The impact of treatment resistance on depressive relapse following electroconvulsive therapy

To the editor: Lauritzen et al. (1) recently reported the results of their study comparing the effacacies of paroxetine, imipramine and placebo in preventing relapse of depression following response to electroconvulsive therapy (ECT). They evaluated two selected groups of patients: patients in group A were randomly assigned to receive either paroxetine or placebo, and patients in group B were randomized to receive either paroxetine or imipramine. After 3 months of continuation treatment, paroxetine was found to be superior (PS0.05) to imipramine and placebo in preventing relapse. However, by the end of 6 months this difference in outcome was observed only for the paroxetine-imipramine comparison. Based on these results, the authors recommended that paroxetine, rather than imipramine, be considered for continuation treatment following ECT. Interpretation of these findings is limited by the fact that the authors did not examine the effect of treatment resistance on outcome. Sackheim et al. (2) and others ( 3 ) have found that patients who fail to respond to adequate pharmacotherapy before ECT are at increased risk of relapse after ECT. Lauritzen et al. noted that the majority of patients in their study had previously received pharmacotherapy for the index episode of depression. However, they did not determine how many of these patients had received an adequate trial of treatment, and whether or not they were equally distributed between the groups. Therefore, it is possible that patients treated with imipramine had a higher rate of relapse because they were a more refractory group. Sackheim (4) has also postulated that the risk of relapse may be higher if, following ECT, patients are prescribed the same medication to which they had previously failed to respond. It is noteworthy, therefore, that by the end of the study, patients treated with paroxetine in group A had a substantially higher rate of relapse than patients treated with paroxetine in group B (47% vs. lo%, respectively). The majority of patients in group A had been given a selective serotonin reuptake inhibitor (SSRI) prior to ECT, whereas most of the patients in group B had previously received a tricyclic antidepressant. Could the inferior outcomes of paroxetine-treated patients in group A and imipramine-treated patients in group B reflect the fact that they had failed to respond to the same class of antidepressant medication before ECT? If so, this would support Sackheim's (4) hypothesis and suggest that (contrary to the recommendation of Lauritzen et al.) SSRIs may not be the ideal choice for continuation treatment for many patients after ECT. There are many unanswered questions about the optimal treatment of depressed patients following response to ECT. Rather than advocating a specific class of antidepressant medication for continuation therapy, it seems more prudent to maintain a flexible approach to management that takes into account the type and adequacy of previous treatment. Alastair Flint The Toronto Hospital (General Division) 8 Eaton North, Room 238 200 Elizabeth Street Toronto Ontario M5G 2C4 Canada