to be evident in about 8.4% of all epilepsy patients [8]. It is not rare for pediatric patients to be observed without any abnormal findings on MRI at the onset of TLE [9-11]. The authors describe a 2-month preterm infant whose temporal lesions disappeared in the serial MRI. Case Report A 3-month-old male was brought to the outpatient clinic with a chief complaint of convulsions. He was a second twin and had been delivered at 33 weeks 3 days gestation (2 months preterm), with a birth weight of 2,354 gm, but neurologic abnormalities, such as neonatal asphyxia, were absent. The first twin had died before birth at 29 weeks gestation. This child experienced seizures several times daily, and the frequency gradually increased. The patient was admitted to the hospital for detailed examination and treatment. The results of blood biochemistry and cerebrospinal fluid tests were normal at the time of admission. No abnormalities were noted on interictal electroencephalogram (EEG). A simultaneous video EEG recording (Fig 1) at the time of seizure was performed. His seizures began with rolling up of both eyeballs, followed by twitching in the face, bending of the left upper extremity, and intermittent seizures involving the right upper extremity. EEG exhibited continuous spikes on the left side, particularly in the middle temporal area, with the background activity on the right side maintained, revealing a marked difference between the left and right sides. In light of these findings, focal epilepsy was diagnosed, and administration of carbamazepine was begun. Two days later, seizures were fully controlled by this treatment.
Results
Magnetic resonance imaging (MRI) studies of temporal lobe epilepsy (TLE) have been thoroughly evaluated using hippocampal volumetric studies, conventional MRI, and the new MRI pulse sequence [1-4]. Mesial temporal sclerosis is one of major origins of TLE and the syndrome is known to be intractable [5-7]. In children, TLE is
MRI findings at the time of admission were as follows. The coronal T1-weighted image (Fig 2A), illustrating the sylvian fissure, revealed clear formation of the corticospinal tract, and myelination appeared to be at the level of 1 month gestation. The left sylvian fissure, however, was markedly dilated in comparison with that on the right, and the left temporal lobe was markedly smaller than that of the contralateral side. The hyperplasia of the cortex and the ectopic gray matter were not observed in the coronal T2-weighted image (Fig 2B). The coronal single-photon computed tomography (SPECT) imaging (Fig 2C), obtained using technetium-99m-labeled hexamethylpropyleneamine oxime during intervals between convulsions 2 weeks after the start of carbamazepine administration, exhibited an area of hypoperfusion in the left temporal lobe corresponding to the region revealed by MRI. In the follow-up MRI at 11 months of age the improvement in the previous abnormal MRI findings was dra-
From the *Department of Pediatrics; Showa General Hospital; Kodaira City; †Department of Pediatrics; Showa University School of Medicine; Shinagawa-Ku, Tokyo, Japan; and ‡Department of Radiology; Center for Magnetic Resonance Research; University of Minnesota Medical School; Minneapolis, Minnesota.
Communications should be addressed to: Dr. Kato; Center for Magnetic Resonance Research; University of Minnesota Medical School; 385 East River Road; Minneapolis, MN 55455. Received January 6, 1998; accepted May 21, 1998.
Furusho J, Kato T, Tazaki I, Iikura Y, Takita S. MRI lesions masked by brain development: A case of infantonset focal epilepsy. Pediatr Neurol 1998;19:377-381.
Introduction
© 1998 by Elsevier Science Inc. All rights reserved. PII S0887-8994(98)00066-6 ● 0887-8994/98/$19.00
Furusho et al: Masked MRI Lesions 377
Figure 1. Simultaneous video electroencephalogram (EEG) recording during a seizure. EEG exhibited continuous spikes on the left side, particularly in the middle temporal area.
