Recent neuroimaging studies on posttraumatic stress disorder (PTSD) have revealed a consistent decrease in thalamic activity, relative to non-PTSD controls. Empirical studies of the past decade have shown the thalamus to be centrally involved in the integration of perceptual, somatosensory, memorial, and cognitive processes (thalamo-cortical-temporal binding). A theoretical model is proposed to suggest that one underlying mechanism of EMDR stimulation (dual-attention stimulation/bilateral stimulation [DAS/BLS] ) is thalamic activation, specifi cally of the ventrolateral and central-lateral nuclei. It is hypothesized that this may facilitate the repair and integration of somatosensory, memorial, cognitive, frontal lobe and synchronized hemispheric functions that are disrupted in PTSD.
This discussion explores current neurobiological findings in the areas of the limbic system, REM-sleep and psychological trauma. The formation and consolidation of memory and emotion are discussed. Research regarding the mediating anatomy and physiology of REM-sleep is explicated, particularly the function of REM-sleep in memory processing. The pathways of trauma are outlined. Speculations are then offered, based on these findings, as to the underlying mechanisms of Eye Movement Desensitization and Reprocessing (EMDR).The speculations considered in this paper are submitted to stimulate further discussion and research about the underlying mechanisms of EMDR. These speculations are derived from recent empirical findings in the areas of the limbic system, the neurobiology of trauma and of REM-sleep. This discussion explores the possibility that EMDR processing gradually enables the capacity of higher, cortical, brain functions to override the input from the limbic structures, thereby facilitating limbic downregulation, reduced kindling and, consequently, an enhanced integration of thalamic, amygadaloid, hippocampal and cortical functioning. This appears to correct hemispheric laterality and allows the brain to maintain balanced interhemispheric functioning on its own. Francine Shapiro posits that one of the simplest ways of describing integrative EMDR effects is to say that the target event has remained unprocessed because the immediate biological responses to, the trauma have left it isolated in neurobiological stasis. The processing mechanism of EMDR is physiologically configured to take misprocessed information to an adaptive level (Shapiro, 1994(Shapiro, , 1995. To comprehend how this takes place at a neurobiological level, I believe that it is imperative to understand the relationship between the amygdala and the following: the other limbic structures; the neocortex; the mediating anatomy, physiology and function of dream sleep; and the specific neurotransmitters that impact on these anatomical connections and functions.
This discussion explores, briefly, the position that the repetitive redirecting of attention in EMDR is capable of turning on the brain's REM sleep system, leading to the activation of specific areas of the the anterior cortex of the cingulate gyrus, facilitating its function as a filter, thereby facilitating the integration of traumatic memory into general semantic networks. This integration is seen to lead to the subsequent reduction in both the strength of hippocampally mediated episodic memories of the traumatic event as well as the amygdaloid mediated negative affect of PTSD. The possibility is suggested that another underlying mechanisms of EMDR stimulation is the activation of the lateral cerebellum. The contribution of the cerebellum to cognitive and language functions is explored. The activation of the dentate nuclei in the lateral neocerebellum is shown to facilitate activation of the ventrolateral and central lateral thalamic nuclei. The activation of the ventrolateral nucleus is shown to lead to the activation of the left dorsolateral prefrontal cortex; further facilitating the integration of traumatic memory into general semantic and other neocortical networks.
Historically, mechanisms of action have often been diffi cult to ascertain. Thus far, the defi nitive discovery of eye movement desensitization and reprocessing (EMDR)'s underlying mechanisms has been equally elusive. We review the neurobiological studies of EMDR, as well as the theoretically driven speculative models that have been posited to date. The speculative theoretically driven models are reviewed historically to illustrate their growth in neurobiological complexity and specifi city. Alternatively, the neurobiological studies of EMDR are reviewed with regard to their object of investigation and categorized as follows: fi ndings before and after EMDR therapy (neuroimaging and psychophysiological studies) and fi ndings during the EMDR set (psychophysiological, neuroimaging, and qEEG studies).
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