Takafumi Shimogawa1, Takato Morioka2, Tetsuro Sayama3, Sei Haga4, Yuka Kanazawa5, Kei Murao6, Shuji Arakawa7, Ayumi Sakata8, Koji Iihara9. 1. Department of Neurosurgery, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan; Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan; Department of Neurosurgery, Fukuoka Children's Hospital, 5-1-1 Kashiiteriha, Higashi-ku, Fukuoka 813-0017, Japan. Electronic address: shimogawa28@gmail.com. 2. Department of Neurosurgery, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan; Department of Neurosurgery, Fukuoka Children's Hospital, 5-1-1 Kashiiteriha, Higashi-ku, Fukuoka 813-0017, Japan. Electronic address: takato@ns.med.kyushu-u.ac.jp. 3. Department of Neurosurgery, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan; Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Electronic address: tsayama@ns.med.kyushu-u.ac.jp. 4. Department of Neurosurgery, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan. Electronic address: sei.haga@gmail.com. 5. Department of Cerebrovascular Disease, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan. Electronic address: yu8850@gmail.com. 6. Department of Cerebrovascular Disease, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan. Electronic address: mrok19840314@gmail.com. 7. Department of Cerebrovascular Disease, Kyushu Rosai Hospital, 1-1 Sonekitamachi, Kokura Minami-Ku, Kitakyushu 800-0296, Japan. Electronic address: shuji6031@gmail.com. 8. Department of Clinical Chemistry and Laboratory Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Electronic address: asakata@med.kyushu-u.ac.jp. 9. Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. Electronic address: kiihara@ns.med.kyushu-u.ac.jp.
Abstract
BACKGROUND: In the diagnosis of nonconvulsive status epilepticus (NCSE), capture of ongoing ictal electroencephalographic (EEG) findings is the gold standard; however, this is practically difficult without continuous EEG monitoring facilities. Magnetic resonance imaging (MRI), including diffusion-weighted imaging (DWI) and perfusion MRI with arterial spin labeling (ASL), have been applied mainly in emergency situations. Recent reports have described that ictal MRI findings, including ictal hyperperfusion on ASL and cortical hyperintensity of cytotoxic edema on DWI, can be obtained from epileptically activated cortex. We demonstrate the characteristics and clinical value of ictal MRI findings. METHODS: Fifteen patients diagnosed as having NCSE (eight had complex partial status epilepticus (SE) and seven subtle SE) who underwent an initial MRI and subsequent EEG confrmation, participated in this study. Follow-up MRI and repeated routine EEG were performed. RESULTS: In 11 patients (73%), ictal MRI findings were obtained on both DWI and ASL, while in four (27%) patients, ictal hyperperfusion was found on ASL without any DWI findings being obtained. In all 10 patients with an epileptogenic lesion, there was a tight topographical relationship between the lesion and the localization of ictal MRI findings. In the other five patients, ictal MRI findings were useful to demonstrate the pathophysiological mechanism of NCSE of non-lesional elderly epilepsy, or 'de novo' NCSE of frontal origin as situation-related NCSE. Ictal MRI findings are generally transient; however, in three cases they still persisted, even though ictal EEG findings had completely improved. CONCLUSION: The present study clearly demonstrates that the initial use of ASL and DWI could help to diagnose partial NCSE and also combined use of the MRI and EEG allows documentation of the pathophysiological mechanism in each patient.
BACKGROUND: In the diagnosis of nonconvulsive status epilepticus (NCSE), capture of ongoing ictal electroencephalographic (EEG) findings is the gold standard; however, this is practically difficult without continuous EEG monitoring facilities. Magnetic resonance imaging (MRI), including diffusion-weighted imaging (DWI) and perfusion MRI with arterial spin labeling (ASL), have been applied mainly in emergency situations. Recent reports have described that ictal MRI findings, including ictal hyperperfusion on ASL and cortical hyperintensity of cytotoxic edema on DWI, can be obtained from epileptically activated cortex. We demonstrate the characteristics and clinical value of ictal MRI findings. METHODS: Fifteen patients diagnosed as having NCSE (eight had complex partial status epilepticus (SE) and seven subtle SE) who underwent an initial MRI and subsequent EEG confrmation, participated in this study. Follow-up MRI and repeated routine EEG were performed. RESULTS: In 11 patients (73%), ictal MRI findings were obtained on both DWI and ASL, while in four (27%) patients, ictal hyperperfusion was found on ASL without any DWI findings being obtained. In all 10 patients with an epileptogenic lesion, there was a tight topographical relationship between the lesion and the localization of ictal MRI findings. In the other five patients, ictal MRI findings were useful to demonstrate the pathophysiological mechanism of NCSE of non-lesional elderly epilepsy, or 'de novo' NCSE of frontal origin as situation-related NCSE. Ictal MRI findings are generally transient; however, in three cases they still persisted, even though ictal EEG findings had completely improved. CONCLUSION: The present study clearly demonstrates that the initial use of ASL and DWI could help to diagnose partial NCSE and also combined use of the MRI and EEG allows documentation of the pathophysiological mechanism in each patient.