Extinction or Reconsolidation
Differences between suppression and transformation in how we recover from traumatic experiences

Memory is central to all learned behavior, and in humans to one’s sense of identity. Sleep and memory processes are deeply entwined. Both are central to our sense of well-being. As Shakespeare wrote in Macbeth,

Sleep that knits up the ravell'd sleeve of care,
The death of each day's life, sore labour's bath,
Balm of hurt minds, great nature's second course,
Chief nourisher in life's feast

Problems with memory processes (and with sleep) are at the root of one of the most pervasive problems in society, posttraumatic stress disorder (PTSD). Those with PTSD suffer from memories they cannot escape nor resolve. They cannot escape into sleep because their memories follow them into recurrent nightmares.

Stickgold and Walker, in a 2007 article reviewing phases of sleep involved with the consolidation and reconsolidation of memory, point out “the term ‘memory’ covers a wide range of memory types, which differ in the kinds of information stored, the brain structures mediating this storage, and, in humans, whether the information is accessible to conscious awareness.” They add, “There is no clear consensus at this time on how many such memory systems there are, and how they should be defined, either in terms of information content or brain structures involved in their storage.”

Their review describes the most widely accepted taxonomy of memory and describes the role of sleep in processes of memory consolidation and reconsolidation.

Figure 1 Stickgold and Walker, 2007

It is generally recognized that traumatic memories are organized differently than normal episodic (autobiographical) memories (van der Kolk, 1994; van der Kolk & Fisler, 1995). As Diamond et al., state “...with strong emotionality, the hippocampus rapidly shifts from a “configural/cognitive map” mode to a ‘flashbulb memory’ mode, which underlies the long-lasting, but fragmented, nature of traumatic memories” (Diamond, et al., 2007).

Since the late 1980s, two methods have emerged as the dominant evidence-based treatments for PTSD –
prolonged imaginal exposure (PE) and Eye Movement Desensitization and Reprocessing (EMDR). Both are recognized as effective treatments for PTSD in numerous national and international treatment guidelines, yet their distinct theoretical models are founded on quite different principles. There is increasing speculation that the neurobiological processes by which they work are also quite different.

Evidence has been mounting for years that Pavlovian
extinction, the mechanism that underlies the documented treatment effects in PE therapy, does not eliminate the original learning, but instead generates new learning which in a sense “sits on top” of the original learning and inhibits it. This evidence is reviewed by Bouton (2004) and Quirk & Mueller (2008) both of whom point out that new learning is especially context-dependent, and thus the original learning can re-appear under the right conditions. “Extinction involves new learning, and it therefore leaves the CS [Conditioned Stimulus] with two available ‘meanings’ or associations with the US [Unconditioned Stimulus]. As is true for an ambiguous word, the context is crucial in selecting between them” (Bouton, 2004, p. 485).

Quirk and Mueller 2008 Neural mechanisms of extinction learning and retrieval

Another, entirely different process, known as
reconsolidation is capable of reorganizing memories and may be the process involved in the documented treatment effects of EMDR therapy. “... reconsolidation is the process of restabilizing the memory trace after it is retrieved or “reactivated” (Taylor, et al., 2009, p. 186). In her Adaptive Information Processing theory Francine Shapiro proposed that effective reprocessing leads to synthesis between maladaptive and adaptive memory networks. This concept of synthesis is clearly distinct from the historic, but unfortunately misleading term “desensitization” that remains embedded in the name of the approach.

In EMDR reprocessing, a target memory is first accessed (reactivated). Then, bilateral eye movements are employed. These eye movements used in EMDR have been shown enhance new associations (Kuiken, 2002). In contrast to the required prolonged periods of exposure in PE, the periods of direct exposure to the selected memory in EMDR tend to be brief. Patients generally are unable to retain a focus on their target memory during periods of eye movements, and they often report spontaneously shifting their attention to other associations.

“Reconsolidation is argued to be a distinct process that occurs over a brief time period after memory is reactivated/retrieved -- when the memory becomes labile and vulnerable to disruption. Reconsolidation is thought to be an independent, perhaps opposing, process to extinction...” (Taylor, et al., 2009, p. 186).

