Ad blocker interference detected!
Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers
Wikia is not accessible if you’ve made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected.
Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
Eye Movement Desensitisation for the Treatment of Post-Traumatic Stress Disorder: Fact and Fiction Edit
Introduction – PTSD and EMDEdit
Post-traumatic stress disorder (PTSD), recognised since 1980 when it was in included as a distinct diagnostic category in the DSM-III (APA, 1980), is a condition that follows an unusually threatening event which, in most instances, is sudden and catastrophic in proportion. It is characterised by;
“… the reexperiencing of an extremely traumatic event accompanied by symptoms of increased arousal and by avoidance of stimuli associated with the trauma” (DSM-IV, APA, 1995; p.403)
Diagnosis of the condition requires a number of factors to be present in each of the following six symptom categories (as outlined in DSM-IV, 1995);
A. The person has been the victim of, or has been exposed to a traumatic event which involved threatened death or serious injury, or the death of others. The person’s response involved intense fear, helplessness or horror.
C. The person persistently avoids stimuli associated with the trauma (e.g. avoidance of places or people that arouse recollections of the trauma) and experiences numbing of general responsiveness (e.g. restricted range of affect, feelings of detachment or estrangement from others).
D. The person experiences persistent symptoms hyperarousal (e.g. difficulty falling or staying asleep, increased irritability, exaggerated startle response).
E. The duration of the disturbance is more than one month.
F. The disturbance causes clinically significant distress or impairment in social, occupational or other important areas of functioning.
Considerable research into effective treatments for PTSD has been carried out since its inclusion in DSM-III in 1980. Exposure techniques, which are based on the assumption that individuals habituate to the anxiety provoking memory with a consequent reduction in anxiety, have been frequently used. However some authors have expressed concern about the use of a technique that generates prolonged high levels of anxiety (Fairbank & Brown, 1987) and requires several sessions to achieve a therapeutic effect (Keane, Fairbank & Cadell, 1989). Further, the failure of exposure to have an effect on some patients has been inadequately explained (Wolpe, 1982; Keane et al., 1989). Further, even when exposure techniques seem to have been effective in dealing with some of the symptoms of PTSD, residual difficulties such as nightmares, social isolation and generalised anxiety often remain after treatment (Vaughan & Tarrier, 1992).
Relatively recently, a new approach to the treatment of PTSD has emerged for which dramatic claims have been made. The technique, Eye Movement Desensitisation (EMD) was apparently developed by chance when Shapiro (1989a, b) noticed in herself that recurring disturbing thoughts disappeared when she simultaneously engaged in automatic ‘multi-saccadic’ eye movements. Rosen (1995) suggests that saccadic eye movements are involuntary and cannot be detected by people even when they are specifically instructed to look for them. Therefore, he argues that the term ‘saccadic’ is inaccurate. However, this assertion has been disputed by Welch (1996) who suggests that Rosen’s understanding of saccadic eye movements is flawed. Regardless of the specific type of eye movement that Shapiro observed, this debate does not detract from Shapiro’s serendipitous discovery that lead her to consider whether the induction of bilateral eye-movements might reduce the intrusion phenomena commonly associated with PTSD.
The essential feature of EMD in the treatment of PTSD is that the patient is required to generate an anxiety-inducing image, associated with the traumatic event, and isolate a thought about that scene. For example, Shapiro (1989b) cites examples including, “I am helpless” or “I have no control”. While the patient repeats the phrase to himself, bilateral eye movements are induced by tracking the therapist’s finger which is held between 9 and 12 inches in front of the patient and moved back and forth across the patient’s visual field at a rate of 1-1 seconds (Shapiro, 1989a). Each complete bilateral eye movement cycle is termed a ‘scad’. Next, the patient is required to revisualise the scene in terms that are more acceptable or preferred and generates a counter anxiety-inducing phrase, e.g. “I am safe now”. Eye movements are then induced again with the new image and phrase. The procedure is repeated with all anxiety-provoking memories until no further anxiety is reported. Shapiro (1989a) claims that EMD will be successful in 60-70% of patients in a single 50-minute session.
Shapiro (1989a) suggests that the traumatic memory is weakened or eradicated when the patient maintains awareness of one or more of the following; (1) an image of the memory, (2) the negative self-statement or assessment of the trauma, (3) the physical anxiety response. She suggests that the optimum response to EMD occurs when the patient is aware of all three but that desensitisation can occur when only one is present.
It should be noted that, in her later work, Shapiro changed the name of the technique “Eye Movement Desensitisation and Reprocessing” to connote the “accelerated information processing” that she assumed to be of major importance in the efficacy of the approach. However, the mechanisms by which the technique works have not been conclusively identified and, as Lohr, Kleinknecht, Tolin & Barrett (1995) point out;
"... there is no empirical evidence of the effects of treatment that justifies the use of the term reprocessing” (p.286)
Lohr et al (1995) chose to adhere to the popular name for the treatment protocol, EMDR, because it is now the most commonly used term. However, it is suggested that incorrect labelling of the technique perpetuates a myth which implies the establishment of a mechanism for the phenomenon. Consequently the original name, eye movement desensitisation (EMD) is used in this review.
