You are currently viewing Therapies of psychological trauma in the light of neuroscience. Reconsolidation of memory  and a new paradigm in the therapeutic process

Therapies of psychological trauma in the light of neuroscience. Reconsolidation of memory and a new paradigm in the therapeutic process

With the kind collaboration of Stéphanie Kahlfa, researcher at the CNRS, at the Institut de Neurosciences – La Timone (Marseille)


As early as the 1960s, neuroscientists highlighted that a recently acquired memory is fragile and must be stabilized to become permanent (consolidation). In the 2000s, they found that old memories become unstable again and susceptible to change when they are reactivated (reconsolidation). In particular, their experiments have shown that it is possible to reduce the emotions of a memory when certain pharmacological substances are administered at the time of reconsolidation. This discovery led them to test new drug approaches (propranolol) to treat psychological disorders generated by traumatic memories. In this article, we examine the effectiveness of three forms of trauma psychotherapy, prolonged exposure, EMDR and hypnosis, in the light of this new paradigm of the therapeutic process.
Keywords: Memory reconsolidation, extinction, propranolol, reconsolidation therapy, EMDR, Behavioral and Cognitive Therapies, prolonged exposure, hypnosis, corrective scenarios


According to recent memory reconsolidation theory, memories are labile and subject to change when reactivated. Through this process of reconsolidation, ancient memories are updated by the integration of current information.

Neuroscientists have shown that it is possible to reduce the emotions of a memory when it is reconsolidated. This discovery opens up interesting therapeutic perspectives for psychological disorders generated by a memory carrying intense negative emotions, such as psychological trauma.

We will discuss the effectiveness of reconsolidation therapy, prolonged exposure, EMDR and hypnosis in the light of this new paradigm of the therapeutic process. In this way, we hope to contribute to a better understanding of the mechanisms at work in the resolution of psychological trauma.

Consolidation and reconsolidation of memory

Memory is a dynamic process. It does not just store memories and then return them unchanged. It builds and transforms them.

Memory consolidation

A recently acquired memory is initially labile and vulnerable to interference and oblivion. To become persistent, it must be consolidated. In cognitive neuroscience, memory consolidation refers to the process by which the newly acquired memory trace is transferred from a short-term memory system to long-term memory where it stabilizes1(Dudai, 2004).

More than a century ago, Müller and Pilzecker, who developed the first theory of consolidation, demonstrated that the presentation of distracting stimuli alters the ability to recall newly acquired information (Müller & Pilzecker, 1900). More recently, Holmes and collaborators have proven the effectiveness of the game Tetris in blocking the emotional consolidation of a shocking scene (Holmes, James, Coode-Bate, & Deeprose, 2009). In addition to distraction, electroshock and certain pharmacological substances also interfere with consolidation2. This is the case of propranolol, a noradrenergic beta-blocker, which has been the focus of attention of researchers in the field of the treatment of psychological trauma for some 20 years. On the other hand, exposure to a stressor within minutes of learning increases memory consolidation.

Consolidation involves two processes, synaptic stabilization and systemic stabilization.


Synaptic stabilization refers to cellular and molecular changes in neurons and synapses. Synaptic consolidation is essential for the migration of the trace to the cortical areas (Davis, Squire, 1984; DeZazzo & Tully, 1995; McGaugh, 2000). This consolidation is rapid. It occurs in a few minutes, at most in a few hours after the memory has been encoded.


According to the classical conception, systemic stabilization concerns the migration of the memory trace from the hippocampus to the cortex. According to the theory of multiple traces (Winocur & Moscovitch, 2011), it implies a strong interaction between the hippocampus and the different cerebral zones3 which leads to the multiplication of the memory trace (Buzsaki, 1996; Wang & Morris, 2010, Lesburguères & Bontempi, 2011). In this perspective, the hippocampus is also, just as much as the cortex, a long-term memory storage structure. Due to its associative capacities, the hippocampus reactivates neocortical zones during so-called offline periods, namely calm wakefulness and sleep (Wittenberg, Sullivan, & Tsien, 2002; Diekelmann & Born, 2010). The reactivation of the trace leads to the creation of a new trace which will in turn be consolidated by the hippocampus and inserted into the cortical network involved in the encoding of the memory. This consolidation is slow, between several weeks and several years. However, according to schema theory (Bartlett, 1932), it can be rapid if the new memory traces are integrated into a pre-existing pattern of previously acquired knowledge.


For a long time, it was believed that once the process of consolidation has been completed, the interconnections that constitute the memory becomes permanent. From then on, it was considered impossible to modify a fully consolidated memory trace. However, an experiment conducted in 1968 by James Misanin and his collaborators invalidated this thesis (Misanin et al., 1968). However, it was not until the 2000s that other teams of researchers became interested in the malleability of an ancient memory and confirmed these early experimental data. Thus, various authors have highlighted that the recall of a consolidated memory makes it labile and subject to changes within a time window of a few hours. To be maintained after being recalled, it must once again be stored and stabilized in long-term memory through protein synthesis (Debiec, LeDoux, 2006; Nader, Schafe, LeDoux, & Sara, 2000). This process, called memory reconsolidation, contrasts with consolidation by the molecular mechanisms, neural circuits and brain areas involved (Alberini, 2005; Dudai & Eisenberg, 2004; Hernandez & Kelley, 2004). During reconsolidation, the memory can be re-encoded as is, reinforced, attenuated or modified. Various phenomena can interfere with reconsolidation, for example through new learning (Forcato, Argibay, Pedreira, & Maldonado, 2009; Schiller et al., 2010), amnestic agents (Nader et al., 2000b) or beta-blocking agents.

In short, consolidation is a process of forming new memories and reconsolidation is the process of updating or modulating (increase or decrease) the weight of old memories that have already been consolidated.

Consolidation, reconsolidation and psychological trauma

Consolidation and emotion

The most vivid and lasting memories are those of events accompanied by strong emotions. Indeed, emotion seems to facilitate the consolidation of a long-term memory trace through stress hormones, adrenaline and norepinephrine (Lupien & McEwen, 1997; McGaugh, 2004; Marin et al., 2010), via adrenergic amygdala receptors (Debiec, Bush & LeDoux, 2011; McGaugh, 2004). The effect of these neuromodulators is related to the alert level, anxiety or stress (Cahill & McGaugh, 1996).

Consolidation and psychological trauma

Studies have shown that the intensity of peri-traumatic distress is correlated with the subsequent development of a psychotraumatic disorder (Vaïva et al., 2001; Fikretoglu, 2007; Jehel et al., 2006). This distress is accompanied by orthosympathetic hyperactivation. This peritraumatic neurovegetative activity contributes to a stronger consolidation of traumatic memories (McCleery & Harvey, 2004; Ducrocq & Vaiva, 2005; Marin et al, 2010), by the release of endogenous stress hormones, in particular noradrenaline (Tully & Bolshakov, 2010), and by an increase, influenced by noradrenergic processes, in the activity of the amygdala, the presumed site of emotional memory (LeDoux, 2000). The result is an over-consolidated traumatic memory, which is very vivid, durable, omnipresent in the memory and easily reactivated. Any remembering in turn leads to a synthesis of stress hormones that further reinforces the persistence of the traumatic memory. Preserving the memory of emotional and traumatic events in the long term is an advantage for the preservation and evolution of the human species by giving man the ability to be aware of dangers and to seek what is beneficial to him.

Orthosympathetic peritraumatic activation and subsequent hyperadrenergic state are now considered to be the true factor of chronicization of disorders and the best predictor of long-term psychotraumatic syndrome (Bryant et al., 2011). Studies have shown that a victim with tachycardia greater than 95 beats per minute or tachypnea of at least 22 breaths per minute4, indicating a prolonged orthosympathetic activation, in the immediate wake of an event, whereas he/she is safe and has been reassured, is predisposed to developing psychotraumatic disorder (Bryant et al., 2008). On the contrary, a heart rate of less than 80 beats per minute would be a good omen (Shalev et al.) Indeed, 95% of people with a heart rate of less than 80 beats per minute within hours of the potentially traumatogenic situation do not subsequently suffer from post-traumatic stress syndrome (Vaiva et al., 2003; Pitman et al., 2002). Besides, clinical research suggests that norepinephrine beta-blockers (propranolol) taken within the post-immediate period of trauma prevent the registration of traumatic memories and reduce the risk of developing post-traumatic syndrome (Vaiva et al., 2003)5.

