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The Effect of EMDR on the Pathophysiology of PTSD Stacy Smith Department of Psychology Loyola College EMDR and the Pathophysiology of PTSD 1 Introduction The process of understanding Posttraumatic Stress Disorder (PTSD) has been a long and difficult one. It is safe to say our understanding of this disorder is incomplete, and our exploration into its pathophysiology is fairly recent. As with any disorder of the brain, the complexities of PTSD are extensive and require integrating cognitive, functional, and chemical components. Given this complexity, it is no wonder that treating PTSD has also been a challenge. Treating a disorder whose components are not fully understood is similar to shooting in the dark. Some shots have hit their mark and some have missed. More than ten years after its conception, the question of whether Eye Movement Desensitization and Reprocessing (EMDR) is a hit or a miss is still debated. If understanding the pathophysiology of PTSD is still recent, understanding the possible physiology behind EMDR is just beginning. This paper will define PTSD, explain some aspects of its physiology, and present some hypotheses at to why EMDR may be a successful treatment for PTSD. Posttraumatic Stress Disorder According to the DSM-IV-TR (APA, 2001), Posttraumatic Stress Disorder starts when a person is confronted by a traumatic event. Such events may include, but are not limited to events where one’s life is in danger, witnessing someone’s death, being in a natural disaster, being raped or otherwise physically assaulted. It is not necessary that the event happen to the individual, or that the individual actually be in danger of dying. The person’s perception of danger or witnessing of trauma can be sufficient. Exposure to this traumatic event evokes feelings of intense fear, helplessness or loss of control. After the event, the person continues to reexperience the event through flashbacks, nightmares, or the feeling that one is reliving the EMDR and the Pathophysiology of PTSD 2 experience. Exposure to any stimuli that reminds the person of the trauma can also trigger these reactions. Because of this, the person avoids anything that reminds him of the event, which may include a variety of people, places, or activities. The individual also experiences increased physiological and emotional arousal that may interfere with sleep or concentration and cause outbursts of anger, exaggerated startle response, and hypervigilance. These symptoms have lasted for at least one month and were not present before the exposure to the trauma or traumas. PTSD is estimated to occur in approximately 8% of the population, while estimates for at-risk groups may be higher. The comorbidity rate for mood disorders, anxiety disorders, somatoform disorders, and substance abuse disorders is higher with individuals suffering from PTSD. It is not uncommon for individuals with PTSD to feel guilt, shame, despair, dissociation, a sense of ineffectiveness, or threatened. Their interpersonal relationships are often compromised, as well as their ability to hold a job or have meaningful social interactions. They are more likely to have somatic complaints and to be involved in impulsive, compulsive, or self- destructive behavior. Posttraumatic stress can also be viewed in a larger context. Even without meeting the criteria for the disorder, posttraumatic stress can play a part in dissociative disorders, acute stress disorder, and brief psychotic disorder. It is also linked with Axis II Borderline personality disorder (Everly, 1995a). Since posttraumatic stress can be brought on by stressors as diverse as a war injury in Afghanistan, a bus accident in Egypt, or a sexual assault in Kentucky, it is clear that the scope of this disorder and its effects can be far-ranging. Pathophysiology of PTSD EMDR and the Pathophysiology of PTSD 3 Even as we note the overall complexity of PTSD, it is also necessary to understand the multi-systemic and interconnected components of its pathophysiology (Stickgold, 2002). Within the biological context, one must still address cognitive, behavioral, structural, functional, and chemical pieces of the puzzle. We shall endeavor to do this by breaking PTSD down into several smaller, more manageable parts. PTSD begins with a traumatic event. As noted in the DSM-IV-TR (APA, 2001), what constitutes a traumatic event depends on the individual. Everly (1995b) notes in his two-factor model of posttraumatic stress that, after an initial reflexive neural surge, cognitive appraisal plays a significant role in whether or not an event is perceived as traumatic. If a cognitive appraisal results in no perception of threat, the person returns to a baseline of functioning. If a threat is perceived, the process continues. Several areas of the brain are involved in appraising the threat of a given situation (Bergmann, 1998). The amygdala, which receives all sensory information and works as the alarm system when a perceived threat arises. The cingulate gyrus is implicated in our ability to differentiate real from imagined threat, and the neo-cortex provides the higher processing