Dissociative disorders

• Dissociative disorders are conditions in which the normal linking together of memory, identity, perception and consciousness is interrupted, usually in the setting of trauma, and these interruptions cause distress or impairment.
• The group includes dissociative amnesia, dissociative identity disorder (DID), depersonalisation derealisation disorder, and the (not otherwise) specified dissociative disorders, together with the dissociative subtype of post-traumatic stress disorder.
• Trauma is almost always part of the story, especially repeated or early trauma, but these conditions are more common than most clinicians suppose (lifetime prevalence of dissociative disorders roughly 9 to 18 per cent) and diagnosis is usually delayed. ^[1]
• Diagnosis is clinical, supported by structured questionnaires and interviews; the goal is to rule in characteristic dissociative features rather than simply to exclude neurological or medical disease.
• Primary treatment is psychotherapy (phase-oriented and relational for DID), often over years; medication is an adjunct for comorbid depression, anxiety or for dissociative symptoms, not a cure.

By the end of this page you should be able to:

1. Describe the dissociative disorders as a group and place each member on the spectrum from a single symptom to identity alteration.
2. Link dissociation to trauma (especially developmental trauma) while keeping the common view that it is "attention seeking" out of the account.
3. Recognise the mental state examination and history findings of each major dissociative disorder.
4. Choose suitable screening and assessment instruments and plan the investigations needed to exclude organic causes.
5. Apply diagnostic reasoning to the main differentials (panic, epilepsy, post-traumatic stress disorder, borderline personality disorder, neurological and substance causes).
6. Outline management for each disorder, including the three-phase model for dissociative identity disorder, medication with realistic expectations, risk management, and follow-up.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR) groups five conditions ^[1]:

• Dissociative identity disorder (DID): disruption of identity with two or more distinct personality (self) states and gaps in the recall of everyday events, personal information or trauma, beyond ordinary forgetting.
• Dissociative amnesia: inability to recall autobiographical information, usually of a traumatic or stressful nature, that is inconsistent with ordinary forgetting; a fugue (unexpected travel with amnesia for one's past or identity) may be specified.
• Depersonalisation derealisation disorder (DPDR): persistent or recurrent depersonalisation (feeling detached from one's own thoughts, body, feelings or actions) and/or derealisation (feeling that the world, people or objects are unreal or distorted), with intact reality testing.
• Other specified dissociative disorder (OSDD): presentations with dissociative features that cause distress but do not meet full criteria (for example, identity alteration without amnesia, or chronic mixed dissociative symptoms).
• Unspecified dissociative disorder: when there is insufficient information or the presentation is atypical, as in an emergency setting.

PTSD also has a dissociative subtype in DSM-5-TR, defined by persistent depersonalisation and derealisation in someone who otherwise meets PTSD criteria ^[1]. ICD-11 places conversion (functional neurological) symptoms among dissociative disorders, which is worth remembering when you compare international classifications; DSM-5-TR places that same condition with somatic symptom and related disorders. This page does not repeat the functional neurological disorder material, but the overlap is real: a patient may have both dissociative and functional neurological features.

Dissociative disorders are commoner than their cultural representation suggests.

• Lifetime prevalence of dissociative disorders as a group is roughly 9 to 18 per cent, and across inpatient and outpatient samples the prevalence is up to 46 per cent ^[1].
• DID affects about 1 per cent (one review) to 1.5 per cent (StatPearls) of adults in the general population, combining to "roughly 1 to 1.5 per cent" depending on source; sources differ, which is itself a clue to diagnostic uncertainty and under-recognition ^[3][4].
• Depersonalisation derealisation disorder is diagnosed in about 1 to 2 per cent of the population, with no clear sex difference and a higher rate in adolescents and young adults ^[2]. Transient derealisation or depersonalisation is much commoner: a lifetime prevalence of transient symptoms around 70 per cent, and about 66 per cent during a traumatic event ^[2].
• Dissociative symptoms are highly prevalent in specific psychiatric groups: 80 to 85 per cent in panic disorder, post-traumatic stress disorder and depression, and about 14.4 per cent of people with PTSD meet criteria for the dissociative subtype in the World Health Organization's surveys across 16 countries ^[1][2].
• Outside clinical settings, trauma exposure itself is common: around 70 per cent of people worldwide report at least one traumatic event, and in a US sample 89.7 per cent of adults reported at least one ^[1].
• Post-traumatic stress disorder has a 12-month US prevalence of about 4.7 per cent ^[1].

