FIGURE 1.5. Increased amygdala function during acquisition of conditioned fear responses in women with early childhood abuse and PTSD. Lighter areas represent bilateral amygdala activation. There was greater amygdala activation with acquisition of fear responses (pairing of conditioned stimulus and unconditioned stimulus) in women with PTSD compared to controls; z > 3.09, p < 0.001. Source: Bremner et al., 2005.
Fewer brain-imaging studies have been performed in children with PTSD. Several studies have shown alterations in electroencephalogram (EEG) measures of brain activity in children with a variety of traumas who were not selected for diagnosis compared to healthy children. About half of the children in these studies had a psychiatric diagnosis. Abnormalities were located in the anterior frontal cortex and temporal lobe and were localized to the left hemisphere (Ito et al., 1993; Schiffer, Teicher, & Papanicolaou, 1995). Two studies have found reductions in brain volume in children with trauma and PTSD symptoms (Carrion et al., 2001; De Bellis et al., 1999b). One group did not find reductions in hippocampal volume either at baseline or over a longitudinal period (De Bellis, Hall, Boring, Frustaci, & Moritz, 2001; De Bellis et al., 1999b) while another group found an 8.5% reduction in hippocampal volume that was not significant after controlling for smaller brain volumes in the PTSD group (Carrion et al., 2001). One study used single-voxel proton magnetic resonance spectroscopy (proton MRS) to measure relative concentration of N-acetylaspartate and creatinine (a marker of neuronal viability) in the anterior cingulate of 11 children with maltreatment-related PTSD and 11 controls. The authors found a reduction in the ratio of N-acetylaspartate to creatinine in PTSD patients relative to controls (De Bellis, Keshavan,
Spencer, & Hall, 2000). Studies have also found smaller size of the corpus callosum in children with abuse and PTSD relative to controls (De Bellis et al., 1999b), as well as larger volume of the superior temporal gyrus (De Bellis et al., 2002). In a study of abused children in whom diagnosis was not specified, there was an increase in T2 relaxation time in the cerebellar vermis, suggesting dysfunction in this brain region (Anderson, Teicher, Polcari, & Renshaw, 2002).
In summary, adults with early-abuse-related mental disorders show evidence of decreased medial prefrontal and hippocampal function and structure, as well as increased amygdala function. Although changes in medial prefrontal and corpus callosum structure were found in children with PTSD, changes in hippocampal volume were not. This is explainable by findings in animals showing that early stress does not manifest as changes in hippocampal structure until adulthood (Brunson, Eghbal-Ahmadi, Bender, Chen, & Baram, 2001; Brunson et al., 2005).
These findings have implications for understanding alterations in memories of abuse in patients with abuse-related PTSD (Bremner, 1999; Bremner, 2001; Bremner, Krystal, Charney, & Southwick, 1996a). This hippocampus plays a role in the integration of the individual elements of memory in the context of space and time (Zola-Morgan & Squire, 1990). Dysfunction of the hippocampus in patients with abuse-related PTSD may lead to an inability to effectively retrieve memories of early abuse.
Dissociation is defined as a breakdown in memory, consciousness, and the sense of self. Dissociation at the time of trauma is often seen in trauma victims, and three studies have now found a correlation between smaller hippocampal volume and dissociative symptom severity (Bremner et al., 2003b; Stein, Koverola, Hanna, Torchia, & McClarty, 1997; Vermetten et al., 2006). We have hypothesized that dissociation at the time of trauma represents a behavioral correlate of stress-induced hippocampal damage (Bremner et al., 1996a). If so, hippocampally mediated dissociative amnesia may represent a mechanism of altered recall of early abuse.
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