- Depersonalization disorder
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. Diagnostic criteria include persistent or recurrent experiences of feeling detached from one's mental processes or body. 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, environment and difficulty relating oneself to reality.
Occasional moments of mild depersonalization are normal; 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 sexual, physical, and emotional 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. 
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.
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. 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. Some factors are identified as relieving symptom severity such as diet or exercise; alcohol and fatigue are listed by others as worsening symptoms.
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. Depersonalization disorder is associated with cognitive disruptions in early perceptual and attentional processes.
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. No laboratory test for depersonalization disorder currently exists.
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.
The Dissociative Experiences Scale (DES) is a simple, quick, self-administered questionnaire that has been widely used to measure dissociative symptoms. It has been used in hundreds of dissociative studies, and can detect depersonalization and derealization experiences.
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. 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.
The diagnostic criteria defined in section 300.6 of the Diagnostic and Statistical Manual of Mental Disorders are as follows:
- 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.
- Reality testing is unimpaired during depersonalization
- Depersonalization causes significant difficulties or distress at work, or social and other important areas of life functioning.
- 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:
- Derealization, experiencing the external world as strange or unreal.
- Macropsia or micropsia, an alteration in the perception of object size or shape.
- A sense that other people seem unfamiliar or mechanical.
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. The most common immediate precipitators of the disorder are severe stress; major depressive disorder and panic; and hallucinogen ingestion. People who live in highly individualistic cultures may be more vulnerable to depersonalization, due to threat hypersensitivity and an external locus of control.
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.
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. A PET scan found functional abnormalities in the visual, auditory, and somatosensory cortex, as well as in areas responsible for an integrated body schema. 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. In a similar test of emotional memory, depersonalization disorder patients did not process emotionally salient material in the same way as did healthy controls. In a test of skin conductance responses to unpleasant stimuli, the subjects showed a selective inhibitory mechanism on emotional processing.
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.
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. 
Men and women are diagnosed in equal numbers with depersonalization disorder. A 1991 study on a sample from Winnipeg, Manitoba estimated the prevalence of depersonalization disorder at 2.4% of the population. A 2008 review of several studies estimated the prevalence between 0.8% and 2%. This disorder is episodic in about one-third of individuals, with each episode lasting from hours to months at a time. Depersonalization can begin episodically, and later become continuous at constant or varying intensity.
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. 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. 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.
Relation to 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.
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 has 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 has aimed to help patients reinterpret their symptoms in a nonthreatening way, leading to an improvement on several standardized measures.
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. 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. To date, no clinical trials have studied the effectiveness of benzodiazepines.
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. 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. A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety. SSRIs have also been used in combination with lamotrigine, an anticonvulsant.
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. 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. 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 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.
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 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 Stevens-Johnson syndrome). This trial was the first double-blind, placebo-controlled trial to demonstrate efficacy of any drug for DPD. However, it is 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.
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?"
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.
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.
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. 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.
Depersonalization and Meditation
Some studies have concluded that meditation can cause depersonalization, although in some cases there is no social or occupational impairment
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. 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. 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.
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- Depersonalization Research Abstracts – List of research articles concerning depersonalization disorder.
- Depersonalization at the Open Directory Project
Mental and behavioral disorders (F 290–319) Neurological/symptomaticOther Psychoactive substances, substance abuse, drug abuse and substance-related disorders Schizophrenia, schizotypal and delusional Psychosis Schizophrenia Mood (affective) Neurotic, stress-related and somatoformOther Physiological/physical behavioralNonorganic
- Postpartum depression
- Postnatal psychosis
Adult personality and behaviorOther Mental disorders diagnosed in childhood
- X-Linked mental retardation
- (Lujan-Fryns syndrome)
Symptoms and uncategorized
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Look at other dictionaries:
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