AccessMyLibrary provides FREE access to over 30 million articles from top publications available through your library.
Create a link to this page
Copy and paste this link tag into your Web page or blog:
Introduction
Neurobiological findings (1-9) and clinical data (10,11) suggest that conditioning processes are inhibited by dissociation. Regarding neurobiological processes, the corticolimbic disconnection model of dissociation (12) hypothesizes that the medial prefrontal cortex inhibits the amygdala, resulting in a reduced emotional experience and a dampened autonomic output. Recent studies have partially confirmed this dissociation model. Individuals with depersonalization disorder showed reduced autonomic and emotional responses to unpleasant pictures (1) and facial expressions of disgust (2) but not to neutral stimuli, suggesting a selective inhibition of emotional processing. They also showed an absence of subjective emotional experience and no activation of brain regions involved in normal emotional processing (insula and occipitotemporal cortex) when viewing aversive pictures (3) or during encoding and recognition of emotional verbal material (4) Similarly, individuals who had posttraumatic stress disorder (PTSD) with present-state dissociative experiences exhibited reduced heart rates and increased activation in the dorsolateral and medial frontal cortices compared with a nondissociative PTSD subgroup in a traumatic script-driven symptomprovocation paradigm. (5,7) Likewise, an inverse relation between dissociation severity and cortisol stress reactivity during a psychosocial stress paradigm has been shown in people with dissociative disorders and people with PTSD. (8) Our group has recently demonstrated that individuals with borderline personality disorder (BPD) exhibit reduced startle response amplitude during states of dissociative experience. (9) This is in accordance with the corticolimbic disconnection model of dissociation, (12) since the startle reflex can be directly modified by the central nucleus of the amygdala. (13)
With respect to clinical findings, dissociative experience has been identified as a predictor of poor outcome in behavioural treatments for panic disorder (10) and obsessive-compulsive disorder. (11) This may be explained by the reduced emotional engagement during dissociative experience, as emotional engagement is thought to be crucial for successful exposure therapy. (14) To our knowledge, there are no experimental studies investigating the influence of dissociation on classical conditioning processes (see Giesbrecht and colleagues (15) for a review on experimental studies on dissociation).
The neural circuitry underlying classical conditioning has been well characterized, and emotional and cognitive/ declarative learning components can be distinguished. (16,17) Emotional learning is largely based on a pathway connecting the amygdala and the medial frontal cortex, (18-21) whereas the cognitive components can be related to the lateral frontal cortex and the hippocampus. (16,17) Accordingly, selective damage of the amygdala in humans leads to impaired emotional learning (no acquisition of skin conductance responses) but intact cognitive/ declarative knowledge, whereas selective damage of the hippocampus leads to impaired cognitive/ declarative knowledge but intact emotional leaming. (16)
To determine whether emotional learning depends on dissociative state, we conducted a differential aversive Pavlovian delay conditioning procedure. We chose to study patients with BPD, in which dissociation is commonly observed clinically and is a diagnostic criterion of this disorder. We assumed that present state dissociative experience would specifically alter amygdala-based emotional learning but not hippocampus-based cognitive/ declarative knowledge. Specifically, we hypothesized that patients with BPD who had high states of dissociative experience during the experiment would exhibit diminished acquisition of differential conditioning regarding emotional learning (valence, arousal, skin conductance response) compared with patients with BPD and healthy controls who did not experience dissociative symptoms during the experiment. We furthermore hypothesized that the groups would not differ with regard to cognitive/declarative knowledge (contingency awareness).
Methods
Participants