What is Dissociative Disorder?

Introduction

Dissociative disorders (DD) are conditions that involve disruptions or breakdowns of memory, awareness, identity, or perception.

People with dissociative disorders use dissociation as a defence mechanism, pathologically and involuntarily. The individual experiences these dissociations to protect themselves. Some dissociative disorders are triggered by psychological trauma, but depersonalisationderealisation disorder may be preceded only by stress, psychoactive substances, or no identifiable trigger at all.

The dissociative disorders listed in the American Psychiatric Association’s DSM-5 are as follows:

  • Dissociative identity disorder (formerly multiple personality disorder): the alternation of two or more distinct personality states with impaired recall among personality states. In extreme cases, the host personality is unaware of the other, alternating personalities; however, the alternate personalities can be aware of all the existing personalities.
  • Dissociative amnesia (formerly psychogenic amnesia): the temporary loss of recall memory, specifically episodic memory, due to a traumatic or stressful event. It is considered the most common dissociative disorder amongst those documented. This disorder can occur abruptly or gradually and may last minutes to years depending on the severity of the trauma and the patient. Dissociative fugue was previously a separate category but is now treated as a specifier for dissociative amnesia.
  • Depersonalisation-derealisation disorder: periods of detachment from self or surrounding which may be experienced as “unreal” (lacking in control of or “outside” self) while retaining awareness that this is only a feeling and not a reality.
  • The old category of dissociative disorder not otherwise specified is now split into two: other specified dissociative disorder, and unspecified dissociative disorder. These categories are used for forms of pathological dissociation that do not fully meet the criteria of the other specified dissociative disorders; or if the correct category has not been determined; or the disorder is transient.

The ICD 11 lists dissociative disorders as:

  • Dissociative neurological symptom disorder.
  • Dissociative amnesia.
  • Dissociative amnesia with dissociative fugue.
  • Trance disorder.
  • Possession trance disorder.
  • Dissociative identity disorder.
  • Partial dissociative identity disorder.
  • Depersonalisation-derealisation disorder.

Cause and Treatment

Dissociative Identity Disorder

Cause

Dissociative identity disorder is caused by ongoing childhood trauma that occurs before the ages of six to nine. People with dissociative identity disorder usually have close relatives who have also had similar experiences.

Treatment

Long-term psychotherapy to improve the patient’s quality of life.

Dissociative Amnesia

Cause

A way to cope with trauma.

Treatment

Psychotherapy (e.g. talk therapy) counselling or psychosocial therapy which involves talking about your disorder and related issues with a mental health provider. Psychotherapy often involves hypnosis (help you remember and work through the trauma); creative art therapy (using creative process to help a person who cannot express his or her thoughts); cognitive therapy (talk therapy to identify unhealthy and negative beliefs/behaviours); and medications (antidepressants, anti-anxiety medications, or sedatives). These medications help control the symptoms associated with the dissociative disorders, but there are no medications yet that specifically treat dissociative disorders. However, the medication pentothal can sometimes help to restore the memories. The length of an event of dissociative amnesia may be a few minutes or several years. If an episode is associated with a traumatic event, the amnesia may clear up when the person is removed from the traumatic situation. Dissociative fugue was a separate category but is now listed as a specifier for dissociative amnesia.

Depersonalisation-Derealisation Disorder

Cause

Dissociative disorders usually develop as a way to cope with trauma. The disorders most often form in children subjected to chronic physical, sexual or emotional abuse or, less frequently, a home environment that is otherwise frightening or highly unpredictable; however, this disorder can also acutely form due to severe traumas such as war or the death of a loved one.

Treatment

Same treatment as dissociative amnesia. An episode of depersonalisationderealisation disorder can be as brief as a few seconds or continue for several years.

Dissociative disorders, especially dissociative identity disorder (DID), while being the result of extraordinary abuse and trauma in childhood, it should not be attributed exotic status. DID would be better examined through a more holistic lens, taking into considering the social, cognitive, and neural components, and how they interact with one another.

Medications

There are no medications to treat dissociative disorders, however, drugs to treat anxiety and depression that may accompany the disorders can be given.