Delay and disability. People with dissociative disorders, and DID in particular, spend an average of 5 to 12.4 years in treatment, often with six or more clinicians, before a correct diagnosis ^[1]. In one sample, 60 per cent of people with dissociative disorders described themselves as disabled ^[1]. Approximately 48 per cent of adults report hospitalisations, 68 per cent of them fewer than five ^[1]. Dissociative disorders made up 34.9 per cent of emergency psychiatric admissions in one series, and adults with DID showed the highest acute care utilisation of any diagnostic group, at 2,300 USD per patient compared with 300 USD or less for other groups in one US study ^[1].

Suicide and self-harm are central to the public health picture: over 70 per cent of outpatients with DID have attempted suicide at least once, and a dissociative disorder is an independent risk factor for multiple suicide attempts and self-injury, even after adjusting for PTSD, depression and personality disorder ^[1]. Dissociation mediates part of the path from trauma exposure to adverse outcomes, which is why it is not a footnote: it is where prevention and treatment matter most ^[1].

The model that best fits the evidence is a diathesis-stress one, applied to early development.

• Stress. Chronic, repetitive trauma in childhood, most often maltreatment by caregivers, is the dominant environmental risk for DID and for severe dissociative symptoms more generally. Physical and emotional abuse, neglect, and disorganised attachment relationships all contribute; higher levels of emotional abuse and lower levels of physical abuse have been associated with increased depersonalisation and derealisation ^[1][2][3]. Dissociation is, in this account, an adaptive response: a "psychic escape" when there is no physical escape, such as the depersonalisation reported during sexual assault ^[1].
• Diathesis. An innate capacity to dissociate deeply and to enter autohypnotic (trance) states is thought to be required; without it, the same trauma does not produce dissociative self-states ^[3]. There are no DID-specific molecular genetic studies, but some links between dissociative symptoms, trauma-related genes and learning and memory genes have been proposed ^[3].
• Trauma timing. The younger the onset of maltreatment and the longer its duration, the greater the likelihood of entrenched dissociation. Epidemiological surveys of childhood abuse support the central role of early adversity ^[1][3].

Risk factors for dissociative disorders in general include: childhood maltreatment and disrupted attachment; female sex for DID (women make up the majority in most DID samples); prior psychiatric diagnosis that masks the picture; high dissociation scores; substance use; and comorbid PTSD, depression, anxiety, borderline personality traits and psychosis-spectrum disorders ^[1].

Depersonalisation derealisation disorder has a somewhat different flavour. Its exact cause is unknown ^[2]. Recognised triggers and associations include intense stress, panic attacks, depression, trauma, fatigue, sleep deprivation, and psychoactive substances (ketamine and other NMDA receptor antagonists, cannabis, hallucinogens, stimulants) ^[2]. Comorbidities in a large case series were anxiety disorders 45 per cent, dissociative spectrum disorders 15 per cent, substance use disorders 15 per cent, interpersonal abuse 10 per cent, borderline personality disorder 5 per cent, schizophrenia or schizophrenia spectrum disorders 5 per cent, and depression 5 per cent ^[2]. Family loading for anxiety is high: in one series 95 per cent of patients had a parent with an anxiety disorder, and the genetic contribution was estimated at about 48 per cent ^[2]. For depersonalisation derealisation disorder, age of onset is commonly before 25 years (earliest reported 16 years), with cases also in later decades ^[2].

