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Published online before print November 8, 2007, 10.1097/PSY.0b013e31815aa325
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Psychosomatic Medicine 70:13-19 (2008)
© 2008 American Psychosomatic Society

ORIGINAL ARTICLES

Changes in Brain Electrical Activity After Cognitive Behavioral Therapy for Posttraumatic Stress Disorder in Patients Injured in Motor Vehicle Accidents

Sirko Rabe, MA, Tanja Zoellner, MA, Andrë Beauducel, PhD, Andreas Maercker, PhD and Anke Karl, PhD

From the Biopsychology (S.R., A.K.), Dresden University of Technology, Dresden, Germany; Saxonian Hospital Groβschweidnitz, Germany; Roseneck Hospital (T.Z.), Prien am Chiemsee, Germany; Personality Psychology (A.B.), University of the Federal Armed Forces, Hamburg, Germany; Department of Abnormal Psychology (A.M.), University of Zurich, Zurich, Switzerland; School of Psychology (A.K.), University of Southampton, Southhampton, UK.

Address correspondence and reprint requests to Anke Karl, School of Psychology, University of Southampton, Southampton, SO171BJ, UK. E-mail: karl{at}soton.ac.uk


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: To explore changes for the first time in neural processing due to effective cognitive behavioral therapy (CBT) in posttraumatic stress disorder (PTSD) after severe motor vehicle accidents. Recent studies have highlighted the role of right hemisphere activation during withdrawal-related emotions (e.g., anxiety). There has been little research on changes in brain function due to cognitive-behavioral interventions in anxiety disorders.

Methods: We conducted a randomized, controlled trial comparing cognitive-behavioral therapy with an assessment-only Wait-list condition. Spontaneous electroencephalographic activity was recorded from left and right anterior and posterior regions in participants with PTSD/subsyndromal PTSD receiving CBT (n = 17) before and after a CBT program. Wait-list controls (n = 18) were investigated before and after 3 months.

Results: At the pretreatment assessment, a pattern of increased right-sided activation during exposure to a trauma-related picture (relative to a neutral picture) was observed in both CBT and Wait-list participants. At posttreatment, there was a greater reduction of right anterior activation in the CBT group as compared with Wait-list controls. Across both groups, PTSD symptom reduction was significantly positively correlated with a decrease in right anterior activation to the trauma stimulus.

Conclusions: These findings suggest that effective CBT treatment of PTSD may be accompanied by adaptive changes in asymmetrical brain function. Future studies are needed to confirm our findings.

Key Words: cognitive-behavioral therapy • posttraumatic stress disorder • electroencephalography • alpha • asymmetry

Abbreviations: CBT = cognitive behavioral therapy; PTSD = posttraumatic stress disorder; EEG = electroencephalography; MDD = major depression; CAPS = Clinician Administered PTSD Scale; PANAS = Positive and Negative Affective Scale; MANOVA = multivariate analysis of variance.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Models of brain asymmetry and emotion proposed that greater left frontal activation is associated with approach motivation, emotion, and behavior, whereas greater right frontal cortical activation is associated with withdrawal motivation, emotion, and behavior (1–4). Evidence for these assumptions comes from research investigating brain asymmetries in the {alpha} band of the electroencephalogram (EEG) as an inverse index of brain activation (5). According to these hypotheses, studies investigating EEG asymmetries in anxiety disorders reported increased right anterior activation during symptom provocation in panic patients (6), social phobics (7), and Vietnam veterans with posttraumatic stress disorder (PTSD) (8). Recently, Metzger et al. (9) reported an association of PTSD arousal symptoms with increased relative right parietal activity during a resting condition in a sample of female Vietnam War nurse veterans. This finding was consistent with the suggestion of Nitschke, Heller, and colleagues (10,11), who proposed that anxious arousal is related to increased right posterior activation.

