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Neurobiology of Rape Trauma (From Rape and Sexual Assault III, P 1-11, 1991, Wolbert Burgess, ed. -- See NCJ-134540)

NCJ Number
134541
Author(s)
C R Hartman; A W Burgess
Date Published
1991
Length
11 pages
Annotation
This paper reviews the emerging evidence that traumatic life events, such as sexual assault, are responsible for basic disrupted adaptive patterns of brain biology; this, in turn, affects cognition and patterns of interpersonal reactions by influencing memory on sensory, perceptual, cognitive, and interpersonal levels.
Abstract
The paper first explains five theoretical models of the biological etiology of trauma based on findings from animal and human research. The research data and the models indicate that three key circuits are activated when a person is confronted with a traumatic stressor. First, the preparatory circuit mobilizes the body for an emergency and is influenced by the locus coeruleus and Raphe nucleus which secrete two catecholamines associated with various states of stress. Second, the stress response circuit increases the secretion of the corticotropin-releasing factor and in some cases cortisol. This is one of the main hormones that mobilizes the body to fight or flight. Third, the blunting circuit is regulated by hormones secreted from the opiod-benzodiazopin system. This response blunts the feeling of pain. Disorder behaviors are assumed to arise out of stress/trauma that overwhelms these adaptive systems so they are thrown into states of disregulation via processes of hyposecretion and hypersecretion. Dysregulation occurs in the primary center for the regulation of major life-engaging functions, e.g., sleep, memory, attachment, sexual behavior, aggression, and self-defense. The paper concludes with a brief discussion of the clinical implications of these findings. 12 references

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