Frontiers in Research Epilepsy research is significantly underrepresented in University Seminar Series and Grand Rounds that take place every week at institutions across the country. In an effort to spread news about innovative research in epilepsy, CURE is pleased to sponsor a University-based invited lectureship program – Frontiers in Research.

The goal of this program is to expose young researchers and clinicians to exciting epilepsy research, and to provide opportunities for young investigators to interact with a senior level epilepsy researcher.
10 each year CURE’s goal in developing this lectureship program is to attract the best and brightest minds into the field of epilepsy research. Approximately 10 seminars will be sponsored at different institutions each academic year with one goal – to present cutting-edge epilepsy research to a wide audience of researchers, clinicians, young investigators, and students.

If you have any questions about the Frontiers in Research Seminar Series program, please contact Liz Higgins at


2016 Locations


Chicago, Illinois
Gene discovery in the epileptic encephalopathies: an update

WHERE: Northwestern University Feinberg School of Medicine
WHEN: Monday, March 21, 2016: 12:00-1:00 PM CT
SPEAKER: Heather Mefford, MD, PhD
HOST: Alfred L. George, Jr., MD & Stephan Schuele, MD

TALK SUMMARY: The introduction of next-generation sequencing technologies in the past 10 years has accelerated our understanding of the genetic architecture of the epilepsies. A significant advance has been the recognition that the epileptic encephalopathies - the most severe of the epilepsy syndromes - are often due to de novo mutations. Numerous genes have been identified in the past decade through both targeted and whole exome sequencing approaches. Dr Mefford will provide an overview of recent advances in gene discovery, with an emphasis on the encephalopathies. Proteins encoded by genes in which mutations cause epilepsy function in a wide variety of cellular processes. Understanding the genetic etiology of disease in patients may lead to more precise therapies as drugs are developed to target specific pathways and processes.



London, England
Targeted interventions in acquired and genetic epilepsies

WHERE: University College London (UCL) School of Pharmacy
WHEN: Friday, April 8, 2016: 12:30-1:30pm GT
SPEAKER: John Huguenard, PhD
HOST: Mala M. Shah, PhD

TALK SUMMARY: Our understanding of the local and extended neural networks implicated in seizure genesis has greatly expanded in recent decades. This, coupled with advances in targeted control (opto- or chemo-genetics), is leading to rather sudden improvement of epilepsy treatment, so far at least in animals. Prof. Huguenard's presentation will describe their work in post-lesional (stroke) epilepsy models as well as genetic generalized epilepsy models (absence epilepsy), with identification and effective therapeutic targeting of key neuronal cell types.



Farmington, Connecticut

WHERE: University of Connecticut Health Center
WHEN: Tuesday, April 26, 2016: 4:00 – 5:00pm ET
SPEAKER: Jack Parent, MD
HOST: Eric Levine, PhD




Waco, Texas

WHERE: Baylor University
WHEN: Wednesday, April 27, 2016
SPEAKER: Amy Brooks-Kayal, MD
HOST: Joaquin Lugo, PhD




Portland, Oregon
The genetic borderland of epilepsy: A novel gene mechanism linking epilepsy and migraine

WHERE: Vollum Institute, Oregon Health and Science University
WHEN: Wednesday, May 18, 2016, 10:00-11:00 AM PT
SPEAKER: Jeff Noebels, MD, PhD
HOST: Gary L. Westbrook, MD, Senior Scientist and Co-Director, Vollum Institute




Madison, Wisconsin

WHERE: University of Wisconsin-Madison
WHEN: Wednesday, May 25, 2016
SPEAKER: Paul Buckmaster, DVM, PhD
HOST: Matt Jones, PhD




Stanford, California

WHERE: Stanford University
WHEN: Saturday, June 18, 2016
SPEAKER: Eleanora Aronica, MD, PhD
HOST: John Huguenard, PhD




Halifax, Nova Scotia

WHERE: Dalhousie University
WHEN: Wednesday, September 21, 2016
SPEAKER: Helen Scharfman, PhD
HOST: Bernd Pohlmann-Eden, MD, PhD



2015 Locations


Riverside, California
Astrocyte structure and function: What are the “other” cells of the brain up to in experimentally-induced epilepsy?