This review will restrict itself to a consideration of the efficacy of EMD in the treatment of PTSD. The review begins with a discussion of early single-case design and uncontrolled studies of applying EMD to the treatment of PTSD. The review then considers both therapeutically successful and unsuccessful controlled outcome studies prior to concluding with a summary that draws the available literature together. Readers wishing to consider how EMD has been applied to other disorders should consult Lohr et al. (1995).
Investigating the Efficacy of EMD Edit
Single-Case and Uncontrolled Studies Edit
Early studies of EMD were typically single-case or uncontrolled studies. The studies by Puk (1991), Marquis (1991), Lipke and Botkin (1992), McCann (1992), Spector and Huthwaite (1993) and Spates and Burnette (1995) all seemed to indicate the efficacy of EMD. However, few of these studies used standardised psychological tests and established diagnostic tools and hence caution should be exercised in interpreting the reported outcomes.
Wolpe and Abrams (1991) utilised the Fear Survey (Wolpe & Lang, 1969) which offers a global rating of overall fear level in their treatment of an individual rape victim. They demonstrated significant improvements in subjective distress and collateral reductions in overall fearfulness and social dysfunction at follow-up. However, the 15-session intervention used a modified EMD procedure including systematic desensitisation and relaxation training which precludes conclusions about EMD being drawn (Renfrey & Spates, 1994). Further, the patient had received psychodynamic therapy and rape counselling prior to receiving EMD. Thus, the fact that several other treatment techniques besides EMD makes it difficult to draw conclusions about the efficacy of EMD per se.
Renfrey & Spates (1994) suggest that the most thorough single case replication of Shapiro’s work was a report concerning the treatment of a 40-year-old counselling psychologist who was the victim of a shooting (Kleinknecht and Morgan, 1992). During the EMD treatment, two further traumatic memories were elicited. The first of these was the memory of a fatal car crash in which the patient (who had been the driver) lost his wife and unborn child. The application of EMD to this trauma elicited a further anxiety provoking memory from the patient’s late teens when he had worried about the effect of imprisonment (for being a conscientious objector to the Vietnam war) on his claustrophobia.
Formal psychological assessments, including the Brief Symptom Inventory (BSI: Derogatis & Spencer, 1982), the State-Trait Anxiety Scale (STAI-Trait Form Y: Spielberger, Gorusch, Luschene, Vagg & Jacobs, 1983) and the Centre for Epidemiological Studies Depression Scale (CES-D: Weismann, Sholomkas, Pottenger, Prusoff & Locke, 1977) were administered pre-treatment and at 4 and 8 month follow up. The patient received two sessions comprising history-taking, relaxation and anxiety management prior to administration of the EMD procedure.
The authors report reductions on all clinical dimensions of the BSI as well as significant improvements on the STAI and CES-D. The patient also made a post-treatment statement in which he claims that previously disturbing visual images were diffuse and no longer emotionally charged. Further, he reported substantial reductions in hypervigilance as well as collateral improvements socially in terms of his self-image and confidence.
Although the study does appear to demonstrate overall clinical improvements, the measures used failed to cover the full range of PTSD symptomatology. There was no assessment of the extent of the patient’s PTSD using a standardised instrument, e.g. the Clinician Administered PTSD Scale (CAPS: Blake, Weathers, Nagy, Kaloupek, Klauminzer, Charney & Keane, 1990). Further, no objective data were available to verify the collateral improvements claimed. Finally, the patient studied was unusual. He had received psychological training that may have offered him an advantage in maximising any help offered. Further, there is no suggestion that he had received previous treatments that had failed. Thus, other treatments may have proved to be equally effective, for example.
While the collection of single-case studies provide a useful indication that EMD maybe a promising treatment for aspects of PTSD that is worthy of further consideration, they offer only limited evidence in evaluating its efficacy. This is because generally, single-case designs are limited in their capacity to validate cause-effect relationships (Kazdin, 1992). Single case designs lack a comparative control and are, therefore, susceptible to ‘false-positive’ results (Type I Error).
Controlled Outcome StudiesEdit
There have been a number of controlled outcome studies of varying quality. Shapiro (1989b) carried out the first systematic investigation of the efficacy of her new treatment method with a patient group of 22 rape and molestation victims, and Vietnam Veterans. She used anxiety levels, the validity of positive self-statements and self-assessments (VoC: Validity of Cognitions ) and presenting complaints as dependent variables. The group varied considerably in the length of time they had experienced the symptoms prior to treatment and the number of years of previous treatment.
