Sodium channel inhibitors

Sodium channel inhibitors

The sodium channel inhibitors preferentially bind the sodium-channels of neurons that are in highly active excitation. So they can distinguish the different states of the channel. In this way they will not bind channels of the normal functioning neurons. Sodium channel inhibitors can be applied in all kinds of epilepsy. The different group members are discussed here:

Phenytoin can be difficult to dose appropriately for a specific patient. It can cause concentration-dependent adverse effects (AEs) such as ataxia, nystagmus, diplopia and at high concentrations cognitive changes and an altered level of consciousness. Within the therapeutic range, the capacity of drug-metabolizing enzymes can be exceeded and result in a disproportionate increase of blood levels and thus toxicity. Chronic AEs include gingival hyperplasia and hirsutism as well as teratogenic effects during pregnancy. Phenytoin should be cautiously used with other drugs as it a potent enzyme-inducer.




Carbamazepine and oxcarbazepine both have enzyme inducing capacities, although oxcarbazepine in lesser extent. Dose-related AEs are similar to phenytoin, idiosyncratic AEs include leukopenia, and hyponatremia (and possible SIADH).

Lamotrigine has no enzyme inducing capacities. It’s dose-related and chronic AEs are similar as carbamazepine.

Zonisamide is a new sodium channel blocker with a long half-life. It might possess other antiepileptic properties as well.

Valproic acid is explained as a separate topic. All these drugs can cause a serious rash.


A 37-year-old man with generalised seizures is seen by his dentist for routine checkup. The dentist observes an overgrowth of gum tissue. The patient was most likely receiving which of the following drugs?


Which monitoring is appropriate for a patient on phenytoin?


Which of the following antiepileptic drugs is an enzyme inducer?