Reconsolidation and psychological trauma

Intrusive symptoms of the traumatic event are pathognomonic manifestations of post-traumatic stress disorder. Flashbacks, repetitive memories, and nightmares are some of these reminiscences6. Flashbacks reproduce all or part of the traumatic scene and suddenly burst into the victim’s consciousness. They are experienced as real for a brief moment, at most for a few seconds. Repetitive and intrusive memories of the traumatic event unexpectedly come to the mind of the traumatized person despite his or her willingness to reject them. Unlike flashbacks, they are recognized as cognitions, distinct from the current reality. Nightmares of repetition bring the traumatic event to life in dreams. Generally, they do not accurately reproduce the deleterious situation but retain its main characteristics and trigger the same violent feelings of helplessness, fear or horror.

Through these revivals, the victim feels brought back to the past and has the feeling he/she is re-experiencing the initial event, or even reliving it. Revivals occur spontaneously or are triggered by stimuli that evoke or symbolize the traumatic event (images on television, newspaper article, smell, noise, physical sensations, etc.)

Chronicization of the psychotraumatic syndrome can be explained, at least partially, by the reconsolidation theory. Through the repetition syndrome, the memory of the traumatic event is recalled multiple times. These iterative reactivations trigger the long-term potentiation process (LTP)7 and continuously increase the persistence of the memory trace. In addition, these recollections evoke strong negative emotions (fear, helplessness, horror, anger, guilt, shame). The orthosympathetic system is activated, regardless of the fact that the person is objectively safe and is aware of his or her safety. The resulting hyperadrenergy contributes to a still stronger reconsolidation of the emotional power of the traumatic event (McCleery & Harvey, 2004). The memory is thus quickly hyperconsolidated. On the other hand, research has shown that the decrease in stress hormone levels through pharmacological substances (propranolol, metyrapone), at the moment of reactivation of a memory, durably reduces the reconsolidation of negative memories (Marin et al., 2011; Brunet et al., 2008; Brunet et al., 2011).

Consolidation, reconsolidation and modification of memories

Contrary to widespread conviction, our memories are not a true reflection of reality and are not the faithfully recorded content of our experiences.

Our memory does not encode events in a neutral and objective way as a camera would. As soon as an event is perceived, it is assessed according to the culture of the person experiencing it, their personality, their past experiences, their cognitive development, their needs, desires, values, beliefs, etc. It gets structured and becomes a memory by getting subtly enriched with hypotheses, theories, interpretations and explanations specific to the subject. According to the schema theory developed by Frederic Bartlett (Bartlett, 1932)8, a memory is not the exact reproduction of a scene but an active imaginative reconstruction of past information and experiences. For the American cognitive psychologist Elizabeth Loftus, a memory specialist, « memories are not the sum of what a person has done, but rather the sum of what they have thought, what they have been told, and what they believe » (Le Monde, 2008).

According to the theory of reconsolidation, a memory is modified with each recall (Winocur & Moscovitch, 2011). It is re-encoded with the new context in which the recovery occurred and is rebuilt in the light of the current needs and knowledge (« updating memory » according to Lee, Nader, & Schiller, 2017). This plasticity is a fundamental adaptive process in the evolution of animal and human species. Elizabeth Loftus has shown that memories can be changed when recalled by the addition of new information (Loftus, 1981). Through several hundred experiments conducted on more than 20,000 people, she has proven that it is possible to modify an autobiographical memory in subjects by simply exposing them to erroneous information (Loftus, 2009). Other authors have also shown that it is possible to modify memories following their reactivation (Nader, Schafe, & LeDoux, 2000b; Przybyslawski & Sara, 1997; Sara, 2000).

Memory Reconsolidation and Trauma Therapies

Scientific studies on the reconsolidation of memory and the possibility of modifying consolidated memories offer a new paradigm for the treatment of psychological trauma.

The fact that it is possible to reduce the emotions of a memory at the time of its reconsolidation (Przybyslawski, Roullet, & Sara, 1999) provides interesting therapeutic perspectives for psychological disorders generated by a memory carrying intense negative emotions such as psychological traumas. We will discuss some of the therapies for which one may reasonably wonder whether their efficiency can be attributed to the blocking of the emotional reconsolidation of traumatic memories.

Reconsolidation therapy™

The effectiveness of propranolol in permanently reducing or even neutralizing a newly acquired or already consolidated traumatic memory has been proven by research. Based on this discovery, Canadian Professor Alain Brunet, a psychiatry associate at McGill University in Montreal, developed the reconsolidation therapy.


Propranolol is a noradrenergic beta-blocker prescribed for high blood pressure, prophylaxis of stress angina attacks, long-term treatment after myocardial infarction, certain cardiovascular rhythm disorders, cardiovascular manifestations of hyperthyroidism, in-depth treatment of migraine and facial vascular algae, prevention of digestive bleeding due to ruptured esophageal varices, essential tremors and cardiac functional manifestations such as tachycardia and palpitations during transient emotional situations (ANSM, 2019).

The first study on the ability of propranolol to reduce the consolidation of emotional memories in healthy subjects was conducted in 1994 (Cahill et al., 1994). From the 2000s onwards, studies have been conducted on people who had been exposed to a traumatic event. They have shown that, given as prophylaxis after a traumatic event, within the time window of consolidation, and at a sufficient dose, propranolol can prevent, or at least reduce, the development of post-traumatic disorder (Pitman et al., 2002).

Despite these convincing results, this research has not produced large-scale care for victims of potentially traumatic situations. Indeed, the prescription of such prophylactic treatment is rarely possible in practice because it is mandatory to take the medication within the first few hours following the harmful event. Since then, studies evaluating the effects of propranolol on consolidated memories in healthy subjects have shown that the molecule is active if administered within the time window of reconsolidation (Kindt et al., 2009; Kroes et al., 2010; Schwabe et al., 2012). Brunet and his collaborators replicated these results with traumatized people. In a first study, a single session of reactivation of a traumatic memory on propranolol reduced the psychophysiological reactivity of the patients (Brunet et al., 2008). In the second, increasing the number of reactivations to six, at a rate of one per week, reduced the severity of post-traumatic stress disorder (Brunet et al., 2011). This improvement was maintained four months after the treatment. By limiting adrenergic impregnation at the time of the recall of the traumatic memory, the beta-blocker modulates its emotional charge without altering its content. The memory is thus reconsolidated without the strong negative emotion that prevailed during the initial encoding.

These studies pave the way for large-scale care of victims through an effective, empirically validated treatment9(Brunet, 2018 ; Boriello, 2019).


Following scientific studies of the blockage of memory reconsolidation under propranolol, Brunet developed the reconsolidation therapy™, a treatment combining the reactivation of traumatic memory under propranolol and psychotherapy by mental re-exposure to the traumatic narrative.

Treatment consists of 6 sessions. During the initial session, the patient writes the memory of the event that caused the trauma, in as precise and detailed a manner as possible, in the first person and in the present. He receives propranolol per os, at a dosage of 1mg/kg. His blood pressure and heart rate are checked, with bradycardia and hypotension being contraindications to treatment. 60 to 75 minutes after taking the beta-blocker, under the active effect of the molecule, he reads his story aloud in the presence of the therapist. This is followed by a brief closing interview during which he is free to express his views on his general state and progress. In order to assess the severity of his psychotraumatic syndrome and to measure the effects of treatment, he is asked to complete evaluation questionnaires.

