Aversive learning and memory processes are common in pain and post-traumatic stress disorder (PTSD) and involve some of the same brain areas such as the amygdala, the insula and the anterior cingulate cortex. It is very likely that the deficient extinction of fear or pain responses is the core deficit in these disorders rather than enhanced acquisition (Flor, 2009; Milad, Rauch, Pitman, & Quirk, 2006). A special role for extinction is played by the prefrontal cortex, which shows structural and functional abnormalities in pain and PTSD (e.g., Daniels et al., 2010; Geha et al., 2008). In addition, severe forms of PTSD are accompanied by dissociative states and research shows that dissociation impedes learning (Ebner-Priemer et al., 2009). This may explain why we often have great difficulties in teaching extinction to those affected by PTSD—they do not process and store new information properly. In addition, the hippocampal deficits that have been observed in patients with PTSD impair context conditioning (Pohlack et al., in press) and this keeps these individuals from differentiating safe and dangerous contexts and subsequently danger cues may prevail and become dominant (Gilbertson et al., 2007). Another interesting phenomenon is the fact that stress analgesia is enhanced in PTSD patients suggesting that they have more attenuation of acute pain in stress situations than traumatized persons without PTSD or healthy controls (Diener et al., 2011; Pitman, van der Kolk, Orr, & Greenberg, 1990). This is in contrast to the enhanced rate of chronic pain problems in this group and not easily explained. Another problem is that cognitive deficits are frequent in chronic pain, PTSD and of, course in TBI (Gualtieri & Morgan, 2008; Moriarty, McGuire, & Finn, in press; Skandsen et al., 2010). How this negatively impacts assessment is not really known and new methods for reporting pain may have to be devised. For example, measures of functioning may be more appropriate. In addition, there may be long-lasting changes in the brain after TBI symptoms have already subsided (Chen, Epstein, & Stern, 2010) and this may also be the case with PTSD and pain making it difficult to predict if being sent to a war zone after recovery might not again trigger the same problem due to the long-lasting cognitive and thus also neuroplastic changes. A special problem in the context of assessment is memory distortion that is frequent in both pain and PTSD and that may lead to wrong conclusions about signs and symptoms. DSM-V might improve on postconcussive symptom definition by including overlap or a new category such as ‘‘combat stress’’ including polytrauma. Sleep disorders are frequent in these multiply affected individuals and we know now that sleep is essential for memory and learning (Diekelmann & Born, 2010) and it can be assumed that sleep deficits are related to both symptoms and difficulty in acquiring new information about fear and pain cues. When addiction is present, the processing of reinforcing stimuli other than those related to addiction may also be impaired and this may enhance anxiety, depression and pain (Park et al., 2010). There is a great need for comparative studies for these disorders and their combination and specifically for the analysis of neuropsychological and neurobiological mechanisms that may partially be overlapping between these disorders. H. Flor (&) Department of Cognitive and Clinical Neuroscience, Central Institute of Mental Health, Heidelberg University, J5, 68159 Mannheim, Germany e-mail: herta.flor@zi-mannheim.de
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