 |
 |

Prevention of Relapse in Residual Depression by Cognitive Therapy
A Controlled Trial
Eugene S. Paykel, MD, FRCP, FRCPsych;
Jan Scott, MD, FRCPsych;
John D. Teasdale, PhD;
Anthony L. Johnson, PhD, CStat;
Anne Garland, BA(Hons), RMN;
Richard Moore, PhD;
Alison Jenaway, MB, MRCPsych;
Peter L. Cornwall, MB, MRCPsych;
Hazel Hayhurst, PhD;
Rosemary Abbott, PhD;
Marie Pope, MSc
Arch Gen Psychiatry. 1999;56:829-835.
Background Previous studies indicate that depressed patients with partial remission and residual symptoms following antidepressant treatment are common and have high rates of relapse. There is evidence that cognitive therapy may reduce relapse rates in depression.
Methods One hundred fifty-eight patients with recent major depression, partially remitted with antidepressant treatment (mean daily doses equivalent to 185 mg of amitriptyline or 33 mg of fluoxetine) but with residual symptoms of 2 to 18 months' duration, were included in a controlled trial. Subjects were randomized to receive clinical management alone or clinical management plus cognitive therapy for 16 sessions during 20 weeks, with 2 subsequent booster sessions. Subjects were assessed regularly throughout the 20 weeks' treatment and for a further year. They received continuation and maintenance antidepressants at the same dose throughout.
Results Cognitive therapy reduced relapse rates for acute major depression and persistent severe residual symptoms, in both intention to treat and treated per protocol samples. The cumulative relapse rate at 68 weeks was reduced significantly, from 47% in the clinical management control group to 29% with cognitive therapy (hazard ratio 0.54; 95% confidence interval, 0.32-0.93; intention to treat analysis). Cognitive therapy also increased full remission rates at 20 weeks but did not significantly improve symptom ratings.
Conclusion In this difficult-to-treat group of patients with residual depression who showed only partial response despite antidepressant treatment, cognitive therapy produced worthwhile benefit.
From the Departments of Psychiatry, University of Cambridge, Cambridge, England (Professor Paykel and Drs Moore, Jenaway, Hayhurst, and Abbott); University of Glasgow, Glasgow, Scotland (Professor Scott); University of Newcastle, Newcastle, England (Dr Cornwall and Mss Garland and Pope); and MRC Cognition and Brain Sciences Unit (Dr Teasdale) and Medical Research Council Biostatistics Unit (Dr Johnson), University of Cambridge Institute of Public Health.
|