36:248 脳卒中 36 巻 4 号 (2014:7) Table 1 Characteristics of MRI intensity change and their frequency Focus of MRI Frequency Laterality hippocampus 4.7% (o

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1 36:247 総説 36: , 2014 MRI 要旨 MRI MRI MRI Key words: seizure, MRI findings, cerebral cortex, hippocampus, corpus callosum, thalamus, cerebellum はじめに MRI 1 8 MRI MRI けいれん発作後に MRI 異常信号を呈する症例の臨床的特徴 MRI MRI arginine vasopressin VP hormone けいれん発作後の MRI 異常信号の画像的特徴 MRI DWI DC-map DC-map 6, 16, , 19, 20 T MR 5, 7, MR T2 FLIR 4, 6, 21 23

2 36:248 脳卒中 36 巻 4 号 (2014:7) Table 1 Characteristics of MRI intensity change and their frequency Focus of MRI Frequency Laterality hippocampus 4.7% (of patients with seizure) 1) bilateral 18.9%, unilateral 81.1% 2) 68.5% (of patients with MRI abnormality ) 2) pulvinar % (of patients with seizure) 1, 30) bilateral 17.6%, unilateral 82.4% 2) 26% (of patients with MRI abnormality) 2) corpus callosum 1, 13, 35) % (of patients with seizure) cerebellum 2.3% (of patients with seizure) 1) contralateral to the cortical focus MRI 号 Milligan 2) ( 11.6 ) MRI 号号 (Table 1) 号 Milligan 2) 86 4 ( 4.7 ) Cianfoni 1) MRI 号 ( 38.5 ) 号 Chatzikonstantinou 3) MRI 号 54 号 37 ( 68.5 ) 号号 30 7 号号 T2 号 2, 24) (abnormalities) 25, 26) MRI MRI 号 27 30) 号 31) 号 Milligan 2) 86 5 (5.8 ) Chatzikonstantinou 3) MRI 号 ( 26 ) 号号 11 号 3 9) ( 7.6 ) 号号号 14 7 号 10 号号 3 2 号 12 15) 32 35) 号 , 15, 36) (ovoid/round) ( lateral portion of SCC) 35) 号 Milligan 2) 86 2 ( 2.3 ) MRI MRI 号 5, 37 41) 40) 号号号号 crossed cerebellar diaschisis(ccd) 23) Fig. 1 6 MRI 号 (Fig ) けいれん発作の伝播経路について Papez Yakovlev 41, 42) 43, 44)

Hypointensity in the same location on the apparent diffusion coefficient (DC) map (arrow) (). C Fig.

3 MRI 36:249 Fig. 1 Hyperintensity in the left temporal tip on an axial diffusion-weighted image (DWI) (TR = 4200; TE = 81, b=1000) (arrow) (). Hypointensity in the same location on the apparent diffusion coefficient (DC) map (arrow) (). C Fig. 2 hyperintense lesion is seen in the left pulvinar on axial DWI (arrow) (). The same location ishypointense on the DC map (arrow) (). Pulvinar abnormal signal is completely disappeared on DWI on Day 9 (C). SPECT CCD けいれんによる神経障害機序と病理変化について excessive

4 Thesplenium of thecorpus callsum is hyperintense on an axial DWI (arrows) (), FLIR image () and T2-weighted image (C).

4 36:250 脳卒中 36 巻 4 号 (2014:7) Fig. 3 ilateral pulvinars as well as cerebral cortex are hyperintense on an axial DWI (arrows) (). These lesions are slightly hypointense on the DC map (arrows) (). D E C Fig. 4 Thesplenium of thecorpus callsum is hyperintense on an axial DWI (arrows) (), FLIR image () and T2-weighted image (C). The same focus is hypointense on the DC map (arrow) (D). The abnormal signal in the corpus callsum is completelydisappeared on DWI on Day 8 (E). excitatory neurotransmitter) N-methyl-D-asparate (NMD)receptors voltage-activated calcium channels catabolic enzymes nitrate reductase (NDH) (Fig. 7)

and FLIR image () andhypointensity is seen ondc map (C). C D Fig.

