Brain deficits develop in children exposed to neglect and abuse. It is critical that researchers and society understand these devastating consequences and how children are impacted later in life. Theoretically, during early brain development, neglect and abuse lead to deprivation of input needed by the infant brain. Thus, subsequent brain functioning is impaired.1
Various studies have been conducted to analyze stress responses to various forms of child maltreatment, some of which appear below.
- When patients’ brains were viewed on PET scans after being presented with vivid accounts of their own traumatic experiences, there was heightened activity in their right amygdala and associated areas of the temporal and frontal cortex, as well as in the right visual cortex. At the same time, the area of the brain concerned with language (Borca’s area) was “turned off.”2 The researchers suggest this provides a neurological illustration of the tendency of people diagnosed with PTSD to re-experience emotions as physical states (flashbacks) rather than as verbal memories.
- In a group of 33 maltreated children aged 4 to 6 years, who were also less socially competent, were shown not to have elevated salivary cortisol levels in situations of stress brought on by conflicted social interactions, which suggests a blunting of the HPA (hypothalamic-pituitary-adrenal) axis. This axis is a major system that controls reactions to stress and regulates many processes such as mood and emotions. This lack of HPA responsiveness may have evolved as a protective factor for the brains of these very vulnerable children.3
- A number of studies were summarized suggesting that some years after experiencing trauma, including sexual abuse, lower cortisol levels were found in conjunction with a possibly enhanced negative feedback in the HPA axis.
- The study of the effects on human infants of extreme deprivation, in particular the emotional and tactile caregiving aspects, was carried out on infants reared in Romanian orphanages. At the age of two years, these children did not show the usual variation of cortisol levels that were found in home-reared children.4
The summary of these studies stated that there is evidence of impairment in the HPA axis following and during continuing experiences of various forms of abuse and neglect. After repeated experiences of child abuse and/or neglect, some aspects of reminders of the experiences become cues capable of evoking apprehension and fear, even when not accompanied by or following the trauma. Several studies reflect on this observation.
- Fear is perceived in the amygdala.5 Children might thus become hyperaroused, experiencing raised heart rate and feelings of anxiety when faced with an apparently neutral occurrence or stimulus, which might include a particular smell or a sound associated with the abuse. The children are often not actually aware of the source of the arousing cue.6
- When interacting with their depressed mothers, infants have been observed to be less active, vocalize less, and show more gaze aversion than a comparable group of infants of non-depressed mothers.7
- A child faced with a frightening experience and unable to escape “resorts” to dissociation, disengaging attention from the present reality.8 In this process the vagus nerve, the parasympathetic part of the autonomic nervous system, becomes activated, leading to a slowing of the heart rate and a fall in blood pressure. It is postulated that as a part of the dissociation process, opiates associated with dopamine systems that arise in the brain stem and are activated by stress, alter the perception of painful stimuli.9
The studies listed here are just a few outlining the effects on a developing child’s brain. This provides more insight into the long-term suffering we encounter as adults of child abuse and neglect.
1 Early Brain Development, http://psychweb.cisat.jmu.edu/graysojh/pdfs/Volume077.pdf
2 Rauch, S., van der Kolk, B., Fisler, R., Alpert, N., Orr, S., Savage, C., Fischman, A., Jenike, M., & Pitman, R. (1996). A symptom provocation study of post-traumatic stress disorder using positron emission tomography and script-driven imagery. Archives of General Psychiatry, 53, 380-387.
3 Hart, J., Gunnar, M. & Cicchetti, D. (1995) Salivary cortisol in maltreated children: Evidence of relations between neuro-endocrine activity and social competence. Development and Psychopathology 7, 11-26.
4 Carlson, M., & Earls, F. (1997) Psychological and neuro-endocrinological sequelae of early social deprivation in institutionalized children in Romania. Annals of the New York Academy of Sciences, 807, 419-428.
5 LeDoux, I. (1994): Emotion, memory and the brain. Scientific American, 270, 32-39.
6 Perry, B., Pollard, R., Blakely, T., Baker, W., & Vigilante, D. (1995) Childhood trauma, the neurobiology of adaptation, and “use-dependent” development of the brain: “How states become traits.” Infant Mental Health Journal, 16, 271-291.
7 Dawson, G., Hessl, D., & Frey, K. (1994) Social influences on early developing biological and behavioral systems related to risk for affective disorder. Development and Psychopathology, 6, 759-779.
8 Perry, B., & Pollard, R. (1998) Homeostasis, stress, trauma, and adaptation: A neurodevelopmental view of childhood trauma. Child and Adolescent Clinics of North America, 7, 33-51.
9 Abercrombie, E. & Jacobs, B. (1988) Systemic naloxone administration potentiated locus coeruleus noradrenergic neuronal activity under stressful but not non-stressful conditions, Brain Research, 441, 362-366.