Between the 4th and 6th session, the majority of patients report a marked regression in their traumatic symptoms. The emotional burden associated with the recollection of the event has decreased; the traumatic memory has turned into a commonplace bad memory.

The patient’s general condition and progress are evaluated twice in post-treatment, one week and seven weeks after the last session10.

Following the terrorist attacks in Paris in 2015 and the large number of psychological victims, France launched a research project for the care of people suffering from psychotraumatic syndrome, based on the model of the reconsolidation therapy™, known as Paris Mémoire Vive (Paris MEM). It was set up under the supervision of Professor Brunet and is promoted by Assistance publique/Hôpitaux de Paris (AP-HP).

Trauma-centred cognitive-behavioral therapy


The effectiveness of trauma-oriented cognitive-behavioral therapies has been empirically validated by numerous controlled studies (Bisson, 2010; Bisson et al., 2007, Schnuur, 2007), justifying their recommendation by the World Health Organization as first-line treatment (WHO, 2013).

Among the various techniques, the prolonged exposure therapy developed by Edna Foa and her team (Foa et al., 2007, McLean, Foa, 2011) has proven to be the most effective, both in reducing post-traumatic symptoms and in reducing comorbid disorders (generalized anxiety, depression, negative emotions such as anger and guilt). As we have seen, it is proposed in the therapy of reconsolidation™ in combination with propranolol administration.


Treatment combines psychoeducation on psychological trauma, learning to relax, repeated and prolonged reactivation of traumatic memory through imaginative exposure and combating avoidance behaviors through in vivo exposure exercises to feared situations (Rauch et al., 2012).

In the case of a simple trauma, treatment generally includes between 8 and 12 90-minute sessions (Foa et al., 2007). It can be prolonged when trauma is multiple or comorbid disorders are significant (Foa et al., 2010).

In the first session, the patient chooses the traumatic event for which he or she wishes to be soothed. If he suffers from multiple traumas, he determines the one he wants to treat first and which causes him the most intense distress or the most significant dysfunction. Most often, he chooses the situation that causes the most frequent and disruptive intrusive symptoms. At the end of the session, the therapist teaches him a slow-breathing relaxation technique that he is encouraged to practice daily at home.

In the second session, the clinician provides information on the reactions commonly experienced by traumatized subjects, which provides the patient with a framework for understanding their symptoms (psychoeducation). It outlines the benefits of mental and in vivo exposure therapy. He explains that avoidance behaviors are effective in reducing anxiety in the short term but maintain symptoms because dodging anxiety situations hampers the process of treating and integrating traumatic memories. With the therapist’s help, the patient draws up a hierarchical list of avoided situations that are sources of fear or discomfort but are objectively risk-free (places, people, objects, etc.) He ranks them according to the degree of distress they generate and gives them a score between 0 and 100. In subsequent sessions, he will select among these situations those he will be dealing with in real life between sessions. This in vivo exposure is generally progressive, from moderately scary to severely frightening situations. The patient is instructed to remain in the anxiety-provoking situation for 45 to 60 minutes or until their anxiety has decreased by at least 50%. The duration of exposure is an important treatment factor. It must be long enough for the patient to associate the feared stimulus with safety and for corrective learning to occur (McClean, Foa, 2011).

During the third session, imaginal exposure phase begins. With their eyes closed, patients are invited to imagine themselves reliving the event that caused their trauma as well as the thoughts, emotions, sensations and behaviors associated with it. While visualizing the event as clearly as possible, he describes his experience in detail, aloud, in the first person and in the present tense. The exposure is repeated several times for 30 to 45 minutes (Foa, et al., 2007; Rauch et al., 2012). It will be reproduced in subsequent sessions and at home, as a daily task, by listening to an audio recording made in the office (McClean, Foa, 2011). The session ends with a 15-20 minute open discussion (post-exposure processing) in which the patient’s experience during exposure, any ideas they consider important or significant, their dysfunctional cognitive patterns (for example, erroneous cognitions such as « I am incompetent » or « the world is extremely dangerous ») and the lessons that have been learned are discussed.

The following sessions begin with the report of the tasks carried out since the last session, continue with the imaginal exposure and close with the choice of the next tasks to be carried out in vivo.

In the final session, clinician and patient assess progress, discuss the lessons learned and establish an action plan to maintain the treatment benefits (Foa et al., 2007).

Extinction_of_the_memory_of fear_vs._reconsolidation

The therapy is effective in the short term for more than 50% of patients (Bradley et al., 2005). As for the long-term benefit, the studies reach contradictory conclusions. One meta-analysis reports sustainable therapeutic gains (Taylor, Harvey, 2009), while another reveals fading over time, with only one-third of patients maintaining significant long-term improvement (Bradley et al., 2005).

A memory whose emotional reconsolidation has been blocked should not cause symptoms or recur later. This leads to the hypothesis that in long-term exposure therapy, the traumatic memory trace may only be masked and not altered. The process at work would therefore be different from reconsolidation.

In long-term exposure therapies, treatment is largely based on extinguishing the memory of fear. However, unlike the blockage of emotional reconsolidation, in extinction, traumatic memory does not disappear but is simply inhibited by the new learning in which the subject has realized that he is now safe (Quirk, 2002). During the extinction process, a new memory trace is created and superimposed on the traumatic memory. This new learning creates new circuits that are distinct from the circuits of traumatic learning. The latter remains in the brain, potentially accessible (Bouton, 1993), and may later reappear spontaneously or as a result of a difficult life experience (Rescorla, 2004; Hermans et al., 2005). This could explain the loss of long term effectiveness of exposure therapy (Poundja, 2012; Thomas, 2014). On the contrary, in reconsolidation, the new learning directly modifies the circuits of traumatic memory. Its synaptic coding is replaced by that of the new learning.
Traumatic memory no longer exists as such and undesirable symptoms no longer appear (Ecker, Ticic, & Hulley, 2012).

Animal research shows that a brief 3-minute exposure leads to emotional modulation of reconsolidation, while a prolonged exposure of half an hour generates an extinction process (Suzuki et al., 2004). Of course, these results cannot be applied to humans without further studies. However, since these two processes, extinction and reconsolidation, are relatively comparable in animals and humans, it is not prohibited to make hypotheses that will have to be studied by research. Thus, it can be assumed that a brief exposure combined with another therapeutic intervention (propranolol, EMDR or hypnosis) would offer more durable results than prolonged exposure.


EMDR was discovered by chance in the United States in 1987 by Francine Shapiro, a PhD in psychology at the Mental Research Institute in Palo Alto, California. This method quickly revolutionized the conception and practice of psychotherapy. Since then, many researches have been carried out and the technique has been constantly improved.

EMDR is the acronym for « Eye Movement desensitization and reprocessing ». The name « EMDR » has been retained even though the method is no longer limited to the use of eye movements.

The effectiveness of EMDR has been scientifically proven by numerous controlled studies. Since 2013, the World Health Organization has been advocating it for the treatment of psychotraumatic disorders as first-line treatment (WHO, 2013).


With the patient’s participation, the therapist identifies the situation that caused the trauma and, if there are several, establishes treatment priorities.

He suggests that the patient determine the negative thinking (for example, « I’m going to die »), emotions (for example, fear, anxiety, terror) and current physical sensations (for example, a knot in the stomach) associated with the disturbing target situation (for example, the truck coming straight at her/his vehicle) and the positive thinking by which she/he wants to replace the negative cognition (for example, « I am safe »). He invites the patient to assess the extent of their distress on a subjective scale from 0 to 10 and the validity of the positive idea on a scale from 1 to 7.

