Depersonalization
![](http://upload.wikimedia.org/wikipedia/commons/thumb/8/89/Depersonalization.jpg/220px-Depersonalization.jpg)
Depersonalization is a dissociative phenomenon 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 from delusions, where individuals firmly believe in false perceptions as genuine truths. Depersonalization is also distinct from derealization, which involves a sense of detachment from the external world rather than from oneself.
Depersonalization/derealization disorder refers to chronic depersonalization, classified as a dissociative disorder[4] in both the DSM-4 and the DSM-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 including dissociative 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 severe trauma or prolonged stress/anxiety. Depersonalization-derealization is the single most important symptom in the spectrum of dissociative disorders, including dissociative identity disorder and "dissociative disorder not otherwise specified" (DD-NOS). It is also a prominent symptom in some other non-dissociative disorders, such as anxiety disorders, clinical depression, bipolar disorder, schizophrenia,[7] schizoid personality disorder, hypothyroidism or endocrine disorders,[8] schizotypal personality disorder, borderline personality disorder, obsessive–compulsive disorder, migraines, and sleep deprivation; it can also be a symptom of some types of neurological seizure, 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]
In social psychology, and in particular self-categorization theory, the term depersonalization has a different meaning and refers to "the stereotypical perception of the self as an example of some defining social category".[9]
Description
[edit]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 a self breaks down (hence the name). Depersonalization can result in very high anxiety levels, which further increase these perceptions.[11]
Depersonalization is a subjective experience of unreality in one's self, while derealization is 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
[edit]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 as panic disorder.[13][14] It can also accompany sleep deprivation (often occurring when experiencing jet lag), migraine, epilepsy (especially temporal lobe epilepsy,[15] complex-partial seizure, both as part of the aura and during the seizure[16]), obsessive-compulsive disorder, severe stress or trauma, anxiety, the use of recreational drugs[17] —especially cannabis, hallucinogens, ketamine, and MDMA, certain types of meditation, deep hypnosis, extended mirror or crystal gazing, sensory deprivation, and mild-to-moderate head injury with little or full loss of consciousness (less likely if unconscious for more than 30 minutes). Interoceptive exposure is a non-pharmacological method that can be used to induce depersonalization.[18][8]
In the general population, transient depersonalization and derealization are common, having a lifetime prevalence between 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 called ipseity disturbance (ipse is Latin for "self" or "itself"[20]) may be part of the core process of schizophrenia spectrum disorders. However, specific to the schizophrenia spectrum seems to be "a dislocation 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 in time and space.[clarification needed][21] A study of undergraduate students found that individuals high on the depersonalization/derealization subscale of the Dissociative Experiences Scale exhibited a more pronounced cortisol response in stress. 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
[edit]Depersonalization can arise from a variety of factors, of both a psychological and physiological nature. Common immediate precipitants include instances of severe stress, depressive episodes, panic attacks, and the consumption of psychoactive substances such as marijuana and hallucinogens. Additionally, there exists a correlation between frequent depersonalization and childhood interpersonal trauma, particularly cases involving emotional maltreatment.[14]
A case-control study conducted at a specialized depersonalization clinic included 164 individuals with chronic depersonalization symptoms, of which 40 linked their symptoms to illicit drug use. Phenomenological similarity between drug-induced and non-drug groups was observed, and comparison with matched controls further 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
[edit]Depersonalization has been described by some as a desirable state, particularly by those that have experienced it under the influence of mood-altering recreational drugs. It is an effect of dissociatives and psychedelics, as well as a possible side effect of caffeine, alcohol, amphetamine, cannabis, and antidepressants.[24][25][26][27][28] It is a classic withdrawal symptom 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 the benzodiazepine withdrawal syndrome.[33][34]
Lieutenant Colonel Dave Grossman, in his book On Killing, suggests that military training artificially creates depersonalization in soldiers, suppressing empathy and 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
[edit]Experiences of depersonalization/derealization occur on a continuum, ranging from momentary episodes in healthy individuals under conditions of stress, fatigue, or drug use, to severe and chronic disorders that can persist for decades.[2] Several studies found that up to 66% of individuals in life-threatening accidents report at least transient depersonalization during or immediately after the accidents.[16]
Several studies, but not all, found age to be a significant factor: adolescents and young adults in 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.
