**5.4 Phenytoin**

Phenytoin has been the most commonly used antiepileptic drug for patients with focal and generalized epilepsies since 1938 [52]. Its mechanism of action is exerted by inactivating voltage-gated Na<sup>+</sup> channels. It also acts by inhibiting the flow of Ca2+ through neuronal membranes, such as it is to be expected at the cardiac level, it also inhibits Na<sup>+</sup> channels, which is why it has toxic effects on the myocardium [53]. Phenytoin is bound to plasma proteins, such as albumin, which is metabolized in the liver, so it can cause liver diseases. Toxic effects are present even if the patient has adequate therapeutic levels, like at concentrations lower than 20 mg/Kg [54, 55]. Among the clinical toxic effects, patients may present nystagmus, ataxia, and numbness [56]. With more severe intoxications, in addition to the

above: dysarthria, ataxia, the patient might not be able to walk, and may present hyperreflexia, besides consciousness usually being inhibited [57]. With higher doses, patients may even display a coma [58].

## **5.5 Lamotrigine**

Lamotrigine is an antiepileptic drug principally used for generalized and partial seizures; it is also used in the adjunctive treatment of refractory crises [59]. Its action mechanism at the cellular level is based on blocking excitatory neurotransmitters, especially glutamate, through its NMDA receptors, as well as inhibiting voltage-dependent Na<sup>+</sup> currents [60]. The toxic effects on patients who take this drug above 600 mg are characterized primarily at the CNS level by difficulty in concentration, showing dysarthria, nystagmus, and blurred or double vision. Patients may even present a loss of balance or coordination [61]. Its absorption is intestinal, its elimination in the urine, metabolized in the liver. Thus, there is idiosyncratic hepatotoxicity that commonly requires liver transplantation [62].