Diagnosis and Prevalence

The lifetime prevalence of dissociative disorders varies from 10% in the general population to 46% in psychiatric inpatients. Diagnosis can be made with the help of structured clinical interviews such as the Dissociative Disorders Interview Schedule (DDIS) and the Structured Clinical Interview for DSM-IV Dissociative Disorders (SCID-D-R), and behavioural observation of dissociative signs during the interview. Additional information can be helpful in diagnosis, including the Dissociative Experiences Scale or other questionnaires, performance-based measures, records from doctors or academic records, and information from partners, parents, or friends. A dissociative disorder cannot be ruled out in a single session and it is common for patients diagnosed with a dissociative disorder to not have a previous dissociative disorder diagnosis due to a lack of clinician training. Some diagnostic tests have also been adapted or developed for use with children and adolescents such as the Adolescent Dissociative Experiences Scale, Children’s Version of the Response Evaluation Measure (REM-Y-71), Child Interview for Subjective Dissociative Experiences, Child Dissociative Checklist (CDC), Child Behaviour Checklist (CBCL) Dissociation Subscale, and the Trauma Symptom Checklist for Children Dissociation Subscale.

Dissociative disorders have been found to be quite prevalent in outpatient populations, as well as within low-income communities. One study found that in a population of poor inner-city outpatients, there was a 29% prevalence of dissociative disorders.

There are problems with classification, diagnosis and therapeutic strategies of dissociative and conversion disorders which can be understood by the historic context of hysteria. Even current systems used to diagnose DD such as the DSM-IV and ICD-10 differ in the way the classification is determined. In most cases mental health professionals are still hesitant to diagnose patients with Dissociative Disorder, because before they are considered to be diagnosed with Dissociative Disorder these patients have more than likely been diagnosed with major depressive disorder, anxiety disorder, and most often post-traumatic stress disorder (PTSD). It has been found from interviews with those who may be afflicted with dissociative disorders may be more effective at getting an accurate diagnosis than self-scoring assessments and scales.

The prevalence of dissociative disorders is not completely understood due to the many difficulties in diagnosing dissociative disorders. Many of these difficulties stem from a misunderstanding of dissociative disorders, from an unfamiliarity diagnosis or symptoms to disbelief in some dissociative disorders entirely. Due to this it has been found that only 28% to 48% of people diagnosed with a dissociative disorder receive treatment for their mental health. Patients who are misdiagnosed are often those more likely to be hospitalised repeatedly, and lack of treatment can result in intensive outpatient treatment and higher rates of disability.

An important concern in the diagnosis of dissociative disorders in forensic interviews is the possibility that the patient may be feigning symptoms in order to escape negative consequences. Young criminal offenders report much higher levels of dissociative disorders, such as amnesia. In one study it was found that 1% of young offenders reported complete amnesia for a violent crime, while 19% claimed partial amnesia. There have also been cases in which people with dissociative identity disorder provide conflicting testimonies in court, depending on the personality that is present. The world-wide prevalence of dissociative disorders is not well understood due to different cultural beliefs surrounding human emotions and the human brain

Children and Adolescents

Dissociative disorders (DD) are widely believed to have roots in adverse childhood experiences including abuse and loss, but the symptoms often go unrecognised or are misdiagnosed in children and adolescents. However, a recent western Chinese study showed an increase in awareness of dissociative disorders present in children These studies show that DD’s have an intricate relationship with the patient’s mental, physical and socio-cultural environments. This study suggested that dissociative disorders are more common in Western, or developing countries, however, some cases have been seen in both clinical and non-clinical Chinese populations. There are several reasons why recognising symptoms of dissociation in children is challenging: it may be difficult for children to describe their internal experiences; caregivers may miss signals or attempt to conceal their own abusive or neglectful behaviours; symptoms can be subtle or fleeting; disturbances of memory, mood, or concentration associated with dissociation may be misinterpreted as symptoms of other disorders.

Another resource, Beacon House, informs us of dissociative disorder in children, suggesting that it is a survival mechanism that often goes unnoticed in children that have been traumatised. Dr. Shoshanah Lyons suggests that traumatised children often continue to dissociate even though they might not be in any danger, and that they are often unaware that they are dissociating. In addition to developing diagnostic tests for children and adolescents (see above), a number of approaches have been developed to improve recognition and understanding of dissociation in children. Recent research has focused on clarifying the neurological basis of symptoms associated with dissociation by studying neurochemical, functional and structural brain abnormalities that can result from childhood trauma. Others in the field have argued that recognising disorganised attachment (DA) in children can help alert clinicians to the possibility of dissociative disorders. In their 2008 article, Rebecca Seligman and Laurence Kirmayer suggest the existence of evidence of linkages between trauma experienced in childhood and the capacity for dissociation or depersonalisation. They also suggest that individuals who are able to utilise dissociative techniques are able to keep this as an extended strategy to cope with stressful situations.

