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Depersonalization
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== Psychobiological mechanisms == {{See also|Symptoms of victimization}} === Proximate mechanism === Depersonalization involves disruptions in the integration of [[interoceptive]] and [[Proprioception|exteroceptive]] signals, particularly in response to acute anxiety or [[Traumatic memories|trauma-related events]]. Studies spanning from 1992 to 2020 have highlighted abnormalities in [[primary somatosensory cortex]] processing and [[Insular cortex|insula]] activity as contributing factors to depersonalization experiences.<ref name=":1" /> Additionally, abnormal [[EEG]] activities, notably in the theta band, suggest potential biomarkers for emotion processing, attention, and working memory, though specific oscillatory signatures associated with depersonalization are yet to be determined.<ref name=":1" /> Reduced brain activities in sensory processing units, along with alterations in visceral signal processing regions, are observed, particularly in the early stages of [[Information processing theory|information processing]].<ref name=":1" /><ref name="Simeon-2004" /> Furthermore, [[Vestibular system|vestibular]] signal processing, crucial for balance and spatial orientation, is increasingly recognized as a factor contributing to feelings of disembodiment during depersonalization experiences. Research suggests that abnormal activity in the [[left hemisphere]] may play a role, although abnormalities in right hemisphere brain activity, responsible for self-awareness and emotion processing, may also contribute to depersonalization symptoms. Higher activity in the [[Parietal lobe|right parietal lobe's]] [[angular gyrus]] has been linked to more severe depersonalisation, supporting this idea.<ref name=":1" /> Potential involvement of [[Serotonin|serotonergic]], [[Opioid|endogenous opioid]], and [[Glutamatergic neurotransmission|glutamatergic NMDA]] pathways has also been proposed, alongside alterations in metabolic activity in the [[Sensory nervous system|sensory association cortex]], [[Prefrontal cortex|prefrontal hyperactivation]], and [[Limbic system|limbic inhibition]] in response to [[aversive stimuli]] revealed by [[brain imaging]] studies.<ref name="Simeon-2004" /> In addition to this, research suggests that individuals with depersonalization often exhibit [[Autonomic nervous system|autonomic blunting]], characterized by reduced physiological responses to stressors or emotional stimuli. This blunting may reflect a diminished capacity to engage with the external world or to experience emotions fully, contributing to the subjective sense of detachment from oneself.<ref name=":0" /> Additionally, dysregulation of the [[HPA axis]], which governs the body's stress response system, is frequently observed in individuals who experience depersonalization. This dysregulation can manifest as alterations in [[Cortisol|cortisol levels]] and responsiveness to stress, potentially exacerbating feelings of detachment and unreality.<ref name=":1" /> === Ultimate mechanism === Depersonalization is a classic response to acute [[Psychological trauma|trauma]], and may be highly prevalent in individuals involved in different traumatic situations including [[motor vehicle collision]] and [[imprisonment]].<ref name=Sadock2017-DPD-Criteria-Change /> Psychologically depersonalization can, just like dissociation in general, be considered a type of coping mechanism, used to decrease the intensity of unpleasant experience, whether that is something as mild as [[Psychological stress|stress]] or something as severe as chronically high [[anxiety]] and [[post-traumatic stress disorder]].<ref name=Domain-Dissociation-1994 /> The decrease in [[anxiety]] and psychobiological hyperarousal helps preserving adaptive behaviors and resources under threat or danger.<ref name=Sadock2017-DPD-Criteria-Change /> Depersonalization is an overgeneralized reaction in that it doesn't diminish just the unpleasant experience, but more or less all experience – leading to a feeling of being detached from the world and experiencing it in a more bland way. An important distinction must be made between depersonalization as a mild, short-term reaction to unpleasant experience and depersonalization as a chronic symptom stemming from a severe mental disorder such as [[PTSD]] or [[dissociative identity disorder]].<ref name="Domain-Dissociation-1994">{{cite book |last1=Cardeña |first1=Etzel |chapter=The Domain of Dissociation |year=1994 |editor1-first=Steven J. |editor1-last=Lynn |editor2-first=Judith W. |editor2-last=Rhue |title=Dissociation: Clinical and theoretical perspectives |pages=15–31 |location=New York |publisher=[[Guilford Press]] |isbn=978-0-89862-186-0}}</ref> Chronic symptoms may represent persistence of depersonalization beyond the situations under threat.<ref name=Sadock2017-DPD-Criteria-Change />
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