Looking into possibilities for my second disease project, I remember lightly looking into Sturge-Weber syndrome a year or two ago. The syndrome affects the development of blood vessels in a newborn, resulting in abnormalities as they grow up. One key staple in identifying this disorder is red “port-wine” marks on the face or limbs, as well as risk of seizures.
The article discusses the effects of Levetiracetem, the generic version of Keppra, an anticonvulsant medication. The article summarizes what happens in the human body during a epilepsy, and the medication’s mechanism of action. The medication binds to the SV2A synaptic vesicle proteins found in the brain. They are characterized by “almost complete absorption, minimal insignificant binding to plasma protein, absence of enzyme induction, absence of interactions with other drugs, and partial metabolism outside the liver.” Connecting back to the originally mentioned syndrome, the blood vessels in the individual develop in such a way that there is random pressure on the trigeminal nerve, causing random episodes of seizures. Following the mechanism of Levetiracetem, how does that properly offset this problem?
The answer is I don’t think it does. The article is a published journal on the effects of Levetiracetem on treatment of Epilepsy. The article mentions how the medication works, and the positive effects, however it does point out that half of patients fail the initial antileptic drug, and 35% are refractive to medical therapy. This means that there is much room for studying and finding more effective ways to deal with convulstion, especially in rare scenarios like Sturge Weber Syndrome.
Abou-Khalil B. (2008). Levetiracetam in the treatment of epilepsy. Neuropsychiatric disease and treatment, 4(3), 507–523. https://doi.org/10.2147/ndt.s2937
Cellular Biology Business 