36:247 総説 36: 247 254, 2014 MRI 1 1 2 1 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 1 8 9 1 MRI 1 2 2013 12 19 2013 12 26 10 11 arginine vasopressin VP hormone 12 15 けいれん発作後の MRI 異常信号の画像的特徴 MRI DWI 18 24 2 1 8 DC-map DC-map 6, 16, 17 18 24 2 3 17, 19, 20 T1 5 14 MR 5, 7, 18 2 1 MR T2 FLIR 4, 6, 21 23
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 5.8 7.6% (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) 0.7 2.3% (of patients with seizure) cerebellum 2.3% (of patients with seizure) 1) contralateral to the cortical focus MRI 号 Milligan 2) 86 10 ( 11.6 ) MRI 号 号 (Table 1) 号 Milligan 2) 86 4 ( 4.7 ) Cianfoni 1) MRI 号 26 10 ( 38.5 ) 号 9 1 10 3 Chatzikonstantinou 3) MRI 号 54 号 37 ( 68.5 ) 号 37 22 15 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 54 14 ( 26 ) 号 号 11 号 3 9) 225 17 ( 7.6 ) 号 号 17 14 3 号 14 7 号 10 号 号 3 2 号 12 15) 32 35) 号 0.7 2.3 2, 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. 2 6 9 41 ) けいれん発作の伝播経路について Papez Yakovlev 41, 42) 43, 44)
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 45 50 CCD けいれんによる神経障害機序と病理変化について excessive
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) 30 60 (Fig. 7)
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.
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36:254 脳卒中 36 巻 4 号 (2014:7) foci with postictal single photon emission computed tomography. nn Neurol 26: 660 668, 1989 50)Runge U, Kirsch G, Petersen, et al: Ictal and interictal ECD- SPECT for focus localization in epilepsy. cta Neurol Scand 96: 271 276, 1997 51)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 833 887 52)Fountain N. Cellular damage and the neuropathology of status epilepticus. In Drislane WF (eds): Status epilepticus clinical perspective. New Jersey, Humana press, 2010, pp 181 193 53)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: 387 390, 2012 54)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: 371 376, 2007 55)Dolinak D, Smith C, Graham DI: Global hypoxia per se is an unusual cause of axonal injury. cta Neuropathol 100: 553 560, 2000 56)Mori F, Nishie M, Houzen H, et al: Hypoglycemic encephalopathy with extensive lesions in the cerebral white matter. Neuropathology 26: 147 152, 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: 247 254, 2014)