In a recent study, we examined brain electrical activity in motor vehicle accident (MVA) survivors with PTSD, subsyndromal PTSD, and without PTSD as well as healthy controls without severe MVA during baseline and during confrontation to neutral, positive, negative, and trauma-related pictures (12). We found that participants with PTSD and subsyndromal PTSD showed a pattern of enhanced right anterior and posterior activation in response to the trauma-related accident picture. This trauma-specific increase in relative right hemisphere activation was correlated with increased negative affect and PTSD symptoms. The findings of increased right hemisphere activation in PTSD were in accordance with neuroimaging findings in PTSD (13,14) and PTSD among other anxiety disorders (15).

The aim of the present study was to examine whether the pattern of increased right hemisphere asymmetry observed in MVA survivors with chronic PTSD and subsyndromal PTSD will change due to treatment with cognitive-behavioral therapy (CBT). There has been little research on changes of brain asymmetry due to therapeutic interventions. In a recent study, Davidson et al. (16) examined changes in brain electrical asymmetry and immune function after a meditation program. They found that the meditation group showed significant larger increases in left-sided anterior activation (during baseline and positive, negative emotion induction) compared with a Wait-list group. The increase in relative left anterior brain activity was associated with an increase in antibody titers to an influenza vaccine received immediately after the training program. In contrast, baseline anterior asymmetry has been found to be stable and unrelated to changes in clinical status due to bright light exposure in seasonal affective disorder (17) and acupuncture treatment for major depression (18). Furthermore, Deldin and Chiu (19) showed that baseline frontal asymmetry is stable in individuals with major depression before and after a cognitive intervention but may predict treatment response.

There are few neuroimaging studies investigating brain changes due to psychotherapy (20). Functional changes of brain activity after successful psychological treatment have been reported for depression (21) and obsessive compulsive disorder (22). There are limited data available showing changes in regional brain activity due to CBT in anxiety disorders as social phobia (23), panic disorder (24), and simple phobia (25). Regarding PTSD, there is only one case study of a man who experienced violence in childhood (26). Brain activation during symptom provocation using script-driven imagery was measured before and after three sessions of eye movement desensitization and reprocessing (with parallel antidepressant treatment). At postassessment, two areas showed an increased activation: the anterior cingulate gyrus and the left frontal lobe.

CBT is an effective psychotherapeutic approach for reducing the symptoms of PTSD (27). It is designed to alter dysfunctional affective processing related to PTSD such as behavioral and emotional avoidance, intrusive recollections, and hyperarousal. Several mechanisms like habituation, change of interpretations of the traumatic event, and a change of maladaptive coping strategies have been suggested to explain the therapeutic effects. To our knowledge, there is no study that investigated the neural correlates of change due to CBT in PTSD. Therefore, we measured EEG activity before and after CBT (in comparison with an assessment-only Wait-list condition) as part of a previously completed controlled, randomized treatment trial for MVA-related PTSD (28). Because CBT leads to a decrease of PTSD symptoms and anxiety, we hypothesized that participants receiving CBT would exhibit a greater decrease in right anterior and posterior activation during exposure to a trauma-related accident picture compared with the Wait-list group.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participant Population
As described elsewhere (28), 42 participants with PTSD or subsyndromal PTSD completed the treatment trial and pre- and postassessments. They were recruited through self-referral local media coverage and advertising. All participants received a comprehensive description of the study and provided written informed consent at the initial diagnostic assessment. The protocol was approved by the ethics board of the Dresden University of Technology.

Current diagnosis of PTSD or subsyndromal PTSD was determined by a German version (29) of the Clinician Administered PTSD Scale (CAPS-DX or CAPS-1) (30). This scale represents a standardized interview that allows generating categorical diagnosis of current and lifetime PTSD as well as a total score obtained by summing the ratings of frequency and severity of each of the 17 PTSD symptoms (CAPS Score) according to the Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) (31). Subjects receiving PTSD diagnosis were required to meet all three symptom clusters (B through D) for PTSD according to the DSM-IV criteria. A diagnosis of subsyndromal PTSD (sub-PTSD) was given if the patients met the DSM-IV criteria B (Intrusion) and either Criterion C (Avoidance/Numbing) or Criterion D (Hyperarousal) following the most prominent definition of subsyndromal PTSD proposed by Blanchard and colleagues (32). Previous research has shown that the diagnosis of subsyndromal PTSD has clinical relevance and is associated with significant distress (33,34).