functions of logic and analysis. A trauma can eventually lead to the two factors in Everly’s model. They are autonomic arousal and intrusive cognitions. How these come about requires exploration of the structural, functional, and neurochemical parts of the brain. Let us begin with the neurochemical response to trauma. After the initial surge of the neurotransmitter norepenephron (NE) as a result of the initial shock, the brain bursts into action. The amygdala signals the hypothalamus to start the pituitary gland secreting corticotropin-releasing factor (Bergman, 1998). The brain begins producing EMDR and the Pathophysiology of PTSD 4 chemicals in abundance. Each fulfills a purpose. Activation of amygdala, hippocampus, and locus coeruleus, lead to increased production of NE, benzodiazapine, serotonin, dopamine, endogenous opiates, and glucocorticoids (Southwick, Krystal, Johnson, & Charney, 1992). NE works to activate and arouse the autonomic nervous system and increases heart rate, blood pressure, blood clotting, and neuromuscular activity. Serotonin, whose regulation is interconnected with NE, may serve to stabilize mood and prevent impulsive behavior. Dopamine serves to focus our attention on the perceived threat (Bergmann, 1998). Endogenous opiates work to decrease pain sensitivity and fear. Benzodiazapine works to modify the effect of the other neurotransmitters in order to keep our behavior within adaptive levels. Correctly regulated and in the short term, these chemicals serve an important function during a stress response. If a stressor is uncontrollable or chronic, these very same systems in excess can become harmful. Excess NE leads to chronic hyperarousal of the autonomic nervous system. Increases in NE can lead to decreases in serotonin, which may cause mood swings and impulsive behavior. Excess dopamine could potentially lead to psychosis. Uncontrollable stress may also inhibit benzodiazapine receptors, which prevents the system from curtailing its own excesses. Activation of the Hypothalamic-Pituitary-Adrenal Axis (HPA axis) may lead to oversecretion of glucocorticoids, which may interfere with learning and memory. Understanding the process of memory may be one key to understanding the physiology of PTSD. When we experience an event, the signal is transferred to the hippocampus from the neo-cortex, which processes and translates it before sending it on to the rest of the limbic system (Bergmann, 1998). Meanwhile, the amygdala is responsible for connecting any emotional components to the memory. This is known as episodic memory Stickgold, 2002). At some point, the episodic memory travels from the limbic system to the neo-cortex, where it is EMDR and the Pathophysiology of PTSD 5 integrated into our overall understanding and encoded as part of semantic, or long-term memory. It is by this process that we assimilate and integrate information for adaptive use in the future. For the PTSD sufferer, it is possible that this process does not work correctly. To understand why, we must also address the process of REM sleep. Stickgold (2002) states that one purpose of REM sleep is to facilitate the process of integrating episodic into semantic memory. Non-REM sleep is most beneficial to strengthening hippocampal memory, while REM sleep is most conducive to processing memories in the neo-cortex. (Plihal & Born, 1997). During REM sleep, information that is ready to be encoded travels to the neo-cortex and is assimilated. During this time, the body stops producing NE and serotonin and starts producing acetylcholine. In the end, the process of transmitting memories to the neo-cortex is contingent on the cessation of NE production. If, as might be the case for an individual with PTSD, NE production continues and the amount of REM sleep declines (Glaubman, Mikulincer, Porat, Wasserman, & Birger, 1990), the system is compromised. Excess NE prevents the attainment of complete REM sleep and keeps the limbic system hyperaroused. Furthermore, a barrier typically separates the hippocampus and the neo-cortex during REM sleep, allowing the neo-cortex to process episodic memories into semantic memory. The hyperarousal of the limbic system compromises this barrier, inhibiting the ability of the neo-cortex to assimilate memories. Stickgold (2002) postulates that the inability to integrate episodic memory into the semantic memory explains the presence of contextually accurate nightmares in the case of PTSD sufferers. Dreams should not contain large chunks of reality-based contextual information, because the neo-cortex should process such information into long-term memory. However, if the barricade between the hippocampus and the neo-cortex is compromised, episodic memory is not processed and integrated into long-term memory. EMDR and the Pathophysiology of PTSD 6 The end result of these processes is PTSD as a self-sustaining disorder. Severe and/or chronic stress leads to an overproduction of NE. Excess NE leads to general hyperarousal in many areas of the brain and body. Oversecretion of NE also prevents REM sleep, which is integral to the processing of traumatic memories. Thus, traumas are reexperienced, hyperarousal