Clinicians and researchers stress the importance of using a developmental model to understand both symptoms and the future course of DDs. In other words, symptoms of dissociation may manifest differently at different stages of child and adolescent development and individuals may be more or less susceptible to developing dissociative symptoms at different ages. Further research into the manifestation of dissociative symptoms and vulnerability throughout development is needed. Related to this developmental approach, more research is required to establish whether a young patient’s recovery will remain stable over time.

Current Debates and the DSM-5

A number of controversies surround DD in adults as well as children. First, there is ongoing debate surrounding the aetiology of dissociative identity disorder (DID). The crux of this debate is if DID is the result of childhood trauma and disorganized attachment. A proposed view is that dissociation has a physiological basis, in that it involves automatically triggered mechanisms such as increased blood pressure and alertness, that would, as Lynn contends, imply its existence as a cross-species disorder. A second area of controversy surrounds the question of whether or not dissociation as a defence versus pathological dissociation are qualitatively or quantitatively different. Experiences and symptoms of dissociation can range from the more mundane to those associated with PTSD or acute stress disorder (ASD) to dissociative disorders. Mirroring this complexity, the DSM-5 workgroup considered grouping dissociative disorders with other trauma/stress disorders, but instead decided to put them in the following chapter to emphasize the close relationship. The DSM-5 also introduced a dissociative subtype of PTSD.

A 2012 review article supports the hypothesis that current or recent trauma may affect an individual’s assessment of the more distant past, changing the experience of the past and resulting in dissociative states. However, experimental research in cognitive science continues to challenge claims concerning the validity of the dissociation construct, which is still based on Janetian notions of structural dissociation. Even the claimed etiological link between trauma/abuse and dissociation has been questioned. Links observed between trauma/abuse and DD are largely only present from a Western cultural context. For non-Western cultures dissociation “may constitute a “normal” psychological capacity”. An alternative model proposes a perspective on dissociation based on a recently established link between a labile sleep-wake cycle and memory errors, cognitive failures, problems in attentional control, and difficulties in distinguishing fantasy from reality.

Debates around DD also stem from Western versus non-Western lenses of viewing the disorder, and associated views of causes of DD. DID was initially believed to be specific to the West, until cross-cultural studies indicated its occurrence worldwide. Conversely, anthropologists have largely done little work on DD in the West relating to its perceptions of possession syndromes that would be present in non-Western societies. While dissociation has been viewed and catalogued by anthropologists differently in the West and non-Western societies, there are aspects of each that show DD has universal characteristics. For example, while shamanic and rituals of non-Western societies may hold dissociative aspects, this is not exclusive as many Christian sects, such as “possession by the Holy Ghost” share similar qualities to those of non-Western trances.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Dissociative_disorder >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Reduced Effect Display?

Introduction

Reduced affect display, sometimes referred to as emotional blunting, is a condition of reduced emotional reactivity in an individual.

It manifests as a failure to express feelings (affect display) either verbally or nonverbally, especially when talking about issues that would normally be expected to engage the emotions. Expressive gestures are rare and there is little animation in facial expression or vocal inflection. Reduced affect can be symptomatic of autism, schizophrenia, depression, posttraumatic stress disorder, depersonalisation disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications (e.g. antipsychotics and antidepressants).

Reduced affect should be distinguished from apathy and anhedonia, which explicitly refer to a lack of emotion, whereas reduced affect is a lack of emotional expression (affect display) regardless of whether emotion (underlying affect) is actually reduced or not.

Types

Constricted Affect

A restricted or constricted affect is a reduction in an individual’s expressive range and the intensity of emotional responses.

Blunted and Flat Affect

Blunted affect is a lack of affect more severe than restricted or constricted affect, but less severe than flat or flattened affect. “The difference between flat and blunted affect is in degree. A person with flat affect has no or nearly no emotional expression. They may not react at all to circumstances that usually evoke strong emotions in others. A person with blunted affect, on the other hand, has a significantly reduced intensity in emotional expression”.

Shallow Affect

Shallow affect has equivalent meaning to blunted affect. Factor 1 of the Psychopathy Checklist identifies shallow affect as a common attribute of psychopathy.

