Post-traumatic Stress Disorder and Voluntary Forgetting of Unwanted Memories.
An fMRI Study.
Implications & Reflections
BA (Hons), MClinPsych, PhD, MAPS, MCClin, QCA
Director – Unit for Neuropsychotherapy, Director –
Mediros Clinical Solutions
School of Psychology, School of Social Work and Human Services
The University of Queensland
Trauma and the Brain
The effects of trauma on the brain have been well documented. Violation of basic needs such as attachment, control and safety, facilitates significant changes on neurochemical and neurostructural levels. Trauma up-regulates the stress chemicals norepinephrine, corticotrophin-releasing factor, adrenocorticotropic hormone, adrenalin and cortisol; at the same time, it can inhibit neural proliferation and facilitate strong neural patterns of distress reactions to relatively small triggers (Schore, 2009). Additionally, trauma inhibits cortical blood flow to executive regions of the brain and as a result hinders problem-solving behaviours; it also enhances pathological patterns linked to anxiety, depression, dissociative disorders and even psychosis. All these symptoms are produced by memory systems formed from negative experiences that shape the brain as a result of its interacting with hostile environments (Grawe, 2007). The implication here is that there is a significant need not only to ascertain how the brain is shaped by these experiences but also to identify strategies to manage or treat the effects of these experiences in order to facilitate effective neurochemical, neural structural and neural network functioning (Kandel, Schwartz, Jessell, Siegelbaum, & Hudspeth, 2013).
Parallel to these recent studies on the effects of trauma on the brain and strategies to facilitate change, is research into memory—more specifically, research on the neural mechanisms of voluntary forgetting—based on information from subjects who have experienced trauma which indicates that not everyone suffers the aftermath of trauma and that some people in fact demonstrate an effective voluntary ability to forget unwanted memories.
The brain and forgetting
The inability to remember—or, in other words, the ability to forget—can be a rather useful tool. Negative or painful experiences are often well-remembered because they activate the formation of memory systems located in the hippocampus and dorsolateral prefrontal cortex. While these memory systems are formed on subconscious and pre-cognition levels, they are subsequently activated by related experiences which act as triggers, and these patterns then form the basis of distress, sometimes referred to collectively as posttraumatic stress disorder (PTSD). The function of these particular memory systems is to act as early warning signals, that is, patterns of protection or survival to inhibit actions (e.g., thoughts, feelings, behaviours) that may resemble the initial trigger or trauma. As a result, protective patterns—predominantly avoidance patterns—are established. The function of these avoidance patterns is to protect the system from re-traumatization in an attempt not to re-live, re-think, re-feel, or re-experience the initial distress. PTSD affects general wellness, as sufferers fall victim to patterns of avoidance that, in turn, lead to cognitive, emotional, social, and behavioural levels of impairment (APA, 2013).
Mechanisms of forgetting
In a recent study, using fMRI, Roland Benoit and Michael Anderson from the MRC Cognition and Brain Sciences Unit, Cambridge, UK, demonstrated two distinct neural mechanisms of intentional forgetting of unwanted memories (Benoit & Anderson, 2012). In this paper the authors argue that when people are confronted by unwelcome reminders of a past events, some are able to exclude the unwanted memory from their awareness by activating a process that impairs retention of suppressed memories. The starting point of their research was the question, “What are the neurocognitive mechanisms of memory suppression?” (Benoit & Anderson, 2012).
One way to inhibit memory retrieval is a process of “direct suppression”. fMRI studies show that some subjects exhibit a reduction of blood-oxygen-level-dependent (BOLD) signals in the hippocampus, that is, evidence of a process limiting awareness of a memory (unlike attempts to recall a memory which trigger an opposite process). At the same time, the researchers also found that attempts to exclude a memory from awareness are associated with increased activation in the right dorsolateral prefrontal cortex, and that recruitment of this region predicts greater subsequent forgetting of the avoided memories (Benoit & Anderson, 2012).
