Sleep and Epilepsy: A Summary of the 2011 Merritt-Putnam Symposium

Abstract

Lennox and Lennox, 1960 (1) Despite the long history of sleep and epilepsy research, the relationship between the two remains poorly understood (2, 3). An abundance of evidence suggests a bidirectional relationship between sleep and epilepsy, where sleep disorders are common comorbidities in individuals with epilepsy; and sleep, slow-wave sleep (SWS) in particular, may provide a physiological milieu for epileptiform activity. Sleep is also critical in postencoding evolution including a range of sleep-dependent memory processes, from simple stabilization of memories to the discovery of insights. The chronobiology of sleep results in the need to understand the chronopharmacology of antiepileptic drug therapy in individuals with epilepsy. At the 2011 Merritt-Putnam Symposium, the dynamic symbiotic relationship between sleep and epilepsy was explored. Objectives of the symposium were to 1) identify distinguishing clinical and EEG features of nocturnal seizures and parasomnias, which allow accurate diagnosis; 2) understand how sleep disturbances can exacerbate epilepsy and epilepsy can adversely alter sleep; 3) review common pathophysiological mechanisms between sleep and epilepsy; 4) recognize the consequences of nocturnal seizures and epileptiform discharges on cognition; and 5) learn to manage nocturnal seizures and epileptiform activity using current treatment options. The symposium addressed one of the NIH research benchmarks: Area III: Prevent, limit, and reverse the comorbidities associated with epilepsy and its treatment (4). Specifically, the topics aimed to prevent or limit other adverse consequences occurring in people with epilepsy, identify the range and

The systemDrive: a Multisite, Multiregion Microdrive with Independent Drive Axis Angling for Chronic Multimodal Systems Neuroscience Recordings in Freely Behaving Animals

“…In addition to its MSMR features, the systemDrive supports multimodal recordings by providing full access to the cranium for other auxiliary implants. A multimodal setup like the one used in the current study would be ideal for the chronic observation of thalamocortical networks thought to be responsible for absence seizures in models of epilepsy (Pearce et al, 2014; Taylor et al, 2017) and the mechanisms relating spike-wave discharges in ictal-like thalamocortical dynamics and sleep (Shaw, 2004; Dewolfe et al, 2013). Other sensor modalities, such as cardiac and respiratory electrodes, and oxygen sensors, could be added to study the relationship between seizures and sudden unexpected death from epilepsy (Ssentongo et al, 2017; Bahari et al, 2018).…”

Role for serotonin2A (5-HT2A) and 2C (5-HT2C) receptors in experimental absence seizures

“…Firstly, since both 5-HT 2 R subtypes are well expressed in the basal ganglia ( Li et al., 2004 ), which indirectly modulate AS generation ( Deransart and Depaulis, 2002 ), the 5-HT 2A R- and 5-HT 2C R-induced reduction in ASs reported in the present study could be a consequence of changes in firing rate in these brain regions. Secondly, since ASs are less common during active wakefulness and non-REM sleep ( Crunelli and Leresche, 2002 , Depaulis and van Luijtelaar, 2006 , Dewolfe et al., 2013 ), the 5-HT 2A R- and 5-HT 2C R-elicited decrease in ASs might be due to changes in wake/sleep states elicited by activation of these 5-HT receptor subtypes. Our study design did not allow us to robustly record circadian sleep which would have required acquiring a stable sleep baseline in GAERS before drug injection and a different habituation protocol.…”

Influence of Sleep and Sleep Deprivation on Ictal and Interictal Epileptiform Activity

“…The spike-wave discharges at 3 Hz with continuous discharges during status are fragmented during NREM sleep. In the absence status, spike discharges and polyspike-wave can be seen isolated [40, 41]. …”