Matthew C. Morris

Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: a systematic review and meta-analysis.

Exposure to traumatic stress is associated with increased risk for posttraumatic stress disorder (PTSD) and alterations of hypothalamic-pituitary-adrenocortical (HPA) function. Research linking traumatic stress with HPA function in PTSD has been inconsistent, however, in part due to (a) the inclusion of trauma-exposed individuals without PTSD (TE) in control groups and (b) a failure to consider comorbid major depressive disorder (MDD) and moderating variables. This meta-analysis of 47 studies (123 effect sizes, N=6008 individuals) revealed that daily cortisol output was lower for PTSD (d=-.36, SE=.15, p=.008) and PTSD+MDD (d=-.65, SE=.25, p=.008) groups relative to no trauma controls (NTC); TE and NTC groups did not differ significantly from each other. Afternoon/evening cortisol was lower in TE (d=-.25, SE=.09, p=.007) and PTSD (d=-.27, SE=.12, p=.021) groups and higher in PTSD+MDD groups (d=.49, SE=.24, p=.041) relative to NTC. Post-DST cortisol levels were lower in PTSD (d=-.40, SE=.12, p<.001), PTSD+MDD (d=-.65, SE=.14, p<.001), and TE groups (d=-.53, SE=.14, p<.001) relative to NTC. HPA effect sizes were moderated by age, sex, time since index event, and developmental timing of trauma exposure. These findings suggest that enhanced HPA feedback function may be a marker of trauma-exposure rather than a specific mechanism of vulnerability for PTSD, whereas lower daily cortisol output may be associated with PTSD in particular.

Cortisol Responses to Psychosocial Stress Predict Depression Trajectories: Social-Evaluative Threat and Prior Depressive Episodes as Moderators

BACKGROUND Alterations of hypothalamic-pituitary-adrenal (HPA) function are well-established in adults with current depression. HPA alterations may persist into remission and confer increased risk for recurrence. METHODS A modified version of the Trier Social Stress Test (TSST) was administered at baseline to 32 young adults with remitted major depressive disorder and 36 never-depressed controls. Participants were randomly assigned to either a "high-stress" condition involving social evaluation or a "low-stress" control condition. Cortisol concentrations were measured in saliva samples throughout the TSST. Participants were assessed again after 6 months for the occurrence of stressful life events and depressive symptoms/disorders during the follow-up period. RESULTS Participants who exhibited enhanced cortisol reactivity in the low-stress condition showed increases in depressive symptoms over follow-up, after controlling for stressful life events during the follow-up period. Anticipatory stress cortisol and cortisol reactivity each interacted with history of depressive episodes to predict depression trajectories. LIMITATIONS The single TSST administration limits conclusions about whether alterations of cortisol reactivity represent trait-like vulnerability factors or consequences (scars") of past depression. CONCLUSIONS These results extend previous findings on stress sensitivity in depression and suggest that altered HPA function during remission could reflect an endophenotype for vulnerability to depression recurrence. Findings support interactive models of risk for depression recurrence implicating HPA function, depression history, and sensitivity to minor stressors. Results may have implications for interventions that match treatment approaches to profiles of HPA function.

A prospective study of the cognitive-stress model of depressive symptoms in adolescents.

This prospective study investigated a cognitive diathesis-stress model of depression in adolescents across the transition from 6th to 7th grade using individual, additive, weakest link, and keystone approaches to operationalizing the cognitive vulnerability. Participants were 240 young adolescents (mean age = 11.87 years, SD = 0.57) who differed in risk for mood disorders based on their mothers history of depression. Results of the hierarchical multiple regression analyses indicated some support for the individual, additive, weakest link, and keystone diatheses. In particular, the weakest link diathesis interacted with stress and gender to predict increases in depressive symptoms in 7th grade; the form of this interaction was consistent with the cognitive diathesis-stress model for boys, whereas for girls the pattern of relations reflected more of a dual-vulnerability model. That is, high levels of depressive symptoms were found for all girls except those with more positive cognitive styles and low stress levels. These findings highlight the utility of examining different approaches to combining measures of cognitive vulnerability in conjunction with stress in predicting depressive symptoms, and the importance of exploring gender differences with regard to the cognitive diathesis-stress model.