Exclusion criteria for the current investigation were 1) a history of neurological problems like epilepsy, brain surgery, brain damage, or severe head injury during the accident; 2) current alcohol and/or substance abuse or dependence; 3) current or past schizophrenic, bipolar, or psychotic disorder; and 4) any current treatment or psychotropic medication for at least 1 month before testing. We did not exclude participants with reversible neurological trauma (concussion and loss of consciousness). All participants were right-handed as assessed by the Edinburgh Handedness Inventory (35). Out of 42 participants of the treatment trial, five were excluded from the current study because they did not meet the inclusion criterion to be off psychotropic medication during the preassessment. Two participants were excluded because of EEG recording errors during the preassessment. The final sample included 35 patients—17 in the CBT group (10 PTSD, 7 sub-PTSD) and 18 in the Wait-list group (7 PTSD, 11 sub-PTSD). The CBT group and the Wait-list group did not differ significantly in the proportion of full PTSD to subsyndromal PTSD [{chi}2(1) = 1.39; p = .24]. EEG preassessment data of these participants have been part of a previous report on differences between persons with PTSD and without PTSD (12).

The Structured Clinical Interview for the DSM-IV (36,37) evaluated the presence of concurrent and lifetime DSM-IV Axis I disorders. Comorbid diagnoses in the CBT group were lifetime but not current major depression disorder (MDD) (n = 3), current MDD (n = 6), panic disorder without agoraphobia (n = 1), agoraphobia without panic disorder (n = 1), social phobia (n = 3), specific phobia (n = 1), obsessive compulsive disorder (n = 1), and lifetime generalized anxiety disorder (n = 1). Additional diagnoses in the Wait-list group were lifetime but not current MDD (n = 3), current MDD (n = 3), panic disorder without agoraphobia (n = 1), social phobia (n = 2), and specific phobia (n = 3).

Treatment Trial and Instruments
A full description of the randomized, controlled treatment trial has been published elsewhere (28). The study was conducted at the University of Technology Dresden, Germany, from April 2002 to February 2005. After the initial assessment, patients were matched into dyads based on CAPS Score, age, and comorbidity. The patients were then randomly assigned to one of two conditions: 1) CBT (n = 17, 15 females) or 2) Wait-list (n = 18, 10 females). The CBT was conducted according to a German adaptation and extension of the CBT manual of Hickling and Blanchard (38) and the work has been published previously (39). The CBT program consisted of 8 to 12 weekly sessions each about 1.5 hours. It includes standard CBT techniques for treatment of PTSD: writing exposure, prolonged imaginal exposure, in vivo exposure, cognitive restructuring, and relaxation training. Additionally, it includes new sections for treatment of guilt or anger and a section on facilitation of posttraumatic growth. The Wait-list control individuals were reassessed after 3 months and received CBT if they were still interested in treatment.

At postassessment, PTSD symptoms were assessed using a German version of the CAPS specifically designed for reassessments (CAPS-2) (40) asking for severity of PTSD symptoms during the last week. Several self-report psychological questionnaires were also utilized including a German version (41) of the Beck Depression Inventory (BDI) (42) for assessment of presence and severity of depressive symptoms. The Impact of Event Scale—Revised (IES-R; German version: Maercker and Schützwohl, 1998) (43) asked for self-reported PTSD symptoms of intrusions, avoidance, and hyperarousal. The German version (44) of the State-Trait Anxiety Inventory (STAI) (45) scored for both state anxiety and trait anxiety. State and trait affect were assessed by an extended German version (46) of the Positive and Negative Affect Schedule (PANAS) (47).

