This most excellent article (1) explains how two main memory systems relate to two manifestations related to PTSD, the enhancement and the impairment of traumatic memory which may be difficult to explain via a unitary model of memory, but these seemingly antagonistic effects can be explained more readily through a multiple memory systems approach.
Under robust emotional arousal, amygdala activation can modulate the relative use of memory systems in a manner that favours habit memory.
“We propose a similar mechanism may underlie the development and persistence of some PTSD symptoms. The traumatic memories of PTSD patients can be deficient in hippocampus-dependent contextual or autobiographical aspects, and enhanced in responding to trauma-related cues, which we suggest may reflect increased involvement of the dorsal striatum.
We briefly consider the potential role of a stress/anxiety induced habit bias with regard to other psychopathologies, including obsessive-compulsive disorder and drug addiction.
Building on these earlier models and considering the modern ‘ multiple brain systems ’ approach to learning and memory, recent theories have proposed that the development and persistence of some psychopathologies may arise from the differential involvement of neuroanatomically distinct memory systems (e.g., White, 1996; McDonald et al., 2004; Packard, 2009). More specifically, it has been suggested that some psychological disorders, particularly those characterized by strong habit-like behavioral features, may reflect a shift from the use of a hippocampal-dependent ‘ cognitive ’ memory system towards a dorsal striatal-dependent ‘ habit ’ memory system.
This anxiety-induced habit bias may be mediated by a dynamic interplay among the amygdala, hippocampus and dorsal striatum (Packard and Wingard, 2004; Elliot and Packard, 2008; Wingard and Packard, 2008; Packard and Gabriele, 2009). Specifically, in some learning situations that occur under high levels of emotional arousal, activation of the amygdala can modulate memory in a manner that favors the use of dorsal striatal-dependent habit memory over hippocampal-dependent cognitive memory.
In post-traumatic stress disorder (PTSD), it is possible that interactions among the amygdala, hippocampus, and dorsal striatum may under lie some aspects of the disorder (Packard, 2009).
We have recently investigated the BLA as a potential neural site of action that mediates the modulatory influence of drug-induced anxiety on the relative use of multiple memory systems. A possible role for this brain region is suggested by evidence that the BLA is involved in mammalian emotional behavior, including the ability of various drugs to produce anxiety (e.g., Kluver and Bucy, 1939; Nagy et al., 1979; Scheel-Kruger and Petersen, 1982; Sanders and Shekhar, 1991). In addition, the BLA exerts a modulatory influence on memory processes occurring in several other brain structures, including the hippocampus and dorsal striatum (Packard et al., 1994, 1996; Packard and Teather 1998; Roozendaal and McGaugh, 1996, 1997).
As suggested in lower animals, the stress/anxietyinduced facilitation of habit memory in humans may also stem from an impairment of hippocampal-dependent memory. Several studies in humans indicate that high levels of stress at the time of encoding or retrieval impair learning in hippocampal-dependent memory tasks (Schwabe et al., 2009; Merz et al., 2010; Schwabe and Wolf, 2010; Thomas et al., 2010).
In humans and lower animals, acute or chronic stress can produce a bias towards the use of striatal-dependent habit memory, at the expense of hippocampal-dependent cognitive memory. The existence of a stress/anxiety-induced habit bias in humans provides further reason for considering the phenomenon as a potential mechanism underlying some human psychopathologies.
Introduction to PTSD symptomatology
The Diagnostic and Statistical Manual of Mental Disorders text revision (DSM IV-TR; American Psychiatric Association, 2000) classifies PTSD as an anxiety disorder that may develop after experiencing a traumatic event. According to the DSM IV-TR, the traumatic episode itself must have included actual or anticipated threats of death or serious injury to oneself or others, and the traumatic episode must have instilled within the patient intense feelings of fear, helplessness or horror. In addition, the patient must persistently re-experience the traumatic episode. This re-experiencing may occur through intrusive recollections of the event (taking the form of mental images, thoughts, or perceptions), a sense that the traumatic event is actually recurring, emotional or physiological reactivity to internal or external cues that somehow represent the traumatic event, or recurrent nightmares of the event. Importantly, these recollections often arise involuntarily. In fact, in many cases, a patient ’ s ability to recall the event voluntarily proves to be impaired.
