Depersonalization disorder: Wikis

  
  

Note: Many of our articles have direct quotes from sources you can cite, within the Wikipedia article! This article doesn't yet, but we're working on it! See more info or our list of citable articles.

Encyclopedia

From Wikipedia, the free encyclopedia

Depersonalization disorder
Classification and external resources
ICD-10 F48.1
ICD-9 300.6
MeSH D003861

Depersonalization disorder (DPD) is a dissociative disorder in which the sufferer is affected by persistent or recurrent feelings of depersonalization and/or derealization. The symptoms include a sense of automation, going through the motions of life but not experiencing it, feeling as though one is in a movie, feeling as though one is in a dream, feeling a disconnection from one's body; out-of-body experience, a detachment from one's body, environment and difficulty relating oneself to reality.

Occasional moments of mild depersonalization are normal;[1] strong, severe persistent or recurrent feelings are not. A diagnosis of a disorder is made when the dissociation is persistent and interferes with the social and occupational functions necessary to everyday living. Depersonalization Disorder is thought to be largely caused by severe traumatic lifetime events including childhood sexual, physical, and emotional abuse, accidents, war, and torture. Drug use may be a mitigating factor. It is unclear whether genetics play a role, however there is evidence of physiological factors with respect to DPD.

Depersonalization disorder can be conceptualized as a defense mechanism as the core symptoms of the disorder are thought to protect the victim from negative stimuli. Depersonalization disorder is often comorbid with anxiety disorders, panic disorders, clinical depression and bipolar disorder.

Although depersonalization disorder is an alteration in the subjective experience of reality, it is by no means related to psychosis as sufferers maintain the ability to distinguish between their own internal experiences and the objective reality of the outside world. Sufferers are able to distinguish between reality and fantasy, during episodic and continuous depersonalization, and do not represent a risk to society since their grasp on reality remains stable at all times.[2]

Contents

Symptoms

The core symptom of depersonalization disorder is the subjective experience of unreality, and as such there are no clinical signs. Common descriptions are: watching oneself from a distance; out-of-body experiences; a sense of just going through the motions; feeling as though one is in a dream or movie; not feeling in control of one's speech or physical movements; and feeling detached from one's own thoughts or emotions.[3] Individuals with the disorder commonly describe a feeling as though time is 'passing' them by and they are not in the notion of the present. These experiences may cause a person to feel uneasy or anxious since they strike at the core of a person's identity and consciousness.

Some of the more common factors that exacerbate dissociative symptoms are negative effects, stress, subjective threatening social interaction, and unfamiliar environments. Factors that tend to diminish symptoms are comforting interpersonal interactions, intense physical or emotional stimulation, and relaxation.[4] Factors identified as relieving symptom severity such as diet, exercise, alcohol and fatigue, are listed by others as worsening symptoms.[5]

Fears of going crazy, brain damage, and losing control are common complaints. Individuals report occupational impairments as they feel they are working below their ability, and interpersonal troubles since they have an emotional disconnection from those they care about. Neuropsychological testing has shown deficits in attention, short-term memory and spatial-temporal reasoning.[6] Depersonalization disorder is associated with cognitive disruptions in early perceptual and attentional processes.[7]

Diagnosis

Diagnosis is based on the self-reported experiences of the person followed by a clinical assessment by a psychiatrist, social worker, clinical psychologist or other mental health professional. Psychiatric assessment includes a psychiatric history and some form of mental status examination. Since some medical and psychiatric conditions mimic the symptoms of DPD, clinicians must differentiate between and rule out the following to establish a precise diagnosis: temporal lobe epilepsy, panic disorder, acute stress disorder, schizophrenia, migraine, drug use, brain tumour or lesion.[3] No laboratory test for depersonalization disorder currently exists.[8]

The diagnosis of DPD can be made with the use of the following interviews and scales: The Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D) is widely used, especially in research settings. This interview takes about 30 minutes to 1.5 hours, depending on individual's experiences.[9]

The Dissociative Experiences Scale (DES) is a simple, quick, self-administered questionnaire that has been widely used to measure dissociative symptoms.[10] It has been used in hundreds of dissociative studies, and can detect depersonalization and derealization experiences.[11]

The Dissociative Disorders Interview Schedule (DDIS) is a highly structured interview which makes DSM-IV diagnoses of somatization disorder, borderline personality disorder and major depressive disorder, as well as all the dissociative disorders.[12] It inquires about positive symptoms of schizophrenia, secondary features of dissociative identity disorder, extrasensory experiences, substance abuse and other items relevant to the dissociative disorders. The DDIS can usually be administered in 30–45 minutes.[12]

DSM-IV-TR criteria

The diagnostic criteria defined in section 300.6 of the Diagnostic and Statistical Manual of Mental Disorders are as follows:[8]

  1. Longstanding or recurring feelings of being detached from one's mental processes or body, as if one is observing them from the outside or in a dream.
  2. Reality testing is unimpaired during depersonalization
  3. Depersonalization causes significant difficulties or distress at work, or social and other important areas of life functioning.
  1. Depersonalization does not only occur while the individual is experiencing another mental disorder, and is not associated with substance use or a medical illness.

