The Clinical Implications of Violence-Related PTSD in Mothers and Their Children

TABLE

Mothers with histories of childhood maltreatment or exposure to domestic and other interpersonal violence (IPV) who have a diagnosis of PTSD display more parenting stress and have greater dysregulation of their hypothalamic-pituitary-adrenal (HPA) axis physiology. Their maternal behavior is characterized by less responsiveness to their very young (aged 12 to 42 months) children, particularly following stressful moments such as separation.^1-3 These findings have now been extended and further elaborated by neuroimaging studies.^4,5

Diagnostic imaging

Functional MRI (fMRI) studies suggest that the emotional, physiological, and behavioral dysregulation associated with maternal IPV-PTSD affects the interaction between mother and child. And this interaction is mirrored in neural activity. The [[{"type":"media","view_mode":"media_crop","fid":"41240","attributes":{"alt":"© majivecka/shutterstock.com","class":"media-image media-image-right","id":"media_crop_3757985246743","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"4316","media_crop_rotate":"0","media_crop_scale_h":"101","media_crop_scale_w":"100","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right;","title":" ","typeof":"foaf:Image"}}]]response of mothers with IPV-PTSD to silent video stimuli of their child and unfamiliar children at the moment of separation and during free play was compared with the response of mothers without PTSD (controls) using fMRI. A characteristic pattern of significantly lower medial and ventral medial prefrontal cortical activity was seen in the IPV-PTSD mothers compared with controls and continuously in relation to their IPV-PTSD symptom severity. This pattern of neural activity has also been associated with the response seen on an MRI scan of mothers with PTSD when traumatic memories are triggered (ie, images associated with violence, trauma scripts, frightened/angry facial expressions).

These findings have helped explain the pioneering clinical observations of Fraiberg and colleagues.⁶ Namely, parents caught in intergenerational cycles of violence and trauma often project onto their children (beginning in infancy) attributes that are inconsistent with the age, size, and capacities of the child. Tiny tots are seen as powerful, controlling, violent, or mean because they show age-appropriate displays of negative emotion and helplessness. The traumatized mother associates these behaviors with the perpetrator-victim relationship that she has previously experienced. She thus often perceives the child as a source of danger to be avoided rather than a source of joy and vulnerability to be embraced and protected, leading to further distress by the child-and sadly, further emotional and sometimes physical distance by the parent.

Characteristic of mothers with PTSD, this perceived danger (from the child) does not diminish over time and may produce enhanced glucocorticoid receptor sensitivity. The resulting HPA axis dysregulation can lead to hypocortisolism and altered reactivity to stressors.^7,8 On the basis of these findings, researchers have begun to turn their attention to epigenetic factors involved in HPA axis response variations.^9-11 Of particular interest is the promoter region of the NR3C1 gene, which codes for the glucocorticoid receptor.

Methylation patterns of the NR3C1 gene

Relatively few studies have looked at how the pathophysiology of PTSD is related to methylation patterns of the NR3C1 gene. A study by Weder and colleagues¹² suggests that epigenetic changes in the NR3C1 gene in combination with PTSD conferred an increased risk of depression in the child. However, only certain types of trauma are associated with specific epigenetic signatures. Adults with histories of childhood maltreatment and domestic violence exposure are at high risk for subsequent violent experience and for PTSD and other forms of psychopathy in adulthood.¹³

Our group⁵ undertook a study to determine the role of NR3C1 methylation in mothers with PTSD related to childhood physical and sexual abuse and domestic violence. The goal was to understand how these factors conferred risk to the mother-child relationship and the child’s social and emotional development.

Our study consisted of 123 women who were recruited from the metropolitan Geneva area and their children aged 12 to 42 months. Many of these women had been exposed to interpersonal violence. The mothers completed 3 videotaped visits over a period of 1 to 2 months. After the screening visit, mothers were interviewed (without their child). The mother was asked to focus on how she perceived her child and to elaborate on the trauma she had experienced. This was followed by structured diagnostic interviews and a series of dimensional measures. One to 2 weeks later, the mother was asked to bring her child for a mother-child interaction procedure involving free play and separation reunion.

This mother-child interaction procedure was followed by administration of measures that focused on the child’s life, symptoms, and development. Saliva samples were taken from both the mother and the child for DNA analysis. Two to 4 weeks after the clinical interview and the mother-child observations, mothers had an MRI scan.

The epigenetic and fMRI data in the study showed that the more severe the mother’s IPV-PTSD, the greater her level of parenting stress and the lower the level of methylation of the NR3C1 gene promoter region. The less methylation of the NR3C1 gene, the more disturbed were the mother-toddler interactions, with markedly less child cooperativeness in play (Table). Associated with these variables, less neural activity in the medial and ventral medial prefrontal cortices was seen in response to video stimuli of separation and play activities of their own child than when they were viewing video of unfamiliar toddlers. These brain areas are implicated in emotion regulation as well as parenting stress and maternal PTSD symptom severity, which predicted less child cooperativeness in mother-child play interactions.

