Domestic violence as a risk factor of maternal filicide.

PURPOSE: This paper will investigate precursors to maternal filicide, focusing on domestic violence. While psychosis is often well described, less frequently explored are the connections between prior trauma, domestic violence, depression, and filicide. We will discuss reasons why a woman may not disclose domestic violence and suggest possible areas for intervention. METHODS: We present a case involving domestic violence, its impact on mental health, and eventual filicide. We then present an alternative scenario of the same case where filicide is considered, but is avoided. RESULTS: The case of the mother who experienced domestic violence and was accused and sentenced for filicide is seen in greater relief by presenting the case in an alternative scenario with effective interventions. It is clear the availability and the ability to access community supports, such as obstetric and pediatric screening, psychiatric treatment, domestic violence shelters, intimate partner violence outreach services, parenting support groups, and hospital social work case management, tragedies such as filicide can be prevented. CONCLUSION: Traumatic early childhood experiences predispose people to a stress-response system that is more prone to inactivity and impulsivity. This can cause women in domestic violence relationships to stay, limit their options for family planning, become increasingly depressed, not seek community support, and risk impulsive action of harming their child. This risk can be mitigated by building stable relationships with their medical team, treating depression, connecting with home visitation programs, and being empowered to access contraception.

Immune and Neural Response to Acute Social Stress in Adolescent Humans and Rodents.

Studies in adults have linked stress-related activation of the immune system to the manifestation of psychiatric conditions. Using a translational design, this study aimed to examine the impact of social stress on immune activity in adolescents and on neuronal activity in a preclinical mouse model. Participants were 31 adolescents (ages 12-19), including 25 with mood and anxiety symptoms. Whole-blood samples were collected before and after the Trier Social Stress Test (TSST), a stress-inducing public speaking task, then cultured for 6 hours in the presence and absence of the inflammatory endotoxin lipopolysaccharide (LPS). Effects of TSST and LPS on 41 immune biomarkers were examined using repeated-measures analysis of variance. Separately, juvenile (8-week-old) male mice were non-stressed or exposed to reminder social defeat then intraperitoneally injected with saline or LPS (n = 6/group). Brains were perfused and collected for immunohistochemistry and confocal microscopy at 0, 1, 6, and 24 hours post-injection. Activity was determined by the density of cFos-positive neurons in the paraventricular hypothalamus, paraventricular thalamus, and basolateral amygdala, regions known to show sustained activation to immunological challenge. Analyses in the adolescent study indicated a strong effect of LPS but no effects of TSST or TSST×LPS interaction on immune biomarkers. Similarly, reminder social defeat did not induce sustained neuronal activity changes comparable to LPS immunological challenge in juvenile mice. Our convergent findings across species suggest that the acute immune response to stress documented in adults is not present in youth. Thus, aging and chronicity effects may play an important role in the inflammatory response to acute psychosocial stress.