Wikipedia

Depersonalization

For social philosophy, seeobjectificationanddehumanization.

Depersonalizationis adissociativephenomenon characterized by a subjective feeling of detachment from oneself, manifesting as a sense of disconnection from one's thoughts, emotions, sensations, or actions, and often accompanied by a feeling of observing oneself from an external perspective.[1][2]Subjects perceive that the world has become vague, dreamlike, surreal, or strange, leading to a diminished sense of individuality or identity. Sufferers often feel as though they are observing the world from a distance,[3]as if separated by a barrier "behind glass".[2]They maintain insight into the subjective nature of their experience, recognizing that it pertains to their own perception rather than altering objective reality. This distinction between subjective experience and objective reality distinguishes depersonalization fromdelusions,where individuals firmly believe in false perceptions as genuine truths. Depersonalization is also distinct fromderealization,which involves a sense of detachment from the external world rather than from oneself.

Individuals who experience depersonalization feel divorced from their own personal self as not belonging to the same identity.

Depersonalization-derealization disorderrefers to chronic depersonalization, classified as adissociative disorder[4]in both theDSM-4and theDSM-5,which underscores its association with disruptions in consciousness, memory, identity, or perception.[5]This classification is based on the findings that depersonalization and derealization are prevalent in other dissociative disorders includingdissociative identity disorder.[6]

Though degrees of depersonalization can happen to anyone who is subject to temporary anxiety or stress, chronic depersonalization is more related to individuals who have experienced a severetraumaor prolonged stress/anxiety. Depersonalization-derealization is the single most important symptom in the spectrum of dissociative disorders, includingdissociative identity disorderand "dissociative disorder not otherwise specified"(DD-NOS). It is also a prominent symptom in some other non-dissociative disorders, such asanxiety disorders,clinical depression,bipolar disorder,schizophrenia,[7]schizoid personality disorder,hypothyroidismor endocrine disorders,[8]schizotypal personality disorder,borderline personality disorder,obsessive–compulsive disorder,migraines,andsleep deprivation;it can also be a symptom of some types of neurologicalseizure,and it has been suggested that there could be common aetiology between depersonalization symptoms and panic disorder, on the basis of their high co-occurrence rates.[2]

Insocial psychology,and in particularself-categorization theory,the termdepersonalizationhas a different meaning and refers to "the stereotypical perception of the self as an example of some defining social category".[9]

Description

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Individuals who experience depersonalization feel divorced from their own personal self by sensing their body sensations, feelings, emotions, behaviors, etc. as not belonging to the same person or identity.[10]Often a person who has experienced depersonalization claims that things seem unreal or hazy. Also, a recognition of aselfbreaks down (hence the name). Depersonalization can result in very highanxietylevels, which further increase these perceptions.[11]

Depersonalization is a subjective experience of unreality in one's self, whilederealizationis unreality of the outside world. Although most authors currently regard depersonalization (personal/self) and derealization (reality/surroundings) as independent constructs, many do not want to separate derealization from depersonalization.[12]

Epidemiology

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Despite the distressing nature of symptoms, estimating the prevalence rates of depersonalization is challenging due to inconsistent definitions and variable timeframes.[2]

Depersonalization is a symptom of anxiety disorders, such aspanic disorder.[13][14]It can also accompanysleep deprivation(often occurring when experiencingjet lag),migraine, epilepsy(especiallytemporal lobe epilepsy,[15] complex-partial seizure,both as part of theauraand during theseizure[16]), obsessive-compulsive disorder,severe stress or trauma,anxiety,the use of recreational drugs[17] —especiallycannabis,hallucinogens,ketamine,andMDMA,certain types ofmeditation,deephypnosis,extended mirror orcrystal gazing,sensory deprivation,and mild-to-moderatehead injurywith little or fullloss of consciousness(less likely if unconscious for more than 30 minutes). Interoceptive exposureis a non-pharmacological method that can be used to induce depersonalization.[18][8]

In the general population, transient depersonalization and derealization are common, having alifetime prevalencebetween 26 and 74%.[2]A random community-based survey of 1,000 adults in the US rural south found a 1-year depersonalization prevalence rate at 19%. Standardized diagnostic interviews have reported prevalence rates of 1.2% to 1.7% over one month in UK samples, and a rate of 2.4% in a single-point Canadian sample.[2]In clinical populations, prevalence rates range from 1% to 16%, with varying rates in specific psychiatric disorders such as panic disorder and unipolar depression.[2]Co-occurrence between depersonalization/derealization and panic disorder is common, suggesting a possible common etiology. Co-morbidity with other disorders does not influence symptom severity consistently.[14]

Depersonalization is reported 2-4 times more in women than in men,[19]but depersonalization/derealization disorder is diagnosed approximately equally across men and women, with symptoms typically emerging around the age of 16.[14]