Dissociation is best understood as a failure of the normal integration of consciousness, memory, identity and emotion, and research is beginning to show the brain correlates.

• Trauma neurobiology. Dissociation in trauma is associated with the over-modulation of emotion: excessive "top-down" prefrontal cortical inhibition of limbic structures (amygdala, periaqueductal grey), so the "brakes" on emotion are on too tightly. This produces the characteristic numbing, unreality, and physical analgesia ^[3].
• Depersonalisation derealisation disorder shows altered white-matter connectivity between emotion and self-processing regions, reduced activity in parts of the temporal cortex and altered activity in parietal and occipital regions; the idea of a "defence mechanism" against overwhelming experience is a working hypothesis, not established ^[2].
• DID. Imaging has identified brain correlates that differ from simulation and support the validity of the diagnosis; detailed treatment-relevant findings are beyond the scope of a clinical review but reassuringly, the condition has real neurobiological correlates rather than being an artifact of suggestion ^[3].
• Neurotransmitters. Kappa-opioid and serotonergic signalling, and glutamatergic signalling (notably NMDA receptors), have been linked to dissociative experiences; opioid and serotonin reuptake systems are pharmacological targets explored in research ^[3].

The exact causal chain from trauma to dissociative symptoms is not settled, and honest uncertainty should be taught and remembered: these are hypotheses supported by converging data, not established mechanisms.

Ask about dissociation directly but gently, because shame and amnesia make these symptoms invisible otherwise. Useful open questions include "Do you ever feel as if you are watching yourself from outside?", "Do parts of your day feel missing?", and "Do you find objects or writings you do not remember making?"

Dissociative amnesia presents as gaps in autobiographical memory that are not explained by ordinary forgetting, head injury, alcohol, drugs or a neurological condition. The memory loss usually concerns traumatic or stressful material, but may be broader; episodes can last from hours to years, and some patients retain skills and facts while losing personal context ^[1]. A dissociative fugue may feature: a patient may be found far from home with no memory of travel, sometimes living under a new name, and returning to baseline over hours to days.

Dissociative identity disorder is the most severe form. In addition to amnesia, the person experiences identity alteration with two or more self-states (often called alters or parts) that recurrently take executive control ^[3]. Key features include ^[1][3]:

• disremembered behaviours and "lost time";
• trance states and "spacing out" (absorption);
• fluctuations in skills, knowledge, writing style or preferences;
• hearing voices or internal commentary (passive influence) that is felt as not-quite-self;
• depersonalisation and derealisation;
• negative hallucinations (failing to perceive something that is there);
• unexplained analgesia, somatic symptoms and sensory changes;
• abrupt or marked changes in mood, preferences or relationships;
• and a profound sense of "puzzlement" or of not knowing oneself ("why am I like this?").

Reality testing remains intact: patients know that an alter is not literally a different person, even though it feels like one, and the condition is not akin to psychosis ^[3]. Children may present with possession-like experiences, which in many cultures are normative rather than pathological; the DSM-5-TR and ICD-11 require distress, impairment and exclusion of cultural practice.

Depersonalisation derealisation disorder is defined by persistent or recurrent episodes in which the person feels detached from self (depersonalisation) or from the surroundings (derealisation), while reality testing is preserved ^[2]. Patients may say "I feel like I am in a dream", "my hands feel like they are not mine", or "the world looks flat or behind glass"; they often worry permanently about brain damage. Capacity for emotion and reality testing are typically intact, and symptoms may last a day, months or years ^[2].

PTSD dissociative subtype should be considered when PTSD criteria are met and the patient has persistent depersonalisation or derealisation on top, since this pattern responds to a somewhat different treatment emphasis ^[1].

