Causes and symptoms

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Depersonalization disorder, like the dissociative disorders in general, has been regarded as the result of severe abuse in childhood. This can be of a physical, emotional, and/or sexual nature.

Findings in 2002 indicate that emotional abuse in particular is a strong predictor of depersonalization disorder in adult life, as well as of depersonalization as a symptom in other mental disorders. Analysis of one study of 49 patients diagnosed with depersonalization disorder indicated much higher scores than the control subjects for the total amount of emotional abuse endured and for the maximum severity of this type of abuse. The researchers concluded that emotional abuse has been relatively neglected by psychiatrists compared to other forms of childhood trauma.

It is thought that abuse in childhood or trauma in adult life may account for the distinctive cognitive (knowledge-related) profile of patients with depersonal-ization disorder. These patients have significant difficulties focusing their attention, with spatial reasoning, and with short-term visual and verbal memory. However, they have intact reality testing. (Reality testing refers to a person's ability to distinguish between their internal experiences and the objective reality of persons and objects in the outside world.) Otherwise stated, a patient with depersonalization disorder may experience his/her body as unreal, but knows that "feelings aren't facts." The DSM-IV-TR specifies intact reality testing as a diagnostic criterion for depersonalization disorder.

The causes of depersonalization disorder are not completely understood. Recent advances in brain imaging and other forms of neurological testing, however, have confirmed that depersonalization disorder is a distinct diagnostic entity and should not be considered a subtype of PTSD.

No specific genes have been associated with susceptibility to depersonalization disorder as of early 2002. It is possible that a genetic factor will be identified in the future.

neurobiological. In the past few years, several features of depersonalization disorder have been traced to differences in brain functioning. A group of British researchers found that the emotional detachment that characterizes depersonalization is associated with a lower level of nerve cell responses in regions of the brain that are responsible for emotional feeling; an increased level of nerve cell responses was found in regions of the brain related to emotional regulation.

A group of American researchers concluded that patients with depersonalization disorder had different patterns of response to tests of the hypothalamic-pitu-itary-adrenal axis (HPA, the part of the brain involved in the "fight-or-flight" reaction to stress) than did patients with PTSD. Other tests by the same research team showed that patients with depersonalization disorder can be clearly distinguished from patients with major depression by tests of the functioning of the HPA axis.

Other neurobiological studies involving positron O

emission tomography (PET) measurements of glucose e

(sugar) metabolism in different areas of the brain found so that patients with depersonalization disorder appear to na have abnormal functioning of the sensory cortex. The z sensory cortex is the part of the brain that governs the ti senses of sight, hearing, and perceptions of the location n of one's body in space. These studies indicate that deper- s sonalization is a symptom that involves differences in d sensory perception and subjective experiences. er historical. Depersonalization disorder may be a reflection of changes in people's sense of self or personal identity within Western cultures since the eighteenth century. Historians of psychiatry have noted that whereas some mental disorders, such as depression, have been reported since the beginnings of Western medicine, no instances of the dissociative disorders were recorded before the 1780s. It seems that changes in social institutions and the structure of the family since the mid-eighteenth century may have produced a psychological structure in Westerners that makes individuals increasingly vulnerable to self disorders—as they are now called. Experiences of the unreality of one's body or one's self, such as those that characterize depersonalization disorder, presuppose a certain notion of how the self is presumed to feel. The emphasis on individualism and detachment from one's family is a mark of adult maturity in contemporary Western societies that appears to be a contributing factor to the frequency of dissociative symptoms and disorders.


The symptoms of depersonalization disorder have been described earlier. Although DSM-IV-TR does not specify a list of primary symptoms of depersonalization, British clinicians generally consider the triad of emotional numbing, changes in visual perception, and altered experience of one's body to be important core symptoms of depersonalization disorder.

DSM-IV-TR notes that patients with depersonaliza-tion disorder frequently score high on measurements of hypnotizability.