The DSM-IV-TR specifically recognizes three possible additional features of depersonalization disorder:

  1. Derealization, experiencing the external world as strange or unreal.
  2. Macropsia or micropsia, an alteration in the perception of object size or shape.
  3. A sense that other people seem unfamiliar or mechanical.

Etiology

The exact cause of depersonalization is unknown, although biopsychosocial correlations and triggers have been identified. Childhood interpersonal trauma, emotional abuse in particular, is a significant predictor of a diagnosis.[13] The most common immediate precipitants of the disorder are severe stress, major depressive disorder and panic, marijuana and hallucinogen ingestion.[14] People who live in highly individualistic cultures may be more vulnerable to depersonalization, due to threat hypersensitivity and an external locus of control.[15]

One cognitive behavioral conceptualization is that misinterpreting normally transient dissociative symptoms as an indication of severe mental illness or neurological impairment leads to the development of the chronic disorder. This leads to a vicious cycle of heightened anxiety and symptoms of depersonalization and derealization.[16]

Not much is known about the neurobiology of depersonalization disorder; however, there is converging evidence that the prefrontal cortex may inhibit neural circuits that normally form the substrate of emotional experience.[17] A PET scan found functional abnormalities in the visual, auditory, and somatosensory cortex, as well as areas responsible for an integrated body schema.[18] In an fMRI study of DPD patients, emotionally aversive scenes activated the right ventral prefrontal cortex. Participants demonstrated a reduced neural response in emotion-sensitive regions, as well as an increased response in regions associated with emotional regulation.[19] In a similar test of emotional memory, depersonalization disorder patients did not process emotionally salient material in the same way as healthy controls.[20] In a test of skin conductance responses to unpleasant stimuli, the subjects showed a selective inhibitory mechanism on emotional processing.[21]

Depersonalization disorder may be associated with dysregulation of the hypothalamic-pituitary-adrenal axis, the area of the brain involved in the "fight-or-flight" response. Patients demonstrate abnormal cortisol levels and basal activity. Studies found that patients with DPD could be distinguished from patients with clinical depression and posttraumatic stress disorder.[22][23]

Epidemiology

Men and women are diagnosed in equal numbers with depersonalization disorder.[5] A 1991 study on a sample from Winnipeg, Manitoba estimated the prevalence of depersonalization disorder at 2.4% of the population.[24] A 2008 review of several studies estimated the prevalence between 0.8% and 2%.[25] This disorder is episodic in about one-third of individuals,[5] with each episode lasting from hours to months at a time. Depersonalization can begin episodically, and later become continuous at constant or varying intensity.[5]

Onset is typically during the teenage years or early 20s, although some report being depersonalized as long as they can remember, and others report a later onset.[4][5] The onset can be acute or insidious. With acute onset, some individuals remember the exact time and place of their first experience of depersonalization. This may follow a prolonged period of severe stress, a traumatic event, an episode of another mental illness, or drug use.[5] Insidious onset may reach back as far as can be remembered, or it may begin with smaller episodes of lesser severity that gradually become stronger. Patients with drug-induced depersonalization do not appear to be a clinically separate group from those with a non-drug precipitant.[26]

Relation to psychiatric disorders

Depersonalization exists as both a primary and secondary phenomenon, although making a clinical distinction appears easy to make but is not absolute. The most common comorbid disorders are depression and anxiety, although cases of depersonalization disorder without symptoms of either do exist. Comorbid obsessive and compulsive behaviours may exist as attempts to deal with depersonalization, such as checking if symptoms have changed and avoiding behavioural and cognitive factors that exacerbate symptoms. Researchers at the Institute of Psychiatry in London, England suggest depersonalization disorder be placed with anxiety and mood disorders, as in the ICD-10, instead of with dissociative disorders as in the DSM-IV-TR.[5]

Treatment

To date, no treatment recommendations or guidelines for depersonalization disorder have been established, and it remains largely resistant to treatment. A variety of psychotherapeutic techniques have been used to treat depersonalization disorder, such as cognitive behavioral therapy, although none of these have established efficacy to date. Clinical pharmacotherapy research continues to explore a number of possible options, including selective serotonin reuptake inhibitors, anticonvulsants, and opioid antagonists.

