Depersonalization disorder is identified as a dissociative disorder characterized by a persistent or recurring experience of unreality, where individuals report an experience akin to living in a movie or dream, feeling detached from their body and emotions, and not being in control of their life.  In addition, some find that what are actually familiar places to be strange and unfamiliar. Individuals experiencing depersonalization demonstrate intact reality testing and an experience of a non-delusional objective reality similar to the general population.
Depersonalization is a dissociative symptom and is often accompanied by derealization, a sense that the exterior world is unreal. Although the symptom profiles often co-occur, they are considered separate. Dissociation is a disruption in the normally integrated functions of memory, cognition, and consciousness.
Most individuals with depersonalization disorder also demonstrate symptoms describing co-occurring anxiety or depression, or co-morbid anxious or depressive disorder. This suggests that depersonalization is potentially symptomatic of other disorders, however, as there are no Axis I or II disorders that demonstrate a unique relationship similar to depersonalization disorder in terms of presence or severity, depersonalization disorder remains identified as a separate diagnostic category.
Note: The American Psychiatric Association, which publishes the Diagnostic and Statistical Manual of Mental Disorders, forbids the unauthorized reproduction of their diagnostic criteria. A narrative of the DSM-IV-TR criteria follows.
The primary characteristic of depersonalization outline by the DSM-IV-TR is an experience of chronic or episodic feelings of detachment from one's own thoughts or body.  The World Health Organization's International Classification of Diseases 10 (ICD-10) has a similar diagnostic label: Depersonalization-derealization syndrome. This syndrome is describe as a change in the quality of a individual's experience of mental activity, body, or surroundings, so that they are described as unreal, remote, or automatized. Both criteria acknoweldge the most frequent complaints as a decrease in emotion, and detachment or alienation from their cognition, body, or the world. Although individuals experiencing these symptoms apparently do maintain the ability to discriminative between reality and non-reality, excluding it from a categorization equivalent to delusion thinking. Depersonalization falls into the classification of a disorder if it causes significant dysfunction in one or more areas of an individual's life. Lastly, the experience of depersonalization is not due to another medical or psychological condition or drug use. Persons experiencing symptoms are aware that this is an "as if" experience, and retain their normal capacity for perception and emotional expression. These same symptoms can occur within the context of several other disorders, including epilepsy, schizophrenia, depression, phobia, or obsessive-compulsive disorder, and in these cases should be a secondary diagnosis.
Current diagnostic methods
- 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 the experience of the interviewer. 
- 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.
- The Dissociative Disorders Interview Schedule (DDIS) is a highly structured interview, administered in 30-45 minutes, that generates a DSM-IV-TR diagnosis template for somatization disorder, borderline personality disorder, and major depressive disorder, as well as related dissociative disorders. The inventory inquires into positive symptomology for schizophrenia, secondary features of dissociative identity disorder, extrasensory experiences, substance abuse and other items that may inform dissociative experience.
Proposed diagnostic criteria
Researchers of depersonalization disorder have found the DSM criteria to be inadequate to properly diagnose or describe the symptoms of the disorder. Dr. Daphne Simeon, a psychiatrist and investigator into depersonalization disorder at a research unit in New York, has proposed five criteria for diagnosis: 'numbing', 'unreality of self', 'perceptual alterations', 'unreality of surroundings', and 'temporal disintegration'. Her position on the DSM-V task force will likely lead to the adoption of these diagnostic criteria for the new manual. These proposed criteria match four dimensions proposed earlier by a research group at the Depersonalization Research Unit in London, England: 'anomalous body experience', 'emotional numbing', 'anomalous subjective recall', and 'alienation from surroundings'. The difference between the two sets of criteria is that Simeon's proposal of 'unreality of self' and 'perceptual alterations' are grouped together within 'anomalous body experience'.
A first person account
I look at my mind from within and feel both trapped and puzzled about the strangeness of my existence. My thoughts swirl round and round constantly probing the strangeness of selfhood - why do I exist? Why am I me and not someone else? At these times, feelings of sweaty panic develop, as if I am having a phobia about my own thoughts. At other times, I don't feel "grounded." I look at this body and can't understand why I am within it. I hear myself having conversations and wonder where the voice is coming from. I imagine myself seeing life as if it were played like a film in a cinema. But in that case, where am I? Who is watching the film? What is the cinema? The worst part is that this seems as if it's the truth, and the periods of my life in which I did not feel like this were delusions.
