Epilepsy and paroxysmal conditions

Advanced search


Full Text:


Every neurologist or epileptologist faces a problem of changing antiepileptic treatment. The goal of the therapy is producing seizure freedom. Many patients fail a first drug due to lack of efficacy or failure to tolerate an initial medication. While monotherapy is preferable in epilepsy treatment we need an alteration in therapy. The preferred method for converting between the first and the second therapy is transitional polytherapy, a process involving initiation of a new antiepileptic drug (AED) and adjuncting it toward a target dose while maintaining or reducing the dose of the baseline medication. This articale reviews practical consensus recommendations from an expert panel for successful monotherapy to monotherapy AED conversions are then summarized. Transitional polytherapy is most successful when clinicians appropriately manage the titration strategy and consider pharmacokinetic factors germane to the baseline and new adjunctive medication. 

About the Author

I. Ju. Kovaleva
Pirogov Russian National Research Medical University, Moscow
Russian Federation

Kovaleva Irina Jur’evna – PhD, Professor of Neurology, Neurosurgery and Medical Genetics, Medical Faculty.

Address: ul. Ostrovityanova, 1, Moscow, Russia, 117997


1. Karlov V.A. Epilepsy in children and adults: men and women: a guide for doctors [Jepilepsija u detej i vzroslyh: zhenshhin i muzhchin: rukovodstvo dlja vrachej (In Russian)]. Moscow. 2010.

2. Rudakova I.G. Epilepsiya i paroksizmal’nye sostoyaniya / Epilepsy and paroxysmal conditions. 2014; 4: 62-66.

3. Albani F., Riva R., Baruzzi A. Carbamazepine clinical pharmacology: a review. Pharmacopsychiatry. 1995; 28 (6): 235-244.

4. Beghi E. Adjunctive therapy versus alternative monotherapy in patients with partial epilepsy failing on a single drug. Epilepsy Res. 2003; 57: 1-13

5. Brodie M.J., Sills G.J. Combining antiepileptic drugs. Rational polytherapy. 2011; 20: 369-375.

6. Deckers CLP. Monotherapy versus polytherapy for epilepsy. Epilepsia. 2001; 42: 1387-94.

7. French J.A., Faught E. Rational polytherapy. Epilepsia. 2009; 50 (8): 63-68.

8. Garnett W.R. et al. Transitional Polytherapy: Tricks of the Trade for Monotherapy to Monotherapy AED Conversions. Current Neuropharmacology. 2009; 7: 83-95.

9. Glauster T., Ben-Menachem E. et al. ILAE treatment guidelines: evidence-based analisis of antiepileptic drug efficacy and effectiveness as initial monotherapy for epileptic seizures and syndromes. Epilepsia. 2006; 47: 1094-1120.

10. Karceski S., Morrell M.J., Carpenter D. Treatment of epilepsy in adults: expert opinion. Epilepsy & Behavior. 2005; 1-64.

11. Kwan P., Brodie M.J. Effectiveness of the first antiepileptic drug. Epilepsia. 2001; 42: 1255-1260.

12. Kwan P., Brodie M.J. Epilepsy after the first drug fails: substitution or add-on? Seizure. 2000; 9: 464-468.

13. Kwan P. Brodie M.J. Early identification of refractory epilepsy. N Engl J Med. 2000; 342: 314-9.

14. Lasoń W., Dudra-Jastrzębska M., Rejdak K., Czuczwar S.J. Basic mechanisms of antiepileptic drugs and their pharmacokinetic / pharmacodynamic interactions: an update. Pharmacol Rep. 2011; 63 (2): 271-92.

15. Löscher W. Basic pharmacology of valproate: a review after 35 years of clinical use for the treatment of epilepsy. CNS Drugs. 2002; 16 (10): 669-94.

16. McTague A., Appleton R. Treatment of difficult epilepsy. Arch Dis Child. 2011; 96: 200-204.

17. Nakken K.O., Eriksson A.S., Kwan P., Brodie M.J. Combination Therapy in Epilepsy. When and What to Use. Drugs. 2006; 66 (14): 18171829.

18. Panayotopoulos C.P. Principles of Therapy in Epilepsies. 2010

19. Perucca E. Clinically relevant drug interactions with antiepileptic drugs. Br J Clin Pharmacol. 2006; 61 (3): 246-55.

20. Privatera M.D., Brodie M.J., Mattson R.H., Chadwick D.W., Neto W., Wang S. EPMN 105 Study Group (2003) Topiramate, carbamazepine, and valproate monotherapy: double-blind comparison in newly diagnosed epilepsy. Acta Neurol. Scan. 107 (3): 165-175.

21. Schmidt D. Drug treatment of epilepsy: options and limitations. Epilepsy Behav. 2009; 15: 56-65.

22. Shank R.P., Gardocki J.F., Streeter A.J., Maryanoff B.E. An overview of the preclinical aspects of topiramate: pharmacology, pharmacokinetics, and mechanism of action. Epilepsia. 2000; 41 (1): 3-9.

23. StLouis E.K., Gidal B.E., Henry T.R., Kaydanova Y., Krumholz A., McCabe P.H., Montouris G.D., Rosenfeld W.E., Smith B.J., Stern J.M., Waterhouse E.J., Schulz R.M., Garnett W.R., Bramley T. Conversions between monotherapies in epilepsy: expert consensus. Epilepsy Behav. 2007; 11: 222234.

24. Surges R. Review: is levetiracetam different from other antiepileptic drugs? Levetiracetam and its cellular mechanism of action in epilepsy revisited. Ther. Adv. Neurol. Disord. 2008; 1 (1): 13-24.

25. Yuen A.W., Land G., Weatherly B.C., Peck A.W. So-dium valproate acutely inhibits lamotrigine metabolism. Br. J. Clin. Pharmacol. 1992; 33 (5): 511-5

For citation:

Kovaleva I.J. CHOICE OF ALTERNATIVE MONOTHERAPY IN EPILEPSY. Epilepsy and paroxysmal conditions. 2015;7(4):50-57. (In Russ.)

Views: 219

ISSN 2077-8333 (Print)
ISSN 2311-4088 (Online)