PMC7736901_01
(A-1, A-2) Electroencephalography (EEG) on the 14th day of hospitalization showing fast spike activity with random spikes from the bilateral frontal areas, and (B-J) changes in brain magnetic resonance imaging (MRI) over time. (B) A high-intensity focal lesion is observed in the left pulvinar nucleus of the thalamus on diffusion-weighted imaging (DWI). (C) The lesion shows slight hypointensity on apparent diffusion coefficient (ADC) maps, and hyperintensity on fluid-attenuated inversion recovery (FLAIR) sequences (D) on the 14th day of hospitalization. Follow-up MRI on the 38th day of hospitalization shows attenuation of abnormal findings on DWI (E), ADC maps (F), and the FLAIR sequence (G). Brain MRI nine months after the first admission shows disappearance of the lesion on DWI (H), ADC maps (I), and on FLAIR sequences (J).
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We were eventually able to obtain two EEGs, one on day 14 and another 7 weeks after the first hospitalization (Fig. 1A-1, 1A-2). Brain magnetic resonance imaging (MRI) revealed a focal lesion on the left thalamic pulvinar nucleus, which appeared hyperintense on diffusion weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) sequences, but slightly hypointense on apparent diffusion coefficient (ADC) mapping (Fig. 1B-D). A follow-up MRI performed three weeks after the first admission showed disappearance of abnormal pulvinar signals on DWI and ADC maps and lesion attenuation on FLAIR-MRI imaging (Fig. 1E-G). In the subsequent 9 months of follow-up, the patient did not experience seizures, and no abnormal signals on DWI, ADC maps, or FLAIR were observed (Fig. 1H-J).
Summary of the clinical course from first admission to final hospital discharge. Various combinations of multiple therapeutic antiseizure drugs were administered during the clinical course. The recurrent epilepsy was finally controlled with levetiracetam, valproic acid, and zonisamide. GCSE: generalized convulsive status epilepticus.
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The clinical course is summarized in Fig. 2.