In general infantry and special forces soldiers, measures of depersonalization and derealization increased significantly after training that includes experiences of uncontrollable stress, semi-starvation, sleep deprivation, as well as lack of control over hygiene, movement, communications, and social interactions.[16]
Psychobiological mechanisms
[edit]Proximate mechanism
[edit]Depersonalization involves disruptions in the integration of interoceptive and exteroceptive signals, particularly in response to acute anxiety or trauma-related events. Studies spanning from 1992 to 2020 have highlighted abnormalities in primary somatosensory cortex processing and insula activity as contributing factors to depersonalization experiences.[5] 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.[5] 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.[5][14]
Furthermore, 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 right parietal lobe's angular gyrus has been linked to more severe depersonalisation, supporting this idea.[5]
Potential involvement of serotonergic, endogenous opioid, and glutamatergic NMDA pathways has also been proposed, alongside alterations in metabolic activity in the sensory association cortex, prefrontal hyperactivation, and limbic inhibition in response to aversive stimuli revealed by brain imaging studies.[14]
In addition to this, research suggests that individuals with depersonalization often exhibit 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.[2] 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 levels and responsiveness to stress, potentially exacerbating feelings of detachment and unreality.[5]
Ultimate mechanism
[edit]Depersonalization is a classic response to acute trauma, and may be highly prevalent in individuals involved in different traumatic situations including motor vehicle collision, and imprisonment.[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 as stress or something as severe as chronically high anxiety and post-traumatic stress disorder.[37]
The decrease in anxiety and 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 as PTSD or dissociative identity disorder.[37]
Chronic symptoms may represent persistence of depersonalization beyond the situations under threat.[6]
Treatment
[edit]Currently, no universally accepted treatment guidelines have been established for depersonalization. Pharmacotherapy remains a primary avenue of treatment, with medications such as clomipramine, fluoxetine, lamotrigine, and opioid antagonists being 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 as trauma-focused therapy and cognitive-behavioral techniques have been utilized, although their efficacy remains uncertain and not firmly established.[14]
![](http://upload.wikimedia.org/wikipedia/commons/thumb/f/ff/Depersonalization_Disorder_by_Boris_D._Og%C3%B1enovich.png/220px-Depersonalization_Disorder_by_Boris_D._Og%C3%B1enovich.png)
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 as amyotrophic lateral sclerosis, Alzheimer's disease, multiple sclerosis (MS), or any other neurological disease affecting the brain.[38][citation needed] For those with both depersonalization and migraine, tricyclic antidepressants are often prescribed.
If depersonalization is a symptom of psychological causes such as developmental trauma, treatment depends on the diagnosis. In case of dissociative identity disorder or DD-NOS as a developmental disorder, in which extreme developmental trauma interferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and—in the case of additional (co-morbid) disorders such as eating disorders—a team of specialists treating such an individual. It can also be a symptom of borderline personality disorder, which can be treated in the long term with proper psychotherapy and psychopharmacology.[39]
The treatment of chronic depersonalization is considered in depersonalization disorder.
A 2001 Russian study showed that naloxone, 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."[40] The anticonvulsant drug lamotrigine has shown some success in treating symptoms of depersonalization, often in combination with a selective serotonin reuptake inhibitor and is the first drug of choice at the depersonalisation research unit at King's College London.[39][41][42]
Research directions
[edit]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 than case studies to 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 of electrophysiological depersonalization-derealization markers are urgently needed, and that future research should use analysis methods that can account for the integration of interoceptive and exteroceptive signals.[5]
The Depersonalisation Research Unit at the Institute of Psychiatry in London conducts research into depersonalization disorder.[43] Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder.