Shapiro claimed that a single session of EMD was sufficient to reduce the mean value of the Subjective Units of Disturbance (SUD) for the cohort from 7.45 to 0.13 compared with no appreciable change in the control group. The effect was maintained at 3-month follow-up when additional behavioural change resulting in collateral symptom alleviation had also occurred. However, treatment was terminated when patients reported a SUD reduction to 0 or 1. Thus, demand characteristics, alone, could explain the impressive improvement. For example, patients may have reported a reduction in SUD scores merely because they knew that this was expected and wished to comply with the therapist’s demands. Further, if patients experienced the revisualisation of their trauma as aversive, they might have been motivated to end the session as quickly as possible by reporting a substantial decrease in their SUD score. Herbert and Mueser (1992) note that the study was further confounded because the requirement for patients to report a SUD score of 0 or 1, in order to terminate the session, was only placed on the experimental group and not upon the control group.
Sanderson and Carpenter (1992) employed a two-treatment crossover design to compare EMD with Image Confrontation (IC). The IC technique was identical to EMD except that these patients were instructed to keep their eyes closed and stationary. Both techniques were applied to patients with a variety of phobic disorders. The authors reported significant and equivalent reductions in the SUD scores associated with both treatments. The 8 patients with trauma symptoms did best. However, standardised psychological tests were not employed and the crossover design precluded the analysis of the unique effects of EMD and IC. Although Shapiro’s (1989b) control group was almost identical in nature to the IC group in Sanderson and Carpenter’s study, she noted a significant difference between the experimental and control group, whilst no such difference between the EMD and IC groups was observed. This may provide further evidence that the extent of the success in the Shapiro study was exaggerated owing to the effects of the demand characteristics already discussed.
Boudewyns, Stwertka, Hyer, Albrecht, & Sperr (1993) used psychological, physiological and standardised diagnostic measures in a controlled study of EMD to treat combat related PTSD in Veterans hospital patients. Prior to treatment, all patients recorded their traumatic experiences on audiotape. Patients were then randomly divided into three groups. One group was treated with EMD, one group received an exposure control procedure and the last group received a milieu control procedure. They noted a significantly greater reduction in SUD scores for the EMD and exposure control groups (with the greatest reductions achieved in the EMD group) than displayed by the milieu control group. When the audiotape was played back to patients following treatment, there was no significant difference in physiological reactivity between the groups. Indeed, none of the treatments appeared to affect physiological reactivity. Further, there were no pre- and post treatment differences for any of the conditions on the CAPS (Blake et al., 1990), Impact of Events Scale (IES: Horowitz, Wilner & Alvarez, 1979) and the Mississippi PTSD Scale (Keane, Cadell & Taylor, 1986).
In evaluating the effectiveness of EMD in the treatment of PTSD, it is imperative that outcome measures have adequate construct validity. For example, Puk (1991) reported that the patient was able to reduce the vividness of his visualisations. However, vividness of the image only relates to one dimension of the PTSD syndrome. Similarly, Richards and Rose (1991) used an exposure approach in their treatment of PTSD. They utilised measures of depression, phobic anxiety and social adjustment as outcome measures. However, if any treatment for PTSD is being evaluated, then its effect on the whole range of PTSD symptoms must be considered. This point has been observed by other authors (Baggaley, 1991; Vaughan, Wiese, Gold, & Tarrier, 1994a).
This issue was addressed by Forbes, Creamer and Rycroft (1994) in a study of eight patients. They used a variety of instruments including a structured interview (SI-PTSD: Davidson, Smith & Kudler, 1989), the SCL-90-R (Derogatis, 1977), the Beck Depression Inventory (BDI: Beck, Rush, Shaw & Emery, 1979) and the Impact of Events Scale (IES: Horowitz, Wilner & Alvarez, 1979). Comorbidity was assessed using the Structured Clinical Interview for DSM-III-R (SCID-NP: Spitzer, Williams, & Gibbon, M, 1987)). The possibility that the EMD protocol has features reminiscent of hypnosis was investigated using the Stanford Hypnotic Clinical Scale (SHCS: Morgan & Hilgard, 1975). The authors reasoned that the dramatic results of EMD might be attributable to suggestibility. Finally, electromyography (EMG) was used to measure possible physiological changes resulting from EMD.
In comparisons between pre- and post treatment scores, the authors found significant decreases in intrusion, avoidance and hyper-arousal on the SI-PTSD and decreases in intrusion and avoidance on the IES. They also observed significant decreases on the BDI and on the Global Severity Index of the SCL-90-R. These improvements were maintained at 3-month follow-up. Although significant improvements were observed in 6 of the 8 patients, 50% continued to meet the criteria for PTSD post-treatment and at follow-up.
