**5.1 Valproic acid**

Since 1978, valproic acid or Na+ valproate has been characterized as an antiepileptic drug that suppresses the neuronal excitation of different types of epilepsy, such as partial seizures and generalized seizures [35]. It appears that valproic acid exerts its inhibition by blocking the reuptake of the neurotransmitter GABA, the main inhibitory neurotransmitter. It also lowers glutamate levels and modifies K+ conductance [36], exerting an inhibition through the voltage-dependent Na+ channels. In this way, it reduces the excitement caused by epileptic seizures [37]. Once this drug reaches the central nervous system (CNS), it binds to plasma proteins and is distributed throughout the extracellular space [38]. It is metabolized in the liver and discharged through the urine. Although it is also eliminated with expirations in the form of CO2 [39]. However, this drug is known to have frequent toxic effects derived from the therapeutic dose in patients with toxic plasma levels greater than 120 μg/ ml [40]. After an overdose, the patient may be lethargic and coma, most likely due


#### **Table 2.**

*Main drugs associated with drugs.*

to inhibition produced in the CNS [41]. Another adverse situation that derives from the consumption of this antiepileptic drug is cerebral edema, probably caused by the overstimulation of the stimulation of NMDA receptors [42]. Cardiovascular alterations such as hypotension with tachycardia, gastric alterations such as pancreatitis, and hepatotoxicity have manifested with elevated transaminases, jaundice, and abdominal pain with inflammation, among others, may also occur [43].