matic. Figure 3A depicts coronal T1-weighted images. The dilatation of the sylvian fissure and differences between the left and right temporal lobes, noted at the time of admission, had improved. Figure 3B depicts coronal T2weighted images. The dilatation of the sylvian fissure is no longer conspicuous. Myelination depicted on the MRI obtained at 9 months gestation was normal without differences between the left and right sides, and there were no findings of abnormalities in cortical formation. Although a follow-up SPECT scan was not performed at 11 months of age, the follow-up EEG was normal. This patient experienced focal motor seizures again at the time of a febrile illness at 2 years of age. The dose of carbamazepine was increased, and the subsequent course has been monitored. To date, no abnormalities have been evident in either mental or motor development. MRI findings were normal at 2 years and 4 years of age. Finally, the developmental disappearance of MRI lesions was proved by serial MRI. However, these SPECT images exhibited an area of slight hypoperfusion in the left temporal lobe at 4 years of age (Fig 3C), and follow-up EEG revealed abnormal focal spikes at the right temporoparietal lobes at 4 years of age. In the serial MRI, EEG, and SPECT, MRI lesions were masked by brain development, and EEG examinations were not consistent with the initial MRI lesions. However, in this case of infant-onset focal epilepsy the abnormal findings with SPECT images did not change with brain development. Discussion The serial MRI in the infant-onset focal seizure confirmed the disappearance of abnormal findings with brain development. The focal delayed development might be
378
PEDIATRIC NEUROLOGY
Vol. 19 No. 5
caused by hypoplastic lesions in the left temporal lobe from perinatal focal hypoxic changes or a microscopic cortical dysplasia that could not be detected by MRI. Because the human cortex usually thickens with brain development, cortical dysplasia might be more visible with development. In this patient the hypoplastic lesions in the middle temporal lobe might be surrounded by the developed superior temporal lobe and the inferior temporal lobe in the second MRI study. This case suggests that the early abnormal MRI lesions become less sensitive with brain development. This observation is consistent with a previous report that positive epileptiform discharges in children with neuronal migration disorders may signal a more dysfunctional cortex, leading to a focal neurologic deficit or a more extended lesion than is detected on MRI [11]. It is difficult to visualize a small cortical dysplasia and cortical damage without high-signal intensity on T2-weighted images and heavily T2-weighted fluid attenuated inversion recovery (FLAIR) images [4]. The unexpected partial catch-up in growth of the affected hemisphere (left sylvian areas) was a very interesting observation. Although it is well known that reversible brain atrophy is usually observed with adrenocorticotropic hormone therapy in West syndrome [12], such partial unexpected development has not been reported previously. Therefore the authors could not explain this result from any basic evidence. One of the possible explanations is the different cerebrospinal fluid (CSF) pressures between the left and right hemispheres. The CSF pressure in the affected hemisphere may be lower than the contralateral hemisphere because there is more space between cerebral tissue and bone in the affected hemisphere. Therefore the volume of the left hemisphere quickly expanded and grew. After the ventricle-peritoneal shunt operation for hydrocephalus, expansion of bilateral hemispheres can be observed. Common temporal lobe lesions in patients with epilepsy include mesial temporal lobe sclerosis; abnormal cortical formation, anomalies, such as angioma, and tumorous lesions based on malformation have also been reported [1-4,6]. Unlike these reports, however, the temporary marked volume difference between the left and right lobes was observed in this patient in early infancy, suggesting that the difference between the left and right lobes was attributable to events in the fetal and perinatal periods and not the result of epilepsy. Many patients with intractable TLE who undergo epilepsy surgery are found to have cortical dysgenesis in the epileptic regions, often despite a normal MRI [2,5,9]. In the present case the abnormal MRI lesions may be masked by the partial volume effect with brain development rather than have disappeared. Because neonatal and infantile brains include more rich water than adult brains, T1- and T2-weighted values of brain tissue reveals much longer tissue than in adults [13]. The small destructive lesions of the primitive myelinating areas or around the ventricular trigone could be depicted using short- and long-echo time fast FLAIR sequences
Figure 2. Magnetic resonance imaging (MRI) and single-photon computed tomography (SPECT) images at 3 months of age. (A) Coronal T1-weighted image (TR: 500 ms, TE: 19 ms). The left sylvian fissure is markedly dilated compared with that on the right, and the left temporal lobe is obviously smaller than that of the contralateral side. In the central semiovale, bilateral myelination is not different. (B) Coronal T2-weighted image (TR: 3,500 ms, TE: 102 ms). There were no lesions with T2 elongation. The left suprasylvian area also revealed the immature development observed in the cerebral hemispheal volume. (C) Coronal SPECT images obtained using technetium-99m-labeled hexamethylpropyleneamine oxime. These images exhibit an area of hypoperfusion in the left temporal lobe corresponding to the abnormal region revealed by MRI. However, the cerebral perfusion in the left suprasylvian area was normal.
