In your mind's eye

Speculations on the neurobiology of Eye Movement Desensitisation and Reprocessing (EMDR)

By Uri Bergmann

 

Francine Shapiro, the originator of Eye Movement Desensitisation and Reprocessing (EMDR), stumbled quite by accident upon the potentially positive effects of eye movements in desensitising negative emotions and cognitions. Ironically, she wasn't the first to do so. These findings had been made almost two decades earlier by Antrobus and his colleagues (Antrobus, 1973; Antrobus, Antrobus, & Singer, 1964). What unified the findings of Shapiro and Antrobus, apart from their agreement on the utility of eye movements, was that there was no theoretical system which could convincingly explain the findings to the skeptical research community to which Shapiro began disclosing her findings. What distinguished their approaches was that Shapiro set out to vigorously sell her belief in their utility in the relative absence of explanations as to why that might be the case. Uri Bergmann, an EMDR Institute Facilitator in New York, has recently put together a speculative neurobiological hypothesis for the effects of EMDR. In this article, he draws on a growing body of research into the area, particularly the ideas of Harvard University sleep researcher Robert Stickgold, who first identified the physiological pathways that link EMDR to REM functioning. Bergmann' offers his thoughts on the matter in a form accessible to the neurologically nave as a first step to understanding the neurobiology of EMDR.

The formation, transfer and integration of episodic memory

Very little of what we have experienced is remembered as episodic memory. In episodic memory, information from the outside world passes first through sensory brain structures which produce separate internal representations of a stimulus in each sensory modality. Visual, olfactory, tactile and auditory inputs are each processed by their respective regions and then passed on to higher processing regions.

As the process of passing on information ensues, information from both perceptual and semantic representations flows into the hippocampal complex. The hippocampus forms much stronger representations of the stimuli, which can now be intentionally recalled. The creation of these hippocampal memories facilitates the ability to recall the events of the day and to remember and subsequently recall addresses, hotel room numbers and names heard only once. This is in part because of the second function of the hippocampus, which is to store memories contextually.

Thus, a hippocampal memory is both strong and integrated, storing together simultaneous inputs for all sensorimotor modalities as well as associated affect, which is mediated by amygdaloid structures.

The formation of semantic memory

In the neocortex, memories are stored in dense highly overlapping neural networks. Hippocampal memories are slowly and repetitively replayed from the hippocampal complex to the cortex where the memories are eventually incorporated and consolidated into one's general semantic knowledge. Thus, cortical memories, in contrast to hippocampal memories (which are sparse and quickly formed) are slowly formed and densely represented. Semantic memories are the extraction, abstraction and storage of critically useful information from the sum total of our experiences. In short, hippocampal memories make us smart and factual, but semantic memories make us wise.

Rapid Eye Movement (REM) sleep, which is that most directly associated with dreaming, has long been associated with internal information processing and memory consolidation. Recent neuroimaging studies have shown that REM sleep may be associated with the activation of several brain structures involved in the mediation of emotion, namely the pontine brain-stem, the amygdaloid complexes and the anterior cortex of the cingulate gyrus. REM sleep may also be associated with a deactivation in regions involved in the executive, mnemonic aspects of cognition. REM sleep may also play a role in the processing of emotion in memory systems.

Sleep and memory consolidation

REM sleep seems most critical for neocortical memories. Information has been found to flow out of the hippocampus and into the cortex during non-REM sleep, with the flow being reversed during REM sleep, from the cortex into the hippocampus. The preferential activation of limbic, and particularly amygdaloid cortices can be seen in the hyper-emotional aspect of dreaming.

So what does this have to do with Post Traumatic Stress Disorder?

While hippocampal outflow to the cortex during non-REM sleep facilitates the reinforcement of old memories, the blocking of hippocampal outflow during REM sleep, and the simultaneous neocortical semantic outflow to the hippocampus, facilitates the formation of new associative links which are essential to understanding the meaning of events in our lives.

In PTSD this system breaks down, due to noradronergic and serotonergic surges. PTSD is marked by the constant, intrusive, replay of hippocampal, episodic memories of the event(s), combined with the associated, primitive, amygdaloid emotions attached to those events, and with a simultaneous absence of the necessary neocortical input which brings some sense of meaning to the traumatic event(s).

The role of REM physiology in EMDR

One of the physiological hallmarks of REM sleep is the waves of electrical activity that take place in the pontine brainstem, the lateral geniculate nucleus of the thalamus and the occipital cortex, collectively known as Pontine Geniculate Occipital (PGO) waves.

Another circumstance that allows for the generation of these PGO waves is the startle reflex. EMDR stimulation (eye movements, auditory tones and tactile stimulation), with its constant alternating shifting of attention, mimics this startle reflex. The cholinergic surge produced by EMDR's alternating stimulation, is believed to facilitate PGO wave activity, the activation of the brain's REM sleep systems and areas of the anterior cingulate cortex, which has affect and cognition areas. The affect area has extensive connections to the amygdala and parts of it project to the autonomic brainstem nuclei. This area is involved in conditioned emotional learning, vocalisations associated with expressing internal states, assessments of motivational content, assigning emotional valence to external and internal stimuli and regulating context-dependent behaviours.

It has been suggested that the anterior cingulate cortex and its connections provide the mechanisms by which affect and intellect can be joined. The anterior cingulate gyrus is seen as both an amplifier and filter, interconnecting the emotional and cognitive components of the mind. EMDR stimulation may jump-start the REM sleep system, opening the processing system that facilitates the flow of information from the neocortex back into the hippocampus, allowing for semantic neocortical input and, by implication, the reprocessing of information that is defective or dysfunctional.

Unlike natural REM sleep, when the neocortex is deactivated, EMDR appears able to activate REM systems and facilitate frontal cortical activation as well as the activation of areas of the anterior cingulate gyrus.

The role of the cerebellum

When the human brain enlarged in the course of its phylogenetic evolution, the cerebellum enlarged more dramatically than any other part of the brain except the cerebral cortex. Within the enlarged, multi-folded, cerebellum, the number of nerve cells apparently exceeds the population in the cerebral cortex, making it the largest structure in the human brain.

Containing billions of nerve cells, this cerebellar mechanism in the hindbrain is connected by millions of nerve fibers to many parts of the brainstem and forebrain, including all the lobes of the cerebral cortex.

 

Continued on the next page ...

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