• Appearance and behaviour: may seem "spaced out", with fluctuating eye contact, inconsistent eye movements, or sudden shifts in posture, voice or handwriting. Watch for trance-like unresponsiveness, which is not drowsiness.
• Speech: may switch style, vocabulary or accent; answers may be inconsistent across the same assessment, sometimes as if different "people" were answering.
• Mood and affect: often incongruent, restricted or rapidly shifting; intense shame is common.
• Thought form: usually normal; there is no formal thought disorder.
• Perception: depersonalisation and derealisation described; voices or internal commentary may be reported but are usually experienced as coming from inside, not from external space.
• Cognition: gaps in autobiographical recall; orientation and intellectual function are generally preserved apart from the memory disturbance. Check retrograde and anterograde memory and date of onset.
• Insight: usually high: patients are often articulate, frightened and puzzled by their own symptoms. They are frequently misdiagnosed, so validate rather than challenge.
• Risk assessment: essential. Enquire about suicidal ideation, intent, plan and recent attempts, self-injury, substance use, and eating difficulties. Stressors, threats and recent triggers matter.

Comorbidity is the rule rather than the exception: anxiety, depression, PTSD, borderline personality traits, substance use and eating problems often accompany dissociative disorders and can mask them ^[1][2].

The key clinical challenge is to distinguish a dissociative disorder from organic causes of memory loss, depersonalisation and altered experience, and from other psychiatric conditions that overlap with it.

There is no single test for a dissociative disorder, and none is required when the presentation is characteristic. Investigations have two aims: to look for organic mimics, and to quantify dissociation and trauma.

Clinical interviewing and questionnaires ^[1]:

• Dissociative Experiences Scale, second version (DES-II): a widely used 28-item self-report; an adolescent version exists. It is a screening tool, not a diagnosis.
• Child Dissociative Checklist for children and adolescents.
• Multiscale dissociation inventories and malingering measures, with normative data to distinguish genuine from simulated DID.
• Semi-structured interviews that can yield a dissociative disorder diagnosis (for example, structured interviews for dissociative disorders).
• Office Mental Status Examination for Dissociation for adults, and a version for children and adolescents.

Medical investigations are guided by presentation. Brain imaging (MRI or CT) and electroencephalography may be used to exclude seizures, structural lesions, and (rarely) organic depersonalisation when presentation or atypical features raise concern; blood and urine tests can include a drug screen ^[2]. Routine imaging is not needed when the clinical picture is typical and there are no red flags.

Psychological assessment should include trauma history (with attention to developmental trauma and safety), dissociative features across memory, identity, perception and consciousness, comorbid symptoms, and risk. Corroboration from records and collateral history is helpful when amnesia is prominent.

Pre-operative or routine medical screening is not applicable; however, in a medical or emergency setting, look for the common triggers (trauma anniversaries, substance use, sleep loss, panic) and for the self-harm and suicide risk that frequently co-exist.

The DSM-5-TR criteria are paraphrased and summarised here; consult the edition used locally for exact wording.

• DID: disruption of identity with two or more distinct personality states (which may be experienced as possession in some cultures), marked discontinuity in sense of self and agency with changes in affect, behaviour, consciousness, memory, perception, cognition and/or sensory-motor functioning; recurrent gaps in recall of everyday events, important personal information and/or traumatic experiences; clinically significant distress or impairment; not part of a broadly accepted cultural or religious practice; not explained by substances, another medical condition, or (in children) an imaginary playmate or fantasy play ^[1][3][4].
• Dissociative amnesia: inability to recall important autobiographical information, usually trauma- or stress-related, beyond ordinary forgetting; exclusion of substances, neurological disease and (where specified) a medical cause; a fugue specifier if there is purposeful travel with amnesia ^[1].
• DPDR: persistent or recurrent depersonalisation, derealisation, or both; intact reality testing; significant distress or impairment; not attributable to a substance, medication or another medical condition; not better explained by another mental disorder ^[2].

The dissociative subtype of PTSD requires PTSD criteria plus persistent depersonalisation and/or derealisation ^[1].

