[Over the last decades, drug therapy for epilepsy has changed substantially, which generated new expectations. The first-line therapy of epilepsies is pharmacological treatment, which is effective in 60 to 70% of patients. Despite this favourable result, even today's drug therapy cannot yet be considered optimal. Prior to 1990, only six major antiepileptics were available for the clinicians, while since then more than ten new drugs have been introduced into the market. The older drugs have the advantage of long-term experience, known efficacy, and lower cost. These first generation drugs, while effective in patients with newly diagnosed epilepsy, share some unfavourable properties. They do not control many patients adequately, while with their long-term use chronic side effects develop. The purpose of this paper is to summarize recent data on the efficacy, safety, and administration of the older and new antiepileptic drugs. The main factors to consider when choosing a drug for treatment include syndromatological classification of the disease, efficacy and tolerability of the drug, and individual patient considerations. Of the first generation antiepileptics, carbamapezine, valproate, ethosuximide, and to some extent the clobazam and clonazepam are still widely used (benzodiazepines only as adjunctive therapy). The use of phenobarbitals, primidone, phenytoin, and sulthiam has diminished because of their side effects and inadequate efficacy. New antiepileptics are more efficient primarily in the therapy of West syndrome, Lennox-Gastaut syndrome, and in idiopathic generalized epilepsies. The pharmacokinetic properties of gabapentin, lamotrigine, levetiracetam, and oxcarbazepine are favourable, and their clinical use is safe. The use of felbamate, vigabatrin, and topiramate requires close attention because of their side effects.]

[Nitric oxide is a key molecule of the human body. Since its discovery, a library of books and papers have been published on its physiological and pathophysiological role. It is involved in almost all pathological processes. In healthy individuals nitric oxide plays a crucial role in the vascular regulation by protecting against atherosclerosis, myocardial infarction and stroke. In the central nervous system, nitric oxide in its function as a neurotransmitter is responsible for synaptic plasticity, long-term potentiation, memory and a number of neuroendocrine control mechanisms. Furthermore, during inflammation and host defense, macrophages and neutrophils produce nitric oxide that has antibacterial, antiviral, and tumour cell killing activity. In pathologic conditions, however, nitric oxide reacts with superoxide anion to form peroxynitrite that damages the enzymes of the mitochondrial respiratory chain, superoxide-dismutase, reduced glutathion and activates or inactivates signalling molecules. During ischaemia- reperfusion, nitric oxide and peroxynitrite contribute to nitrative/nitrosative stress, DNAfragmentation and consequent polyADP-ribosepolymerase- 1 enzyme activation both in coronary thrombosis and ischaemic stroke.]