He invites the patient to keep in mind the target situation, negative thought, emotions and associated physical sensations. Then comes the phase of alternating bilateral stimuli11. These stimuli are achieved through eye movements (the patient follows the therapist’s fingers or a moving object with his eyes), tactile stimuli (the therapist alternately taps the patient’s hands or knees or asks him to hold vibrating balls in his hand) or sound stimuli (he clicks fingers alternately to the right and the left or uses a sound beep transmitter). The therapist interrupts the stimuli, encourages the patient to express what is happening in them (emotions, physical sensations, a modification of memory, a sequence of memories linked to the first by an associative chain, the emergence of a new positive cognition, etc.). He then asks them to evaluate their level of disturbance on the scale introduced in the previous phase. During this phase of bilateral stimulation, the patient may experience intense emotions. The therapist repeats the stimulation sets until the patient evaluates his distress at 0 or 1.

Once the target is « desensitized », the reprocessing phase begins. The therapist uses bilateral stimuli to set up the positive idea. He continues the sets until the patient assesses the validity of positive cognition at 6 or 7.

The therapist then checks that the negative thought associated with the target image no longer disturbs the patient. He asks him to perform a « body scan » by reviewing all his body sensations from head to toe. The purpose of this phase is to identify any remaining tensions or negative sensations that will then be eliminated by means of new series of bilateral stimuli.

The therapist ends the session with a small debriefing.


Shapiro postulates that there is an adaptive information processing system that assimilates new experiences through neurophysiological mechanisms into existing memory networks. Experience is automatically processed by this innate system that sorts new data and links them to related elements already stored in our brain (Shapiro, 2007a; Cotraccia, 2013). Through this connection to what the subject already knows, he/she can make sense of them. What is useful is stored with the appropriate emotions, and constitutes constructive learning for the future (Shapiro, 2007a).

When a person is confronted with a deleterious event, an imbalance occurs in the nervous system. The information processing system is hindered, and the information acquired at the time of the event, including images, sounds, affect and physical sensations is maintained neurologically in its disruptive state. Information is frozen in time, trapped in its own neural network and unable to connect to other memory networks containing adaptive information (Shapiro, 1995, 2006, 2007a). This original material inspires inappropriate emotional, cognitive and behavioral reactions and overt symptoms.

EMDR involves accessing dysfunctionally stored information, stimulating the information processing system through standardized protocols and procedures, and facilitating dynamic links with adaptive memory networks. The memory information thus linked finds an adapted resolution (Solomon, Shapiro, 2008).

The adaptive information processing hypothesis is consistent with neurobiological memory reconsolidation theories that suggest that accessible memory becomes labile and can be restored in a modified form.


A large number of studies compare EMDR with trauma-focused behavioral-cognitive therapy. They show higher and/or faster results with EMDR (Ironson, 2002; Power, 2002; Rothbaum, 2005; Kahn, 2018) and a lower dropout rate. In addition, unlike exposure therapies, the therapeutic benefit obtained with EMDR appears to be constant and sustainable (Solomon, Shapiro, 2008), capable of generalizing to similar future events (Rost, Hoffman, & Wheeler, in Zaghout-Hodali & Dodgson, 2008). This supports the hypothesis that different processes are at work in the two techniques.

The disadvantage of exposure therapy is that it requires patients to perform exposure tasks, both imaginatively and in vivo, between sessions. In addition to the fact that these exercises require many hours a week, they are also a major source of distress. This could explain the high dropout rate during treatment, ranging from 25 to 30% depending on the studies (Bisson et al., 2007; Bradley et al., 2005). During the EMDR therapy session, exposure to traumatic memory is of short duration, about 30 seconds. The patient is not required to describe the problematic situation in detail and does not remain focused on it. New thoughts, emotions, memories and associations freely emerge during the reprocessing phase and become the new focus for the next set of bilateral stimuli. According to cognitive-behavioral therapy researchers, exposure must be prolonged to be effective; brief exposures reinforce patient difficulties (Marks et al., 1998). Prolonged exposure is likely to be necessary to complete the extinction process. The fact that the results are comparable or even better with EMDR reinforces the idea that the processes governing the two techniques are different.

As we have seen, extinction and reconsolidation have different neurobiological mechanisms (Suzuki, 2004). Prolonged exposure would promote the extinction of the memory of fear, while EMDR would, according to researchers, promote the reconsolidation of a modified version of the initial memory trace of the disturbing situation (Shapiro, 2007b; Solomon, Shapiro, 2008 ; Oren, Solomon, 2012 ; Khalfa, Touzet, 2017).


The main characteristic of the hypnotic or hypnotic trance state is a highly focused attention to an idea, internal images, sensations, bodily functions or emotions to the point that the subject is momentarily indifferent to most aspects of external reality. Some of its psychic functions are put on hold in favor of other processes, especially unconscious ones. His perceptions and understanding of reality are modified, allowing him to function mentally in a different way and to be more open to himself.

There are many techniques of hypnosis. Corrective scenarios are, according to the author’s clinical experience, among the most effective.


Pierre Janet, in the 1880s, discovered corrective scenarios and their effectiveness on patients suffering from trauma and dissociative disorders. This method is applicable in current hypnotherapy practices, particularly under the name of « scenario change », and shares common principles with the EMDR technique known as « resource development and installation » T12.

The technique of the corrective scenario as we use it, just as Pierre Janet was already doing, consists in revisiting past traumatic events and associating new emotions, ideas and sensations with them. This subjective reconstruction is developed by introducing resources in the form of supportive persons and/or capacities or possibilities for action and reaction that the patient was deprived of at the time of the trauma. By combining a set of resources with traumatic memories, the patient is able to overcome the loneliness, helplessness, terror, horror, shame and/or guilt she experienced at the time of the event. By revisiting the situation in this way, she does not « relive » it in a traumatic way because she now has the means needed to deal with it. Symptoms, painful emotions and negative cognitions are attributed to the dramatic event while another part, consisting of the psychic areas which remained undamaged by the traumatic impact, identifies with its struggle against this influence13.

Corrective scenarios bring thought into traumatic memories; they promote spontaneous awareness and the creation of connections between the recalled episode and other non-traumatic situations, or even with positive resources and emotions. They are integrated into the consciousness, making it possible to initiate a maieutic language through what Janet calls the « act of memory ». Thanks to this cognitive rebuilding process, deleterious situations are reinterpreted and made into a narrative. Thinking frees itself from events and places them in a temporal perspective with which they cease to merge. It is thus rebuilt in its function as a container and becomes an effective means of counteracting the impact of trauma.
In the hypnosis session, the therapist asks the patient to go back to the deleterious situation and then, based on his or her current learning and resources, helps the patient to construct, reconsider and redesign another scenario so that it will lose its traumatogenic charge.


The situation that caused the traumatic disorders is identified during the interview. The therapist invites the patient to assess the extent of his distress on a subjective scale calibrated from 0 to 10.

The hypnosis session itself begins with an induction. Induction is nothing more than a technique designed to help the person enter a state of inner focus. There are many methods for inducing the hypnotic state, all of which have in common that attention is focused on an object (an object that the patient freely chooses in his visual space, a point drawn on one of his hands, etc.), physical sensations (the progressive heaviness of the body, the lightness of a hand, breathing, etc.), emotions (for example, the joy inspired by the success of a test) or mental images (a pleasant memory, a safe place, etc.)

Once the hypnotic state is induced, the therapist reactivates the traumatic memory. He instructs the patient to go back to the moment of the trauma and retrieve the deleterious situation perceptually (what she sees, hears, smells), emotionally (what she feels), somatically (what she feels in her body) and cognitively (what she thinks). He accompanies the patient through the memory until she knows that the event has ended and that she has survived. Studies show that psychotherapies are more effective when they focus on exploring traumatic events than on developing present or past aspects other than traumatic events (Bisson, 2010; Bisson et al., 2007). This should stimulate hypnotherapists to address directly traumatic memories in hypnosis. Too often, indeed, they prefer to help their patients manage stress and anxiety, regain satisfactory sleep or rebuild a positive future for themselves, avoiding any direct exposure to traumatic images. This phase of reactivation of the disturbing memory is of short duration and usually does not exceed two or three minutes.

