翻译|Bree & Shirly & Renee & Lydia 审校|高淑媛
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-5 it was combined with Derealization Disorder and renamed to Depersonalization/Derealization Disorder.
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 an neurotic disorder.
Common descriptions of symptoms from sufferers include feeling disconnected from one's physicality or body, feeling detached from one's own thoughts or emotions, feeling as if one is disconnected from the reality of one's self, and a sense of feeling as if one is dreaming or in a dreamlike state.
In some cases, a person may feel an inability to accept their reflection as their own, or they may even have out-of-body experiences.
The disorder can also be described as suffering from recurrent episodes of surreal experiences, which may in some cases be reminiscent of panic attacks.
In addition to these DPD symptoms, the inner turmoil created by the disorder can result in depression,self-harm, low self-esteem, anxiety attacks, panic attacks, extreme phobias (especially of losing their mind), etc. It can also cause a variety of physical symptoms, including chest pain, blurry vision, nausea, and pins and needles.
Diagnostic criteria for depersonalization disorder includes, among other symptoms, persistent or recurrent feelings of detachment from one's mental or bodily processes.
A diagnosis is made when the dissociation is persistent and interferes with the social and/or occupational functions necessary for everyday living.
Providing an accurate description through investigation has however proved challenging due to the subjective nature of depersonalization, sufferers' ambiguous use of language when describing episodes of depersonalization, and because the experiences of depersonalization overlap with those of derealization—a separate disorder.
Depersonalization disorder is thought to be caused largely by severe traumatic lifetime events, including childhood abuse, accidents, natural disasters, 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.
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 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, lifetime experiences with the disorder are common in approximately 1%–2% of the general populace.
Chronic depersonalization disorder has a reported prevelence ranging from 0.1 to 1.9%.
While these numbers may seem small, depersonalization experiences were frequently reported by a majority of the population to varying degrees of intensity.
Whist experiencing brief episodes of depersonalization can be considered fairly common within the general population, in some individuals it may last much longer, progressing into a disorder.
• 1 Symptoms/症状
• 2 Assessment/评估
• 3 Diagnosis/诊断
o 3.1 DSM-IV-TR/诊断标准
o 3.2 ICD-10/国际疾病分类第10版
• 4 Causes/病因
o 4.1 Cannabis/大麻
• 5 Prevalence/患病率
o 5.1 Relation to other psychiatric disorders/和其他精神疾病的联系
• 6 Treatment/治疗
o 6.1 Cognitive behavior therapy/认知行为疗法
o 6.2 Iboga total alkaloid/伊博格碱
o 6.3 Medications/药物治疗
o 6.4 Transcranial magnetic stimulation/经颅磁刺激
• 7 History/历史
• 8 Depersonalization and meditation/人格解体和冥想
• 9 Society and culture/社会和文化
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.
People who are diagnosed with 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; feeling "weird" being alive; and even out-of-body experiences.
Some 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.
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 others as to cause worsening of 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, and obsession, 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:
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.
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.
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 abnormalcortisol 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.
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.
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 认知行为疗法
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.
Iboga total alkaloid Iboga 伊博格总生物碱（抗抑郁药）
Anecdotal reports of DPD sufferers as well as iboga treatment centers, and others have claimed that treatment with iboga total alkaloid has reversed depersonalization in those with DPD who did the treatment. Anecdotal reports occasionally appear of people claiming to find relief from DPD through iboga TA treatment. Given the theorized connection between depersonalization/derealization and the disruption of normal kappa and mu opioid receptor agonization and antagonization, outlined in the book "Inside Depersonalization: The Hidden Epidemic" and the scientifically proven ability of large flood doses of iboga TA to reset the opioid system, which is the mechanism of action in its primary use of treating addiction, it appears clear the effect of iboga TA on opioid receptors to restore their 'factory reset' is responsible for its ability to successfully treat depersonalization and derealization disorder.
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. Although Naloxone is usually administered intraveneously, it can also be administered intramuscularly, subcutaneously, and intranasally. Given that the latter generally is not practiced, long-term treatment may be 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.
