**Author details**

Several earlier interesting observations seem to be related to these findings to a certain extent. Turkdogan et al. (2002) found that increased lipid peroxidation in plasma may be causally related to the presence of abnormal structural changes as assessed by brain magnetic resonance (MR), rather, than to the treatment of epilepsy with focal or generalized epileptic discharges in the EEG, duration of epilepsy, or seizure frequency (more or fewer than 1 seizure a month). The authors found an increase in plasma lipid peroxidation in 52 children with epilepsy, treated with one or more AEDs and abnormal brain MR, compared with 16 healthy children (the difference was significant, p<0.05). No significant differences in anti-oxidant enzymes were found in either group. Patients with well-controlled seizures and children with drugresistant seizures but normal MRs had a higher SOD activity than children in the control group (p<0.05). GSH-Px (an antioxidant) activity was not significantly different in the children with

This interesting and heterogeneous picture of enzymatic activity in children with epilepsy and control children suggests that the relationship between various laboratory tests and numerous variables associated with the heterogeneity and treatment of epilepsy are very complex. Although the authors took seizure frequency into consideration, they did not state when blood tests were undertaken relative to seizure occurrence or to an imminent seizure, nor do they report EEG epileptic activity prior to the blood test. This makes it very difficult to monitor the causal relationships between the results of the various tests and their epileptic correlates.

Study of oxygen stress markers in the neocortex of drug-resistant epilepsy patients submitted to epilepsy surgery, supported human findings being in agreement with those found in animal models (Rumia et al., 2013). The concurrent increase in catalase (p<0.01) and decrease in GPx (p<0.05) together with unchanged SOD levels, suggests catalase as the main anti-oxidant enzyme in human epileptic cortex. The substantial increase in the levels of oxidants – 02 (-) and 8-oxo-dG in epileptic patients – in comparison with non-epileptic cortex samples – supports a

**1.** It seems that oxygen stress and its products may play an essential role in earliest stage of epileptogenesis. However, antioxidants as well as antiepiletic drugs do not prevent epileptogenesis. In seizure or epilepsy animal models, at best, both antioxidants or antepileptic drugs can delay the first seizure occurrence and diminish seizures' severity.

**2.** Research on animal models and patients with epilepsy suggests that epileptic seizures, epileptiform discharges and some AEDs (especially polytherapy) may produce oxygen

**3.** AEDs and the drug dosages have differential effects on oxygen stress. In epileptic patients (and in animal models of seizures) CBZ, OXC, PB, PHT and VPA produce oxygen stress. In experimental models of seizures, the majority of new generation AEDs has no or minor effects on oxygen stress; usually they have a more favourable effect on the oxidation and

stress and have a negative effect on the oxidation – anti-oxidation balance.

connection between chronic seizures and ROS-mediated neuronal damage.

epilepsy compared to the control group.

26 Pharmacology and Nutritional Intervention in the Treatment of Disease

**11. Conclusions**

Jerzy Majkowski\*

Address all correspondence to: fundacja@epilepsy.pl

Epilepsy Diagnostic and Therapeutic Center, Foundation of Epileptology, Warsaw, Poland

The authors have no conflict of interest to disclose.
