|Classification and external resources|
Depersonalization disorder (DPD) is a mental disorder in which the sufferer has persistent or recurrent feelings of depersonalization and/or derealization. In the DSM-5 it was combined with Derealization Disorder and renamed to Depersonalization/Derealization Disorder (DDPD). In the DSM-5 it remains classified as a dissociative disorder, while in the ICD-10 it is called depersonalization-derealization syndrome and classified as a neurotic disorder.
Symptoms can be classified as either depersonalization or derealization. Depersonalization is described as feeling disconnected or estranged from one's body, thoughts, or emotions. Individuals experiencing depersonalization may report feeling as if they are in a dream or are watching themselves in a movie. They may feel like an outside observer of their own thoughts or body, and often report feeling a loss of control over their thoughts or actions. In some cases, individuals may be unable to accept their reflection as their own, or they may have out-of-body experiences. While depersonalization is a sense of detachment from one's self, derealization is described as detachment from one's surroundings. Individuals experiencing derealization may report perceiving the world around them as foggy, dreamlike/surreal, or visually distorted.
In addition to these depersonalization-derealization disorder symptoms, the inner turmoil created by the disorder can result in depression, self-harm, low self-esteem, anxiety attacks, panic attacks, phobias, etc. It can also cause a variety of physical symptoms, including chest pain, blurry vision, nausea, and the sensation of pins and needles in one's arms or legs.
Diagnostic criteria for depersonalization-derealization disorder includes, among other symptoms, persistent or recurrent feelings of detachment from one's mental or bodily processes or from one's surroundings. A diagnosis is made when the dissociation is persistent and interferes with the social and/or occupational functions of daily life. However, accurate descriptions of the symptoms are hard to provide due to the subjective nature of depersonalization/derealization and sufferers' ambiguous use of language when describing these episodes.
Depersonalization-derealization disorder is thought to be caused largely by severe traumatic lifetime events, including childhood abuse, accidents, natural disasters, war, torture, 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. The disorder is typically associated with cognitive disruptions in early perceptual and attentional processes.
Although the disorder is an alteration in the subjective experience of reality, it is not a form of 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 can distinguish between reality and fantasy. In other words, their grasp on reality remains stable at all times.
While depersonalization-derealization disorder was once considered rare, lifetime experiences with the disorder occur in approximately 1%–2% of the general population. The chronic form of this disorder has a reported prevalence of 0.1 to 1.9% While these numbers may seem small, depersonalization/derealization experiences have been reported by a majority of the general population, with varying degrees of intensity. While brief episodes of depersonalization or derealization can be common in the general population, the disorder is only diagnosed when these symptoms cause significant distress or impair social, occupational, or other important areas of functioning.
- 1 Symptoms
- 2 Causes
- 3 Diagnosis
- 4 Treatment
- 5 Epidemiology
- 6 History
- 7 Depersonalization and meditation
- 8 Society and culture
- 9 See also
- 10 References
- 11 External links
The core symptom of depersonalization-derealization disorder is the subjective experience of "unreality in one's sense of self," or detachment from one's surroundings. People who are diagnosed with depersonalization also experience an urge to question and think critically about the nature of reality and existence.
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 themselves. As such, a recognition of one's self breaks down. Depersonalization can result in very high anxiety levels, which can intensify these perceptions even further.
Individuals with depersonalization describe feeling disconnected from their physicality; feeling as if they are not completely occupying their own body; feeling as if their speech or physical movements are out of their control; feeling detached from their own thoughts or emotions; and experiencing themselves and their lives from a distance. While depersonalization involves detachment from one's self, individuals with derealization feel detached from their surroundings, as if the world around them is foggy, dreamlike, or visually distorted. Some people suffering from depersonalization disorder also have visual alterations such as rapid fluctuations in light. While the exact cause of these perceptual changes has not been determined, it is thought that they may be due to previous drug use. These perceptual changes differ from true hallucinatory phenomena, as they are closer to being optical distortions or illusions rather than psychotic breaks from reality. 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. Distracting oneself (by engaging in conversation or watching a movie, for example) may also provide temporary relief. Some other factors that are identified as relieving symptom severity are diet and/or exercise, while alcohol and fatigue are listed by some as worsening their 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-derealization 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, and obsession, which contributes to the worsening of symptoms.
Occasional, brief moments of mild depersonalization can be experienced by many members of the general population; however, depersonalization-derealization disorder occurs when these feelings are strong, severe, persistent, or recurrent and when these feelings interfere with daily functioning.
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.
In some cases, the use of cannabis can lead to dissociative states such as depersonalization, and derealization. Sometimes these effects can remain persistent and result in continual depersonalization or derealization disorder. When cannabis is consumed in a high dose during adolescence it increases the risk of acquiring depersonalization disorder, this occurs especially in cases where the individual is predisposed to psychosis or cannabis consumption is proceeded by a panic attack during cannabis intoxication. Cannabis induced depersonalization disorder usually occurs in adolescence and is more common with boys. Overall, the majority of cases of depersonalization disorder induced by cannabis typically begin between the ages of 15 and 19.
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.
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-derealization disorder currently exists.
The diagnosis of depersonalization disorder 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. One limitation is that the scale does not allow for the differentiation between past and present episodes of depersonalization. It should also be noted that it may be difficult for the individual to describe the duration of a depersonalization episode, and thus the scale may lack accuracy. The project was conducted in the hope that it would stimulate further scientific investigations into depersonalization disorder.
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.
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:
- 1. one of the following:
- depersonalization symptoms, i.e. the individual feels that his or her feelings and/or experiences are detached, distant, etc.
- derealization symptoms, i.e. objects, people, and/or surroundings seem unreal, distant, artificial, colourless, lifeless, etc.
- 2. an acceptance that this is a subjective and spontaneous change, not imposed by outside forces or other people (i.e. insight)
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.
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. However, recognizing and diagnosing the condition may in itself have therapeutic benefits, considering many patients express their problems as baffling and unique to them, but are in fact, one: recognized and described by psychiatry, and two: those affected by it are not the only individuals to suffer from the condition. 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.
Cognitive behavior therapy
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.
Neither antidepressants nor antipsychotics have been found to be useful. To date, no clinical trials have studied the effectiveness of benzodiazepines. Tentative evidence supports naloxone and naltrexone.
A combination of an SSRI and a benzodiazepine has been proposed to be useful for DPD patients with anxiety.
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 (those who have attentional impairments, under-arousal and hypersomnia). However, clinical trials have not been conducted.
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 1.9%. 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 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.
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 is 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.
Depersonalization and meditation
The outcome of one study on meditation and depersonalization concluded the following
- Meditation can sometimes lead to the experience of depersonalization
- The meditator's understanding and meaning regarding the experience of depersonalization will greatly determine whether anxiety is present as part of the experience
- A meditator who interprets depersonalization with catastrophic interpretations will likely experience significant panic/anxiety
- The meditator's depersonalization does not need to have significant anxiety or impairment on social or occupational functioning.
- The meditator's depersonalized state can become a permanent mode of functioning
- People who wish to reduce Depersonalization Disorder may be treated by changing the meanings associated with depersonalization in the mind of the patient, thereby reducing anxiety and functional 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 suffer 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.
- ADHD predominantly inattentive
- Cotard's syndrome
- Daphne Simeon
- Frederick T. Melges
- Solipsism syndrome
- Sluggish cognitive tempo
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