Electrophysiological (Begic et al., 2001) and neuroimaging (Bremner et al., 1999; Pitman et al., 2001) data support the concept of an alteration of hippocampal functioning in relation to PTSD. Functional brain imaging data also argue for the involvement of the amygdala and the medial prefrontal cortex in the mechanisms underlying the expression of PTSD symptoms. Whereas neuronal activity increases in the amygdala during symptom provocation (Shin et al., 1997), the medial prefrontal cortex exhibits, on the contrary, decreased neuronal activity (Bremner et al., 1999). Although prefrontal data, both from animal and human studies, have yielded contradictory conclusions, more recent electrophysiological (Herry and Garcia, 2002) and neuroimaging (Fernandez et al., 2001) studies deserve, however, a little more consideration as potential tools for predicting treatment dropout. Indeed, following a complete elimination of PTSD-symptoms via an exposure therapy, follow-up data indicate that up to 40 % of treated individuals still display the original affective changes (Tarrier et al., 1999). If, as shown by Fernandez et al. (2001), extinction of PTSD symptoms is associated with a disappearance of depression in prefrontal neuronal activity, and if this plasticity signals low risk of symptom return, as shown in mice (Herry and Garcia, 2002), then post-treatment neuroimaging analyses might predict the long-term outcome of the treatment. This prediction would be defined by the restoration of amygdalar neuronal activity (Levin et al., 1999), and a restoration or potentiation of hippocampal and prefrontal neuronal activities (note: hippocampal neuronal activity is reduced in PTSD patients during symptom provocation; Bremner et al., 1999).
However, maintenance of depression of neuronal activity in the hippocampus and the medial prefrontal cortex, despite restoration of amygdalar activity and complete extinction of PTSD symptoms, would be predictive of treatment dropout. Hence, brain-mapping methods associated with PTSD treatment will not only provide insights into the basic mechanisms of this disorder but also improve diagnostics of potential relapses.
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