Risk comes first. People with dissociative disorders have high rates of suicidal ideation, self-injury, substance use, revictimisation, and hospitalisation; self-harm often occurs with only partial awareness of triggers ^[1]. Every assessment should include a written risk plan: means restriction, safety planning, identified triggers, crisis contacts, and involvement of trusted supports. Hospital admission is sometimes needed for safety, but prolonged inpatient treatment without a clear plan can reinforce dissociation; community-based specialist care is preferred where it exists.

How the diagnosis is delivered matters as much as the label. Explain that dissociation is a common, understandable response to overwhelming experience; that it is a survival strategy rather than a sign of weakness or "madness"; and that the person is not "faking" or "making it up". Naming the process often reduces shame and time lost in investigation. Many patients have spent years being disbelieved; being heard and validated is itself an intervention ^[1].

Dissociative amnesia. There is no medication that restores missing memories. Treatment emphasises safety, stabilisation, and psychotherapy that allows memories to return at a rate the patient can tolerate. Do not press for, or "recover", memories through suggestion, hypnosis-for-recall or abreaction; contamination and false memory are real risks, and the emphasis is on present-day functioning and processing what does emerge, with trauma-focused work only when the patient is stable. Treat comorbid depression, anxiety and substance use.

Depersonalisation derealisation disorder. Cognitive behavioural therapy is the first-line psychotherapy for most newly diagnosed patients, because it targets the thoughts and behaviours that maintain unreality experiences ^[2]. Dialectical behaviour therapy contributes emotion regulation and distress tolerance; grounding, mindfulness-based and body-based approaches are often helpful. Long-term prognosis is better with prompt and consistent treatment, especially when comorbid conditions are treated ^[2].

Dissociative identity disorder. Expert consensus supports a long-term, relational, phase-oriented psychotherapy ^[3][5]:

• Phase 1 - Safety and stabilisation. Build a trusting therapeutic relationship with firm boundaries; develop a shared, non-pathologising language for dissociation; teach grounding, containment and emotion-regulation skills; reduce self-harm and suicidality; address housing, safety from ongoing abuse, substance use and comorbid conditions. The manualised workbook programmes described in the research literature (for example, Finding Solid Ground and trauma-focused Phase 1 programmes) can be delivered within individual therapy and reach people who lack access to specialist services ^[3].
• Phase 2 - Trauma processing and mourning. Once dissociation is no longer the primary reflexive way of coping, trauma-related memories, emotions and sensations are approached gradually, within the patient's window of tolerance. Phased trauma processing integrates cognitive processing therapy or EMDR techniques within a relational framework; hypnotic and dissociative skills can be used to build self-efficacy and manage switching, but the work is paced by safety. Self-hypnosis training may be a useful adjunct ^[3].
• Phase 3 - Reconnection. The focus shifts to living a life less organised around trauma and dissociation: consolidating a sense of ownership ("it was me, after all"), building relationships, work and meaning, and managing residual triggers. Completion of trauma processing is a beginning, not an end, and Phase 3 often takes as long as the first two ^[3].

Frequency is typically one to three sessions per week over several years for adults; in one summary, the mean duration of treatment for DID was 6 years, although children and adolescents can respond more quickly ^[1]. A strong, bounded therapeutic relationship is an essential ingredient, and working through traumatic transference and countertransference is part of the work ^[3].

There is no medication that specifically treats a dissociative disorder or the identity alteration of DID; drugs are adjuncts ^[1][3]. Evidence-based use:

• Treat comorbid depression, anxiety, PTSD and sleep disorder with standard agents chosen for the individual (selective serotonin reuptake inhibitors, serotonin noradrenaline reuptake inhibitors, and so on), with careful monitoring.
• For DPDR, selective serotonin reuptake inhibitors and serotonin noradrenaline reuptake inhibitors are commonly used when anxiety or depression co-exist, and low-dose antipsychotics or anxiolytics may be used in select cases ^[2].
• A small research literature has shown opioid antagonists (naloxone) and the SSRI paroxetine to beat placebo for dissociative symptoms in other conditions; these are not approved or established treatments for DID, and DID-specific pharmacological trials do not yet exist ^[3]. Watch for fads: most of the pharmacological claims for dissociation come from small or non-DID studies.
• Avoid benzodiazepines as a long-term strategy: they worsen dissociation, memory, and accident risk, and promote dependence.
• Medication management should be coordinated with the psychotherapist and monitored for splitting (different clinicians being played against each other), for non-adherence, and for interactions with substance use.

