A theoretical framework for the neurobiology of chronic traumatization

This issue of the Acta Psychiatrica Scandinavica features an article by Lanius et al. (1) that provides the first comprehensive framework for the complex symptom constellation experienced by individuals who have suffered chronic traumatization. These symptoms include difficulties with emotional awareness, emotion regulation, self-reflection, and the experience of an often fragmented and ⁄or intensely self-loathing sense of self. Such a theoretical framework is of great importance because many of these symptoms have often not been emphasized by traditional studies in posttraumatic stress disorders. However, the complex clinical picture described in this review including problems with emotion regulation and an altered sense of self is consistent with the revisions of the post-traumatic stress disorder criteria that have been proposed for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Specifically, the DSM-5 proposal suggests that patients may experience persistent and exaggerated negative expectations about one s self, others, or the world and persistent distorted blame of self or others about the cause or consequences of the traumatic event(s) . In addition, ‘reckless or self-destructive behavior, ‘pervasive negative emotional state – for example: fear, horror, anger, guilt, or shame, and ‘persistent inability to experience positive emotions have been proposed to be part of the new criteria for post-traumatic stress disorder (2). Building on advances in social cognitive and affective neuroscience, Lanius et al. (1) have proposed that a core set of brain regions, including cortical midline structures, amygdala, insula, posterior parietal cortex, and temporal poles, is vulnerable to psychological trauma. With chronic exposure to trauma, functions associated with these regions such as emotional ⁄ self-awareness, emotion regulation, social emotional processing, and ⁄or self-referential processing can be adversely affected. While investigations are clearly at an early stage of development, it is striking how well brain imaging anomalies in patients exposed to chronic traumatization map onto these regions. The role of the dorsomedial prefrontal cortex and the posterior cingulate in self-referential processing and anomalies in related regions in the default mode network in patients with post-traumatic stress disorder are highlighted, adding to the burgeoning literature on the default mode network and disorders of mentalizing. A distinction is also made between patients who show significant symptoms of depersonalization, derealization, and analgesia and patients who predominantly exhibit re-experiencing and flashback-type symptoms; the latter demonstrated a failure of prefrontal inhibition of limbic regions, and the former showed increased prefrontal inhibition of limbic regions (3). Parsing out the components of the emotional processing dysfunction in patients with posttraumatic stress disorder is much more than an academic exercise. The presence of emotional dysregulation can have treatment implications whether it arises from fear conditioning (4) or the unavailability of a responsive attachment figure during childhood (5). Successful exposure therapies depend on the ability of the patient to form a therapeutic alliance and fully emotionally engage with the traumatic material. A failure to address deficits in emotion regulation or emotional awareness before exposure-based treatments interferes with the therapeutic process leading to less than satisfactory outcomes. Recognizing these complex adaptations to psychological trauma will have important implications for the assessment, treatment, and furthering the understanding of the neurobiological underpinnings of this devastating disorder. It may be too much to expect that brain imaging correlates of trauma could lead to the ability to predict which patients are at particular risk or the type of Acta Psychiatr Scand 2011: 124: 329–330 All rights reserved DOI: 10.1111/j.1600-0447.2011. 01770.x 2011 John Wiley & Sons A/S