**2. Pharmacotherapy of epilepsy-Valproic acid**

There are a large range of antiepileptic drugs with different mechanisms of action, pharma‐ cokinetics, pharmacology, and important side effects. Pharmacotherapy of epilepsy is symp‐ tomatic.

Valproic acid (VPA) which is an eight-carbon branched-chain fatty acid, is one of the most widely used effective antiepileptic drugs. The main mechanism of the action includes a blockade of sodium channels, activating calcium dependent potassium conductance and GABAergic effect [7]. VPA is metabolized by microsomal glucuronide conjugation, mitochon‐ drial beta-oxidation and cytochrome P450-dependent omega-, (omega-1)-and (omega-2) oxidation [8]. Therefore, an involvement of lipid peroxidation seems to be probable during pharmacotherapy with VPA.

Serious side effects are relatively rare but include fatal hepatotoxicity and acute haemorrhag‐ ic pancreatitis. They occur mainly in children on polypharmacy and those with organic brain disease. Hyperammonaemic encephalopathy has been reported in patients with urea cycle disorder. Benign elevation of liver enzymes is common during valproate therapy and dose depended. Thrombocytopenia and other haematological abnormalities should be control‐ led. Other troublesome adverse effects are weight gain, gastrointestinal disturbances, hair loss and tremors. Hormonal disturbances with polycystic ovary syndrome and risk of teratogenicity, including a 1 to 3% risk of neural tube defects, make the use of VPA in some women undesirable [7].

In numerous studies there was found to be an imbalance in oxidative status of the patient with epilepsy treated with VPA [9].
