Depersonalization disorder

Depersonalization disorder (DPD) is characterized by a persistent or recurring experience of unreality. People commonly report this experience as 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 what are typically familiar places to be strange and unfamiliar.

The Diagnostic and Statistical Manual of Mental Disorders classifies DPD as a dissociative disorder. Dissociation is a disruption in the normally integrated functions of memory, cognition, and consciousness. Depersonalization is often accompanied by derealization, a sense that the exterior world is unreal. Although these dissociative symptoms often occur simultaneously, they are considered separate symptoms.

Individuals diagnosed with depersonalization disorder demonstrate intact reality testing and, sharing the same objective reality as those not diagnosed as such, are not considered delusional.

Most individuals diagnosed with depersonalization disorder exhibit symptoms for co-occurring anxiety or depression, or a co-morbid anxious or depressive disorder. This has led many mental health professionals to suggest that depersonalization is a symptom of other disorders. On the other hand, the diagnostic criteria for depersonalization disorder have been included in the Diagnostic and Statistical Manual of Mental Disorders since the third edition. Further, there are no Axis I or II disorders that demonstrate a unique relationship similar to depersonalization disorder in terms of presence or severity. These factors present support for DPD as a separate diagnostic category.

Diagnostic criteria

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.

Diagnostic narrative

The primary characteristic of depersonalization is an experience of chronic or episodic feelings of detachment from one's own thoughts or body. Despite this experience, individuals do maintain the ability to discriminative between reality and non-reality, converse 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.

Diagnostic methods

1. 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.
2. 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.
3. 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.

Causes

Although the exact cause of depersonalization disorder is unknown, an association has been suggested with childhood abuse. Emotional abuse is a significant predictor of depersonalization symptoms. In addition, the symptomolgy of the disorder may have several etiologies, both drug induced, and psychological.

Depersonalization is the third most common psychological experience, after feelings of anxiety and feelings of depression, and often occurs after life threatening experiences, such as accidents, assault, or serious illness or injury. The most common immediate precipitants of the disorder are stress, as well as cannabis or hallucinogen ingestion. Depersonalization commonly exists as a symptom in epilepsy, schizophrenia, and several anxiety disorders, such as panic attacks, and should not be considered a separate disorder in this case.

Clinical Presentation

Men and women are affected equally by DPD. The average age of onset is 16 years of age, although some report being depersonalized as long as they can remember, and others report an onset in their 20s, 30s, or even 40s. One study estimates the prevalence of depersonalization disorder at 2.4% of the population. 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 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 have an emotional disconnection from those they care about. Neuropsychological testing has shown deficits in attention, short-term memory and spatial ability.

Pathophysiology

Not much is known about the neurobiology of depersonalization disorder, however a few studies may explain the subjective sense of detachment that forms the core of this dissociative experience. A PET scan found functional abnormalities in the visual, auditory, and somatosensory cortex, as well as 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 similiar test of emotional memory, depersonalization disorder patients did not process emotionally salient material in the same way as 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 system involved in the "fight-or-flight" response. Patients demonstrate abnormal cortisol levels and basal activity. Two studies found patients with DPD could be distinguished from patients with clinical depression and posttraumatic stress disorder.

Management

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. Both of these disorders, in turn, can worsen symptoms of depersonalization.

Psychotherapy

Cognitive behavioral therapy is effective for both depression and anxiety, and suggests effectiveness for depersonalization disorder by improving overall symptoms on measures of psychopathology. Many patients experience tremendous relief when their disturbing and seemingly inexplicable symptoms form a well-defined syndrome.

Therapists can help patients by reevaluating their experiences as less threatening, reducing avoidances, safety behaviours, and symptom monitoring. It is important for patients to understand that their feeling of being less real is not an indication of severe psychiatric illness or neurological damage. Since anxiety tends to increase the severity of depersonalization, many people avoid certain situations and activities. The most commonly avoided are social situations. Many individuals attempt to mask their disorder by behaving normally, although adopting a role tends to increase the sense of detachment. An obsessive focus on symptoms leads to symptom monitoring and checking. An increased focus on the self tends to exacerbate experiences of depersonalization.

Pharmacotherapy

In terms of medication, serotonin reuptake inhibitor treatment can create an overall improvement in participants, but only by reducing anxiety and depression. The only placebo-controlled trial failed to show benefit with fluoxetine in fifty four patients with depersonalization disorder. 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 DPD, the majority of benzodiazepine trials were reported to have led to slight or definite improvement. Some individuals anecdotally appear to 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.

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.