Response to “Treatment compliance and effectiveness in complex PTSD patients with co-morbid personality disorder undergoing stabilizing cognitive behavioral group treatment: a preliminary study” – authors’ reply

I n a response to our article ‘‘Treatment compliance and effectiveness in complex PTSD patients with personality disorders ( . . .)’’ (Dorrepaal et al., 2013), Dr. A de Jongh and Dr. E ten Broeke express their concern ‘‘that conclusions on data derived from an analysis of a sample of complex PTSD patients previously published in the Journal of Psychosomatics and Psychotherapy (Dorrepaal, et al., 2012), could prematurely encourage clinicians, as well as investigators, to offer their patients similar stabilization programs in affiliated mental health institutions. ’’ In this reply, we would like to explain what we actually encourage clinicians and researchers to do, and why: 1) stabilize when PTSD patients drop-out from, or cannot be included in, first-line treatments due to complexity and comorbidity; 2) conduct treatment effect studies on complex PTSD patients with comorbid severe personality disorder(s) (PD) before generalizing the effectiveness of first-line treatments to this understudied group; and 3) use stabilization treatment to prepare complex PTSD patients with comorbid PD for first-line treatments and as such increase the net number of patients profiting from these treatments. De Jongh and ten Broeke question the conclusions that we drew from our data, citing ‘‘while significant superiority on change scores was absent, responder analysis suggested clinical meaningfulness of adding group treatment. ’’ As we reported in the article describing our clinical trial that they referred to (Dorrepaal et al., 2012), our results were ambiguous and were described accordingly. The authors appear to have misread our conclusions as being based on an analysis of patients completing treatment only, whereas they were based on intention-to-treat (ITT) analyses as well as analyses of completers (Dorrepaal et al., 2012, tables 3 4). Change scores were significant at trend level only, probably because we based our power calculation on Zlotnick et al.’s (1997) randomized controlled trial. These authors found a very low effect size in their treatment as usual comparison condition (TAU: d 0.1), while TAU in our trial achieved a medium effect size. Had we initially based the power of our study on a medium effect size within TAU, almost double the number of patients would have been required to demonstrate significant results. Alternatively, we could have applied a more powerful onetailed test to our data, which would have yielded statistically significant results as well. Importantly, the secondary responders’ analysis on PTSD symptoms (ITT; p 0.03) was statistically significant and indicated clinical meaningfulness. Moreover, our results are supported by our neuroimaging study showing improvement in terms of increased selective attention and decreased emotional arousal, associated with normalized activation in the dorsal anterior cingulate cortex and anterior insula after adding stabilizing treatment (Thomaes et al., 2012). Therefore, we do not agree that our carefully phrased conclusion of ‘‘clinical meaningfulness’’ is an overstatement of the effectiveness of the intervention, especially in this population. We agree with De Jongh and ten Broeke’s concern that ‘‘the effect of (the experimental treatment) over TAU could be considered as ‘placebo effects’’’, since our design did not include a comparison to a gold standard treatment or placebo (Dorrepaal et al., 2012). However, we disagree with their suggestion that the effect of the treatment over TAU may have been caused by spontaneous improvement or symptom fluctuation as these would likely affect both conditions, which is obviously the reason to compare such conditions in a controlled trial. Moreover, regression to the mean cannot explain the difference between conditions in our trial, since high symptomatic patients and low symptomatic patients profited equally from the treatment. De Jongh and ten Broeke considered the attrition rate to be relatively high (although they misread the attrition rate, which was 16% in the total group of 71 patients described in Dorrepaal et al., 2012, 18% in the subgroup of 38 patients receiving the stabilizing treatment described in Dorrepaal et al., 2013, and 15% in the subgroup of 33 patients receiving TAU). However, our attrition rate in this complex population is similar to, and not higher than, the mean attrition reported previously for various PTSD PSYCHOTRAUMATOLOGY EUROPEAN JOURNAL OF