Sarah L. Halligan

Posttraumatic stress disorder following assault: the role of cognitive processing, trauma memory, and appraisals

Two studies of assault victims examined the roles of (a) disorganized trauma memories in the development of posttraumatic stress disorder (PTSD), (b) peritraumatic cognitive processing in the development of problematic memories and PTSD, and (c) ongoing dissociation and negative appraisals of memories in maintaining symptomatology. In the cross-sectional study (n = 81), comparisons of current, past, and no-PTSD groups suggested that peritraumatic cognitive processing is related to the development of disorganized memories and PTSD. Ongoing dissociation and negative appraisals served to maintain PTSD symptoms. The prospective study (n = 73) replicated these findings longitudinally. Cognitive and memory assessments completed within 12-weeks postassault predicted 6-month symptoms. Assault severity measures explained 22% of symptom variance; measures of cognitive processing, memory disorganization, and appraisals increased prediction accuracy to 71%.

Childhood trauma and risk for PTSD:relationship to intergenerational effects of trauma, parental PTSD and cortisol excretion

Among the adverse mental health consequences of childhood trauma is the risk related to the development of posttraumatic stress disorder (PTSD) in adulthood. Other risk factors for PTSD. including parental trauma exposure and parental PTSD, can also contribute to the experience of child trauma. We examined associations between childhood trauma and PTSD in 51 adult children of Holocaust survivors and 41 comparison subjects. in consideration of parental trauma exposure and parental PTSD. We also examined these variables in relation to 24-hr urinary cortisol levels. Adult offspring of Holocaust survivors showed significantly higher levels of self-reported childhood trauma, particularly emotional abuse and neglect. relative to comparison subjects. The difference was largely attributable to parental PTSD. Self-reported childhood trauma was also related to severity of PTSD in subjects, and emotional abuse was significantly associated with 24-hr mean urinary cortisol secretion. We conclude that the experience of childhood trauma may be an important factor in the transmission of PTSD from parent to child.

Exposure to postnatal depression predicts elevated cortisol in adolescent offspring

BACKGROUND Animal research shows that early adverse experience results in altered glucocorticoid levels in adulthood, either raised basal levels or accentuated responses to stress. If a similar phenomenon operates in humans, this suggests a biological mechanism whereby early adversity might transmit risk for major depression, glucocorticoid elevations being associated with the development of this disorder. METHODS We measured salivary cortisol at 8:00 am and 8:00 pm over 10 days in 13-year-old adolescents who had (n = 48) or had not (n = 39) been exposed to postnatal maternal depression. RESULTS Maternal postnatal depression was associated with higher, more variable morning cortisol in offspring, a pattern previously found to predict major depression. CONCLUSIONS Early adverse experiences might alter later steroid levels in humans. Because maternal depression confers added risk for depression to children, these alterations might provide a link between early events and later psychopathology.

Maternal Postnatal Depression and the Development of Depression in Offspring Up to 16 Years of Age

OBJECTIVE The aim of this study was to determine the developmental risk pathway to depression by 16 years in offspring of postnatally depressed mothers. METHOD This was a prospective longitudinal study of offspring of postnatally depressed and nondepressed mothers; child and family assessments were made from infancy to 16 years. A total of 702 mothers were screened, and probable cases interviewed. In all, 58 depressed mothers (95% of identified cases) and 42 nondepressed controls were recruited. A total of 93% were assessed through to 16-year follow-up. The main study outcome was offspring lifetime clinical depression (major depression episode and dysthymia) by 16 years, assessed via interview at 8, 13, and 16 years. It was analysed in relation to postnatal depression, repeated measures of child vulnerability (insecure infant attachment and lower childhood resilience), and family adversity. RESULTS Children of index mothers were more likely than controls to experience depression by 16 years (41.5% versus 12.5%; odds ratio = 4.99; 95% confidence interval = 1.68-14.70). Lower childhood resilience predicted adolescent depression, and insecure infant attachment influenced adolescent depression via lower resilience (model R(2) = 31%). Family adversity added further to offspring risk (expanded model R(2) = 43%). CONCLUSIONS Offspring of postnatally depressed mothers are at increased risk for depression by 16 years of age. This may be partially explained by within child vulnerability established in infancy and the early years, and by exposure to family adversity. Routine screening for postnatal depression, and parenting support for postnatally depressed mothers, might reduce offspring developmental risks for clinical depression in childhood and adolescence.

Relationship of parental trauma exposure and PTSD to PTSD, depressive and anxiety disorders in offspring

This study examined the relationship of parental trauma exposure and PTSD to the development of posttraumatic stress disorder (PTSD), depressive and anxiety disorders in the adult offspring of Holocaust survivors. One hundred and thirty-five subjects (55 men and 80 women) were divided into three groups according to parental trauma exposure and PTSD: 60 subjects were offspring of Holocaust survivors who endorsed having at least one parent with PTSD, 33 were offspring of Holocaust survivors who reported having no parent with PTSD, and 42 were demographically similar subjects with no parental Holocaust exposure. All subjects underwent a comprehensive psychiatric interview in which information about lifetime psychiatric diagnoses and exposure to traumatic events was obtained. Subjects also completed a checklist based on the 17 DSM-IV symptoms of PTSD, to estimate the symptom severity of PTSD in their parents. A presumptive diagnosis of parental PTSD was assigned according to DSM-IV criteria. Forward and forced entry stepwise logistic regression analyses were used to determine the effects of parental exposure, parental PTSD, and the subjects own history of trauma in the development of PTSD, depressive, and anxiety disorders in the offspring. The findings demonstrate a specific association between parental PTSD and the occurrence of PTSD in offspring. Additionally, parental trauma exposure, more than parental PTSD, was found to be significantly associated with lifetime depressive disorder. The identification of parental PTSD as a risk factor for PTSD in offspring of Holocaust survivors defines a sample in which the biological and psychological correlates of risk for PTSD can be further examined.