Psychobiology of PTSD in the acute aftermath of trauma: Integrating research on coping, HPA function and sympathetic nervous system activity.

Research on the psychobiological sequelae of trauma has typically focused on long-term alterations in individuals with chronic posttraumatic stress disorder (PTSD). Far less is known about the nature and course of psychobiological risk factors for PTSD during the acute aftermath of trauma. In this review, we summarize data from prospective studies focusing on the relationships among sympathetic nervous system activity, hypothalamic-pituitary-adrenal function, coping strategies and PTSD symptoms during the early recovery (or non-recovery) phase. Findings from pertinent studies are integrated to inform psychobiological profiles of PTSD-risk in children and adults in the context of existing models of PTSD-onset and maintenance. Data regarding bidirectional relations between coping strategies and stress hormones is reviewed. Limitations of existing literature and recommendations for future research are discussed.

Interactive models of depression vulnerability: the role of childhood trauma, dysfunctional attitudes, and coping.

OBJECTIVES This prospective study investigated whether within-individual relations between depression vulnerability factors (childhood trauma, dysfunctional attitudes, maladaptive coping) and depressive symptom trajectories varied as a function of the number of prior major depressive episodes (MDEs) experienced in their lifetime. DESIGN Participants were 68 young adults who varied with regard to their history of depression; 32 were remitted depressed and 36 were never depressed. METHODS Depressive symptoms and disorders were assessed using semi-structured psychiatric interviews conducted twice over a 6-month period; interviews yielded weekly ratings of depressive symptoms during the follow-up interval. Childhood trauma, dysfunctional attitudes and coping were assessed with self-report measures. Data analyses were conducted using time-lagged multilevel models. RESULTS Individuals with more previous MDEs who reported greater childhood trauma exposure, more dysfunctional attitudes, or greater use of maladaptive coping strategies experienced more rapid increases in depressive symptoms during the follow-up period. A significant interaction of coping, number of previous MDEs, and time was found indicating that among individuals with less adaptive coping (i.e., lower primary or lower secondary control coping scores), depressive symptoms rating (DSR) increased significantly in relation to number of prior depressive episodes; no change in DSR was observed for never-depressed individuals. Among individuals with higher primary control coping scores, significant increases in DSR scores were observed for individuals with ≥3 prior MDEs only. CONCLUSIONS Findings highlight the need for treatment and prevention programmes that target stress reactivity and coping strategies early in the course of depression.

Cortisol response to psychosocial stress during a depressive episode and remission

Abstract This study compared cortisol responses to a standardized psychosocial stressor during a major depressive episode (MDE) and again during remission in adolescents and young adults. Twenty-six individuals with no personal or family history of a major psychiatric disorder (NC) and 24 individuals with a diagnosis of major depressive disorder (MDD) at Time 1 participated in the study. The MDD group showed robust cortisol responses during their index episode and after recovery. In contrast, the NC group showed habituation to the repeated psychosocial stressor, as evident in a flatter cortisol response profile at Time 2. Within the MDD group, net peak cortisol during the first stress test was positively associated with the duration of the index MDE and negatively associated with the total duration of all MDEs. Whereas summary indices of cortisol responses were relatively stable across repeated stress tasks within the MDD group, this was not the case for NC. Results demonstrate that cortisol responses fail to habituate to repeated psychosocial stress during recovery from an MDE and could reflect a trait-like marker of risk for recurrence.

Race effects on temporal summation to heat pain in youth.

Abstract Racial differences in pain responsiveness have been demonstrated in adults. However, it is unclear whether racial differences are also present in youth and whether they extend to experimental pain indices assessing temporal summation of second pain (TSSP). Temporal summation of second pain provides an index of pain sensitivity and may be especially relevant in determining risk for chronic pain. This study assessed pain tolerance and TSSP to evoked thermal pain in 78 healthy youth (age range, 10-17), 51% of whom were African American and 49% were non-Hispanic white. Multilevel models revealed within-individual increases in pain ratings during the temporal summation task in non-Hispanic white youth that were consistent with TSSP. Pain ratings did not change significantly during the temporal summation task in African-American youth. Baseline evoked pain ratings were significantly higher in African-American compared with non-Hispanic white youth. These findings suggest that enhanced responsiveness to evoked thermal pain in African Americans is present in adolescence but is unlikely to be related to elevated TSSP. These results may have implications for understanding racial differences in chronic pain experience in adulthood.