In general, extinction effects require prolonged exposure while reconsolidation requires only brief exposure to reactivate the memory. “Recent studies have suggested that brief and/or weak exposures to a conditioned cue lead to reconsolidation whereas more prolonged or repeated retrieval events, or weaker conditioning, results in extinction (Pedreira and Maldonado, 2003; Eisenberg et al., 2003; Suzuki et al., 2004; Power et al., 2006; Tronson et al., 2006)” (Taylor, et al., 2009, p. 189).

Thus the neurobiological process of reconsolidation, which involves the reorganization of the original learning, appears more similar to the theoretical model proposed by Shapiro (1991).

In spite of the claims of some who remain skeptical of the unique contributions of EMDR and the AIP model, EMDR should not be viewed as just another form of exposure therapy. As pointed out by Rogers & Silver (2002), “EMDR conflicts with some of the specific assumptions of the Emotional Processing Model [used in PE], with several of the procedural guidelines for exposure therapy for trauma, and with previous exposure research. It produces symptom relief by using brief, high-intensity exposures, by using incomplete exposure to the details of the target experience, and by using a nondirective approach that allows client behaviors previously thought to reduce treatment effectiveness.”

This distinction in underlying processes (mechanism) is important for several reasons. The first is that by making use of procedures that enhance reconsolidation, EMDR does not leave the original learning in a form in which it can be restimulated by subsequent contexts or cues. Prolonged Exposure, relying on extinction, leaves the original learning in place and relies on inhibitory mechanism and other brain systems to “chose” the new learning over the original learning. This suggests that EMDR may produce treatment effects that are essentially invulnerable to changes in context.

The second reason this distinction is important is that skeptics of the empirical evidence for EMDR’s treatment effects have claimed that it merely makes use of “exposure” with unnecessary eye movements. (See a discussion in Perkins and Rouanzoin, 2002). As stated above, Rogers and Silver (2002) reviewed the evidence and concluded that EMDR is in fact not an “exposure” based therapy but is correctly classified as an information processing form of therapy.

In an intriguing and as yet unpublished paper, presented at the 2001 annual meeting of the Association for the Advancement of Behavior Therapy, Rogers & Lanius explored evidence from treatment trials using naltrexone – an opioid antagonist – to identify a possible difference in neurobiological processes in exposure/extinction treatment (for phobia) and in EMDR reprocessing treatment (for PTSD). “Research with spider phobics indicate that opiate blockade inhibits the effectiveness of exposure for phobia, yet a recent case series suggests that blockade enhances the effectiveness of EMDR with dissociative trauma clients.”

Another reason it is important to recognize that EMDR achieves its treatment effects through reconsolidation rather than through extinction is because this leads to a consideration of the additional conditions for which EMDR is likely to be found effective. A major clinical challenge is the treatment of co-occurring PTSD and substance abuse. A secondary analysis of National Institute on Drug Abuse (NIDA) data concluded, “PTSD severity reductions were more likely to be associated with substance use improvement, with minimal evidence of substance use symptom reduction improving PTSD symptoms. Results support the self-medication model of coping with PTSD symptoms and an empirical basis for integrated interventions for improved substance use outcomes in patients with severe symptomatology.” (Hein et al., 2010).

Taylor, et al., (2009) “review behavioral and pharmacological studies outlining novel methods of effective and persistent reductions in cue-induced relapse behavior in animal models.” They “hypothesize that a combined approach aimed at both enhancing the consolidation of cue-drug extinction and interfering with the reconsolidation of cue-drug memories will have a greater potential for persistently inhibiting cue-induced relapse than either treatment alone.”

Only limited, but promising treatment trials have been conducted of EMDR for these commonly co-occurring conditions (Brown, & Gilman, 2008; Brown, Gilman & Kelso, 2008; Hase, Schallmayer & Sack, 2008; Popky, 2005). These suggest that larger and controlled studies are warranted. Given the role of reconsolidation processes in the maintenance and treatment of substance abuse there is reason to be optimistic that EMDR has an important role to play in the treatment of those who suffer from these co-occurring conditions.


