Archived AES Symposia 2005
Plenary III - Maladaptive Neuroplasticity in Stress and Epilepsy
Program Length: 1 hrs 22 min
Acute stress may promote epilepsy and facilitate seizures by evoking a chain of molecular events that promote amygdala and hippocampal hyperexcitability. In addition, both chronic stress and recurrent seizures (epilepsy) elicit adaptive responses directed toward maintaining homeostasis. This functional (and in some cases structural) plasticity is evident within single neurons, neuronal ensemblies and the whole brain. However, by altering neuronal interaction, the consequences of this neuroplasticity may be maladaptive, resulting in cognitive impairment and emotional disorders (e.g., depression). The effects of chronic stress on hippocampal neuronal structure, and the responsible molecular mechanisms, will be reviewed by Dr. McEwen. Neurosteroids, molecular mediators involved in the acute effects of stress on limbic excitability, will be discussed by Dr. Rogawski. The mechanisms of the long-lasting neuroplasticity of hippocampal neurons evoked by chronic early-life stress will be reviewed by Dr. Baram. Finally, the role of stress-mediators in epilepsy-related depressive disorders will be discussed by Dr. Gilliam.
At the conclusion of this activity, participants should be able to:
- Identify the effects of chronic stress on hippocampal neurons, particularly dendritic remodeling
- Recognize the origin of neurosteroids and their effects on limbic excitability
- Understand the structural and functional neuronal changes provoked by stress early in life, and the relevance of these changes to epilepsy
- Be aware of the role of stress-mediators in epilepsy-related depression, and the potential therapeutic implications.
Chair: Tallie Z. Baram, M.D., Ph.D.
Basic scientists interested in neuronal plasticity stress and epilepsy; adult and pediatric neurologists and epileptologists, pharmacists and healthcare providers who deal with comorbid problems in individuals with epilepsy.
Disclosure: It is the policy of the American Epilepsy Society that all faculty participating in continuing medical education activities are expected to disclose to the program audience (1) any real or apparent conflict(s) of interest related to the content of their presentation and (2) discussions of unlabeled or unapproved uses of drugs or medical devices. The American Epilepsy Society adheres to the ACCMEs Essential Areas and Policies regarding industry support of continuing medical education. Disclosure by faculty of commercial relationships, if any, and discussions of unlabeled or unapproved uses will be made.
Tallie Z. Baram, M.D., Ph.D. has disclosed she has no real or apparent conflicts of interest to report.
Frank G. Gilliam, M.D., M.P.H. has disclosed he has no real or apparent conflicts of interest to report.
David M. Labiner, M.D. (liaison reviewer) has disclosed that he has received consulting fees from Cyberonics, GlaxoSmithKline, Novartis, Ortho McNeil Neurologics, Pfizer Inc. and UCB Pharma, Inc. Dr. Labiner has also disclosed he has received fees for non-CME services from Abbott Laboratories, Cyberonics, Eisai, Inc., GlaxoSmithKline, Novartis, Ortho-McNeil Neurologics, Pfizer Inc., Shire and UCB Pharma, Inc. and has contracted research with Abbott Laboratories, Cyberonics, GlaxoSmithKline, Novartis, Ortho-McNeil Neurologics, Pfizer Inc., and UCB Pharma, Inc.
Bruce S. McEwen, Ph.D. has disclosed he has no real or apparent conflicts of interest to report.
Michael A. Rogawski, M.D., Ph.D. has disclosed he has no real or apparent conflicts of interest to report.
Disclaimer: Opinions expressed with regard to unapproved uses of products are solely those of the faculty and are not endorsed by the American Epilepsy Society or any manufacturers of pharmaceuticals.