continues, the overproduction of NE continues, and the system perpetuates itself. Although cognitive and structural variables play a part, excess NE appears to play the biggest role in transforming the systems from functioning to dysfunctional. The Role of EMDR in the Pathophysiology of PTSD In the span of time since EMDR began, there has been an enormous body of literature addressing its efficacy in treating people suffering from PTSD and other trauma-related disorders. Independent reviewers working under the auspices of the American Psychological Association Division 12 task force on psychological interventions recognized EMDR as one of two useful treatments for PTSD (Chambless, et al 1998). Although there has been some strong evidence to suggest that EMDR is an effective treatment, the question of why it may work has not been conclusively answered. In this section, I will begin by outlining the EMDR procedure then try to fit some recent hypotheses into the context of a pathophysiological explanation of PTSD. The following is a summary of the EMDR treatment protocol from Shapiro (1989). An EMDR treatment begins by asking the client to retrieve a traumatic memory and isolate a single picture that symbolizes the memory. At the same time, the individual should provide a thought or phrase that goes with the picture. The thought or phrase is most commonly a negative one. The person is asked to assign a Subjective Units of Disturbance (SUD) score (0-10) to the picture EMDR and the Pathophysiology of PTSD 7 and thought. Then the person is asked to provide a positive thought or statement they would prefer to be having in regards to the picture. They should report how true they feel this positive statement to be on a 7 point Validity of Cognition (VOC) scale. After being informed that they should be accurate in reporting their subsequent experiences and being assured against any pressure to perform in a specific manner, the therapist would begin facilitating eye movements. As the client continued to visualize the image, the therapist would begin a series of movements with the index finger. There would be 10-20 bilaterally saccadic movements about 12-14 inches from the face moving from extreme right to extreme left at a rate of two full sweeps per second. After this has been accomplished, the client is asked to blank out the picture, attempt to clear the mind, and take a deep breath. After retrieving the picture and accompanying thought, the subject would provide another SUD level. The procedure would be repeated until the SUD level was at 0 or 1. At that point, the therapist would ask the client to provide a VOC score for the positive statement that was originally identified as preferable. Originally, the key to EMDR was considered to be the eye movements. Shapiro (1989) contended that the bilateral, rhythmic, saccadic eye movements allowed the brain to process the traumatic event, although she was uncertain as to how this came about. Despite continued controversy, many therapists and researchers have also attained positive results with alternating finger tapping and other stimuli (Bergmann, 1998). What then, may cause this process to work? For hypotheses on that matter, we must return to REM sleep. Stickgold (2002) posits that EMDR works because it mimics the movements our eyes make during REM sleep. He suggests that the constant shifts of attention all EMDR treatments have in common is the key. These shifts, which are similar to what occurs in REM sleep, allow the brain to activate the areas central to processing episodic into semantic memories. In essence, it serves to “jump start” the EMDR and the Pathophysiology of PTSD 8 processing procedure. As a result, the traumatic memory that has remained as episodic memory is processed and integrated into the individual’s overall life experience. This also allows the neo-cortex to signal the hippocampus to allow the event to deteriorate from episodic memory. Thus, along with being able to assimilate the trauma and put it in context, the individual no longer experiences it as an ongoing, intrusive phenomenon. Bergmann (1998) also believes that EMDR works similarly to REM sleep. He suggests that the phases of alternating attention serve to resynchronize areas of the brain that have become asymmetrical in functioning. EMDR may help to activate certain pacemaker cells in the brain, which facilitate hemispheric interaction and allow for the downregulation of the limbic system. This provides the neo-cortex with its higher function capacities to take over from the hypoaroused limbic system. The limbic system arousal decreases, and regular brain functioning is restored. On a simpler note, Levin et al., (1999) suggest that EMDR does indeed lead to a resynchronization of the brain. This, in turn, allows the cingulate gyrus to function effectively. A properly functioning cingulate gyrus is better able to distinguish real threat from perceived threat. Once it has established that a real threat no longer exists, the brain begins to hyperreact less frequently. While these explanations are tantalizing and interesting, empirical evidence for them has been somewhat sparse and