Race Effects on Conditioned Pain Modulation in Youth.

Race and ethnicity shape the experience of pain in adults. African Americans typically exhibit greater pain intensity and evoked pain responsiveness than non-Hispanic whites. However, it remains unclear whether there are racial differences in conditioned pain modulation (CPM) and if these are present in youth. CPM refers to a reduction in perceived pain intensity for a test stimulus during application of a conditioning stimulus and may be especially relevant in determining risk for chronic pain. The present study assessed CPM to evoked thermal pain in 78 healthy youth (ages 10-17 years), 51% of whom were African American and 49% of whom were non-Hispanic white. African American youth reported lower mean conditioning pain ratings than non-Hispanic white youth, controlling for mean preconditioning pain ratings, which is consistent with stronger CPM. Multilevel models demonstrated stronger CPM effects in African American than non-Hispanic white youth, as evident in more rapid within-person decreases in pain ratings during the conditioning phase. These findings suggest that diminished CPM likely does not account for the enhanced responsiveness to evoked thermal pain observed in African American youth. These results may have implications for understanding racial differences in chronic pain experienced in adulthood. Perspective: This study evaluated conditioned pain modulation to evoked thermal pain in African American and non-Hispanic white youth. Findings could have implications for the development of personalized chronic pain treatment strategies that are informed by race and ethnicity.

Cortisol, heart rate, and blood pressure as early markers of PTSD risk: A systematic review and meta-analysis.

Individuals with posttraumatic stress disorder (PTSD) typically exhibit altered hypothalamic-pituitary-adrenal (HPA) function and sympathetic nervous system (SNS) activity. The goals of this study were to determine whether HPA and SNS alterations in the immediate aftermath of trauma predict subsequent PTSD symptom development and whether inconsistencies observed between studies can be explained by key demographic and methodological factors. This work informs secondary prevention of PTSD by identifying subgroups of trauma survivors at risk for PTSD. This meta-analysis (26 studies, N=5186 individuals) revealed that higher heart rate measured soon after trauma exposure was associated with higher PTSD symptoms subsequently (r=0.13). Neither cortisol (r=-0.07) nor blood pressure (diastolic: r=-0.01; systolic: r=0.02) were associated with PTSD symptoms which may be influenced by methodological limitations. Associations between risk markers (heart rate, cortisol, systolic blood pressure) and PTSD symptoms were in the positive direction for younger samples and negative direction for older samples. These findings extend developmental traumatology models of PTSD by revealing an age-related shift in the presentation of early risk markers. More work will be needed to identify risk markers and pathways to PTSD while addressing methodological limitations in order to shape and target preventive interventions.

Heightened Temporal Summation of Pain in Patients with Functional Gastrointestinal Disorders and History of Trauma.

BackgroundIndividuals with functional gastrointestinal disorders (FGIDs) report experiencing trauma more often than healthy controls, but little is known regarding psychophysical correlates.PurposeThe purpose of this study was to test the hypothesis that adolescents and young adults with FGIDs since childhood and a trauma history (n = 38) would exhibit heightened temporal summation to thermal pain stimuli, an index of central sensitization, and greater clinical symptoms compared to patients with FGIDs and no trauma history (n = 95) and healthy controls (n = 135).MethodsParticipants completed self-report measures, an experimental pain protocol, and psychiatric diagnostic interview as part of a larger longitudinal study.ResultsFGID + Trauma patients exhibited greater temporal summation than FGID + No Trauma patients and healthy controls. Additionally, FGID + Trauma patients exhibited greater gastrointestinal and non-gastrointestinal symptom severity, number of chronic pain sites, and disability.ConclusionsAssessing for trauma history in patients with FGIDs could identify a subset at risk for greater central sensitization and pain-related symptoms.