Brain structures

Individuals with schizophrenia with blunted affect show different regional brain activity in fMRI scans when presented with emotional stimuli compared to individuals with schizophrenia without blunted affect. Individuals with schizophrenia without blunted affect show activation in the following brain areas when shown emotionally negative pictures: midbrain, pons, anterior cingulate cortex, insula, ventrolateral orbitofrontal cortex, anterior temporal pole, amygdala, medial prefrontal cortex, and extrastriate visual cortex. Individuals with schizophrenia with blunted affect show activation in the following brain regions when shown emotionally negative pictures: midbrain, pons, anterior temporal pole, and extrastriate visual cortex.

Limbic Structures

Individuals with schizophrenia with flat affect show decreased activation in the limbic system when viewing emotional stimuli. In individuals with schizophrenia with blunted affect neural processes begin in the occipitotemporal region of the brain and go through the ventral visual pathway and the limbic structures until they reach the inferior frontal areas. Damage to the amygdala of adult rhesus macaques early in life can permanently alter affective processing. Lesioning the amygdala causes blunted affect responses to both positive and negative stimuli. This effect is irreversible in the rhesus macaques; neonatal damage produces the same effect as damage that occurs later in life. The macaques’ brain cannot compensate for early amygdala damage even though significant neuronal growth may occur. There is some evidence that blunted affect symptoms in schizophrenia patients are not a result of just amygdala responsiveness, but a result of the amygdala not being integrated with other areas of the brain associated with emotional processing, particularly in amygdala-prefrontal cortex coupling. Damage in the limbic region prevents the amygdala from correctly interpreting emotional stimuli in individuals with schizophrenia by compromising the link between the amygdala and other brain regions associated with emotion.

Brainstem

Parts of the brainstem are responsible for passive emotional coping strategies that are characterised by disengagement or withdrawal from the external environment (quiescence, immobility, hyporeactivity), similar to what is seen in blunted affect. Individuals with schizophrenia with blunted affect show activation of the brainstem during fMRI scans, particularly the right medulla and the left pons, when shown “sad” film excerpts. The bilateral midbrain is also activated in individuals with schizophrenia diagnosed with blunted affect. Activation of the midbrain is thought to be related to autonomic responses associated with perceptual processing of emotional stimuli. This region usually becomes activated in diverse emotional states. When the connectivity between the midbrain and the medial prefrontal cortex is compromised in individuals with schizophrenia with blunted affect an absence of emotional reaction to external stimuli results.

Prefrontal Cortex

Individuals with schizophrenia, as well as patients being successfully reconditioned with quetiapine for blunted affect, show activation of the prefrontal cortex (PFC). Failure to activate the PFC is possibly involved in impaired emotional processing in individuals with schizophrenia with blunted affect. The mesial PFC is activated in aver individuals in response to external emotional stimuli. This structure possibly receives information from the limbic structures to regulate emotional experiences and behaviour. Individuals being reconditioned with quetiapine, who show reduced symptoms, show activation in other areas of the PFC as well, including the right medial prefrontal gyrus and the left orbitofrontal gyrus.

Anterior Cingulate Cortex

A positive correlation has been found between activation of the anterior cingulate cortex and the reported magnitude of sad feelings evoked by viewing sad film excerpts. The rostral subdivision of this region is possibly involved in detecting emotional signals. This region is different in individuals with schizophrenia with blunted affect.

Diagnoses

Schizophrenia

Flat and blunted affect is a defining characteristic in the presentation of schizophrenia. To reiterate, these individuals have a decrease in observed vocal and facial expression as well as the use of gestures. One study of flat affect in schizophrenia found that “flat affect was more common in men, and was associated with worse current quality of life” as well as having “an adverse effect on course of illness”.

The study also reported a “dissociation between reported experience of emotion and its display” – supporting the suggestion made elsewhere that “blunted affect, including flattened facial expressiveness and lack of vocal inflection … often disguises an individual’s true feelings.” Thus, feelings may merely be unexpressed, rather than totally lacking. On the other hand, “a lack of emotions which is due not to mere repression but to a real loss of contact with the objective world gives the observer a specific impression of ‘queerness’ … the remainders of emotions or the substitutes for emotions usually refer to rage and aggressiveness”. In the most extreme cases, there is a complete “dissociation from affective states”. To further support this idea, a study examining emotion dysregulation found that individuals with schizophrenia could not exaggerate their emotional expression as healthy controls could. Participants were asked to express whatever emotions they had during a clip of a film, and the participants with schizophrenia showed deficits in behavioural expression of their emotions.

