Interrater reliability for CSP slice count in the current sample was .88 (intraclass correlation coefficient).
Magnetic resonance imaging data were unavailable in four combat-exposed, PTSD subjects for the following reasons: two had shrapnel that prohibited scanning, one developed an acute medical condition that precluded scanning, and one developed claustrophobia in the scanner. Magnetic resonance imaging data were unusable in one exposed twin without PTSD who had a brain tumor and in one unexposed co-twin (of an exposed twin with PTSD) who had had past brain surgery.
presents the remaining subjects’ demographic, psychometric, whole brain volume, and CSP data, along with the results of the statistical analyses. There were no significant main effects or interactions for age or education. As would be expected, exposed PTSD subjects had larger total combat-related CAPS scores than exposed, non-PTSD subjects. Although the PTSD diagnosis × combat exposure interaction for whole brain volume showed a trend toward statistical significance (p = .07), the pattern of the PTSD veterans’ and the co-twins of the non-PTSD veterans’ mean whole brain volumes both being lower than those of the non-PTSD veterans and the co-twins of the PTSD veterans makes this trend uninterpretable and unlikely to be of any significance. With regard to the proportion of subjects with an abnormal CSP, the PTSD diagnosis main effect was χ2 = 2.8, p = .09 (two-sided), or p < .05 (one-sided). In contrast, the combat exposure main effect and the PTSD diagnosis × combat exposure interaction were not significant.
Group Mean (SD) Demographic, Psychometric, and Cavum Septum Pellucidum Data
The correlation between presence (or absence) of an abnormal CSP in exposed and unexposed twins collapsed across exposed twin’s PTSD diagnosis was calculated by means of the Φ coefficient (which is the equivalent of a Pearson product moment correlation between two dichotomous variables and also referred to as Yule’s d). For this analysis, Φ = .35, n = 42, p = .01 (one-sided). There was no difference in mean (SD) hippocampal volume in the 20 subjects with an abnormal CSP: 7.4 (1.3) mL versus the 67 subjects without an abnormal CSP: 7.3 (.8) mL, t(85) = .4, p = .67 (hippocampal volume data missing in three subjects).