WHERE: University of California, Riverside
WHEN: Tuesday, February 24, 2015: 4:00 – 5:00pm PT
SPEAKER: Karen Wilcox, PhD
HOST: Todd Fiacco, PhD and Devin Binder, MD, PhD

TALK SUMMARY: Temporal lobe epilepsy (TLE) is a devastating seizure disorder that is difficult to control with currently available anti-seizure drugs. Decades of research in animal models have generated vast knowledge regarding functional changes in neurons in TLE. However very little is currently known about the role in TLE of astrocytes, the other major cell type of the brain. Furthermore, epilepsy is recognized as a ‘circuit’ disorder. Thus innovative ways to evaluate the contributions that both neurons and astrocytes make to aberrant excitatory circuit activity will be critical for the understanding of the emergent network activity that results in seizures. Dr. Wilcox will describe recent findings from her laboratory that have identified structural and functional changes in astrocytes soon after a TLE-inducing insult. In addition, she will present recent genetic approaches the she and her collaborators have taken to image calcium signals, a marker of activity in both neurons and glial cells, both in vivo and ex vivo. It is anticipated that this work will lead to novel insights into the process of epileptogenesis at the network level and may identify disease-modifying therapeutic targets that have been missed due to a largely neurocentric view of seizure generation.



Toronto, Canada
Sudden Unexpected Death in Epilepsy: What are we missing?

WHERE: University of Toronto, Toronto Western Hospital
WHEN: Thursday, April 2, 2015
SPEAKER: Orrin Devinsky, MD
HOST: Danielle Andrade, MD, MSc.

TALK SUMMARY: Sudden unexpected death in epilepsy is a leading cause of mortality in people with epilepsy. The past decade has brought significant advances in our understanding of the epidemiology, risk factors, and the role of seizures in leading to the cascade of terminal physiological changes. However, we remain uncertain about the specific mechanisms that lead a rare minority of seizures to become fatal while the vast majority of similar intensity seizures are followed by full recovery. Dr Devinsky will provide a broad overview on our current knowledge of SUDEP from both clinical and research perspectives, including the role of serotonergic function and respiratory dysfunction. One focus will be areas of current thinking that may restrict our recognition of SUDEP - from limitations of definition and diagnosis that likely lead to a significant underestimate of SUDEP, the role of status as a model of SUDEP, and Sudden Unexplained Death in Childhood where the rate of febrile seizures is ten-fold higher than population controls. He will discuss the recently funded NINDS Center for SUDEP Research (CSR) and its portfolio of studies, the North American SUDEP Registry, as well as other research efforts that are ongoing. Finally, he will present current research on SUDEP prevention - from education to reduce risk factors to monitoring devices to detect seizures.



Sodium channels and epilepsy:
New insights, challenges and opportunities

Sacramento, California

WHERE: UC Davis Medical Center (Sacramento)
WHEN: Thursday, June 4, 2015: 1:00 – 2:00pm PT
SPEAKER: Andrew Escayg, PhD
HOST: Christoph Lossin, PhD and James Trimmer, PhD

Davis, California

WHERE: University of California, Davis
WHEN: Friday, June 5, 2015
SPEAKER: Andrew Escayg, PhD
HOST: Christoph Lossin, PhD and James Trimmer, PhD

TALK SUMMARY: Voltage-gated sodium channels (VGSCs) have emerged as important epilepsy genes with mutations in the major brain isoforms, SCN1A, SCN2A, SCN3A and SCN8A, associated with a growing list of epilepsy subtypes. This presentation will focus on recent findings from the analysis of SCN1A and SCN8A mutations. The emerging data highlights the complexity of seizure generation, but importantly, also provides new opportunities for the development of improved treatments.



