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While new-onset status epilepticus (NOSE) is a harbinger of chronic epilepsy, prospective medical data are sparse in terms of specifying whether the evolution of status epilepticus (SE) and seizure expression in NOSE resembles what occurs in patients who have already been diagnosed with epilepsy [non-inaugural SE (NISE)] in all aspects apart from its inaugural nature. The aim of this study was to compare the clinical, MRI, and EEG features that could distinguish NOSE from NISE. We conducted a prospective monocentric study in which all patients ≥18 years admitted for SE over a 6-month period were included. A total of 109 patients (63 NISE and 46 NOSE cases) were included. Despite similar modified Rankin scores before SE, several aspects of the clinical history distinguished NOSE from NISE patients. NOSE patients were older and frequently had neurological comorbidity and preexisting cognitive decline, but they had a similar prevalence of alcohol consumption to NISE patients. NOSE and NISE evolve in the same proportions as refractory SE (62.5% NOSE, 61% NISE) and share common features such as the same incidence (33% NOSE, 42% NISE, and p = 0.53) and volumes of peri-ictal abnormalities on MRI. However, in NOSE patients, we observed greater non-convulsive semiology (21.7% NOSE, 6% NISE, and p = 0.02), more periodic lateral discharges on EEG ( p = 0.004), later diagnosis, and higher severity according to the STESS and EMSE scales ( p < 0.0001). Mortality occurred in 32.6% of NOSE patients and 21% of NISE patients at 1 year ( p = 0.19), but with different causes of death occurring at different time points: more early deaths directly linked to SE at 1 month occurred in the NOSE group, while there were more remote deaths linked to causal brain lesions in the NISE group at final follow-up. In survivors, 43.6% of the NOSE cases developed into epilepsy. Despite acute causal brain lesions, the novelty related to its inaugural nature is still too often associated with a delay in diagnosing SE and a poorer outcome, which justifies the need to more clearly specify the various types of SE to constantly raise awareness among clinicians. These results highlight the relevance of including novelty-related criteria, clinical history, and temporality of occurrence in the nosology of SE., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Benaiteau, Valton, Gardy, Denuelle, Debs, Wucher, Rulquin, Barbeau, Bonneville, Pariente and Curot.)

The observation that a pathophysiological link might exist between Alzheimer's disease (AD) and epilepsy dates back to the identification of the first cases of the pathology itself and is now strongly supported by an ever-increasing mountain of literature. An overwhelming majority of data suggests not only a higher prevalence of epilepsy in Alzheimer's disease compared to healthy aging, but also that AD patients with a comorbid epileptic syndrome, even subclinical, have a steeper cognitive decline. Moreover, clinical and preclinical investigations have revealed a marked sleep-related increase in the frequency of epileptic activities. This characteristic might provide clues to the pathophysiological pathways underlying this comorbidity. Furthermore, the preferential sleep-related occurrence of epileptic events opens up the possibility that they might hasten cognitive decline by interfering with the delicately orchestrated synchrony of oscillatory activities implicated in sleep-related memory consolidation. Therefore, we scrutinized the literature for mechanisms that might promote sleep-related epileptic activity in AD and, possibly dementia onset in epilepsy, and we also aimed to determine to what degree and through which processes such events might alter the progression of AD. Finally, we discuss the implications for patient care and try to identify a common basis for methodological considerations for future research and clinical practice., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 B. Szabo, Cretin, Gérard, Curot, J. Barbeau, Pariente, Dahan and Valton.)

Introduction: Patients with psychogenic nonepileptic seizures (PNESs) have often been exposed to traumatic events, which is a risk factor for suicidal behavior. This would suggest that the severity of suicidal ideation is greater in PNES than in patients suffering only from epileptic seizures (ESs). However, these psychiatric symptoms may be underestimated in the ES population. The specific features or similarities between the psychiatric clinical profiles of these two groups should be elaborated to improve therapeutic management. Our study is the first to compare suicidal ideation, suicide risk, posttraumatic stress disorder (PTSD), and depression disorder simultaneously in both groups, in a tertiary care epilepsy center. Material and methods: We prospectively enrolled patients hospitalized for video-electroencephalography (EEG) monitoring to assess repeated seizures before an ES or a PNES diagnosis was made. During the psychiatric consultation that accompanied the video EEG, we rated the severity of suicidal ideation and depressive symptoms, suicidal risk, traumatic exposure history, and PTSD symptoms. Results: Eighteen subjects were enrolled and diagnosed with PNES, and 42, with ES. The PNES group reported more exposures to traumatic events and more intense PTSD symptoms (median: 17 vs. 27; p = 0.001). The severity of suicidal ideation did not differ significantly between the two groups. Conclusion: It is the severity of PTSD symptoms in PNES patients that differentiates them from ES patients, although exposure to traumatic events is also frequent in ES patients. We demonstrated that suicidal ideation and suicide risk are equally high in the ES and PNES groups. Therefore, both groups require extreme vigilance in terms of suicidal risk.