Then begins the corrective scenarios phase. The therapist suggests that the patient return to the beginning of the traumatic scene. It helps her to identify the resources that have been lacking at the critical moment (protection, emotional security, control, etc.) and encourages her to transform the traumatic scene by introducing into it the chosen solutions (a person who is supportive, protective or who brings essential values such as ethics, respect, justice, etc.; capacity or opportunity for action and reaction, an ability to understand, neutralization of images, alternative feelings, etc.) If necessary, he proposes — in the form of questions, a less directive approach than direct suggestions — the means that would spontaneously emerge if the patient could freely access them. In this type of session, the therapist is active. His presence plays an essential role in the fact that the patient experiences the event in a different way from what they experienced at the time of the event. These considerations are all the more valid if the event occurred in childhood; the highly dissociated patient relives it with the physical and mental resources he or she had at an early age. If he is 5 years old, he is helpless and needs to be rescued. Without the therapist’s intervention, he would feel reduced to impotence.

As an illustration, among the many possible corrective scenarios, let us take the example of self-parenting. Self-reliance is when the person of today, secure, controlling his/her life, able to protect himself, alive, recovering from his injuries, etc., protects, reassures, consoles, supports the victim he/she once was, tells him /her how the situation will improve and explains how he/she will succeed in getting out of this bad situation. The therapist asks, « Can the adult you are today come and help the little girl you were then? ». If the person answers positively, he can ask then « What is she doing? What does she say to the child? ». If the patient answers, « She takes the little girl in her arms and consoles her. She explains that she’s going to get her out of there and that this bad dad will never hurt her again », the therapist asks about the help received by the child: » What is going on? How is the little one reacting? », etc.

The corrective scenario experienced in a hypnotic state has an intensity and quality of reality that the simple fact of imagining has not. In parenting, the victim patient truly experiences being protected or reassured by the adult he or she has become. The experience seems real to him, which is very convincing. We hypothesize that imaginary experiments can create new neural circuits and new responses as the emotional centers of the sub-cortex do not discriminate between internal and external perceptions (Ecker et al., 2012).

After each scenario, the therapist asks the patient to reassess his or her distress. He repeats the method until it is 0 or 1. Let’s take the case of a person who was physically abused in childhood by his father. The first scenario could, for example, involve a grandparent who takes him out of danger (being protected, getting back to safety); a second scenario could involve the adult he has become to comfort him (being emotionally secure) and a third scenario could allow the child to defend himself after becoming hyper-powerful through the ingestion of a magic potion (coming out of impotence).

Corrective_scenarios_and adaptive_information_processing

The effectiveness of the corrective scenario technique is consistent with Francine Shapiro’s theory of adaptive information processing (Shapiro, 2007a). Indeed, the patient revisits his painful past using his current and adaptive resources. We believe that this technique promotes the connection between the dysfunctional memory network that contains the traumatic event and adaptive information stored in other memory networks.

Hypnosis and reconsolidation

In corrective scenarios, the patient re-enters the traumatic event. The exposure is of short duration, a few minutes at most, but sufficient for the memory to be reactivated. According to the reconsolidation theory, it can be modulated before it stabilizes again as a long-term memory. We hypothesize that restorative scenarios reduce the reconsolidation of traumatic memory. In our opinion, the ideas injected during the scenarios specifically attenuate the reconsolidation of emotional elements but have little effect on all the memory data. When the treatment is over, patients remember the traumatic event but the intense emotion has disappeared or has at least significantly decreased.


Alice had wept so much that her tears had formed a pool in which she as well as many animals had fallen. On the advice of the Dodo bird, they organized a race to dry themselves. When they were dry, the Dodo ended the test. The participants asked who the winner was and after careful consideration, he replied: « Everyone has won, and we all have to receive prizes ».

We owe to the American psychologist Saul Rosenzweig the dodo bird verdict (or dodo bird conjecture), a notion inspired by this excerpt from Lewis Carroll’s Alice in Wonderland (Rosenzweig, 1936). In a 1936 article on the comparative effectiveness of psychotherapies, he demonstrated that they had comparable effectiveness regardless of the technique and theoretical models underlying them. In the race to healing, all have proven beneficial, but none has demonstrated superiority over the others. Rosenzweig concluded that the factors common to the various forms of psychotherapy were more important than the technique itself. In 1975, his compatriot Lester Luborsky and his team confirmed this hypothesis (Luborsky et al., 1975). These two studies were largely controversial and provoked heated debates. Although questionable in many respects, they have had the merit of highlighting pantheoretical factors of effectiveness such as the therapeutic alliance.

We would certainly not go so far as to claim that current psychotherapies are equally effective in treating psychological trauma. However, how can it be explained that techniques as different as reconsolidation therapy, EMDR and hypnosis can all achieve excellent therapeutic effects? Would the effectiveness of these approaches depend on the processes they share rather than on the processes that differentiate them? Is blocking the reconsolidation of traumatic memories the common factor in their effectiveness? We hope that future research will focus on answering this question. 