Men and women are diagnosed at equal rates with depersonalization disorder. The onset most commonly occurs during the teenage years or early 20s, although cases have been reported at all ages, and some even report being depersonalized for as long as they can remember. The prevalence is estimated at 0.8-2% of the population, while exact numbers are difficult to obtain due to clinician unfamiliarity, patient reluctance to divulge symptoms (for fear of appearing "crazy"), or depersonalization is diagnosed as a secondary pathology. The onset of depersonalization 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 gradually become stronger. 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.
Fears of going crazy, brain damage, and losing control are common complaints. Individuals report occupational impairments as they feel they are working below their ability, and interpersonal troubles since they feel emotionally disconnected from those they care about.
The pathophysiology of depersonalization disorder appears to be dysfunction in the reception, processing, and multi-modal integration of sensory information. This may have several etiologies, including both drug induced and psychological. Although not much is known about the neurology of the disorder, a few studies may explain the subjective sense of detachment that forms the core of this dissociative experience.
The most commonly reported triggers of the disorder are stress and cannabis or hallucinogen ingestion.
Childhood abuse, especially emotional abuse, is a significant predictor of depersonalization symptoms. Certain elements of individualistic cultures may predispose a person to be vulnerable to depersonalization.
Emotional detachment is a core feature of depersonalization disorder. In functional magnetic resonance imaging studies of emotional memory, depersonalization disorder patients did not process emotionally salient material in the same way as healthy controls. Emotionally aversive scenes showed a reduced neural response in emotion-sensitive regions, as well as increased activity in regions associated with emotion regulation. 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 system involved in the "fight-or-flight" response. Patients demonstrate abnormal basal cortisol levels and activity. Two studies found patients with depersonalization disorder could be distinguished from patients with clinical depression and posttraumatic stress disorder.
Neuropsychological testing has shown deficits in attention, short-term memory and spatial ability on two- and three-dimensional stimuli. A later study of these same cognitive deficits found that despite intact overall intelligence, difficulty arises from information processing. Compared to the control group, subjects showed slower processing speed, organized perceptual information more poorly, and were vulnerable to distraction. The authors suggest that deficits in immediate recall on memory tasks are due to disturbances in attention and perception, rather than memory, since the subjects had no problems with delayed recall.
There are no treatment modalities specific to depersonalization disorder, although therapy and medication may be helpful. Most people who have this disorder also have depression or an anxiety disorder which can, in turn, worsen symptoms of depersonalization. Many individuals experience tremendous relief simply by learning their symptoms have a label.
Cognitive behavioral therapy is effective for both depression and anxiety, and suggests effectiveness for depersonalization disorder by improving overall symptoms on measures of psychopathology. For depersonalization disorder, therapists can help patients to reevaluate their experiences as less threatening, and to reduce safety behaviours and symptom monitoring. Obsessively ruminating on symptoms leads to symptom monitoring and checking, and this increased focus on the self tends to exacerbate dissociation. Many individuals attempt to mask their disorder by behaving normally, although adopting a role tends to increase the sense of detachment. It is important for patients to understand that feeling less real is not an indication of severe psychiatric illness or neurological damage. Anxiety tends to increase the severity of depersonalization leading many people avoid certain situations and activities that make them feel anxious, most commonly social situations.
In terms of medication, serotonin reuptake inhibitors can facilitate an overall improvement in participants, but only by reducing anxiety and depression. The only placebo-controlled trial of an SRI (fluoxetine) in fifty four patients failed to show benefit. 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 significant improvement of DPD.
In a retrospective report of subjects with depersonalization disorder, the majority of benzodiazepine trials were reported to have led to slight or definite improvement. Some individuals anecdotally benefit from clonazepam in particular. These drugs are not known to specifically affect the symptoms of dissociation; however, they do target the often co-morbid anxiety and stress experienced by those with DPD. To date no clinical trials have studied the effectiveness of benzodiazepines.
A placebo-controlled study of lamotrigine failed to show efficacy in treating depersonalization. While lamotrigine may not work on its own, it has been suggested that it may work when combined with a selective serotonin reuptake inhibitor. A second proposed combination is of an SSRI and a benzodiazepine proposed to be useful for patients with anxiety.
Opiate drugs, specifically those that agonize the kappa receptor, can cause similar sensations of the numb and detached feelings in depersonalization disorder. Opiate antagonists may reduce these symptoms. Naloxone and naltrexone are opioid antagonists that have been tested specifically on individuals with DPD. Naloxone was tested on eleven patients, 10 of which experienced complete remession or marked improvement. Naltrexone was used on fourteen individuals with DPD, four of which experienced much improvement, with a 30% decrease in depersonalization symptoms. Naltrexone has also been found to reduce general dissociation in borderline personality disorder.
