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Mr. D, age 45, presents to his primary care physician with panic attacks, nausea, shortness of breath, nightmares, and dizziness 6 months after being assaulted and robbed at an ATM. Following a routine medical workup, the physician diagnoses posttraumatic stress disorder (PTSD) and refers Mr. D for exposure and response prevention therapy.
During graded exposure sessions, Mr. D’s eyes sometimes glaze over and he seems to “float away” from the discussion. When the therapist asks about these symptoms, Mr. D reports having had them as long as he can remember. In school, he says, teachers thought he was a slow learner, a daydreamer, or had attention-deficit/hyperactivity disorder. From what he can recall of his childhood, he describes a history of trauma and neglect with a violent, drug-abusing father and absent mother.
Patients with a history of early abuse or neglect are at risk for dissociative phenomena and other trauma-related psychiatric disorders.1 The heterogeneous dissociative disorders are often hidden and unrecognized2 —as in Mr. D’s case—or present with unfamiliar or atypical symptoms. Understanding and identifying dissociative symptoms is important because:
- Dissociative symptoms worsen prognosis, whether patients have conversion disorders1 or psychogenic seizures3 or are in psychotherapy.4
- Dissociative states may impair memory encoding5 and decrease patients’ ability to remember therapeutic information.
- Symptoms (such as hearing voices in multiple personality disorder) can be confused with those of disorders with different treatment strategies (such as psychotic disorders).6
- Peritraumatic dissociation may be a risk factor for PTSD.7
This article presents a practical model for understanding dissociation, reviews clinical characteristics of this family of symptoms, and offers suggestions for assessing and treating patients with dissociative disorders.
Coming together, falling apart
Since Pierre Janet’s first reports on dissociative disorders, a number of theories and models of dissociation have been proposed,8 including empirically based, taxonomic models that address DSM-IV-TR categories (Table 1). The model I propose—which attaches a visual metaphor to dissociative phenomena—answers the question, “What is ‘dissociated’ in dissociation disorders?”
Table 1
DSM-IV-TR classification of dissociative disorders
Disorder | Symptoms |
---|---|
Dissociative amnesia | A reversible loss of memory, typically preceded by a stressor |
Dissociative fugue | Loss of memory and identity, along with travel away from home |
Dissociative identity disorder (formerly multiple personality disorder) | Presence of different identity states, often with lack of connection between them; current models highlight the presence of recurrent dissociative intrusions into many aspects of executive function and self |
Depersonalization disorder | Detachment from oneself as a present, feeling person (depersonalization) and the world (derealization) |
Dissociative identity disorder NOS | Functionally disturbing dissociative symptoms that do not fit into any of the above |
NOS: not otherwise specified | |
Source: Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
One paired component is a detached “observer” and a more embodied, feeling “experiencer.” The observer is a perspective that begets metacognition (thinking about one’s inner world) and self-observation; it resides in the same body as soma-based “feelings” that unconsciously contribute to the sense of “being present” with oneself and the world in the moment.9
A second component is voluntary access to one’s autobiographical memories (memories about the self in time), which are constantly “updated” and integrated with current experiences. This component allows one to distinguish between remembered (past) experiences and “firsthand” (present) experience.
Three other components of normal consciousness are:
- a sense of agency and voluntary control over one’s mental contents, mental activity, and bodily movements
- an ongoing connection with one’s body and mind and an understanding of where sensations and images come from
- a sense of sequential experience, with relatively smooth transitions (from self at work to self at home, self a week ago to self today, etc) that have a singular referent (an identity).
- separation of the “observer” and “experiencer” occurs in depersonalization disorder
- reversible loss of ability to access memories characterizes dissociative amnesia
- disconnection between sequential experiences is a part of dissociative identity disorder.
10 Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).
From a neurophysiologic perspective, mental states may be viewed as arising from synchronized integration of the activity of functionally specialized brain regions. Functional neuroimaging of dissociation supports an understanding of these symptoms as ‘disconnection syndromes.’
Functional neuroimaging. Different ‘identities’—sometimes called a traumatic personality state and neutral personality state—demonstrate different patterns of cerebral blood flow, subjective reports, and peripheral physiologic parameters (blood pressure, heart rate).a
Functional imaging of traumatic dissociation shows active suppression of limbic regions (amygdala) and increased activity in dorsolateral prefrontal areas.b Similarly, neuroimaging of depersonalization disorder show increased neural activity in prefrontal regions associated with affect regulation and decreased activity in emotion-related areas.c,d
Speed. Dissociative responses occur extremely rapidly. Using EEG, which allows finer temporal resolution than functional imaging studies, Kirino et ale showed reversible attenuation of a specific EEG signal within 300 msec during dissociative episodes. This ultra-rapid neural reflex was correlated with allocation of attentional and working memory resources, perhaps with the goal of minimizing memory activation and resurgence of affect-laden memories.e
Hormonal. Stress-related disorders cause perturbations in neurohormonal function. Simeon et alf found a distinct pattern of stress-induced HPA axis dysregulation in dissociative patients compared with PTSD patients and healthy controls. Similar results were seen in patients with borderline personality disorder and dissociative symptoms.g
Structural imaging. Stress-related neurohormonal perturbations are known to affect critical neural structures, including the hippocampus. Using MRI, Vermetten et alh found significantly decreased amygdala and hippocampal volumes in patients with dissociative identity disorder.
EEG: electroencephalography; HPA: hypothalamic-pituitary-adrenal; PTSD: posttraumatic stress disorder
Reference Citations: click here
Causes of dissociative disorders
As with many psychiatric disorders, the etiology of dissociative phenomena is thought to include the individual patient’s temperamental or constitutional predispositions11 as well as a strong contribution of environmental trauma (early abuse, neglect).12
Constitutional predisposition for developing a dissociative disorder may include personality traits such as being easily hypnotized, mental absorption, suggestibility, and a tendency to fantasize.13 These characteristics fueled concerns in the 1990s that therapists may contribute to dissociative identity disorder by “digging” for repressed memories in susceptible patients and creating “pseudomemories” of events that did not happen.14
The issue of repressed traumatic memory and its role in therapy is extremely controversial and contributes to the complexity of psychotherapeutic treatment of dissociation.15
- shame and secrecy of early sexual or physical abuse and potential for victims to repress traumatic memories
- lability of memory, potential for suggestibility, and difficulty with verification.14
- early relationships are one of the primary ways that humans learn to regulate distress
- early trauma frequently includes pathology in caregiving relationships, including overt role reversal, abuse, and neglect.
Finally, remember that transient dissociative symptoms can be considered normal in high-stress situations. Intensive military training has been found to be associated with a very high incidence (96%) of dissociative symptoms in army recruits.17
Identifying ‘hidden’ phenomena
Dissociative disorders have been called “diseases of hiddenness”18 because:
- Many of their clinical characteristics— sense of identity, memory, connectedness, somatosensory phenomena—are alterations in subjective phenomena that lack clearly observable symptoms.