-ANSM (Agence Nationale de Sécurité du Médicament et des produits de santé) (2019). Propranolol. Retrieved from:
-Alberini, C. M. (2005). Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends in Neurosciences, 28(1), 51-56.
-Bartlett, C. (1932, ed. 1995). Chapter X: Remembering: A Study in Experimental and Social Psychology. Cambridge University Press. Retrieved from: jose/courses/578_mem_learn/2012/readings/Bartlett_1932.pdf
-Bisson, J. I. (2010). Post-traumatic stress disorder. Clinical Evidence, 02:1005.
Retrieved from:
-Bisson, J. I., Ehlers, A., Matthews, R., Pilling, S., Richards, D., & Turner S. (2007). Psychological treatments for chronic post-traumatic stress disorder. Systematic review and meta-analysis. The British Journal of Psychiatry: The Journal of Mental Science, 190, 97-104. Retrieved from:
-Boriello C. (2019). Étude de l’impact du protocole “ Paris Mémoire Vive ” chez des victimes souffrant de Trouble de Stress Post Traumatique : traitement par blocage de la reconsolidation mnésique ou thérapie d’exposition. Médecine humaine et pathologie. 2019. ffdumas-02186197f
-Bouton, M. E. (1993). Context, time, and memory retrieval in the interference paradigms of Pavlovian learning. Psychological Bulletin, 114(1), 80-99.
-Bradley R., Greene J., Russ E., Dutra L., Westen, D. (2005). A multidimensional meta-analysis of psychotherapy for PTSD. The American Journal of Psychiatry, 162(2), 214-227. Retrieved from:
-Brunet, A., Orr, S. P., Tremblay, J., Robertson, K., Nader, K., & Pitman, R. K. (2008). Effect of post-retrieval propranolol on psychophysiologic responding during subsequent script-driven traumatic imagery in post-traumatic stress disorder. Journal of Psychiatric Research, 42(6), 503-506.
-Brunet A, Poundja J, Tremblay J, Bui E, Thomas E, Orr SP, Azzoug A, Birmes P, Pitman RK. (2011). Trauma reactivation under the influence of propranolol decreases posttraumatic stress symptoms and disorder: 3 open-label trials. J Clin Psychopharmacol. 2011 Aug;31(4):547-50. doi: 10.1097/JCP.0b013e318222f360. PMID: 21720237.
-Brunet, A., et al. (2018). Reduction of PTSD Symptoms With Pre-Reactivation Propranolol Therapy: a Randomized Controlled Trial. The American Journal of Psychiatry, vol. 175, no. 5, 2018, pp. 427-433
-Bryant, R. A., Creamer, M., O’Donnell, M., Silove, D., & McFarlane, AC. (2008). A multisite study of initial respiration rate and heart rate as predictors of posttraumatic stress disorder. J Clin Psychiatry, 69(11): 1694-1701.
-Bryant, R. A., Brooks, R., Silove, D., Creamer, M., O’Donnell, M., & McFarlane, A. C. (2011). Peritraumatic dissociation mediates the relationship between acute panic and chronic posttraumatic stress disorder. Behaviour Research and Therapy, 49, 346-351.
-Buzsaki, G. (1996). The hippocampo-neocortical dialogue. Cereb. Cortex 1996 ; 6: 81–92.
Retrieved from:
-Cahill, L., Prins, B., Weber, M., & McGaugh, J. L. (1994). Beta-adrenergic activation and memory for emotional events. Nature, 371(6499), 702-704.
Retrieved from:
-Cahill, L., & McGaugh, J. L. (1996). Modulation of memory storage. Current Opinion in Neurobiology, 6(2), 237-242.
-Cotraccia, J. A. (2013). Le traitement adaptatif de l’information et un modèle biopsychosocial systémique [Adaptive Information Processing and a Systemic Biopsychosocial Model]. Journal of EMDR Practice and Research 7(4): 96-106 November 2013
-Davis, H. P., & Squire, L. R. (1984). Protein synthesis and memory: a review. Psychological Bulletin, 96(3), 518-559. Retrieved from:
-Debiec, J., & LeDoux, J. E. (2006). Noradrenergic signaling in the amygdala contributes to the reconsolidation of fear memory: treatment implications for PTSD. Annals of the New York Academy of Sciences, 1071, 521-524.
-Debiec, J., Bush, D. E., & LeDoux, J. E. (2011). Noradrenergic enhancement of reconsolidation in the amygdala impairs extinction of conditioned fear in rats – a possible mechanism for the persistence of traumatic memories in PTSD. Depression and Anxiety, 28(3), 186-193.
-Delucchi, D. S., Weiss, J., Fagan, A. Liberman, C., & Marmar, R. (2007). Peritraumatic fear, helplessness and horror and peritraumatic dissociation: Do physical and cognitive symptoms of panic mediate the relationship between the two? Behav. Res. Ther. 2007 Jan. 45(1): 39-47
-DeZazzo, J., & Tully, T. (1995). Dissection of memory formation: from behavioral pharmacology to molecular genetics. Trends in Neurosciences, 18(5), 212-218.
-Diekelmann, S., & Born, J. (2010). The memory function of sleep. Nat. Rev. Neurosci., 2010 ; 11: 114–126.
-Ducrocq, F., & Vaiva, G. (2005). From the biology of trauma to secondary preventive pharmacological measures for post-traumatic stress disorders. L’Encéphale, 31(2), 212 226.
-Dudai, Y. (2004). The neurobiology of consolidations, or, how stable is the engram?. Annu. Rev. Psychol., 2004; 55: 51–86. Retrieved from:
-Dudai, Y., & Eisenberg, M. (2004). Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron, 44(1), 93-100. Retrieved from:
-Ecker, B., Ticic, R., & Hulley, L. (2012). Unlocking the Emotional Brain: Eliminating Symptoms at Their Roots Using Memory Reconsolidation. Routledge.
-Eichenbaum, H. (1997). Memory: old questions, new perspectives. Current Biology, 7(1), R53-55.
Retrieved from:
-Fikretoglu, D., Brunet, A., Suzanne, R., Best, T. J., Metzler, T., Delucchi, K., Weiss, D. S., Fagan, J., & Marmar, C. (2006). The relationship between peritraumatic distress and peritraumatic dissociation: an examination of two competing models. The Journal of Nervous and Mental Disease, 194(11), 853-858.
-Foa, E. B., Keane, T. M., Friedman, M. J., & Cohen, J. A. (2010, sd. ed.). Effective Treatments for PTSD: Practical Guidelines from the International Society for Traumatic Stress Studies. New York: The Guilford Press.
-Foa, E. B., Hembree, E. A., & Rothbaum, B. O. (2007). Prolonged Exposure Therapy for PTSD: Emotional Processing of Traumatic Experiences Therapist Guide: Oxford University Press.
-Forcato, C., Argibay, P. F., Pedreira, M. E., & Maldonado,H. (2009). Human reconsolidation does not always occur when a memory is retrieved: the relevance of the reminder structure. Neurobiology of Learning and Memory, 91(1), 50-57. Retrieved from:
-Hermans, D., Dirikx, T., Vansteenwege, D., Baeyens, F., Van den Bergh, O., & Eelen, P. (2005). Reinstatement of fear responses in human aversive conditioning. Behaviour Research and Therapy, 43(4), 533-551.
-Hernandez, P. J., & Kelley, A. E. (2004). Long-term memory for instrumental responses does not undergo protein synthesis-dependent reconsolidation upon retrieval. Learning & Memory, 11(6), 748-754. Retrieved from:
-Holmes, E. A., James, E. L., Coode-Bate, T., & Deeprose, C. (2009). Can playing the computer game « Tetris » reduce the build-up of flashbacks for trauma? A proposal from cognitive science. PLoS One 2009; 4(1): e4153.
Retrieved from:
-Hornsveld, K. H., de Jongh, A., & ten Broeke, E. (2012). Stop using eye movements in the development and installation of resources until their added value is proven: reply to Leeds and Korn. Journal of EMDR Practice and Research, 08/2013 ; 7(3):68-73
-Ironson, G. I., Freund, B., Strauss, J. L., & Williams, J. (2002). Comparison of two treatments for traumatic stress: A community-based study of EMDR and prolonged exposure. Journal of Clinical Psychology, 58, 113-128.
-Janet, P. (1889), L’automatisme psychologique. Essai de psychologie expérimentale sur les formes inférieures de l’activité humaine. Première partie: Automatisme total, Félix Alcan, Paris. Retrieved from:
-Janet, P. (1889), L’automatisme psychologique. Essai de psychologie expérimentale sur les formes inférieures de l’activité humaine. Deuxième partie : Automatisme partiel, Félix Alcan, Paris. Retrieved from:
-Jehel, L., Paterniti, S., Brunet, A., Louville, P., & Guelfi, J.-D (2006). L’intensité de la détresse péritraumatique prédit la survenue des symptômes post-traumatiques parmi des victimes d’agressions [Intensity of peritraumatic distress as predictor of development of posttraumatic symptoms among assault victims]. L’Encéphale, Vol 32, N° 6. Retrieved from:
-Josse, É. (2007). Le pouvoir des histoires thérapeutiques. L’hypnose éricksonienne dans la guérison des traumatismes psychiques [The power of therapeutic stories. Ericksonian hypnosis to heal psychological trauma]. Paris: La Méridienne/Desclée De Brouwer.
-Josse, É., & Dubois, V. (2009). Interventions en santé mentale dans les violences de masse [Mental health interventions in context of mass violence]. Brussels: De Boeck.
-Josse, É. (2011). Le traumatisme psychique chez le nourrisson, l’enfant et l’adolescent [Psychological trauma in infants, children and adolescents]. De Boeck, coll. Le Point sur: Brussels.
-Josse, É. (2016). Les scénarii réparateurs des mnésies traumatiques par hypnose et EMDR [Corrective scenarios for traumatic memories in hypnosis and EMDR], in Psychothérapies de la dissociation, Smith, J., Ed., Paris: Dunod.
-Josse, É. (2017). Histoire du psychotraumatisme [History of psychotrauma] in Pratique de la psychothérapie EMDR, Tarquinio, C., Ed., Paris: Dunod.
-Josse, É. (2017). Conception classique du psychotraumatisme [Classical view of psychotrauma], in Pratique de la psychothérapie EMDR, Tarquinio, C., Ed., Paris: Dunod.
-Josse, É. (2017). Le traumatisme complexe [ Complex psychotrauma], in Pratique de la psychothérapie EMDR, Tarquinio, C., Ed., Paris: Dunod.
-Josse, É. (2017). Les traumatismes psychiques chez le nourrisson et l’enfant en bas-âge [Psychotrauma in infants and toddlers], in Aide-mémoire – Psychiatrie et psychopathologie périnatales en 51 notions, Bayle, B., Ed., Paris: Dunod.
-Josse, É., & Maes, J.-C. (2018). Se protéger du radicalisme [How to protect oneself against radicalism]. Couleur livres: Brussels
-Josse, É. (2nd ed. 2019). Le traumatisme psychique chez l’adulte [Psychotrauma in adults]. De Boeck, coll. Le Point sur: Brussels.
-Khalfa, S., & Touzet, C. F. (2017). EMDR Therapy Mechanisms Explained by the Theory of Neural Cognition. J Trauma Stress Disor Treat 2017, 6:4. Retrieved from:
-Khan, A. M., Dar, S., Ahmed, R., Bachu, R., Adnan, M., & Kotapati, V. P. (2018). Cognitive Behavioral Therapy versus Eye Movement Desensitization and Reprocessing in Patients with Post-traumatic Stress Disorder: Systematic Review and Meta-analysis of Randomized Clinical Trials. Cureus, 10(9), e3250. doi:10.7759/cureus.3250. Retrieved from:
-Kindt, M., Soeter, M., & Vervliet, B. (2009). Beyond extinction: erasing human fear responses and preventing the return of fear. Nature Neuroscience, 12(3), 256-258.
-Kroes, M. C., Strange, B. A., & Dolan, R. J. (2010). Beta-adrenergic blockade during memory retrieval in humans evokes a sustained reduction of declarative emotional memory enhancement. The Journal of Neuroscience, 30(11), 3959-3963