Many people improve substantially over years of consistent, dissociation-targeted treatment: reductions in PTSD and dissociative symptoms, less self-harm and hospitalisation, fewer revictimisations, better functioning, and reduced costs ^[1][3]. Structured follow-up reviews (for example every three to six months) should track frequency of dissociative experiences, switches and amnesia, self-harm, substance use, safety, social and occupational functioning, and medication. Be explicit that treatment is usually measured in years, not weeks, and celebrate behavioural evidence of change rather than demanding proof of "integration".

Refer promptly to mental health services, and ideally to a clinician with experience in trauma and dissociation, when:

• there is dissociative amnesia with functional impact, obvious safety concerns, or a suspected fugue;
• DID or OSDD is suspected;
• there is self-harm, suicidal ideation, eating disorder or substance dependence;
• a patient has repeated emergency or hospital presentations without explanation;
• or the patient is not responding to standard treatment for the comorbid condition (anxiety, depression) despite good engagement.

Urgent referral (same day) is needed for current suicidal intent or plan, self-harm requiring medical attention, dissociation with confusion suggestive of an organic cause, suspected substance withdrawal or overdose, or a recent head injury.

• Self-harm and suicidal behaviour, the leading complication and cause of death; dissociative disorder is an independent risk factor even after controlling for PTSD and depression ^[1].
• Revictimisation: dissociation impairs danger cue processing and is linked to higher rates of re-traumatisation, intimate partner violence and sexual assault ^[1].
• Physical health: chronic pain, somatic symptoms, and reduced pain thresholds are common; trauma and dissociation affect stress axis and immune responding ^[1].
• Substance use: often used for "grounding" or numbing, and it worsens dissociation and memory.
• Disability and social exclusion: difficulties maintaining work, relationships, education and housing ^[1].
• Misdiagnosis and iatrogenic harm: years of unnecessary investigations, invalidation, and treatments that never targeted the dissociation ^[1].
• Costs and service use: high rates of emergency care and hospitalisation; accurate diagnosis and specialist treatment reduce costs substantially (from about 10 to 4 years of treatment length in one summary) ^[1].
• Family and caregiving burden, including in adolescence where onset often occurs.

Prognosis improves markedly with accurate diagnosis, validation and consistent, dissociation-targeted treatment; without it, symptoms tend to persist or worsen ^[1][3]. Younger patients and those who receive treatment closer to onset do better ^[2]. Even after years of treatment, a significant minority retain relationship, employment or health difficulties, and "integration" in the strict sense is not necessary for a worthwhile life ^[3]. For DPDR, prognosis varies from episodic to persistent, with better outcomes when comorbid conditions are treated and intervention is early ^[2]. Set honest expectations and avoid both dismissiveness and infinite dependence.

There is no primary prevention that targets dissociation itself; prevention means trauma prevention, safe caregiving and attachment-informed early intervention. Secondary prevention means training clinicians to recognise dissociation, using low-cost screening tools such as the DES-II, and acting early in adolescence, when dissociative disorders commonly first present. Because trauma is common and dissociation mediates downstream harm, routine enquiry about trauma in primary care and mental health settings is justified, done safely (a private setting, permission, preparation for distress and follow-up) ^[1].

