|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-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 a 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 prevalence 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. Whilst 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
- 2 Assessment
- 3 Diagnosis
- 4 Causes
- 5 Prevalence
- 6 Treatment
- 7 History
- 8 Depersonalization and meditation
- 9 Society and culture
- 10 See also
- 11 References
- 12 External links
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:
- 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.
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.
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
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
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.
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
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.
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.
- ADHD predominantly inattentive
- Cotard's syndrome
- Daphne Simeon
- Frederick T. Melges
- Solipsism syndrome
- Sluggish cognitive tempo
American Psychiatric Association (05). Desk reference to the Diagnostic criteria for the DSM5. APA. ISBN 9780890425541. Check date values in:
- APA 2013.
- World Health Organisation http://apps.who.int/classifications/icd10/browse/2010/en#/F48.1
- Simeon D (2004). "Depersonalisation Disorder: A Contemporary Overview". CNS Drugs 18 (6): 343–354. doi:10.2165/00023210-200418060-00002. PMID 15089102.
- Depersonalization Disorder, (DSM-IV 300.6, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition)
- Blevins, Christy A.; Weathers, Frank W.; Mason, Elizabeth A. (1 October 2012). "Construct Validity of Three Depersonalization Measures in Trauma-Exposed College Students". Journal of Trauma & Dissociation 13 (5): 539–553. doi:10.1080/15299732.2012.678470.
- Simeon, Daphne. "Depersonalisation Disorder: A Contemporary Overview". Adis International. Retrieved 2011-10-13.
- Guralnik O, Giesbrecht T, Knutelska M, Sirroff B, Simeon D (December 2007). "Cognitive functioning in depersonalization disorder". J. Nerv. Ment. Dis. 195 (12): 983–8. doi:10.1097/NMD.0b013e31815c19cd. PMID 18091191.
- Simeon and Abugel p. 32 & 133
- Cannabis-induced depersonalization disorder in adolescence. Hürlimann F1, Kupferschmid S, Simon AE. ("Although depersonalization disorder has a low prevalence, with a reported prevalence ranging from 0.8 to 1.9%")
- Sierra, Mauricio; Medford, Nick; Wyatt, Geddes; David, Anthony S. (1 May 2012). "Depersonalization disorder and anxiety: A special relationship?". Psychiatry Research 197 (1–2): 123–127. doi:10.1016/j.psychres.2011.12.017. PMID 22414660.
- Radovic F (2002). Feelings of Unreality: A Conceptual and Phenomenological Analysis of the Language of Depersonalization. Philosophy, Psychiatry, & Psychology. pp. 9: 271–279.
- Simeon D, Knutelska M, Nelson D, Guralnik O (2003). "Feeling unreal: a depersonalization disorder update of 117 cases". Journal of Clinical Psychiatry 64 (9): 990–7. doi:10.4088/JCP.v64n0903. PMID 14628973.
- Baker D, Hunter E, Lawrence E et al. (May 2003). "Depersonalisation disorder: clinical features of 204 cases". The British Journal of Psychiatry 182 (5): 428–33. doi:10.1192/bjp.182.5.428. PMID 12724246.
- Sacco, Robert G. (December 2010). "The Circumplex Structure of Depersonalization/Derealization". International Journal of Psychological Studies 2 (2): 26–40.
- Simeon, D., & Abugel, J. (2006). Feeling Unreal: Depersonalization Disorder and the Loss of the Self. New York, NY: Oxford University Press. (p. 3)
- Steinberg M: Interviewers Guide to the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D). Washington, DC, American Psychiatric Press, 1994.
- Bernstein EM, Putnam FW (1986). "Development, reliability, and validity of a dissociation scale". J. Nerv. Ment. Dis. 174 (12): 727–35. doi:10.1097/00005053-198612000-00004. PMID 3783140.
- Simeon and Abugel p. 73-4
- Saxe GN, van der Kolk BA, Berkowitz R et al. (July 1993). "Dissociative disorders in psychiatric inpatients". Am J Psychiatry 150 (7): 1037–42. doi:10.1176/ajp.150.7.1037. PMID 8317573.