-LeDoux J. E. (2000). Emotion circuits in the brain. Annual Review of Neuroscience, 23, 155-184. Retrieved from:
-Le Monde (2008). Tous les souvenirs sont faux. 16 juillet 2008. Retrieved from:
-Lee, J. L. C., Nader K., Schiller D. (2017). An Update on Memory Reconsolidation Updating. Trends Cogn Sci. 2017 Jul; 21(7):531-545. Retrieved from:
-Lee C., Gavriel, H., Drummond, P., Richards, J., & Greenwald, R. (2002). Treatment of post-traumatic stress disorder: A comparison of stress inoculation training with prolonged exposure and eye movement desensitization and reprocessing. Journal of Clinical Psychology, 58, 1071-1089.
-Lesburguères, E., & Bontempi, B. (2011). Mécanismes de consolidation de la mémoire. Importance de l’étiquetage précoce des neurones du néocortex. [Mechanisms of memory consolidation. Why early labelling of neocortex neurons is important]. Med Sci (Paris) 2011; 27: 1048–1050. Retrieved from:
-Loftus, E. F. (1981). Natural and unnatural cognition. Cognition, 10(1-3), 193-196
-Loftus, E. (2009). Les illusions de la mémoire, conférence [The illusions of memory, lecture]. Retrieved from:
-Luborsky, L., Rosenthal, R., Diguer, L., Andrusyna, T. P., Berman, J. S., Levitt, J. T., Seligman, D. A., & Krause, E. D. (1975). The dodo bird verdict is alive and well — mostly. Clinical Psychology: Science and Practice, 9(1), 2-12.
Retrieved from:
-Lupien, S. J., & McEwen, B. S. (1997). The acute effects of corticosteroids on cognition: integration of animal and human model studies. Brain Research. Brain Research Reviews, 24(1), 1-27.
-Mallet, C. (2018). Les cauchemars dans l’état de stress post-traumatique. Impact des séances de blocage de la reconsolidation mnésique sous propranolol sur les cauchemars post-traumatiques. [Nightmares in posttraumatic stress disorder. Impact of propranolol memory reconsolidation blockage sessions on posttraumatic nightmares]. Médecine humaine et pathologie. 2018. dumas-01903535. Retrieved from:
-Marin, M. F., Pilgrim, K., & Lupien, S. J. (2010). Modulatory effects of stress on reactivated emotional memories. Psychoneuroendocrinology, 35(9), 1388-1396.
Retrieved from:
-Marin, M. F., Hupbach, A., Maheu, F. S., Nader, K., & Lupien, S. J. (2011). Metyrapone administration reduces the strength of an emotional memory trace in a long-lasting manner. Journal of Clinical Endocrinology and Metabolism, 96(8). Retrieved from:
-Marks, I., Lovell, K., Noshirvani, H., Livanou, M., & Thrasher, S. (1998). Treatment of posttraumatic stress disorder by exposure and/or cognitive restructuring: a controlled study. Archives of General Psychiatry, 55(4), 317-325.
-McLean, C. P., & Foa, E. B. (2011). Prolonged exposure therapy for post-traumatic stress disorder: a review of evidence and dissemination, Expert Rev. Neurother. 11(8), 1151–1163 (2011).
Retrieved from:
-McCleery, J. M., & Harvey, A. G. (2004). Integration of psychological and biological approaches to trauma memory: implications for pharmacological prevention of PTSD. Journal of Traumatic Stress, 17(6), 485-496.
-McGaugh, J. L. (2000). Memory – a century of consolidation. Science, 287(5451), 248-251.
-McGaugh, J. L. (2004). The amygdala modulates the consolidation of memories of emotionally arousing experiences. Annual Review of Neuroscience, 27, 1-28.
-Misanin, J. R., Miller, R. R., & Lewis, D. J. (1968). Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace. Science, 160(3827), 554-555.
Retrieved from:
-Müller, G. E., & Pilzecker, A. (1900). Experimenteller Beitrag zur Lehre vom Gedächtnis. (Experimental contribution to the science of memory). Zeitschrift für Psychology. Ergänzungsband (Suppl.1), 1-300.
-Myers, C. S. (2011, 1ère éd. 1940), Shell shock in France, 1914-1918. Cambridge University Press.
-Nader, K., Schafe, G. E., & LeDoux, J. E. (2000a). Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature, 406(6797), 722-726.
-Nader, K., Schafe, G. E., & LeDoux, J. E. (2000b). The labile nature of consolidation theory. Nature Reviews. Neuroscience, 1(3), 216-219. Retrieved from:
-Nijenhuis, E., van der Hart, O., Steel, K., de Soir, E., & Matthess, H. (2006). Dissociation structurelle de la personnalité et trauma (Structural dissociation of the Personality and Trauma). Stress et Trauma, 2006, 6(3):125-139
-Oren, E., & Solomon, R. (2012). EMDR therapy: An overview of its development and mechanisms of action. Revue Européenne de Psychologie Appliquée/EuropeanReview of Applied Psychology. Volume 62, Issue 4, October 2012, pp. 197-203
-Poundja, J. (2012). Le blocage de la reconsolidation des souvenirs, une avenue possible pour le traitement du trouble de stress post-traumatique ? [Is blocking the reconsolidation of memories a possible approach for treating post-traumatic stress disorder?] Thèse présentée à la Faculté des études supérieures et postdoctorales en vue de l’obtention du grade de Ph. D. en psychologie. Option recherche et intervention clinique. Retrieved from:
-Power, K. G., McGoldrick, T., Brown, K., et al. (2002). A controlled comparison of eye movement desensitization and reprocessing versus exposure plus cognitive restructuring, versus waiting list in the treatment of post-traumatic stress disorder. Journal of Clinical Psychology and Psychotherapy, 9, 299-318.
-Przybyslawski, J., & Sara, S. J. (1997). Reconsolidation of memory after its reactivation. Behavioural Brain Research, 84(1-2), 241-246
-Przybyslawski, J., Roullet, P., & Sara, S. J. (1999). Attenuation of emotional and nonemotional memories after their reactivation: role of beta adrenergic receptors. Journal of Neuroscience, 19(15), 6623-6628. Retrieved from:
-Quirk, G. J. (2002). Memory for extinction of conditioned fear is long-lasting and persists following spontaneous recovery. Learning & Memory, 9(6), 402-407. Retrieved from:
-Rauch, S. A. M., Eftekhari, A., & Ruzek J. I. (2012). Review of exposure therapy: A gold standard for PTSD treatment. JRRD Volume 49, Number 5, 2012, pp. 679–688
-Rescorla, R. A. (2004). Spontaneous recovery. Learning & Memory, 11(5), 501-509. Retrieved from:
-Rosenzweig, S. (1936). Some implicit common factors in diverse methods of psychotherapy. American Journal of Orthopsychiatry, 6(3), 412-415.
-Rothbaum, B. O., Astin, M. C., & Marsteller, F. (2005). Prolonged exposure versus eye movement desensitization (EMDR) for PTSD rape victims. Journal of Traumatic Stress, 18, 607-616.
-Sara, S. J. (2000). Retrieval and reconsolidation: toward a neurobiology of remembering. Learning and Memory, 7(2), 73-84. Retrieved from:
-Schiller, D., Monfils, M. H., Raio, C. M., Johnson, D. C., Ledoux, J. E., & Phelps, E. A.(2010). Preventing the return of fear in humans using reconsolidation update mechanisms. Nature, 463(7277), 49-53. Retrieved from:
-Schnurr, P. P., Friedman, M. J., Engel, C. C., Foa, E. B., Shea, M. T., Chow, B. K., Resick, P. A., Thurston, V., Orsillo, S. M., Haug, R., Turner, C., & Bernardy, N. (2007). Cognitive behavioral therapy for posttraumatic stress disorder in women: A randomized controlled trial. JAMA. 2007; 297(8): 820–30.
-Schwabe, L., Nader, K., Wolf, O. T., Beaudry, T., &Pruessner, J. C. (2012). Neural signature of reconsolidation impairments by propranolol in humans. Biological Psychiatry, 71(4), 380-386. Retrieved from:
-Servan-Schreiber, D., Schooler, J., Dew Mary, A., Carter, C., & Bartone, P. (2006). Eye Movement Desensitization and Reprocessing for Posttraumatic Stress Disorder: A Pilot Blinded, Randomized Study of Stimulation Type, Psychother Psychosom 2006; 75:290–297. Retrieved from:
-Shalev, A. Y., Sahar, T., Freedman, S. et al. (1998). A prospective study of heart rate response and the subsequent development of posttraumatic stress disorder. Archive of General Psychiatry, 55(6), 553-9.
-Shapiro, F. (2018). Eye Movement Desensitization and Reprocessing (EMDR) Therapy, Third Edition: Basic Principles, Protocols, and Procedures. New York: Guilford
-Shapiro, F. (2007b). EMDR and case conceptualization from an adaptive information processing perspective. In F. Shapiro, F. Kaslow, L. Maxfield (Eds.), Handbook of EMDR and family therapy processes (pp. 3–36). New York: Wiley.
Solomon, R. M., & Shapiro, F. (2008). EMDR and the Adaptive Information Processing Model Potential Mechanisms of Change. Journal of EMDR Practice and Research Vol 2 Issue 4.
-Suzuki, A., Josselyn, S. A., Frankland, P. W., Masushige, S., Silva, A. J., & Kida, S. (2004). Memory reconsolidation and extinction have distinct temporal andbiochemical signatures. The Journal of Neuroscience, 24(20), 4787-4795. Retrieved from:
-Taylor, J. E., & Harvey, S. T. (2010). A meta-analysis of the effects of psychotherapy with adults sexually abused in childhood. Clinical Psychology Review, 30(6), 749-767.
-Thomas, E. (2014). Le blocage de la consolidation et de la reconsolidation des souvenirs émotionnels chez l’humain à l’aide du propranolol. Thèse présentée à la Faculté des Études Supérieures et Postdoctorales de Montreal en vue de l’obtention du grade de Ph. D. en psychologie. [Blocking the consolidation and reconsolidation of emotional memories in humans with propranolol. Thesis presented at the Faculty of Graduate and Postdoctoral Studies of Montreal for a PhD degree in Psychology.] Recherche et Intervention option Neuropsychologie clinique. Retrieved from:
-Tully, K., & Bolshakov, V. Y. (2010). Emotional enhancement of memory: how norepinephrine enables synaptic plasticity. Molecular Brain, 3, 15. Retrieved from:
-Vaïva, G., Lebigot, F., Boss, V., Ducrocq, F., Legru, H., Cottencin, O., Devos, P., Lestavel, P., Laffargue, P., & Goudemand, M. (2001). Peritraumatic distress after a serious traffic accident: Predictive value for a PTSD two months later. Revue francophone du stress et du trauma, vol. 1, no 5, Princeps, Issy les Moulineaux, France.
-Vaïva, G., Ducrocq, F., Jezequel, K., Averland, B., Lestavel, P., Brunet, A., & Marmar, C. R. (2003). Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma. Biol Psychiatry. 2003 Nov 1; 54(9):947-9.
-Wang, S. H., & Morris, RG. (2010). Hippocampal-neocortical interactions in memory formation, consolidation, and reconsolidation. Annu Rev Psychol 61: 49–79.
WHO (2013). WHO guidelines on conditions specifically related to stress. Retrieved from:;jsessionid=621D409EB8D06514DE59077B6443B661?sequence=1
-Winocur, G., & Moscovitch, M. (2011). Memory Transformation and Systems Consolidation. Journal of the International Neuropsychological Society, June 2011. Retrieved from:
Wittenberg, G. M, Sullivan, M. R., & Tsien, J. Z. (2002). Synaptic reentry reinforcement based network model for long-term memory consolidation. Hippocampus 2002 ; 12: 637–647.
Retrieved from:
-Zaghout-Hodali, M., Alissa, F., & Dodgson, P. (2008). EMDR and resilience in children in ongoing trauma. Journal of EMDR Practice and Research, 1, 106–113.

