Over the past 20 years, our research has focused on elucidating the developmental effects of child abuse (CA) at the behavioral and neurobiologi-cal levels. In parallel, a cadre of behavioral scientists and neuroscientists has collectively established a substantial body of work on the etiology, course, and outcome of CA (for reviews, see Glaser, 2000; Heim & Nemeroff, 2002; Kaufman & Charney, 2001; Putnam, 2003; Tarullo & Gunnar, 2006; Teicher et al., 2003; Teicher, Tomoda, & Andersen, 2006). From a nosological perspective, CA is considered a traumatic stressor and precursor to the development of post-traumatic stress disorder (PTSD) as defined in the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.) (DSM-IV-TR) (American Psychiatric Association, 2000). In addition, several other psychiatric conditions are associated with CA— most notably depression, anxiety, borderline personality disorder, dissociation, and substance use disorders. The central tenet to our work (and that of others) is that the stress that results from CA has an unfavorable effect on neurodevelopment and, consequently, behavioral development.
In this chapter, we will review what is known about the clinical neuroscience of CA and provide new findings on neuroanatomical effects of CA and their relation with memory processes.
Child abuse is but one of many forms of early adverse experiences. Sigmund Freud (1896/1959) outlined one of the first theories of the causal role that sexual abuse during childhood plays in the development of psychopathology. Historically, CA has also included physical abuse and neglect. Precise definitions notwithstanding, these types of maltreatment are common worldwide and are the primary problems that child protective/social services address. More recently, researchers have a renewed interest in understanding the impact of emotional abuse—typically manifested as either verbal abuse/aggression or the witnessing of domestic violence—on mental health. In fact, initial evidence suggests that emotional abuse also functions as a traumatic stressor; is a marked risk factor for later psychopathology; and may prove to have more detrimental effects than the traditional forms of CA (Grilo & Masheb, 2001; Kaplan & Klinetob, 2000; Simeon, Guralnik, Schmeidler, Sirof, & Knutelska, 2001; Teicher, Samson, Polcari, & McGreenery, 2006).
Our research endeavors have been predicated on the conjecture that stress in the form of CA negatively affects neurodevelopment, which in turn can result in disordered behavior, thought, and emotion. In support of this contention, a vast array of preclinical studies have demonstrated that brain development is sculpted by early experience and that specific brain regions are particularly sensitive to the effects of early stress (Kaufman, Plotsky, Nemeroff, & Charney, 2000; Teicher, Tomoda, et al., 2006). For example, initial work by Berrebi, Fitch, Ralphe, Denenberg, Friedrich, and Denenberg (1988) showed that early handling influences corpus callosum development, particularly in male rats. Not surprisingly, human studies have provided evidence that the corpus callosum is particularly sensitive to the effects of CA (De Bellis et al., 1999; De Bellis et al., 2002; Teicher et al., 2004; Teicher et al., 1997). Utilizing a hypothetico-deductive approach, we proposed a clinical model in which a cascade of events produces CA effects and that this succession is primarily mediated by stress that results in the release of stress hormones (cortisol, adrenalin, and vasopressin) and enhances the turnover of neurotransmitters (e.g., dopamine, serotonin, and norepi-nephrine) in key brain regions (Teicher, 2000; Teicher, Andersen, Polcari, Anderson,& Navalta,2002;Teicher et al.,2003). Such stress-induced neurochemical alterations effect modifications in myelination, synaptogenesis, and neurogenesis. This model hinges on the premise that CA is perceived and responded to as a stressor, regardless of the parameters of the adverse experience, which directly impacts neurodevelopment.
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