In some circumstances memories may be updated when they are recalled
Reconsolidation is a biomolecular mechanism mediating specific protein synthesis
The method allows the change of emotions, negative automatic thoughts and dysfunctional schemas
Can be integrated into various forms of psychotherapy
Partly following references by Marie-H Monfils 2012
Reconsolidation in psychotherapy at a glance
The patient recalls memory in emotional detail. The patient’s recall of memory is mediated by using techniques the therapist is in control and comfortable with - the procedure is not allowed to develop into so-called catharsis sessions: increased prefrontal cognitive control is one of the central components. When an old memory is recalled, the reconsolidation window opens and becomes temporarily and optimally amenable to change for one hour, up to about 5-6 hours. The therapist helps the patient to pinpoint the problem and find alternative emotional components that can be used to "overwrite" the previous memory.
Unlocking / mismatch
When the molecular window is open, the memory trace is also changeable. Prepared alternative emotional memories and verbal explanatory models is presented or exposed imaginary or in vivo.
New memory modules "overwrite" previous emotional memories. Research shows that for a sustained effect, the procedure needs to be repeated up to six times during a session, ie in the optimal change window.
More research is needed.
Click to enlarge graph
A therapeutic program with a neuropsychological evidence based profile
Unlocking the Emotional Brain
- Eliminating Symptoms at Their Roots Using Memory Reconsolidation
by Bruce Ecker, Robin Ticic and Laurel Hulley
Psychotherapy that regularly yields liberating, lasting change was, in the last century, a futuristic vision, but it has now become reality, thanks to a convergence of remarkable advances in clinical knowledge and brain science. In Unlocking the Emotional Brain, authors Ecker, Ticic and Hulley equip readers to carry out focused, empathic therapy using the process found by researchers to induce memory reconsolidation, the recently discovered and only known process for actually unlocking emotional memory at the synaptic level. Emotional memory's tenacity is the familiar bane of therapists, and researchers have long believed that emotional memory forms indelible learning. Reconsolidation has overturned these views. It allows new learning to erase, not just suppress, the deep, unconscious, intensely problematic emotional learnings that form during childhood or in later tribulations and generate most of the symptoms that bring people to therapy. Readers will learn methods that precisely eliminate unwanted, ingrained emotional responses-whether moods, behaviors or thought patterns-causing no loss of ordinary narrative memory, while restoring clients' well-being.
Dissertation from University of Uppsala, Sweden
Agren, T. (2012). Erasing Fear: Effect of Disrupting Fear Memory Reconsolidation on Central and Peripheral Nervous System Activity. Dissertation. Acta Universitatis Upsaliensis, Sweden.
Fear memories, here defined as learned associations between a stimulus and a physiological fear reaction, are formed through fear conditioning. In animals, fear memories, present in the lateral amygdala, undergo reconsolidation after recall. Moreover, this reconsolidation process can be disrupted both pharmacologically and behaviourally, resulting in a reduced fear response to the stimulus. This thesis examines the attenuation of fear memories by disrupting reconsolidation in humans, using measures of both the central and peripheral nervous system activity. Serotonergic and dopaminergic genes have previously been tied to both fear conditioning and anxiety disorders, where fear conditioning mechanisms are important. In order to evaluate the possible role of fear memory reconsolidation mechanims in the effect on fear and anxiety by these genes, this thesis also compare the reconsolidation disruption effect between different serotonergic and dopaminergic genotypes.
Study I examined the attentuation of fear memories by disrupting reconsolidation in humans using reacquisition as a measure of the return of fear. Moreover, study I investigated the impact of differences in serotonergic and dopaminergic alleles on this process.
Study II examined the attentuation of fear memories by disrupting reconsolidation in humans using reinstatement as a measure of the return of fear. Study II also investigated the impact of differences in serotonergic and dopaminergic alleles on the process of fear memory reconsolidation.
Study III used psychophysiology and fMRI to localize the functional neural activity mediating the fear memory reconsolidation disruption effect.
In summary, this thesis provides evidence that fear memories are attenuated by reconsolidation disruption in humans and that serotonergic and dopaminergic alleles influence this process. Moreover, this thesis support that human fear memory reconsolidation is amygdaladependent, suggesting an evolutionary shared memory mechanism.
Download the dissertation: Agren, T. (2012)
Agren, T. (2014). Human reconsolidation: a reactivation and update. Brain Res Bull. Jun ;105:70-82.
The Amygdala, Fear and Reconsolidation
Neural and Behavioral Effects of Retrieval-Extinction in Fear Conditioning and Spider Phobia
Dissertation from University of Uppsala, Sweden
Björkstrand, J. (2017) The Amygdala, Fear and Reconsolidation
Neural and Behavioral Effects of Retrieval-Extinction in Fear Conditioning and Spider Phobia. Dissertation. Acta Universitatis Upsaliensis, Sweden.
The amygdala is crucially involved in the acquisition and retention of fear memories. Experimental research on fear conditioning has shown that memory retrieval shortly followed by pharmacological manipulations or extinction, thereby interfering with memory reconsolidation, decreases later fear expression. Fear memory reconsolidation depends on synaptic plasticity in the amygdala, which has been demonstrated in rodents using both pharmacological manipulations and retrieval-extinction procedures. The retrieval-extinction procedure decreases fear expression also in humans, but the underlying neural mechanism have not been studied. Interfering with reconsolidation is held to alter the original fear memory representation, resulting in long-term reductions in fear responses, and might therefore be used in the treatment of anxiety disorders, but few studies have directly investigated this question. The aim of this thesis was to examine the effects of the retrieval-extinction procedure on amygdala activity and behavioral fear expression in humans. The work presented here also investigated whether findings from studies on recent fear memories, established through fear conditioning, extends to naturally occurring long-term phobic fears. Study I, combining fear conditioning and a retrieval-extinction procedure with functional magnetic resonance imaging (fMRI), demonstrated that memory retrieval shortly followed by extinction reduces later amygdala activity and fear expression in healthy subjects. In Study II, these subjects were re-tested 18 months later. The results showed that the effects on fear expression were still present and that initial amygdala activity predicted long-term fear expression. Using an adapted version of the retrieval-extinction procedure, Study III showed that memory retrieval shortly followed by exposure to spider pictures, attenuates subsequent amygdala activity and increases approach behavior in subjects with life-long fear of spiders. In Study IV, these subjects were re-tested 6 months later, and the results showed that effects on amygdala activity as well as approach behavior were maintained. In summation, retrieval-extinction leads to long-lasting reductions in amygdala activity and fear expression. These findings are consistent with the hypothesis that retrieval-extinction alters an amygdala dependent fear memory. Retrieval-extinction can also attenuate long-term phobic fears, indicating that this manipulation could be used to enhance exposure-based treatments for anxiety disorders.
Download the dissertation: Bjorkstrand, J. (2017)
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