Notes et références

  1. According to another theory, not all information would go through short-term memory before being recorded in long-term memory. So, there would be two types of consolidation, one serial (information would go first into short-term memory and then into long-term memory) and the other parallel (direct inscription of information in the long-term memory) (Eichenbaum, 1997).
  2. See below.
  3. For example, an autobiographical memory involves the interconnection of different areas of the brain: the prefrontal lobe, the lateral temporal lobe, the hippocampus and the parieto-occipital regions.
  4. Tachypnea refers to accelerated pulmonary ventilation. In an adult, resting breathing is 12 to 18 breathing movements per minute.
  5. See below.
  6. For a detailed description of the clinical picture of psychological trauma, see the author’s book Le traumatisme psychique chez l’adulte (Josse, 2019).
  7. At the cellular level, learning and memory are based on a form of plasticity called LTP, long-term potentiation. The brain stores information in neural networks connected by their synapses and retrieves it by activating these networks. Repeated activation of a network permanently modifies the efficiency of synaptic transmission of the neurons involved.
  8. For Bartlett, a schema is an organized structure that integrates an individual’s knowledge and expectations of an aspect of the world (Bartlett, 1932).
  9. It should be noted, however, that research has shown a decrease in traumatic symptomatology and not a complete resolution.
  10. Detailed protocol in Claire Mallet’s thesis (Mallet, 2018)
  11. Studies have shown that alternative rhythmic sensory stimuli are more effective than simultaneous stimuli or continuous stimuli, which are also more effective but to a lesser extent (Servan-Schreiber et al. 2006).
  12. his technique was developed in 1995 by Andrew Leeds and Deborah Korn
  13. This concept is consistent with the model of personality dissociation developed in 1940 by English psychologist Charles Myers (Myers, 1940, ed. 2011) and developed under the name « structural personality dissociation » by Ellert Nijenhuis, Onno van der Hart, Kathy Steele and their collaborators in the early 2000s (Nijenhuis E., 2006). According to this model, a major threat can cause a dissociation leading to a particular psychological organization in which different psychobiological subsystems of the personality coexist. EPP, the emotional part of the personality, stuck in the traumatic experience, consists of painful sensorimotor experiences and charged with painful affects. ANPP, the apparently normal part of the personality, assumes the tasks needed for the daily life and the survival of the species. In 1889, Janet already mentioned « successive psychological existences » corresponding to fragments of experiences that could not be integrated into the memory system to which a unified personality refers (Janet P., 1889).

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