LeDoux's work with fear/amygdala learning: a link?

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Yes, there is a link between LeDoux"s work and our understanding of the underlying mechanisms of EMDR. His work, Bessel van der Kolk's and Rachel Yehudah's (to mention just a few) have given us a good understanding of PTSD and dissociation. A great deal of these research findings is outlined in my paper, Speculations on the Neurobiology of EMDR ,1998, Traumatology, vol. 4, Issue 1 (an electronic version can be accessed at www.fsu.edu/~trauma/).

For instance, we know from LeDoux's work that that when people are under severe stress, they secrete endogenous stress hormones that effect the strength of memory consolidation.  Bessel van der Kolk posits that massive secretion of neurohormones at the time of the trauma plays a role in the long-term potentiation (and thus the overconsolidation) of traumatic memories.  He cites LeDouxšs work in noting that this phenomenon is largely mediated by the input of norepinephrine to the amygdala. This excessive stimulation of the amygdala interferes with hippocampal functioning, inhibiting cognitive evaluation of experience and semantic representation.  Memories are then stored in sensorimotor modalities, somatic sensations and visual images. This would appear to be one of the underlying mechanisms of primary dissociation and PTSD.

It has long been known that many potent emotional memories date from the first few years of life. During this early period brain structures, like the hippocampus, which is crucial for forming consciously accessible memories and, therefore, narrative memory, as well as the neocortex, have yet to fully develope. The hippocampus is not fully myelinated until the third or fourth year of life.   The amygdala, by contrast, matures very early in the infantšs brain development (LeDoux, 1994;  van der Kolk, 1994 ) .  As the central nervous system matures, memory storage shifts from primarily sensorimotor and perceptual representations to symbolic and linguistic organization of mental experience (Piaget, 1962;  van der Kolk, 1994). LeDoux posits this as support for the position that psychodynamic psychology has taken; that the experience of lifešs earliest years lays down a set of emotional lessons based on the level of atunement between infant and caretaker.  This sheds light on the difficulty traditional psychotherapy has had in ameliorating neuroses and personality disorders.  These early interactions are so potent and difficult to understand and work through from the vantage point of adult life, because they are stored in the amygdala as rough, wordless blueprints for emotional life (LeDoux, 1992, 1994).

Is there a link between this and EMDR? Given the speed and depth of its information processing abilities, there must be. Every aspect of treatment, from simple, acute, PTSD to chronic/dissociative (adult survivors of long-term childhood sexual abuse) has been greatly accelerated by EMDR.

Does EMDR facilitate learning at the level of the amygdala? We have no way of knowing, yet. Our only hard scientific evidence comes from van der Kolk's SPECT scan studies of EMDR treatment. Baseline scans were performed prior to the EMDR treatment.  The results showed the following: after three EMDR treatment sessions, the anterior cortex of the cingulate gyrus evidenced increased activity, bilaterally;  and Brocašs area, in the left prefrontal lobe, evidenced increased activity.

Given the fact that the study lacked a control group and only six subjects were tested, the findings are considered as preliminary . However, they begin to shed light on the following hypotheses:  that EMDR does appear to correct the marked asymmetry in lateralization, evidenced by the increased activation of Brocašs area;  that the lateralization may be further corrected by the increased bilateral activation of the anterior cingulate cortex, facilitating a more realistic differentiation between real and perceived threat and concomitant reduction in hypervigilence;  and that EMDR processing, in general, gradually enables the capacity of higher brain functions to override the input from the limbic structures charged with the initial appraisal of the degree of threat posed by incoming stimuli. Rather than downregulate the amygdala, EMDR may be upregulating Broca's area (left prefrontal cortex) and the anterior cortex of the cingulate gyrus. The emotional amygdaloid material can then be analyzed and put into emotional perspective.

Robert Stickgold (Professor of neuropsychology and REM researcher at Harvard) will soon be submitting a paper outlining the connection between EMDR and REM physiology. He will posit that the rhythmic, alternating bilateral stimulation of EMDR causes a cholinergic surge, thereby downregulating norepinehrine output and causing the pons to begin the cycle of GTF neural activity and subsequent PGO neural activity that are the underlying mechanisms of REM functioning. The end product, other than REM sleep, is the activation of the anterior cingulate. Other papers, still in development, will try to outline the pathways to the activation of Broca's area.

This is a sketchy response to your question. Details can be found in my paper, as well as the referances.

Uri Bergmann, LCSW, BCD

UBergmann@worldnet.att.net

• Correction of error by Uri Bergmann, LCSW, BCD, 1/14/99