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Psychosomatic Medicine 68:307-311 (2006)
© 2006 American Psychosomatic Society

ORIGINAL ARTICLES

Extinction Learning Before Trauma and Subsequent Posttraumatic Stress

Rachel M. Guthrie, PhD and Richard A. Bryant, PhD

From the School of Psychology, University of New South Wales, Australia.

Address correspondence and reprint requests to Richard A. Bryant, PhD, School of Psychology, University of New South Wales, Sydney NSW 2052, Australia. E-mail: R.Bryant{at}unsw.edu.au


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Objective: Fear conditioning theories propose that persistent stress reactions may occur as a result of impaired extinction learning, and a poor capacity for extinction learning may predispose some individuals to posttraumatic stress disorder development. This study indexed the extent to which deficits in extinction learning before trauma exposure are a risk factor for persistent posttraumatic stress after trauma exposure.

Methods: Eighty-four firefighters were assessed during cadet training (before trauma) and 70 were reassessed within 24 months of commencing active firefighting duties (after trauma). Measures of posttraumatic stress were used before and after trauma exposure. In addition, skin conductance and corrugator electromyogram (EMG) responses were obtained during fear conditioning and extinction paradigms before trauma exposure.

Results: Reduced extinction of an aversively conditioned corrugator EMG response pretrauma predicted 31% of the variance in posttraumatic stress severity.

Conclusions: This result provides preliminary support for reduced extinction of a conditioned emotional response as a vulnerability factor for posttraumatic stress.

Key Words: posttraumatic stress • fear conditioning • prospective

Abbreviations: PTSD = posttraumatic stress disorder; HR = heart rate; EMG = electromyogram; CS = conditioned stimulus.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Posttraumaticstress disorder (PTSD) involves reexperiencing symptoms, avoidance of trauma reminders, and elevated arousal (1). Although most people display an array of PTSD-type reactions in the initial weeks after trauma exposure, most people adapt in the following 3 months (2). Across studies of people directly exposed to threat, approximately only 20% of people develop persistent PTSD (3). This pattern has led to considerable research into the characteristics of people who develop PTSD (4).

Biological theories posit that PTSD is the result of strong associative learning in which individuals initially react to a traumatic event (unconditioned stimulus) with arousal and fear (unconditioned response), and that individuals who develop PTSD continue to show arousal (conditioned response) when confronted with reminders of the trauma (conditioned stimuli). This theory holds that extreme sympathetic nervous system arousal at the time of a trauma results in the release of stress neurochemicals (including norepinephrine and epinephrine) into the cortex, mediating an overconsolidation of trauma memories (5). This model proposes that successful adaptation to a trauma involves extinction learning, which refers to a decrement in conditioned responding when there are repeated exposures to the conditioned stimulus in the absence of the aversive consequence (6). Extinction of conditioned emotional responses may explain normal adaptation following trauma exposure, with conditioned emotional responses to trauma-related stimuli gradually declining over time in the absence of the threatening consequences when people are exposed to trauma reminders. Converging evidence demonstrates a crucial role of the amygdala in the acquisition and expression of conditioned fear and possibly that a failure of extinction of the conditioned emotional response may result from impaired cortical inhibition of amygdala following trauma (5). Supporting this model is evidence that larger skin conductance (SC), heart rate (HR), and facial electromyogram (EMG) responses to trauma reminders are observed in individuals with PTSD compared with trauma-exposed individuals without PTSD (7–10).