Boston, Massachusetts
A dendritic mechanism underlying epileptogenesis in temporal lobe epilepsy: Implications for therapy

WHERE: Tufts University
WHEN: Wednesday, June 17, 2015: 4:00 – 5:00pm ET
SPEAKER: Heinz Beck, MD, PhD
HOST: Jamie Maguire, PhD and Chris Dulla, PhD

TALK SUMMARY: The input-output relationship of neuronal networks depends both on their synaptic connectivity and on the intrinsic properties of their neuronal elements. In addition to altered synaptic properties, profound changes in intrinsic neuronal properties are observed in many CNS disorders. We have found pronounced changes in intrinsic excitability in experimental epilepsy, consisting of a transient conversion of regular firing to burst-firing hippocampal neurons. This conversion is due to a selective functional up-regulation of T-type Cav3.2 channels in CA1 dendrites, mediated via specific Zn2+-dependent transcriptional mechanisms. Importantly, genetic deletion of Cav3.2 subunits, or transient application of the Cav3.2 blocking anticonvulsant eslicarbazepine, strongly attenuated the development of chronic epilepsy. These results suggest that Cav3.2-dependent increases in intrinsic excitability may be an important mechanism for epileptogenesis that can be influenced by a clinically employed anticonvulsant drug.



Cleveland, Ohio
Adult Neurogenesis, mTOR signaling and the Development of Temporal Lobe Epilepsy

WHERE: Cleveland Clinic
WHEN: Thursday, August 27, 2015: 1:00 – 2:00pm ET
SPEAKER: Steve Danzer, PhD
HOST: Hoonkyo Suh, PhD

TALK SUMMARY: Aberrant integration of adult-generated dentate granule cells is implicated in the development of temporal lobe epilepsy. It has been known for decades that the hippocampal dentate gyrus rewires in animals and humans with temporal lobe epilepsy, and physiological evidence indicates that this rewiring promotes hyperexcitability. More recently, it has been established that adult-generated neurons are responsible for much of this rewiring, directly implicating these new cells in epileptogenesis. While substantial correlative evidence now exists suggesting a role for aberrantly integrated adult-generated cells in epilepsy, however, direct evidence is limited. Dr. Danzer’s research program is aimed at establishing whether adult-neurogenesis plays a causative role in the development of temporal lobe epilepsy, and whether these cells can be manipulated to develop novel therapies. Dr. Danzer will show new data characterizing the origination of these cells from distinct granule cell progenitors, and will present pre-clinical data aimed at determining whether manipulating these cells can have disease-modifying effects in epilepsy. Findings focus on clonal analysis studies of granule cell progenitors, and on results demonstrating that genetically ablating adult-generated cells after an epileptogenic brain injury can mitigate epileptogenesis. Studies designed to establish the cell signaling pathways responsibility for aberrant cell integration, with particular emphasis on the mammalian target of rapamycin (mTOR) pathway, will also be discussed.



Atlanta, Georgia
Developmental Effects of Antiepileptic Drugs

WHERE: Georgia State University
WHEN: Friday, September 18, 2015: 10:00 - 11:00am ET
SPEAKER: Kimford J. Meador, MD
HOST: Mukesh Dhamala, PhD

TALK SUMMARY: Antiepileptic Drugs (AEDs) have been known to be teratogens for over 50 years, but our knowledge of differential AED effects has developed predominately in the last decades. AED-induced teratogenicity includes both anatomical and behavioral effects. Typical major congenital malformations include heart defects, orofacial clefts, skeletal, urological and neural tube defects. The highest risk of malformations exists for valproate with intermediate risks for phenobarbital and topiramate. Overall, the lowest known risks of malformations are seen with carbamazepine, lamotrigine, levetiracetam, and oxcarbazepine. However, carbamazepine is associated with an increased risk of neural tube defects although less than valproate. Further, the risks of many AED monotherapies and polytherapy combinations remain unknown. Fetal AED exposure may also affect cognitive and behavioral outcomes. The highest risk exists for fetal valproate exposure, which has dose-dependent associations with reduced cognitive abilities across a range of domains. Valproate has also been linked to a risk for autism. Phenobarbital has also been associated with reduced cognitive outcomes. The lowest risks for adverse cognitive outcomes exist for carbamazepine, lamotrigine and levetiracetam. The behavioral/cognitive risks for other AEDs are unclear. The mechanisms by which AEDs affect developmental outcomes are not well defined. A prominent hypothesis for AED-induced malformations is that they are the result of free radical intermediate metabolites in the first trimester. In regards to behavioral teratogenesis, AED-induced apoptosis and impaired synaptogenesis in the 3rd trimester is a leading hypothesis. Additional research is critically needed to better understand the risks and mechanisms of AED-induced teratogenesis.