An open study of cognitive behavior therapy aimed to help patients re-interpret their symptoms in a non-threatening way, which lead to an improvement on several standardized measures.[27]

In a retrospective report of 117 subjects with DPD, 18 of 35 benzodiazepine subjects, reported slight or definite improvement with benzodiazepines and clonazepam in particular.[4] Benzodiazepines are not known to reduce dissociative symptoms, however they do target the often co-morbid anxiety and stress experienced by those with DPD, and thus lead to global improvement.[4] To date no clinical trials have studied the effectiveness of benzodiazepines.[2]

A series of small studies have suggested a possible role of selective serotonin reuptake inhibitors in treating primary depersonalization disorder. However, a placebo-controlled trial failed to show benefit with fluoxetine in 54 patients with depersonalization disorder.[28] SSRI treatment created an overall improvement in participants, but only by reducing anxiety and depression. Clomipramine is a tricyclic antidepressant that is helpful with both depression and obsessional disorders. In a study of four subjects treated with clomipramine, two showed clinically significant improvement of DPD.[29] A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.[25] SSRIs have also been used in combination with lamotrigine, an anticonvulsant.[30]

Naloxone, an antagonist used primarily for the treatment of opiate overdose, was used in a pilot study in 11 patients with chronic DPD. Of the 11 patients, three experienced complete remission, and seven had marked improvement of depersonalization symptoms.[31] The study only reported immediate treatment results, which makes the efficacy of continued treatment unknown. Naloxone can only be administered intravenously, which makes long-term treatment difficult. Naltrexone was used in a preliminary study in 14 individuals with DPD.[32] Participants were treated for 6–10 weeks, at a fairly high average dose of 120 milligrams per day. Three individuals were very much improved, another one was much improved, and on average a 30% decrease in depersonalization symptoms were reported. In another study in borderline personality disorder, doses of 200 milligrams per day of naltrexone was reported to decrease general dissociative symptoms over a 2-week period of treatment.[33]

History

The word depersonalization itself was first used by Henri Frédéric Amiel in The Journal Intime. The July 8, 1880 entry reads:

"I find myself regarding existence as though from beyond the tomb, from another world; all is strange to me; I am, as it were, outside my own body and individuality; I am depersonalized, detached, cut adrift. Is this madness?"[34]

Depersonalization was first used as a clinical term by Ludovic Dugas in 1898 to refer to "a state in which there is the feeling or sensation that thoughts and acts elude the self and become strange; there is an alienation of personality; in other words a depersonalization". This description refers to personalization as a psychical synthesis of attribution of states to the self.[35]

Early theories of the cause of depersonalization focused on sensory impairment. Maurice Krishaber proposed depersonalization was the result of pathological changes to the body's sensory modalities which lead to experiences of "self-strangeness" and the description of one patient who "feels that he is no longer himself". One of Carl Wernicke's students suggested all sensations were composed of a sensory component and a related muscular sensation that came from the movement itself and served to guide the sensory apparatus to the stimulus. In depersonalized patients these two components were not synchronized, and the myogenic sensation failed to reach consciousness. The sensory hypothesis was challenged by others who suggested that patient complaints were being taken too literally and that some descriptions were metaphors; attempts describe experiences that are difficult to articulate in words. Pierre Janet approached the theory by pointing out his patients with clear sensory pathology did not complain of symptoms of unreality, and that those who suffered from depersonalization were normal from a sensory viewpoint.[35]

Psychodynamic theory formed the basis for the conceptualization of dissociation as a defense mechanism. Within this framework, depersonalization is understood as a defense against a variety of negative feelings, conflicts, or experiences. Sigmund Freud himself experienced fleeting derealization when visiting the Acropolis in person; having read about it for years and knowing it existed, seeing the real thing was overwhelming and proved difficult for him to perceive it as real.[36] Freudian theory is the basis for the description of depersonalization as a dissociative reaction, placed within the category of psychoneurotic disorders, in the first two editions of the Diagnostic and Statistical Manual of Mental Disorders.[37]