In a 2020 article in the Journal 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
[edit]- Alienation
- Brain fog
- Catatonic state
- Cognition
- Derealization
- Dissociation (psychology)
- Ego death
- Falling (sensation)
- Hallucinogen persisting perception disorder
- Human spirit
- Nina Searl
- Out-of-body experience
- Post-assault treatment of sexual assault victims
- Post-traumatic stress disorder
- Psychedelic experience
- Psychological trauma
- Śūnyatā
- Spiritual crisis
- Weltschmerz
References
[edit]- ^ Sierra, M.; Berrios, G. E. (2001). "The phenomenological stability of depersonalization: Comparing the old with the new". The Journal of Nervous and Mental Disease. 189 (9): 629–36. doi:10.1097/00005053-200109000-00010. PMID 11580008. S2CID 22920376.
- ^ a b c d e f g h i j k Hunter, E. C. M.; Sierra, M.; David, A. S. (2004-01-01). "The epidemiology of depersonalisation and derealisation". Social Psychiatry and Psychiatric Epidemiology. 39 (1): 9–18. doi:10.1007/s00127-004-0701-4. ISSN 1433-9285. PMID 15022041.
- ^ "Depersonalization-derealization disorder - Symptoms and causes". Mayo Clinic. Archived from the original on 2017-10-08. Retrieved 2022-03-28.
- ^ American Psychiatry Association (2013). "Dissociative Disorders". Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington: American Psychiatric Publishing. pp. 291-307. ISBN 978-0-89042-555-8.
- ^ a b c d e f g Salami, Abbas; Andreu-Perez, Javier; Gillmeister, Helge (November 2020). "Symptoms of depersonalisation/derealisation disorder as measured by brain electrical activity: A systematic review". Neuroscience & Biobehavioral Reviews. 118: 524–537. arXiv:2111.06126. doi:10.1016/j.neubiorev.2020.08.011. ISSN 0149-7634. PMID 32846163. Archived from the original on 2024-04-12. Retrieved 2024-03-29.
- ^ a b c d Dissociative Disorders (2017), CHANGES IN DIAGNOSTIC CRITERIA TO THE DISSOCIATIVE DISORDERS, Changes to the Diagnostic Criteria for Depersonalization Disorder
- ^ a b Sass, Louis; Pienkos, Elizabeth; Nelson, Barnaby; Medford, Nick (2013). "Anomalous self-experience in depersonalization and schizophrenia: A comparative investigation". Consciousness and Cognition. 22 (2): 430–441. doi:10.1016/j.concog.2013.01.009. PMID 23454432. S2CID 13551169.
- ^ a b Sharma, Kirti; Behera, Joshil Kumar; Sood, Sushma; Rajput, Rajesh; Satpal; Praveen, Prashant (2014). "Study of cognitive functions in newly diagnosed cases of subclinical and clinical hypothyroidism". Journal of Natural Science, Biology, and Medicine. 5 (1): 63–66. doi:10.4103/0976-9668.127290. ISSN 0976-9668. PMC 3961955. PMID 24678200.
- ^ Turner, John; Oakes, Penny (1986). "The significance of the social identity concept for social psychology with reference to individualism, interactionism and social influence". British Journal of Social Psychology. 25 (3): 237–52. doi:10.1111/j.2044-8309.1986.tb00732.x.
- ^ Depersonalization Disorder at Merck Manual of Diagnosis and Therapy Home Edition [permanent dead link]
- ^ Hall-Flavin, Daniel. "Depersonalization disorder: A feeling of being 'outside' your body". Archived from the original on 2007-09-29. Retrieved 2007-09-08.
- ^ Radovic, F.; Radovic, S. (2002). "Feelings of Unreality: A Conceptual and Phenomenological Analysis of the Language of Depersonalization". Philosophy, Psychiatry, & Psychology. 9 (3): 271–9. doi:10.1353/ppp.2003.0048. S2CID 145074433.
- ^ Sierra-Siegert M, David AS (December 2007). "Depersonalization and individualism: the effect of culture on symptom profiles in panic disorder". Journal of Nervous and Mental Disease. 195 (12): 989–95. doi:10.1097/NMD.0b013e31815c19f7. PMID 18091192. S2CID 7182322.
- ^ a b c d e f g h i Simeon D (2004). "Depersonalisation Disorder: A Contemporary Overview". CNS Drugs. 18 (6): 343–54. doi:10.2165/00023210-200418060-00002. PMID 15089102. S2CID 18506672.