Another way of excluding an unwanted memory from awareness is to activate a substitute thought, similar to another memory. As thought substitution specifically requires an alternative memory, it would engage processing in the hippocampus—in contrast to disengaging it—indicating that the activated neural system has to select between the substitute memory and the unwanted memory. Thus, thought substitution is an active process of change rather than a process of suppression. Previous studies have found weakening of memories in the presence of selective retrieval (Andersen, Bjork, & Bjork, 1994; Norman, Newman, & Detre, 2007).
Retrieval of information occurs via activation of sections of the prefrontal cortex. Nee and Jonides (2008) found that greater activation of the caudal prefrontal cortex restricts intruding memories. An example would be a student day-dreaming in class while new information is being discussed, with the implication that new information is suppressed due to a shift in attention and the activation of alternative memory systems. Clearly this process is unhelpful in some situations but can be very beneficial in others. A second structure in the prefrontal cortex, the mid-ventrolateral prefrontal cortex, is linked to the identification of a substitute memory—hence the effective management of unwanted memories using thought substitution takes place through the interplay of the dorsal and mid-ventrolateral prefrontal cortex.In an interesting experimental design, the researchers tested this process and observed that distinct neural processes were activated, reflecting the two systems of forgetting. On the one hand, they found that attempts to suppress retrieval of memories were associated with increased activity in the dorsolateral prefrontal cortex (DLPFC), that activation was stronger in individuals who induced greater “below-baseline forgetting” of unwanted memories, and that it was stronger in this group than for the thought suppression group (Benoit & Anderson, 2012). On the other hand, they also found that the suppression pattern was associated with reduced hippocampal activation. These findings strengthen the hypothesis that neural activation to inhibit retrieval is supported by a neural pattern that effectively activates to inhibit retrieval of unwanted memories. In contrast, the researchers found that actions to suppress unwanted memories with thought substitution were associated with engagement of the two prefrontal neural areas and these actions associated with increased hippocampal activation.
Forgetting and disaster – new perspectives
The study offers new perspectives on understanding how we manage intrusive memories and is significant for understanding both the effects of trauma and its management. Importantly, thought substitution is associated with increased hippocampal prefrontal cortical activity. A recent study by Lyoo and colleagues points towards the positive effect of thought substitution from greater connectivity in this region of the brain. In this study, the authors found that survivors of a subway disaster who showed greater thickening in the DLPFC also showed the greatest reduction in PTSD symptoms (Lyoo et al., 2011). Shin et al. (1999) also demonstrated reduced DLPFC activation by this group when triggers of the incident were presented, indicating effective thought substitution. They also found the DLPFC volume normalized within 3 years to levels similar to the controls, thus indicating the pathway of the neural recovery process.
Unlike with thought substitution, hippocampal disengagement during the process of memory suppression leads to a systematic disruption of memory retrieval. Although benefits of the thought substitution process have been demonstrated it is still unclear whether the benefits of suppression remain long-term. Clearly, the effects of hippocampal disengagement need to be explored further.
A shortcoming of this fascinating study is a lack of attention to neurochemical indicators. Up- or down-regulation of the hypothalamus-pituitary-adrenal (HPA) system with the release of the stress chemicals norepinephrine, corticotrophin-releasing factor, adrenocorticotropic hormone, adrenalin and cortisol may provide critical information as to the neurochemical indicators of system distress or control (Rossouw, 2012). A reasonable hypothesis could be that—given the outcomes of the studies with survivors of the subway disaster—thought substitution as a strategy of forgetting would be linked to HPA down-regulation, hence providing a greater sense of control and reduction in PTSD symptoms; and therefore that suppression may go hand in hand with HPA up-regulation. One would hypothesise that hippocampal activation that is associated with thought substitution as a process of forgetting down-regulates the amygdala and HPA activation, that less intrusive thoughts are experienced and higher levels of control demonstrated. One would also hypothesise that reduced hippocampal activation would up-regulate HPA activation (i.e., increased stress responses) as suppression, as this strategy of forgetting does not effectively activate connectivity in the hippocampal prefrontal cortex.
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