Chronic adversity, including neighborhood socioeconomic disadvantage and childhood maltreatment, has been linked to alterations in brain structure and increased risk for psychopathology. While prior research has focused largely on cortical and limbic regions, the cerebellum is increasingly recognized for its role in cognitive and affective processes and may be particularly sensitive to prolonged stress. The present study examined associations between chronic adversity and cerebellar volume in a sample of trauma-exposed adults. Participants (N = 220) were recruited following acute traumatic injury and completed structural magnetic resonance imaging (MRI) post-trauma, along with assessments of neighborhood disadvantage (Area Deprivation Index) and childhood maltreatment (Childhood Trauma Questionnaire). Greater neighborhood disadvantage was significantly associated with smaller total cerebellar volume after adjusting for age, gender, and intracranial volume (p < .001). Greater childhood maltreatment was also associated with smaller total cerebellar volume (p = .043), although effects were more modest. Exploratory analyses indicated that neighborhood disadvantage was associated with widespread reductions across multiple cerebellar subregions, whereas childhood maltreatment showed more limited and attenuated associations after covariate adjustment. Mediation analyses revealed that total cerebellar volume did not significantly mediate associations between adversity and PTSD symptom severity. These findings suggest that both environmental and interpersonal forms of chronic adversity are associated with reduced cerebellar volume in adulthood. The cerebellum may represent a neural substrate through which chronic adversity becomes biologically embedded.
Across species, caregivers regulate offspring fear learning and expression of conditioned fear responses. Rodent studies additionally demonstrate that pups exposed to rough maternal care show disruptions in this adaptive learning mechanism. An analogous experience, early life threat (i.e., interpersonal violence), is strongly associated with developmental outcomes in children. However, we do not understand the extent to which early life threat is associated with fear learning in the context of caregivers in children, although this may be an important mechanism shaping development. The present study utilized data from 219 children who completed a novel fear learning paradigm, in which conditioned fear responses to caregivers and strangers were measured using skin conductance responses. First, we show that children show differential skin conductance responses to stranger stimuli, but not to caregiver stimuli. Second, we find subtle associations between early life threat and conditioned fear responses to caregiver stimuli. Specifically, early life threat was associated with small increases in skin conductance responses to the caregiver-safety cue compared to the caregiver-threat cue. These data show similarities with the rodent literature and identify a potential mechanism by which early life threat may shape child development.
The phenomenological closeness of post-traumatic stress disorder (PTSD) and dissociative disorders has been re-emphasized in recent diagnostic nomenclature, but their common neural pathogenesis is not yet clarified. Moreover, conventional neuroimaging studies have been observational, making it fundamentally difficult to establish causal relationships between abnormalities in specific brain regions and clinical symptoms. Here, we reviewed psychiatric symptoms in human limbic epilepsy, PTSD and dissociative disorders, together with findings from animal studies of limbic circuits, in order to explore causal links between limbic dysfunction and symptoms resembling those of PTSD and dissociative disorders. In human limbic epilepsy, epileptogenic activity arises within limbic-centered networks involving regions such as the hippocampus, amygdala and cingulate cortices, providing a clinical condition in which psychiatric symptoms can be linked to relatively identifiable neural disturbances. These symptoms overlap with key clinical domains of PTSD and dissociative disorders, including intrusive or altered memories, affective dysregulation, depersonalization/derealization, disturbances of consciousness and functional motor phenomena. This overlap raises the possibility that abnormal limbic activity may contribute to similar symptoms in PTSD and dissociative disorders. Animal studies further suggest that experimental manipulation of limbic structures and related circuits can produce PTSD-like and dissociation-like phenomena. Therefore, human limbic epilepsy and animal studies of limbic circuits complement observational neuroimaging studies by offering a framework for examining possible causal links between limbic dysfunction and PTSD- and dissociation-like symptoms.
Background Psychological stress has been implicated in gut microbiome variation, but human evidence remains inconsistent and often does not distinguish exposure to stressful contexts from individual differences in physiological stress reactivity. This repeated-measures study examined whether naturalistic examination stress and post-awakening cortisol reactivity were associated with gut microbiome diversity, community composition, and species-level differential abundance. Methods Thirty-nine healthy university students were assessed during examination and non-examination periods. At each assessment, participants completed validated measures of perceived stress, anxiety, affect, self-esteem, sleep, diet, and physical activity; provided salivary cortisol samples at awakening, 30 min, and 45 min post-awakening; and collected a stool sample for whole-metagenome shotgun sequencing. Post-awakening cortisol reactivity was indexed using area under the curve with respect to increase. Results Examination stress was associated with increased perceived stress, state and trait anxiety, negative affect, poorer subjective sleep, and amplified post-awakening cortisol reactivity. Alpha and beta diversity of the gut microbiome did not differ between examination and non-examination periods, and within-subject changes in community composition were not associated with changes in cortisol reactivity. However, exploratory species-level analyses identified nominal selective microbial differences. Examination stress was associated with higher relative abundance of Dialister massiliensis and Lawsonibacter asaccharolyticus, alongside lower Duodenibacillus massiliensis and Sutterella wadsworthensis. Cortisol reactivity showed distinct associations with higher Roseburia hominis and Ruminococcus bicirculans, and lower Methanobrevibacter smithii. Within-subject increases in cortisol reactivity also covaried with higher Dabirmavirus hominis, Phascolarctobacterium succinatutens and lower Coprococcus catus. Conclusions Short-term examination stress was associated with marked psychological and endocrine responses but was not accompanied by broad restructuring of the adult gut microbiome. Instead, exploratory findings suggest that examination stress and cortisol reactivity may be reflected in selective species-level microbial variation, supporting further longitudinal and functional investigation of stress-related microbiome dynamics.
