Paroxetine treatment resulted in a mean 54% reduction (85.3% [SD 22.45%] to 38.6% [SD 28.2%]) in PTSD symptoms as measured with mean changes from baseline on the CAPS total score [t(1,22) = 7.10, p = .000] among study completers. Improvement was equally strong on all symptom cluster scores (re-experiencing, avoidance/ numbing, hyperarousal) ().
Changes in the Clinician-Administered Posttraumatic Stress Disorder (PTSD) Scale (CAPS) after long-term treatment.
Treatment also resulted in significant improvements in verbal declarative memory, as measured with the WMS-R paragraph recall, for delayed recall [22.1–27.7, t(1,22) = −5.755, p = .000] and percent retention [80.2–91.1, t(1,22) = −3.41, p = .003] but not immediate recall [27.3–30.3, t(1,22) = −1.842, p = .079). Visuospatial memory on the WMS-R significantly improved for immediate [32.5–35.8, t(1,21) = −2.857, p = .009] but not for delayed recall [23.6–30.6, t(1,21) = −2.723, p = .13] nor for percent retention [72.6–84.4; t(1,20) = −1.96, p= .064]. Improvements were significant on all subscales of the verbal component of the SRT, including long-term retrieval and delayed recall, which was not significant in the visual component of the scale [11.6–11.7; t(1,22) =−.646, p = .525] (see ).
Memory Performance before and after Long-Term Treatment with Paroxetine in Posttraumatic Stress Disorder
The individual pretreatment and posttreatment effects per patient are displayed in .
Individual difference in memory performance on Wechsler Memory Scale (paragraph), delayed recall, before and after treatment. Each line connects the individual score pre- and posttreatment. The horizontal lines indicate the mean group score.
Repeated-measures ANOVA with side as the repeated measure showed a main effect for treatment related to a 4.6% increase in mean hippocampal volume (1857.3 mm3 [SD 225.6] to 1942.9 mm3 [SD 243.2]) with treatment [F(1,36) = 8.775, p = .005]. Increased hippocampal volume was seen for both left (5.6%) (1807.6 mm3 [SD 255.5, p = .025] to 1909.3 mm3 [SD 236.9]) and right (3.7%) (1906.9 mm3 [SD 195.8] to 1976.7 mm3 [SD 249.6, p = .046]) hippocampus. There was no main effect for side (left/right) [F(1,36) = .413, p = .525]. There was no change in whole brain volume with treatment (360,871 mm3 to 359,932 mm3) (p = .17). Increase in hippocampal volume was significant after adding whole brain volume before and after treatment to the model. Individual pretreatment and posttreatment effects per patient are displayed in .
Individual differences in hippocampal volume before and after treatment. Each line connects the individual score of pre- and posttreatment. The horizontal lines indicate the mean group volume.
There was no correlation between change in CAPS or memory and change in hippocampal volume with treatment. There were no significant gender-specific differences in the patients on the visual memory components of WMS-R or SRT. Analyzing the data per gender did not change the specificity of the improvement in delayed verbal memory as opposed to visual memory. No significant relationships were found between age, ETI index score, trauma onset, and WAIS-R with memory improvement. A positive relationship was found between ETI index score and improvement with treatment on the CAPS avoidance subscale [F(1,17) = 4.78, p < .05]. A positive correlation was found between absence of lifetime depression and improvement on CAPS [F(1,18) = 2,72, p = .007]. There was no correlation with increase in hippocampal volume in this group.