- Patients are often reluctant to seek help or divulge their symptoms to clinicians.
- When dissociative symptoms are obvious—such as multiple personalities or sudden loss of memories—they may be dismissed or evoke skepticism because of their dramatic presentation.
For more targeted screening, the self-report Dissociative Experiences Scale (DES)21 is useful for clinical assessment in conjunction with the clinician-administered diagnostic Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D).22
Table 2
With these findings, consider screening for dissociation
Posttraumatic stress disorder |
Certain personality disorders (especially borderline personality disorder) |
Somatoform disorders (conversion disorders and nonepileptic seizures) |
Eating disorders |
Substance use disorders |
Extensive history of trauma or neglect |
Self-harm behavior |
As in Mr. D’s case, dissociative phenomena may attenuate the benefit of post-trauma therapeutic interventions, especially those involving exposure. Therefore:
- assess post-trauma patients for dissociation before you start treatment
- make specific alterations in psychotherapy for such patients, as described below.
Table 3
Differential diagnosis: Dissociation ‘look-alikes’
Dissociation symptom | Can be confused with: |
---|---|
Visual or auditory hallucinations, other ‘first-rank’ psychotic symptoms in dissociative identity disorder | Psychotic disorder |
‘Blanking out’ (cognitive disruption) | ADHD, seizures |
Somatoform (conversion) symptoms | A variety of nonpsychiatric medical problems, including pelvic or abdominal pathology and headaches |
Dissociative memory lapses | Learning disability, not paying attention |
‘Switching’ between states | Bipolar disorder, rapid cycling |
Lack of emotional reaction to traumatic stimuli(numbing response) | Healthy coping |
ADHD: attention-deficit/hyperactivity disorder |
Recreational drugs such as ketamine, methylenedioxymethamphetamine (“Ecstasy”), hallucinogens, marijuana, and dextromethorphan also can induce dissociative states. Consider evaluating for use of these substances, some of which may not be detected on a routine drug screen.24
CASE CONTINUED: A tactical shift
Internal distress—such as when remembering painful events—clearly is linked with the appearance of Mr. D’s symptoms. The therapist—recognizing unacknowledged dissociative phenomena—changes Mr. D’s therapeutic strategy from exposure therapy to affect and anxiety regulation, with an explicit focus on attachment security (safety).
The therapist explains to Mr. D that dissociation symptoms are a response to distress, and he can learn more adaptive distress regulation in therapy. The in-session focus shifts to include more direct attention to components of the therapy relationship, including overt disclosure of the therapist’s positive regard and commitment to help the patient and frequent pauses to “check in” that the patient feels present, safe, and understood. With this new focus, Mr. D’s dissociative symptoms resolve and he feels more ready to face and overcome his fear and avoided memories.
Psychotherapy: Putting pieces together
Psychotherapy is the primary treatment, based on understanding dissociative disorders as manifestations of distress-related, traumatic fragmentation of the sense of self, interpersonal relatedness, and capacity for adaptive affect regulation (Table 4).
Table 4
Tips for conceptualizing dissociative disorders
Ground your understanding of this class of disorders as distress-related breakdowns in functional connection and integration among components of normal consciousness |
Consider the overlap among dissociation, certain somatoform disorders (conversion symptoms, pseudoseizures), and PTSD |
Maintain a high index of suspicion for dissociative symptoms in patients with early trauma or neglect (consider screening for this); do further evaluation with dissociative-specific tools |
Avoid the tendency to assume that reversible, unfamiliar, or peculiar symptoms imply volition or lack of an organic basis |
PTSD: posttraumatic stress disorder |
Safety, stabilization, and symptom reduction. Providing a safe therapeutic relationship is a primary and necessary part of DID treatment. On that platform, a first step in reintegrating distressing material into the self involves building the patient’s capacity for conscious, flexible affect regulation. This keeps anxiety and distress within a therapeutic “window.”
Integration of identity and person. Treatment ends when formerly unintegrated or dissociated experiences or parts of the self are integrated into a coherent whole, and the patient can deal adaptively with inter-personal relationships and distress without fragmentation.
Adjunctive medications
Few studies have addressed using psychopharmacologic interventions in the heterogeneous dissociative disorders. GABAA antagonism and 5-HT2a/2c agonism have induced psychotic and dissociative-like symptoms in healthy men,29 and alterations in enzymes such as catechol-O-methyltransferase (COMT) may explain individual vulnerability to trauma.30 Reports of dissociation related to ketamine31 and marijuana32 implicate other neurotransmitter systems in their etiology.
DID. Similar to guidelines for borderline personality disorder,33 guidelines for DID suggest using medications to treat the most prominent symptom clusters such as insomnia, affective instability, and posttraumatic intrusions.
Depersonalization disorder. Trials of fluoxetine and lamotrigine showed no benefit in depersonalization disorder.34,35 In an open trial of 14 patients, naloxone (mean 120 mg/d) reduced depersonalization symptoms by 30%, as measured by 3 validated scales.36
Related Resources
- International Society for the Study of Trauma and Dissociation. Site for professionals. www.isst-d.org
- National Alliance on Mental Illness (NAMI). Patient education on dissociative disorders. www.nami.org/Content/ContentGroups/Helpline1/Dissociative_Disorders.htm
- Fluoxetine • Prozac
- Lamotrigine • Lamictal
- Naloxone • Narcan
- Paroxetine • Paxil
Dr. MacDonald is a speaker for Eli Lilly and Company, Janssen, L.P., and Pfizer Inc.
1. Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004;161:2271-6.
2. Foote B, Smolin Y, Kaplan M, et al. Prevalence of dissociative disorders in psychiatric outpatients. Am J Psychiatry 2006;163:623-9.
3. Reuber M, Pukrop R, Bauer J, et al. Outcome in psychogenic nonepileptic seizures: 1 to 10-year follow-up in 164 patients. Ann Neurol 2003;53:305-11.
4. Spitzer C, Barnow S, Freyberger HJ, Grabe HJ. Dissociation predicts symptom-related treatment outcome in short-term inpatient psychotherapy. Aust N Z J Psychiatry 2007;41:682-7.
5. Allen JG, Console DA, Lewis L. Dissociative detachment and memory impairment: reversible amnesia or encoding failure? Compr Psychiatry 1999;40:160-71.
6. Dell PF. A new model of dissociative identity disorder. Psychiatr Clin North Am 2006;29:1-26.
7. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective evaluation. Am J Psychiatry 2005;162:1188-91.
8. Steinberg M, Rounsaville B, Cicchetti DV. The Structured Clinical Interview for DSM-III-R Dissociative Disorders: preliminary report on a new diagnostic instrument. Am J Psychiatry 1990;147:76-82.
9. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York, NY: Harcourt, Inc; 1999.
