| Početna strana | Uredništvo | Časopis  | Uputstvo autorima  | Kodeks u  kliničkom i eksperimentalnom radu | Kontakt  |  
| Home page | Editorial  board | About the Journal | Instructions for Authors | Peer Review Policy | Clinical and Experimental Work Code | Contact  |


Acta Medica Medianae
Vol. 51, No 1, March, 2012

UDK 61
ISSN 0365-4478(Printed version)
ISSN 1821-2794(Online)


Correspondence to:

Stevo Lukic

Clinical Centre Niš

Clinic for Neurology

Bul. dr Zorana Djindjića 48

18000 Niš, Serbia

E-mail: slukic@medfak.ni.ac.rs

Review article                                                                    

UDC: 616.853-092:615.213




Pathophysiological or empirical approach to the pharmacotherapy of epilepsy?


Srdjan Ljubisavljević1, Mirjana Spasić2, Vladmila Bojanić1 and Stevo Lukić2


University of Niš, Faculty of Medicine, Institute for Pathophysiology, Niš, Serbia1

Clinical Centre Niš, Clinic for Neurology, Niš, Serbia2


The knowledge of etiopathogenesis of epilepsy and the therapeutic treatment of this disease has evolved from the mechanistic approach to the time when a lot is known about the pathophisyological basis of this disease, the mechanisms of epileptogenesis and the propagation of seizures.

The aim of this review article is to point to some analyses about the ways the understanding of the mechanisms of action of antiepileptic drugs (AEDs) can help with the prediction of the clinical response to AEDs, and, therefore, ultimately improve the treatment of epilepsy.

In contrast to other therapeutic areas, epilepsy is still an area where therapeutic algorithms cannot be designed through pathophysiological mechanistic approach. It is very unlikely that in the near future doctors will be advised to treat the given epileptic syndrome with a “sodium channel blocker”, “AMPA receptor antagonist”, “GABA transmission blocker”, or the “combination of sodium channel blocker and P glycoprotein inhibitor”.

Preliminary evidence suggest that, when it comes to patients with refractory epilepsy, the cause can be a disorder at the level of ionic channels which are insensible to the effects of the medication used, or the genetically determined abnormality of a receptor subunit. According to this evidence, dysfunctional ionic channels may be the new target of antiepileptic treatments. Acta Medica Medianae 2012; 51(1):59-65.


      Key words: epilepsy, epileptogenesis, antiepileptic therapy