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NEUROLOGY

Clinical, Cognitive, and Neurophysiologic Correlates of Short-Term Treatment with Carbamazepine, Oxcarbazepine, and Levetiracetam in Healthy Volunteers

Specialist in Neurophysiopathology, Assistant Professor of Neurophysiopathology, Department of Neurological Sciences, La Sapienza University, Rome, Italy

Edoardo Vicenzini, MD

Specialist in Neurology, Research Fellow, Department of Neurological Sciences, La Sapienza University

Patrizia Pulitano, MD

Specialist in Neurophysiopathology, Research Fellow, Department of Neurological Sciences, La Sapienza University

Nicola Vanacore, MD

Specialist in Neurophysiopathology, Researcher, National Centre of Epidemiology, National Institute for Health, Rome

Francesco Saverio Romolo, MSc

Research Fellow, Department of Legal Medicine, Forensic Toxicology Section, La Sapienza University

Vittorio Di Piero, MD PhD

Specialist in Neurology, Assistant Professor of Neurology, Department of Neurological Sciences, La Sapienza University

Gian Luigi Lenzi, MD

Specialist in Neurology, Professor of Neurology, Department of Neurological Sciences, La Sapienza University

Neri Accornero, MD

Specialist in Neurology, Professor of Neurology, Department of Neurological Sciences, La Sapienza University

Reprints: Oriano Mecarelli MD, University of Rome, La Sapienza, Department of Neurological Sciences, Viale Regina Elena 336, 00161 Rome, Italy, fax 39-6-49912657, oriano.mecarelli{at}uniroma1.it

BACKGROUND: The adverse effects of the antiepileptic drugs (AEDs) originally developed are well known, while those of the newer AEDs remain unclear.

OBJECTIVE: To investigate clinical, cognitive, and neurophysiologic effects of carbamazepine, oxcarbazepine, and levetiracetam in healthy volunteers.

METHODS: A double-blind crossover study was conducted in 10 volunteers. Eight-day treatment with carbamazepine, oxcarbazepine, levetiracetam, or placebo was administered in random order. Drug doses were titrated gradually to the daily target doses on day 7: carbamazepine 800 mg, oxcarbazepine 1200 mg, and levetiracetam 1500 mg. At baseline and at the end of each treatment period, participants underwent cognitive and neurophysiologic assessment. A washout period of 14 days between treatment periods was conducted.

RESULTS: More adverse events were self-reported with carbamazepine (63%) than the other treatments (oxcarbazepine 12%, levetiracetam 20%, placebo 5%; p < 0.001 between the 4 groups). Carbamazepine induced the greatest motor slowing (p = 0.002), followed by oxcarbazepine (p = 0.01). Levetiracetam left baseline motor speed unchanged. All AEDs increased attention span from baseline values as shown on the Stroop test. Quantitative electroencephalogram (EEG) analysis showed that carbamazepine significantly increased the delta–theta power and reduced the frequency of alpha rhythm; oxcarbazepine induced smaller changes than carbamazepine. Levetiracetam did not change any EEG measurements. On color visually evoked potential (VEP) tests, carbamazepine induced a constant slowing of P1 latency, while oxcarbazepine induced changes only after the blue–black pattern. All color VEP measures for volunteers receiving levetiracetam were almost unchanged.

CONCLUSIONS: After short-term treatment in healthy volunteers, carbamazepine induced major clinical and neurophysiologic changes. Oxcarbazepine was better tolerated than carbamazepine. Levetiracetam interfered least with clinical and neurophysiologic test results.

Key Words: carbamazepine, levetiracetam, oxcarbazepine, short-term treatment

Published Online, September 14, 2004. www.theannals.com, DOI 10.1345/aph.1E136

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