Can anyone who understands neuroscience or EMDR explain parts of this article to me

Factual Questions
1

http://www.mindspaces.org/uploads/EMDR_EEG_published_on_web_page.pdf

This is what I’m able to gather. This article is about the neuroscience of why EMDR works for trauma and PTSD.

An intensely trauamtic event can overload the basolateral complex of the amygdala. This results in long term potentation between neurons via AMPA receptors. The article implies they more or less max out at about 84 AMPA receptor sites in a post synaptic density. The brain is supposed to process traumas via the hippocampus and anterior cingulate cortex but due to this overload, the memory gets stuck in the amygdala where it retains its emotional impact and cannot be processed cognitively.

Bilateral stimulation (EMDR) can depotentate the neural connections in the basolateral complex, which allows traumas to be processed properly in the ACC and hippocampus. EMDR causes delta brain waves, and studies on both EMDR therapy and electrical stimulation in animal models finds you need about 900 bilateral stimulations to depotentate neural connections enough to reverse PTSD.

That is just the synopsis. I don’t know if anyone is going to bother to read this article, but what exactly does it mean that a memory gets stuck in the amygdala due to too much LTP between neurons? How do they even know what ‘a fear memory’ is? And what mechanism allows bilateral stimulation to break the connections between neurons in that area? And why does that result in the memory being able to be processed by the ACC and hippocampus? Why would too much LTP in the basolateral complex of the amygdala cause a traumatic memory to get ‘stuck’?

2

Allow me to preface that I have a moderately strong interest in neuroscience and have had some interest in EMDR as my wife is a therapist who does some EMDR. And that most of what I have read about the neuroscience explanation for why EMDR works seems like hooey. It does however work. Some claim that it works only by virtue of being a form of cognitive behavioral therapy; I read the evidence as pretty solid that it works a bit differently than that, but that is a different discussion.

This article briefly reviews some past speculations as to how EMDR works and then proposes a different mechanism using quantitative EEG brain mapping changes during EMDR as evidence.

The background basic concept is that the hippocampus is integrally involved forming (or possibly accessing) new episodic and declarative memories (as opposed to learning and accessing new procedural memories, like how to play a piano song). The amygdala is integrally involved in placing emotional value on those memories, especially fear and reward value.

They go into stating some things as established facts that are actually quite speculative … but it is pretty widely accepted if not obvious that PTSD is the result of a highly stressful circumstance keeping the fear response to a traumatic event highly salient and easily triggered by a wide range of stimuli, wider than the specific memory alone. Exactly how that happens may not be as well establihsed as they present it and following the long term potentiation 84 AMPA receptor bit is immaterial really. Their point is that fear memories normally can be processed and down-regulated by certain sorts of low frequency stimulation originating elsewhere in the brain and their claim is that EMDR triggers that sot of stimulation to occur. They believe that their qEEG data supports that claim. I do not have enough of a critical understanding of the limits of qEEG data to critically evaluate that claim but that is the argument made.

The fear memory being “stuck” means the intensity of fear reaction/sensation (mediated by the amygdala) being kept very high for the memory and for a range of stimuli similar to the memory. The concept they espouse is that LTP has resulted in very strong synaptic connections between the fear reponse and the episodic memory (causing an intense fear memeory to be associated with the memory and similar stimuli) and that low level repeating stimulation (at least 900 of them they claim) of those synapses can down-regulate the strength of the connections (that’s their bit on “cycling of the receptors on the post-synaptic membrane at the stimulation frequency (usually from 1 to 5 Hz), and results in depotentiation of the AMPA receptors as the calcium concentration in the synapses decreases during the long interstimulus interval …” They cite animal studies that accomplish that with direct stimulation and claim that EMDR causes the same sort of cycles to occur. The previously over-intense fear response associated with the memory prevented it from being oterwise processed in a more narrative (declarative memory) fashion. Intuitively that is easy to understand: during severe fear you not going to process what is happening/happened the same way as you do upon somewhat calmer reflection of the event. Decreasing that fear valance by deceasing the strength of the connections to the fear response (extinguishing the fear response/depotentiating the receptors/normalizing the response) allows for that reflection to occur (even if that “reflection” is less a conscious process than a processing that occurs during certain sleep phases).

Make sense?

Thank you for the link by the way. Very interesting.

3

The published version of that article is here: http://www.researchgate.net/publication/202172255_On_the_neural_basis_of_EMDR_therapy_Insight_from_qEEG_studies/file/015ee071742371740a97619469fcbe86.pdf

As DSeid says, there is fairly good evidence that EMDR works (to some extent, at least - that is to say, it is no miracle cure, but it does seem to help, and to be better than a number of other PTSD therapies that have been tried) but there is no very satisfactory theory of how it works. There are a bunch of theoretical suggestions, but none that seems entirely satisfactory, or that has very convincing evidential support.