- American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders. American Psychiatric Press: Washington DC
- 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. PMID 3783140.
- Simeon D, Kozin DS, Segal K, Lerch B, Dujour R, Giesbrecht T (2008). "De-constructing depersonalization: Further evidence for symptom clusters". Psychiatry Res 157 (1-3): 303–6. DOI:10.1016/j.psychres.2007.07.007. PMID 17959254. Research Blogging.
- Sierra M, Baker D, Medford N, David AS (2005). "Unpacking the depersonalization syndrome: an exploratory factor analysis on the Cambridge Depersonalization Scale". Psychol Med 35 (10): 1523–32. DOI:10.1017/S0033291705005325. PMID 16164776. Research Blogging.
- Jeffrey Abugel; Simeon, Daphne (2006). Feeling unreal: depersonalization disorder and the loss of the self. Oxford [Oxfordshire]: Oxford University Press, 15. ISBN 0-19-517022-9.
- Baker D, Hunter E, Lawrence E, et al. Depersonalization disorder: clinical features of 204 cases. British Journal of Psychiatry 2003; 182: 428-33. PMID 12724246 Full text available.
- 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 PMID 14628973
- Sierra M (2008). "Depersonalization disorder: pharmacological approaches". Expert Rev Neurother 8 (1): 19–26. DOI:10.1586/14737188.8.131.52. PMID 18088198. Research Blogging.
- 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. PMID 11431223.
- Sierra-Siegert M, David AS (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. Research Blogging.
- Simeon D, Guralnik O, Hazlett EA, Spiegel-Cohen J, Hollander E, Buchsbaum MS. (2000) Feeling unreal: a PET study of depersonalization disorder. American Journal of Psychiatry 157(11): 1782-8. PMID 11058475 Full text available.
- Medford N, Brierley B, Brammer M, Bullmore ET, David AS, Phillips ML. (2006) Emotional memory in depersonalization disorder: a functional MRI study. Psychiatry Research, 148(2-3):93-102. PMID 17085021 Full text available PDF.
- Phillips ML, Medford N, Senior C, Bullmore ET, Suckling J, Brammer MJ, Andrew C, Sierra M, Williams SC, David AS. (2001) Depersonalization disorder: thinking without feeling. Psychiatry Research: Neuroimaging, 108, 145-160 PMID 11756013
- Sierra M, Senior C, Dalton J, McDonough M, Bond A, Phillips ML, O'Dwyer AM, David AS. (2002) Autonomic response in depersonalization disorder. Archives of General Psychiatry. 59(9): 833-8. PMID 12215083 Full text available.
- 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. Research Blogging.
- 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. PMID 11600192.
- Curran HV, Morgan C (2000). "Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later". Addiction 95 (4): 575–90. PMID 10829333.
- Anand A, Charney DS, Oren DA, et al (2000). "Attenuation of the neuropsychiatric effects of ketamine with lamotrigine: support for hyperglutamatergic effects of N-methyl-D-aspartate receptor antagonists". Arch. Gen. Psychiatry 57 (3): 270–6. PMID 10711913.
- Guralnik O, Schmeidler J, Simeon D (2000). "Feeling unreal: cognitive processes in depersonalization". Am J Psychiatry 157 (1): 103–9. PMID 10618020.
- Guralnik O, Giesbrecht T, Knutelska M, Sirroff B, Simeon D (2007). "Cognitive functioning in depersonalization disorder". J. Nerv. Ment. Dis. 195 (12): 983–8. DOI:10.1097/NMD.0b013e31815c19cd. PMID 18091191. Research Blogging.
- Hunter EC, Baker D, Phillips ML, Sierra M, David AS (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. Research Blogging.
- 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 PMID 15231553
- Simeon D, Stein DJ, Hollander E. (1998) Treatment of depersonalization disorder with clomipramine. Biological Psychiatry, 44, 302-303. PMID 9715363
- Sierra M, Phillips ML, Ivin G, Krystal J, David AS (2003). "A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder". J. Psychopharmacol. (Oxford) 17 (1): 103–5. PMID 12680746.
- 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. Research Blogging.
- 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. PMID 11448093
- Simeon D, Knutelska M. (2005). An open trial of naltrexone in the treatment of depersonalization disorder. Journal of clinical Psychopharmacology, 25, 267-270. 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. PMID 10520978
- Jiménez-Genchi AM (2004). "Repetitive transcranial magnetic stimulation improves depersonalization: a case report". CNS Spectr 9 (5): 375–6. PMID 15115950.
- New York State Psychiatric Institute Study Treatment of Depersonalization Disorder With TMS