Electrophysiological Recording Procedure and Analysis
The procedure for measurement of EEG activity during baseline and mood induction was described in our previous report (12) and was identical between pre- and postassessments. Measures of EEG activity were obtained before assignment to each of the two treatment groups and then after completion of CBT (or after 3 months for Wait-list controls). EEG was recorded during an 8-minute baseline condition (48), followed by a presentation of four pictures, 1 minute each (neutral, positive, negative, and trauma-related). The accident picture was a photograph from a crashed car lying on the roof. The positive (two bunnies), negative (a barking dog), and neutral (spoon) pictures were taken from the International Affective Picture System (49). Following baseline and after viewing each picture, subjects rated their actual mood with the PANAS-state questionnaire.

EEG was recorded from 28 scalp placements (Fp1, Fp2, F7, F3, Fz, F4, F8, Fc5, Fc1, Fc2, Fc6, T7, C3, Cz, C4, T8, Cp5, Cp1, Cp2, Cp6, P7, P3, Pz, P4, P8, POz, O1, O2) according to the extended 10 to 20 system (50) using a stretchable electro cap (FMS, Falk Minow Services, Munich, Germany). Moreover, we recorded EEG activity at linked mastoid positions (A1, A2). All sites were online referenced to a computer averaged F3/F4 reference and grounded at AFz. Impedances were maintained below 5 k{Omega} and within 500 {Omega} at homologous sites. The EEG signal was recorded by a Nihon Kohden amplifier (NeuroFileII system, Tokyo, Japan), filtered with a time constant of 10 seconds and a high-frequency cut-off (300 Hz) and digitized online at 1024 Hz and stored at 256 Hz. A linked-mastoids reference was rederived off-line. Before further data processing, EEG artifacts (eye blinks and muscle artifacts) were removed by applying independent component analysis (51) to the EEG segments of interest. Before artifact screening, an off-line bandpass filter (1–30 Hz) was applied. Continuous EEG data were divided offline in 4-second epochs (50% overlap) and again visually inspected for artifacts. All epochs free of artifacts were subjected to a fast Fourier transformation using a Hamming window over the distal 50% of each epoch. By averaging segments, estimates of spectral power (µV2) were derived for 0.25 Hz bins, averaged between 8 and 13 Hz, and normalized (natural log) to obtain ln power density (ln µV2/Hz) in the {alpha} band. The {alpha} power is considered to be inversely related to cortical activity, with decreases in {alpha} power reflecting increases in activation (52,53).

To examine the emotion-induced activation relative to the neutral condition, we computed neutral-minus-emotion-condition change scores by subtracting {alpha} activity during the three emotional conditions (positive, negative, and trauma-related) from that of the neutral condition. Whereas a decrease in {alpha} power is inversely related to activity, positive change scores indicate greater activation during emotion compared with neutral condition. All reported effects are based on these change scores. This approach has the advantage of controlling individual differences in the total amount of recorded {alpha} power, e.g., produced by individual differences in skull thickness or occasion specific fluctuations. Furthermore, it allows examining changes in brain activation within one hemisphere instead of only comparing asymmetry sores (right – left). Similarly to our previous report, we assessed {alpha} activity in four quadrants of the scalp. Therefore, we averaged electrode sites within left anterior (F3, F7, T7), right anterior (F4, F8, T8), left posterior (Cp5, P3, P7), and right posterior (Cp6, P4, P8) regions. This has the advantage of reducing the amount of data; according to the Spearman-Brown prophecy formula, it increases the reliability of anterior and posterior brain asymmetry measures.

Statistical Analyses
In this report, we examined the changes in brain electrical activation during viewing the trauma-related accident picture, because this was the only condition previously shown to discriminate symptomatic (PTSD, subsyndromal PTSD), and nonsymptomatic MVA victims and non-MVA controls (12). The statistical analysis focused on the interactions between Treatment-Group (CBT/Wait-list) and Time (Pre, Post). Repeated-measures multivariate analyses of variance (MANOVAs) were computed for anterior and posterior regions. Follow-up MANOVAs were performed for each group separately to examine changes in hemispheric activity.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Pretreatment Evaluation
CBT and Wait-list groups did not differ in age (CBT: mean = 38.65, SD = 11.47; Wait-list: mean = 41.89, SD = 11.03), and time since accident in months (CBT: mean = 74.18, SD = 114.61; Wait-list: mean = 41.39, SD = 32.77). There were no differences between groups in PTSD severity (CAPS Score) and questionnaire data (all t < 0.89, p > .34) (Table 1).