- Sugiura, Miyuki; Hirosawa, Masataka; Tanaka, Sumio; Nishi, Yasunobu; Yamada, Yasuyuki; Mizuno, Motoki (1 June 2009). "Reliability and validity of a Japanese version of the Cambridge depersonalization scale as a screening instrument for depersonalization disorder". Psychiatry and Clinical Neurosciences 63 (3): 314–321. doi:10.1111/j.1440-1819.2009.01939.x. PMID 19566762.
- Simeon D, Guralnik O, Schmeidler J, Sirof B, Knutelska M (2001). "The role of childhood interpersonal trauma in depersonalization disorder". The American Journal of Psychiatry 158 (7): 1027–33. doi:10.1176/appi.ajp.158.7.1027. PMID 11431223.
- Simeon D: Depersonalisation disorder: a contemporary overview. CNS Drugs. 2004.
- Sierra-Siegert M, David AS (December 2007). "Depersonalization and individualism: the effect of culture on symptom profiles in panic disorder". J. Nerv. Ment. Dis. 195 (12): 989–95. doi:10.1097/NMD.0b013e31815c19f7. PMID 18091192.
- Hunter EC, Phillips ML, Chalder T, Sierra M, David AS (December 2003). "Depersonalisation disorder: a cognitive-behavioural conceptualisation". Behav Res Ther 41 (12): 1451–67. doi:10.1016/S0005-7967(03)00066-4. PMID 14583413.
- Medford N, Sierra M, Baker D, David A. (2005). "Understanding and treating depersonalisation disorder". Advances in Psychiatric Treatment (Royal College of Psychiatrists) 11 (2): 92–100. doi:10.1192/apt.11.2.92.
- Simeon D, Guralnik O, Hazlett EA, Spiegel-Cohen J, Hollander E, Buchsbaum MS (November 2000). "Feeling unreal: a PET study of depersonalization disorder". The American Journal of Psychiatry 157 (11): 1782–8. doi:10.1176/appi.ajp.157.11.1782. PMID 11058475.
- Phillips ML, Medford N, Senior C, Bullmore ET, Suckling J, Brammer MJ, Andrew C, Sierra M, Williams SC et al. (2001). "Depersonalization disorder: thinking without feeling". Psychiatry Research: Neuroimaging 108 (3): 145–160. doi:10.1016/S0925-4927(01)00119-6. PMID 11756013.
- Medford N, Brierley B, Brammer M, Bullmore ET, David AS, Phillips ML (December 2006). "Emotional memory in depersonalization disorder: A functional MRI study" (PDF). Psychiatry Research: Neuroimaging 148 (2–3): 93–102. doi:10.1016/j.pscychresns.2006.05.007. PMID 17085021.
- Sierra M, Senior C, Dalton J et al. (September 2002). "Autonomic response in depersonalization disorder". Archives of General Psychiatry 59 (9): 833–8. doi:10.1001/archpsyc.59.9.833. PMID 12215083.
- Simeon D, Guralnik O, Knutelska M, Hollander E, Schmeidler J (2001). "Hypothalamic-pituitary-adrenal axis dysregulation in depersonalization disorder". Neuropsychopharmacology 25 (5): 793–5. doi:10.1016/S0893-133X(01)00288-3. PMID 11682263.
- Stanton BR, David AS, Cleare AJ et al. (2001). "Basal activity of the hypothalamic-pituitary-adrenal axis in patients with depersonalization disorder". Psychiatry Research 104 (1): 85–9. doi:10.1016/S0165-1781(01)00291-8. PMID 11600192.
- Leedy, Melissa J., Jackson, Melissa, Callahan, Jennifer L (2007). "Treating Depression and Compensatory Narcissistic Personality Style in a Man With Chronic Lyme Disease". Clinical Case Studies 6 (5): 430–42. doi:10.1177/1534650106295847.
- Strohle, A., Kumpfel, T., Sonntag, A. (2000). "Paroxetine for Depersonalization Associated With Multiple Sclerosis". Am. J. Psychiatry 157 (1): 150. doi:10.1176/ajp.157.1.150.
- "Medication-Associated Depersonalization Symptoms"
- Shufman, E; Lerner, A; Witztum, E (2005). "Depersonalization after withdrawal from cannabis usage" (PDF). Harefuah (in Hebrew) 144 (4): 249–51, 303. PMID 15889607.