EMG results indicated a decrease in physiological reactivity with progressive EMD treatments although these results did not correlate significantly with SI-PTSD data. The authors found a modest positive correlation between overall symptom reduction (i.e. the total SI-PTSD score) and suggestibility as measured by the Stanford Hypnotic Clinical Scale (SHCS: Morgan & Hilgard, 1975). The authors submit that suggestibility is a measure of the degree to which patients can generate images. Consequently, treatment success may depend of the ability of patients to visualise traumatic scenes. Finally a negative relationship between chronicity and longer term response to treatment was observed, supporting the view that chronic forms of PTSD are more resistant to treatment (Peterson, Prout and Schwartz, 1991). Although the study offers support for the efficacy of EMD, the small sample size used in the study and the absence of any form of control group are reasons to be cautious about over-interpretation.
In a study of 10 patients, Vaughan, Wiese, Gold, & Tarrier (1994a) found EMD effective for the re-experiencing, hyper-arousal and avoidance categories of the DSM-III-R. A significant reduction in depression was also seen although this and the hyper-arousal results were not maintained at follow-up.
Vaughan, Armstrong, Gold, O’Connor, Jenneke, & Tarrier (1994b) compared EMD with image habituation training (IHT) and applied muscle relaxation (AMR) in 36 randomly assigned PTSD patients. In IHT, patients were required to listen to continuous audiotaped loops of descriptions of their trauma. They then recorded cognitions and anxiety levels on a homework sheet. The treatment took approximately 60 minutes per day. It has been reported as being effective in PTSD by Vaughan and Tarrier (1992). Patients in the AMR group were taught to recognise their own symptoms of anxiety so that they could apply Ost’s (1987) progressive relaxation technique. The relaxation was practised for two 20-minute sessions each day.
Patients in all three groups were initially assessed using the SI-PTSD (Davidson, Smith & Kudler, 1989), the STAI (Spielberger, 1983), the BDI (Beck, 1978) and the IES (Horowitz, Wilner & Alvarez, 1979). Comorbidity was also assessed using the Anxiety Disorders Interview Schedule (ADIS-R: Di Nardo & Barlow, 1988) and the Hamilton Rating Scale for Depression (HRSD: Hamilton, 1960). Seventeen of the patients were initially assigned to a waiting list after assessment and then reassessed two to three weeks later prior to undergoing treatment. The groups were balanced with respect to number of treatment sessions, demographic and trauma-related variables.
Significant reductions in hyper-arousal and avoidance symptoms between waiting list and post-treatment assessment occurred for all three groups. However, at post-treatment, 47% of patients still met the criteria for PTSD. At 3-month follow-up this had fallen further to 30%. Significant reductions in total PTSD symptoms for all three groups were observed. Further, reductions in hyperarousal were seen in the EMD and IHT groups. Although improvements were seen across all three groups with regard to re-experiencing and intrusive symptoms, only EMD produced significant improvements in ‘flashbacks’, nightmares and avoidance symptoms. Patients perceived therapists in the EMD group to show more ‘warmth’ than in the other two conditions although they did not report differences in genuineness or empathy. EMD may rely on greater patient-therapist interaction than does IHT or AMR. If so, this could account for the difference in perceived warmth.
The absence of a true placebo condition is a flaw in the methodology given that placebo treatments have been shown to be superior to waiting lists (McConaghy, 1990). Additionally, although all patients had symptoms identified in the DSM-III criteria, 22% failed to meet all the criteria required for a diagnosis of PTSD. Small numbers in each group in the study make it difficult to draw clear conclusions about the relative effectiveness of one treatment over another. However, given that EMD was superior with respect to nightmares and flashbacks and that it does not require the homework commitment associated with IHT and AMR, it may be that EMD is at least as effective as these alternatives and in less treatment time, too.
Wilson, Becker and Tinker (1995) assigned 80 patients to either an immediate treatment, or delayed treatment, group. Only 37 of the patients met the criteria for a diagnosis of PTSD. The key criterion for inclusion in the study was that patients had to have experienced some traumatic memory that interfered with their lives. Both groups of patients received 3 EMD sessions. The SUDS, VoC, IES, STAI and SCL-90-R were used as process or outcome measures. Patients assigned to each of the groups were matched demographically and for length of trauma. The demand characteristics issue was addressed by using an independent assessor. They found a decrease in SUDS and concomitant increase in VoC, which were maintained at 90-day follow-up. However, as has been the case with many studies, comorbidity was inadequately assessed. The authors suggest that whilst EMD may be effective for the treatment of specific intrusive and avoidant aspects of PTSD, the impact of the technique on more general psychological functioning (as measured by the SCL-90-R, for example) is less clear.
Unsuccessful treatments using EMDEdit
A number of studies are reported in the literature that describe unsuccessful treatments using EMD. However, without exception, these are fraught with methodological flaws that do not support the notion that EMD may be a non-efficacious treatment for PTSD.
