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A recent 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."<ref>{{Cite journal | last1 = Nuller | first1 = Yuri L. | last2 = Morozova | first2 = Marina G. | last3 = Kushnir | first3 = Olga N. | last4 = Hamper | first4 = Nikita | year = 2001 | title = Effect of naloxone therapy on depersonalization: a pilot study | place = Bekhterev Psychoneurological Research Institute. St-Petersburg, Russia | publisher = Journal of Psychopharmacology | pmid = 11448093 | volume = 15 | issue = 2 | pages = 93–95 | url = http://jop.sagepub.com/cgi/content/abstract/15/2/93 | doi =10.1177/026988110101500205 | accessdate = 9 August 2009 | journal = Journal of Psychopharmacology | postscript = <!--None-->}}</ref>
A recent 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."<ref>{{Cite journal | last1 = Nuller | first1 = Yuri L. | last2 = Morozova | first2 = Marina G. | last3 = Kushnir | first3 = Olga N. | last4 = Hamper | first4 = Nikita | year = 2001 | title = Effect of naloxone therapy on depersonalization: a pilot study | place = Bekhterev Psychoneurological Research Institute. St-Petersburg, Russia | publisher = Journal of Psychopharmacology | pmid = 11448093 | volume = 15 | issue = 2 | pages = 93–95 | url = http://jop.sagepub.com/cgi/content/abstract/15/2/93 | doi =10.1177/026988110101500205 | accessdate = 9 August 2009 | journal = Journal of Psychopharmacology | postscript = <!--None-->}}</ref>


Depersonalization therapy with [[phenazepam]] <ref>{{cite web|url=http://psychiatry.spsma.spb.ru/lib/nuller/depersonalization.htm|title=Depersonalization diagnostics and treatment (in Russian), author - prof. [[Yuri Nuller]]}}</ref>(developed by prof. [[Yuri Nuller]], [[Saint Petersburg State Medical Academy]]). Depersonalization is characterized by high therapeutic resistance: in overwhelming majority of cases treatment with antidepressants and neuroleptics (antipsychotics) renders no effect. If quite massive depersonalization appears against the background of other psychic illness - depression or schizophrenia, the therapy usually prescribed at these disturbances also appears ineffective. Only after depersonalization reduction these diseases yield to treatment with traditional agents. Appearing from time to time individual reports about successful application of some antidepressants and neuroleptics further were not confirmed. Part of these cases may be explained by the fact that depersonalization, which appeared within some or other psychic disturbance did not play dominant role in syndrome structure, and underlying disease therapy led to reduction of syndrome depersonalization component. However, such observations were few, and applied psychotropic preparations had significant anxiolytic effect: Insidon or Larivon from antidepressants group, and Clozapine (Azaleptin), antipsychotic preparation with powerful anxiolytic and sedative effect.
Electroconvulsive therapy (ECT) is not effective in depersonalization treatment, and in such patient it more often than in endogenous depression patients leads to side effects, at first place to memory disturbances. This is obviously caused by the fact that depersonalization patients often present with organic brain pathology.
Various psychotherapeutic methods also appear inefficient.
Until present the only effective depersonalization treatment is benzodiazepine tranquilizers. Such therapy is usually started with diazepine test, and its positive result, on the one hand, indicates good prognosis, and on the other hand is signal for treatment start.
From benzodiazepine group preparations [[Phenazepam]] and [[Diazepam]] are used. Phenazepam is used in high (4 – 8 mg) and very high in specific cases up to 20 mg daily doses (max. daily dosage that was used – 36 mg<ref>{{cite web|url=http://psychiatry.spsma.spb.ru/lib/files/deprderson.zip|title=Depression and depersonalization (in Russian), author - prof. [[Yuri Nuller]]}}</ref>.). Diazepam is applied intravenously as 30 – 40 mg a day. Such high doses are caused by the fact that depersonalization patients are resistant not only to benzodiazepines therapeutic action, but also to their side effects. Thus one patient with severe depersonalization tolerated without side effects (muscles relaxation, somnolence) Diazepam in the dose 75 mg intravenous, and other patients did not demonstrate side effects during intake of Phenazepam 15 – 10 mg per os. Interesting to note that after depersonalization reduction the preparation side effects present themselves at the same or lower preparation doses.