[14]. In conventional spin echo sequences, for example, it was difficult to differentiate between small periventricular lesions and normal persistent areas of long T2-weighted relaxation times, which were seen superior and dorsal to the ventricular trigone in all neonates and infants. Therefore, in infant-onset focal epilepsy, scheduled examinations are necessary, even after obtaining normal findings on MRI during the stages of early brain development. Although in this case MRI with FLAIR sequences were not performed, the necessity of performing such sequences should be emphasized. In the serial MRI [2] and EEG [16], similar to those in previous reports, the results were not consistent with the
initial MRI lesions. Surprisingly, follow-up SPECT images revealed the persistent abnormal findings in the left hemisphere, although the hypoperfusion in the temporal lobe with infants may be misread easily as a false-positive finding. Perfusion imaging techniques, including SPECT, might be very useful in diagnosis and treatment planning. In addition, functional MRI recently has been developed as a powerful noninvasive research tool for studying human hippocampal long-term sustained response during memory processing [17]. Functional MRI should be applied to cases such as this one for the detection of the physiologic hippocampal changes and the abnormalities of temporal lobe function.
Furusho et al: Masked MRI Lesions 379
Figure 3. Follow-up MRI at 11 months and SPECT at 4 years of age. (A) Coronal T1-weighted image (TR: 500 ms, TE: 19 ms). (B) Coronal T2-weighted image (TR: 3,500 ms, TE: 102 ms). The abnormal MRI findings (dilatation of the sylvian fissure and the differences between the left and right temporal lobes) at 3 months of age at the time of admission had obviously improved. (C) Follow-up coronal SPECT images obtained using technetium-99m-labeled hexamethylpropyleneamine oxime at 4 years of age. MRI findings were normal at 2 and 4 years of age. However, these SPECT images exhibit similar hypoperfusion in the left temporal lobe as was observed in the MRI at 3 months of age.
The authors thank Dr. Yasuto Sasaki for technical support, Dr. Kazunobu Fujita for detail editing, and Drs. Takashi Endo, Kumi Oto, and Akinobu Iwasaki for their clinical discussion.
References [1] Jackson GD, Berkovic SF, Tress BM, Kalnis RM, Fabinyi GCA, Bladin PF. Hippocampal sclerosis can be reliably detected by magnetic resonance imaging. Neurology 1990;40:1869-75. [2] Kuzniecky R, Garcia JH, Faught E, Morawetz RB. Cortical dysplasia in temporal lobe epilepsy: Magnetic resonance imaging correlations. Ann Neurol 1991;29:293-8. [3] Bergin PS, Fish DR, Shorvon SD, Oatridge A, de Souza NM, Bydder GM. Magnetic resonance imaging in partial epilepsy: Additional abnormalities shown with the fluid attenuated inversion recovery (FLAIR) pulse sequence. J Neurol Neurosurg Psychiatry 1995;58:439-43. [4] Kato T, Yamanouchi H, Sugai K, Takashima S. Improved detection of cortical and subcortical tubers in tuberous sclerosis by
380
PEDIATRIC NEUROLOGY
Vol. 19 No. 5
fluid-attenuated inversion recovery MRI. Neuroradiology 1997;39:37880. [5] Engel J Jr. Update on surgical treatment of the epilepsies: Summary of the second international Palm Desert conference on the surgical treatment of the epilepsies. Neurology 1993;43:1612-8. [6] Gloor P. Mesial temporal sclerosis: Historical background and an overview from a modern perspective. In: Luders H, ed. Epilepsy surgery. New York: Raven Press, 1991;689-703. [7] Sagar HJ, Oxbury JM. Hippocampal neuron loss in temporal lobe epilepsy: Correlation with early childhood convulsions. Ann Neurol 1987;22:334-40. [8] Aso K, Watanabe K, Maeda N, Negoro T, Miura T. Temporal lobe epilepsy of childhood onset. Jpn J Psychiatry Neurol 1994;48:21720. [9] Harbord MG, Manson JI. Temporal lobe epilepsy in childhood: Reappraisal of etiology and outcome. Pediatr Neurol 1987;3:263-8. [10] Cendes F, Anderman E, Dubeau F, et al. Early childhood prolonged febrile convulsion, atrophy and sclerosis of mesial structures, and temporal lobe epilepsy. Neurology 1993;43:1083-7.