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  		TABLE 1. Pre- and Posttreatment Values (mean ± SD) for Symptom Severity Measures and State Negative Affect for the Trauma-Related Picture

 

Treatment Outcome Measures
For the assessment of differences in treatment outcome, we calculated a two-way repeated measures MANOVA on the CAPS Score with Time (Pre, Post) as within-subject factor and Treatment-Group (CBT, Wait-list) as between-subject-factor. This analysis revealed a significant interaction of Group x Time (F(1,33) = 25.32, p < .001, {eta}2 = 0.434) indicating a greater decrease in PTSD severity in the CBT group. Furthermore, there were significant Group x Time interactions for self-report measures of PTSD severity (IES-R), depression (BDI), anxiety (STAI), and trait negative affect (PANAS) (Table 1). There was no significant Group x Time interaction for ratings of state negative affect (PANAS) during exposure to the accident picture (F(1,33) = 1.78, p = .19). Because we a priori predicted a decrease in negative affect in the CBT group, we examined the change over time for each group separately. There was a significant reduction in negative affect (PANAS) in the CBT group (t(16) = .49, p = .003) but not for Wait-list participants (t(17) = 1.23, p = .24).

Electrophysiology
Based on our previous finding of increased right anterior and posterior activation during exposure to a trauma-related picture in PTSD and subsyndromal PTSD subjects, we predicted a greater decrease in right hemisphere activation in patients receiving CBT. We computed a repeated-measures MANOVA with Treatment-Group x Time x Hemisphere on {alpha} power change scores (neutral-trauma-related) for the anterior and posterior regions separately.1 For the anterior region, this analysis revealed a marginally significant Time x Hemisphere interaction [F(1,33) = 3.65, p = .06, {eta}2 = 0.100] and a trend for the predicted Treatment-Group x Time x Hemisphere interaction [F(1,33) = 3.49, p = .07, {eta}2 = 0.096].2 As can be seen in Figure 1, there was a greater reduction in relative right anterior activation in the CBT patients when compared with Wait-list controls. To test our prediction that the CBT group shows a decrease in hemispheric asymmetry, we conducted Time x Hemisphere MANOVAs for each group separately. For the CBT group, there was a significant Time x Hemisphere interaction [F(1,16) = 7.90, p = .01, {eta}2 = 0.331] indicating a shift in hemispheric asymmetry. This interaction was mainly an effect of a decrease in activity in the right [t(16) = 2.33, p = .03] but not the left anterior region [t(16) = 0.69, p = .50]. The Wait-list showed no change in hemispheric activity over time [Time x Hemisphere interaction: F(1,17) = 0.01, p = .98]. For the posterior region, there was a tendency for the Time x Hemisphere interaction [F(1,33) = 3.17, p = .08, {eta}2 = 0.088] but no significant Treatment-Group x Time x Hemisphere interaction [F(1,33) = 0.13, p = .72]. Analyses for each group separately revealed no significant Time x Hemisphere interactions for the CBT group [F(1,16) = 2.78, p = .12] and Wait-list [F(1,17) = 0.87, p = .36] for the posterior region.


Figure 13
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  		Figure 1. EEG {alpha} power change scores (neutral minus trauma condition) for the left and right anterior (upper panel) and posterior regions (lower panel) for CBT group and Wait-list controls. Whereas EEG {alpha} power is inversely related to activity, positive change score values denote increased activation during exposure to the accident picture. Left = left hemisphere; Right = right hemisphere; CBT = cognitive-behavioral therapy; pre = preassessment; post = postassessment. Error bars represent standard errors of the mean.