Several mechanisms have been postulated to account for the persistence of PTSD symptoms in some individuals but not others after trauma exposure. The proposed pathways to PTSD include: 1) a greater responsivity (e.g., UCRs) during traumatic events (11); 2) a greater acquisition of CRs (12), and 3) slower extinction of CRs (5). Some people may develop persistent stress reactions after trauma because they are more conditionable before trauma exposure and they suffer reduced extinction learning after the trauma. Recent studies have used aversive classical conditioning paradigms using novel stimuli that were not direct trauma reminders to explore these hypotheses in individuals with PTSD. Orr et al. (12) found that individuals with PTSD had higher sympathetic nervous system arousal during the conditioning task, heightened acquisition of SC, HR, and corrugator EMG conditioned responses, and reduced extinction of SC conditioned responses, compared with controls. Elevated SC responsiveness to both neutral and aversive stimuli and reduced extinction of SC and HR conditioned responses has also been demonstrated in individuals with PTSD (13). These findings provide some evidence for a heightened "conditionability" in individuals with PTSD (12).

The hypothesis that posttraumatic stress may occur because some people are more conditionable remains untested, however, because this issue requires assessment of trauma survivors’ conditioned responses and extinction before trauma exposure to index its influence on subsequent stress reactions. We tested the proposition that impaired extinction learning before trauma exposure is a risk factor for subsequent posttraumatic stress by administering an aversive conditioning and extinction learning paradigm to a cohort of firefighters during their cadet training and before active firefighting duties, and subsequently assessed them for posttraumatic stress within 24 months of their commencement of firefighting duties (and exposure to trauma). We predicted that posttraumatic stress would be predicted by the degree of impaired extinction learning before trauma exposure.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 
Participants
Eligible participants were 87 successive male recruits (mean age = 30.1 years, SD = 5.1 years) to the NSW Fire Brigade who were receiving class-based instruction at the time of recruitment; 3 (3%) participants declined to participate in the study. Participants were initially evaluated before commencing active firefighting duties (Time 1: between June and October, 2001), and then attempts were made to reassess all participants within 24 months of the initial assessment (Time 2; between June and October, 2003). Nonparticipation in the follow-up assessment occurred because 1 participant had moved to a rural area, 2 participants were on physical injury-related Workers’ Compensation, and 11 refused to be reassessed. In total, 70 participants completed both assessments; however, data from 3 participants were excluded from analysis due to technical problems resulting in the loss of psychophysiologic data. The final sample consisted of 67 (80%) participants who completed both assessments and had valid psychophysiologic data. Participants in the study (n = 70) did not differ from nonparticipants (n = 17) on demographic or initial psychometric responses.

Following the Time 1 assessment, the experimenters monitored participants’ trauma exposure on a weekly basis via the Fire Brigade’s emergency calls database. At Time 2, all participants had been exposed to a Fire Brigade-related traumatic event that involved direct exposure to an event that involved actual or threatened death or serious injury to the participant or others. In terms of the traumatic events experienced by participants, 72% (n = 48) had attended a motor vehicle accident, 57% (n = 38) had been exposed to a fire, and 6% (n = 4) had attended the scene of a suicide. With regards to the most traumatic Fire Brigade-related event participants had been exposed to since Time 1, 54% (n = 36) rated a motor vehicle accident, 40% (n = 27) rated a fire, and 6% (n = 4) rated attending the scene of a suicide. The mean number of Fire Brigade-related traumatic events experienced by the cohort in the interval between Time 1 and Time 2 was 2.4 (SD = 1.6).

Measures
At the initial assessment, a clinical psychologist administered participants the Structured Clinical Interview for DSM-IV (SCID-IV) (14) to assess for current Axis I disorders, and the Clinician Administered PTSD Scale (CAPS) (15,16) to index current PTSD diagnosis. Participants were also administered the Traumatic Events Questionnaire (TEQ) (17) to assess prior traumatic events, the Trait version of the State Trait Anxiety Inventory (STAI-T) (18) to assess trait anxiety, the Beck Anxiety Inventory (BAI) (19) to index state anxiety, the Beck Depression Inventory, Version 2 (BDI-II) (20) to index depressive symptoms, and the Alcohol Use Disorders Identification Test (AUDIT) (21) to assess current alcohol use.

At the follow-up assessment, participants were readministered the SCID-IV, CAPS, BDI-II, BAI, STAI-T, and the AUDIT. In addition, they were administered the Impact of Event Scale (IES) (22) to assess intrusive and avoidance posttraumatic stress symptoms.

