Spike Dynamic and Epigenetic Malfunctions in Epilepsy: A Tale of Two Codes

the disruption of conscious perception during an absence seizure is not due to an obliteration of information transfer in the thalamocortical system. The authors state, “Our findings thus dispute the widely accepted assumption that synchronized oscillations in thalamocortical loops disrupt conscious perception by filtering-out external sensory inputs and/or disallowing their allocation to the appropriate cortical assemblies.” Rather, they suggest that the loss of consciousness during absence seizures may be caused by a disruption of the normal information processing in large-scale brain networks. Stefan and Lopes da Silva (2013) argue that the concept of “local” and “generalized” epilepsies is now outmoded. They add that there is now compelling evidence, even in the case of Ideopathic Generalized Seizures and Childhood Absence Seizures, that seizures start in a well-defined brain area and spread at great speed to connected brain areas recruiting specific neuronal networks into typical oscillatory behavior. These accounts, however, consider only corticocortical and corticothalamic interactions; in none of these review papers is the claustrum even mentioned. Recent work, however, may throw some light on this mystery. Koubeissi et al. (2012) have demonstrated that electrical stimulation of the claustrum, in a conscious patient with intractable complex partial epilepsy undergoing a preoperative investigation, produces a clinical state of immobility and complete lack of interaction with the environment, but retainment of some automatic movements, quite similar to cases of partial complex seizures. No such result was obtained when the nearby insula or white matter surrounding the claustrum IntroductIon The cellular processes that underlie the genesis and spread of epileptic seizures are currently poorly understood. This paper explores two hypotheses that seek to fill in some of these gaps. The first hypothesis relates to the role of the claustrum in the genesis of both complex partial and grand mal seizures in light of new and unique clinical data, and in modulating and integrating synchronized gamma oscillations in corticoclaustral circuits. The second hypothesis explores the possible role of epigenetic transcription factors, microRNAs, and exosomes in the kindling phenomenon. The conclusion is that the brain may possess two coding systems – one based on synchronized spikes for its software, the other on epigenetic processes that may modulate its dynamic hardware.