Disturbances in morning cortisol secretion in association with maternal postnatal depression predict subsequent depressive symptomatology in adolescents.

BACKGROUND We have previously reported higher and more variable salivary morning cortisol in 13-year-old adolescents whose mothers were depressed in the postnatal period, compared with control group adolescents whose mothers did not develop postnatal depression (PND). This observation suggested a biological mechanism by which intrafamilial risk for depressive disorder may be transmitted. In the current article, we examined whether the cortisol disturbances observed at 13 years could predict depressive symptomatology in adolescents at 16 years of age. METHODS We measured self-reported depressive symptoms in 16-year-old adolescents who had (n = 48) or had not (n = 39) been exposed to postnatal maternal depression and examined their prediction by morning and evening cortisol indices obtained via 10 days of salivary collections at 13 years. RESULTS Elevated morning cortisol secretion at 13 years, and particularly the maximum level recorded over 10 days of collection, predicted elevated depressive symptoms at 16 years over and above 13-year depressive symptom levels and other possible confounding factors. Morning cortisol secretion mediated an association between maternal PND and symptomatology in 16-year-old offspring. CONCLUSIONS Alterations in steroid secretion observed in association with maternal PND may provide a mechanism by which risk for depression is transmitted from mother to offspring.

Cognitive processing, memory, and the development of PTSD symptoms: Two experimental analogue studies.

Memory deficits are implicated in the development of posttraumatic stress disorder (PTSD). Intentional recall of trauma memories is frequently disorganised or incomplete, whilst involuntary memory fragments are easily triggered by perceptual cues. Ehlers and Clark (Behaviour Research and Therapy 38 (2000) 319-345) propose that a predominance of data-driven processing (i.e., processing sensory impressions) during the trauma contributes to the development of this memory pattern, and therefore, predicts PTSD symptoms after trauma. Two experimental studies examined these hypotheses. Student volunteers viewed a distressing videotape as an analogue for a traumatic event. In Study 1, cognitive processing was manipulated; in Study 2, extreme scorers on a processing screening questionnaire were pre-selected. The results indicated that data-driven processing is associated with the development of PTSD-like memories and analogue symptoms.

The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder

BACKGROUND Because alterations in cortisol negative feedback inhibition associated with aging are generally opposite of those observed in posttraumatic stress disorder (PTSD), we examined the cortisol and glucocorticoid receptor (GR) response to dexamethasone (DEX) in older trauma survivors. METHODS Twenty-three Holocaust survivors (9 men, 14 women), 27 combat veterans (all male), and 10 comparison subjects (7 men, 3 women) provided samples for plasma or salivary cortisol and glucocorticoid receptor determination in mononuclear leukocytes at 8:00 AM on the day of, and following, 0.5 mg of DEX at 11:00 PM. RESULTS Greater percent suppression of cortisol and lymphocyte GR was observed in older trauma survivors with PTSD compared to survivors without PTSD and comparison subjects. There was a significant main effect of depression in the direction of reduced suppression following DEX, consistent with the effects of DEX in major depressive disorder patients. Responses to DEX were uncorrelated with PTSD symptom severity, but cortisol suppression was associated with years elapsed since the most recent, but not focal, traumatic event. CONCLUSIONS The response to DEX is generally similar in older and younger trauma survivors, but the findings suggest that age, symptom severity, and lifetime trauma exposure characteristics may influence this response.

Learning and memory in Holocaust survivors with posttraumatic stress disorder

BACKGROUND Impairments in explicit memory have been observed in Holocaust survivors with posttraumatic stress disorder. METHODS To evaluate which memory components are preferentially affected, the California Verbal Learning Test was administered to Holocaust survivors with (n = 36) and without (n = 26) posttraumatic stress disorder, and subjects not exposed to the Holocaust (n = 40). RESULTS Posttraumatic stress disorder subjects showed impairments in learning and short-term and delayed retention compared to nonexposed subjects; survivors without posttraumatic stress disorder did not. Impairments in learning, but not retention, were retained after controlling for intelligence quotient. Older age was associated with poorer learning and memory performance in the posttraumatic stress disorder group only. CONCLUSIONS The most robust impairment observed in posttraumatic stress disorder was in verbal learning, which may be a risk factor for or consequence of chronic posttraumatic stress disorder. The negative association between performance and age may reflect accelerated cognitive decline in posttraumatic stress disorder.

Socioemotional development in adolescents at risk for depression: The role of maternal depression and attachment style

We examined the impact on adolescent socioemotional functioning of maternal postnatal depression (PND) and attachment style. We also investigated the role of earlier aspects of the childs development-attachment in infancy, and 5-year representations of family relationships. Ninety-one mother-child pairs, recruited in the postnatal period, were followed up at 13 years. Adolescents were interviewed about their friendships, and their level of emotional sensitivity and maturity were rated. Emotional sensitivity was heightened in girls whose mothers experienced PND; notably, its occurrence was also linked to insecure attachment in infancy and raised awareness of emotional components of family relationships at 5 years. High emotional sensitivity was also associated with adolescent depressed mood. Raised social maturity was predicted by a secure maternal attachment style and, for girls, by exposure to maternal PND. Precursors of adolescent social maturity were evident in the narrative coherence of 5-year family representations. Higher social maturity in the friendship interview was also associated with overall good adjustment.