[11] Otsubo H, Steinlin M, Hwang PA, et al. Positive epileptiform discharges in children with neuronal migration disorders. Pediatr Neurol 1997;16:23-31. [12] Konishi Y, Yasujima M, Kuriyama M, et al. Magnetic resonance imaging in infantile spasms: Effects of hormonal therapy. Epilepsia 1992;33:304-9. [13] Holland BA, Haas DK, Norman D, Brant-Zawadzki M, Newton TH. MRI of normal brain maturation. Am J Neuroradiol 1986;7:201-8. [14] Kato T, Sasaki Y, Oto K, et al. Advantage of short/long echo
fast FLAIR in the neonatal and infant brain. Proc Soc Magn Reson Med 1995;2:1281. [15] Quirk JA, Kendall B, Kingsley DPE, Boyd SG, Pitt MC. EEG features of cortical dysplasia in children. Neuropediatrics 1993;24:193-9. [16] Kato T, Okuyama K. Assessment of maturation and impairment of the brain by I-123 iodoamphetamine SPECT and MR imaging in children. Showa Univ J Med Sci 1993;5:99-114. [17] Kato T, Erhard P, Takayama Y, et al. Human hippocampal long-term sustained response during word memory processing. Neuroreport 1998;9:1041-47.
Furusho et al: Masked MRI Lesions 381
reported to be evident in about 8.4% of all epilepsy patients [8]. It is not rare for pediatric patients to be observed without any abnormal findings on MRI at the onset of TLE [9-11]. The authors describe a 2-month preterm infant whose temporal lesions disappeared in the serial MRI. Case Report A 3-month-old male was brought to the outpatient clinic with a chief complaint of convulsions. He was a second twin and had been delivered at 33 weeks 3 days gestation (2 months preterm), with a birth weight of 2,354 gm, but neurologic abnormalities, such as neonatal asphyxia, were absent. The first twin had died before birth at 29 weeks gestation. This child experienced seizures several times daily, and the frequency gradually increased. The patient was admitted to the hospital for detailed examination and treatment. The results of blood biochemistry and cerebrospinal fluid tests were normal at the time of admission. No abnormalities were noted on interictal electroencephalogram (EEG). A simultaneous video EEG recording (Fig 1) at the time of seizure was performed. His seizures began with rolling up of both eyeballs, followed by twitching in the face, bending of the left upper extremity, and intermittent seizures involving the right upper extremity. EEG exhibited continuous spikes on the left side, particularly in the middle temporal area, with the background activity on the right side maintained, revealing a marked difference between the left and right sides. In light of these findings, focal epilepsy was diagnosed, and administration of carbamazepine was begun. Two days later, seizures were fully controlled by this treatment.