- Johnson, BA (1990). "Psychopharmacological effects of cannabis". British journal of hospital medicine 43 (2): 114–6, 118–20, 122. PMID 2178712.
- Cannabis-induced depersonalization disorder in adolescence. Hürlimann F1, Kupferschmid S, Simon AE. ("One evening at the age of 15 he smoked cannabis repeatedly and instantly began to feel very anxious. Ever since he has felt like a stranger in his own world and his awareness")("Immediately after the consumption he felt like he was ‘far off’ and sometimes even out of the world. He felt the environment detached from him and was 'afraid of going insane")("At that time he withdrew markedly from his social environment, and when he realized that he had developed sociophobic symptoms, he decided to stop smoking cannabis. One day after cessation of cannabis use, he felt as if people around him were actors and wearing masks")("Patient C is a 16-year-old male who, according to his mother, had little contact with other children in his childhood as he often felt insecure. During a 3-month period at the age of 15, he started smoking cannabis several times a week. He then developed anxiety and a ‘strange feeling in his mind’ that he was unable to better describe, and further developed an altered sense of time")("Patient D is a 19-year-old male who smoked cannabis between the ages of 16 and 18 as he was feeling insecure in social situations")
- Cannabis-induced depersonalization disorder in adolescence. Hürlimann F1, Kupferschmid S, Simon AE. ("All reported cases describe onset of depersonalization disorder in adolescence. While this condition is in general equally distributed between genders drug induced depersonalization disorder is usually associated with younger age at onset and with male gender")
- Cannabis-induced depersonalization disorder in adolescence. Hürlimann F1, Kupferschmid S, Simon AE. ("Overall, however, the majority of cases with depersonalization disorder claim that the condition began during adolescence, typically between the ages of 15 and 19. Bak- er et al."
- Ross CA (1991). "Epidemiology of multiple personality disorder and dissociation". Psychiatric Clinics of North America 14 (3): 503–17. PMID 1946021.
- Sierra M (January 2008). "Depersonalization disorder: pharmacological approaches". Expert Rev Neurother 8 (1): 19–26. doi:10.1586/1473718.104.22.168. PMID 18088198.
- Medford N, Baker D, Hunter E et al. (December 2003). "Chronic depersonalization following illicit drug use: a controlled analysis of 40 cases". Addiction 98 (12): 1731–6. doi:10.1111/j.1360-0443.2003.00548.x. PMID 14651505.
- Medford N, Sierra M, Baker D, David AS (2005). "Understanding and treating depersonalization disorder". advances in psychiatric treatment 11 (5): 92–100. doi:10.1192/apt.11.2.92.
- Hunter EC, Baker D, Phillips ML, Sierra M, David AS (September 2005). "Cognitive-behaviour therapy for depersonalisation disorder: an open study". Behav Res Ther 43 (9): 1121–30. doi:10.1016/j.brat.2004.08.003. PMID 16005701.
- Bar, E., & Minnen van, A. (2011). Protocollaire behandeling van de depersonalisatiestoornis. In: G.P.J. Keijsers, A.van Minnen, & C.A.L. Hoogduin (red.). Protocollaire behandelingen voor volwassenen met psychische klachten. Arnhem, Boom Cure & Care publishers.
- Depersonalization: A New Look at a Neglected Syndrome by Mauricio Sierra (Aug 16, 2012)
- Stranger To My Self: Inside Depersonalization: The Hidden Epidemic by Jeffrey Abugel (Jan 21, 2011)
- Brewer, Sara. "An anti-addiction drug?." essays and reflections from an amsterdam graduate programme: 105.*"Researchers currently theorize that Ibogaine fills the opiate receptor sites that stop addiction cravings and “effectively hits the reset button on the brain's neurotransmitter mechanisms")
- Pablo, John P., and Deborah C. Mash. "Noribogaine stimulates naloxone-sensitive [35S] GTP [gamma] S binding." Neuroreport 9.1 (1998): 109-114.("The capacity of noribogaine to reset multiple opioid receptors and the 5-HT transporter mechanisms may explain...")
