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This page contains information and summaries of published research that are intended for people with professional training in mental health.  We urge caution since it may be difficult to know how to interpret the information without advanced training in psychology or psychiatry.

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BEHAVIORAL AND COGNITIVE THEORIES

People with ASD and PTSD show a more disorganized structure in their narratives possibly implying less cohesion and organizations of their memories (Harvey & Bryant, 2002).

Ø       This lack of cohesion may mean that it is more difficult to access and resolve trauma memories since retrieval is impaired by poor organization

Ø       ASD and PTSD are also associated with poor recall of past positive experiences, which may make it difficult to place traumatic events in a broader, less threatening context

Studies that have been published indicate that treatment based on prolonged exposure may reduce fragmentation of trauma survivors’ narratives.  However, further examination has noted that these improvements occur independently of treatment outcome, and are probably an artifact of the process of exposure-based treatment rather than a curative factor (van Minnen et al., 2002).

In summarizing effects of thought suppression in ASD and PTSD, Harvey & Bryant (2002) offer the following synthesis of research to date:

In a study modeled after the thought suppression paradigm developed by Wegner, Schneider, Carter, and White (1987) , we ( Harvey & Bryant, 1998b ) asked trauma survivors with and without ASD to monitor the frequency of their trauma memories over 3—5 min thought periods in which (a) they were told to think about anything, (b) they were administered suppression or nonsuppression instructions, and (c) they were again asked to think about anything. During each period, participants were asked to indicate via button press each time a thought relating to their trauma came to mind. ASD participants who were instructed to suppress their memories during the second thought period displayed a delayed increase in the frequency of their memories during the third thought period. This finding is consistent with the proposal that trauma reactions are, at least in part, maintained by thought suppression ( Ehlers & Clark, 2000 ). In a replication of this design with ASD and non-ASD participants who either suppressed or monitored their trauma-related thoughts over three 24-hr periods, Guthrie and Bryant (2000) found no increase in intrusions following attempted suppression. This finding apparently occurred because many of the acutely traumatized participants suppressed their unwanted memories, regardless of the experimental instructions. This study found that over this extended period, participants reverted to their preferred cognitive strategies, which were characterized by avoidance and distraction. Furthermore, these avoidant strategies were correlated with anxiety, attempted suppression, and frequency of intrusions. These findings replicate an earlier observation that ASD participants use punishment and worry (which are conceptualized as avoidance strategies) more often than non-ASD participants to manage their traumatic memories ( Warda & Bryant, 1998b ). Furthermore, the association between frequency of intrusions and distraction is consistent with Salkovskis and Campbell's (1994) report that general distraction was associated with a delayed enhancement of naturally occurring intrusions, whereas distraction in the form of an interesting and engaging alternative cognitive task was associated with fewer intrusions.

Cognitive appraisal about one’s symptoms and about the future may also contribute to the likelihood of PTSD (Harvey & Bryant, 2002).  These appraisals include:

Ø       Negative attributions about intrusive symptoms

Ø       Over-estimation of the probability of negative future events and the likelihood that they will have negative effects.

Ø       Cognitive biases for events related to external harm, somatic sensations, and social concerns

However, in a study comparing exposure therapy vs. cognitive restructuring vs. both (Livanou et al, 2002) as treatments for PTSD found that:

Ø       Pre-treatment cognitions (e.g., beliefs about mistrust, helplessness, meaninglessness, and unjustness of the world) were associated with pre-treatment Sx severity, but not treatment outcome

Ø       Symptoms changed before cognitions, with no cognitions that were assessed changing before behavioral symptoms changed

Ø        Following treatment, sense of control and attribution of gains to personal efforts predicted maintenance of gains at follow up

Mowrer’s Two Factor Theory (see Falls & Davis, 1995 for an excellent summary)

Step 1: Classical Conditioning.

Unconditioned stimulus (threat to life or well being) results in unconditioned response (fear).  Intensity of UCS-UCR pairing is strong enough for single trial learning.  (Example: car crash results in person fearing for their life)

Previously neutral stimuli associated with the US become conditioned, and evoke a conditioned emotional response (CER).  (Example: the intersection where the crash occurred evokes fear, hearing screeching tires evokes fear)

Other, previously neutral stimuli come become associated with a CER through generalization and second order conditioning (Example: all intersections evoke fear; going to get in a car or thinking about driving evokes fear)

Step 2: Operant Conditioning.

The person learns to act in ways (conditioned response) that help them avoid the things they have learned to fear (conditioned stimuli).  (Example: by not getting in a car, the person avoids the anxiety associated with going through intersections)

Through operant conditioning, the person learns increasingly sophisticated avoidance responses.  This avoidance results in negative reinforcement (e.g., since avoidance temporarily reduces anxiety, it is processed as being a good thing to do and the habit of avoidance is strengthened, as is the idea that the stimulus being avoided is dangerous. (Example: fear of getting in a car increases)

Since the person does not get experience in learning that the CS is not necessarily associated with UCS, s/he does not learn that her or his conditioned responses may be excessive (Example: since the person never gets in a car, s/he never learns through new experiences that cars are not always dangerous)

Extinction/habituation of this conditioning occurs when person confronts situations, thoughts, feelings, or memories without the UCS occurring (From the Prior Example: the person is confronted with a feared stimulus, either through imaginal exposure or riding in a car, for prolonged periods of time until their anxiety decreases.  Through this process they are repeatedly exposed to experiences that show that being in a car does not always mean that they are going to be in a crash)

In their study of PTSD and habituation to startling tones, Shalev et al. (2000) noted, “At 4 months, they were assessed for PTSD and depression. At 1 week posttrauma, the responses of the groups were comparable. However, at 1 and 4 months posttrauma, the heart rate response to startling tones of the subjects with PTSD had become larger than those of the subjects without PTSD. The subjects with PTSD also showed less decline over the follow-up sessions than the subjects without PTSD in the number of trials required to reach the skin conductance nonresponse criterion, and they showed an increase in the number of trials needed to reach the EMG nonresponse criterion. . .”

The pattern of group differences in physiological response in subjects with PTSD to the startling tones observed here at 1 and 4 months after the traumatic event resembles that previously found in subjects with chronic PTSD, including Vietnam veterans 20 years after combat, Israeli civilians 10 years after exposure to a variety of traumatic events, Israeli prisoners of war 20 years after captivity, and adult women sexually abused as children.”   

The differences in physiological responding appear to be consistent with behavioral concomitants of progressive neuronal sensitization in PTSD.

Although I have not yet read the article, there are reports of a study recently published in Nature by Milad & Quirk (Milad, M.R. & Quirk, G.J. (2002) “Neurons in the medial prefrontal cortex signal memory for fear extinction.” Nature, 420, 70-74) that indicate researchers continue to find confirmatory information about the role of the medial prefrontal cortex in extinction.

Lang’s (1979) Bioinformational Theory of Emotion

Emotional Processing Theory (Foa and Kozak, 1986)

“Two conditions are required for the reduction of fear.  First, fear-relevant information must be available in a manner that will activate the fear memory. . . Next, information made available must include elements that are incompatible with some of those that exist in the fear structure, so that a new memory can be formed.  This new information, which is at once cognitive and affective, has to be integrated into the evoked information structure for an emotional change to occur” (Foa and Kozak, 1986).

 “Shattered Assumptions” (Janoff-Bulman, 1992)

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The information posted on this site reflects our understanding of peer-reviewed research and generally accepted principles in psychology.  It is not intended to be used for self-treatment or as a substitute for individualized assessment and treatment by a licensed professional, and should not be construed as professional advice.

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