Phoenix, Arizona
Perinatal hypoxic-ischemic encephalopathy: neonatal seizures, EEG suppression, and epilepsy

WHERE: Barrow Neurological Institute at Phoenix Children’s Hospital
WHEN: Monday, October 5, 2015: 7:30 – 8:30am MT
SPEAKER: Edward Dudek, PhD
HOST: Matthew M. Troester, DO

TALK SUMMARY: At the conclusion of this session, participants will be able to:
Understand cellular mechanisms that are believed to contribute to acute seizures and chronic epileps, know hypothetical mechanisms underlying pediatric epilepsy after neonatal hypoxic-ischemic insults, and understand principles and controversies concerning the role of neonatal seizures and/or brain injury in acquired epilepsy.



Frankfurt am Main, Germany
Epilepsy therapies of the future: The latest translational research

WHERE: Rhein-Main Epilepsy Center (Opening ceremony)
WHEN: Wednesday, October 14, 2015
SPEAKER: Professor Matthew Walker, University College London
HOST: Braxton Norwood, PhD

TALK SUMMARY: Approximately 30% of people with epilepsy do not fully respond to our present drugs yet fewer than 10% of these people are suitable for curative epilepsy surgery, often because the epileptogenic zone is too widespread or overlaps with eloquent cortex. An alternative approach to resective surgery is the use of gene therapy to reduce the excitability of excitatory neurons or to increase the excitability of inhibitory neurons in the focus. There have been considerable advances in the development of viral vectors that self-inactivate and are not immunogenic, providing safe and effective methods for gene therapy. We have successfully used a lentiviral vector to overexpress an endogenous gene that encodes the potassium channel Kv1.1 and so have cured epilepsy in a model of focal neocortical epilepsy. A different approach is to express proteins that can be modulated on demand. We have used optogenetic (the expression of channels and ion pumps that are activated by coloured light) in order to increase or decrease neuronal excitability in specific neurons. Using a system in which an implanted light is activated when a seizure is detected, it is possible through optogenetics to suppress seizure activity. Rather than using light sensitive proteins, receptors have been developed that are activated by specific drugs – Designer Receptors Exclusively Activated by Designer Drugs (DREADDs). Using gene therapy to express in specific neurons a DREADD that is sensitive to an otherwise inert synthetic ligand, clozapine-N-oxide (CNO), we have been able to suppress seizure activity by the administration of CNO. Although human trials are some way off, there is a clear route to translation and it is likely that trials of gene therapy in the treatment of epilepsy will occur within the next decade.



Lebanon, New Hampshire
Spatial and Temporal Prediction of Seizures in Human Focal Epilepsy

WHERE: Dartmouth-Hitchcock Medical Center
WHEN: Friday, November 6, 2015: 12:00 – 1:00pm ET
SPEAKER: Greg Worrell, MD, PhD
HOST: Barbara Jobst, MD

TALK SUMMARY: Advances in computation, recording technology, and devices are poised to transform how patients with drug resistant epilepsy are evaluated for epilepsy surgery and brain stimulation devices. In this talk Dr. Worrell will review recent advances, clinical applications, and future directions.