There is still some debate regarding the source of flat affect in schizophrenia. However, some literature indicates abnormalities in the dorsal executive and ventral affective systems; it is argued that dorsal hypoactivation and ventral hyperactivation may be the source of flat affect. Further, the authors found deficits in the mirror neuron system may also contribute to flat affect in that the deficits may cause disruptions in the control of facial expression.

Another study found that when speaking, individuals with schizophrenia with flat affect demonstrate less inflection than normal controls and appear to be less fluent. Normal subjects appear to express themselves using more complex syntax, whereas flat affect subjects speak with fewer words, and fewer words per sentence. Flat affect individuals’ use of context-appropriate words in both sad and happy narratives are similar to that of controls. It is very likely that flat affect is a result of deficits in motor expression as opposed to emotional processing. The moods of display are compromised, but subjective, autonomic, and contextual aspects of emotion are left intact.

Post-Traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) was previously known to cause negative feelings, such as depressed mood, re-experiencing and hyperarousal. However, recently, psychologists have started to focus their attention on the blunted affects and also the decrease in feeling and expressing positive emotions in PTSD patients. Blunted affect, or emotional numbness, is considered one of the consequences of PTSD because it causes a diminished interest in activities that produce pleasure (anhedonia) and produces feelings of detachment from others, restricted emotional expression and a reduced tendency to express emotions behaviourally. Blunted affect is often seen in veterans as a consequence of the psychological stressful experiences that caused PTSD. Blunted affect is a response to PTSD, it is considered one of the central symptoms in post-traumatic stress disorders and it is often seen in veterans who served in combat zones. In PTSD, blunted affect can be considered a psychological response to PTSD as a way to combat overwhelming anxiety that the patients feel. In blunted affect, there are abnormalities in circuits that also include the prefrontal cortex.

Assessment

In making assessments of mood and affect the clinician is cautioned that “it is important to keep in mind that demonstrative expression can be influenced by cultural differences, medication, or situational factors”; while the layperson is warned to beware of applying the criterion lightly to “friends, otherwise [he or she] is likely to make false judgments, in view of the prevalence of schizoid and cyclothymic personalities in our ‘normal’ population, and our [US] tendency to psychological hypochondriasis”.

R.D. Laing in particular stressed that “such ‘clinical’ categories as schizoid, autistic, ‘impoverished’ affect … all presuppose that there are reliable, valid impersonal criteria for making attributions about the other person’s relation to [his or her] actions. There are no such reliable or valid criteria”.

Differential Diagnosis

Blunted affect is very similar to anhedonia, which is the decrease or cessation of all feelings of pleasure (which thus affects enjoyment, happiness, fun, interest, and satisfaction). In the case of anhedonia, emotions relating to pleasure will not be expressed as much or at all because they are literally not experienced or are decreased. Both blunted affect and anhedonia are considered negative symptoms of schizophrenia, meaning that they are indicative of a lack of something. There are some other negative symptoms of schizophrenia which include avolition, alogia and catatonic behaviour.

Closely related is alexithymia – a condition describing people who “lack words for their feelings. They seem to lack feelings altogether, although this may actually be because of their inability to express emotion rather than from an absence of emotion altogether”. Alexithymic patients however can provide clues via assessment presentation which may be indicative of emotional arousal.

“If the amygdala is severed from the rest of the brain, the result is a striking inability to gauge the emotional significance of events; this condition is sometimes called ‘affective blindness'”. In some cases, blunted affect can fade, but there is no conclusive evidence of why this can occur.

What is Dissociative Disorder Not Otherwise Specified?

Introduction

Dissociative disorder not otherwise specified (DDNOS) is a mental health diagnosis for pathological dissociation that matches the DSM-5 criteria for a dissociative disorder, but does not fit the full criteria for any of the specifically identified subtypes, which include dissociative identity disorder, dissociative amnesia, and depersonalisation/derealisation disorder, and the reasons why the previous diagnoses were not met are specified.

Refer to Depressive Disorder Not Otherwise Specified (DD-NOS).

Background

“Unspecified dissociative disorder” is given when the clinician does not give a reason. The International Statistical Classification of Diseases and Related Health Problems (ICD-10) refers to the diagnosis as “Other dissociative and conversion disorders”.

