Although the scientific discourse tends to associate memories that create intrusions with criterion A events and the definition of PTSD, non-criterion A events have been shown to create even more intrusions than criterion A events (Gold et al., 2005). Additionally, data from a survey of 832 adult subjects indicated that stressful life events can generate at least as many PTSD symptoms as traumatic events (Kendler et al., 2003). McFarlane (2010) showed that stressful life experiences can lead to intrusions without a fully developed PTSD. McFarlane (2010) also demonstrated that these intrusions relate to many mental disorders and poor health in general. Following these findings intrusions seem to be a common memory-based symptom, which is not necessarily linked with a PTSD diagnosis or criterion A event. Nevertheless, intrusions indicate a memory-based pathology beyond PTSD that can be linked with other mental disorders. This is consistent with a publication of Heinz et al. (2016) discussing basic learning mechanisms as representations of a basic dimension of mental disorders. They advocate for a research focus on such basic dimensions rather than pursuing a narrow focus on single disorders.
Centonze et al. (2005) described the importance of pathogenic memories from a theoretical perspective. There approach is based on the increasing acceptance of theories that relate the origin of many psychiatric symptoms to the formation and consolidation of implicit dysfunctional memory (Centonze et al., 2005). Since their publication other prominent authors have engaged in this discussion. Alberini and LeDoux (2013) summarize research on memory reconsolidation and dwell on the therapeutic perspective. In their opinion further research on memory reconsilidation could help to ameliorate maladaptive memories and potentiate adaptive behaviors in psychopathology (Alberini and LeDoux, 2013). Sillivan et al. (2015) explore the possibilities of latest research on epigenetic modification. They advocate for a recognition of the contribution of epigenetic mechanisms to how pathological memories associated with addiction and PTSD are stored, expressed, and subsequently modified, possibly leading to novel therapeutic targets (Sillivan et al., 2015).
Summarizing current neurobiological research, Centonze et al. (2005) state: “Experimental research examining the neural bases of non-declarative memory (such as habit formation, classical conditioning, and fear conditioning) has offered intriguing insight into how functional and dysfunctional implicit learning affects the brain.” They give evidence on the importance of long-term modification of synaptic transmission in particular as the most plausible mechanisms underlying memory trace encoding compulsions, addiction, anxiety, and phobias. Compulsions and other stereotypies are viewed as pathological habits (nearly automated implicit motor abilities) encoded as aberrant synaptic plasticity in the corticobasal ganglia loop. Centonze et al. (2005) refer to addictive drugs abusing the molecular mechanisms of reward-based associative learning by inducing long-term changes in synaptic effectiveness in those brain areas serving basic biological needs, such as feeding and sexual interaction. Finally, anxiety, panic disorder, and phobias are viewed as uncontrolled and repetitive defensive reactions secondary to abnormal fear conditioning – a form of implicit associative learning, encoded as long-term potentiation (LTP) in the lateral amygdala. In consequence, Centonze et al. (2005) propose that an effective psychotherapy must be directed to erase maladaptive pathogenic memories and research should focus on the development of techniques to remove pathogenic memories. Although they mentioned neither the AIP model, nor EMDR therapy, the concept of pathogenic memories could probably open another view on recent developments in EMDR research.
It seems to be of interest to explore the overlap of the theory of pathogenic memory and the AIP model, regarding practical implications for EMDR therapy in reprocessing maladaptive implicit memories, especially as the cited authors are advocating for the developments of therapeutic tools to modify pathogenic memories. As Centonze et al. (2005) coined the term “pathogenic memory” but did not give a precise definition, one should start here.