The lifetime prevalence of depersonalization disorder in the general population is unknown, possibly because many people are made anxious by episodes of depersonalization and afraid to discuss them with a primary care physician. One survey done by the National Institutes of Mental Health (NIMH) indicates that about half of the adults in the U.S. have had one or two brief episodes of depersonalization in their lifetimes, usually

<u resulting from severe stress. About a third of people "I exposed to life-threatening dangers develop brief peri™ ods of depersonalization, as do 40% of psychiatric n inpatients.

Depersonalization disorder is diagnosed about twice

™ as often in women as in men. It is not known, however, re on whether this sex ratio indicates that women are at greater ers risk for the disorder or if they are more likely to seek help ^ for its symptoms, or both. Little information is available

O about the incidence of the disorder in different racial or ethnic groups.


The diagnosis of depersonalization disorder is usually a diagnosis of exclusion. The doctor will take a detailed medical history, give the patient a physical examination, and order blood and urine tests in order to rule out depersonalization resulting from epilepsy, substance abuse, medication side effects, or recent periods of sleep deprivation.

There are several standard diagnostic questionnaires that may be given to evaluate the presence of a dissociative disorder. The Dissociative Experiences Scale, or DES, is a frequently administered self-report screener for dissociation. The Structured Clinical Interview for DSM-IV Dissociative Disorders, or SCID-D, can be used to make the diagnosis of depersonalization disorder distinct from the other dissociative disorders defined by DSM-IV. The SCID-D is a semi-structured interview, which means that the examiner's questions are open-ended and allow the patient to describe experiences of depersonalization in some detail—distinct from simple "yes" or "no" answers.

In addition to these instruments, a six-item Deper-sonalization Severity Scale, or DSS, has been developed to discriminate between depersonalization disorder and other dissociative or post-traumatic disorders, and to measure the effects of treatment in patients.


Depersonalization disorder sometimes resolves on its own without treatment. Specialized treatment is recommended only if the symptoms are persistent, recurrent, or upsetting to the patient. Insight-oriented psychody-namic psychotherapy, cognitive-behavioral therapy, and hypnosis have been demonstrated to be effective with some patients. There is, however, no single form of psychotherapy that is effective in treating all patients diagnosed with depersonalization disorder.

Medications that have been helpful to patients with depersonalization disorder include the benzodiazepine tranquilizers, such as lorazepam (Ativan), clo-razepate (Tranxene), and alprazolam (Xanax), and the tricyclic antidepressants, such as amitriptyline (Elavil), doxepin (Sinequan), and desipramine (Norpramin). As of 1999, newer, promising medications called selective serotonin reuptake inhibitors (SSRIs) became available. Some SSRIs include fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil). SSRIs act on brain chemicals that nerve cells use to send messages to each another. These chemical messengers (neurotransmitters) are released by one nerve cell and taken up by others. Those that are not taken up by other cells are taken up by the ones that released them. This is called "reuptake." SSRIs work by preventing the reuptake of serotonin—an action which allows more serotonin to be taken up by nerve cells.

Unfortunately, there have been very few well-designed studies comparing different medications for depersonalization disorder. Because depersonalization disorder is frequently associated with trauma, effective treatment must include other stress-related symptoms, as well.

Relaxation techniques have been reported to be a beneficial adjunctive treatment for persons diagnosed with depersonalization disorder, particularly for those who are worried about their sanity.


The prognosis for recovery from depersonalization disorder is good. Most patients recover completely, particularly those who developed the disorder in connection with traumas that can be explored and resolved in treatment. A few patients develop a chronic form of the disorder; this is characterized by periodic episodes of depersonalization in connection with stressful events in their lives.


Some clinicians think that depersonalization disorder has an undetected onset in childhood, even though most patients first appear for treatment as adolescents or young adults. Preventive strategies could include the development of screening techniques for identifying children at risk, as well as further research into the effects of emotional abuse on children.

It is also hopeful that further neurobiological research will lead to the development of medications or other treatment modalities for preventing, as well as treating, depersonalization.

Resources books

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th edition, text revised. Washington, DC: American Psychiatric Association, 2000.

