Actual Driving Performance and Psychomotor Function in Healthy Subjects After Acute and Subchronic Treatment With Escitalopram, Mirtazapine, and Placebo: A Crossover Trial

Marleen Wingen, M.Sc.; John Bothmer, Ph.D.; Stefan Langer, M.Sc.; and Johannes G. Ramaekers, Ph.D.

Objective: The effects of escitalopram 10 to 20 mg/day and mirtazapine 30 to 45 mg/day on actual driving and psychomotor performance of 18 healthy subjects were determined in a randomized, double-blind, placebo-controlled, multiple-dose, 3-way crossover trial.

Method: Each treatment period lasted for 15 days and was separated from the next period by a washout period of at least 13 days. Subjects received an evening dose of escitalopram 10 mg, mirtazapine 30 mg, or placebo from days 1 to 7 and an evening dose of escitalopram 20 mg, mirtazapine 45 mg, or placebo from days 8 to 15. On days 2, 9, and 16, reflecting acute period, dose increase, and steady state, respectively, the Road Tracking Test was performed. The main parameter was standard deviation of lateral position. Psychomotor performance was also assessed on days 2, 9, and 16 by laboratory computer tasks. Subjective sleep quality was measured with the Groninger Sleep Quality Scale, and mood was measured by visual analogue scales.

Results: Treatment differences were apparent during the acute treatment period, in which subjects treated with mirtazapine 30 mg performed less well on the driving test as compared to placebo. The Divided Attention Task results also revealed a significant increase in tracking error after a single dose of mirtazapine 30 mg as compared to placebo. Mirtazapine decreased feelings of alertness and contentedness. Mirtazapine did not affect performance on days 9 and 16 of treatment. Escitalopram did not affect driving, psychomotor performance, or subjective mood throughout treatment.

Conclusion: Driving performance, as well as psychomotor functioning, was not affected by escitalopram treatment in healthy subjects. Driving performance was significantly impaired after ingestion of mirtazapine 30 mg during the acute treatment period.

(J Clin Psychiatry 2005;66:436-443)

Received Dec. 2, 2004; accepted Jan. 27, 2005. From the Experimental Psychopharmacology Unit, Brain & Behaviour Institute, University of Maastricht, Maastricht, the Netherlands (Ms. Wingen and Dr. Ramaekers); and Lundbeck GmbH, Hamburg, Germany (Dr. Bothmer and Mr. Langer).

This study was sponsored by H. Lundbeck A/S, Copenhagen, Denmark.

The results have previously been presented (as a poster) at the 25th Congress of the College of International Neuropsychopharmacology, Paris, France, June 20-24, 2004, and at the 17th congress of the European College of Neuropsychopharmacology, Stockholm, Sweden, October 9-13, 2004.

We are thankful to A. van Oers; P. van Ruitenbeek, M.Sc.; M. Klomp; J. van Hoogh, M.Sc.; and C. J. van Leeuwen, M.D., for their assistance in the data collection.

Corresponding author and reprints: Marleen Wingen, M.Sc., Maastricht University, Faculty of Psychology, Department of Neurocognition (Experimental Psychopharmacology Unit), P.O. Box 616, 6200 MD Maastricht, the Netherlands (e-mail: m.wingen@psychology.unimaas.nl).