Clinical implications

Early-onset, long-term, and repeated exposure to interpersonal violence that leads to PTSD can affect the parent and, in turn, the parent-child relationship at multiple levels-including behavior, physiology, epigenetics, and neural activity during the early, most sensitive periods of child development. Clinical interventions for such traumatized parents with young children must address the child’s developmental needs, the parent’s psychopathology, and the parent-child relationship.¹⁴

New methods to address disturbances in the parent-child relationship are being developed that integrate elements of prolonged exposure therapy and evidence-based infant-parent interventions. One such model, the Clinician Assisted Videofeedback Exposure Session(s) (CAVES), uses video feedback of parent-toddler interactions and recontextualization of trauma-associated memory traces evoked by those interactions in the present.⁸ For example, a mother who sees her child as “being aggressive and trying to control her” by his distressed protest when she leaves the room is asked to watch a video clip with the therapist, who helps her mentalize the process. The therapist asks the mother to think about what is going on in the mind of both child and mother during that moment in the video and how that moment might remind the mother of her past. Therapy also focuses on the mother’s and therapist’s reactions in the present.

Recontextualizing the times and places of these different experiences helps the mother see that her small child is genuinely feeling helpless and frightened and that the mother is stressed by the child’s emotional state. Mothers come to understand that this vulnerable state of mind reminds them of the painful and emotionally dysregulating violent experiences they have avoided thinking about.

The CAVES model shows promising changes in mothers, who begin to see their children less negatively.⁸ The question remains, however, whether patterns of neural activity and functioning of the HPA axis and associated epigenetics reflect the psychological and behavioral changes observed. If such an intervention can support and model competent parenting by traumatized mothers, the child’s distress can be alleviated and a break in familial cycles of violence and trauma becomes ever more likely.¹⁵

Disclosures:

Dr Schechter is Senior Lecturer in Psychiatry at the University of Geneva Faculty of Medicine in Switzerland; he serves as Director of the Pediatric Psychiatric Consult-Liaison Unit and Parent-Child Research and is Deputy Chief of Child and Adolescent Psychiatry at the University of Geneva Hospitals. In addition, Dr Schechter is Adjunct Assistant Professor of Psychiatry in the division of developmental neurosciences at Columbia University College of Physicians and Surgeons in New York. He reports no conflicts of interest concerning the subject matter of this article.

References:

1. Schechter DS, Willheim E, Hinojosa C, et al. Subjective and objective measures of parent-child relationship dysfunction, child separation distress, and joint attention. Psychiatry. 2010;73:130-144.

2. Pat-Horenczyk R, Cohen S, Ziv Y, et al. Emotion regulation in mothers and young children faced with trauma. Infant Ment Health J. 2015;36:337-348.

3. Martinez-Torteya C, Dayton CJ, Beeghly M, et al. Maternal parenting predicts infant biobehavioral regulation among women with a history of childhood maltreatment. Dev Psychopathol. 2014;26:379-392.

4. Schechter DS, Moser DA, Wang Z, et al. An fMRI study of the brain responses of traumatized mothers to viewing their toddlers during separation and play. Soc Cogn Affect Neurosci. 2012;7:969-979.

5. Schechter DS, Moser DA, Paoloni-Giacobino A, et al. Methylation of NR3C1 is related to maternal PTSD, parenting stress and maternal medial prefrontal cortical activity in response to child separation among mothers with histories of violence exposure. Front Psychol. 2015;6:690-701.

6. Fraiberg S, Adelson E, Shapiro V. Ghosts in the nursery: a psychoanalytic approach to the problems of impaired infant-mother relationships. J Am Acad Child Psychiatry. 1975;14:387-421.

7. Schechter DS, Zeanah CH Jr, Myers MM, et al. Psychobiological dysregulation in violence-exposed mothers: salivary cortisol of mothers with very young children pre- and post-separation stress. Bull Menninger Clin. 2004;68:319-336.

8. Schechter DS, Moser DA, Reliford A, et al. Negative and distorted attributions towards child, self, and primary attachment figure among posttraumatically stressed mothers: what changes with Clinician Assisted Videofeedback Exposure Sessions (CAVES). Child Psychiatry Hum Dev. 2015;46:10-20.

9. Yehuda R, Teicher MH, Seckl JR, et al. Parental posttraumatic stress disorder as a vulnerability factor for low cortisol trait in offspring of holocaust survivors. Arch Gen Psychiatry. 2007;64:1040-1048.

10. McGowan PO, Sasaki A, D’Alessio AC, et al. Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nat Neurosci. 2009;12:342-348.

11. Tyrka AR, Price LH, Marsit C, et al. Childhood adversity and epigenetic modulation of the leukocyte glucocorticoid receptor: preliminary findings in healthy adults. PLoS One. 2012;7:e30148.

12. Weder N, Zhang H, Jensen K, et al. Child abuse, depression, and methylation in genes involved with stress, neural plasticity, and brain circuitry. J Am Acad Child Adolesc Psychiatry. 2014;53:417-424.

13. Breslau N. The epidemiology of trauma, PTSD, and other posttrauma disorders. Trauma Violence Abuse. 2009;10:198-210.

14. Schechter DS, Willheim E. When parenting becomes unthinkable: intervening with traumatized parents and their toddlers. J Am Acad Child Adolesc Psychiatry. 2009;48:249-253.

15. Côté SM, Vaillancourt T, LeBlanc JC, et al. The development of physical aggression from toddlerhood to pre-adolescence: a nation wide longitudinal study of Canadian children. J Abnorm Child Psychol. 2006;34:71-85.

16. Spieker S, Crittenden PM. Comparing two attachment classification methods applied to preschool strange situations. Clin Child Psychol Psychiatry. 2010;15:97-120.