 

Relationship of Change in PTSD Severity and Electrophysiological Measures
To examine the relationship between changes in EEG measures and PTSD severity, we calculated pre- and post-change scores for measures of a) activation asymmetry, b) activity within the right and left hemisphere, and c) change in PTSD severity (CAPS Score). For these analyses, we combined participants from CBT and Wait-list groups (n = 35). There was a significant correlation between the decrease in PTSD severity and the total decrease in right anterior activation (r = .39, p = .02) (Figure 2). However, there were no significant correlations between change in PTSD severity and total decrease of left hemisphere activation (r = .26, p = .13) or change in anterior asymmetry (r = .08, p = .44). For the posterior region, there was no significant correlation between change in PTSD severity and change in left or right activity and asymmetry (all r < .18, p > .31).


Figure 23
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  		Figure 2. Scatterplot of the association between the reduction in right anterior activation (pre minus post) with the change in PTSD severity (CAPS score). Higher activation change scores indicate greater reduction in activation.

 


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
This study examined whether increased right-sided hemispheric activation during exposure to a trauma-related accident picture in patients with PTSD and subsyndromal PTSD which was reported previously (12) would change due to a CBT. Therefore, we compared EEG activity before and after CBT (in comparison with an assessment-only Wait-list condition). Our results showed a trend for differences in the change of anterior activation asymmetry as a result of treatment. At preassessment, the CBT group and Wait-list showed a comparable pattern of increased right hemisphere activation. The CBT group showed a shift of hemispheric activity from pre- to postassessment, which was mainly a result of a decrease in right anterior activation. The pattern of hemispheric activation in the CBT group at postassessment was similar to that observed for MVA victims without PTSD (12). For the Wait-list, there was no significant change in hemispheric anterior activation over time. The observed treatment-group differences in changes in anterior brain asymmetry were not modulated by a differential change in depression. When statistically controlling for change in scores of BDI-depression, the results did not change. Correlational analysis showed that the decrease in PTSD severity was associated with the reduction in total right anterior activation. For posterior cortical regions, there was a trend for a reduction in right hemisphere (Time x Hemisphere interaction) activation, which was not significantly different between treatment groups. Furthermore, changes in posterior asymmetry or left/right activation were not related to changes in PTSD severity. The reduction of negative affect during viewing the accident picture was significant only for the CBT group, but did not differ significantly from Wait-list controls.

Our results are consistent with a report of functional brain changes due to CBT in patients with spider phobia (25). The authors reported a reduction of activation in the right dorsolateral prefrontal cortex (PFC) post CBT, a region which was activated before CBT during exposure to spider videos. They suggested that changes in dorsolateral PFC activation might reflect changes in avoidance and cognitive strategies for the regulation of fear and anxiety evoked by the phobogenic stimulus. Similarly, Prasko et al. (24) reported a decrease of resting glucose metabolism in right hemisphere prefrontal regions in panic patients.

With regard to models of brain asymmetry and emotion (1–3,54), the reduction in right prefrontal cortical activation might reflect a decrease in anxiety-related withdrawal tendencies in the CBT group. The group-independent reduction in posterior asymmetry might reflect reduced anxious arousal (10,11) in both groups.

The treatment-related alterations of the cortical activation pattern might be associated with changes in the processing of trauma-related information. The right PFC is involved in cognitive processes such as episodic memory retrieval, sustained attention, and visual vigilance (55). Accordingly, increased right anterior activation in patients with PTSD and subsyndromal PTSD (before CBT) during exposure to trauma-related stimuli might be a correlate of altered information processing associated with symptoms of intrusion and hypervigilance. In psychological models of PTSD, externally or internally triggered intrusive memories have been described as mostly visual, very vivid, and associated with negative emotions (56–58) in contrast to the structured, verbally accessible nature of "normal" autobiographical memories. Thus, a reduction in right anterior activation—as observed in our study—could reflect a normalization of these processes due to cognitive-behavioral interventions. The described changes in brain activation may be the neurobiological underlying of enhanced top-down regulation and reduced bottom-up triggering.

CBT has been shown to produce different brain changes than pharmacotherapy in depression (21). Goldapple et al. argued that CBT seems to affect clinical recovery by top-down mechanisms that modulate the functioning of specific brain regions (e.g., PFC and hippocampus). In contrast, pharmacotherapy may target bottom-up processes that are associated with changes in limbic and subcortical brain regions. Future research is warranted comparing psychological therapies for PTSD with pharmacological interventions.