5 MRI 36:251 C Fig. 5 Hyperintensity is seen in thesplenium of thecorpus callsum on an axial DWI (arrows) () and FLIR image () andhypointensity is seen ondc map (C). C D Fig. 6 Hyperintense lesionsare confirmed in the left frontal lobe and the right cerebellum on DWI (, ) and on FLIR image (C, D). Cerebellar abnormal signals indicate crossed cerebellar diaschisis.

6 36:252 脳卒中 36 巻 4 号 (2014:7) Fig. 7 Schematic representation of the process of the neuron damage caused by seizure. 51, 52) ( 2 4 ) ( ) 51 56) C1 C3 C4 51) stratum oriens 53, 56) おわりに MRI 号 MRI 号 MRI 号号 : 参考文献 1)Cianfoni, Caulo M, Cerase, et al: Seizure-induced brain lesions: a wide spectrum of variably reversible MRI abnormalities. Eur J Radiol 82: , )Milligan T, Zamani, romfield E: Frequency and patterns of MRI abnormalities due to status epilepticus. Seizure 18: , )Chatzikonstantinou, Gass, Förster, et al: Features of acute DWI abnormalities related to status epilepticus. Epilepsy Res 97: 45 51, )Szabo K, Poepel, Pohlmann-Eden, et al: Diffusion-weighted and perfusion MRI demonstrates parenchymal changes in complex partial status epilepticus. rain 128: , )Lansberg MG, O rien MW, Norbash M, et al: MRI abnormalities associated with partial status epilepticus. Neurology 52: , )Parmar H, Lim SH, Tan NC, et al: cute symptomatic seizures and hippocampus damage: DWI and MRS findings. Neurology 66: , )Toledo M, Munuera J, Sueiras M, et al: MRI findings in aphasic status epilepticus. Epilepsia 49: , )Katramados M, urdette D, Patel SC, et al: Periictal diffusion abnormalities of the thalamus in partial status epilepticus. Epilepsia 50: , )Ohe Y, Hayashi T, Deguchi I, et al: MRI abnormality of the pulvinar in patients with status epilepticus. J Neuroradiol pii: S (13) , )Wieshmann UC, Clark C, Symms MR, et al: Water diffusion in the human hippocampus in epilepsy. Magn Reson Imaging 17: 29 36, )voli M: brief history on the oscillating roles of thalamus and cortex in absence seizures. Epilepsia 53: , )Kim SS, Chang KH, Kim ST, et al: Focal lesion in the splenium of the corpus callosum in epileptic patients: antiepileptic drug

