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Depersonalization disorder

Depersonalization disorder
Depersonalization
disorder
Classification and external resources
[1]

ICD-10

F48.1

ICD-9

300.6

MeSH

D003861

[2]
[3]

Depersonalization disorder (DPD) is a dissociative disorder (ICD-10 classifies the disorder as an anxiety disorder)
in which the sufferer is affected by persistent or recurrent feelings of depersonalization and/or derealization.
Diagnostic criteria include persistent or recurrent experiences of feeling detached from one's mental processes or
body.[4] 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, loss of conviction with one's identity, 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), inability to accept ones
reflection as one's own, and difficulty relating oneself to reality and the environment.
Occasional moments of mild depersonalization are normal;[5] 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 for everyday living. Depersonalization disorder is thought to be largely caused by severe
traumatic lifetime events including childhood abuse, accidents, war, torture, panic attacks and bad drug experiences.
It is unclear whether genetics play a role; however, there are many neurochemical and hormonal changes in
individuals suffering with depersonalization disorder.[6]
As the core symptoms of the disorder are thought to protect the victim from negative stimuli, depersonalization
disorder can be conceptualized as a defense mechanism. 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 not related to
psychosis, as sufferers maintain the ability to distinguish between their own internal experiences and the objective
reality of the outside world. During episodic and continuous depersonalization, sufferers are able to distinguish
between reality and fantasy, and their grasp on reality remains stable at all times.[7]

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.[8] 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 which strike at the core of a person's identity and consciousness may cause a person to feel uneasy or
anxious.
Some of the more common factors that exacerbate dissociative symptoms are negative stimuli, 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.[9] Some factors are identified as
relieving symptom severity such as diet or exercise; alcohol and fatigue are listed by others as worsening
symptoms.[10]

Depersonalization disorder
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.[11] Depersonalization disorder is associated with cognitive
disruptions in early perceptual and attentional processes.[12]

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.[13] No laboratory test for depersonalization disorder currently exists.[4]
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.[14]
The Dissociative Experiences Scale (DES) is a simple, quick, self-administered questionnaire that has been widely
used to measure dissociative symptoms.[15] It has been used in hundreds of dissociative studies, and can detect
depersonalization and derealization experiences.[16]
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.[17] 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 3045 minutes.[17]

DSM-IV-TR criteria
The diagnostic criteria defined in section 300.6 of the Diagnostic and Statistical Manual of Mental Disorders are as
follows:[4]
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.
4. 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.

Depersonalization disorder

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.[18] The most common immediate precipitators of the disorder are severe stress; major depressive disorder
and panic; and hallucinogen ingestion.[19] People who live in highly individualistic cultures may be more vulnerable
to depersonalization, due to threat hypersensitivity and an external locus of control.[20]
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.[21]
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.[22] A
PET scan found functional abnormalities in the visual, auditory, and somatosensory cortex, as well as in areas
responsible for an integrated body schema.[23] 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.[24] In a
similar test of emotional memory, depersonalization disorder patients did not process emotionally salient material in
the same way as did healthy controls.[25] In a test of skin conductance responses to unpleasant stimuli, the subjects
showed a selective inhibitory mechanism on emotional processing.[26]
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.[27][28]
The symptoms are sometimes described by sufferers from neurological organic diseases, such as amyotrophic lateral
sclerosis, Alzheimer's, multiple sclerosis (MS), neuroborreliosis (Lyme disease), etc., that directly affect brain
tissue.[29] [30]

Epidemiology
Men and women are diagnosed in equal numbers with depersonalization disorder.[31] A 1991 study on a sample from
Winnipeg, Manitoba estimated the prevalence of depersonalization disorder at 2.4% of the population.[32] A 2008
review of several studies estimated the prevalence between 0.8% and 2%.[33] This disorder is episodic in about
one-third of individuals,[10] with each episode lasting from hours to months at a time. Depersonalization can begin
episodically, and later become continuous at constant or varying intensity.[10]
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.[34][10] 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.[10] Insidious
onset may reach back as far as can be remembered, or it may begin with smaller episodes of lesser severity that
become gradually stronger. Patients with drug-induced depersonalization do not appear to be a clinically separate
group from those with a non-drug precipitant.[35]

Depersonalization disorder

Relation to other psychiatric disorders


Depersonalization exists as both a primary and secondary phenomenon, although making a clinical distinction
appears easy 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 whether 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.[10]

