Abstract: The present chapter will review childhood PTSD with specific focus on neurobiological sequelae of childhood trauma and present some preliminary evidence of altered functioning of brainstem catecholamine systems in childhood PTSD. In specific, it is hypothesized that the abnormal patterns of catecholamine activity associated with prolonged ‘alarm reactions’ induced by traumatic events during infancy and childhood can result in altered development of the central nervous system (CNS). Furthermore, it is hypothesized that this altered development includes a ‘dysregulated’ brainstem which in turn results in a host of signs and symptoms related to abnormal brainstem functioning, including altered cardiovascular regulation, affective lability, behavioral impulsivity, increased anxiety, increased startle response and sleep abnormalities. Finally, early life experience is discussed, in context of childhood trauma, as an ‘expresser of genetic predispositions.
Perry, B. D. (1996). Neurodevelopmental Adaptations to Violence: How Children Survive the Intragenerational Vortex of Violence. In Violence and Childhood Trauma: Understanding and Responding to the Effects of Violence on Young Children. Cleveland, Ohio: Gund Foundation Publishers, pp.67-80.
Perry, B. D. (1997). Incubated in Terror: Neurodevelopmental Factors in the “Cycle of Violence.” In J. Osofsky (Ed.). Children, Youth and Violence: The Search for Solutions . (pp. 124-148). New York: Guilford Press.
How violence alters the brain and nervous system of the developing child.
Perry, B. D. (1997). Altered Brain Development Following Global Neglect in Early Childhood. (1997). Academy version of a paper presented at the Society for Neuroscience Annual Meeting, New Orleans.
Perry, B. D. (1998). Neurophysiological Aspects of Anxiety Disorders in Children. In: Textbook of Pediatric Neuropsychiatry. In C.E. Coffey & R.A. Brumback (Eds.), Textbook of Pediatric Neuropsychiatry. (pp. 579-594). Washington, D.C: American Psychiatric Press, Inc.
Perry, B.D. (1999). Memories of fear: How the Brain Stores and Retrieves Physiologic States, Feelings, Behaviors and Thoughts from Traumatic Events. In J.M. Goodwin & R. Attias (Eds.), Splintered Reflections: Images of the Body In Trauma. (pp. 9-38). New York: Basic Books.
Perry, B.D. (1999). Violence and Childhood: How Persisting Fear Can Alter the Developing Child’s Brain.
Perry, B. D. (2000). Traumatized children: How childhood trauma influences brain development. The Journal of the California Alliance for the Mentally Ill 11(1), 48-51.
Perry, B.D. (2001). The neurodevelopmental impact of violence in childhood. In D. Schetky & E. Benedek (Eds.), Textbook of Child and Adolescent Forensic Psychiatry. Washington, D.C.: American Psychiatric Press, Inc.
Perry, B.D. (2001) The neuroarcheology of childhood maltreatment: The neurodevelopmental costs of adverse childhood events. In B. Geffner (Ed.), The Cost of Child Maltreatment: Who Pays? We All Do. San Diego, CA: Family Violence & Sexual Assault Institute.
Perry, B.D. (2001). Trauma and Terror in Childhood: The Neuropsychiatric Impact of Childhood Trauma. In Ed., I. Schulz, S. Carella & D.O. Brady (Eds.). Handbook of Psychological Injuries: Evaluation, Treatment and Compensable Damages. American Bar Association Publishing.
Perry, B.D. (2002). Childhood Experience and the Expression of Genetic Potential: What Childhood Neglect Tells Us About Nature and Nurture. Brain and Mind, 3, 79-100,
Abstract. Studies of childhood abuse and neglect have important lessons for considerations of nature and nurture. While each child has unique genetic potentials, both human and animal studies point to important needs that every child has, and severe long-term consequences for brain function if those needs are not met. The effects of the childhood environment, favorable or unfavorable, interact with all the processes of neurodevelopment (neurogenesis, migration, differentiation, apoptosis, arborization, synaptogenesis, synaptic sculpting, and myelination). The time courses of all these neural processes are reviewed here along with statements of core principles for both genetic and environmental influences on all of these processes. Evidence is presented that development of synaptic pathways tends to be a “use it or lose it” proposition. Abuse studies from the author’s laboratory, studies of children in orphanages who lacked emotional contact, and a large number of animal deprivation and enrichment studies point to the need for children and young nonhuman mammals to have both stable emotional attachments with and touch from primary adult caregivers, and spontaneous interactions with peers. If these connections are lacking, brain development both of caring behavior and cognitive capacities is damaged in a lasting fashion. These effects of experience on the brain imply that effects of modern technology can be positive but need to be monitored. While technology has raised opportunities for children to become economically secure and literate, more recent inadvertent impacts of technology have spawned declines in extended families, family meals, and spontaneous peer interactions. The latter changes have deprived many children of experiences that promote positive growth of the cognitive and caring potentials of their developing brains.
Perry, B.D. (in press). Sexual Abuse of Infants. A five-part question focusing on sexual abuse during infancy
Perry, B. D., Conroy, L., & Ravitz, A. (1991). Persisting psychophysiological effects of traumatic stress: The memory of “states”. Violence Update, 1(8), 1-11.
Perry, B. D., & Marcellus, J. E. (1997). The Impact of Abuse and Neglect on the Developing Brain. Colleagues for Children, 7, 1-4. [Missouri Chapter of the National Committee to Prevent Child Abuse]
Perry, B. D., & Pollard, R. Altered brain development following global neglect in early childhood. Society For Neuroscience: Proceedings from Annual Meeting , New Orleans, 1997)
Perry, B.D., & Pollard, R. (1998). Homeostasis, stress, trauma, and adaptation: A neurodevelopmental view of childhood trauma. Child and Adolescent Psychiatric Clinics of North America , 7, 33-51.