- ^ Michelle V. Lambert; Mauricio Sierra; Mary L. Phillips; Anthony S. David (May 2002). "The Spectrum of Organic Depersonalization: A Review Plus Four New Cases". The Journal of Neuropsychiatry and Clinical Neurosciences. 14 (2): 141–54. doi:10.1176/appi.neuropsych.14.2.141. PMID 11983788.
- ^ a b c Dissociative Disorders (2017), GENERAL POPULATION STUDIES OF DISSOCIATIVE DISORDERS, Epidemiology of Depersonalization and Derealization Symptoms.
- ^ "Depersonalization-derealization disorder - Symptoms and causes". Mayo Clinic. Archived from the original on 2017-10-08. Retrieved 2019-11-20.
- ^ Lickel J; Nelson E; Lickel A H; Brett Deacon (2008). "Interoceptive Exposure Exercises for Evoking Depersonalization and Derealization: A Pilot Study". Journal of Cognitive Psychotherapy. 22 (4): 321–30. doi:10.1891/0889-8391.22.4.321. S2CID 12746427.
- ^ Sadock, BJ; Sadock, VA (2015). "12: Dissociative Disorders". Kaplan and Sadock's Synopsis of Psychiatry (11th ed.). Wolters Kluwer. DEPERSONALIZATION/DEREALIZATION DISORDER, Epidemiology, pp. 454-455. ISBN 978-1-60913-971-1.
- ^ Sass, Louis A.; Parnas, Josef (2003). "Schizophrenia, Consciousness, and the Self". Schizophrenia Bulletin. 29 (3): 427–44. doi:10.1093/oxfordjournals.schbul.a007017. PMID 14609238.
- ^ Sierra, Mauricio; Berrios, German E. (2000). "The Cambridge Depersonalisation Scale: A new instrument for the measurement of depersonalisation". Psychiatry Research. 93 (2): 153–164. doi:10.1016/S0165-1781(00)00100-1. PMID 10725532. S2CID 206024895.
- ^ Giesbrecht, T.; T. Smeets; H. Merckelbac; M. Jelicic (2007). "Depersonalization experiences in undergraduates are related to heightened stress cortisol responses". Journal of Nervous and Mental Disease. 195 (4): 282–87. doi:10.1097/01.nmd.0000253822.60618.60. PMID 17435477. S2CID 9283387.
- ^ Medford, Nicholas; Baker, Dawn; Hunter, Elaine; Sierra, Mauricio; Lawrence, Emma; Phillips, Mary L.; David, Anthony S. (December 2003). "Chronic depersonalization following illicit drug use: a controlled analysis of 40 cases". Addiction. 98 (12): 1731–1736. doi:10.1111/j.1360-0443.2003.00548.x. ISSN 0965-2140. PMID 14651505. Archived from the original on 2023-04-30. Retrieved 2024-03-30.
- ^ Stein, M. B.; Uhde, TW (July 1989). "Depersonalization Disorder: Effects of Caffeine and Response to Pharmacotherapy". Biological Psychiatry. 26 (3): 315–20. doi:10.1016/0006-3223(89)90044-9. PMID 2742946. S2CID 34396397. Archived from the original on 2024-01-26. Retrieved 2019-07-12.
- ^ Raimo, E. B.; R. A. Roemer; M. Moster; Y. Shan (June 1999). "Alcohol-Induced Depersonalization". Biological Psychiatry. 45 (11): 1523–6. doi:10.1016/S0006-3223(98)00257-1. PMID 10356638. S2CID 34049706.
- ^ Cohen, P. R. (2004). "Medication-associated depersonalization symptoms: report of transient depersonalization symptoms induced by minocycline". Southern Medical Journal. 97 (1): 70–73. doi:10.1097/01.SMJ.0000083857.98870.98. PMID 14746427. S2CID 27125601.
- ^ "Medication-Associated Depersonalization Symptoms". medscape.com. Archived from the original on 2015-02-14. Retrieved 2009-03-30.
