Inhibition/Suppression of Cognitive Processes

Dissociation reflects the culturally and neuro-biologically patterned regulation of attentional mechanisms. It involves the process of inhibiting or suppressing specific perceptual and cognitive processes. Intense fear, threat or trauma can provoke and intensify this self-regulatory process, leading individuals to experience dissociation more frequently or persistently. Dissociation reflects a compartmentalization of memory and experience or an inhibition of the normal integration of otherwise fragmentary or punctuated awareness. In the context of stress, higher order integration might fail to take place, and in fact might be actively inhibited from occurring, because coping with a stressful experience may be more effective that way. In other words, a general ability to narrowly focus attention might be recruited in the context of stress because it helps people to cope. Narrowing of attention and alterations in awareness may also occur in the context of stress simply because the stressor forces itself on attention in such a way that other aspects of awareness are suppressed. Only an approach that encompasses both neuropsychological mechanisms and the social, rhetorical shaping of experience and positioning of the self can hope to capture the complex dynamics of dissociative behavior and experience. [8]

DPDR Implicated Brain Regions

Increased Brain Activity:
  • Default Mode Network
    • Functional Hubs: Medial Prefrontal Cortex
  • Salience Network:
    • Primary Hubs: Dorsal Anterior Cingulate Cortex
  • Right Anterior Cingulate Cortex, Right Ventral Prefrontal Cortex
Decreased Brain Activity:
  • Salience Network
    • Primary Hubs: Anterior Insula
    • Subcortical Structures: Limbic regions (i.e. Amygdala, Hypothalamus)
  • Occipito-temporal Cortex

Hypoarousal/Hyperarousal

The neural correlates of hyperarousal vs. hypoarousal in patients with PTSD showed the opposite patterns of activation in brain regions that are implicated in arousal modulation and emotion regulation. In particular these differential patterns are found in the medial prefrontal cortex and the limbic system, including the anterior cingulate cortex and the amygdala. [6]

Primary dissociation refers to the re-experiencing/hyperaroused type of dissociation and includes the classic PTSD symptoms including intrusive recall, flashbacks, and nightmares. In contrast, secondary dissociation [DPDR/Hypoarousal] is characterized by such symptoms as numbness, depersonalization, derealization, and analgesia responses. [7]

Hypoarousal

  • Neuroimaging studies have demonstrated diminished subcortical limbic activity in response to increasingly intense happy and sad face stimuli and may underlie the dampened emotional responses in [DPDR]. An additional study demonstrated increased activation of the right anterior cingulate and medial prefrontal cortex during self vs stranger face processing; activation in the medial prefrontal cortex positively correlated with depersonalization symptoms. [6]
  • During traumatic memory recall, dissociated individuals exhibited abnormally high activation in the anterior cingulate cortex and the medial prefrontal cortex. The dissociative response was negatively correlated with right anterior insula activation and positively correlated with activation in the medial prefrontal cortex and dorsal anterior cingulate cortex. These results provided the neurobiological basis of the dissociative hypoarousal-subtype of PTSD which focuses on symptoms of depersonalization and derealization. [6]

Hyperarousal

  • Research shows increased activation of the limbic system, especially the amygdala, which is involved in fear conditioning, and direct inhibitory influence of the prefrontal cortex on the emotional limbic system among hyperaroused PTSD patients. These symptoms are a form of emotion dysregulation that involves emotional undermodulation, mediated by failure of prefrontal inhibition of limbic regions. [6]

DPDR & fMRI Brain Scans

  • Shown emotionally relevant images, control groups showed significantly greater activation in the insula and occipito-temporal cortex. DP patients activated the right ventral prefrontal cortex when shown the same images. The insula was activated only by neutral scenes in the dissociated group, indicating that a core phenomenon of depersonalization–absent subjective experience of emotion–is associated with reduced neural responses in emotion-sensitive regions, and increased responses in regions associated with emotion regulation. [1]
  • Depersonalization has been associated with abnormal decreases in limbic activity to increasingly intense emotional expressions, and increases in dorsal prefrontal cortical activity to emotionally arousing stimuli. [2]
  • Depersonalization appears to be associated with functional abnormalities along sequential hierarchical areas, secondary and cross-modal, of the sensory cortex, as well as areas responsible for an integrated body schema. [3]
  • Dissociative participants demonstrated weaker connectivity between the amygdala and right interior insula in response to trauma-relevant images. Their overall cognitive profiles are similar to low-dissociative people in a neutral context, but experience difficulties with attentional control in the context of emotionally evocative stimuli. In a non-neutral context, dissociated individuals demonstrated better performance on an executive functioning task and worse performance on a task of visual memory. [4]
  • The attenuation of emotional experience was associated with reduced activity of the insula, whereas clinical improvement in DPD symptoms was associated with increased insula activity. An area of right ventrolateral prefrontal cortex emerged as particularly implicated region in the inhibition of emotional responses. The core of the depersonalized state, subjective alteration of experience, may be rooted in a lack of anterior insula activity. [5]
  • During virtual maze performance, patients with Dissociative Disorders showed less activation of the cingulate cortex, insula, and inferior parietal cortex as compared to controls, and the performance of Dissociated patients improved as a function of increasing dissociative disorder severity. [6]