Foundation Launch Phase

Fighting for Hope. Driving Awareness.

Supporting families, advancing research, and raising awareness for a rare and severe form of epilepsy caused by SCN1A Gain-of-Function mutations.

The Critical Gap in SCN1A Research

Most SCN1A mutations—such as those causing Dravet Syndrome—result in a "loss" of sodium channel function. However, in Gain of Function (GoF), the sodium channels in the brain are overactive or "stuck open."

Because SCN1A is widely synonymous with Dravet in clinical settings, GoF children are frequently misdiagnosed. This is a life-altering distinction: standard Dravet treatments can be ineffective or even harmful for GoF patients, who require a fundamentally different medical approach.

"We are the first foundation dedicated exclusively to these families, ensuring they aren't left behind by medical research that wasn't built for them."
11%
Rarity
Of all SCN1A-related diagnoses are Gain of Function. This represents a distinct medical population from Dravet Syndrome.
SCB
Treatment Paradox
Unlike Dravet, GoF patients may benefit from Sodium Channel Blockers (like oxcarbazepine), which are usually avoided.
DEE
Phenotype
Characterized by neonatal onset (0-3 months) and the 'Philadelphia Variant' (p.Thr226Met).

The Diagnostic Timeline

Understanding the critical clinical window where SCN1A Gain-of-Function fundamentally diverges from Dravet Syndrome.

0 - 3 Months

Neonatal Onset (EIDEE)

Unlike standard SCN1A variants which typically present around 6 months, GoF mutations frequently present earlier as severe, early infantile developmental and epileptic encephalopathy (EIDEE).

The Critical Gap

The Dravet Assumption

Because SCN1A is synonymous with Dravet Syndrome in many clinical settings, neonates are often incorrectly placed on standard Loss-of-Function protocols.

The Testing Window

Timing of Genetic Panels

Standard genetic epilepsy panels can take weeks to return. Advocating for Rapid Whole Exome Sequencing (rWES) in the NICU is critical during this window to minimize the infant's exposure to contraindicated medications.

Differentiation

Genetic Confirmation

Advanced genetic sequencing reveals specific mutations, such as p.Thr226Met (The Philadelphia Variant), identifying the sodium channel as "stuck open" rather than missing.

Clinical Action

The Treatment Paradox

Upon GoF confirmation, clinicians must often pivot protocols entirely. Paradoxically, these 11% of patients may respond significantly to Sodium Channel Blockers which are strictly contraindicated in the other 89%.

Family-Led Mission

About the Foundation

Founded by parents of children diagnosed with SCN1A Gain-of-Function epilepsy, we are a family-led organization dedicated to supporting others on this exact journey. Our mission is to fill the critical gap left by traditional SCN1A advocacy.

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Raising Awareness

We work to educate clinicians, advocate for accurate genetic differentiation, and bring public attention to the unique needs of the SCN1A GoF community.

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Supporting Families

We offer guidance, educational resources, and a growing community for caregivers navigating the terrifying reality of a rare EIDEE diagnosis.

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Advancing Research

We actively fund and support cutting-edge institutional research aimed at better understanding GoF mutations and unlocking targeted treatments.

Are you part of the 11%?

Whether you are a researcher studying EIDEE, a clinician treating a patient, or a family navigating a new GoF diagnosis, you are no longer alone. Let's map this together.