- ^ Arehart-Treichel, Joan (2003-08-15). "Depersonalization Again Finds Psychiatric Spotlight". Psychiatric News. 38 (16): 18–30. doi:10.1176/pn.38.16.0018.
- ^ Marriott, S.; P. Tyrer (1993). "Benzodiazepine dependence: avoidance and withdrawal". Drug Safety. 9 (2): 93–103. doi:10.2165/00002018-199309020-00003. PMID 8104417. S2CID 8550990.
- ^ Shufman, E.; A. Lerner; E. Witztum (2005). "Depersonalization after withdrawal from cannabis usage" [Depersonalization after withdrawal from cannabis usage]. Harefuah (in Hebrew). 144 (4): 249–51 and 303. PMID 15889607.
- ^ Djenderedjian, A.; R. Tashjian (1982). "Agoraphobia following amphetamine withdrawal". The Journal of Clinical Psychiatry. 43 (6): 248–49. PMID 7085580.
- ^ Mourad, I.; M. Lejoyeux; J. Adès (1998). "Evaluation prospective du sevrage des antidépresseurs" [Prospective evaluation of antidepressant discontinuation]. L'Encéphale (in French). 24 (3): 215–22. PMID 9696914.
- ^ Ashton, Heather (1991). "Protracted withdrawal syndromes from benzodiazepines". Journal of Substance Abuse Treatment. 8 (1–2): 19–28. doi:10.1016/0740-5472(91)90023-4. PMID 1675688.
- ^ Terao T; Yoshimura R; Terao M; Abe K (1992-01-15). "Depersonalization following nitrazepam withdrawal". Biological Psychiatry. 31 (2): 212–3. doi:10.1016/0006-3223(92)90209-I. PMID 1737083. S2CID 26522217.
- ^ Grossman, Dave (1996). On Killing: The Psychological Cost of Learning to Kill in War and Society. Back Bay Books. ISBN 978-0-316-33000-8.
- ^ Reed, Graham (1972). The Psychology of Anomalous Experience. Hutchinson. p. 127. ISBN 9780091132408.
- ^ a b Cardeña, Etzel (1994). "The Domain of Dissociation". In Lynn, Steven J.; Rhue, Judith W. (eds.). Dissociation: Clinical and theoretical perspectives. New York: Guilford Press. pp. 15–31. ISBN 978-0-89862-186-0.
- ^ "Overview of Child Neglect and Abuse - Overview of Child Neglect and Abuse". MSD Manual Consumer Version. Retrieved 28 June 2024.
- ^ a b Sierra, Mauricio; Baker, Dawn; Medford, Nicholas; Lawrence, Emma; Patel, Maxine; Phillips, Mary L.; David, Anthony S. (2006). "Lamotrigine as an Add-on Treatment for Depersonalization Disorder". Clinical Neuropharmacology. 29 (5): 253–258. doi:10.1097/01.WNF.0000228368.17970.DA. PMID 16960469. S2CID 38595510.
- ^ Nuller, Yuri L.; Morozova, Marina G.; Kushnir, Olga N.; Hamper, Nikita (2001). "Effect of naloxone therapy on depersonalization: A pilot study". Journal of Psychopharmacology. 15 (2): 93–95. doi:10.1177/026988110101500205. PMID 11448093. S2CID 22934937.
- ^ Somer, Eli; Amos-Williams, Taryn; Stein, Dan J. (2013). "Evidence-based treatment for Depersonalisation-derealisation Disorder (DPRD)". BMC Psychology. 1 (1): 20. doi:10.1186/2050-7283-1-20. PMC 4269982. PMID 25566370.
- ^ Medford, Nick; Sierra, Mauricio; Baker, Dawn; David, Anthony S. (2005). "Understanding and treating depersonalisation disorder". Advances in Psychiatric Treatment. 11 (2): 92–100. doi:10.1192/apt.11.2.92.
- ^ "Depersonalisation Research Unit - Institute of Psychiatry, London". Archived from the original on 2007-01-18. Retrieved 2006-11-07.
Other references
[edit]- 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. ISBN 978-1-4511-0047-1.