A similar and overlapping concept calledipseity disturbance(ipse is Latin for "self" or "itself"[20]) may be part of the core process ofschizophreniaspectrum disorders. However, specific to the schizophrenia spectrum seems to be "adislocation of first-person perspective such that self and other or self and world may seem to be non-distinguishable, or in which the individual self or field of consciousness takes on an inordinate significance in relation to the objective or intersubjective world "(emphasis in original).[7]

For the purposes of evaluation and measurement depersonalization can be conceived of as a construct and scales are now available to map its dimensions intime and space.[clarification needed][21]A study of undergraduate students found that individuals high on the depersonalization/derealization subscale of theDissociative Experiences Scaleexhibited a more pronouncedcortisolresponse instress.Individuals high on the absorption subscale, which measures a subject's experiences of concentration to the exclusion of awareness of other events, showed weaker cortisol responses.[22]

Causes

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Depersonalization can arise from a variety of factors, of both a psychological and physiological nature. Common immediate precipitants include instances ofsevere stress,depressive episodes,panic attacks,and the consumption of psychoactive substances such asmarijuanaandhallucinogens.Additionally, there exists a correlation between frequent depersonalization andchildhood interpersonal trauma,particularly cases involvingemotional maltreatment.[14]

Acase-control studyconducted at a specialized depersonalization clinic included 164 individuals with chronic depersonalization symptoms, of which 40 linked their symptoms to illicit drug use.Phenomenologicalsimilarity between drug-induced and non-drug groups was observed, and comparison withmatched controlsfurther supported the lack of distinction. The severity of clinical depersonalization symptoms remains consistent regardless of whether they are triggered by illicit drugs or psychological factors.[23]

Pharmacological

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Depersonalization has been described by some as a desirable state, particularly by those that have experienced it under the influence of mood-alteringrecreational drugs.It is an effect ofdissociativesandpsychedelics,as well as a possible side effect ofcaffeine,alcohol,amphetamine,cannabis,andantidepressants.[24][25][26][27][28]It is a classicwithdrawalsymptom from many drugs.[29][30][31][32]

Benzodiazepine dependence,which can occur with long-term use of benzodiazepines, can induce chronic depersonalization symptomatology and perceptual disturbances in some people, even in those who are taking a stable daily dosage, and it can also become a protracted feature of thebenzodiazepine withdrawal syndrome.[33][34]

Lieutenant ColonelDave Grossman,in his bookOn Killing,suggests that military training artificially creates depersonalization in soldiers, suppressingempathyand making it easier for them to kill other human beings.[35]

Graham Reed(1974) claimed that depersonalization occurs in relation to the experience of falling in love.[36]

Situational

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Experiences of depersonalization/derealization occur on a continuum, ranging from momentary episodes in healthy individuals under conditions ofstress,fatigue,ordrug use,to severe and chronic disorders that can persist for decades.[2]Several studies found that up to 66% of individuals inlife-threatening accidentsreport at least transient depersonalization during or immediately after the accidents.[16]

Several studies, but not all, found age to be a significant factor:adolescentsandyoung adultsin the normal population reported the highest rate. In a study, 46% of college students reported at least one significant episode in the previous year. In another study, 20% of patients with minor head injury experience significant depersonalization and derealization.

Ingeneral infantryandspecial forcessoldiers, measures of depersonalization and derealization increased significantly aftertrainingthat includes experiences of uncontrollable stress, semi-starvation,sleep deprivation,as well as lack of control overhygiene,movement,communications,andsocial interactions.[16]

Biological

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Studies have linked dysregulation of theimmune systemwith depersonalisation.[37]Researchers compared protein expression in serum samples of individuals withdepersonalisation/derealization disorder(DPDR, DDD) and healthy controls, and found that many key proteins involved in maintaininghomeostasiswere present at altered levels. Decreased levels ofC-reactive protein (CRP),complement C1q subcomponent subunit B,and apolipoprotein A-IV, and increased levels of alpha-1-antichymotrypsin (SERPINA3) were observed in patients with DPDR. Furthermore, expressions of CRP and SERPINA3 were found to be linked with the ability to inhibit cognitive interference of DPDR.