Left corrugator EMG and SC were recorded with a Coulbourn Lablinc V System (Coulbourn Instruments, Allentown, PA). EMG was recorded through 4-mm (sensor diameter) Ag/AgCl surface electrodes filled with Microlyte gel (Coulbourn Instruments) and attached with adhesive collars over the corrugator site, in accordance with recommendations (23). The raw EMG signal was amplified by 50,000 and filtered so as to retain the 90- to 1000-Hz frequency range by a Coulbourn Isolated Bioamplifier (V75-04). The EMG signal was rectified and integrated by a Coulbourn Multi-function Integrator (V76-23A) using a 10-ms time constant. Skin conductance was measured directly by a Coulbourn Isolated Skin Conductance Coupler (V71-23) using a constant 0.5 V through 8 mm Ag/AgCl electrodes. Electrodes were filled with Microlyte gel and attached with adhesive collars to the subject’s nondominant distal phalanges of the index and middle fingers, in accordance with published guidelines (24). The Coulbourn instruments were interfaced with an IBM-compatible computer through a Coulbourn general purpose Lablinc port (V19-16). All physiologic analog signals were digitized at 1 KHz. An IBM-compatible computer with a Coulbourn Lablinc Computer Interface (L18-16) was used for sampling and storing the digitized physiologic signals.

Procedure
All procedures were approved by the University of New South Wales Human Ethics Committee. The experiment employed a classical aversive conditioning paradigm conducted at Time 1. The conditioned stimuli (paired = CS+; unpaired = CS–) were two different colored 15.2-cm-diameter circles, randomly selected for each participant from four options (red, blue, green, or yellow) and presented for 8 s. The conditioned stimuli were computer-generated and displayed on a 28.5 x 21.5 cm monitor positioned 1 m in front of the participant, at the level of his face. A Coulbourn Video-Splitter (VGA-SPL-4) and Real World Interface (V19-91) controlled the presentation of the CS+ and CS– to the participant’s monitor. The unconditioned stimulus (UCS) was a 500-ms electric shock, delivered through electrodes attached to the fourth finger of the nondominant hand, which the participant had chosen as "highly annoying but not painful." The shock was generated by a Coulbourn Transcutaneous Aversive Finger Stimulator (E13-22), which used a 9-cell battery attached to an adjustable step-up transformer and was electrically isolated from line current.

Following written informed consent, electrodes for recording physiologic measures and administering the electrical UCS were then attached. Participants were asked to rate their current anxiety level (0 = very calm; 12 = very anxious) and mood (0 = very happy; 12 = very sad). The experimenter then set the UCS intensity level selected by the participant, which ranged from 0.5 to 5.0 mA. The Habituation phase consisted of five presentations each of the colored circles to be used as CS stimuli throughout the experiment, without the UCS. This was followed immediately by the first acquisition (Acquisition I) phase that consisted of four presentations each of the CS+ and CS– stimuli. During the Acquisition I phase, the UCS occurred immediately following each CS+ offset. Following the Habituation and Acquisition I phases, the experimenter assessed the participant’s knowledge of the CS-UCS relationship, using a short post–conditioning recognition questionnaire (25). The participants were asked to indicate whether the electrical stimuli were associated with (a) CS+, (b) CS–, (c) both CS+ and CS–, or (d) they did not know. Participants were also asked to rate their degree of confidence in their response on a 6-point scale (1 = "completely certain," to 6 = "completely uncertain"). The experimenter administered a second acquisition (Acquisition II) phase and an Extinction phase. Before these phases, the participant was instructed that a contingency existed between one of the colors and the shock, but they were not told which color (26). The participant was also instructed to use a 10-point button panel (0 = "certain no shock," to 100 = "certain shock") to indicate expectancy of shock. This method has previously been utilized as a valid concurrent measure of the development of contingency learning (27,28). The Acquisition II phase consisted of three presentations each of the CS+ and CS– stimuli, which were different colored circles from those used in the Habituation and Acquisition I phases. The UCS occurred immediately following each CS+ offset during the Acquisition II phase. The instructions for the Acquisition II phase were intended to maximize the number of participants who became aware of the CS-UCS contingency before the Extinction phase of the experiment. The Extinction phase followed immediately after the Acquisition II phase, and consisted of 10 nonreinforced presentations each of the conditioned stimuli used in the Acquisition II phase. Throughout the experiment, the CS+ and CS– stimuli were presented in a quasi-random order within each phase, with the constraint that no more than three consecutive presentations of the CS+ or CS– were allowed. The intertrial interval was 20 ± 5 s, randomly determined by the computer. The dependent physiologic measures were sampled at 1K Hz.