"Depersonalization Disorder." Section 15, Chapter 188, in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers, MD, and Robert Berkow, MD. Whitehouse Station, NJ: Merck Research Laboratories, 2001.

Ellenberger, Henri. The Discovery of the Unconscious. New York: Basic Books, Inc., 1970.

Herman, Judith, MD. Trauma and Recovery. 2nd ed., revised. New York: Basic Books, 1997.

Medical Economics staff. Physicians' Desk Reference. 56th ed. Montvale, NJ: Medical Economics Company, 2002.

Stout, Martha, PhD. The Myth of Sanity: Tales of Multiple Personality in Everyday Life. New York: Penguin Books, 2001.


Berrios, G. E., and M. Sierra. "Depersonalization: A Conceptual History." Historical Psychiatry 8 (June 1997): 213-229.

Guralnik, O., J. Schmeidler, and D. Simeon. "Feeling Unreal: Cognitive Processes in Depersonalization." American Journal of Psychiatry 157 (January 2000): 103-109.

Lambert, M. V., C. Senior, M. L. Phillips, and others. "Visual Imagery and Depersonalisation." Psychopathology 34 (September-October 2001): 259-264.

Phillips, M. L., N. Medford, C. Senior, and others.

"Depersonalization Disorder: Thinking Without Feeling." Psychiatry Research 108 (December 30, 2001): 145-160.

Sierra, M., and others. "Lamotrigine in the Treatment of Depersonalization Disorder." Journal of Clinical Psychiatry 62 (October 2001): 826-827.

Sierra, M., and G. E. Berrios. "The Phenomenological

Stability of Depersonalization: Comparing the Old with the New." Journal of Nervous and Mental Disorders 189 (September 2001): 629-636.

Simeon, D., and others. "Personality Factors Associated with Dissociation: Temperament, Defenses, and Cognitive Schemata." American Journal of Psychiatry 159 (March 2002): 489-491.

Simeon, D., O. Guralnik, E. A. Hazlett, and others. "Feeling Unreal: A PET Study of Depersonalization Disorder." American Journal of Psychiatry 157 (November 2000): 1782-1788.

Simeon, D., O. Guralnik, M. Knutelska, and others.

"Hypothalamic-Pituitary-Adrenal Axis Dysregulation in Depersonalization Disorder." Neuropsychopharmacology 25 (November 2001): 793-795.

Simeon, D., O. Guralnik, and J. Schmeidler. "Development of a Depersonalization Severity Scale." Journal of Traumatic Stress 14 (April 2001): 341-349.

Simeon, D., O. Guralnik, J. Schmeidler, and others. "The Role O

of Childhood Interpersonal Trauma in Depersonalization p

Disorder." American Journal of Psychiatry 158 (July s

Simeon, D., D. J. Stein, and E. Hollander. "Treatment of 3

Depersonalization Disorder with Clomipramine." d

Biological Psychiatry 44 (August 15, 1998): 302-303. d

Stanton, B. R., A. S. David, A. J. Cleare, and others. "Basal -o

Activity of the Hypothalamic-Pituitary-Adrenal Axis in s Patients with Depersonalization Disorder." Psychiatry

Research 104 (October 2001): 85-89. d

Zanarini, M. C., and others. "The Dissociative Experiences of O

Borderline Patients." Comparative Psychiatry 41 (May- d

s organizations

International Society for the Study of Dissociation (ISSD). 60 Revere Drive, Suite 500, Northbrook, IL 60062. (847) 480-0899. Fax: (847) 480-9282. <>. National Institute of Mental Health. 6001 Executive Boulevard, Room 8184, MSC 9663, Bethesda, MD 20892-9663. (301) 443-4513. <>. National Organization for Rare Disorders, Inc. P. O. Box 8923, New Fairfield, CT 06812-8923. (203 ) 746-6518. <>. Society for Traumatic Stress Studies. 60 Revere Dr., Ste. 500, Northbrook, IL 60062. (708) 480-9080.

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