Results
Magnetic resonance imaging (MRI) studies of temporal lobe epilepsy (TLE) have been thoroughly evaluated using hippocampal volumetric studies, conventional MRI, and the new MRI pulse sequence [1-4]. Mesial temporal sclerosis is one of major origins of TLE and the syndrome is known to be intractable [5-7]. In children, TLE is
MRI findings at the time of admission were as follows. The coronal T1-weighted image (Fig 2A), illustrating the sylvian fissure, revealed clear formation of the corticospinal tract, and myelination appeared to be at the level of 1 month gestation. The left sylvian fissure, however, was markedly dilated in comparison with that on the right, and the left temporal lobe was markedly smaller than that of the contralateral side. The hyperplasia of the cortex and the ectopic gray matter were not observed in the coronal T2-weighted image (Fig 2B). The coronal single-photon computed tomography (SPECT) imaging (Fig 2C), obtained using technetium-99m-labeled hexamethylpropyleneamine oxime during intervals between convulsions 2 weeks after the start of carbamazepine administration, exhibited an area of hypoperfusion in the left temporal lobe corresponding to the region revealed by MRI. In the follow-up MRI at 11 months of age the improvement in the previous abnormal MRI findings was dra-
From the *Department of Pediatrics; Showa General Hospital; Kodaira City; †Department of Pediatrics; Showa University School of Medicine; Shinagawa-Ku, Tokyo, Japan; and ‡Department of Radiology; Center for Magnetic Resonance Research; University of Minnesota Medical School; Minneapolis, Minnesota.
Communications should be addressed to: Dr. Kato; Center for Magnetic Resonance Research; University of Minnesota Medical School; 385 East River Road; Minneapolis, MN 55455. Received January 6, 1998; accepted May 21, 1998.
Furusho J, Kato T, Tazaki I, Iikura Y, Takita S. MRI lesions masked by brain development: A case of infantonset focal epilepsy. Pediatr Neurol 1998;19:377-381.
Introduction
© 1998 by Elsevier Science Inc. All rights reserved. PII S0887-8994(98)00066-6 ● 0887-8994/98/$19.00
Furusho et al: Masked MRI Lesions 377
Figure 1. Simultaneous video electroencephalogram (EEG) recording during a seizure. EEG exhibited continuous spikes on the left side, particularly in the middle temporal area.
matic. Figure 3A depicts coronal T1-weighted images. The dilatation of the sylvian fissure and differences between the left and right temporal lobes, noted at the time of admission, had improved. Figure 3B depicts coronal T2weighted images. The dilatation of the sylvian fissure is no longer conspicuous. Myelination depicted on the MRI obtained at 9 months gestation was normal without differences between the left and right sides, and there were no findings of abnormalities in cortical formation. Although a follow-up SPECT scan was not performed at 11 months of age, the follow-up EEG was normal. This patient experienced focal motor seizures again at the time of a febrile illness at 2 years of age. The dose of carbamazepine was increased, and the subsequent course has been monitored. To date, no abnormalities have been evident in either mental or motor development. MRI findings were normal at 2 years and 4 years of age. Finally, the developmental disappearance of MRI lesions was proved by serial MRI. However, these SPECT images exhibited an area of slight hypoperfusion in the left temporal lobe at 4 years of age (Fig 3C), and follow-up EEG revealed abnormal focal spikes at the right temporoparietal lobes at 4 years of age. In the serial MRI, EEG, and SPECT, MRI lesions were masked by brain development, and EEG examinations were not consistent with the initial MRI lesions. However, in this case of infant-onset focal epilepsy the abnormal findings with SPECT images did not change with brain development. Discussion The serial MRI in the infant-onset focal seizure confirmed the disappearance of abnormal findings with brain development. The focal delayed development might be
378
PEDIATRIC NEUROLOGY
Vol. 19 No. 5
caused by hypoplastic lesions in the left temporal lobe from perinatal focal hypoxic changes or a microscopic cortical dysplasia that could not be detected by MRI. Because the human cortex usually thickens with brain development, cortical dysplasia might be more visible with development. In this patient the hypoplastic lesions in the middle temporal lobe might be surrounded by the developed superior temporal lobe and the inferior temporal lobe in the second MRI study. This case suggests that the early abnormal MRI lesions become less sensitive with brain development. This observation is consistent with a previous report that positive epileptiform discharges in children with neuronal migration disorders may signal a more dysfunctional cortex, leading to a focal neurologic deficit or a more extended lesion than is detected on MRI [11]. It is difficult to visualize a small cortical dysplasia and cortical damage without high-signal intensity on T2-weighted images and heavily T2-weighted fluid attenuated inversion recovery (FLAIR) images [4]. The unexpected partial catch-up in growth of the affected hemisphere (left sylvian areas) was a very interesting observation. Although it is well known that reversible brain atrophy is usually observed with adrenocorticotropic hormone therapy in West syndrome [12], such partial unexpected development has not been reported previously. Therefore the authors could not explain this result from any basic evidence. One of the possible explanations is the different cerebrospinal fluid (CSF) pressures between the left and right hemispheres. The CSF pressure in the affected hemisphere may be lower than the contralateral hemisphere because there is more space between cerebral tissue and bone in the affected hemisphere. Therefore the volume of the left hemisphere quickly expanded and grew. After the ventricle-peritoneal shunt operation for hydrocephalus, expansion of bilateral hemispheres can be observed. Common temporal lobe lesions in patients with epilepsy include mesial temporal lobe sclerosis; abnormal cortical formation, anomalies, such as angioma, and tumorous lesions based on malformation have also been reported [1-4,6]. Unlike these reports, however, the temporary marked volume difference between the left and right lobes was observed in this patient in early infancy, suggesting that the difference between the left and right lobes was attributable to events in the fetal and perinatal periods and not the result of epilepsy. Many patients with intractable TLE who undergo epilepsy surgery are found to have cortical dysgenesis in the epileptic regions, often despite a normal MRI [2,5,9]. In the present case the abnormal MRI lesions may be masked by the partial volume effect with brain development rather than have disappeared. Because neonatal and infantile brains include more rich water than adult brains, T1- and T2-weighted values of brain tissue reveals much longer tissue than in adults [13]. The small destructive lesions of the primitive myelinating areas or around the ventricular trigone could be depicted using short- and long-echo time fast FLAIR sequences
Figure 2. Magnetic resonance imaging (MRI) and single-photon computed tomography (SPECT) images at 3 months of age. (A) Coronal T1-weighted image (TR: 500 ms, TE: 19 ms). The left sylvian fissure is markedly dilated compared with that on the right, and the left temporal lobe is obviously smaller than that of the contralateral side. In the central semiovale, bilateral myelination is not different. (B) Coronal T2-weighted image (TR: 3,500 ms, TE: 102 ms). There were no lesions with T2 elongation. The left suprasylvian area also revealed the immature development observed in the cerebral hemispheal volume. (C) Coronal SPECT images obtained using technetium-99m-labeled hexamethylpropyleneamine oxime. These images exhibit an area of hypoperfusion in the left temporal lobe corresponding to the abnormal region revealed by MRI. However, the cerebral perfusion in the left suprasylvian area was normal.
[14]. In conventional spin echo sequences, for example, it was difficult to differentiate between small periventricular lesions and normal persistent areas of long T2-weighted relaxation times, which were seen superior and dorsal to the ventricular trigone in all neonates and infants. Therefore, in infant-onset focal epilepsy, scheduled examinations are necessary, even after obtaining normal findings on MRI during the stages of early brain development. Although in this case MRI with FLAIR sequences were not performed, the necessity of performing such sequences should be emphasized. In the serial MRI [2] and EEG [16], similar to those in previous reports, the results were not consistent with the
initial MRI lesions. Surprisingly, follow-up SPECT images revealed the persistent abnormal findings in the left hemisphere, although the hypoperfusion in the temporal lobe with infants may be misread easily as a false-positive finding. Perfusion imaging techniques, including SPECT, might be very useful in diagnosis and treatment planning. In addition, functional MRI recently has been developed as a powerful noninvasive research tool for studying human hippocampal long-term sustained response during memory processing [17]. Functional MRI should be applied to cases such as this one for the detection of the physiologic hippocampal changes and the abnormalities of temporal lobe function.
Furusho et al: Masked MRI Lesions 379
Figure 3. Follow-up MRI at 11 months and SPECT at 4 years of age. (A) Coronal T1-weighted image (TR: 500 ms, TE: 19 ms). (B) Coronal T2-weighted image (TR: 3,500 ms, TE: 102 ms). The abnormal MRI findings (dilatation of the sylvian fissure and the differences between the left and right temporal lobes) at 3 months of age at the time of admission had obviously improved. (C) Follow-up coronal SPECT images obtained using technetium-99m-labeled hexamethylpropyleneamine oxime at 4 years of age. MRI findings were normal at 2 and 4 years of age. However, these SPECT images exhibit similar hypoperfusion in the left temporal lobe as was observed in the MRI at 3 months of age.