Charlottesville, Virginia
Epilepsy Genetics--From Discovery to Precision Medicine

WHERE: University of Virginia
WHEN: Friday, November 20, 2015: 12:00 – 1:00pm ET
SPEAKER: Ann Poduri, MD
HOST: Laura Jansen, MD


2014 Locations


Montreal, Canada
If Pascal had only known: Genes for Arrhythmias of Heart and Brain

WHERE: McGill University
WHEN: Thursday, March 6, 2014: 4:00 - 5:00pm ET
SPEAKER: Jeff Noebels, MD, PhD
HOST: Massimo Avoli, MD, PhD

TALK SUMMARY: The dimensions and urgency of preventing sudden unexpected death in epilepsy (SUDEP) have grown rapidly in the last two decades. At least 3,000 SUDEP deaths occur each year in North America. Like its close relatives, SIDS (Sudden Infant Death), SUDY (Sudden Death in the Young), and SADS (Sudden Arrhythmogenic Death Syndrome), all of which may include seizures, the causes are mysterious to family, physician, and medical examiner alike. SUDEP strikes without warning, not as the result of the first or even longest seizure in a person’s life, but within minutes or hours, as a tragic outcome of the last. It is the most common cause of premature mortality in human epilepsy. Recent advances in the molecular genetics of brain circuits controlling cardiorespiratory pacemakers reveal that mutations in specific genes co-expressed in the brain and heart dramatically raise the risk of SUDEP. Expanding this list of predictive risk genes, understanding their mechanisms, and identifying gene-specific treatments may soon dramatically alter our ability to save lives and improve the well-being of patients and family members living with epilepsy.


St Lake City

Salt Lake City, UT
Large-Scale Team Science and Epilepsy Genetics: The EPGP and Epi4K Experience

WHERE: University of Utah
WHEN: Monday, March 17, 2014
SPEAKER: Dan Lowenstein, MD
HOST: Karen Wilcox, PhD

TALK SUMMARY: Dr. Lowenstein’s major research interest is focused on understanding the genetic basis of the more common forms of human epilepsy, and translating these findings into the direct care of the patient. Over the last ten years, he has been a principal organizer of two large-scale, international efforts to study the complex genetics of epilepsy: the “Epilepsy Phenome/Genome Project” and “Epi4K: Gene Discovery in 4,000 Genomes”, both of which are funded by NIH and have already yielded discoveries that are bringing us closer to the era of precision medicine in epilepsy.

Video See a video from the seminar here


St. Louis

St. Louis, MO
Using Patient-Derived Neurons To Study Genetic Epilepsies

WHERE: Washington University
WHEN: Friday, March 28, 2014
SPEAKER: Jack Parent, MD
HOST: Michael Wong, MD, PhD

TALK SUMMARY: Many childhood-onset epilepsies are extremely difficult to treat and have a poor prognosis. Dr. Parent has been working on understanding the causes underlying some of severe pediatric epilepsies using a new approach to model the disorders – induced stem cells – in which a patient’s own cells can be studied. The induced stem cell method involves taking skin biopsies from patients and turning their skin cells into stem cells. Then those stem cells can be turned into neurons to study the causes of epilepsy and test new therapies. In some cases, the stem cells can also be turned into hear cells and used to study the causes of SUDEP in these patients.

Dr. Parent’s talk will describe the use of this approach to explore two devastating types of epilepsy, Dravet Syndrome and Pretzel Syndrome. He will present data showing the generation of patient-specific neurons and heart cells to study epilepsy and SUDEP, respectively. This approach represents a powerful new research strategy to uncover how epilepsy develops and identify new and potentially individualized therapies.



Seattle, WA
Are You Only Using 75% of Your Brain?