Examples of DDNOS include chronic and recurrent syndromes of mixed dissociative symptoms, identity disturbance due to prolonged and intense coercive persuasion, disorders similar to dissociative identity disorder, acute dissociative reactions to stressful events, and dissociative trance.

DDNOS is the most common dissociative disorder and is diagnosed in 40% of dissociative disorder cases. It is often co-morbid with other mental illnesses such as complex posttraumatic stress disorder, major depressive disorder, generalised anxiety disorder, personality disorders, substance use disorders, and eating disorders.

What is Depersonalisation?

Introduction

Depersonalisation can consist of a detachment within the self, regarding one’s mind or body, or being a detached observer of oneself.

Subjects feel they have changed and that the world has become vague, dreamlike, less real, lacking in significance or being outside reality while looking in. Chronic depersonalisation refers to depersonalisation/derealisation disorder, which is classified by the DSM-5 as a dissociative disorder, based on the findings that depersonalisation and derealisation are prevalent in other dissociative disorders including dissociative identity disorder.

Though degrees of depersonalisation and derealisation can happen to anyone who is subject to temporary anxiety or stress, chronic depersonalisation is more related to individuals who have experienced a severe trauma or prolonged stress/anxiety. Depersonalisation-derealisation is the single most important symptom in the spectrum of dissociative disorders, including dissociative identity disorder and “dissociative disorder not otherwise specified” (DD-NOS). It is also a prominent symptom in some other non-dissociative disorders, such as anxiety disorders, clinical depression, bipolar disorder, schizophrenia, schizoid personality disorder, hypothyroidism or endocrine disorders, schizotypal personality disorder, borderline personality disorder, obsessive compulsive disorder, migraines, and sleep deprivation; it can also be a symptom of some types of neurological seizure.

In social psychology, and in particular self-categorisation theory, the term depersonalisation has a different meaning and refers to “the stereotypical perception of the self as an example of some defining social category”.

Description

Individuals who experience depersonalisation feel divorced from their own personal self by sensing their body sensations, feelings, emotions, behaviours etc. as not belonging to the same person or identity. Often a person who has experienced depersonalisation claims that things seem unreal or hazy. Also, a recognition of a self breaks down (hence the name). Depersonalisation can result in very high anxiety levels, which further increase these perceptions.

Depersonalisation is a subjective experience of unreality in one’s self, while derealisation is unreality of the outside world. Although most authors currently regard depersonalisation (self) and derealisation (surroundings) as independent constructs, many do not want to separate derealisation from depersonalisation.

Prevalence

Depersonalisation is a symptom of anxiety disorders, such as panic disorder. It can also accompany sleep deprivation (often occurring when suffering from jet lag), migraine, epilepsy (especially temporal lobe epilepsy, complex-partial seizure, both as part of the aura and during the seizure), obsessive compulsive disorder, severe stress or trauma, anxiety, the use of recreational drugs – especially cannabis, hallucinogens, ketamine, and MDMA, certain types of meditation, deep hypnosis, extended mirror or crystal gazing, sensory deprivation, and mild-to-moderate head injury with little or full loss of consciousness (less likely if unconscious for more than 30 mins). Interoceptive exposure is a non-pharmacological method that can be used to induce depersonalisation.

In the general population, transient depersonalisation/derealisation are common, having a lifetime prevalence between 26-74%. A random community-based survey of 1,000 adults in the US rural south found a 1-year depersonalisation prevalence rate at 19%. Several studies, but not all, found age to be a significant factor: adolescents and young adults in the normal population reported the highest rate. In a study, 46% of college students reported at least one significant episode in the previous year. In another study, 20% of patients with minor head injury experience significant depersonalisation and derealisation. Several studies found that up to 66% of individuals in life-threatening accidents report transient depersonalisation at minimum during or immediately after the accidents. Depersonalisation occurs 2-4 times more in women than in men.

A similar and overlapping concept called ipseity disturbance (ipse is Latin for “self” or “itself”) may be part of the core process of schizophrenia spectrum disorders. However, specific to the schizophrenia spectrum seems to be “a dislocation of first-person perspective such that self and other or self and world may seem to be non-distinguishable, or in which the individual self or field of consciousness takes on an inordinate significance in relation to the objective or intersubjective world” (emphasis in original).