Therapy method. As stated above, the most optimal is to start treatment with diazepam test on the same, or start therapy the next day. Phenazepam starting dose is 3-4 mg taken 2 or 3 times daily.) In case depersonalization is not reduced completely or there is no abrupt and significant improvement, the dose is elevated by 1-2 mg daily every 2-3 days until depersonalization symptoms would not completely disappear, or decrease considerably (by 75-80% by depersonalization scale). Therapeutic doses may be as high as 5-10 mg daily, and in certain cases even higher. After the complete therapeutic effect is achieved the same preparation dose should be maintained minimum 7 days, and then it should be gradually reduced by 1-2 mg every 3-4 days. In case of even insignificant worsening the dose should be escalated to the previous level, or more, and only after depersonalization manifestations disappear again, and patient condition remains stable for 7-10 days Phenazepam dose may be cautiously decreased again – by 1 mg every 4 days. If against the background of depersonalization symptoms absence the patient would present with sleep disturbances and/or anxiety, tranquilizers intake should not be stopped. In sleep disturbances Phenazepam may be substituted by [[Nitrazepam]] 5-10 mg at bedtime.
In cases of acute depersonalization, which appeared relatively recently (several weeks or 2-3 months), accompanied by anxiety and mental anguish feeling, positive effect of Phenazepam therapy was noted in approximately 75% of patients; at that depersonalization symptoms completely disappeared in 40% of cases. In prolonged months-long and long-term depersonalization conditions Phenazepam therapy was less effective: positive effect was achieved only in 40% of patients, and complete depersonalization reduction was noted only in individual cases.
Frequent argument against prolonged use of high doses of benzodiazepine tranquilizers is threat of drug dependence formation. However in spite of months-long application of high Phenazepam doses depersonalization patient did not demonstrate narcotic dependence. Some patients feared preparation abolition afraid of depersonalization relapse, but in case of preparation abolition there was no abstinence.
Besides Phenazepam positive therapeutic effect in depersonalization syndrome provides benzodiazepine preparation [[Lorazepam]] (Temesta). [[Diazepam]] (Valium, Seduxen, Sibazone), is less suitable for depersonalization course treatment: its main advantage – rapid effect in intravenous administration can not be used for long time, because the preparation solution in case of frequent injections may induce veins obliteration. Additionally, due to more strong Diazepam relaxing effect comparing to Phenazepam doses of equally efficiency there is considerable danger of drug dependence development.


==Research==
==Research==

Revision as of 11:59, 11 February 2012

This article is about the psychological symptom. For the diagnosis, see depersonalization disorder.

Depersonalization (or depersonalisation) is an anomaly of the mechanism by which an individual has self-awareness. It is a feeling of watching oneself act, while having no control over a situation.[1] Sufferers feel they have changed, and the world has become less real, vague, dreamlike, or lacking in significance. It can be a disturbing experience, since many feel that, indeed, they are living in a "dream". Chronic depersonalization refers to depersonalization disorder, which is classified by the DSM-IV as a dissociative disorder. Though degrees of depersonalization and derealization can happen to anyone who is subject to temporary anxiety/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, borderline personality disorder, obsessive-compulsive disorder, migraine and sleep deprivation. It can be considered desirable, such as in the use of recreational drugs.

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".[2]

Description

Individuals who experience depersonalization feel divorced from their own personal physicality by sensing their body sensations, feelings, emotions and behaviors as not belonging to the same person or identity.[3] Often a person who has experienced depersonalization claims that things seem unreal or hazy. Also, a recognition of self breaks down (hence the name). Depersonalization can result in very high anxiety levels, which further increase these perceptions.[4] Individuals with Depersonalization often find it hard to remember anything they saw or experienced while in third person.

Depersonalization is a subjective experience of unreality in one's sense of self, while derealization is unreality of the outside world. Although most authors currently regard depersonalization (self) and derealization (surroundings) as independent constructs, many do not want to separate derealization from depersonalization.[5]

Prevalence

Depersonalization is the third most common psychological symptom, after feelings of anxiety and feelings of depression.[6] Depersonalization is a symptom of anxiety disorders, such as panic disorder.[7] It can also accompany sleep deprivation (often occurring when suffering from jet lag), migraine, epilepsy (especially temporal lobe epilepsy)[8], obsessive-compulsive disorder, stress, and anxiety; Interoceptive exposure is a non-pharmacological method that can be used to induce depersonalization.[9]

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. 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.[10]

Pharmacological and situational causes

Depersonalization may also be a desirable effect, such as in the case of recreational drugs. It is an effect of dissociatives and psychedelics, as well as possible side effect of caffeine, alcohol, cannabis, and minocycline.[11][12][13][14][15] It is a classic withdrawal symptom from many drugs.[16][17][18][19]

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.[20][21]

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.[22]

A hypothesis, posited by writer David Zweig, called Fiction Depersonalization Syndrome, suggests that depersonalization may be triggered by being immersed in a highly mediated environment. [23]

Treatment

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, multiple sclerosis (MS), neuroborreliosis (Lyme disease), or any other neurological disease affecting the brain. For those suffering from depersonalization with 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—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.[24]

The treatment of chronic depersonalization is considered in depersonalization disorder.