Treatment
A variety of psychotherapeutic techniques have been used to treat depersonalization disorder, such as cognitive
behavioral therapy. 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 has aimed to help patients reinterpret their symptoms in a
nonthreatening way, leading to an improvement on several standardized measures.[36] A standardized treatment for
DPD based on cognitive behavioral principles has recently been published in The Netherlands[37].
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.[9] Benzodiazepines are not known to reduce
dissociative symptoms; however, they do target the often comorbid anxiety and stress experienced by those with
DPD and, thus, lead to global improvement.[9] To date, no clinical trials have studied the effectiveness of
benzodiazepines.[7]
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 DPD.[38] 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.[39] A
combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.[33]
SSRIs have also been used in combination with lamotrigine, an anticonvulsant.[40]
Naloxone, an antagonist used primarily for the treatment of opiate overdose, was used in a pilot study in 14 patients
with chronic DPD. Of the 14 patients, three experienced complete remission, and seven had marked improvement of
depersonalization symptoms.[41] The study reported only immediate treatment results, which makes the efficacy of
continued treatment unknown. Naloxone can only be administered intravenously, making long-term treatment
difficult. Naltrexone was used in a preliminary study in 14 individuals with DPD.[42] Participants were treated for
610 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 was reported. In
another study in borderline personality disorder, naltrexone doses of 200 milligrams/day were reported to decrease
general dissociative symptoms over a two-week period of treatment.[43]
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.
A 2011 study involving lamotrigine[44] demonstrated efficacy in treating depersonalization disorder in a double-blind
placebo-controlled trial. In particular, of the 36 lamotrigine-treated patients, 26 were classified as responders by
week 12 versus 6 of the 38 in the placebo-treated participants. The most common and problematic adverse effect in
the lamotrigine group was rash (potentially important because of the possibility of StevensJohnson syndrome). This
trial was the first double-blind, placebo-controlled trial to demonstrate efficacy of any drug for DPD. However, it is

Depersonalization disorder
not clear how robust the study methodology was. Patients did not receive any antidepressant or anticonvulsant drugs
for 2 months before the commencement of the study, however the patients were allowed to take up to 4mg per day
of clonazepam for insomnia, and hydroxyzine of 25mg 3 times per day during 7 days for the treatment of rash. As
noted above, clonazepam itself is a potential treatment for depersonalization, and hydroxyzine has been shown to be
an effective anxiolytic. Therefore it is unclear whether the benefits in the study are due to the lamotrigine or the
clonazepam. The study does not appear to control for the effect of clonazepam or hydroxyzine administration.
Modafinil used alone has been reported to be effective in a subgroup of individuals with depersonalisation disorder;
the subgroup of people with depersonalisation disorder most likely to respond are those who have attentional
impairments, under-arousal and hypersomnia. However, clinical trials have not been conducted.[45] Dr. Evan Torch
calls a combination of an SSRI and Modafinil "the hidden pearl that can really help depersonalization disorder".[46]

History
The word depersonalization itself was first used by Henri Frdric 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?"[47]
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.[48]
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 to 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.[48]
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.[49] 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.[50]

Depersonalization disorder

Depersonalization and Meditation


Some studies have concluded that meditation can cause depersonalization, although in some cases there is no social
or occupational impairment[51]

Society and culture


Depersonalization disorder has appeared in a variety of media. 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. Norwegian painter
Edvard Munch's famous masterpiece The Scream may have been inspired by depersonalization disorder.[52] In Glen
Hirshberg's novel The Snowman's Children, main female plot characters throughout the book suffers from a
condition that is revealed to be depersonalization disorder.[53] Suzanne Segal had an episode in her 20s that was
diagnosed by several psychologists as depersonalization disorder, though Segal herself interpreted it through the lens
of Buddhism as a spiritual experience.[54]

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Depersonalization disorder
[49] Mayer-Gross W. (1935). "On depersonalization." British Journal of Medicine and Psychology (15)103-126.
[50] Simeon and Abugel p. 12 & 58
[51] R. Castillo, "Depersonalization and Meditation," Psychiatry_, Vol. 53, May 1990, pages 158-167
[52] Simeon, D; Abugel J (2006). "The Blow of the Void: Depersonalization in Literature and Philosophy". Feeling unreal: depersonalization
disorder and the loss of the self. United States: Oxford University Press. pp. 12758 (http:/ / books. google. com/
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[53] Hirshberg, Glen (2003). The Snowman's Children: A Novel. New York, NY: Carroll & Graf. ISBN0-7867-1253-8.
[54] Suzanne Segal (1996). Collision With the Infinite: A Life Beyond the Personal Self. Blue Dove Press. ISBN1-884997-27-9.

External links
Depersonalization Research Abstracts (http://www.iop.kcl.ac.uk/departments/?locator=911&context=720)
List of research articles concerning depersonalization disorder.
Depersonalization (http://www.dmoz.org//Health/Mental_Health/Disorders/Somatoform/Depersonalization/
/) at the Open Directory Project

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