Recent studies have found a significant association between PTSD and low heart rate variability (HRV), a biomarker of autonomic dysregulation. Research indicates that respiratory sinus arrhythmia (RSA) biofeedback increases HRV while reducing related pathological symptoms. This controlled pilot study compared RSA biofeedback to progressive muscle relaxation (PMR) as adjunctive interventions for 38 persons with PTSD symptoms in a residential treatment facility for a substance use disorder. Both groups were assessed at pre-intervention and 4-week post-intervention. Group x time interactions revealed significantly greater reductions in depressive symptoms and increases in HRV indices for the RSA group. Both groups significantly reduced PTSD and insomnia symptoms and a statistical trend was observed for reduced substance craving for the RSA group. Increases in HRV were significantly associated with PTSD symptom reduction. Overall, these results provide preliminary support for the efficacy of RSA biofeedback in improving physiological and psychological health for individuals with PTSD.

Studies have shown differences in neuropsychological functioning between groups with posttraumatic stress disorder (PTSD) and control participants. Because individuals with PTSD often have a history of comorbid alcohol abuse, the extent to which an alcohol confound is responsible for these differences remains a concern. The current study compares neuropsychological testing scores in 4 groups of veterans with and without PTSD (PTSD+ and PTSD-, respectively) and with and without a history of alcohol abuse (ETOH+ and ETOH-, respectively): n for PTSD+/ETOH- = 30, n for PTSD+/ETOH- = 37, n for PTSD-/ETOH+ = 30, and n for PTSD-/ETOH- = 31. Results showed that PTSD, when alcohol, educational level, vocabulary, and depression are controlled for, was associated with decreased verbal memory, attention, and processing speed performance. Alcohol abuse history was associated with decreased visual memory performance. By controlling for alcohol and depression, the authors can more conclusively demonstrate that verbal memory and attention differences are associated with PTSD.

Magnetic resonance spectroscopic imaging (MRSI) studies suggest hippocampal abnormalities in posttraumatic stress disorder (PTSD), whereas findings of volume deficits in the hippocampus, as revealed with magnetic resonance imaging (MRI), have been inconsistent. Co-morbidities of PTSD, notably alcohol abuse, may have contributed to the inconsistency. The objective was to determine whether volumetric and metabolic abnormalities in the hippocampus and other brain regions are present in PTSD, independent of alcohol abuse. Four groups of subjects, PTSD patients with (n=28) and without (n=27) alcohol abuse and subjects negative for PTSD with (n=23) and without (n=26) alcohol abuse, were enrolled in this observational MRI and MRSI study of structural and metabolic brain abnormalities in PTSD. PTSD was associated with reduced N-acetylaspartate (NAA) in both the left and right hippocampus, though only when normalized to creatine levels in the absence of significant hippocampal volume reduction. Furthermore, PTSD was associated with reduced NAA in the right anterior cingulate cortex regardless of creatine. NAA appears to be a more sensitive marker for neuronal abnormality in PTSD than brain volume. The alteration in the anterior cingulate cortex in PTSD has implications for fear conditioning and extinction.

Posttraumatic stress disorder (PTSD) has been associated with deficits in the areas of verbal memory and learning, executive functioning, working memory, and attention in adults. Findings have been less consistent in the few studies examining neuropsychological functioning in childhood PTSD, which are often limited by comparing children with PTSD to children without trauma histories, making it unclear whether observed neuropsychological deficits are related to trauma exposure or to PTSD symptomatology. In an ethnically diverse sample of 62 children who witnessed intimate partner violence (n = 27 PTSD+ and 35 PTSD-), children with PTSD exhibited slower and less effective learning, heightened sensitivity to interference, and impaired effect of rehearsal on memory acquisition on the California Verbal Learning Test - Children's Version, a word list learning task. Both groups performed in the below average range on measures of executive functioning, attention, and intellectual ability.

SUMMARY Background Inflammation may reduce hippocampal volume by blocking neurogenesis and promoting neurodegeneration. Posttraumatic stress disorder (PTSD) has been linked with both elevated inflammation and reduced hippocampal volume. However, few studies have examined associations between inflammatory markers and hippocampal volume, and none have examined these associations in the context of PTSD. Methods We measured levels of the inflammatory markers interleukin-6 (IL-6) and soluble receptor II for tumor necrosis factor (sTNF-RII) as well as hippocampal volume in 246 Gulf War veterans with and without current and past PTSD as assessed with the Clinician Administered PTSD Scale (CAPS). Enzyme-linked immunosorbent assays were used to measure inflammatory markers, and 1.5 Tesla magnetic resonance imaging (MRI) and Freesurfer version 4.5 were used to quantify hippocampal volume. Hierarchical linear regression and analysis of covariance models were used to examine if hippocampal volume and PTSD status would be associated with elevated levels of IL-6 and sTNF-RII. Results Increased sTNF-RII, but not IL-6, was significantly associated with reduced hippocampal volume (β = −.14, p = .01). The relationship between sTNF-RII and hippocampal volume was independent of potential confounds and covariates, including PTSD status. Although we observed no PTSD diagnosis-related differences in either IL-6 or sTNF-RII, higher PTSD severity was associated with significantly increased sTNF-RII (β = .24, p = .04) and reduced IL-6 levels (β = −.24, p = .04). Conclusions Our results indicate that specific inflammatory proteins may be associated with brain structure and function as indexed by hippocampal volume and PTSD symptoms.

Results highlight the need to target parenting stress in interventions with trauma-exposed families.

In this cohort of veterans under age 65 years without known neurologic disease, patients with versus without PTSD had significantly poorer performance in several domains of cognitive function, particularly in tests involving processing speed, executive function, and learning. These cognitive deficits were largely explained by modifiable risk factors. Interventions targeted at these risk factors might minimize the impact of PTSD on cognitive decline and dementia risk as patients age.

Recently researchers have begun to explore the extent to which children's cognitive development is influenced by experiences in the family environment. Assessing mother-child dyads exposed to intimate partner violence (IPV), a population at risk for emotional and neurocognitive problems, we examined relationships between maternal emotional regulation, parenting, and children's executive functioning (including working memory, inhibitory control, cognitve flexibility and set shifting, and planning). Positive parenting practices, as reported by the children, were correlated with children's planning and problem solving performance. Controlling for children's own emotion regulation and gender, mothers' self-reported emotion regulation abilities predicted children's performance on a task of cognitive flexibility. Girls exhibited superior emotion regulation and executive functioning performance compared to boys, and mothers of girls reported better emotion regulation abilities compared to mothers of boys. These findings add to a nascent literature suggesting that parenting and parental emotional functioning may play important roles in children's neurocognitive functioning. In addition, they help to explain the mechanisms by which children exposed to IPV experience executive functioning deficits.