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Lacosamide, sold under the brand name Vimpat among others, is a medication used for the treatment of Focal-onset seizures and primary generalized tonic-clonic seizures. It is used by mouth or intravenously.
Read the full article on WikipediaIntractable focal onset seizures Clinical criteria: Treatment Phase: Continuing treatment Patient must have previously received PBS-subsidised treatment with this drug for this condition.
Idiopathic generalised epilepsy with primary generalised tonic-clonic seizures Clinical criteria: Treatment criteria: Must be treated by a neurologist; OR Must be treated by a paediatrician; OR Must be treated by an eligible practitioner type who has consulted at least one of the above mentioned specialist types, with agreement reached that the patient should be treated with this pharmaceutical benefit on this occasion. The condition must have failed to be controlled satisfactorily by at least two antiseizure medications prior to when the drug is/was first commenced, AND The treatment must be (for initiating treatment)/have been (for continuing treatment) in combination with at least one PBS-subsidised antiseizure medication at the time the drug is/was first commenced.
“Lacosamide is a functionalized amino acid that produces activity in the maximal electroshock seizure (MES) test, that, like some other antiepileptic drugs (AEDs), are believed to act through voltage-gated sodium channels. Lacosamide enhances the slow inactivation of voltage-gated sodium channels without affecting the fast inactivation of voltage-gated sodium channels. This inactivation prevents the channel from opening, helping end the action potential. Many antiepileptic drugs, like carbamazepine or lamotrigine, slow the recovery from inactivation and hence reduce the ability of neurons to fire action potentials. Inactivation only occurs in neurons firing action potentials; this means that drugs that modulate fast inactivation selectively reduce the firing in active cells. Slow inactivation is similar but does not produce complete blockade of voltage gated sodium channels, with both activation and inactivation occurring over hundreds of milliseconds or more. Lacosamide makes this inactivation happen at less depolarized membrane potentials. This means that lacosamide only affects neurons which are depolarized or active for long periods of time, typical of neurons at the focus of epilepsy. Lacosamide administration results in the inhibition of repetitive neuronal firing, the stabilization of hyperexcitable neuronal membranes, and the reduction of long-term channel availability, but does not affect physiological function. Lacosamide has a dual mechanism of action. It also modulates collapsin response mediator protein 2 (CRMP-2), preventing the formation of abnormal neuronal connections in the brain.”
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