10. Alkire MT, Miller J. General anesthesia and the neural correlates of consciousness. Prog Brain Res 2005;150:229-44.
11. Simeon D, Guralnik O, Knutelska M, Schmeidler J. Personality factors associated with dissociation: temperament, defenses, and cognitive schemata. Am J Psychiatry 2002;159(3):489-91.
12. Kihlstrom JF. Dissociative disorders. Annu Rev Clin Psychol 2005;1:227-53.
13. Isaac M, Chand PK. Dissociative and conversion disorders: defining boundaries. Curr Opin Psychiatry 2006;19(1):61-6.
14. Laney C, Loftus EF. Traumatic memories are not necessarily accurate memories. Can J Psychiatry 2005;50(13):823-8.
15. Loftus EF, Davis D. Recovered memories. Annu Rev Clin Psychol 2006;2:469-98.
16. Lyons-Ruth K, Dutra L, Schuder MR, Bianchi I. From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences? Psychiatr Clin North Am 2006;29(1):63-86.
17. Morgan CA, 3rd, Hazlett G, Wang S, et al. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry 2001;158(8):1239-47.
18. Spiegel D. Recognizing traumatic dissociation. Am J Psychiatry 2006;163(4):566-8.
19. Scher CD, Stein MB, Asmundson GJ, et al. The childhood trauma questionnaire in a community sample: psychometric properties and normative data. J Trauma Stress 2001;14:843-57.
20. Teicher MH, Andersen SL, Polcari A, et al. The neurobiological consequences of early stress and childhood maltreatment. Neurosci Biobehav Rev 2003;27:33-44.
21. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation scale. J Nerv Ment Dis 1986;174(12):727-35.
22. Steinberg M, Rounsaville B, Cicchetti D. Detection of dissociative disorders in psychiatric patients by a screening instrument and a structured diagnostic interview. Am J Psychiatry 1991;148(8):1050-4.
23. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology 1989;39:835-40.
24. Schonenberg M, Reichwald U, Domes G, et al. Effects of peritraumatic ketamine medication on early and sustained posttraumatic stress symptoms in moderately injured accident victims. Psychopharmacology (Berl) 2005;182(3):420-5.
25. Hunter EC, Phillips ML, Chalder T, et al. Depersonalisation disorder: a cognitive-behavioural conceptualisation. Behav Res Ther 2003;41:1451-67.
26. Guidelines for treating dissociative identity disorder in adults (2005). J Trauma Dissociation 2005;6(4):69-149.
27. van der Hart O, Nijenhuis E. Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found. Aust N Z J Psychiatry 2001;35:589-600.
28. Holmes EA, Brown RJ, Mansell W, et al. Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin Psychol Rev 2005;25(1):1-23.
29. D’Souza DC, Gil RB, Zuzarte E, et al. gamma-Aminobutyric acid-serotonin interactions in healthy men: implications for network models of psychosis and dissociation. Biol Psychiatry 2006;59(2):128-37.
30. Savitz JB, van der Merwe L, Newman TK, et al. The relationship between childhood abuse and dissociation. Is it influenced by catechol-O-methyltransferase (COMT) activity? Int J Neuropsychopharmacol 2008;11:149-61.
31. Curran HV, Morgan C. Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later. Addiction 2000;95:575-90.
32. Mathew RJ, Wilson WH, Humphreys D, et al. Depersonalization after marijuana smoking. Biol Psychiatry 1993;33:431-41.
33. American Psychiatric Association. Practice guideline for the treatment of patients with borderline personality disorder. Am J Psychiatry 2001;158(10 suppl):1-52.
34. Sierra M, Phillips ML, Ivin G, et al. A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder. J Psychopharmacol 2003;17:103-5.
35. Simeon D, Guralnik O, Schmeidler J, Knutelska M. Fluoxetine therapy in depersonalisation disorder: randomised controlled trial. Br J Psychiatry 2004;185:31-6.
36. Simeon D, Knutelska M. An open trial of naltrexone in the treatment of depersonalization disorder. J Clin Psychopharmacol 2005;25:267-70.
37. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2006(1):CD002795.-
38. Marshall RD, Lewis-Fernandez R, Blanco C, et al. A controlled trial of paroxetine for chronic PTSD, dissociation, and interpersonal problems in mostly minority adults. Depress Anxiety 2007;24:77-84.
Mr. D, age 45, presents to his primary care physician with panic attacks, nausea, shortness of breath, nightmares, and dizziness 6 months after being assaulted and robbed at an ATM. Following a routine medical workup, the physician diagnoses posttraumatic stress disorder (PTSD) and refers Mr. D for exposure and response prevention therapy.
During graded exposure sessions, Mr. D’s eyes sometimes glaze over and he seems to “float away” from the discussion. When the therapist asks about these symptoms, Mr. D reports having had them as long as he can remember. In school, he says, teachers thought he was a slow learner, a daydreamer, or had attention-deficit/hyperactivity disorder. From what he can recall of his childhood, he describes a history of trauma and neglect with a violent, drug-abusing father and absent mother.
Patients with a history of early abuse or neglect are at risk for dissociative phenomena and other trauma-related psychiatric disorders.1 The heterogeneous dissociative disorders are often hidden and unrecognized2 —as in Mr. D’s case—or present with unfamiliar or atypical symptoms. Understanding and identifying dissociative symptoms is important because:
- Dissociative symptoms worsen prognosis, whether patients have conversion disorders1 or psychogenic seizures3 or are in psychotherapy.4
- Dissociative states may impair memory encoding5 and decrease patients’ ability to remember therapeutic information.
- Symptoms (such as hearing voices in multiple personality disorder) can be confused with those of disorders with different treatment strategies (such as psychotic disorders).6
- Peritraumatic dissociation may be a risk factor for PTSD.7
This article presents a practical model for understanding dissociation, reviews clinical characteristics of this family of symptoms, and offers suggestions for assessing and treating patients with dissociative disorders.
Coming together, falling apart
Since Pierre Janet’s first reports on dissociative disorders, a number of theories and models of dissociation have been proposed,8 including empirically based, taxonomic models that address DSM-IV-TR categories (Table 1). The model I propose—which attaches a visual metaphor to dissociative phenomena—answers the question, “What is ‘dissociated’ in dissociation disorders?”