Response Scores
Square root transformations were performed on each participant’s SC and EMG responses before statistical analyses to reduce the variance due to irregular responses (29). An SC response was calculated by subtracting the mean level for the 2 s immediately before CS onset from the highest SC value recorded during the 8-s CS interval. A SC response score for the interval containing the unconditioned response was calculated by subtracting the average SC level within 6 to 8 s following CS onset from the maximum increase in SC level during the 6-s interval following CS offset, corresponding to the onset of the UCS. Data reduction for corrugator EMG was identical to that for SC. The mean of each individual’s response to the first CS+ and CS– trial during the Habituation phase was calculated as an estimate of SC orienting response magnitude (12).

Previous research has shown that participants who are unaware of the CS–UCS contingency fail to discriminate between cues on either skin conductance or expectancy measures (30,31). Participants were therefore classified as either "aware" or "unaware" of the contingencies during the Acquisition I phase based on their responses to the short postconditioning recognition questionnaire Participants who were able to correctly identify the CS+ and only the CS+ as having been followed by the shock were classified as "aware." Participants were classified as "unaware" if they did not rate only the CS+ as having been followed by the shock with at least fair certainty during the postconditioning questioning. For the Acquisition II phase, participants were categorized as being aware of the contingency if he expressed both a positive expectancy of the UCS during CS+ trials (expectancy of shock ≥70) and a negative expectancy of the UCS during CS– trials (expectancy of shock ≤30) by the end of the Acquisition II phase.

Data Analysis
A stepwise multiple regression analysis was performed to identify the Time 1 predictors of Time 2 psychopathology. The dimensional measure of Time 2 psychopathology was IES total score. This measure was chosen as the dependent variable because there was a floor effect in CAPS scores; in contrast, there was greater variance in IES scores. Participants were included in the analysis if they showed CS-UCS contingency awareness by the end of the Acquisition I and II phases at Time 1 (n = 45). To identify a subset of potential predictors, Pearson product-moment correlations (which adopted an adjusted alpha of 0.01) were calculated between the IES total score and the Time 1 psychometric and psychophysiologic (SC and corrugator EMG) variables. The specific psychophysiologic variables were: orienting response, UCR (mean response during the UCS interval of Acquisition I phase CS+ trials), differential acquisition response (mean response during the CS interval of CS+ trials minus mean response during the CS interval of CS– trials for the Acquisition I phase), and differential extinction response (mean response during the CS interval of CS+ trials minus mean response during the CS interval of CS– trials for the Extinction phase (12). Responses to the Acquisition I phase were used to calculate the differential acquisition response, as the Acquisition I phase was a measure of spontaneous learning. The Time 1 psychometric variable and psychophysiologic variable that correlated the highest with Time 2 IES total score were then entered into the regression equation, along with the interval between Time 1 and Time 2, and the interval between the worst trauma experienced and Time 2.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 NOTES
 REFERENCES
 
Participant Characteristics
Mean demographic and psychometric data for the total sample at Times 1 and 2 are presented in Table 1. No participants met criteria for a current diagnosis of PTSD at either assessment. Two participants met criteria for a non-PTSD anxiety disorder at Time 1, which in each case was a specific phobia. At Time 2, three participants met criteria for a non-PTSD anxiety disorder, which was a specific phobia for 2 participants and generalized anxiety disorder for 1 participant.