The authors thank Dr. Yasuto Sasaki for technical support, Dr. Kazunobu Fujita for detail editing, and Drs. Takashi Endo, Kumi Oto, and Akinobu Iwasaki for their clinical discussion.
References [1] Jackson GD, Berkovic SF, Tress BM, Kalnis RM, Fabinyi GCA, Bladin PF. Hippocampal sclerosis can be reliably detected by magnetic resonance imaging. Neurology 1990;40:1869-75. [2] Kuzniecky R, Garcia JH, Faught E, Morawetz RB. Cortical dysplasia in temporal lobe epilepsy: Magnetic resonance imaging correlations. Ann Neurol 1991;29:293-8. [3] Bergin PS, Fish DR, Shorvon SD, Oatridge A, de Souza NM, Bydder GM. Magnetic resonance imaging in partial epilepsy: Additional abnormalities shown with the fluid attenuated inversion recovery (FLAIR) pulse sequence. J Neurol Neurosurg Psychiatry 1995;58:439-43. [4] Kato T, Yamanouchi H, Sugai K, Takashima S. Improved detection of cortical and subcortical tubers in tuberous sclerosis by
380
PEDIATRIC NEUROLOGY
Vol. 19 No. 5
fluid-attenuated inversion recovery MRI. Neuroradiology 1997;39:37880. [5] Engel J Jr. Update on surgical treatment of the epilepsies: Summary of the second international Palm Desert conference on the surgical treatment of the epilepsies. Neurology 1993;43:1612-8. [6] Gloor P. Mesial temporal sclerosis: Historical background and an overview from a modern perspective. In: Luders H, ed. Epilepsy surgery. New York: Raven Press, 1991;689-703. [7] Sagar HJ, Oxbury JM. Hippocampal neuron loss in temporal lobe epilepsy: Correlation with early childhood convulsions. Ann Neurol 1987;22:334-40. [8] Aso K, Watanabe K, Maeda N, Negoro T, Miura T. Temporal lobe epilepsy of childhood onset. Jpn J Psychiatry Neurol 1994;48:21720. [9] Harbord MG, Manson JI. Temporal lobe epilepsy in childhood: Reappraisal of etiology and outcome. Pediatr Neurol 1987;3:263-8. [10] Cendes F, Anderman E, Dubeau F, et al. Early childhood prolonged febrile convulsion, atrophy and sclerosis of mesial structures, and temporal lobe epilepsy. Neurology 1993;43:1083-7.
[11] Otsubo H, Steinlin M, Hwang PA, et al. Positive epileptiform discharges in children with neuronal migration disorders. Pediatr Neurol 1997;16:23-31. [12] Konishi Y, Yasujima M, Kuriyama M, et al. Magnetic resonance imaging in infantile spasms: Effects of hormonal therapy. Epilepsia 1992;33:304-9. [13] Holland BA, Haas DK, Norman D, Brant-Zawadzki M, Newton TH. MRI of normal brain maturation. Am J Neuroradiol 1986;7:201-8. [14] Kato T, Sasaki Y, Oto K, et al. Advantage of short/long echo
fast FLAIR in the neonatal and infant brain. Proc Soc Magn Reson Med 1995;2:1281. [15] Quirk JA, Kendall B, Kingsley DPE, Boyd SG, Pitt MC. EEG features of cortical dysplasia in children. Neuropediatrics 1993;24:193-9. [16] Kato T, Okuyama K. Assessment of maturation and impairment of the brain by I-123 iodoamphetamine SPECT and MR imaging in children. Showa Univ J Med Sci 1993;5:99-114. [17] Kato T, Erhard P, Takayama Y, et al. Human hippocampal long-term sustained response during word memory processing. Neuroreport 1998;9:1041-47.
Furusho et al: Masked MRI Lesions 381