Bouton, M. E. (2004). Context and behavioral processes in extinction. Learn Mem, 11(5), 485-94.

Brown, S., & Gilman, S. G. (2008). Executive summary: An integrated trauma treatment program (EMDR and seeking safety) as an ehancement in the thurston county drug court program. EMDRIA Annual Conference. Phoenix, AZ.

Brown, S., Gilman, S. G., & Kelso, T. (2008). Integrated trauma treatment program: A novel EMDR approach for PTSD and substance abuse . EMDRIA Annual Conference. Phoenix, AZ.

Diamond, D. M., Campbell, A. M., Park, C. R., Halonen, J., & Zoladz, P. R. (2007).
The temporal dynamics model of emotional memory processing: A synthesis on the neurobiological basis of stress-induced amnesia, flashbulb and traumatic memories, and the yerkes-dodson law. Neural Plast, 2007, 60803.

Hase, M., Schallmayer, S., & Sack, M. (2008). EMDR reprocessing of the addiction memory: Pretreatment, posttreatment, and 1-month follow-up.
Journal of EMDR Practice and Research, 2(3), 170-179.

Hien, D. A., Jiang, H., Campbell, A. N., Hu, M. C., Miele, G. M., Cohen, L. R., et al. (2010).
Do treatment improvements in PTSD severity affect substance use outcomes? A secondary analysis from a randomized clinical trial in NIDA's clinical trials network. Am J Psychiatry, 167(1), 95-101.

Kuiken, D., Bears, M., Miall, D., & Smith, L. (2002). Eye movement desensitization reprocessing facilitates attentional orienting.
Imagination, Cognition and Personality, 21(1), 3-20.

Perkins, B. R., & Rouanzoin, C. C. (2002).
A critical evaluation of current views regarding eye movement desensitization and reprocessing (EMDR): Clarifying points of confusion. J Clin Psychol, 58(1), 77-97.

Popky, A. J. (2005). Detur, an urge reduction protocol for addictions and dysfunctional behaviors. In R. Shapiro (Ed.),
EMDR solutions: Pathways to healing. (pp. 167-88). New York: W. W. Norton.

Quirk, G. J., & Mueller, D. (2008).
Neural mechanisms of extinction learning and retrieval. Neuropsychopharmacology, 33(1), 56-72.

Rogers, S., & Lanius, U. F. (2001). Phobia, PTSD, endogenous opioids and EMDR treatment response. Poster presented at the annual meeting of the Association for the Advancement of Behavior Therapy. Philadelphia.

Rogers, S., & Silver, S. M. (2002).
Is EMDR an exposure therapy? A review of trauma protocols. Journal of Clinical Psychology, 58(1), 43-59.

Schwabe, L., & Wolf, O. T. (2009).
New episodic learning interferes with the reconsolidation of autobiographical memories. Plos ONE, 4(10), e7519.

Shapiro, F. (1991). Eye movement desensitization and reprocessing: From EMD to EMD/R - a new treatment model for anxiety and related traumata. Behavior Therapist, 14, 133-135.

Shapiro, F., & Maxfield, L. (2002).
Eye movement desensitization and reprocessing (EMDR): Information processing in the treatment of trauma. J Clin Psychol, 58(8), 933-46.

Stickgold, R., & Walker, M. P. (2007).
Sleep-Dependent memory consolidation and reconsolidation. Sleep Med, 8(4), 331-43.

Taylor, J. R., Olausson, P., Quinn, J. J., & Torregrossa, M. M. (2009).
Targeting extinction and reconsolidation mechanisms to combat the impact of drug cues on addiction. Neuropharmacology, 56 Suppl 1, 186-95.

van der Kolk, B. A. (1994).
The body keeps the score: Memory and the evolving psychobiology of posttraumatic stress. Harv Rev Psychiatry, 1(5), 253-65.

van der Kolk, B., & Fisler, R. (1995).
Dissociation and the fragmentary nature of traumatic memories: Overview and exploratory study. Journal of Traumatic Stress, 8(4), 505-525.