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  		TABLE 1. Total Sample Means and Standard Deviations for the Demographic and Psychometric Measures at Times 1 and Time 2

 

Predicting Posttraumatic Stress
Table 2 presents Pearson product-moment correlations between Time 2 IES total score and Time 1 psychometric and psychophysiologic variables. To predict Time 2 IES total, the variables entered into the regression equation were Time 1 corrugator EMG differential extinction response, TEQ score, the interval between Time 1 and Time 2, and the interval between the worst trauma and Time 2. Time 1 corrugator EMG differential extinction response was the only significant predictor, explaining 31% of the variance (ß = 0.6, SE = 1.5, t = 4.5, p < .001).


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  		TABLE 2. Pearson Product-Moment Correlations Between Selected Conditioning Psychophysiologic Measures and Psychometric Responses at Time 1 and IES Score at Time 2 for the Total Sample

 


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
NOTES
 REFERENCES
 
In the current study, pretrauma reduced extinction of an aversively conditioned corrugator EMG response predicted 31% of the variance in posttrauma IES scores. Corrugator EMG activity has been found to be a sensitive and specific measure of negative affect (32). Therefore, reduced extinction of a conditioned emotional response may be a pretrauma vulnerability factor for posttraumatic stress reactions. This finding is consistent with the proposal that a reduced capacity to extinguish aversively conditioned responses may represent a potential pathway underlying the pathogenesis of PTSD following trauma (5). Importantly, preexisting distress did not predict posttraumatic distress, as Time 1 CAPS score did not contribute significantly to the variance in posttrauma IES score.

Recent neuroimaging studies have demonstrated reduced activation in the medial prefrontal regions, thought to regulate amygdala activity, in PTSD patients in response to trauma-relevant stimuli (33). Reduced extinction, as a pretrauma risk factor for posttraumatic stress, could possibly represent a deficit in the inhibitory control of the amygdala by the medial prefrontal regions (34). Future neuroimaging studies may help to determine the precise neural pathways that may underlie reduced extinction as a risk factor for posttraumatic stress.

In contrast to corrugator EMG responses, reduced extinction of an aversively conditioned SC response was not a significant predictor of posttrauma IES scores. This finding highlights that these psychophysiologic measures are indexing different response systems. Specifically, SC is a measure of sympathetic arousal (35), whereas corrugator EMG is a measure of negative affect (32).

There are a number of limitations to the conclusions of this study. First, the lack of PTSD cases necessitated a focus on posttraumatic stress symptom severity rather than diagnosis. Previous research has demonstrated that response bias leads firefighters to minimize symptom reporting (36). Second, we recognize that the sample size is small and needs to be replicated with a larger cohort. Third, the dimensional measure of posttraumatic distress used at Time 2 was the IES. The main limitations of the IES are that it is a self-report measure of intrusive and avoidance symptoms associated with posttraumatic stress and it does not assess hyperarousal symptoms. Fourth, firefighters may represent a specific population, and the conclusions may not necessarily be generalized to other trauma-exposed populations. Despite these limitations, the present data offer preliminary evidence for the role of reduced extinction of a conditioned emotional response as a pretrauma risk factor for the development of posttraumatic stress symptoms. Identification of reduced extinction learning as a pretrauma vulnerability factor provides insight into the emergence of posttraumatic stress in only a subset of trauma-exposed individuals and suggests a promising direction for further investigation into the biological mechanisms of posttraumatic stress reactions.


   NOTES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
REFERENCES
 
Supported by an NHMRC Program Grant (No. 300304) and an Australian Postgraduate Award.

DOI:10.1097/01.psy.0000208629.67653.cc


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 NOTES
 REFERENCES
 

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