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|Classification and external resources|
Depersonalization disorder (DPD) is a mental disorder in which the sufferer is affected by persistent or recurrent feelings of depersonalization and/or derealization. In the DSM-IV-TR this disorder is classified as a dissociative disorder; in the ICD-10 it is called depersonalization-derealization syndrome and classified as an independent neurotic disorder. Common descriptions of symptoms are: feeling disconnected from one's physicality; feeling as though one is not completely occupying the body; not feeling in control of one's speech or physical movements; feeling detached from one's own thoughts or emotions; a sense of automation, going through the motions of life but not experiencing it or participating in it; loss of conviction with one's identity; feeling a disconnection from one's body; inability to accept one's reflection as one's own; difficulty relating oneself to reality and the environment; feeling as though one is in a dream; and out-of-body experiences. Depersonalization is described as suffering from episodes of surreal experiences. Some of these experiences have been also reminiscent of panic attacks and paroxysmal anxiety. While many people experience brief moments of depersonalization, in others it may last much longer and can become a persistent problem. Diagnostic criteria for Depersonalization disorder include, among others, persistent or recurrent experiences of feeling detached from one's mental processes or body. A diagnosis is made when the dissociation is persistent and interferes with the social and occupational functions necessary for everyday living. Providing an accurate description through investigation has proved challenging due to the subjective nature of depersonalization, the ambiguity of the language used to describe episodes of depersonalization and because the experiences of depersonalization overlap with those of derealization, which are two separate disorders.
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.
Although the 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.
While depersonalization disorder was once considered rare among the general population, lifetime experiences with the disorder are common in about 1%-2% of the general populace. While these numbers may seem small, depersonalization experiences were frequently described by a majority of the population but in varying intensities.
Depersonalization disorder is associated with cognitive disruptions in early perceptual and attentional processes.
The core symptom of depersonalization disorder is the subjective experience of "unreality in one's sense of self", and as such there are no clinical signs. Patients who suffer from depersonalization also experience an almost uncontrollable urge to question and think about the nature of reality and existence as well as other deeply philosophical questions.
Individuals who experience depersonalization can 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. Also, a recognition of self breaks down (hence the name). Depersonalization can result in very high anxiety levels, which can intensify these perceptions even further.
Common descriptions: Feeling disconnected from one's physicality; feeling like one is not completely occupying the body; not feeling in control of one's speech or physical movements; and feeling detached from one's own thoughts or emotions; experiencing one's self and life from a distance; a sense of just going through the motions; feeling as though one is in a dream or movie; and even out-of-body experiences. Patients suffering from depersonalization disorder have also certain visual stimulations such as hallucinations and rapid fluctuations in lighting. While the exact cause of these hallucinations has not yet been determined, it is generally accepted that patients suffering from them is caused by previous drug usage. These hallucinations differ from true hallucinatory phenomena as they are closer to being optical distortions or illusions rather than psychotic breaks. 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.
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.
First experiences with depersonalization may be frightening, with patients fearing loss of control, dissociation from the rest of society and functional impairment. The majority of patients suffering from depersonalization disorder misinterpret the symptoms, thinking that they are signs of serious mental illness or brain dysfunction. This commonly leads to an increase of anxiety experienced by the patient which contributes to the worsening of symptoms.
Occasional moments of mild depersonalization are normal; strong, severe, persistent, or recurrent feelings are not.
Diagnosis is based on the self-reported experiences of the person followed by a clinical assessment. 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 Cambridge Depersonalization Scale (CDS) is a method for determining the severity of depersonalization disorder patients may suffer from. It has been proven and accepted as a valid tool for the diagnosis of depersonalization disorder in a clinical setting. It was validated through trials with a sample of patients who had been confirmed to be suffering from depersonalization disorder. It is also used in a clinical setting to differentiate minor episodes of depersonalization from suffering from actual symptoms of the disorder. Due to the success of the CDS, a group of Japanese researchers underwent the effort to translate the CDS into the J-CDS or the Japanese Cambridge Depersonalization Scale. Through clinical trials the Japanese research team successfully tested their scale and determined its accuracy. They did discover a limitation that the scale did not allow for the differentiation between past and present episodes of depersonalization. It should also be noted that it may be difficult for the patient to describe the duration of depersonalization episodes and thus the scale lacks some degree of accuracy. The project was conducted in the hope that it would stimulate further scientific investigations into depersonalization disorder.
Depersonalization disorder is classified differently in the DSM-IV-TR and in the ICD-10: In the DSM-IV-TR this disorder it is seen as a dissociative disorder; in the ICD-10 as an independent neurotic disorder. Whether depersonalization disorder should be characterized as a dissociative disorder can be discussed; it relies very much upon how dissociative is being described.
The diagnostic criteria defined in section 300.6 of the Diagnostic and Statistical Manual of Mental Disorders are as follows:
The DSM-IV-TR specifically recognizes three possible additional features of depersonalization disorder:
Dissociation is defined as a "disruption in the usually integrated functions of consciousness, memory, identity and perception, leading to a fragmentation of the coherence, unity and continuity of the sense of self. Depersonalisation is a particular type of dissociation involving a disrupted integration of self-perceptions with the sense of self, so that individuals experiencing depersonalisation are in a subjective state of feeling estranged, detached or disconnected from their own being."
In ICD-10, this disorder is called depersonalization-derealization syndrome F48.1. The diagnostic criteria are as follows:
The diagnosis should not be given in certain specified conditions, for instance when intoxicated by alcohol or drugs, or together with schizophrenia, mood disorders and anxiety disorders.
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.
It has been thought that depersonalization has been caused by a biological response to dangerous or life-threatening situations which causes heightened senses and emotional neutrality. If this response is applied in real life, non-threatening situations, the result can be shocking to the individual.
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.
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.
Primary depersonalization disorder is mostly refractory to current treatments. The disorder lacks effective treatment in part because it has been neglected by the psychiatric community because funding has mainly been allocated to the search for cures of other illnesses, like alcoholism. 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. A standardized treatment for DPD based on cognitive behavioral principles has recently been published in The Netherlands.
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 14 patients with chronic DPD. Of the 14 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 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 4 mg per day of clonazepam for insomnia, and hydroxyzine of 25 mg 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 depersonalization disorder; the subgroup of people with depersonalization disorder most likely to respond are those who have attentional impairments, under-arousal and hypersomnia. However, clinical trials have not been conducted. Dr. Evan Torch calls a combination of an SSRI and Modafinil "the hidden pearl that can really help depersonalization disorder".
Antipsychotics typically have a paradoxical effect and worsen symptoms of depersonalisation.
A 2011 study has shown positive effects from transcranial magnetic stimulation (TMS) to treat depersonalization disorder. Currently, however, the FDA has not approved TMS to treat depersonalization disorder.
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.
Arguments have been brought forth by researchers that despite the fact that depersonalization and derealization are both impairments to one’s ability to distinguish reality and thus they fall into the same disorder and are merely two facets of it. Depersonalization also differs from delusion in the sense that the patient is able to differentiate between reality and the symptoms they may experience. The ability to sense that something is unreal it maintained when experiencing symptoms of the disorder. The problem with properly defining depersonalization also lies within the understanding of what reality actually is. In order to comprehend the nature of reality we must incorporate all the subjective experiences throughout and thus the problem of obtaining an objective definition is brought about again.
The outcome of one study on meditation and depersonalization concluded the following
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. The song "Is Happiness Just A Word?" by Hip-Hop artist and rapper Vinnie Paz describes his struggle with Depersonalization disorder.