• Children and adolescents. Onset is usually in childhood. Presentation may be possession-like or somatic rather than the "multiple personalities" of popular culture. Screening tools such as the Child Dissociative Checklist exist. Treatment tends to be quicker than in adults, and early intervention improves long-term outcomes; ISSTD publishes separate guidance for children and adolescents ^[1][5]. Be alert to ongoing safeguarding concerns.
• Older adults. Dissociation may first be misread as dementia or cerebrovascular disease; careful cognitive assessment and a trauma history are essential, and the capacity to process trauma may still be present.
• Pregnancy and the postpartum. Dissociation may flare around childbirth when body sensations and loss of control echo previous trauma; trauma-informed obstetric care, continuity, control, and avoidance of triggering practices help. Coordinate with perinatal mental health services; see "perinatal mental health" topic (plain reference).
• Immunocompromised or medically unwell patients. Somatic symptoms may be over-attributed to the physical illness; depersonalisation is common in severe anxiety and medical crises and should not be over-medicalised, but neither should a genuine dissociative disorder be missed.

• A careful clinical interview plus a free self-report screen (DES-II) is enough to begin; specialist instruments are a bonus, not a requirement.
• Most healthcare systems have no dedicated dissociation services. Train primary-care and mental-health staff in recognition, basic psychoeducation and stabilisation; the Phase 1 focus on safety and emotion regulation can be taught in group or primary-care formats.
• Avoid unnecessary neurological imaging and repeated emergency presentations by explaining the diagnosis and agreeing a consistent plan.
• Medication access is usually limited to antidepressants and basic antipsychotics; use them for comorbidity, not for dissociation itself, and avoid benzodiazepines.
• There is no ISSTD-trained therapist everywhere, and telehealth or manualised materials can bridge part of the gap. ISSTD treatment guidelines, adopted originally in 1994 and now in their third (2011) revision, focus on DID and similar conditions and were explicitly written not to replace clinical judgement ^[5].
• Care for revictimisation risk is universal: safety planning, confidential spaces, and links to protection and social services matter as much as any therapy.

• Dissociative disorders are disruptions of the normal integration of memory, identity, perception and consciousness, usually linked to trauma, and are common, under-recognised and disabling.
• The group contains dissociative amnesia (with fugue specifier), dissociative identity disorder, depersonalisation derealisation disorder, other specified and unspecified dissociative disorders, plus the dissociative subtype of PTSD.
• Trauma (especially early, repetitive trauma) and disrupted attachment are the dominant risks for DID and severe dissociation; diathesis (innate capacity to dissociate) and stress together explain why not everyone who is traumatised develops DID.
• Diagnosis is clinical, supported by instruments (DES-II and others) and by exclusion of organic, substance and psychiatric mimics; reality testing is preserved.
• Over 70 per cent of outpatients with DID have attempted suicide, and dissociation independently raises self-harm and revictimisation risk, so risk assessment is not optional.
• Prevalence: dissociative disorders roughly 9 to 18 per cent lifetime; DID about 1 to 1.5 per cent; DPDR 1 to 2 per cent; PTSD dissociative subtype about 14.4 per cent of PTSD.
• Primary treatment is psychotherapy: phase-oriented relational therapy for DID, support and trauma-processing for amnesia, and CBT with emotion-regulation skills for DPDR.
• No drug cures a dissociative disorder; medication treats comorbidity; CBT is first-line for DPDR and phase-oriented psychotherapy for DID; avoid long-term benzodiazepines.
• Expect treatment to take years; neurobiological and pharmacological research is active but no DID-specific drug yet exists.
• Delivery of the diagnosis with validation is a treatment in itself; many patients spend 5 to 12.4 years before being correctly diagnosed.
• Low-resource practice: clinical skills, free screening, consistent plans, safety; ISSTD guidelines (1994, third revision 2011) are the principal international reference for DID.

• Post-traumatic stress disorder and acute stress disorder
• Somatic symptom and related disorders
• Personality disorders and defence mechanisms
• Substance use disorders
• Suicidality and self-harm
• Seizures and epilepsy (functional dissociative seizure)
• Common mental health problems in primary care