A recently-completed study at Columbia University in New York City has shown positive effects from transcranial magnetic stimulation (TMS) to treat depersonalization disorder. Currently, however, the FDA has not approved TMS to treat DP. [citation needed]

A recent 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."[25]


Depersonalization therapy with phenazepam [26](developed by prof. Yuri Nuller, Saint Petersburg State Medical Academy). Depersonalization is characterized by high therapeutic resistance: in overwhelming majority of cases treatment with antidepressants and neuroleptics (antipsychotics) renders no effect. If quite massive depersonalization appears against the background of other psychic illness - depression or schizophrenia, the therapy usually prescribed at these disturbances also appears ineffective. Only after depersonalization reduction these diseases yield to treatment with traditional agents. Appearing from time to time individual reports about successful application of some antidepressants and neuroleptics further were not confirmed. Part of these cases may be explained by the fact that depersonalization, which appeared within some or other psychic disturbance did not play dominant role in syndrome structure, and underlying disease therapy led to reduction of syndrome depersonalization component. However, such observations were few, and applied psychotropic preparations had significant anxiolytic effect: Insidon or Larivon from antidepressants group, and Clozapine (Azaleptin), antipsychotic preparation with powerful anxiolytic and sedative effect. Electroconvulsive therapy (ECT) is not effective in depersonalization treatment, and in such patient it more often than in endogenous depression patients leads to side effects, at first place to memory disturbances. This is obviously caused by the fact that depersonalization patients often present with organic brain pathology. Various psychotherapeutic methods also appear inefficient. Until present the only effective depersonalization treatment is benzodiazepine tranquilizers. Such therapy is usually started with diazepine test, and its positive result, on the one hand, indicates good prognosis, and on the other hand is signal for treatment start. From benzodiazepine group preparations Phenazepam and Diazepam are used. Phenazepam is used in high (4 – 8 mg) and very high in specific cases up to 20 mg daily doses (max. daily dosage that was used – 36 mg[27].). Diazepam is applied intravenously as 30 – 40 mg a day. Such high doses are caused by the fact that depersonalization patients are resistant not only to benzodiazepines therapeutic action, but also to their side effects. Thus one patient with severe depersonalization tolerated without side effects (muscles relaxation, somnolence) Diazepam in the dose 75 mg intravenous, and other patients did not demonstrate side effects during intake of Phenazepam 15 – 10 mg per os. Interesting to note that after depersonalization reduction the preparation side effects present themselves at the same or lower preparation doses.

Therapy method. As stated above, the most optimal is to start treatment with diazepam test on the same, or start therapy the next day. Phenazepam starting dose is 3-4 mg taken 2 or 3 times daily.) In case depersonalization is not reduced completely or there is no abrupt and significant improvement, the dose is elevated by 1-2 mg daily every 2-3 days until depersonalization symptoms would not completely disappear, or decrease considerably (by 75-80% by depersonalization scale). Therapeutic doses may be as high as 5-10 mg daily, and in certain cases even higher. After the complete therapeutic effect is achieved the same preparation dose should be maintained minimum 7 days, and then it should be gradually reduced by 1-2 mg every 3-4 days. In case of even insignificant worsening the dose should be escalated to the previous level, or more, and only after depersonalization manifestations disappear again, and patient condition remains stable for 7-10 days Phenazepam dose may be cautiously decreased again – by 1 mg every 4 days. If against the background of depersonalization symptoms absence the patient would present with sleep disturbances and/or anxiety, tranquilizers intake should not be stopped. In sleep disturbances Phenazepam may be substituted by Nitrazepam 5-10 mg at bedtime. In cases of acute depersonalization, which appeared relatively recently (several weeks or 2-3 months), accompanied by anxiety and mental anguish feeling, positive effect of Phenazepam therapy was noted in approximately 75% of patients; at that depersonalization symptoms completely disappeared in 40% of cases. In prolonged months-long and long-term depersonalization conditions Phenazepam therapy was less effective: positive effect was achieved only in 40% of patients, and complete depersonalization reduction was noted only in individual cases. Frequent argument against prolonged use of high doses of benzodiazepine tranquilizers is threat of drug dependence formation. However in spite of months-long application of high Phenazepam doses depersonalization patient did not demonstrate narcotic dependence. Some patients feared preparation abolition afraid of depersonalization relapse, but in case of preparation abolition there was no abstinence. Besides Phenazepam positive therapeutic effect in depersonalization syndrome provides benzodiazepine preparation Lorazepam (Temesta). Diazepam (Valium, Seduxen, Sibazone), is less suitable for depersonalization course treatment: its main advantage – rapid effect in intravenous administration can not be used for long time, because the preparation solution in case of frequent injections may induce veins obliteration. Additionally, due to more strong Diazepam relaxing effect comparing to Phenazepam doses of equally efficiency there is considerable danger of drug dependence development.

