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  • The International Journal of Neuropsychopharmacology, Volume 9, Issue 5
  • October 2006, pp. 495-505

Prevention of relapse in generalized anxiety disorder by escitalopram treatment

  • Christer Allgulander (a1), Ioana Florea (a2) and Anna K. Trap Huusom (a2)
  • DOI: http://dx.doi.org/10.1017/S1461145705005973
  • Published online: 01 September 2005
Abstract

Escitalopram has demonstrated a robust and dose-dependent efficacy in the treatment of generalized anxiety disorder (GAD) for up to 3 months. In the present study, the efficacy and tolerability of escitalopram in the prevention of relapse in GAD was investigated. A total of 491 patients with a primary diagnosis of GAD and a Hamilton Anxiety (HAMA) total score [ges ]20 received 12 wk of open-label treatment with a fixed dose of escitalopram (20 mg/d). Of these, 375 patients responded (HAMA total score [les ]10) and were randomized to double-blind treatment with 20 mg/d escitalopram (n=187) or placebo (n=188). Treatment was continued for 24–76 wk unless the patient relapsed or was withdrawn for other reasons. Relapse was defined as either an increase in HAMA total score to [ges ]15, or lack of efficacy, as judged by the investigator. The results of the primary analysis showed a clear beneficial effect of escitalopram relative to placebo on the time to relapse of GAD (log-rank test, p<0.001). The risk of relapse was 4.04 times higher for placebo-treated patients than for escitalopram-treated patients; the proportion of patients who relapsed was statistically significantly higher in the placebo group (56%) than in the escitalopram group (19%) (p<0.001). Escitalopram was well tolerated and 7% of the escitalopram-treated patients withdrew due to adverse events, vs. 8% of the placebo patients. The incidence of discontinuation symptoms with escitalopram during tapered withdrawal was low; the symptoms primarily being dizziness (10–12%), nervousness (2–6%), and insomnia (2–6%). Escitalopram 20 mg/d significantly reduced the risk of relapse and was well tolerated in patients with GAD.

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Corresponding author
Karolinska Institutet, Department of Clinical Neuroscience, Division of Psychiatry at Karolinska University Hospital, SE-141 86 Stockholm, Sweden. Tel.: +468-585-85797 E-mail: christer.allgulander@neurotec.ki.se
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The International Journal of Neuropsychopharmacology
  • ISSN: 1461-1457
  • EISSN: 1469-5111
  • URL: /core/journals/the-international-journal-of-neuropsychopharmacology
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