The study by Oswalt, Anderson, Hagstrom & Berkowitz (1993) on the EMD treatment of 8 patients provides an early attempt to replicate the findings of Shapiro. Only 3 patients were judged to have been successfully treated and they were regarded by the authors to have the least pathology. However, the study can be considered methodologically unsound for the following reasons: The patients were recruited via an advert in a campus newspaper. Of the eight who responded, 5 were hospital inpatients who had been diagnosed as having PTSD. However, no independent assessment of the cohort's PTSD status was made. Further, no account was taken of the patient’s mental health status in general and whether they were suffering from any form of psychiatric disorder that would have precluded them from a well designed study (e.g. personality disorder, psychosis etc.). In fact, the only criterion for inclusion in the study was a report of intrusive traumatic memories. Although Oswalt et al. (1993) claim to have followed Shapiro’s method exactly, this was not the case. In addition to therapist and patient being present in the room, a researcher and psychology student were also present to make observations. The study failed to use standardised psychological tests to assess treatment effect (using only the SUD scale and patient post-treatment reports about whether the memories were still ‘bothersome’). Additionally, there was no indication that the Validity of Cognitions scale (VoC) was used as in the original Shapiro method. Finally, in contrast to Shapiro’s (1989b) study, the authors failed to include a control group in their study. In view of the shortcomings of this study, it fails to qualify as a reasonable replication of Shapiro’s work and tells us nothing about the efficacy of EMD. It does suggest that a degree of caution must be adopted in the selection of patients who might benefit from the approach.
In a laboratory experiment to test whether EMD reduces the aversiveness of visual imagery, Merckelbach, Hogervorst, Kampman and de Jongh (1994) found no significant reduction in heart rate, ability to visualise an aversive stimulus or the perceived aversiveness of the stimulus after EMD. Further, there was no difference between the experimental group and a finger-tapping control group. However, it could be argued that the experimental situation differs markedly from a ‘real life’ traumatic situation in that PTSD victims have to contend with considerably more than a simple aversive visual stimulus. For example, some authors have argued that in PTSD a classically conditioned association is produced between the emotional response to the situation and the entire contents of the memory buffer that occurs during the trauma (Pearce, 1987; Dyck, 1993). Further, recent evidence from a study of PTSD (using Positron Emission Tomography (PET scan) and script-driven imagery) suggests that the emotions associated with PTSD are mediated within the limbic and paralimbic systems within the right hemisphere (Rauch, van der Kolk, Fisler, Alpert, Orr, Savage, Fischman, Jenike & Pitman, 1996). One implication from this study is that information processing in PTSD may not comprise a verbal component. Thus, it is possible that information processing, in the case of highly personalised trauma, is different to that involved in dealing with a non-personal aversive stimulus. It is unlikely that the aversive stimulus evoked personal cognitive statements (e.g. “I am helpless” or “I am going to die”) as is the case with PTSD. This precluded an essential aspect of EMD treatment (Shapiro, 1991) which is the ‘reprocessing’ of these cognitions.
Jensen (1994) examined 25 Vietnam veterans who met the criteria for PTSD. All patients received a pre-treatment structured interview prior to random assignment to the treatment or control group. The SUD scale was utilised as was the VoC scale. Post-treatment measures included the Mississippi PTSD Scale (Keane, Cadell & Taylor, 1986) and Goal Attainment Scaling (Kiresuk & Sherman, 1968). The control group comprised a group of veterans who simply accessed Veteran Administration services ad libitum. The experimental group received two treatment sessions of EMD within a 10-day period. Jensen reports no significant differences on the post-treatment measures between the groups although there was a significant reduction in SUD scores in the treatment group when compared with the control group. However, Lohr et al. (1995) suggest that the Mississippi PTSD Scale is based on historical information and may not be a sensitive measure of symptom change. Further, a number of authors have noted a negative correlation between chronicity of PTSD and successful treatment outcome (Peterson, Prout and Schwartz, 1991; Forbes, Creamer & Rycroft, 1994). Finally, EMD requires that the procedure be repeated for each traumatic image. Whilst is possible that some of the patients may have only required one or two sessions, it is likely that many would have required several sessions if there was to be any reasonable chance of the EMD being effective. Nevertheless, the study does suggest that Shapiro’s claim that 60-70% of patients will improve after a single session cannot be generalised to all PTSD populations. Furthermore, the efficacy of EMD with combat veterans suffering from chronic PTSD has yet to be established.
Summary and ConclusionsEdit
Of the seventeen studies considered in this review, 13 (7 single-case design and 6 controlled outcome studies) found evidence to suggest that EMD may be a useful technique in the treatment of PTSD.
Three studies found no evidence to support the use of EMD in the treatment of PTSD. The first of these (Oswalt et al., 1993) was severely methodologically flawed. The researchers used a small highly selected group (respondents to an advertisement) of which 5 patients were hospitalised psychiatric patients. No account of comorbidity was taken. Furthermore, the authors failed to independently assess the subjects’ PTSD status using a standardised assessment. The only measure used was the SUD scale. Finally, the procedure used failed to include central aspects of the EMD treatment (i.e. use of the VoC scale) and the patients were required to undergo the treatment with an audience of at least three people, two of whom were unknown to them.
