Cited by 607Child Abuse and TraumaStress Responses and CortisolPosttraumatic Stress Disorder Research

Developmental neurobiology of childhood stress and trauma

Teicher, Martin H, Andersen, Susan L, Polcari, Ann, Anderson, Carl M, Navalta, Carryl P·2002·Psychiatric Clinics of North America

Abstract

Severe early stress and maltreatment produces a cascade of events that have the potential to alter brain development. The first stage of the cascade involves the stress-induced programming of the glucocorticoid, noradrenergic, and vasopressin-oxytocin stress response systems to augment stress responses. These neurohumors then produce effects on neurogenesis, synaptic overproduction and pruning, and myelination during specific sensitive periods. Major consequences include reduced size of the mid-portions of the corpus callosum; attenuated development of the left neocortex, hippocampus, and amygdala along with abnormal frontotemporal electrical activity; and reduced functional activity of the cerebellar vermis. These alterations, in turn, provide the neurobiological framework through which early abuse increases the risk of developing post-traumatic stress disorder (PTSD), depression, symptoms of attention-deficit/hyperactivity, borderline personality disorder, dissociative identity disorder, and substance abuse.

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Crossref · 10.1016/s0193-953x(01)00003-x

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19 of 19 references verified0 citation errors · 0 not checkable

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  • The fight-or-flight response among children exposed to extreme, traumatic, or repetitive stressors, and the attendant release of endogenous catecholamines and adrenal corticosteroids, are both uncontrollable and invisible.

    “Likewise, the fight-or-flight response among children exposed to these types of stressors, and the attendant release of endogenous catecholamines and adrenal corticosteroids are both uncontrollable and invisible (Perry 1998; Teicher 2002; De Bellis 1994, 1997; Scaer 2001).”
  • Neurobiological evidence supports the hypothesis of dysfunction in hippocampus, amygdala, medial prefrontal cortex, and other limbic structures believed to mediate anxiety and mood dysregulation following early abuse.

    “Neurobiological evidence supports the hypothesis of dysfunction in hippocampus, amygdala, medial prefrontal cortex, and other limbic structures believed to mediate anxiety and mood dysregulation following early abuse (Teicher 2002).”

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Authors
Teicher, M. H., Andersen, S. L., Polcari, A., Anderson, C. M., & Navalta, C. P.
Affiliations
  • Harvard University (US)
  • McLean Hospital (US)
Venue
Psychiatric Clinics of North America
Publisher
Elsevier BV
Published
2002-06
Volume
25
Issue
2
Pages
397-426
ISSN
0193-953X (ISSN-L)
OpenAlex
W2040075391
Cited by
607
References
19
Citations by year
2026: 11 · 2025: 18 · 2024: 22 · 2023: 15 · 2022: 18 · 2021: 29 · 2020: 30 · 2019: 29 · 2018: 36 · 2017: 27 · 2016: 28 · 2015: 39 · 2014: 35 · 2013: 43 · 2012: 29
FWCI
2.80
Type
journal article
Language
en
Open access
closed
Locations
  • Psychiatric Clinics of North America (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01mh043743-14, 5r01mh053636-04)
  • National Institute of Mental Health (MH 53636, R01 MH43743)
Topics
  • Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
Keywords
childhood stress, childhood trauma, maltreatment, brain development, glucocorticoid stress response, neurogenesis, synaptic pruning, myelination, corpus callosum, hippocampus, amygdala, cerebellar vermis, post-traumatic stress disorder, depression, attention deficit hyperactivity disorder, borderline personality disorder, dissociative identity disorder, substance abuse
MeSH terms
Brain, Child, Child Abuse, Child Development, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Life Change Events, Pituitary-Adrenal System, Stress Disorders, Post-Traumatic, Stress, Psychological, Neurotransmitter Agents

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