77, P= 0.191, . None of the three covariates were significantly related to working memory performance.

A series of mediation analyses were conducted to test if anxiety, depression, and combat exposure scores each served as total or partial mediators of the relationship between PTSD diagnosis and impaired working memory. Using the Freedman and Schatzkin (1992) test for partial mediation, neither depression, t (42) = 0.29, P > 0.05, anxiety, t (42) = 0.28, P > 0.05, nor combat exposure, t (42) = 0.31, P > 0.05, proved to meet the criteria for partial mediators of the relationship between PTSD diagnosis and working memory scores. Antidepressant #GSK1349572 solubility dmso keyword# use The effects of antidepressant use upon working memory as measured by collapsed BDI scores were examined. Due to the low numbers of participants in the Inhibitors,research,lifescience,medical control group who reported taking some form of antidepressant medication at the time of data collection (n= 2), only data from participants diagnosed with PTSD were included for analysis.

Among PTSD-diagnosed participants, there was no difference with regard to working memory as measured by collapsed BDS scores between those participants having reported using antidepressant medication (n= 11) at the time of data collection and those participants Inhibitors,research,lifescience,medical not reporting the use of antidepressant medication (n= 10), t (19) = 0.65, P > 0.05. Prior concussions and working memory To assess possible additive effects of having a prior concussion, individuals in the PTSD group were placed into one of two subgroups based on reporting having a LOC from a head injury: (1) PTSD with a LOC (PTSD + LOC; n= 9) from a prior head injury and (2) PTSD with no LOC (PTSD – LOC; n= 12). BDS scores from both of these subgroups were compared against each other and with the control Inhibitors,research,lifescience,medical group. The results indicated that, although, both the PTSD + LOC group and PTSD – LOC Inhibitors,research,lifescience,medical group were significantly different from the control group, t (30) = 3.46, P < 0.05; t (33) = 2.41, P < 0.05; respectively; the difference between the PTSD + LOC and PTSD – LOC groups was not significant, t (19) =–1.16, P > 0.05. In as such, the results do not suggest there was a significant contribution

of prior concussions on working memory function above and beyond that of PTSD alone. However, GPX6 one of the limitations is the small sample size of the subgroups. Therefore, future studies should continue to explore the main effects and interactions of PTSD and concussion comorbidity on neurocognitive functioning. Working memory: individual phases A series of t-tests were conducted to determine if a relationship existed between PTSD and working memory on each of the individual string lengths (4, 5, 6, 7, and 8 digits) for reverse recall. The Holm procedure was used to correct for familywise error rate. For all string lengths, participants diagnosed with PTSD exhibited poorer working memory than participants in the control group (Fig. 1).