7 MRI 36:253 toxicity? JNR m J Neuroradiol 20: , Mirsattari SM, Lee DH, Jones MW, et al: Transient lesion in the splenium of the corpus callosum in an epileptic patient. Neurology 60: , Maeda M, Shiroyama T, Tsukahara H, et al: Transient splenial lesion of the corpus callosum associated with antiepileptic drugs: evaluation by diffusion-weighted MR imaging. Eur Radiol 13: , Nelles M, ien CG, Kurthen M, et al: Transient splenium lesions in presurgical epilepsy patients: incidence and pathogenesis. Neuroradiology 48: , Cole J: Status epilepticus and periictal imaging. Epilepsia 45 Suppl 4: 72 77, Scott RC, King MD, Gadian DG, et al: Prolonged febrile seizures are associated with hippocampal vasogenic edema and developmental changes. Epilepsia 47: , Hong KS, Cho YJ, Lee SK, et al: Diffusion changes suggesting predominant vasogenic oedema during partial status epilepticus. Seizure 13: , Righini, Pierpaoli C, lger JR, et al: rain parenchyma apparent diffusion coefficient alterations associated with experimental complex partial status epilepticus. Magn Reson Imaging 12: , Nakasu Y, Nakasu S, Morikawa S, et al: Diffusion-weighted MR in experimental sustained seizures elicited with kainic acid. JNR m J Neuroradiol 16: , Tschampa HJ, Greschus S, Sassen R, et al: Thalamus lesions in chronic and acute seizure disorders. Neuroradiology 53: , Seidenberg M, Hermann, Pulsipher D, et al: Thalamic atrophy and cognition in unilateral temporal lobe epilepsy. J Int Neuropsychol Soc 14: , Tien RD, shdown C: Crossed cerebellar diaschisis and crossed cerebellar atrophy: correlation of MRI findings, clinical symptoms and supratentorial diseases in 26 patients. m J Roentgenology 58: , riellmann RS, Newton MR, Wellard RM, et al: Hippocampal sclerosis following brief generalized seizures in adulthood. Neurology 57: , Jackson GD, Chambers R, erkovic SF: Hippocampal sclerosis: development in adult life. Dev Neurosci 21: , VanLandingham KE, Heinz ER, Cavazos JE, et al: Magnetic resonance imaging evidence of hippocampal injury after prolonged focal febrile convulsions. nn Neurol 43: , Nohria V, Lee N, Tien RD, et al: Magnetic resonance imaging evidence of hippocampal sclerosis in progression: a case report. Epilepsia 35: , Farina L, ergqvist C, Zimmerman R, et al: cute diffusion abnormalities in the hippocampus of children with new-onset seizures: the development of mesial temporal sclerosis. Neuroradiology 46: , Chevret L, Husson, Nguefack S, et al: Prolonged refractory status epilepticus with early and persistent restricted hippocampal signal MRI abnormality. J Neurol 255: , Cox JE, Mathews VP, Santos CC, et al: Seizure-induced transient hippocampal abnormalities on MR: correlation with positron emission tomography and electroencephalography. JNR m J Neuroradiol 16: , Shipp S: The functional logic of cortico-pulvinar connections. Philos Trans R Soc Lond iol Sci 358: , Takanashi J, arkovich J, Yamaguchi K, et al: Influenzaassociated encephalitis/encephalopathy with a reversible lesion in the splenium of the corpus callosum: a case report and literature review. JNR m J Neuroradiol 25: , Kobata R, Tsukahara H, Nakai, et al: Transient MR signal changes in the splenium of the corpus callosum in rotavirus encephalopathy: value of diffusion-weighted imaging. J Comput ssist Tomogr 26: , Ogura H, Takaoka M, Kishi M, et al: Reversible MR findings of hemolytic uremic syndrome with mild encephalopathy. JNR m J Neuroradiol 19: , Tada H, Takanashi J, arkovich J, et al: Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 63: , Gröppel G, Gallmetzer P, Prayer D, et al: Focal lesions in the splenium of the corpus callosum in patients with epilepsy. Epilepsia 50: , Thajeb P, Shih F, Wu MC: Crossed cerebellar diaschisis in herpes simplex encephalitis. Eur J Radiol 38: 55 58, Stübgen JP: Crossed cerebellar diaschisis related to recurrent focal seizures. Epilepsia 36: , Nagasaka T, Shindo K, Hiraide M, et al: Ipsilateral thalamic MRI abnormality in an epilepsy patient. Neurology 58: , l-jafen N, lanazy MH, Scott JN, et al: Magnetic resonance imaging of crossed cerebellar diaschisis and bright pulvinar in status epilepticus. Neurosciences (Riyadh) 17: , Ohe Y, Hayashi T, Deguchi I, et al: case of non-convulsive status epilepticus with crossed cerebellar diaschisis temporal change of MRI and SPECT findings. J Stroke Cerebrovasc Dis 2013 Jul 30. doi:pii: S (13) /j.jstrokec erebrovasdis Hope O, lumenfeld H. Cellular physiology of status epilepticus. In Drislane WF (ed): Status epilepticus clinical perspective, New Jersey, Humana press, 2010, pp Hogan RE, Kaiboriboon K, ertrand ME, et al: Composite SISCOM perfusion patterns in right and left temporal seizures. rch Neurol 63: , SPECT 51: , Won JH, Lee JD, Chung TS, et al: Increased contralateral cerebellar uptake of technetium-99m-hmpo on ictal brain SPECT. J Nucl Med 37: , Umemura, Suzuka T: Crossed cerebellar hyperperfusion in symptomatic epilepsy two case reports. Neurol Med Chir (Tokyo) 40: 65 68, Harvey S, Hopkins IJ, owe JM, et al: Frontal lobe epilepsy: clinical seizure characteristics and localization with ictal 99mTc- HMPO SPECT. Neurology 43: , Marks D, Katz, Hoffer P, et al: Localization of extratemporal epileptic foci during ictal single photon emission computed tomography. nn Neurol 31: , Rowe CC, erkovic SF, Sia ST, et al: Localization of epileptic

