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2014 NINDS Benchmarks for Epilepsy Research


On April 17-19, 2013, NINDS hosted Curing the Epilepsies 2013: Pathways Forward, the third in a series of Curing the Epilepsies conferences held in partnership with epilepsy advocacy and professional organizations to assess progress in epilepsy research and help set an agenda for future years. As an important outcome, these conferences have led to the development of Benchmarks for Epilepsy Research, which reflect priorities shared across the epilepsy community for research toward clinically meaningful advances in understanding and treating the epilepsies. Since their initial development in 2000, the Benchmarks have brought attention to goals such as preventing epileptogenesis, addressing aspects of epilepsy beyond seizures, and confronting the challenge of sudden unexpected death in epilepsy (SUDEP).

With input received during and prior to the April 2013 conference, NINDS has developed 2014 Benchmarks for Epilepsy Research as a framework for focusing research and benchmarking progress over the next five to ten years. The final 2014 Benchmarks incorporate revisions in response to public comments on a draft posted in October 2013. 


2014 NINDS Benchmarks for Epilepsy Research

  1. Collapsable minus sign. When the image is clicked on the exposed links that are in bulleted fashion will be hidden. Understand the causes of the epilepsies and epilepsy-related neurologic, psychiatric, and somatic conditions.
    1. Identify new genes and pathways associated with the epilepsies and epilepsy-related conditions.
    2. Identify new infectious, immune, age-related, environmental, or other causes and risk factors associated with the epilepsies and epilepsy-related conditions.
    3. Determine whether factors related to age, gender, race/ethnicity, socioeconomic status, and other features of specific populations affect risk and mechanisms of epilepsy and epilepsy-related conditions.
    4. Determine whether the bi-directional relationships that exist between the epilepsies and several co-occurring conditions (e.g., neuropsychiatric or neurodevelopmental disorders) result from the same underlying causal mechanisms, interacting mechanisms, or are a consequence of the first presenting condition.

  2. Collapsable minus sign. When the image is clicked on the exposed links that are in bulleted fashion will be hidden. Prevent epilepsy and its progression.
    1. Understand epileptogenic processes involved in epilepsies with neurodevelopmental origins, including those due to genetic or presumed genetic causes.
    2. Understand epileptogenic processes involved in the development of epilepsy following traumatic brain injury, stroke, brain tumor, infections, neurodegeneration, or other insults to the brain.
    3. Identify biomarkers that will aid in identifying, predicting, and monitoring epileptogenesis and disease progression, including markers early after injury/insult that identify those people at risk for epilepsy.
    4. Develop or refine models aligned with the etiologies of human epilepsies to enable improved understanding of epileptogenesis and rigorous preclinical therapy development for epilepsy prevention or disease modification.
    5. Identify new targets and develop interventions to prevent or modify epileptogenesis and the progression of epilepsy and epilepsy-related conditions.

  3. Collapsable minus sign. When the image is clicked on the exposed links that are in bulleted fashion will be hidden. Improve treatment options for controlling seizures and epilepsy-related conditions without side effects.
    1. Understand the initiation, propagation, and termination of seizures at the network level in different forms of epilepsy.
    2. Identify biomarkers for assessing or predicting treatment response, including markers that may identify specific populations that are likely to have good outcomes or develop adverse responses.
    3. Develop or refine models that are aligned with etiologies and clinical features of human epilepsies, especially treatment resistant forms, to enable improved understanding of ictogenesis and preclinical development to improve seizure control with fewer side effects. Establish the sensitivity and specificity of these models with regard to current therapies.
    4. Identify, develop, and improve interventions to detect, predict, prevent, or terminate seizures, including approaches suitable for use in the home and other non-medical settings.
    5. Identify, develop, and improve anti-seizure therapies that target (either alone, or in combination) novel or multiple seizure mechanisms.
    6. Develop, improve, and implement interventions for effective self-management, including treatment adherence.
    7. Develop and validate objective patient-centered outcome metrics for clinical studies.

  4. Collapsable minus sign. When the image is clicked on the exposed links that are in bulleted fashion will be hidden. Limit or prevent adverse consequences of seizures and their treatment across the lifespan.
    1. Understand and limit adverse impacts of seizures on quality of life, including effects on neurodevelopment, mental health, intellectual abilities, and other neurological and non-neurological functions.
    2. Understand and limit adverse impacts of anti-seizure treatments (medical, surgical, or other interventions) on quality of life, including effects on neurodevelopment, mental health, intellectual abilities, and other neurological and non-neurological functions.
    3. Understand risk factors and mechanisms involved in non-epileptic seizures (NES). Develop effective approaches for earlier and accurate diagnosis and treatment.
    4. Identify causes, risk factors, and potential preventive strategies for sudden unexpected death in epilepsy (SUDEP) and other epilepsy-related mortality (for example, suicide) in people with epilepsy.
    5. Identify the impact of pharmacological treatment of the epilepsies on fetal and neonatal development. Develop strategies to control seizures in pregnancy without causing harm to either the mother or child.

View 2014 Benchmarks with introductory preamble: (PDF, 320 kB)


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Last updated December 6, 2013