circumstantial. Although there appears to be some agreement that EMDR and REM sleep may share certain properties, a consensus on which systems are affected has yet to be reached. EMDR and the Pathophysiology of PTSD 9 Empirical Review As one might imagine for such a controversial topic, the literature on EMDR is vast. Up until recently, however, the main focus appeared to be on the question of treatment efficacy. Literature on the mechanisms of why EMDR works has been sparse and somewhat speculative. In order to keep this literature review salient to my topic, my focus will be on those studies that address areas discussed in this particular paper. Kolb (1987) studied over 300 Vietnam veterans and others with chronic or delayed PTSD. Most had long and high level combat exposure. Many had symptoms of dissociation or psychosomatic complaints. The author found that these veterans had a persisting conditioned emotional response to stimuli reminiscent of combat. These men had both perceptual abnormalities and also excessive autonomic arousal. After introducing combat sounds to veterans with PTSD, as well as sounds of music, or silence, several significant changes were noted. Namely, combat sounds produced a higher heart rate and an increase in systolic and diastolic blood pressure. Schiffer (1997) used electroencephalography (EEG) with auditory stressors to study patterns of hemispheric lateralization with a group of victims of abuse and a control group. The traumatized group showed increased activation in the right hemisphere and deceased activity in the left hemisphere. The control group showed no significant laterality during the recall of distressing memories. This appears to show a split in brain functioning for those with PTSD. Uncontrollable stress leads to the productions of endogenous opiates (Hemingway and Reigle, 1987). Endogenous opiates provide a feeling of numbness, or lack of sensitivity to pain. Repeating an uncontrollable stressor at a lower intensity is found to result in the same level of opiates being released. This suggests that the system becomes hypersensitive to uncontrollable EMDR and the Pathophysiology of PTSD 10 stress and does not appropriately regulate the amount of opiates needed. Such numbing is characteristic of PTSD sufferers. In 1989, Francine Shapiro published her first paper on EMDR. In it, she described the procedure, as well as the study she used to empirically verify the results. This study made two comparisons: treatment vs. control (between-group) and placebo vs. treatment (within-group) within the control group. The mean SUD of the treatment group prior to EMD was 7.45. After treatment it was 0.13 and remained below 1.0 at one and three month follow-ups. The SUD for the delayed treatment group was 6.77, and after placebo it was 8.31. Before delayed treatment it was 7.54, and after it was 0.18. It remained below 1.0 at one and three month follow-ups. Since her first landmark study, research on the efficacy of EMDR has been plentiful. The results, however, have been somewhat mixed and although EMDR has gained greater popular acceptance, controversy over its efficacy still exists. Davidson and Parker (2001) performed a meta-analysis to address the efficacy of EMDR treatment. They used literature found by searching on MedLine and PsycInfo from 1988 to April of 2000. Current Contents was also searched from 1997 to March 2000. They searched under EMDR and eye movement desensitization and only treatment studies were included. Any follow-up data was not included. In all, there were a total of 34 studies. This study reflected the literature by looking at both between-group and within-group comparisons. The authors used outcome and process measures to define the effectiveness of EMDR. The SUD and VOC levels were the process measures used, and the outcome measures included various types of psychometric tests, as well as physiological, and behavioral measures. The authors compared EMDR with a variety of treatments including non-specific treatment, eyes fixed treatments (EFixDR), and other treatments (Othdism). Non-specific treatment was defined as applied EMDR and the Pathophysiology of PTSD 11 relaxation, biofeedback, active listening, or rapid induction. OthDism was defined as a procedure similar to EMDR, with a component other than the eye movements changed. When using outcome measures, 28 studies were included in the meta-analysis. EMDR was effective using a pre-test and post-test comparison. It was also effective compared to wait-list, non- specific treatment, and no treatment control groups. It was not more effective than exposure therapies. Eighteen of the studies had information on process measures. Using process measures, EMDR was only effective in a pre/post situation, but was not shown to be more effective than any other therapy. Outcome and process measures were also considered comparing EMDR to EfixDR. EfixDR is defined as EMDR with a fixed eye component instead of movement. The end result was that EMDR and EfixDR were found to be equally effective in process and outcome measures. In conclusion, EMDR was found to be effective when compared to no treatment, non- specific