Prevention of relapse in generalized anxiety disorder by escitalopram treatment
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 [gt-or-equal, slanted]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 [less-than-or-eq, slant]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 Treatment was continued for 24–76 wk unless the patient relapsed or was withdrawn for other reasons.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 [gt-or-equal, slanted]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.(Received April 19 2005)
(Reviewed June 13 2005)
(Revised June 25 2005)
(Accepted June 26 2005)
(Published Online September 6 2005)
Key Words: Anxiety; clinical trial; escitalopram; placebo-controlled; relapse prevention.
c1 Karolinska Institutet, Department of Clinical Neuroscience, Division of Psychiatry at Karolinska University Hospital, SE-141 86 Stockholm, Sweden. Tel.: +468-585-85797 E-mail: firstname.lastname@example.org