8 36:254 脳卒中 36 巻 4 号 (2014:7) foci with postictal single photon emission computed tomography. nn Neurol 26: , )Runge U, Kirsch G, Petersen, et al: Ictal and interictal ECD- SPECT for focus localization in epilepsy. cta Neurol Scand 96: , )Thom M, Sisodiya S, Najm I. Neuropathology of epilepsy. In Love S, et al (eds): Greenfield s Neuropathology, 8th ed, London, Hodder rnold, 2008, pp )Fountain N. Cellular damage and the neuropathology of status epilepticus. In Drislane WF (eds): Status epilepticus clinical perspective. New Jersey, Humana press, 2010, pp )Mori F, Tanji K, Miki Y, et al: Status epilepticus associated with extensive axonal swelling in the unilateral cerebral cortex and hippocampus. Neuropathol ppl Neurobiol 38: , )uvin S, Devisme L, Maurage C, et al: Neuropathological and MRI findings in an acute presentation of hemiconvulsionhemiplegia: a report with pathophysiological implications. Seizure 16: , )Dolinak D, Smith C, Graham DI: Global hypoxia per se is an unusual cause of axonal injury. cta Neuropathol 100: , )Mori F, Nishie M, Houzen H, et al: Hypoglycemic encephalopathy with extensive lesions in the cerebral white matter. Neuropathology 26: , 2006 bstract MRI abnormal signal after seizures Yasuko Ohe, M.D., 1) Takeshi Hayashi, M.D., 1) kira Uchino, M.D., 2) and Norio Tanahashi, M.D. 1) 1) Department of Neurology and Cerebrovascular Medicine, Saitama Medical University International Medical Center 2) Department of Diagnostic Radiology, Saitama Medical University International Medical Center s MRI become widely available, we often encounter signal changes in the brain of patients with epileptic seizures. These lesions are variable for each patient, such as cerebral cortex, hippocampus, corpus callosum, thalamus, and cerebellum. It is noteworthy that not only the primary epileptic region but also fiber connection with the primary region show intensity changes. These signal changes indicate vasogenic and/or cytotoxic edema in acute phase of seizures. They are generally transient, but severe and refractory seizures may bring irreversible damage and atrophy of these lesions. In this article, we review clinical, radiological, and pathological characteristics of these lesions with abnormal signal after epileptic seizures. Key words: seizure, MRI findings, cerebral cortex, hippocampus, corpus callosum, thalamus, cerebellum (Jpn J Stroke 36: , 2014)

MRI demonstrates brain edema due to hyperperfusion with NCSE 39:447 CT MRI 7 DWI ADC-map FLAIR DWI Fig. 1 MRA 2 MRI DWI ADC-map FLAIR Fig. 2 3 FLAIR F

MRI demonstrates brain edema due to hyperperfusion with NCSE 39:447 CT MRI 7 DWI ADC-map FLAIR DWI Fig. 1 MRA 2 MRI DWI ADC-map FLAIR Fig. 2 3 FLAIR F 39:446 症例報告 39: 446 450, 2017 MRI 1 1 2 3 要旨 84 MRI 2 MRI ADC-map FLAIR 3 ASL MRA MCA 16 MRI MRI ASL Key words: nonconvulsive status epilepticus, mimicking cerebral infarction, magnetic resonance imaging,