Society and culture

The director of the autobiographical documentary Tarnation, Jonathan Caouette, suffers from depersonalization disorder. The screenwriter for the 2007 film Numb suffers from depersonalization disorder, as does the film's protagonist played by Matthew Perry. In print, the novel The Stranger by Albert Camus has a protagonist who displays an emotional deadness and views the world as absurd, which is reminiscent of depersonalization disorder.[38]

References

  1. ^ Simeon, D., & Abugel, J. (2006). Feeling Unreal: Depersonalization Disorder and the Loss of the Self. New York, NY: Oxford University Press. (p. 3)
  2. ^ a b Simeon and Abugel p. 32 & 133
  3. ^ a b Simeon D, (2004) Depersonalisation Disorder: A Contemporary Overview. CNS Drugs 18(6): 343-354. PMID 15089102
  4. ^ a b c d Simeon D, Knutelska M, Nelson D & Guralnik O. (2003) Feeling unreal: a depersonalization disorder update of 117 cases. Journal of Clinical Psychiatry 64 (9): 990-7 PMID 14628973
  5. ^ a b c d e f g Baker D, Hunter E, Lawrence E, Medford N, Patel M, Senior C, Sierra M, Lambert MV, Phillips ML, David AS. (2003) Depersonalization disorder: clinical features of 204 cases. British Journal of Psychiatry 2003; 182: 428-33. PMID 12724246 Full text available.
  6. ^ Guralnik O, Schmeidler J, Simeon D. (2003) Feeling unreal: cognitive processes in depersonalization. American Journal of Psychiatry; 157: 103-9. PMID 10618020 Full text available.
  7. ^ Guralnik O, Giesbrecht T, Knutelska M, Sirroff B, Simeon D (December 2007). "Cognitive functioning in depersonalization disorder". J. Nerv. Ment. Dis. 195 (12): 983–8. doi:10.1097/NMD.0b013e31815c19cd. PMID 18091191. 
  8. ^ a b Depersonalization Disorder, ( DSM-IV 300.6, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition)
  9. ^ Steinberg M: Interviewers Guide to the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D). Washington, DC, American Psychiatric Press, 1994.
  10. ^ Bernstein EM, Putnam FW (1986). "Development, reliability, and validity of a dissociation scale". J. Nerv. Ment. Dis. 174 (12): 727–35. doi:10.1097/00005053-198612000-00004. PMID 3783140. 
  11. ^ Simeon and Abugel p. 73-4
  12. ^ a b Saxe GN, van der Kolk BA, Berkowitz R, et al. (July 1993). "Dissociative disorders in psychiatric inpatients". Am J Psychiatry 150 (7): 1037–42. PMID 8317573. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=8317573. 
  13. ^ Simeon D, Guralnik O, Schmeidler J, Sirof B, Knutelska M (2001). "The role of childhood interpersonal trauma in depersonalization disorder". The American journal of psychiatry 158 (7): 1027–33. doi:10.1176/appi.ajp.158.7.1027. PMID 11431223. 
  14. ^ Simeon D: Depersonalisation disorder: a contemporary overview. CNS Drugs. 2004.
  15. ^ Sierra-Siegert M, David AS (December 2007). "Depersonalization and individualism: the effect of culture on symptom profiles in panic disorder". J. Nerv. Ment. Dis. 195 (12): 989–95. doi:10.1097/NMD.0b013e31815c19f7. PMID 18091192. 
  16. ^ Hunter EC, Phillips ML, Chalder T, Sierra M, David AS (December 2003). "Depersonalisation disorder: a cognitive-behavioural conceptualisation". Behav Res Ther 41 (12): 1451–67. doi:10.1016/S0005-7967(03)00066-4. PMID 14583413. http://linkinghub.elsevier.com/retrieve/pii/S0005796703000664. 
  17. ^ Medford N, Sierra M, Baker D, David A. (2005) Understanding and treating depersonalisation disorder. Advances in Psychiatric Treatment 11: 92-100 Full text available.
  18. ^ Simeon D, Guralnik O, Hazlett EA, Spiegel-Cohen J, Hollander E, Buchsbaum MS. (2000) Feeling unreal: a PET study of depersonalization disorder. American Journal of Psychiatry 157(11): 1782-8. PMID 11058475 Full text available.
  19. ^ Phillips ML, Medford N, Senior C, Bullmore ET, Suckling J, Brammer MJ, Andrew C, Sierra M, Williams SC, David AS. (2001) Depersonalization disorder: thinking without feeling. Psychiatry Research: Neuroimaging, 108, 145-160 PMID 11756013