There are a few limitations of our study, however. First, we used a trauma sample of MVA survivors. Replication of our results is needed using other trauma samples. Our samples consisted of a higher percentage of women and the distribution of gender was slightly different between CBT and Wait-list controls. Some patients had comorbid disorders, although a high rate of comorbidity is typical of PTSD (59) and exclusion would have resulted in a nonrepresentative sample. Future studies using larger samples are warranted to examine the effects of gender and comorbidity on treatment-related changes of brain activity. However, the CBT and Wait-list controls did not differ in the severity of PTSD symptoms, so that effects due to differential statistical regression to the mean can be ruled out.

Second, the use of identical pictures at pre- and postassessments might have led to a treatment independent habituation to this stimulus. This might be the reason for a failure to find differences between treatment groups in change of posterior asymmetry and affective ratings of the trauma picture.

Third, the spatial resolution of our scalp recorded electrophysiology is limited and allows coarse distinctions of anterior/posterior and left/right cortical activation. Neuroimaging studies of PTSD revealed that PTSD is also associated with dysfunctions in regions not detectable with EEG such as hippocampus and amygdala (60,61). Accordingly, there is need for additional research on brain changes due to CBT in PTSD using neuroimaging techniques with higher spatial resolution. However, the EEG has the advantage of being inexpensive and totally noninvasive, which makes it ideally suited for studies of repeated measures and larger samples.

In conclusion, this is the first study reporting changes in brain activity in PTSD in a randomized, controlled trial of CBT. PTSD severity was significantly reduced after CBT in comparison to Wait-list controls. Participants receiving CBT displayed a pattern of reduced right anterior cortical activation after treatment, which has been ascribed a crucial role in experience of withdrawal emotions. The amount of reduction in the right anterior region was associated with reduction in PTSD severity. A highly interesting question for future research might be how different components of psychological therapy of PTSD (e.g., cognitive restructuring, imaginal/behavioral exposure, or relaxation training) are related to changes in brain function.

We thank Hans-Ulrich Wittchen and Jürgen Hoyer for their support with access to treatment facilities at the Outpatient Clinic for Clinical Psychology and Psychotherapy at the University of Technology Dresden. We appreciate the helpful comments of Annett Hentschel on previous versions of this manuscript. We thank Katrin Pöttrich, Dorion Kruska, Hang Fang, Kerstin Bader, Susanne Leiberg, Robert Langner, Constanze Nennewitz, and Denise Dörfel, for help with data collection. The authors would like to thank Edward B. Blanchard and Edward J. Hickling for many helpful suggestions at various stages of our treatment study. We would also like to thank our colleagues, Anne Boos, Andrea Hähnel, and Michael Klose, for serving as therapists, and Silvia Lemke, Andreas Poldrack, and Frank Schirmer for supervisory activities.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
1For better interpretability of {alpha} power change scores, we investigated EEG {alpha} activity for each condition separately. There were no treatment-related group differences in brain asymmetry (interactions with Treatment-Group or Time with Hemisphere) for the baseline, neutral, positive, and negative conditions (all p > .19). Only for the trauma-related picture, there was a significant Treatment-Group x Time x Hemisphere interaction for the anterior region (F(1,33) = 4.63, p = .04, {eta}2 = .123). There were no group differences present for the posterior region. Back

2Also using the change in BDI-depression score (pre-post) in an analysis of covariance (ANCOVA), the results did not change. Again, for the anterior region, there was a tendency for the Treatment-Group x Time x Hemisphere interaction (F(1,32) = 3.24, p = .08, {eta}2 = .096). There was no main effect or interaction with BDI-change (all p > .5). Back

Received for publication October 16, 2006; revision received July 29, 2007.

This study was supported by the Deutsche Forschungsgemeinschaft (KA 1476/3).

DOI:10.1097/PSY.0b013e31815aa325


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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