Abstracts

With limited available [italic]in vivo[/italic] microphysiology, the neuronal mechanisms underlying the initiation and propagation of focal seizures in humans remain unclear. Yet this type of detailed information is important in the design of new therapeutic approaches to epilepsy. To more completely characterize the physiological evolution of seizures and how neuronal populations contribute to the development and spread of synchrony we recorded interictal and ictal activity in epileptic patients using intracortical linear microelectrode arrays, depth and subdural grid macroelectrodes., Microelectrode arrays measure potential gradient (PG), current source density (CSD) and multi-unit activity (MUA) from a restricted region of cortex [sim]300 [mu]m in diameter. These parameters, when combined, present a view of active microcircuitry during a given event. This information is complemented by macroelectrodes which provide contextual information about widespread cortical activity. We analyzed interictal discharges and 13 seizures from 7 patients who were undergoing intracranial investigation for intractable temporal or frontal lobe epilepsy of different etiologies including mesial temporal sclerosis, dysplasias, tumors and structural lesions., Microelectrode recordings of some ictal events showed similarities to the PG, CSD and MUA profiles of interictal events. During most seizures, however, there was a progression in this profile suggesting changes in the cellular substrates underlying ictal spike generation. In particular, large amplitude burst discharges toward the seizure[apos]s end involved more robust participation of deeper cortical layers and greater population neuronal firing. Seizures also exhibited differing phase characteristics during their evolution: trains of ictal discharges recorded either from two laminar microelectrode arrays or from different points on the subdural grid showed phase locking during some epochs in the seizure but were phase variable at others. Likewise, interictal events often showed inconsistent onsets and spread patterns., These results lead us to speculate that network synchrony is achieved and then spreads by different modes during focal seizures in humans; epileptiform activity is generated not from a single cellular source but from different micro-circuitry networks and propagation relies on a variety of pathways. Furthermore, it is likely that both local and distributed processes interact to shape the overall spatio-temporal evolution and synchronization features of the seizure. This type of [italic]in vivo[/italic] data may influence future designs of surgical procedures and brain stimulation paradigms., (Supported by NIH, AES, Grass Foundation.)