Psychobiological mechanisms

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See also:Symptoms of victimization

Proximate mechanism

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Depersonalization involves disruptions in the integration ofinteroceptiveandexteroceptivesignals, particularly in response to acute anxiety ortrauma-related events.Studies spanning from 1992 to 2020 have highlighted abnormalities inprimary somatosensory cortexprocessing andinsulaactivity as contributing factors to depersonalization experiences.[5]Additionally, abnormalEEGactivities, 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.[5]Reduced brain activities in sensory processing units, along with alterations in visceral signal processing regions, are observed, particularly in the early stages ofinformation processing.[5][14]

Furthermore,vestibularsignal 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 theleft hemispheremay 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 theright parietal lobe'sangular gyrushas been linked to more severe depersonalisation, supporting this idea.[5]

Potential involvement ofserotonergic,endogenous opioid,andglutamatergic NMDApathways has also been proposed, alongside alterations in metabolic activity in thesensory association cortex,prefrontal hyperactivation,andlimbic inhibitionin response toaversive stimulirevealed bybrain imagingstudies.[14]

In addition to this, research suggests that individuals with depersonalization often exhibitautonomic 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.[2]Additionally, dysregulation of theHPA axis,which governs the body's stress response system, is frequently observed in individuals who experience depersonalization. This dysregulation can manifest as alterations incortisol levelsand responsiveness to stress, potentially exacerbating feelings of detachment and unreality.[5]

Ultimate mechanism

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Depersonalization is a classic response to acutetrauma,and may be highly prevalent in individuals involved in different traumatic situations includingmotor vehicle collisionandimprisonment.[6]

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 asstressor something as severe as chronically highanxietyandpost-traumatic stress disorder.[38]

The decrease inanxietyand psychobiological hyperarousal helps preserving adaptive behaviors and resources under threat or danger.[6]

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 asPTSDordissociative identity disorder.[38]

Chronic symptoms may represent persistence of depersonalization beyond the situations under threat.[6]

Treatment

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Currently, no universally accepted treatment guidelines have been established for depersonalization. Pharmacotherapy remains a primary avenue of treatment, with medications such asclomipramine,fluoxetine,lamotrigine,andopioid antagonistsbeing commonly prescribed. However, it is important to note that none of these medications have demonstrated a potent anti-dissociative effect in managing symptoms.[14]

In addition to pharmacological interventions, various psychotherapeutic techniques have been employed in attempts to alleviate depersonalization symptoms. Modalities such astrauma-focused therapyandcognitive-behavioral techniqueshave been utilized, although their efficacy remains uncertain and not firmly established.[14]

An attempt at a visual representation of depersonalization

Treatment is dependent on the underlying cause, whether it is organic or psychological in origin. If depersonalization is a symptom of neurological disease, then diagnosis and treatment of the specific disease is the first approach. Depersonalization can be a cognitive symptom of such diseases asamyotrophic lateral sclerosis,Alzheimer's disease,multiple sclerosis(MS), or any other neurological disease affecting the brain.[39][40]For those with both depersonalization andmigraine,tricyclic antidepressantsare often prescribed.

If depersonalization is a symptom of psychological causes such as developmental trauma, treatment depends on the diagnosis. In case ofdissociative identity disorderor DD-NOS as a developmental disorder, in which extreme developmentaltraumainterferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and—in the case of additional (co-morbid) disorders such aseating disorders—a team of specialists treating such an individual. It can also be a symptom ofborderline personality disorder,which can be treated in the long term with proper psychotherapy and psychopharmacology.[41]

The treatment of chronic depersonalization is considered indepersonalization disorder.

A 2001 Russian study showed thatnaloxone,a drug used to reverse the intoxicating effects of opioid drugs, can successfully treat depersonalization disorder. According to the study: "In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization."[42]The anticonvulsant druglamotriginehas shown some success in treating symptoms of depersonalization, often in combination with aselective serotonin reuptake inhibitorand is the first drug of choice at the depersonalisation research unit at King's College London.[41][43][44]

Research directions

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Interest in DPDR has increased over the past few decades, leading to a large accumulation of literature on dissociative disorders. There has been a shift towards the use of research studies, rather thancase studiesto understand depersonalization.[2]However, there remains a lack of solid consensus on its definition and scales used for assessment.[2][14]Salami and colleagues argued that studies ofelectrophysiologicaldepersonalization-derealization markers are urgently needed, and that future research should use analysis methods that can account for the integration ofinteroceptiveandexteroceptivesignals.[5]

The Depersonalisation Research Unit at the Institute of Psychiatry in London conducts research intodepersonalization disorder.[45]Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder.

In a 2020 article in theJournal Nature,Vesuna, et al. describe experimental findings which show that layer 5 of the retrosplenial cortex is likely responsible for dissociative states of consciousness in mammals.

See also

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References

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Other references

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  • Loewenstein, Richard J; Frewen, Paul; Lewis-Fernández, Roberto (2017). "20 Dissociative Disorders". In Sadock, Virginia A; Sadock, Benjamin J; Ruiz, Pedro (eds.).Kaplan & Sadock's Comprehensive Textbook of Psychiatry(10th ed.). Wolters Kluwer.ISBN978-1-4511-0047-1.
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