Table 1
DSM-IV-TR classification of dissociative disorders
Disorder | Symptoms |
---|---|
Dissociative amnesia | A reversible loss of memory, typically preceded by a stressor |
Dissociative fugue | Loss of memory and identity, along with travel away from home |
Dissociative identity disorder (formerly multiple personality disorder) | Presence of different identity states, often with lack of connection between them; current models highlight the presence of recurrent dissociative intrusions into many aspects of executive function and self |
Depersonalization disorder | Detachment from oneself as a present, feeling person (depersonalization) and the world (derealization) |
Dissociative identity disorder NOS | Functionally disturbing dissociative symptoms that do not fit into any of the above |
NOS: not otherwise specified | |
Source: Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
One paired component is a detached “observer” and a more embodied, feeling “experiencer.” The observer is a perspective that begets metacognition (thinking about one’s inner world) and self-observation; it resides in the same body as soma-based “feelings” that unconsciously contribute to the sense of “being present” with oneself and the world in the moment.9
A second component is voluntary access to one’s autobiographical memories (memories about the self in time), which are constantly “updated” and integrated with current experiences. This component allows one to distinguish between remembered (past) experiences and “firsthand” (present) experience.
Three other components of normal consciousness are:
- a sense of agency and voluntary control over one’s mental contents, mental activity, and bodily movements
- an ongoing connection with one’s body and mind and an understanding of where sensations and images come from
- a sense of sequential experience, with relatively smooth transitions (from self at work to self at home, self a week ago to self today, etc) that have a singular referent (an identity).
- separation of the “observer” and “experiencer” occurs in depersonalization disorder
- reversible loss of ability to access memories characterizes dissociative amnesia
- disconnection between sequential experiences is a part of dissociative identity disorder.
10 Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).
From a neurophysiologic perspective, mental states may be viewed as arising from synchronized integration of the activity of functionally specialized brain regions. Functional neuroimaging of dissociation supports an understanding of these symptoms as ‘disconnection syndromes.’
Functional neuroimaging. Different ‘identities’—sometimes called a traumatic personality state and neutral personality state—demonstrate different patterns of cerebral blood flow, subjective reports, and peripheral physiologic parameters (blood pressure, heart rate).a
Functional imaging of traumatic dissociation shows active suppression of limbic regions (amygdala) and increased activity in dorsolateral prefrontal areas.b Similarly, neuroimaging of depersonalization disorder show increased neural activity in prefrontal regions associated with affect regulation and decreased activity in emotion-related areas.c,d
Speed. Dissociative responses occur extremely rapidly. Using EEG, which allows finer temporal resolution than functional imaging studies, Kirino et ale showed reversible attenuation of a specific EEG signal within 300 msec during dissociative episodes. This ultra-rapid neural reflex was correlated with allocation of attentional and working memory resources, perhaps with the goal of minimizing memory activation and resurgence of affect-laden memories.e
Hormonal. Stress-related disorders cause perturbations in neurohormonal function. Simeon et alf found a distinct pattern of stress-induced HPA axis dysregulation in dissociative patients compared with PTSD patients and healthy controls. Similar results were seen in patients with borderline personality disorder and dissociative symptoms.g
Structural imaging. Stress-related neurohormonal perturbations are known to affect critical neural structures, including the hippocampus. Using MRI, Vermetten et alh found significantly decreased amygdala and hippocampal volumes in patients with dissociative identity disorder.
EEG: electroencephalography; HPA: hypothalamic-pituitary-adrenal; PTSD: posttraumatic stress disorder
Reference Citations: click here
Causes of dissociative disorders
As with many psychiatric disorders, the etiology of dissociative phenomena is thought to include the individual patient’s temperamental or constitutional predispositions11 as well as a strong contribution of environmental trauma (early abuse, neglect).12
Constitutional predisposition for developing a dissociative disorder may include personality traits such as being easily hypnotized, mental absorption, suggestibility, and a tendency to fantasize.13 These characteristics fueled concerns in the 1990s that therapists may contribute to dissociative identity disorder by “digging” for repressed memories in susceptible patients and creating “pseudomemories” of events that did not happen.14
The issue of repressed traumatic memory and its role in therapy is extremely controversial and contributes to the complexity of psychotherapeutic treatment of dissociation.15
- shame and secrecy of early sexual or physical abuse and potential for victims to repress traumatic memories
- lability of memory, potential for suggestibility, and difficulty with verification.14
- early relationships are one of the primary ways that humans learn to regulate distress
- early trauma frequently includes pathology in caregiving relationships, including overt role reversal, abuse, and neglect.
Finally, remember that transient dissociative symptoms can be considered normal in high-stress situations. Intensive military training has been found to be associated with a very high incidence (96%) of dissociative symptoms in army recruits.17
Identifying ‘hidden’ phenomena
Dissociative disorders have been called “diseases of hiddenness”18 because:
- Many of their clinical characteristics— sense of identity, memory, connectedness, somatosensory phenomena—are alterations in subjective phenomena that lack clearly observable symptoms.
- Patients are often reluctant to seek help or divulge their symptoms to clinicians.
- When dissociative symptoms are obvious—such as multiple personalities or sudden loss of memories—they may be dismissed or evoke skepticism because of their dramatic presentation.
For more targeted screening, the self-report Dissociative Experiences Scale (DES)21 is useful for clinical assessment in conjunction with the clinician-administered diagnostic Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D).22
Table 2
With these findings, consider screening for dissociation
Posttraumatic stress disorder |
Certain personality disorders (especially borderline personality disorder) |
Somatoform disorders (conversion disorders and nonepileptic seizures) |
Eating disorders |
Substance use disorders |
Extensive history of trauma or neglect |
Self-harm behavior |
As in Mr. D’s case, dissociative phenomena may attenuate the benefit of post-trauma therapeutic interventions, especially those involving exposure. Therefore:
- assess post-trauma patients for dissociation before you start treatment
- make specific alterations in psychotherapy for such patients, as described below.
Table 3
Differential diagnosis: Dissociation ‘look-alikes’
Dissociation symptom | Can be confused with: |
---|---|
Visual or auditory hallucinations, other ‘first-rank’ psychotic symptoms in dissociative identity disorder | Psychotic disorder |
‘Blanking out’ (cognitive disruption) | ADHD, seizures |
Somatoform (conversion) symptoms | A variety of nonpsychiatric medical problems, including pelvic or abdominal pathology and headaches |
Dissociative memory lapses | Learning disability, not paying attention |
‘Switching’ between states | Bipolar disorder, rapid cycling |
Lack of emotional reaction to traumatic stimuli(numbing response) | Healthy coping |
ADHD: attention-deficit/hyperactivity disorder |
Recreational drugs such as ketamine, methylenedioxymethamphetamine (“Ecstasy”), hallucinogens, marijuana, and dextromethorphan also can induce dissociative states. Consider evaluating for use of these substances, some of which may not be detected on a routine drug screen.24
CASE CONTINUED: A tactical shift
Internal distress—such as when remembering painful events—clearly is linked with the appearance of Mr. D’s symptoms. The therapist—recognizing unacknowledged dissociative phenomena—changes Mr. D’s therapeutic strategy from exposure therapy to affect and anxiety regulation, with an explicit focus on attachment security (safety).