WHERE: University of Washington
WHEN: Thursday, April 24, 2014
SPEAKER: Kevin Staley, MD
HOST: Nick Poolos, MD, PhD

TALK SUMMARY: Is loss of inhibition of neurons the cause of seizures? Answering that question would be easier if we knew how neurons lose their inhibitions. One idea is that the chloride isn’t balanced in the brain of patients with epilepsy and chloride is important for inhibition. Imbalance of chloride can actually make neurons that are supposed to be inhibitory, behave as excitatory instead. This could lead to a seizures. Chloride balance is mostly regulated by large, relatively immobile negatively charged proteins (called anions) that can get bigger or smaller very quickly. If these anions stay in place and don’t change in size, chloride will be in balance in the brain. But things like injuries and swelling can cause these anions to leak out of cells or to change size, and this can lead to a chloride imbalance and subsequent seizures.

Interestingly, one quarter of the brain’s volume is made up of these anions and very little is known about how they work. This talk will address how we are now learning that these anions and chloride play a role in brain injury that leads to seizures.

Video Watch video from the seminar here



San Francisco, CA
Born Another Day: The critical timing of an epilepsy-inducing brain injury during the development of newly born neurons

WHERE: University of California, San Francisco
WHEN: Wednesday, May 28, 2014
SPEAKER: Istvan Mody
HOST: Scott Baraban

TALK SUMMARY: A region deep inside in the brain called the dentate gyrus is capable of producing new nerve cells throughout life. Temporal lobe epilepsy (TLE) frequently develops after some time following a brain insult that includes prolonged seizures, inflammation, head trauma, or stroke. When the newly born cells in the dentate gyrus are "caught" by the insult at a specific time during their development, their normal development becomes derailed, and these neurons get transformed into key contributors to the development of TLE.

Video Watch video from the seminar here



Little Rock, AR
Noninvasive Localization of Epileptic Foci During Interictal Recordings: Clinical MEG and EEG-fMRI in the Evaluation of Intractable Epilepsies

WHERE: University of Arkansas for Medical Sciences
WHEN: Friday, August 29, 2014: 8:00 - 9:00am CT
SPEAKER: Andreas Alexopoulos, MD, MPH
HOST: Demitre Serletis, MD, PhD

TALK SUMMARY: Up to 40% of individuals with epilepsy will exhibit medical refractoriness to all available antiepileptic medications. Most of these patients are destined to lead a life of disruptive, uncontrolled seizures and undesirable medication side effects. Resective epilepsy surgery may be offered in select cases where the epileptogenic focus can be localized and targeted, with excellent clinical outcomes. Therefore, accurate localization of the epileptogenic zone is essential and underscores the need for an extensive work-up in patients with refractory epilepsy. In the most complex cases of epilepsy, localization of the epileptogenic network can be challenging especially when EEG and imaging studies are inconclusive. In this context, newer tools - such as magnetoencephalography (MEG) and EEG-correlated functional MRI (EEG/fMRI) - are needed, and have been employed, to improve the noninvasive estimation of the epileptogenic network. Both are considered interictal studies as they rely on measures of electromagnetic signals during the interictal state. This presentation will discuss selected concepts and limitations of recording MEG and EEG/fMRI signals in refractory epilepsy patients. It will also review some of the earlier studies that have explored the use of MEG and EEG/fMRI in clinical epilepsy, and examine preliminary results from our laboratory. Ultimately, this type of research seeks to guide future applications of these modalities that will in turn advance our understanding of the initiation and propagation of seizures at the network level in different types of epilepsy.



Calgary, Canada
Improving Outcomes in Early Onset Epilepsies

WHERE: University of Calgary
WHEN: Monday, September 8, 2014: 8:00 - 9:00am MT
SPEAKER: Helen Cross, PhD
HOST: Jong Rho, MD

TALK SUMMARY: Epilepsy with onset under two years of age in general has a poor prognosis for both seizure control as well as neurodevelopmental outcome. A prominent predictor of outcome remains aetiology, although the epileptic seizures will have a compounding effect, and seizure control is likely to lead to improved outcome. However, in many our treatments remain unsuccessful. Increasingly we are determining causes of the epilepsies in this age group, specifically genetic and structural causes, and consequently our approach to this group of disorders is moving forward. Treatments are therefore being increasingly targeted at the underlying cause. Resective surgery should be considered early in the presence of focal brain lesions, likely to be the cause of seizures even where generalised features are apparent electroclinically. There is increasing evidence for improved neurodevelopmental outcomes in this group the presence of seizure control. Neurometabolic disorders will demand specific treatments, such as in pyridoxine dependency and Glucose Transporter defects (ketogenic diet). Genetic discovery has widened our insight into this group of disorders, and is likely to lead to other possible targeted treatments in the future.



