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Background: Traditional brain activity monitoring via scalp electroencephalography (EEG) offers limited resolution and is susceptible to artifacts. Endovascular electroencephalography (eEEG) emerged in the 1990s. Despite early successes and potential for detecting epileptiform activity, eEEG has remained clinically unutilized. This study aimed to further test the capabilities of eEEG in detecting lateralized epileptic discharges in animal models. We hypothesized that eEEG would be able to detect lateralization. The purpose of this study was to measure epileptiform discharges with eEEG in animal models with lateralization in epileptogenicity. Materials and methods: We inserted eEEG electrodes into the transverse sinuses of three pigs, and subdural electrodes (SDs) on the surfaces of the left and right hemispheres. We induced epileptogenicity with penicillin in the left brain of pigs F00001 and F00003, and in the right brain of pig F00002. The resulting epileptiform discharges were measured by eEEG electrodes placed in the left and right transverse sinuses, and conducted comparisons with epileptiform discharges from SDs. We also had 12 neurological physicians interpret measurement results from eEEG alone and determine the side (left or right) of epileptogenicity. Results: Three pigs were evaluated for epileptiform discharge detection using eEEG: F00001 (7 months old, 14.0 kg), F00002 (8 months old, 15.6 kg), and F00003 (8 months old, 14.4 kg). The eEEG readings were compared with results from SDs, showing significant alignment across all subjects (p 0.93) and PPV (>0.95) that appear equivalent to those of subdural EEG in the three pigs. This lateralization was also discernible by neurological physicians on visual inspection.

We report a case of superficial siderosis (SS) of the central nervous system that developed approximately 8 years after the treatment of cerebral arteriovenous malformation (AVM). A 17-year-old boy was diagnosed with cerebral AVM in the right frontal lobe, which was treated with embolization and radiation therapy. Radiation-induced encephalopathy occurred 5 years later, and the lesion was resected. Although the patient could walk with a cane following the surgery and rehabilitation, he exhibited complete paresis of the left upper extremity. In the course of the next 9 years, he showed cognitive function decline, paresis of the lower right extremity, and the inability to walk. He also exhibited dysarthria and paresis of the right arm. Respiratory failure developed at age 39 years, necessitating mechanical ventilation. Cerebral angiography revealed no recurrence of cerebral AVM; however, brain and spinal magnetic resonance imaging revealed broad hemosiderin deposition, which is characteristic of SS, and the presence of a postoperative cyst that was suspected to be the bleeding source. While eliminating the source of the bleeding is considered the best line of treatment for SS, this was not pursued due to the patient's irreversible neurological condition. Thus, clinicians should consider SS as a differential diagnosis for patients that exhibit gradual and progressive neurological defects several years after successful AVM treatment. Keywords: Superficial siderosis, Radiation-induced encephalopathy, Arteriovenous malformation

Introduction: Intracranial subdural empyema (ISDE) can cause drug-resistant epilepsy. We attempted to cure post-ISDE refractory epilepsy by operative surgery and assessed the neuropathological findings. Patient and method: A 23-year-old right-handed man with refractory epilepsy had ISDE on the right temporal and occipital areas at 14 years old. He underwent ISDE drainage operation at the time. A week after the infection, he developed epileptic seizure, which consisted of epigastric sensation, followed by loss of awareness with gelastic seizure. This type of seizure occurred around five times a day. He underwent right posterior disconnection and the temporal lobe was submitted to histopathological examination. Result: The patient has remained seizure-free for more than 3 months. Histopathological diagnosis showed focal cortical dysplasia (FCD) type IB. Conclusion: We cured post-ISDE refractory epilepsy by posterior quadrant disconnection. Epileptogenicity of FCD might be triggered by ISDE. Keywords: Subdural empyema, Focal cortical dysplasia, Posterior quadrant disconnection, Refractory epilepsy