The therapist explains to Mr. D that dissociation symptoms are a response to distress, and he can learn more adaptive distress regulation in therapy. The in-session focus shifts to include more direct attention to components of the therapy relationship, including overt disclosure of the therapist’s positive regard and commitment to help the patient and frequent pauses to “check in” that the patient feels present, safe, and understood. With this new focus, Mr. D’s dissociative symptoms resolve and he feels more ready to face and overcome his fear and avoided memories.
Psychotherapy: Putting pieces together
Psychotherapy is the primary treatment, based on understanding dissociative disorders as manifestations of distress-related, traumatic fragmentation of the sense of self, interpersonal relatedness, and capacity for adaptive affect regulation (Table 4).
Table 4
Tips for conceptualizing dissociative disorders
Ground your understanding of this class of disorders as distress-related breakdowns in functional connection and integration among components of normal consciousness |
Consider the overlap among dissociation, certain somatoform disorders (conversion symptoms, pseudoseizures), and PTSD |
Maintain a high index of suspicion for dissociative symptoms in patients with early trauma or neglect (consider screening for this); do further evaluation with dissociative-specific tools |
Avoid the tendency to assume that reversible, unfamiliar, or peculiar symptoms imply volition or lack of an organic basis |
PTSD: posttraumatic stress disorder |
Safety, stabilization, and symptom reduction. Providing a safe therapeutic relationship is a primary and necessary part of DID treatment. On that platform, a first step in reintegrating distressing material into the self involves building the patient’s capacity for conscious, flexible affect regulation. This keeps anxiety and distress within a therapeutic “window.”
Integration of identity and person. Treatment ends when formerly unintegrated or dissociated experiences or parts of the self are integrated into a coherent whole, and the patient can deal adaptively with inter-personal relationships and distress without fragmentation.
Adjunctive medications
Few studies have addressed using psychopharmacologic interventions in the heterogeneous dissociative disorders. GABAA antagonism and 5-HT2a/2c agonism have induced psychotic and dissociative-like symptoms in healthy men,29 and alterations in enzymes such as catechol-O-methyltransferase (COMT) may explain individual vulnerability to trauma.30 Reports of dissociation related to ketamine31 and marijuana32 implicate other neurotransmitter systems in their etiology.
DID. Similar to guidelines for borderline personality disorder,33 guidelines for DID suggest using medications to treat the most prominent symptom clusters such as insomnia, affective instability, and posttraumatic intrusions.
Depersonalization disorder. Trials of fluoxetine and lamotrigine showed no benefit in depersonalization disorder.34,35 In an open trial of 14 patients, naloxone (mean 120 mg/d) reduced depersonalization symptoms by 30%, as measured by 3 validated scales.36
Related Resources
- International Society for the Study of Trauma and Dissociation. Site for professionals. www.isst-d.org
- National Alliance on Mental Illness (NAMI). Patient education on dissociative disorders. www.nami.org/Content/ContentGroups/Helpline1/Dissociative_Disorders.htm
- Fluoxetine • Prozac
- Lamotrigine • Lamictal
- Naloxone • Narcan
- Paroxetine • Paxil
Dr. MacDonald is a speaker for Eli Lilly and Company, Janssen, L.P., and Pfizer Inc.
Mr. D, age 45, presents to his primary care physician with panic attacks, nausea, shortness of breath, nightmares, and dizziness 6 months after being assaulted and robbed at an ATM. Following a routine medical workup, the physician diagnoses posttraumatic stress disorder (PTSD) and refers Mr. D for exposure and response prevention therapy.
During graded exposure sessions, Mr. D’s eyes sometimes glaze over and he seems to “float away” from the discussion. When the therapist asks about these symptoms, Mr. D reports having had them as long as he can remember. In school, he says, teachers thought he was a slow learner, a daydreamer, or had attention-deficit/hyperactivity disorder. From what he can recall of his childhood, he describes a history of trauma and neglect with a violent, drug-abusing father and absent mother.
Patients with a history of early abuse or neglect are at risk for dissociative phenomena and other trauma-related psychiatric disorders.1 The heterogeneous dissociative disorders are often hidden and unrecognized2 —as in Mr. D’s case—or present with unfamiliar or atypical symptoms. Understanding and identifying dissociative symptoms is important because:
- Dissociative symptoms worsen prognosis, whether patients have conversion disorders1 or psychogenic seizures3 or are in psychotherapy.4
- Dissociative states may impair memory encoding5 and decrease patients’ ability to remember therapeutic information.
- Symptoms (such as hearing voices in multiple personality disorder) can be confused with those of disorders with different treatment strategies (such as psychotic disorders).6
- Peritraumatic dissociation may be a risk factor for PTSD.7
This article presents a practical model for understanding dissociation, reviews clinical characteristics of this family of symptoms, and offers suggestions for assessing and treating patients with dissociative disorders.
Coming together, falling apart
Since Pierre Janet’s first reports on dissociative disorders, a number of theories and models of dissociation have been proposed,8 including empirically based, taxonomic models that address DSM-IV-TR categories (Table 1). The model I propose—which attaches a visual metaphor to dissociative phenomena—answers the question, “What is ‘dissociated’ in dissociation disorders?”
Table 1
DSM-IV-TR classification of dissociative disorders
Disorder | Symptoms |
---|---|
Dissociative amnesia | A reversible loss of memory, typically preceded by a stressor |
Dissociative fugue | Loss of memory and identity, along with travel away from home |
Dissociative identity disorder (formerly multiple personality disorder) | Presence of different identity states, often with lack of connection between them; current models highlight the presence of recurrent dissociative intrusions into many aspects of executive function and self |
Depersonalization disorder | Detachment from oneself as a present, feeling person (depersonalization) and the world (derealization) |
Dissociative identity disorder NOS | Functionally disturbing dissociative symptoms that do not fit into any of the above |
NOS: not otherwise specified | |
Source: Diagnostic and statistical manual of mental disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000 |
One paired component is a detached “observer” and a more embodied, feeling “experiencer.” The observer is a perspective that begets metacognition (thinking about one’s inner world) and self-observation; it resides in the same body as soma-based “feelings” that unconsciously contribute to the sense of “being present” with oneself and the world in the moment.9
A second component is voluntary access to one’s autobiographical memories (memories about the self in time), which are constantly “updated” and integrated with current experiences. This component allows one to distinguish between remembered (past) experiences and “firsthand” (present) experience.
Three other components of normal consciousness are:
- a sense of agency and voluntary control over one’s mental contents, mental activity, and bodily movements
- an ongoing connection with one’s body and mind and an understanding of where sensations and images come from
- a sense of sequential experience, with relatively smooth transitions (from self at work to self at home, self a week ago to self today, etc) that have a singular referent (an identity).
- separation of the “observer” and “experiencer” occurs in depersonalization disorder
- reversible loss of ability to access memories characterizes dissociative amnesia
- disconnection between sequential experiences is a part of dissociative identity disorder.
10 Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).