New York, NY
Toward the development of new therapies for intractable epilepsies

WHERE: Columbia University
WHEN: Friday, September 19, 2014
SPEAKER: Scott Baraban, PhD
HOST: Guy M. McKhann, MD

TALK SUMMARY: Epilepsy is a neurological disorder characterized by spontaneous recurrent seizures. An estimated 3 million Americans suffer with epilepsy making it more common than multiple sclerosis, cerebral palsy, muscular dystrophy and Parkinson’s disease combined. Seizures can be life-threatening events and uncontrolled seizures, especially in children, result in significant developmental delay and cognitive deficit. The ultimate goal of epilepsy treatment (and CURE) is to control seizures, with no side effects. However, despite the availability of more than twenty-five FDA-approved antiepileptic drugs, surgical resection and vagal nerve stimulator options, 30% to 40% of all epilepsy patients remain drug resistant and continue to suffer with uncontrolled seizures. These individuals have intractable epilepsy and, as defined by the Institute of Medicine, represent an "urgent and unmet clinical need". Unfortunately, this is approximately the same number of intractable epilepsy patients as were reported over fifty years ago. In the Baraban laboratory, we are developing novel therapeutic approaches targeted toward this patient population. These follow two parallel paths: one, is to use cell transplantation of GABA neural progenitors to generate new functionally integrated inhibitory interneurons in mice and the second, incorporates a “precision medicine” strategy that capitalizes on the genetic tractability and drug screening advantages of a simple vertebrate species (zebrafish). In this seminar, our current progress in pursuing these two pre-clinical research programs will be discussed.



Miami, FL
Epilepsy Plus: Epidemiology of psychiatric disorders and migraine in epilepsy

WHERE: University of Miami, Miller School of Medicine
WHEN: Friday, October 17, 2014, 12:00 – 1:15pm ET
SPEAKER: Dale Hesdorffer, PhD
HOST: Andres Kanner, MD

TALK SUMMARY: Epilepsy is the fourth most common neurological disease in the United States. But seizures are not the only manifestation of epilepsy. Comorbid conditions, such as psychiatric disorders, suicidal behaviors and migraine, are often seen in people with epilepsy and may have a greater impact on the individual than the seizures themselves.

Epilepsy comorbidities have been known since the first half of the second millennium BC through ancient Babylonian texts describing the overlap of epilepsy and psychosis and through the texts by Hippocrates, mentioning the melancholia of epilepsy. Much later, psychiatric disorders were described in association with epilepsy in cross-sectional studies and the interpretation was given that the burden of having epilepsy was associated with the development of disorders such as depression. Since the 1990's, however, new studies have accumulated, revising this story and revealing that psychiatric disorders and migraine are associated with an increased risk for developing epilepsy and that new onset epilepsy is associated with an increased risk for developing psychiatric disorders and migraine. These findings have spurred studies on the impact of pre-existing comorbid conditions on the course of epilepsy (e.g., continued seizures and mortality), quality of life, and feelings of stigma. This presentation will describe the evolution and impact newer findings on epilepsy comorbidities, focusing on psychiatric disorders, suicidal behavior and migraine.