It is true that the laboratory study by Merckelbach et al. (1994) which failed to find reductions in heart rate or the ability to visualise an aversive stimulus following EMD did not specifically set out to evaluate EMD as a treatment for PTSD.
Nevertheless, it does serve as a warning about the limitations of analogue studies. PTSD is a highly personal syndrome in which the patient was confronted by a situation involving actual or threatened death or severe injury. All of the symptoms of PTSD are based upon this fundamental aspect of the disorder. Thus, it is possible that information from an aversive stimulus that is not considered personal will be processed in a different way to intensely personal traumatic information. Consequently, this study neither supports nor refutes the claimed efficacy of EMD as a procedure for treating PTSD.
The study by Jensen (1994) suggests that Shapiro’s claim that EMD is effective 60-70% of patients after the first session is excessive, at least when war veterans with chronic PTSD are considered. It also lends further weight to the assertion of other authors that there is a negative correlation between chronicity and successful outcome when EMD is applied to PTSD (Peterson, Prout and Schwartz, 1991; Forbes, Creamer & Rycroft, 1994).
Owing to the variability in research designs employed by the various authors reviewed, it is difficult to fully evaluate the efficacy of EMD in the treatment of PTSD. Even so, a number of observations can be drawn from the literature. To begin with, none of the studies provided conclusive evidence that EMD is a comprehensive treatment for all aspects of PTSD. Indeed, evidence from some studies suggests that as many as 50% of patients continued to meet the criteria for PTSD post-treatment (e.g. Forbes, Creamer & Rycroft, 1994; Vaughan et al., 1994b). Additionally, the effect of EMD on general psychological functioning remains unclear. Whilst some authors report reductions in depression and anxiety (e.g. Renfrey & Spates, 1994; Forbes, Creamer & Rycroft, 1994) others suggest that their results were less clear (e.g. Boudewyns et al., 1993; Wilson, Becker & Tinker, 1995). There is also clear evidence that alternative approaches to EMD are effective in reducing some of the symptoms associated with PTSD (Sanderson & Carpenter, 1992; Boudewyns et al., 1993; Vaughan et al., 1994b). Finally, as has been stated, it may transpire that EMD is of limited utility in patients with long-term PTSD.
There are a number of positive indications that emerge from the literature. Thus, several authors agree that EMD seems to be particularly effective in reducing intrusion and avoidance symptoms in PTSD (e.g. Shapiro, 1989; Puk, 1991; Renfrey & Spates, 1994; Sanderson & Carpenter, 1992; Forbes, Creamer & Rycroft, 1994; Vaughan et al., 1994; Wilson, Becker & Tinker, 1995). Further, whilst other treatments were shown to be effective in reducing these symptoms (Sanderson & Carpenter, 1992, Boudewyns et al., 1993; Vaughan et al., 1994b), EMD appears to have been more effective than these alternatives. Finally, when effective, EMD seems to require less treatment time than any of the alternatives examined (e.g. Vaughan et al., 1994b).
There are practical advantages to a technique that requires relatively few sessions (thus preventing prolonged high levels of anxiety) and does not require the (unreliable) compliance associated with homework. The fact that EMD appears to be an effective treatment for some aspects of PTSD and not others, may be evidence for the multi-factorial structure of the PTSD syndrome. It is suggested that there is sufficient evidence to warrant continuing research into the application of EMD for treating PTSD. Future research should address itself to the deconstruction of the EMD procedure to establish exactly how the technique produces its effects. The development of a clear theoretical basis for the technique may result in it being better targeted and, consequently, more effective.
American Psychiatric Association (1980). Diagnostic and Statistical Manual for Mental Disorders (3rd Edition) (DSM-III). Washington DC: APA.
American Psychiatric Association (1995). Diagnostic and Statistical Manual for Mental Disorders (3rd Edition) (DSM-IV). Washington DC: APA.
Beck, A. T., Rush, A. J., Shaw, B. F. & Emery, G. (1977). Cognitive Therapy of Depression. New York: Guilford Press.
Beck, A. T. (1978). Depression Inventory. Philadelphia: Centre for Cognitive Therapy. Baggaley, M. R. (1991). Exposure therapy for PTSD (letter). British Journal of Psychiatry, 159, 732-733.
Blake, D. D., Weathers, F. W., Nagy, L. M., Kaloupek, D. G., Klauminzer, G., Charney, D. S. & Keane, T. M. (1990). A clinical rating scale for assessing current and lifetime PTSD. The Behavior Therapist, 13, 187-188.