- Hayes, Gary. "Ibogaine-poison or panacea?." Drugs and Alcohol Today 4.3 (2004): 16-24. (In a way, ibogaine hits a 'reset' button)
- Simeon D, Gurainik O, Schmeidler J, Knutelska M (2004). "Fluoxetine is not efficacious in depersonalisation disorders: a randomized controlled trial". British Journal of Psychiatry 185: 31–36. doi:10.1192/bjp.185.1.31. PMID 15231553.
- Simeon D, Stein DJ, Hollander E (1998). "Treatment of depersonalization disorder with clomipramine". Biological Psychiatry 44 (4): 302–303. doi:10.1016/S0006-3223(98)00023-7. PMID 9715363.
- Sierra M, Baker D, Medford N et al. (2006). "Lamotrigine as an add-on treatment for depersonalization disorder: a retrospective study of 32 cases". Clin Neuropharmacol 29 (5): 253–8. doi:10.1097/01.WNF.0000228368.17970.DA. PMID 16960469.
- Nuller YL, Morozova MG, Kushnir ON, Hamper N (2001). "Effect of naloxone therapy on depersonalization: a pilot study". Journal of Psychopharmacology 15 (2): 93–95. doi:10.1177/026988110101500205. PMID 11448093.
- Simeon D, Knutelska M (2005). "An open trial of naltrexone in the treatment of depersonalization disorder". Journal of Clinical Psychopharmacology 25 (3): 267–270. doi:10.1097/01.jcp.0000162803.61700.4f. PMID 15876908.
- Bohus MJ, Landwehrmeyer GB, Stiglmayr CE, Limberger MF, Böhme R, Schmahl CG (1999). "Naltrexone in the treatment of dissociative symptoms in patients with borderline personality disorder: an open-label trial". Journal of Clinical Psychiatry 60 (9): 598–603. doi:10.4088/JCP.v60n0906. PMID 10520978.
- Aliyev NA, Aliyev ZN (2011). "Lamotrigine in the immediate treatment of outpatients with depersonalization disorder without psychiatric comorbidity: randomized, double-blind, placebo-controlled study". Journal of Clinical Psychopharmacology 31 (1): 61–65. doi:10.1097/JCP.0b013e31820428e1. PMID 21192145.
- Mauricio Sierra (13 August 2009). Depersonalization: A New Look at a Neglected Syndrome. Cambridge, UK: Cambridge University Press. p. 120. ISBN 0-521-87498-X.
- Simeon, Daphne; Abugel, Jeffrey (2006). Feeling Unreal: Depersonalization Disorder and the Loss of the Self. p. 256. ISBN 978-0-19-517022-1.
- Mantovani A, Simeon D, Urban N, Bulow P, Allart A, Lisanby S. (2011). "Temporo-parietal junction stimulation in the treatment of depersonalization disorder". Psychiatry Res 186 (1): 138–40. doi:10.1016/j.psychres.2010.08.022. PMID 20837362.
- Henri Frédéric Amiel's The Journal Intime Retrieved June 2, 2007
- Berrios GE, Sierra M (June 1997). "Depersonalization: a conceptual history". Hist Psychiatry 8 (30 Pt 2): 213–29. doi:10.1177/0957154X9700803002. PMID 11619439.
- Mayer-Gross W. (1935). "On depersonalization." British Journal of Medicine and Psychology (15)103–126.
- Simeon and Abugel p. 12 & 58
- Sogomy, Varga (June 2012). "Depersonalization and the Sense of Realness". Philosophy, Psychiatry, & Psychology 19 (2).
- R. Castillo, "Depersonalization and Meditation," Psychiatry_, Vol. 53, May 1990, pages 158–167
- Simeon, D; Abugel J (2006). "The Blow of the Void: Depersonalization in Literature and Philosophy". Feeling unreal: depersonalization disorder and the loss of the self. United States: Oxford University Press. pp. 127–58. ISBN 0-19-517022-9.
- Hirshberg, Glen (2003). The Snowman's Children: A Novel. New York, NY: Carroll & Graf. ISBN 0-7867-1253-8.
- Suzanne Segal (1996). Collision With the Infinite: A Life Beyond the Personal Self. Blue Dove Press. ISBN 1-884997-27-9.
- Depersonalization Research Abstracts – List of research articles concerning depersonalization disorder.
- Depersonalization at DMOZ