Boston, MA
Epilepsy Genetics and Clinical Practice: Impact of the $1000 Genome

WHERE: Harvard University
WHEN: Thursday, December 11, 2014
SPEAKER: Samuel Berkovic, MD, PhD
HOST: Andrew Cole, MD

TALK SUMMARY: Genetic factors play a role in essentially every patient with epilepsy, although these vary from crucial to clinically trivial. Enormous progress has recently occurred in the understanding of epilepsy genetics, both at clinical genetic and basic science levels. Currently, genetic defects underlying epilepsies can be identified in an important minority of cases. Many epilepsy genes discovered to date encode ion channel subunits, leading to the concept that the genetic epilepsies are, at least in part, a family of channelopathies. Non-ion channels genes are also emerging as important, notably the gene encoding the glucose transporter GLUT-1 and the mTOR regulator DEPDC5. In the infantile epileptic encephalopathies, remarkable advances have revealed a group of causative genes for a major group of hitherto ill-understood cases. The new wave of technology is resulting in rapid solving of Mendelian epilepsies and, for epilepsies with complex inheritance, is generating an avalanche of data, with challenges for pragmatic interpretation. This technology, with its enormous power and diminishing cost, will shortly lead to major advances in the utility and widespread applicability of genetics at the clinic.


2013 Locations


Denver, CO
Cell-type Specific Control of Neuronal Circuits in Epilepsy

WHERE: University of Colorado
WHEN: Tuesday, October 22, 2013: 12:00 - 1:00pm MT
SPEAKER: Ivan Soltesz, PhD
HOST: Manisha Patel, PhD

TALK SUMMARY: Dr. Soltesz's major research interest is focused on GABAergic interneuronal microcircuits, neuronal oscillations, and the cellular and synaptic basis of epilepsy. His laboratory employs closely integrated experimental and theoretical techniques, including closed-loop in vivo optogenetics, paired patch clamp recordings, in vivo recordings from identified interneurons in awake mice, optical imaging, and large-scale computational modeling methods using supercomputers.

Video Watch video from the seminar here



Houston, TX
Does Human Papilloma Virus Cause Brain Malformations?

WHERE: Baylor College of Medicine
WHEN: Monday, November 18, 2013
SPEAKER: Peter Crino, MD, PhD
HOST: Jeff Noebels, MD, PhD

TALK SUMMARY: Focal cortical dysplasia (FCD) is the most common brain malformation associated with intractable epilepsy. Some FCDs arise from gene mutations whereas others result from unknown causes. Many FCD subtypes are associated with abnormalities in mammalian target of rapamycin (mTOR) signaling. We have recently found that the human papilloma virus 16 (HPV16) oncoprotein E6, which is the most common cause of cervical dysplasia and cancer, is expressed in brain tissue of patients with FCD and this leads to disruption of mTOR signaling. These results suggest some FCDs are caused by HPV16 infection and may be preventable.

Video See a video from the seminar here



Bronx, NY
Optogenetics: Tools for Mapping and Controlling Brain Dynamics

WHERE: Einstein College of Medicine
WHEN: Friday, December 20, 2013: 4:00 - 5:00pm ET
SPEAKER: Ed Boyden, PhD
HOST: Aristea Galanapoulou, PhD

TALK SUMMARY: The brain is a complex, densely wired circuit made out of heterogeneous cells, which vary in their shapes, molecular composition, and patterns of connectivity. In order to help discover how neural circuits implement brain functions, and how these computations go awry in brain disorders such as epilepsy, we invent technologies to enable the scalable, systematic observation and control of biological structures and processes in the living brain. We have developed genetically-encoded reagents that, when expressed in specific neuron types in the nervous system, enable their electrical activities to be precisely driven or silenced in response to millisecond timescale pulses of light. Often working in interdisciplinary collaborations, we have developed microfabricated hardware to enable complex and distributed neural circuits to be controlled and observed in a fully 3-D fashion, as well as robots that can automatically record neurons intracellularly and integratively in live brain, and strategies for building 3-D brain circuits in vitro. These tools are in widespread use to enable systematic analysis of neural circuit functions, are also opening up new frontiers on the understanding and treatment of brain disorders, and may serve as components of new platforms for diagnosing and treating brain disease. In particular, we will discuss how such technologies are being used to open up new frontiers on the understanding and potential treatment of epilepsy.

Video See videos from the seminar here