… a patient must display several avoidance behaviors; this avoidance may include efforts to avoid stimuli that might incite involuntary recollection, or may manifest itself as the inability to voluntarily recall important aspects of the traumatic event.
Specifically, the DSM IV-TR suggests that PTSD patients may potentially exhibit both enhanced and impaired memory of the traumatic event. Enhancements of the traumatic memory become evident through the exceptionally vivid and involuntary re-experiencing, or ‘ flashbacks ’ , of the event. Such flashbacks are characterized as being triggered by trauma-related internal cues (e.g., anxiety) or external cues (e.g., loud noises) and as containing vivid perceptual features from the event, such as sounds, smells, and images. Importantly, when a patient experiences a flashback, he or she feels the event is actually recurring, as if it were part of the present instead of the past. These observations suggest that the version of the traumatic memory that is readily and involuntarily invoked by cues fails to acknowledge the spatial or temporal context in which the event originally took place. This lack of contextual content may be viewed as one of the many impairments commonly observed in traumatic memories.
Other impairments in traumatic memory become evident through the patient ’ s inability to recall certain aspects of the event. Thus, amnesia, memory gaps and fragmentary recall of the traumatic event are relatively common features in PTSD (van der Kolk and Fisler, 1995; Koss et al., 1996; Shalev et al., 1996; Tichenor et al., 1996; Mechanic et al., 1998; Yovell et al., 2003). Although a concomitant enhancement and impairment of traumatic memory may be difficult to explain via a unitary model of memory, these seemingly antagonistic effects may be explained more readily through a multiple memory systems approach.
Thus, one memory system may be highly active and lead to biased encoding of certain features, and another memory system may be relatively inactive and fail to encode other features of the traumatic event.
For example, in one case study, a 19-year-old male developed PTSD symptoms after a motor vehicle accident that caused TBI and consequent amnesia of the event (see Podoll et al., 2000a). Despite having no memory of the accident, the patient experienced recurrent nightmares involving ‘ two lights appearing like the headlights of an approaching motor vehicle ’ and ‘ the feeling of a shock or concussion going through the whole body ’ . The patient would also experience intense psychological distress when driving past the location of the accident or when seeing another accident on the road, and he avoided riding in vehicles of the same make and model as the one he was driving during the crash. The patient displayed all these symptoms without having any conscious memory of the accident.
Case studies such as this suggest that although a traumatic memory may not be stored or recalled at a conscious level, some remnants of the event may be preserved at a comparatively less conscious level. This view is consistent with the idea of at least two distinct memory systems: one mediating conscious memory of the event (a cognitive, declarative, explicit system) and another mediating latent memory of the event (a habit, non-declarative, implicit system).
There are several neurobiological models of PTSD that incorporate more than one memory system (Layton and Wardi-Zonna, 1995; Nadel and Jacobs, 1998; Brewin, 2001; Layton and Krikorian, 2002; Rauch et al., 2006). These neurobiological theories suggest, in part, that the concomitant impairment and enhancement of traumatic memory observed in PTSD may be explained through differential involvement of the hippocampus and amygdala. For example, Layton and Krikorian (2002) propose that as a situation increases in emotional intensity the amygdala becomes progressively more involved in the encoding process. At moderate levels of arousal, the amygdala enhances hippocampal function, thus strengthening the consolidation of aspects of the event dependent on the hippocampus (e.g., contextual aspects, integration of the event into autobiographical memory, etc.). However, at extreme levels of emotional intensity (such as those experienced under trauma) the amygdala inhibits hippocampal function, thus leading to impairments in the consolidation of hippocampal-dependent features of the event. At the same time, the amygdala encodes and consolidates its own version of the traumatic event, serving as the predominant locus of consolidation of the traumatic memory. According to this hypothesis, the traumatic memory mediated by the amygdala remains noncontexual and highly emotional (two characteristics that are common to PTSD flashbacks).
1. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.