From a neurophysiologic perspective, mental states may be viewed as arising from synchronized integration of the activity of functionally specialized brain regions. Functional neuroimaging of dissociation supports an understanding of these symptoms as ‘disconnection syndromes.’
Functional neuroimaging. Different ‘identities’—sometimes called a traumatic personality state and neutral personality state—demonstrate different patterns of cerebral blood flow, subjective reports, and peripheral physiologic parameters (blood pressure, heart rate).a
Functional imaging of traumatic dissociation shows active suppression of limbic regions (amygdala) and increased activity in dorsolateral prefrontal areas.b Similarly, neuroimaging of depersonalization disorder show increased neural activity in prefrontal regions associated with affect regulation and decreased activity in emotion-related areas.c,d
Speed. Dissociative responses occur extremely rapidly. Using EEG, which allows finer temporal resolution than functional imaging studies, Kirino et ale showed reversible attenuation of a specific EEG signal within 300 msec during dissociative episodes. This ultra-rapid neural reflex was correlated with allocation of attentional and working memory resources, perhaps with the goal of minimizing memory activation and resurgence of affect-laden memories.e
Hormonal. Stress-related disorders cause perturbations in neurohormonal function. Simeon et alf found a distinct pattern of stress-induced HPA axis dysregulation in dissociative patients compared with PTSD patients and healthy controls. Similar results were seen in patients with borderline personality disorder and dissociative symptoms.g
Structural imaging. Stress-related neurohormonal perturbations are known to affect critical neural structures, including the hippocampus. Using MRI, Vermetten et alh found significantly decreased amygdala and hippocampal volumes in patients with dissociative identity disorder.
EEG: electroencephalography; HPA: hypothalamic-pituitary-adrenal; PTSD: posttraumatic stress disorder
Reference Citations: click here
Causes of dissociative disorders
As with many psychiatric disorders, the etiology of dissociative phenomena is thought to include the individual patient’s temperamental or constitutional predispositions11 as well as a strong contribution of environmental trauma (early abuse, neglect).12
Constitutional predisposition for developing a dissociative disorder may include personality traits such as being easily hypnotized, mental absorption, suggestibility, and a tendency to fantasize.13 These characteristics fueled concerns in the 1990s that therapists may contribute to dissociative identity disorder by “digging” for repressed memories in susceptible patients and creating “pseudomemories” of events that did not happen.14
The issue of repressed traumatic memory and its role in therapy is extremely controversial and contributes to the complexity of psychotherapeutic treatment of dissociation.15
- shame and secrecy of early sexual or physical abuse and potential for victims to repress traumatic memories
- lability of memory, potential for suggestibility, and difficulty with verification.14
- early relationships are one of the primary ways that humans learn to regulate distress
- early trauma frequently includes pathology in caregiving relationships, including overt role reversal, abuse, and neglect.
Finally, remember that transient dissociative symptoms can be considered normal in high-stress situations. Intensive military training has been found to be associated with a very high incidence (96%) of dissociative symptoms in army recruits.17
Identifying ‘hidden’ phenomena
Dissociative disorders have been called “diseases of hiddenness”18 because:
- Many of their clinical characteristics— sense of identity, memory, connectedness, somatosensory phenomena—are alterations in subjective phenomena that lack clearly observable symptoms.
- Patients are often reluctant to seek help or divulge their symptoms to clinicians.
- When dissociative symptoms are obvious—such as multiple personalities or sudden loss of memories—they may be dismissed or evoke skepticism because of their dramatic presentation.
For more targeted screening, the self-report Dissociative Experiences Scale (DES)21 is useful for clinical assessment in conjunction with the clinician-administered diagnostic Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D).22
Table 2
With these findings, consider screening for dissociation
Posttraumatic stress disorder |
Certain personality disorders (especially borderline personality disorder) |
Somatoform disorders (conversion disorders and nonepileptic seizures) |
Eating disorders |
Substance use disorders |
Extensive history of trauma or neglect |
Self-harm behavior |
As in Mr. D’s case, dissociative phenomena may attenuate the benefit of post-trauma therapeutic interventions, especially those involving exposure. Therefore:
- assess post-trauma patients for dissociation before you start treatment
- make specific alterations in psychotherapy for such patients, as described below.
Table 3
Differential diagnosis: Dissociation ‘look-alikes’
Dissociation symptom | Can be confused with: |
---|---|
Visual or auditory hallucinations, other ‘first-rank’ psychotic symptoms in dissociative identity disorder | Psychotic disorder |
‘Blanking out’ (cognitive disruption) | ADHD, seizures |
Somatoform (conversion) symptoms | A variety of nonpsychiatric medical problems, including pelvic or abdominal pathology and headaches |
Dissociative memory lapses | Learning disability, not paying attention |
‘Switching’ between states | Bipolar disorder, rapid cycling |
Lack of emotional reaction to traumatic stimuli(numbing response) | Healthy coping |
ADHD: attention-deficit/hyperactivity disorder |
Recreational drugs such as ketamine, methylenedioxymethamphetamine (“Ecstasy”), hallucinogens, marijuana, and dextromethorphan also can induce dissociative states. Consider evaluating for use of these substances, some of which may not be detected on a routine drug screen.24
CASE CONTINUED: A tactical shift
Internal distress—such as when remembering painful events—clearly is linked with the appearance of Mr. D’s symptoms. The therapist—recognizing unacknowledged dissociative phenomena—changes Mr. D’s therapeutic strategy from exposure therapy to affect and anxiety regulation, with an explicit focus on attachment security (safety).
The therapist explains to Mr. D that dissociation symptoms are a response to distress, and he can learn more adaptive distress regulation in therapy. The in-session focus shifts to include more direct attention to components of the therapy relationship, including overt disclosure of the therapist’s positive regard and commitment to help the patient and frequent pauses to “check in” that the patient feels present, safe, and understood. With this new focus, Mr. D’s dissociative symptoms resolve and he feels more ready to face and overcome his fear and avoided memories.
Psychotherapy: Putting pieces together
Psychotherapy is the primary treatment, based on understanding dissociative disorders as manifestations of distress-related, traumatic fragmentation of the sense of self, interpersonal relatedness, and capacity for adaptive affect regulation (Table 4).
Table 4
Tips for conceptualizing dissociative disorders
Ground your understanding of this class of disorders as distress-related breakdowns in functional connection and integration among components of normal consciousness |
Consider the overlap among dissociation, certain somatoform disorders (conversion symptoms, pseudoseizures), and PTSD |
Maintain a high index of suspicion for dissociative symptoms in patients with early trauma or neglect (consider screening for this); do further evaluation with dissociative-specific tools |
Avoid the tendency to assume that reversible, unfamiliar, or peculiar symptoms imply volition or lack of an organic basis |
PTSD: posttraumatic stress disorder |
Safety, stabilization, and symptom reduction. Providing a safe therapeutic relationship is a primary and necessary part of DID treatment. On that platform, a first step in reintegrating distressing material into the self involves building the patient’s capacity for conscious, flexible affect regulation. This keeps anxiety and distress within a therapeutic “window.”
