Interestingly, excitatory magnetic stimulation over the same prefrontal areas has been shown to give rise to DPD symptoms in a treatment-resistant depressed patient 29. Two case studies 25, 26 and two trials 27, 28 demonstrated the directionality and causality of the fronto-insular inhibitory circuit by reporting temporary reduction in DPD symptoms immediately after the delivery of inhibitory magnetic stimulation over the lateral prefrontal cortex. This fronto-insular inhibitory mechanism has also been observed in healthy individuals during voluntary negative affect suppression tasks, thus suggesting that the emotional detachment manifested in DPD may be the result of a pathological enhancement of an otherwise healthy control mechanism 24. Accordingly, DPD patients exhibit autonomic responses to negative emotional stimuli that are blunted compared to those of healthy controls 22, and inversely related to lateral prefrontal activation 23, thus supporting the hypothesis of an inhibitory role carried out by frontal areas. As put forward in Sierra and David's model, in DPD lateral prefrontal cortices employ an excessive inhibitory control over the insula, dampening the emotional experience and giving rise to a subjective “feeling of unreality" 11 (p. Conversely, lateral prefrontal cortices are largely involved in emotion and action regulation 15, 16, 17, inhibitory control 18, 19, as well as goal-appropriate response selection 20, 21 and are thought to exert inhibitory control over the insula. The insula is a cortical area receiving information about the internal state of the body and it is considered a key region of emotional and bodily awareness processing 14. This idea is based on the observation of a reduction of anterior insula (AI) activation in response to emotional stimuli, together with increased lateral prefrontal activation in DPD patients as compared to healthy controls 12, 13. One model, developed by Sierra and David 11, suggests that DPD may arise as a consequence of an increased cognitive control of the subjective affective experience. Several attempts to explain the aetiology of DPD have been made in recent years 10. Despite the vivid nature of such feelings of detachment, patients' ability to distinguish between subjective and objective reality remains intact. More serious forms of DPD may be associated with a previous history of anxiety and panic disorder 6, 7, 8, and symptoms of depersonalisation frequently accompany psychiatric conditions such as post-traumatic stress disorder, schizophrenia, panic disorder and depression 5, 9. Mild and transient DPD episodes are a common phenomenon, with a life prevalence estimated at 74%, and often results from stress and fatigue 5.
DPD symptomatology is mainly characterised by emotional numbing (i.e., “de-affectualisation" 1, 2, 3), together with a feeling of detachment from one's own body 4. Finally, our simulation shows that repeated exposure to similar situations over time will lead the agent to increasingly disengage from bodily responses even in the face of a less triggering situation, explaining how a single episode of depersonalization can lead to chronic DPD.ĭepersonalisation disorder (DPD) is a psychopathological condition characterised by a persistent and distressing alteration in the quality of a person's subjective experience of themselves (depersonalisation), which can be accompanied by a modified perception of one's surroundings (derealisation). Such interoceptive silencing would force the agent to over-rely on exteroceptive information and would ultimately lead to the DPD phenomenology. The simulation showed how a similar condition, if perceived as inescapable, would result in a downregulation of interoceptive signals, whilst leaving the exteroceptive ones unaffected. We simulated the behaviour of an agent subjected to a situation of high interoceptive activation despite the absence of a perceivable threat in the external environment. Specifically, we describe DPD as arising from disrupted interoceptive processing at higher levels of the cortical hierarchy where the interoceptive and exteroceptive streams are integrated. Here we present a computational and neurobiologically plausible model of DPD within the active inference framework.
However, the precise mechanisms that drive this ‘interoceptive silencing’ are yet to be clarified. Depersonalisation disorder (DPD) is a psychopathological condition characterised by a feeling of detachment from one's own body and surrounding, and it is understood as emerging from the downregulation of interoceptive afferents.
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