Boudewyns, P. A., Stwertka, S. A., Hyer, L. A., Albrecht, J. W. & Sperr, E. (1993). Eye movement desensitization for PTSD of combat: a treatment outcome pilot study. The Behavior Therapist, 13, 187-188.
Davidson, J., Smith, R. & Kudler, H. (1989). Validity and reliability of the DSM-III criteria for posttraumatic stress disorder. Experience with a structured interview. Journal of Mental and Nervous Disease, 177, 336-341.
Derogatis, L. R. (1977). SCL-90-R: Administration, scoring and procedures manual - II. Towson, MD: Clinical Psychometric Research.
Derogatis, L. R. & Spencer, P. M. (1982). The Brief Symptom Inventory: administration, scoring & procedures manual - I. Baltimore: Clinical Psychometric Research.
Di Nardo, P. A., & Barlow, D. H. (1988). Anxiety Disorders Interview Schedule Revised (ADIS-R). Albany, N.Y.: Centre for Stress and Anxiety Disorders.
Dyck, M. J. (1993). A proposal for a conditioning model of eye movement desensitization treatment for posttraumatic stress disorder. Journal of Behavior Therapy and Experimental Psychiatry, 24, 201-210.
Fairbank, A. J. & Brown, T. A. (1987). Current behavioral approaches to the treatment of posttraumatic stress disorder. Behavior Therapist, 3, 57-64.
Forbes, D., Creamer, M. & Rycroft, P. (1994). Eye movement desensitization and reprocessing in posttraumatic stress disorder: a pilot study using assessment measures. Journal of Behavior Therapy and Experimental Psychiatry, 25, 113-120.
Herbert, J. D. & Mueser, K. T. (1992). Eye movement desensitization: a critique of the evidence. Journal of Behavior Therapy and Experimental Psychiatry, 23, 169-174.
Horowitz, M. D., Wilner, N. & Alvarez, W. (1979). Impact of event scale: a measure of subjective stress. Psychosomatic Medicine, 41, 209-218.
Jensen, J. A. (1994) An investigation of Eye Movement Desensitisation and Reprocessing (EMD/R) as a treatment of post-traumatic stress disorder (PTSD) symptoms of Vietnam combat veterans. Behavior Therapy, 25, 311-325.
Kazdin, A. (1992). Research design in clinical psychology: Second Edition. General Psychology Series. Allyn & Bacon.
Keane, T. M., Cadell, J. M. & Taylor, K. L. (1986). The Mississippi Scale for Combat-related PTSD: three studies in reliability and validity. Journal of Consulting and Clinical Psychology, 56, 85-90.
Keane, T. M., Fairbank, J. A., Cadell, J. M. et al.(1989). Implosive (flooding) therapy reduces symptoms of PTSD in Vietnam combat veterans. Behavior Therapy, 20, 245-260.
Kiresuk, T. J., & Sherman, R. E. (1968). Goal Attainment Scaling: general method for evaluating comprehensive community mental health programmes. Community Mental Health, 4, 443-453.
Kleinknecht, R. A. & Morgan, M. P. (1992). Treatment of posttraumatic stress disorder with eye movement desensitization. Journal of Behavior Therapy and Experimental Psychiatry, 23, 43-49.
Lipke, H. J. & Botkin, A. L. (1992). Case studies of eye movement desensitisation and reprocessing (EMDR) with chronic post-traumatic stress disorder. Psychotherapy, 29, 591-595.
Lohr, J. M., Kleinknecht, R. A., Tolin, D. F. & Barrett, R. H. (1995). The empirical status of the clinical application of eye movement desensitization and reprocessing. Journal of Behavior Therapy & Experimental Psychiatry, 26, 285-302.
Marquis, J. N. (1991). A report on seventy-eight cases treated by eye movement desensitisation. Journal of Behavior Therapy and Experimental Psychiatry, 22, 187-192. McCann, D. L. (1992). Post-traumatic stress disorder due to devastating burns overcome by a single session of eye movement desensitization. Journal of Behavior Therapy and Experimental Psychiatry, 23, 319-323.
McConaghy, N (1990). Can reliance be placed on a single meta-analysis? Australian and New Zealand Journal of Psychiatry, 24, 405-418.
Merckelbach, H., Hogervorst, E., Kampman, M. & de Jongh, A. (1994). Effects of “Eye Movement Desensitisation” on emotional processing in normal subjects. Behavioural and Cognitive Psychotherapy, 22, 331-335.
Morgan, A. H. & Hilgard, J. R. (1975). The Stanford Hypnotic Clinical Scale. In E. R. Hilgard and J. R. Hilgard Hypnosis in the Relief of Pain. Los Altos, California: William Kauffman.
Ost, L. G. (1987). Applied relaxation: description of a coping technique and review of controlled studies. Behavior Research and Therapy, 25, 397-409. Oswalt, R., Anderson, M., Hagstrom, K. & Berkowitz, B. (1993). Evaluation of the one-session eye-movement desensitization reprocessing procedure for eliminating traumatic memories. Psychological Reports, 73, 99-104.
