|Neurobiological aspects of EMDR|
Given the infancy of the field of neurobiology, the physiological foundations of all psychotherapies are currently unknown, and therefore, all neurobiological models of psychotherapy are speculative. Testing of hypotheses about EMDR’s neurological mechanisms awaits the development of advanced brain imaging techniques. Hypotheses concerning EMDR’s neurobiological mechanisms are, at this time, purely speculative.
Neuroimaging post-EMDR findings have been noted with respect to left frontal lobe activation (Lansing et al., 2005; Levin et al., 1999; Oh & Choi, 2007), decreased occipital activation (Lansing et al., 2005; Pagani et al., 2007), and decreased temporal lobe activation (Oh & Choi, 2007; Pagani et al., 2007). These findings are indicative of the following: (a) emotional regulation due to increased activity of the prefrontal lobe, (b) inhibition of limbic over-stimulation by increased regulation of the association cortex, (c) reduction in the intrusion and over-consolidation of traumatic episodic memory due to the reduction of temporal lobe activity, (d) the reduction of occipitally mediated flashbacks, and (e) the induction of a functional balance between the limbic and prefrontal areas. Recent modifications in neuroimaging paradigms have illustrated findings of bilateral dorsolateral prefrontal activation (Oh & Choi, 2007), as well as left orbitofrontal (Lansing et al., 2005) and right ventromedial prefrontal activation (Richardson et al., 2009). The implications of these findings have yet to be fully understood, but suggest repair in memorial function, working memory/concentration, and affect regulation, respectively. In addition, the finding of increased thalamic activation following successful EMDR treatment (Richardson et al., 2009) was noted for the first time. The consequence of such a change suggests the repair of failures in cognitive, memorial, affective, somatosensory, and interhemispheric integration, which are disrupted in PTSD. Additionally, structural hippocampal growth was also noted following EMDR treatment (Bossini et al., 2007, 2011).
EEG findings of EMDR treatment have shown increases in amplitude (Grbesa et al., 2010), enhanced left hemispheric function (Pagani et al., 2011), as well as decreased limbic activation and enhanced cortical activation (Pagani et al., 2012). These findings are indicative of desensitization, and cortical inhibition of neural kindling.
Psychophysiological studies of EMDR have yielded findings of parasympathetic relaxation responses (Wilson et al, 1996; Sack et al., 2008), increased HRV parasympathetic tone (Sack et al., 2007, 2008; Frustaci et al., 2010), reduced electrodermal function (Aubert-Khalfa et al., 2008; Schubert et al., 2011), reduced EEG P3a function (Lamprecht et al., 2004), and increased vagal parasympathetic function (Elofsson et al., 2008). These findings suggest that EMDR mediates directly on affect regulatory systems, inducing an initial "compelling” parasympathetic state change that facilitates information processing and neural linkage repair and the eventual stable trait change that is seen as a result of successful EMDR treatment.
Aubert-Khalfa, S., Roques, J. & Blin, O. (2008). Evidence of a decrease in heart rate and skin conductance responses in PTSD patients after a single EMDR session. Journal of EMDR Practice and Research, 2, 51-56.
Oh, D.-H., & Choi, J. (2007). Changes in the regional cerebral perfusion after Eye Movement Desensitization and Reprocessing: A SPECT study of two cases. Journal of EMDR Practice and Research, 1(1), 24–30.
Pagani, M., Hogberg, G., Salmaso, D., Nardo, D., Sundin, O., Jonsson, C., et al. (2007). Effects of EMDR psychotherapy on 99m Tc-HMPAO distribution in occupation-related post-traumatic stress disorder. Nuclear Medicine Communications, 28(10), 757–765
Pagani M, Di Lorenzo G, Verardo AR, Nicolais G, Monaco L, et al. (2012). Neurobiological Correlates of EMDR Monitoring – An EEG Study. PLoS ONE 7(9): 45753. doi:10.1371/journal.pone.0045753
Richardson, R., Williams, S. R., Hepenstall, S., Gregory, L., McKie, S., & Corrigan, F. (2009). A single-case fMRI study EMDR treatment of a patient with posttraumatic stress disorder. Journal of EMDR Practice and Research, 3(1), 10–23.
Sack, M., Lempa, W., & Lemprecht, W. (2007). Assessment of psychophysiological stress reactions during a traumatic reminder in patients treated with EMDR. Journal of EMDR Practice and Research, 1, 15-23.
Sack, M., Hofmann, A., Wizelman, L., & Lempa, W. (2008). Psychophysiological changes during EMDR and treatment outcome. Journal of EMDR Practice and Research, 2, 239-246
Harper, M. L., Rasolkhani-Kalhorn, T., & Drozd, J. F. (2009). On the neural basis of EMDR therapy: Insights from qeeg studies. Traumatology, 15, 81-95.
Landin-Romero, R., et al. (2013). EMDR therapy modulates the default mode network in a subsyndromal, traumatized bipolar patient. Neuropsychobiology, 67, 181-184.
Nardo D et al. (2009, in press). Gray matter density in limbic and paralimbic cortices is associated with trauma load and EMDR outcome in PTSD patients. Journal of Psychiatric Research. doi:10.1016/j.jpsychires.2009.10.014
Propper, R., Pierce, J.P., Geisler, M.W., Christman, S.D., & Bellorado, N. (2007). Effect of bilateral eye movements on frontal interhemispheric gamma EEG coherence: Implications for EMDR therapy. Journal of Nervous and Mental Disease, 195, 785-788.
Sack, M., Nickel, L., Lempa, W., & Lamprecht, F. (2003) Psychophysiological regulation in patients suffering from PTSD: Changes after EMDR treatment. Journal of Psychotraumatology and Psychological Medicine, 1, 47 -57. (German)
van der Kolk, B., Burbridge, J., & Suzuki, J. (1997). The psychobiology of traumatic memory: Clinical implications of neuroimaging studies. Annals of the New York Academy of Sciences, 821, 99-113
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