Abstracts

Rationale: The concept of Secondary Epileptogenesis (SE) was introduced by Frank Morrell (Morrell, 1989). The secondary epileptogenic zone (SEZ) is a cortical area that has become epileptogenic due to the influence of epileptogenic activity in a primary epileptogenic zone (PEZ). The most likely mechanism responsible for secondary epileptogenesis is kindling, which is the tendency of the brain to become progressively more epileptogenic when stimulated repeatedly. It is difficult to provide conclusive proof of kindling and secondary epileptogenesis in humans (Lüders, 2001). We present a case of a patient with refractory epilepsy and ictal intermediate secondary epileptogenesis proven by stereotactically placed depth electrodes and 8 years of clinical follow up.  Methods: Case report of a patient with refractory epilepsy,ictal intermediate secondary epileptogenesis and literature review. Results: 52 year-old right-handed woman with intractable epilepsy since age 45 was referred to our center for presurgical evaluation. She described her seizures as a sudden sensation of familiarity and abdominal rising sensation lasting for seconds to 1 minute. Next thing she remembers is being confused and tired. Her husband described these episodes as unresponsiveness along with repetitive mouth and tongue movements. Her seizure frequency was 2-3 times every month which evolved into a generalized tonic- clonic seizure once a month. Multiple antiepileptic medications failed to control her seizures.  Her only risk factor for epilepsy was a motor vehicle accident with a severe closed head injury at age 17. Her MRI showed areas of cystic encephalomalacia and gliosis of the right inferior frontal lobe and anterior aspect of the right insula. Scalp VEEG showed automotor seizures with ictal onset zone maximum over F8-T8. No interictal epileptiform abnormalities were recorded on scalp EEG.  She underwent stereotactic implantation of depth electrodes (image 1) located around the right frontal cystic encephalomalacia, right insula and temporal lobe (mesial structures, lateral and tip). Irritative zone was extensive (frontal around the lesion, insular cortex and mesial temporal structures). She had 6 automotor seizures arising from the right orbitofrontal area anterior, medial and lateral to the lesion (Image 1), and multiple electrographic seizures arising from the right mesial temporal areas (Image 2). After a discussion in a multidisciplinary conference, the following was recommended:  resection of the right orbitofrontal epileptogenic lesion, leaving the right temporal lobe intact. She has remained seizure free for a total of 8 years, completely off all antiepileptic medications.  Conclusions: The epileptogenic zone in our patient was the right orbitofrontal lesion. Nevertheless, depth electrodes clearly showed an additional seizure onset zone in the right amygdala and hippocampus. Only the right frontal epileptogenic lesion was removed preserving the right mesial temporal lobe. This patient has been seizure free, off AEDs, for 8 years. This suggests the right mesial temporal structure is a SEZ.  Funding: None.