Indication
Seizures associated with tuberous sclerosis complex
Seizures associated with tuberous sclerosis complex represent the primary neurological manifestation of an autosomal dominant genetic neurocutaneous disorder caused by inactivating mutations in either the TSC1 or TSC2 genes. Read more about Seizures associated with tuberous sclerosis complex
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Common Seizures associated with tuberous sclerosis complex therapies.
EPIDIOLEX (cannabidiol (CBD))
EPIDIOLEX (cannabidiol (CBD))
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Coming soonSeizures associated with tuberous sclerosis complex represent the primary neurological manifestation of an autosomal dominant genetic neurocutaneous disorder caused by inactivating mutations in either the TSC1 or TSC2 genes.
These genetic variants cause hyperactivation of the mechanistic target of rapamycin signaling pathway, leading to abnormal cellular proliferation, disordered neuronal migration, and the development of benign hamartomatous glioneuronal lesions known as cortical tubers and subependymal nodules.
Clinically affecting pediatric and adult patients, these seizures often begin in infancy as epileptic spasms and frequently evolve into focal or multifocal seizures that demonstrate high rates of pharmacoresistance and correlate with neurodevelopmental and cognitive impairments.
- nih.gov
Seizures associated with tuberous sclerosis complex represent the primary neurological manifestation of an autosomal dominant genetic neurocutaneous disorder caused by inactivating mutations in either the TSC1 or TSC2 genes These genetic variants cause hyperactivation of the mechanistic target of rapamycin signaling pathway, leading to abnormal cellular proliferation, disordered neuronal migration, and the development of benign hamartomatous glioneuronal lesions known as cortical tubers and sube...
- ovid.com
Seizures associated with tuberous sclerosis complex represent the primary neurological manifestation of an autosomal dominant genetic neurocutaneous disorder caused by inactivating mutations in either the TSC1 or TSC2 genes These genetic variants cause hyperactivation of the mechanistic target of rapamycin signaling pathway, leading to abnormal cellular proliferation, disordered neuronal migration, and the development of benign hamartomatous glioneuronal lesions known as cortical tubers and sube...
- nih.gov
These genetic variants cause hyperactivation of the mechanistic target of rapamycin signaling pathway, leading to abnormal cellular proliferation, disordered neuronal migration, and the development of benign hamartomatous glioneuronal lesions known as cortical tubers and subependymal nodules
- nih.gov
Clinically affecting pediatric and adult patients, these seizures often begin in infancy as epileptic spasms and frequently evolve into focal or multifocal seizures that demonstrate high rates of pharmacoresistance and correlate with neurodevelopmental and cognitive impairments
- nih.gov
Clinically affecting pediatric and adult patients, these seizures often begin in infancy as epileptic spasms and frequently evolve into focal or multifocal seizures that demonstrate high rates of pharmacoresistance and correlate with neurodevelopmental and cognitive impairments
- neurologylive.com
Clinically affecting pediatric and adult patients, these seizures often begin in infancy as epileptic spasms and frequently evolve into focal or multifocal seizures that demonstrate high rates of pharmacoresistance and correlate with neurodevelopmental and cognitive impairments
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