Integration of identity and person. Treatment ends when formerly unintegrated or dissociated experiences or parts of the self are integrated into a coherent whole, and the patient can deal adaptively with inter-personal relationships and distress without fragmentation.
Adjunctive medications
Few studies have addressed using psychopharmacologic interventions in the heterogeneous dissociative disorders. GABAA antagonism and 5-HT2a/2c agonism have induced psychotic and dissociative-like symptoms in healthy men,29 and alterations in enzymes such as catechol-O-methyltransferase (COMT) may explain individual vulnerability to trauma.30 Reports of dissociation related to ketamine31 and marijuana32 implicate other neurotransmitter systems in their etiology.
DID. Similar to guidelines for borderline personality disorder,33 guidelines for DID suggest using medications to treat the most prominent symptom clusters such as insomnia, affective instability, and posttraumatic intrusions.
Depersonalization disorder. Trials of fluoxetine and lamotrigine showed no benefit in depersonalization disorder.34,35 In an open trial of 14 patients, naloxone (mean 120 mg/d) reduced depersonalization symptoms by 30%, as measured by 3 validated scales.36
Related Resources
- International Society for the Study of Trauma and Dissociation. Site for professionals. www.isst-d.org
- National Alliance on Mental Illness (NAMI). Patient education on dissociative disorders. www.nami.org/Content/ContentGroups/Helpline1/Dissociative_Disorders.htm
- Fluoxetine • Prozac
- Lamotrigine • Lamictal
- Naloxone • Narcan
- Paroxetine • Paxil
Dr. MacDonald is a speaker for Eli Lilly and Company, Janssen, L.P., and Pfizer Inc.
1. Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004;161:2271-6.
2. Foote B, Smolin Y, Kaplan M, et al. Prevalence of dissociative disorders in psychiatric outpatients. Am J Psychiatry 2006;163:623-9.
3. Reuber M, Pukrop R, Bauer J, et al. Outcome in psychogenic nonepileptic seizures: 1 to 10-year follow-up in 164 patients. Ann Neurol 2003;53:305-11.
4. Spitzer C, Barnow S, Freyberger HJ, Grabe HJ. Dissociation predicts symptom-related treatment outcome in short-term inpatient psychotherapy. Aust N Z J Psychiatry 2007;41:682-7.
5. Allen JG, Console DA, Lewis L. Dissociative detachment and memory impairment: reversible amnesia or encoding failure? Compr Psychiatry 1999;40:160-71.
6. Dell PF. A new model of dissociative identity disorder. Psychiatr Clin North Am 2006;29:1-26.
7. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective evaluation. Am J Psychiatry 2005;162:1188-91.
8. Steinberg M, Rounsaville B, Cicchetti DV. The Structured Clinical Interview for DSM-III-R Dissociative Disorders: preliminary report on a new diagnostic instrument. Am J Psychiatry 1990;147:76-82.
9. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York, NY: Harcourt, Inc; 1999.
10. Alkire MT, Miller J. General anesthesia and the neural correlates of consciousness. Prog Brain Res 2005;150:229-44.
11. Simeon D, Guralnik O, Knutelska M, Schmeidler J. Personality factors associated with dissociation: temperament, defenses, and cognitive schemata. Am J Psychiatry 2002;159(3):489-91.
12. Kihlstrom JF. Dissociative disorders. Annu Rev Clin Psychol 2005;1:227-53.
13. Isaac M, Chand PK. Dissociative and conversion disorders: defining boundaries. Curr Opin Psychiatry 2006;19(1):61-6.
14. Laney C, Loftus EF. Traumatic memories are not necessarily accurate memories. Can J Psychiatry 2005;50(13):823-8.
15. Loftus EF, Davis D. Recovered memories. Annu Rev Clin Psychol 2006;2:469-98.
16. Lyons-Ruth K, Dutra L, Schuder MR, Bianchi I. From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences? Psychiatr Clin North Am 2006;29(1):63-86.
17. Morgan CA, 3rd, Hazlett G, Wang S, et al. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry 2001;158(8):1239-47.
18. Spiegel D. Recognizing traumatic dissociation. Am J Psychiatry 2006;163(4):566-8.
19. Scher CD, Stein MB, Asmundson GJ, et al. The childhood trauma questionnaire in a community sample: psychometric properties and normative data. J Trauma Stress 2001;14:843-57.
20. Teicher MH, Andersen SL, Polcari A, et al. The neurobiological consequences of early stress and childhood maltreatment. Neurosci Biobehav Rev 2003;27:33-44.
21. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation scale. J Nerv Ment Dis 1986;174(12):727-35.
22. Steinberg M, Rounsaville B, Cicchetti D. Detection of dissociative disorders in psychiatric patients by a screening instrument and a structured diagnostic interview. Am J Psychiatry 1991;148(8):1050-4.
23. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology 1989;39:835-40.
24. Schonenberg M, Reichwald U, Domes G, et al. Effects of peritraumatic ketamine medication on early and sustained posttraumatic stress symptoms in moderately injured accident victims. Psychopharmacology (Berl) 2005;182(3):420-5.
25. Hunter EC, Phillips ML, Chalder T, et al. Depersonalisation disorder: a cognitive-behavioural conceptualisation. Behav Res Ther 2003;41:1451-67.
26. Guidelines for treating dissociative identity disorder in adults (2005). J Trauma Dissociation 2005;6(4):69-149.
27. van der Hart O, Nijenhuis E. Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found. Aust N Z J Psychiatry 2001;35:589-600.
28. Holmes EA, Brown RJ, Mansell W, et al. Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin Psychol Rev 2005;25(1):1-23.
29. D’Souza DC, Gil RB, Zuzarte E, et al. gamma-Aminobutyric acid-serotonin interactions in healthy men: implications for network models of psychosis and dissociation. Biol Psychiatry 2006;59(2):128-37.
30. Savitz JB, van der Merwe L, Newman TK, et al. The relationship between childhood abuse and dissociation. Is it influenced by catechol-O-methyltransferase (COMT) activity? Int J Neuropsychopharmacol 2008;11:149-61.
31. Curran HV, Morgan C. Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later. Addiction 2000;95:575-90.
32. Mathew RJ, Wilson WH, Humphreys D, et al. Depersonalization after marijuana smoking. Biol Psychiatry 1993;33:431-41.
33. American Psychiatric Association. Practice guideline for the treatment of patients with borderline personality disorder. Am J Psychiatry 2001;158(10 suppl):1-52.
34. Sierra M, Phillips ML, Ivin G, et al. A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder. J Psychopharmacol 2003;17:103-5.