treatment, and pre-post test comparisons. EMDR was not found to be better than other exposure based treatments. The eye-movement component of EMDR was not found to be necessary to the treatment Devilly and Spence (1999) also took on the question of EMDR efficacy. This study looked at 23 participants, all of which were diagnosed with PTSD. They were divided into two treatment groups, one with a Cognitive-Behavior technique Trauma Treatment Protocol (TTP), and one with EMDR. The subjects were tested pre-treatment, post treatment, at two weeks and at three months by an extensive array of psychological measures. The TTP uses a combination of cognitive restructuring and behavioral experiments as its basis. Both groups were statistically the same in the pre-treatment testing consistent with random assignment. Following the treatment, 10 of the 12 subjects in the TTP groups did not meet the DSM-III-R EMDR and the Pathophysiology of PTSD 12 criteria for PTSD, while only 4 of the 11 EMDR participants had the same results. At a 3-month follow-up, the effect was generally the same. Merckelbach, Hogerrvorst, Kampman and De Jongh (1994) studied the effect of eye movement and retrieval of aversive information. A slide showing a mutilated hand was shown to 40 participants. The group was then split and half underwent an eye movement protocol as they recalled the information, and half utilized a finger tapping procedure (the control). Information on heart rate as well as other self-report data were collected before and after the intervention while concurrently visualizing the aversive slide. The authors found that eye movement did not decrease the strength of the emotional response. The authors suggest that this indicates there is no basis for the claim that eye movements are critical to EMDR success. It should be noted, however, that the subjects of this study had not been diagnosed with PTSD, and their ability to process information would most likely be intact. Also, an argument could be made that viewing the slid of a mangled hand is not fundamentally similar to the kinds of trauma experienced by people with PTSD. There is little in the way of personal context, and the perception of helplessness or loss of control seems unlikely. Finally, Levin, Lazrove, and van der Kolk (1999) examined 6 subjects with PTSD. The study used a within-subject design and did not use a control group. Subjects were given standard psychological tests, including scales for depression, PTSD, traumatic memories and impact of life events. The Rorschach Ink Blot test and Single Photon Emission Computed Tomography (SPECT) were also given, both before and after three EMDR sessions. The article presents a case study of one of the subjects. Comparing the results before and after the EMDR sessions showed a number of changes. There was decline in scores on PTSD and depression scales and the subject’s hypervigilance scale went from positive to negative. A post-EMDR Rorschach test EMDR and the Pathophysiology of PTSD 13 confirmed these changes. SPECT scanning showed two areas of the brain were more active after EMDR treatment. The anterior cingulate gyrus and the left frontal lobe both showed signs of increased blood flow. The authors suggest that EMDR treatment did not decrease arousal in the limbic system, but increased the subject’s ability to distinguish real from imagined threat. Conclusion Understanding the intricacies of a disorder as complex as PTSD provides us with a unique challenge. It requires that we be willing to give up our single factor models and accept that PTSD involves many interrelated and interconnected variables. The recent advances in understanding the pathophysiology of PTSD should help to bring the picture into clearer focus. The hypotheses of the EMDR mechanism are not as clear. As preliminary findings, they are tantalizing, but stronger empirical support is still needed. Current theories emphasize the similarities between EMDR and REM sleep. The brain reacts to alternating stimuli and REM sleep in similar ways. Research has suggested that such similarities allow PTSD sufferers to process traumatic episodic memories during EMDR treatment. There is much literature however that suggests the use of alternating stimuli during EMDR treatment is not necessary and does not increase it’s effectiveness. If this is true, then research must address this inconsistency between the theoretical and empirical literature. Given this uncertainty, it is difficult to know whether EMDR would be valuable to me. At this time, explanations about the mechanisms behind EMDR are like so much Swiss cheese. There are still a great many holes to fill. EMDR and the Pathophysiology of PTSD 14 References American Psychiatric Association. (2001). Diagnostic and Statistical Manual, Version IV-TR. Washington, DC: Authors. Bergmann, U. (1998). Speculations on the neurobiology of EMDR. Traumatology, 4, Article 2. Boudewyns, P.A., & Hyer, L.A. (2001). Eye movement desensitization and reprocessing (EMDR) as treatment for posttraumatic stress disorder (PTSD). Clinical Psychology and Psychotherapy, 3, 185-195. 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