2011年的研究，在治疗自我丢失症双盲安慰剂对照试验中，加入拉莫三嗪证实疗效。36位用拉莫三嗪治疗的患者，其中的26位在第12周产生积极反应，而在安慰剂对照组，38人中有6人反响良好。拉莫三嗪组中最常见的和急需解决的的不利影响是皮疹（非常重要因为可能导致Stevens–Johnson 综合症）。这项试验是用来证明药物对DPD功效的第一个双盲，安慰剂对照试验，。不过，目前尚不清楚该研究方法效果是否强劲。患者在研究开始前2个月内没有使用任何抗抑郁药或抗惊厥药物，但是患者们可以每天使用4毫克的高达氯硝西泮用于治疗失眠，在治疗皮疹期间每天可以用25毫克羟嗪 ，每日3次持续7天。如上所述，氯硝西泮本身是自我感丧失的一种潜在的治疗，并且羟嗪已被证明是一种有效的抗焦虑药物。因此，目前还不清楚研究中的药效是由拉莫三嗪或氯硝西泮带来的。该研究目的不在于测试氯硝西泮或羟的效果。
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. 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. However evidence suggests that the antipsychotic Aripiprazole could have a therapeutic effect in combating Depersonalization disorder.
Transcranial magnetic stimulation 经颅磁刺激
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.
自我感丧失这一词本身是由Henri Frédéric Amiel在The Journal Intime中第一次使用。1880年7月8日的记录写道："我发现自己仿佛穿越坟墓或是从另一世界看待万物。对我来说，一切都很陌生。我自己, 就好像是，不在我的身体里，不是我自己； 我丧失了自我，被分离了，被分割然后漂浮着。这是疯了吗？"而在1898年，Ludovic Dugas是首次将自我感丧失作为临床词汇运用的。它指的是"一种觉得自己的想法和行动逃离自我并且开始变得怪异的感觉或是感知，也就是人格异化 –换句话说，也就是自我感丧失。“这将自我感描述为反应自我状态属性的心理综合状况。
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.
早期研究自我感丧失的病因的理论集中在感官机能受损。Maurice Krishaber提出自我感受丧失是由身体中多种感觉通道的病理性改变引起的，这种病理改变导致了“自我陌生感”的经历，病人描述的“感觉他再也不是自己了”。Carl Wernicke的一个学生建议说所有的感官都是由感觉组件和肌肉知觉组成，肌肉知觉则来自肌肉本身的运动并且能引导感觉器官应对刺激。而自我感丧失的病人这两个组件是不同步且肌源性的知觉不能被意识感知。这一理论受到了其他研究者的质疑，他们认为对病人的抱怨的理解过于字面化了，而且有些描述还运用了比喻的手法---尝试去面描述很难清晰明了的表达出来的经历。对于这一理论，Pierre Janet 持赞同观点，他指出感觉系统患病者并没有报告他们有感觉不现实的症状，而那些被诊断为自我感丧失的病人却拥有着正常的感觉系统。
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.
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 social or occupational functioning as a result of depersonalization need not have significant anxiety or impairment.
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.
自我感丧失症已经在许多媒体中出现了。自传纪录片《诅咒》（英文：Tarnation）的导演 Jonathan Caouette就患有自我感丧失症。2007年上映的电影《麻木》（英文： Numb）的编剧就像片中由Matthew Perry出演的主角一样也患有自我感丧失症，。挪威画家Edvard Munch的著作《呐喊》（英文：The Scream）就有可能是受到了自我感丧失症的启发所画。在Glen Hirshberg所著的小说《雪人的孩子》（英文： The Snowman's Children）中，女主人公在整篇作品中遭受的症状也被认定为自我感丧失症。 Suzanne Segal在她20多岁的那段经历中被数名心理学家诊断为自我感丧失症，虽然她自己解释说从佛教的uddhism的角度来看，这是一种精神历程。由嘻哈艺术家，说唱歌手Vinnie Paz创作的歌曲《幸福只是一个词吗？》（英文： "Is Happiness Just A Word?"）也描述了自己与自我感丧失症抗争的经历。
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