dpdr excerpt

Dissociation during traumatic events (also referred to as peritraumatic dissociation [18]) can be considered an adaptive defense mechanism to cope with overwhelming threat that cannot be prevented or escaped [3, 11•]. States of subjective detachment (e.g., depersonalization, derealization, and numbing) may help to create an inner distance to the overwhelming experience by dampening unbearable emotions and reducing conscious awareness of the event. The traumatic situation may be perceived as an unreal film-like scene that is not happening to oneself but observed from a wider distance. Somatoform symptoms such as analgesia and out of body experiences (e.g., the sense of floating above one’s body) may reduce awareness of physical injury [16].

While direct translations between animal and human studies are difficult [21], some models have conceptualized peritraumatic dissociation analogous to the freezing response observed in animals (see, e.g., [16]). The proximity of threat may at first elicit an orienting response, preparing the organism for an active defense mechanism (fight or flight reaction [22]), associated with increased sympathetic nervous system activation (e.g., in heart rate, blood pressure, and release of stress hormones). In situations that cannot be controlled or escaped, the threatened organism may more likely engage in a passive defense mode, accompanied by tonic immobility, increased parasympathic activity, and a “shut-down” of the arousal system [14, 16, 21, 23]. Passive reactions (i.e, tonic immobility) in the face of unescapable threat may enhance survival when the chance of escaping or winning a fight is low or impossible, e.g., by reducing the risk of being detected [23, 24]. As pointed out before, however, translations from animal to human research are complicated by conceptual and methodological differences (see, e.g., [21]).

There is evidence that peritraumatic dissociation increases the risk of subsequent PTSD [18, 25–30]. Although the precise mechanisms remain elusive [18, 28], disturbed information processing, most prominently memory alterations, may play an important role in this relationship [31–34]. Dissociation is thought to interfere with a coherent encoding of salient events [35–37], leading to a fragmentation (compartmentalization) of memory: sensory, affective, and cognitive aspects of the traumatic event are encoded and stored as separate elements, which may later reoccur as implicit intrusive flashback memories, accompanied by strong sensory impressions as if the traumatic event was happening again in the present [29, 38–42].

Sierra and Berrios proposed that symptoms of depersonalization may be associated with a “disconnection” of a cortico-limbic brain system, involving the amygdala, anterior cingulate cortex (ACC), and prefrontal structures. In this model, depersonalization is more broadly conceptualized as a state of subjective detachment, involving emotional numbing, emptiness of thoughts, analgesia, and hypervigilance [62]. It is assumed that these symptoms are associated with increased activity in the medial prefrontal cortex (mPFC), dorsolateral prefrontal cortex (dlPFC), and ACC [63], brain areas implicated in attention, cognitive control, and arousal modulation. Increased recruitment of the PFC may (both directly and indirectly via the ACC) lead to dampened activity in the amygdala and a marked attenuation of automatic responses, comparable to “shutting down the affective system” [62, 64–66]. The amygdala is fundamentally involved in salience detection and emotion processing such as the initiation of stress and fear responses [63, 67–69]. States of detachment (e.g., numbing) may thus be associated with reduced reactivity in this area [70].

                      Annegret Krause-Utz, Rachel Frost, Dorina Winter, and Bernet M. Elzinga