Depersonalization disorder

Depersonalization Disorder (DPD) is a persistent or recurring feeling of being unreal. 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. Some find familiar places strange and unfamiliar.

In the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM), DPD is classified 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 separate symptoms.

Individuals with depersonalization disorder demonstrate intact reality testing. This means they share the same objective reality about objects and people in the outside world as healthy people. Individuals diagnosed with depersonalization disorder are not delusional.

Most of the people with depersonalization disorder also have an anxiety disorder or depression. This leads many mental health professionals to believe that depersonalization is only a symptom of another disorder. The diagnosis of depersonalization disorder has existed in the Diagnostic and Statistical Manual of Mental Disorders since the third edition. As well, there are no Axis I or II disorders that show a unique relationship in terms of presence or severity of depersonalization disorder. This supports DPD’s existence as a separate diagnosis.

Diagnosis

As with any mental disorder, a diagnosis can only be made by a properly trained mental health professional, usually a psychiatrist or psychologist. According to the DSM-IV-TR, a diagnosis of depersonalization disorder is made using the following criteria:

• Persistent, recurring feeling of being detached from one’s mental processes or body; as if an observer
• During depersonalization, reality testing is intact
• Depersonalization causes significant distress, and impairment in social, occupational, or other functioning
• Depersonalization is not related to another disorder, substance use, or general medical condition

Differential diagnoses include epilepsy, schizophrenia, drug use, and anxiety disorders.

Some structured interviews and scales may aid diagnosis. 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. 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.

Causes

Although the exact cause of depersonalization disorder is unknown, it has been associated with childhood abuse. Emotional abuse is a significant predictor of depersonalization symptoms. This 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 severe stress, depression, panic, cannabis and hallucinogen ingestion.

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 area of the brain 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 guidelines for 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.