Neurobiological Basis of EMDR
Posted on February 19th, 2016

Ruwan M Jayatunge M.D.

In 1987 an accidental discovery revealed an association between certain eye movements and reduced levels of distress resulting from traumatic memories. The result was a new psychological intervention, eye movement desensitization and reprocessing (EMDR) (Blore, 1996). The American Psychiatric Association Practice Guideline (2004) has recommended EMDR as one of the first-line treatments of trauma. The Department of Veterans Affairs & Department of Defense (2010) have placed EMDR as one of the most effective PTSD psychotherapies. EMDR is now considered evidence based practice in the treatment of trauma symptoms (Lee & Cuijpers, 2013).

EMDR has received widely divergent reactions from the scientific and professional community (Perkins et al., 2002). However its mechanism of action remains unclear and much controversy exists about whether eye movements or other forms of bilateral kinesthetic stimulation contribute to its clinical effects beyond the exposure elements of the procedure (Servan-Schreiber et al., 2006). Therefore EMDR requires explanation (Hassard, 1996).

The search for EMDR’s mechanisms of action began in the early 1990s, initially proceeding slowly and tentatively (Bergmann, 2010). There are a number of theories that attempt to explain the mechanism of EMDR.

Adaptive Information Processing

EMDR is a therapeutic approach guided by the adaptive information processing (AIP) model (Solomon & Shapiro, 2008). The AIP model portrays an innate healing system hypothesized to be composed of neurophysiological mechanisms of action causally related to the resolution of disturbing life experiences (Cotraccia, 2012). According to Shapiro (2001) when trauma is overwhelming strong negative feelings or dissociation interfere with information processing. Therefore dysfunctionally stored memories with inappropriate associative connections impact the PTSD victim. EMDR transmute the dysfunctionally stored experiences into an adaptive resolution promoting psychological health (Bergmann, 2010). Hence in EMDR traumatic memories lose their emotional charge (de Jongh et al., 2013).

The REM Effect

Eye movements during recall of an aversive memory are a treatment element unique to EMDR (Leer et al., 2014). Eye movements are known to improve episodic memory retrieval in healthy adults and to facilitate the processing of traumatic memories in EMDR therapy (Samara et al., 2011). Furthermore Shapiro, in her original description of EMDR, proposed that its directed eye movements mimic the saccades of rapid eye movement sleep (REM) (Stickgold, 2002).  Eye movements during EMDR activate cholinergic and inhibit sympathetic systems and this reactivity has similarities with the pattern during REM-sleep (Elofsson et al., 2008).

REM sleep is physiologically different from the other phases of sleep (Ezenwanne, 2015) and has been associated with gains in semantic and emotional memory (Gujar et al., 2011) and the regulation of emotional reactivity (Nishida et al., 2009).

A recent study suggested that REM sleep is associated with modulation of expectation-mediated placebo analgesia (Chouchou et al., 2015). REM sleep is punctuated and immediately preceded by ponto-geniculo-occipital waves (PGO) waves, bursts of electrical activity originating in the brain stem (Steriade & McCarley, 1990). In addition REM sleep is suspected to have a memory consolidation function and induced eye movements could generate ponto-geniculo-occipital equivalent spikes and EMDR could be explained as a focused and artificial exploitation of the rapid-eye-movement sleep mechanism (Hassard, 1996).

Ponto-geniculo-occipital potentials appear in the brainstem, thalamus and cerebral cortex during rapid eye movement sleep (Amzica & Steriade, 1996) and play an important role in triggering and maintaining rapid eye movement sleep. Ponto-geniculo-occipital waves have been implicated in several important functions such as sensorimotor integration, learning, cognition, development of the visual system, visual hallucination, and startle response (Datta & Hobson, 1995).

Jeffries and Davis (2013) hypothesized that eye movements may be more effective at reducing distress. Bilateral ocular stimulation activates orbito-frontal, prefrontal and anterior cingulate cortex (Pagani et al., 2012). The findings by Leer and team (2014) suggested that recall with eye movements causes 24-h changes in memory vividness/emotionality, which may explain part of the EMDR treatment effect, and these effects are related to intervention duration. Eye movement also decreases the memory’s image clarity and the accompanying excitement (Zarghi, Zali & Tehranidost, 2013).

Stickgold (2002) proposed that the repetitive redirecting of attention in EMDR induces a neurobiological state, similar to that of REM sleep, which is optimally configured to support the cortical integration of traumatic memories into general semantic networks.

Rosas Uribe and colleagues (2010) denoted that EMDR has positive effect on emotional cognitive processing and   long-term memory conceptual organization.

EMDR facilitates accessing and processing of negative material while presumably creating new associative links (Herkt et al, 2014).

Some researchers have speculated that series of horizontal saccadic eye movements increase the functional connectivity of the two brain hemispheres (Samara et al., 20111).

A variety of nervous system components such as medulla, pons, midbrain, cerebellum, basal ganglia, parietal, frontal and occipital lobes have role in EMDR processes (Zarghi et al., 2013). Farina and team (2015) found a significant increase of alpha power in the left inferior temporal gyrus after administering EMDR.   Herkt et al (2014) found increased activation of the amygdala upon bilateral EMDR stimulation even in healthy subjects.

Activation of Benzodiazepine Receptor

There is accumulating evidence that benzodiazepines agents widely used as anxiolytics and hypnotics-could be regarded as “natural” drugs since they have been found in trace amounts also in plants, various tissues of different animal species and even humans (Klotz, 1991). Möhler and Okada (1977) found natural   benzodiazepine receptor in the brain. As described by Möhler and Okada (1978) the receptor is mainly localized in the synaptic membrane fraction and has its highest density in cortical areas of the brain. Naturally occurring benzodiazepines and benzodiazepine-like molecules in brain are involved in the modulation of memory processes (Medina, Paladini & Izquierdo, 1993). Jayatune (2008) hypothesized that EMDR activates natural benzodiazepine receptor in the brain.

Concluding Thoughts

EMDR is an effective mode of psychotherapy. There are several theoretical explanations of how EMDR might work. According to one explanation EMDR mimics the saccades of rapid eye movement sleep. Another theory elucidates that EMDR transmute the dysfunctionally stored experiences into an adaptive resolution. In addition activation of benzodiazepine receptor in the brain following EMDR is another hypothesis.

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