  20. ^ Medford N, Brierley B, Brammer M, Bullmore ET, David AS, Phillips ML. (2006) Emotional memory in depersonalization disorder: a functional MRI study. Psychiatry Research, 148(2-3):93-102. PMID 17085021 Full text available PDF.
  21. ^ Sierra M, Senior C, Dalton J, McDonough M, Bond A, Phillips ML, O'Dwyer AM, David AS. (2002) Autonomic response in depersonalization disorder. Archives of General Psychiatry. 59(9): 833-8. PMID 12215083 Full text available.
  22. ^ Simeon D, Guralnik O, Knutelska M, Hollander E, Schmeidler J (2001). "Hypothalamic-pituitary-adrenal axis dysregulation in depersonalization disorder". Neuropsychopharmacology 25 (5): 793–5. doi:10.1016/S0893-133X(01)00288-3. PMID 11682263. 
  23. ^ Stanton BR, David AS, Cleare AJ, et al. (2001). "Basal activity of the hypothalamic-pituitary-adrenal axis in patients with depersonalization disorder". Psychiatry research 104 (1): 85–9. doi:10.1016/S0165-1781(01)00291-8. PMID 11600192. 
  24. ^ Ross CA. (1991) Epidemiology of multiple personality disorder and dissociation. Psychiatric Clinics of North America 14: 503-17. PMID 1946021
  25. ^ a b Sierra M (January 2008). "Depersonalization disorder: pharmacological approaches". Expert Rev Neurother 8 (1): 19–26. doi:10.1586/14737175.8.1.19. PMID 18088198. http://www.future-drugs.com/doi/abs/10.1586/14737175.8.1.19?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov. 
  26. ^ Medford N, Baker D, Hunter E, et al. (December 2003). "Chronic depersonalization following illicit drug use: a controlled analysis of 40 cases". Addiction 98 (12): 1731–6. doi:10.1111/j.1360-0443.2003.00548.x. PMID 14651505. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0965-2140&date=2003&volume=98&issue=12&spage=1731. 
  27. ^ Hunter EC, Baker D, Phillips ML, Sierra M, David AS (September 2005). "Cognitive-behaviour therapy for depersonalisation disorder: an open study". Behav Res Ther 43 (9): 1121–30. doi:10.1016/j.brat.2004.08.003. PMID 16005701. 
  28. ^ Simeon D, Gurainik O, Schmeidler J, Knutelska M. (2004) Fluoxetine is not efficacious in depersonalisation disorders: a randomized controlled trial. British Journal of Psychiatry, 185: 31-36 PMID 15231553
  29. ^ Simeon D, Stein DJ, Hollander E. (1998) Treatment of depersonalization disorder with clomipramine. Biological Psychiatry, 44, 302-303. PMID 9715363
  30. ^ Sierra M, Baker D, Medford N, et al. (2006). "Lamotrigine as an add-on treatment for depersonalization disorder: a retrospective study of 32 cases". Clin Neuropharmacol 29 (5): 253–8. doi:10.1097/01.WNF.0000228368.17970.DA. PMID 16960469. 
  31. ^ Nuller YL, Morozova MG, Kushnir ON, Hamper N. (2001) Effect of naloxone therapy on depersonalization: a pilot study. Journal of Psychopharmacology. 15(2) 93-95. PMID 11448093
  32. ^ Simeon D, Knutelska M. (2005). An open trial of naltrexone in the treatment of depersonalization disorder. Journal of clinical Psychopharmacology, 25, 267-270. PMID 15876908
  33. ^ Bohus MJ, Landwehrmeyer GB, Stiglmayr CE, Limberger MF, Böhme R, Schmahl CG. (1999). Naltrexone in the treatment of dissociative symptoms in patients with borderline personality disorder: an open-label trial. Journal of Clinical Psychiatry 60(9), 598-603. PMID 10520978
  34. ^ Henri Frédéric Amiel's The Journal Intime Retrieved June 2, 2007
  35. ^ a b Berrios GE, Sierra M (June 1997). "Depersonalization: a conceptual history". Hist Psychiatry 8 (30 Pt 2): 213–29. doi:10.1177/0957154X9700803002. PMID 11619439. 
  36. ^ Mayer-Gross W. (1935). "On depersonalization." British Journal of Medicine and Psychology (15)103-126.
  37. ^ Simeon and Abugel p. 12 & 58
  38. ^ Simeon and Abugel p. 138-9

External links








Got something to say? Make a comment.
Your name
Your email address
Message