Cognitive deficits are prevalent in individuals with epilepsy and negatively impact functional capacity and quality of life. Further, a substantial proportion of those with pharmacoresistant epilepsy experience clinically significant declines in cognitive functions, such as memory and language, following epilepsy surgery. Patients are often referred for speech therapy or cognitive rehabilitation to treat these deficits and improve function. Yet, to date, there is little empirical evidence for the efficacy of such interventions in epilepsy; and almost no evidence in children. This session will:
- Review the state of knowledge on cognitive
SIG: Seizures in Autoimmune Encephalitis: Seizures and Epilepsy Accompanying Neuroimmunological Disorders
This year’s SIG will discuss clinical manifestations and EEG patterns in patients with autoimmune encephalitis. It will also address treatment protocols for refractory status epilepticus in patients with autoimmune encephalitis by discussing illustrative cases. Finally we will conclude with audience participation via questions and answers.
The substrates and triggers for SUDEP remain unknown; the events leading up to SUDEP are often not captured. This session will include a review of novel technologies for capturing the physiological changes (e.g., autonomic, serotonergic, and cardiac) surrounding non-fatal and fatal seizures, and recent therapeutic interventions. In addition, this session will review recent pathological markers for SUDEP identified using novel technologies. Talks will include recent translational studies that apply computational approaches, accelerometry, ECGs, videos, and multimodal technologies to characterize the physiological state and postictal changes associated with SUDEP. The SIG
Negotiation skills can help you access the job and the resources that will allow you to thrive throughout your career. This session will focus on advice and training for those seeking new employment opportunities in any sector of epilepsy, with a panel of leading professionals from common sectors of research and clinical care professions.
Neurological disorders with increased burden of phosphorylated Tau, e.g. Alzheimer's Disease, are characterized by neuronal hyperexcitability and elevated lifetime risk of seizures. Vice versa, recent work suggests that reducing Tau burden in animal models of epilepsy decreases neuronal excitability and inhibits seizures. These studies suggest that drugs targeting Tau could be therapeutic in epilepsy. Despite this progress in the field, the underlying mechanisms are unclear, and it is controversial if Tau hyperphosphorylation is cause or consequence of seizures, or both. This proposed SIG will shed light on these questions by