For the purposes of evaluation and measurement depersonalisation can be conceived of as a construct and scales are now available to map its dimensions in time and space. A study of undergraduate students found that individuals high on the depersonalisation/derealisation subscale of the Dissociative Experiences Scale exhibited a more pronounced cortisol response in stress. Individuals high on the absorption subscale, which measures a subject’s experiences of concentration to the exclusion of awareness of other events, showed weaker cortisol responses.

In general infantry and special forces soldiers, measures of depersonalisation and derealisation increased significantly after training that includes experiences of uncontrollable stress, semi-starvation, sleep deprivation, as well as lack of control over hygiene, movement, communications, and social interactions.

Pharmacological and Situational Causes

Depersonalisation has been described by some as a desirable state, particularly by those that have experienced it under the influence of mood-altering recreational drugs. It is an effect of dissociatives and psychedelics, as well as a possible side effect of caffeine, alcohol, amphetamine, cannabis, and antidepressants. It is a classic withdrawal symptom from many drugs.

Benzodiazepine dependence, which can occur with long-term use of benzodiazepines, can induce chronic depersonalisation symptomatology and perceptual disturbances in some people, even in those who are taking a stable daily dosage, and it can also become a protracted feature of the benzodiazepine withdrawal syndrome.

Lieutenant Colonel Dave Grossman, in his book On Killing, suggests that military training artificially creates depersonalisation in soldiers, suppressing empathy and making it easier for them to kill other human beings.

Graham Reed (1974) claimed that depersonalisation occurs in relation to the experience of falling in love.

Depersonalisation as a Psychobiological Mechanism

Depersonalisation is a classic response to acute trauma, and may be highly prevalent in individuals involved in different traumatic situations including motor vehicle accident, and imprisonment.

Psychologically depersonalisation can, just like dissociation in general, be considered a type of coping mechanism. Depersonalisation is in that case unconsciously used to decrease the intensity of unpleasant experience, whether that is something as mild as stress or something as severe as chronically high anxiety and post-traumatic stress disorder. The decrease in anxiety and psychobiological hyperarousal helps preserving adaptive behaviours and resources under threat or danger. Depersonalisation is an overgeneralised reaction in that it does not diminish just the unpleasant experience, but more or less all experience – leading to a feeling of being detached from the world and experiencing it in a more bland way. An important distinction must be made between depersonalisation as a mild, short term reaction to unpleasant experience and depersonalisation as a chronic symptom stemming from a severe mental disorder such as PTSD or Dissociative Identity Disorder. Chronic symptoms may represent persistence of depersonalization beyond the situations under threat.

Treatment

Treatment is dependent on the underlying cause, whether it is organic or psychological in origin. If depersonalisation is a symptom of neurological disease, then diagnosis and treatment of the specific disease is the first approach. Depersonalisation can be a cognitive symptom of such diseases as amyotrophic lateral sclerosis, Alzheimer’s, multiple sclerosis (MS), or any other neurological disease affecting the brain. For those suffering from depersonalisation with migraine, tricyclic antidepressants are often prescribed.

If depersonalization is a symptom of psychological causes such as developmental trauma, treatment depends on the diagnosis. In case of dissociative identity disorder or DD-NOS as a developmental disorder, in which extreme developmental trauma interferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and – in the case of additional (co-morbid) disorders such as eating disorders – a team of specialists treating such an individual. It can also be a symptom of borderline personality disorder, which can be treated in the long term with proper psychotherapy and psychopharmacology.

The treatment of chronic depersonalisation is considered in depersonalisation disorder.

A recently completed study at Columbia University in New York City has shown positive effects from transcranial magnetic stimulation (TMS) to treat depersonalisation disorder. Currently, however, the FDA has not approved TMS to treat DP.

A 2001 Russian study showed that naloxone, a drug used to reverse the intoxicating effects of opioid drugs, can successfully treat depersonalization disorder. According to the study: “In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization.” The anti convulsion drug Lamotrigine has shown some success in treating symptoms of depersonalisation, often in combination with a Selective serotonin reuptake inhibitor and is the first drug of choice at the depersonalisation research unit at King’s College London.

Research

The Depersonalisation Research Unit at the Institute of Psychiatry in London conducts research into depersonalization disorder. Researchers there use the acronym DPAFU (Depersonalisation and Feelings of Unreality) as a shortened label for the disorder. In a 2020 article in the journal Nature, Vesuna, et al. describe experimental findings which show that layer 5 of the retrosplenial cortex is likely responsible for dissociative states of consciousness in mammals.