35. Simeon D, Guralnik O, Schmeidler J, Knutelska M. Fluoxetine therapy in depersonalisation disorder: randomised controlled trial. Br J Psychiatry 2004;185:31-6.
36. Simeon D, Knutelska M. An open trial of naltrexone in the treatment of depersonalization disorder. J Clin Psychopharmacol 2005;25:267-70.
37. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2006(1):CD002795.-
38. Marshall RD, Lewis-Fernandez R, Blanco C, et al. A controlled trial of paroxetine for chronic PTSD, dissociation, and interpersonal problems in mostly minority adults. Depress Anxiety 2007;24:77-84.
1. Sar V, Akyuz G, Kundakci T, et al. Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004;161:2271-6.
2. Foote B, Smolin Y, Kaplan M, et al. Prevalence of dissociative disorders in psychiatric outpatients. Am J Psychiatry 2006;163:623-9.
3. Reuber M, Pukrop R, Bauer J, et al. Outcome in psychogenic nonepileptic seizures: 1 to 10-year follow-up in 164 patients. Ann Neurol 2003;53:305-11.
4. Spitzer C, Barnow S, Freyberger HJ, Grabe HJ. Dissociation predicts symptom-related treatment outcome in short-term inpatient psychotherapy. Aust N Z J Psychiatry 2007;41:682-7.
5. Allen JG, Console DA, Lewis L. Dissociative detachment and memory impairment: reversible amnesia or encoding failure? Compr Psychiatry 1999;40:160-71.
6. Dell PF. A new model of dissociative identity disorder. Psychiatr Clin North Am 2006;29:1-26.
7. Shalev AY, Freedman S. PTSD following terrorist attacks: a prospective evaluation. Am J Psychiatry 2005;162:1188-91.
8. Steinberg M, Rounsaville B, Cicchetti DV. The Structured Clinical Interview for DSM-III-R Dissociative Disorders: preliminary report on a new diagnostic instrument. Am J Psychiatry 1990;147:76-82.
9. Damasio A. The feeling of what happens: body and emotion in the making of consciousness. New York, NY: Harcourt, Inc; 1999.
10. Alkire MT, Miller J. General anesthesia and the neural correlates of consciousness. Prog Brain Res 2005;150:229-44.
11. Simeon D, Guralnik O, Knutelska M, Schmeidler J. Personality factors associated with dissociation: temperament, defenses, and cognitive schemata. Am J Psychiatry 2002;159(3):489-91.
12. Kihlstrom JF. Dissociative disorders. Annu Rev Clin Psychol 2005;1:227-53.
13. Isaac M, Chand PK. Dissociative and conversion disorders: defining boundaries. Curr Opin Psychiatry 2006;19(1):61-6.
14. Laney C, Loftus EF. Traumatic memories are not necessarily accurate memories. Can J Psychiatry 2005;50(13):823-8.
15. Loftus EF, Davis D. Recovered memories. Annu Rev Clin Psychol 2006;2:469-98.
16. Lyons-Ruth K, Dutra L, Schuder MR, Bianchi I. From infant attachment disorganization to adult dissociation: relational adaptations or traumatic experiences? Psychiatr Clin North Am 2006;29(1):63-86.
17. Morgan CA, 3rd, Hazlett G, Wang S, et al. Symptoms of dissociation in humans experiencing acute, uncontrollable stress: a prospective investigation. Am J Psychiatry 2001;158(8):1239-47.
18. Spiegel D. Recognizing traumatic dissociation. Am J Psychiatry 2006;163(4):566-8.
19. Scher CD, Stein MB, Asmundson GJ, et al. The childhood trauma questionnaire in a community sample: psychometric properties and normative data. J Trauma Stress 2001;14:843-57.
20. Teicher MH, Andersen SL, Polcari A, et al. The neurobiological consequences of early stress and childhood maltreatment. Neurosci Biobehav Rev 2003;27:33-44.
21. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation scale. J Nerv Ment Dis 1986;174(12):727-35.
22. Steinberg M, Rounsaville B, Cicchetti D. Detection of dissociative disorders in psychiatric patients by a screening instrument and a structured diagnostic interview. Am J Psychiatry 1991;148(8):1050-4.
23. Devinsky O, Putnam F, Grafman J, et al. Dissociative states and epilepsy. Neurology 1989;39:835-40.
24. Schonenberg M, Reichwald U, Domes G, et al. Effects of peritraumatic ketamine medication on early and sustained posttraumatic stress symptoms in moderately injured accident victims. Psychopharmacology (Berl) 2005;182(3):420-5.
25. Hunter EC, Phillips ML, Chalder T, et al. Depersonalisation disorder: a cognitive-behavioural conceptualisation. Behav Res Ther 2003;41:1451-67.
26. Guidelines for treating dissociative identity disorder in adults (2005). J Trauma Dissociation 2005;6(4):69-149.
27. van der Hart O, Nijenhuis E. Generalized dissociative amnesia: episodic, semantic and procedural memories lost and found. Aust N Z J Psychiatry 2001;35:589-600.
28. Holmes EA, Brown RJ, Mansell W, et al. Are there two qualitatively distinct forms of dissociation? A review and some clinical implications. Clin Psychol Rev 2005;25(1):1-23.
29. D’Souza DC, Gil RB, Zuzarte E, et al. gamma-Aminobutyric acid-serotonin interactions in healthy men: implications for network models of psychosis and dissociation. Biol Psychiatry 2006;59(2):128-37.
30. Savitz JB, van der Merwe L, Newman TK, et al. The relationship between childhood abuse and dissociation. Is it influenced by catechol-O-methyltransferase (COMT) activity? Int J Neuropsychopharmacol 2008;11:149-61.
31. Curran HV, Morgan C. Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later. Addiction 2000;95:575-90.
32. Mathew RJ, Wilson WH, Humphreys D, et al. Depersonalization after marijuana smoking. Biol Psychiatry 1993;33:431-41.
33. American Psychiatric Association. Practice guideline for the treatment of patients with borderline personality disorder. Am J Psychiatry 2001;158(10 suppl):1-52.
34. Sierra M, Phillips ML, Ivin G, et al. A placebo-controlled, cross-over trial of lamotrigine in depersonalization disorder. J Psychopharmacol 2003;17:103-5.
35. Simeon D, Guralnik O, Schmeidler J, Knutelska M. Fluoxetine therapy in depersonalisation disorder: randomised controlled trial. Br J Psychiatry 2004;185:31-6.
36. Simeon D, Knutelska M. An open trial of naltrexone in the treatment of depersonalization disorder. J Clin Psychopharmacol 2005;25:267-70.
37. Stein DJ, Ipser JC, Seedat S. Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database Syst Rev 2006(1):CD002795.-
38. Marshall RD, Lewis-Fernandez R, Blanco C, et al. A controlled trial of paroxetine for chronic PTSD, dissociation, and interpersonal problems in mostly minority adults. Depress Anxiety 2007;24:77-84.