Pearce, J. (1987). A model for stimulus generalisation in Pavlovian conditioning. Psychological Review, 94, 61-73.
Peterson, K. C., Prout, M. F. & Schwartz, R. A. (1991). Post-traumatic stress disorder: a clinician’s guide. Plenum Press, New York.
Puk, G. (1991). Treating traumatic memories: a case report on the eye movement desensitisation procedure. Journal of Behavior Therapy and Experimental Psychiatry, 22, 149-151.
Rauch, S. L., van der Kolk, B. A., Fisler, R. E., Alpert, N. M., Orr, S. P., Savage, C. R., Fischman, A. J., Jenike, M. A. & Pitman, R. K. (1996). A symptom provocation study of posttraumatic stress disorder using positron emission tomography and script-driven imagery. Archives of General Psychiatry. 53, 380-387.
Renfrey, G. & Spates, C.R. (1994). Eye Movement Desensitization: A Partial Dismantling Study. Journal of Behavior Therapy and Experimental Psychiatry, 25, 231-239.
Richards, D. A. & Rose, J. S. (1991). Exposure therapy for post-traumatic Stress Disorder. Four case studies. British Journal of Psychiatry, 158, 836-840. Rosen, G. M. (1995). On the origin of eye movement desensitization. Journal of Behavior Therapy and Experimental Psychiatry, 26, 121-122.
Sanderson, A. & Carpenter, R. (1992). Eye movement desensitization versus image confrontation: a single session crossover study of 58 phobic subjects. Journal of Behavior Therapy and Experimental Psychiatry, 23, 269-275.
Shapiro, F. (1989a). Eye movement desensitisation: a new treatment for post-traumatic stress disorder. Journal of Behavior Therapy and Experimental Psychiatry, 20, 211-217. Shapiro, F. (1989b). Efficacy of the eye movement desensitisation procedure in the treatment of traumatic memories. Journal of Traumatic Stress, 2, 199-223.
Shapiro, F. (1991). Eye movement desensitization and reprocessing: from EMD to EMD/R - a new treatment model for anxiety and related traumata. The Behavior Therapist, 14, 133-135.
Spates, C. R. & Burnette, M. M. (1995). Eye movement desensitization: three unusual cases. Journal of Behavior Therapy and Experimental Psychiatry, 26, 51-55.
Spector, J. & Huthwaite, M. (1993). Eye movement desensitisation to overcome post-traumatic stress disorder. British Journal of Psychiatry, 163, 106-108.
Spielberger, C., Gorusch, R. L., Luschene, R., Vagg, P. R. & Jacobs, G. A. (1983). Manual for the Stait-Trait Anxiety Inventory (STAI (Form Y)). Palo Alto. CA: Consulting Psychologist Press.
Spitzer, R. L., Williams, J. B., & Gibbon, M. (1987). Structured Clinical Interview for DSM-III-R (SCID). New York: Biometrics Research Department, New York State Psychiatric Institute.
Vaughan, K. & Tarrier, N. (1992). The use of image habituation training with post-traumatic stress disorders. British Journal of Psychiatry, 161, 658-664.
Vaughan. K., Wiese, M., Gold, R. & Tarrier, N. (1994a). Eye-Movement Desensitisation: Symptom Change in Post-Traumatic Stress Disorder. British Journal of Psychiatry. 164, 533-541.
Vaughan, K., Armstrong, M. S., Gold, R., O’Connor, Jenneke, W., & Tarrier, N. (1994b). A trial of eye movement desensitisation compared to image habituation training and applied muscle relaxation in post-traumatic stress disorder. Journal of Behavior Therapy and Experimental Psychiatry, 25, 283-291.
Welch, R. B. (1996). On the origin of eye movement desensitization and reprocessing: A response to Rosen. Journal of Behaviour Therapy and Experimental Psychiatry. 27, 175-179.
Weismann, M., Sholomkas, D., Pottenger, M., Prusoff, B. & Locke, B. (1977). Assessing depressive symptoms in five psychiatric populations: A validation study. American Journal of Epidemiology, 106, 203-214.
Wilson, S. A., Becker, L. A. & Tinker, R. H. (1995). Eye movement desensitisation and reprocessing (EMDR) treatment for psychologically traumatized individuals. Journal of Consulting and Clinical Psychology, 6, 928-937.
Wolpe, J. (1982). The Practice of Behavior Therapy. New York: Pergamon.
Wolpe, J. & Abrams, J. (1991). Post-traumatic stress disorder overcome by eye-movement desensitisation: a case report. Journal of Behavior Therapy and Experimental Psychiatry, 22, 39-43.
Wolpe, J. & Lang, P. J. (1969). Fear Survey Schedule, San Diego, CA: Educational and Industrial Testing Service.