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Cardiac arrhythmias are a frequent complication related to seizures [1]. Most are benign although some, such as high-grade atrioventricular block, asystole, atrial fibrillation (AF), and ventricular fibrillation are potentially harmful. Indeed, several studies suggest that cardiac dysfunction may be the primary underlying cause of sudden unexpected death in epilepsy (SUDEP). Post-ictal atrial fibrillation (PIAF) is a very rare cardiac arrhythmia associated with seizures, and its relevance is currently unknown. AF characteristics include: 1) irregular R-R intervals, 2) absence of distinct repeating P waves, and 3) erratic atrial activity [2]. Atrial flutter is differentiated from AF because of the characteristic “saw tooth” waves on the ECG instead of the chaotic atrial rhythm of the AF. In fact, there are only four reported cases of PIAF diagnosed during video-EEG monitoring (VEM) [1], [3], [4]. We report a case of PIAF identified during long-term VEM, with recurrent episodes corroborated by Holter-ECG monitoring

Atypical antipsychotic drugs (APDs) used to treat positive and negative symptoms in schizophrenia block serotonin receptors 5-HT2AR and dopamine receptors D2R and stimulate 5-HT1AR directly or indirectly. However, the exact cellular mechanisms mediating their therapeutic actions remain unresolved. We recorded neural activity in the prefrontal cortex (PFC) and hippocampus (HPC) of freely-moving mice before and after acute administration of 5-HT1AR, 5-HT2AR and D2R selective agonists and antagonists and atypical APD risperidone. We then investigated the contribution of the three receptors to the actions of risperidone on brain activity via statistical modeling and pharmacological reversal (risperidone + 5-HT1AR antagonist WAY-100635, risperidone + 5-HT2A/2CR agonist DOI, risperidone + D2R agonist quinpirole). Risperidone, 5-HT1AR agonism with 8-OH-DPAT, 5-HT2AR antagonism with M100907, and D2R antagonism with haloperidol reduced locomotor activity of mice that correlated with a suppression of neural spiking, power of theta and gamma oscillations in PFC and HPC, and reduction of PFC-HPC theta phase synchronization. By contrast, activation of 5-HT2AR with DOI enhanced high-gamma oscillations in PFC and PFC-HPC high gamma functional connectivity, likely related to its hallucinogenic effects. Together, power changes, regression modeling and pharmacological reversals suggest an important role of 5-HT1AR agonism and 5-HT2AR antagonism in risperidone-induced alterations of delta, beta and gamma oscillations, while D2R antagonism may contribute to risperidone-mediated changes in delta oscillations. This study provides novel insight into the neural mechanisms for widely prescribed psychiatric medication targeting the serotonin and dopamine systems in two regions involved in the pathophysiology of schizophrenia. This work was supported by the Brain and Behavior Research Foundation (NARSAD Young Investigator Award 23014), SAF2013-49129-C2-2-R and SAF2016-80726-R (AEI / FEDER, UE) by the Spanish Ministry of Economy and Competitiveness (MINECO; to MVP). M.V. Puig is a Ramon y Cajal Investigator (RyC-2012-10042), M. Alemany a FPI predoctoral fellow (BES-2014-070429) from MINECO, and C. Delgado a FI predoctoral fellow (2018FI_B_00112)from the Generalitat de Catalunya (AGAUR)

OBJECTIVE: We introduce a method that quantifies the consistent involvement of intracranially monitored regions in recurrent focal seizures. METHODS: We evaluated the consistency of two ictal spectral activation patterns (mean power change and power change onset time) in intracranial recordings across focal seizures from seven patients with clinically marked seizure onset zone (SOZ). We examined SOZ discrimination using both patterns in different frequency bands and periods of interest. RESULTS: Activation patterns were proved to be consistent across more than 80% of recurrent ictal epochs. In all patients, whole-seizure mean activations were significantly higher for SOZ than non-SOZ regions (P