To my eye (and at first glance - I have not read it carefully, yet) the theory being pushed in this paper looks to be very speculative, and perhaps a bit whacky, but it has gathered 11 citations according to Google scholar, so it is not being dismissed. It does not look to me like cutting-edge neuroscience. fMRI is where it is (mostly) at these days, not EEG.

My impression is that the nearest thing to a mainstream theory of EMDR is the visuospatial working memory interference theory, but even that is less than entirely satisfying. It is expressed primarily in cognitive rather than neurological terms, but, frankly, that is probably a more appropriate theoretical level at which to address the problem, especially given our current relatively primitive understanding of EMDR in particular, and the brain’s workings in general.

4

Re fMRI … eh. It is the tool du jour and has gotten a bit trendy being used sometimes just because and not in service a particular question. Right tool for the right job. Again, my understanding of the limits of qEEG data is not deep, but it does tell different information than fMRI. In this case the question of interest is not so much precisely which anatomical area is active when but the frequency of the activity. fMRI studies can tell us that the amygdala is hyperresponsive in PTSD, even show us what brain regions are more or less active asa result of an EMDR protocol, but it does not answer the question about the pattern of stimulation.

5

I personally wonder if it has something to do with why people going off of SSRIs can get “brain zaps” from rapid eye movement. Somehow the eye movements stimulate some part of the brain that other actions do not.

6

The term “a memory gets stuck in the amygdala due to too much LTP between neurons” is a metaphoric or heuristic statement that was utilized a great deal in the middle to late 90s. From more recent research we now know that memories are not contained in any one part of the brain, but rather are stored in fragmented forms in the various distributed neural networks that were active when the event (to be remembered) was first encoded. It appears that the Engram (the neural map of the various distributed sites containing the fragments of information that was processed during the encoding of the experience and which requires reactivation in order to produce the experience of remembering something) is mediated in the hippocampus and para-hippocampal regions.

While the limbic system, and the amygdala within it, are certainly very important brain areas when it comes to our experience of emotions, neuroscientific research makes it clear that our emotionality is not restricted to these areas alone. Richard Davidson’s research has demonstrated that the right frontal lobe of the brain is highly involved in distressed emotion (Davidson & Begley 2012), and evidence provided by Panksepp & Biven (2012) makes it clear that areas of the brainstem are also highly important. In fact, Panksepp states that, “we know from neuroanatomy that the most important area for emotions is not the amygdala, as some people have marketed, but it is in the mid-brain, at the very core of the brain area called periaqueductal gray, because that’s where we get emotional behaviors at the lowest amount of electricity for deep brain stimulation.” (2012). Panksepp & Biven (2012) discuss the neurological fear circuit, which includes the periaqueductal gray, in addition to the amygdala, as well as the frontal lobes.

Information processing/consciousness (sensation, perception, cognition, memory, emotion, and somatosensory integration) are mediated by neural linkage and neural temporal binding When memory is accessed adaptively, it is linked with emotional, cognitive, somato-sensorial and semantic networks which facilitate its accuracy and appropriateness with respect to time, place and contextual situation. When processed traumatically, or under fearful circumstances, experiences appearto be encoded, but unlinked to existing neural networks. Pathology/PTSD results when the linkage/binding systems in the information processing system are impaired. Therefore, experiences are inadequately processed and unlinked to somatosensory, cognitive , emotional and memorial networks, thereby becoming susceptible to inappropriate access and experienced in fragmented form, with respect to time, place and context. This phenomenon of PTSD is what used to get characterized as “memory stuck in the amygdala” prior to our current understanding of neural linkage and binding.

The exact mechanisms of EMDR’s amelioration of PTSD symptoms is not as yet known. What appears to be clear from the outside, is that it appears to mediate the following: desensitization/depotentiation of fear circuits (encompassing areas of the brainstem, midbrain and limbic areas, anterior cingulate gyrus, and orbitofrontal cortex); and the facilitation of neural linkage of somatosensory, cognitive , emotional and memorial networks and the temporal binding of these areas.

Just exactly how bilateral sensory stimulation, combined with clinical procedures, accomplishes all of this is yet to be inferred empirically. The article referenced in your question attempts to explain the desensitization/depotentiation, utilizing data from a qEEG examination of EMDR.

7

I only opened this to say “I can’t explain it, but it worked for me :).” Took about two or three years to work the PTSD into something manageable, but am now pretty much symptom free.

:slight_smile:

8

I am pretty sure it is not correct to equate EMDR with bilateral sensory stimulation. Other forms of bilateral sensory stimulation that have been tried, such as playing tones alternately to each ear, in an otherwise similar therapeutic context, have not proven to effective in clinical trials in the way that true EMDR is. It is much more likely that the effective aspect of EMDR (over other therapies) is the deliberate, voluntary moving of the eyes whilst visualizing. The fact that this causes the subject to receive visual stimulation alternately from either side (because, for reasons of convenience and tradition, EMDR normally empolys side-to-side eye movements) is probably merely incidental.