Research

The Depersonalisation Research Unit at the Institute of Psychiatry in London is a world leader in research in depersonalization disorder.[28] Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder.

See also

References

  1. ^ American Psychiatric Association (2004). Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR (Text Revision). American Psychiatric Association. ISBN 0-89042-024-6.
  2. ^ 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): 237–252.
  3. ^ Depersonalization Disorder at Merck Manual of Diagnosis and Therapy Home Edition
  4. ^ Daniel. "Depersonalization disorder: A feeling of being 'outside' your body". Retrieved 2007-09-08.
  5. ^ Radovic F., Radovic S. (2002). "Feelings of Unreality: A Conceptual and Phenomenological Analysis of the Language of Depersonalization". Philosophy, Psychiatry, & Psychology. 9: 271–279. doi:10.1353/ppp.2003.0048.
  6. ^ Simeon D (2004). "Depersonalisation Disorder: A Contemporary Overview". CNS Drugs. 18 (6): 343–354. PMID 15089102.
  7. ^ Sierra-Siegert M, David AS (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. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ Michelle V. Lambert, Mauricio Sierra, Mary L. Phillips, and Anthony S. David. The Spectrum of Organic Depersonalization: A Review Plus Four New Cases J Neuropsychiatry Clin Neurosci, May 2002; 14: 141 - 154.
  9. ^ 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: an International Quarterly. 22: 4.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ Giesbrecht, T. (2007). "Depersonalization experiences in undergraduates are related to heightened stress cortisol responses". J. Nerv. Ment. Dis. 195 (4): 282–87. doi:10.1097/01.nmd.0000253822.60618.60. PMID 17435477. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  11. ^ Stein, M. B.; Uhde, TW (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. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Raimo, E. B. (1999). "Alcohol-Induced Depersonalization". Biological Psychiatry. 45 (11): 1523–6. doi:10.1016/S0006-3223(98)00257-1. PMID 10356638. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  13. ^ 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.
  14. ^ "Medication-Associated Depersonalization Symptoms".
  15. ^ "Depersonalization Again Finds Psychiatric Spotlight".
  16. ^ Marriott, S. (1993). "Benzodiazepine dependence: avoidance and withdrawal". Drug Safety. 9 (2): 93–103. doi:10.2165/00002018-199309020-00003. PMID 8104417. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  17. ^ Shufman, E. (2005). "[Depersonalization after withdrawal from cannabis usage]". Harefuah (in Hebrew). 144 (4): 249–51 and 303. PMID 15889607. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  18. ^ Djenderedjian, A. (1982). "Agoraphobia following amphetamine withdrawal". The Journal of Clinical Psychiatry. 43 (6): 248–49. PMID 7085580. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  19. ^ Mourad, I. (1998). "[Prospective evaluation of antidepressant discontinuation]". L'Encéphale (in French). 24 (3): 215–22. PMID 9696914. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  20. ^ Ashton H (1991). "Protracted withdrawal syndromes from benzodiazepines". J Subst Abuse Treat. 8 (1–2). benzo.org.uk: 19–28. doi:10.1016/0740-5472(91)90023-4. PMID 1675688.
  21. ^ Terao T (January 15, 1992). "Depersonalization following nitrazepam withdrawal". Biol Psychiatry. 31 (2): 212–3. doi:10.1016/0006-3223(92)90209-I. PMID 1737083. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  22. ^ Grossman, Dave (1996). On Killing: The Psychological Cost of Learning to Kill in War and Society. Back Bay Books. ISBN 0-316-33000-0.
  23. ^ Fiction Depersonalization Syndrome
  24. ^ 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. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  25. ^ 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). Bekhterev Psychoneurological Research Institute. St-Petersburg, Russia: Journal of Psychopharmacology: 93–95. doi:10.1177/026988110101500205. PMID 11448093. Retrieved 9 August 2009.
  26. ^ "Depersonalization diagnostics and treatment (in Russian), author - prof. [[Yuri Nuller]]". {{cite web}}: URL–wikilink conflict (help)
  27. ^ "Depression and depersonalization (in Russian), author - prof. [[Yuri Nuller]]". {{cite web}}: URL–wikilink conflict (help)
  28. ^ Depersonalisation Research Unit - Institute of Psychiatry, London
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