Evidence-Based Reviews

Dissociative disorders unclear? Think ‘rainbows from pain blows’

Current Psychiatry. 2008 May;7(5):73-85

References

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.

¹⁰ Functional neuroimaging of dissociation supports an understanding of these symptoms as “disconnection syndromes” (Box).

Box

Dissociation’s neurobiology: Evidence of brain ‘disconnections’

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 al^e 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 al^f 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 al^h 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

Clinical Point

To reduce shame about not fighting back, educate abused patients that detachment is a normal response to threat

Early trauma. Factors that make it difficult to define the specific role of early trauma in dissociative disorders include:

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

Some experts—influenced by attachment theory—view dissociative phenomena as manifestations of an innate, reflexive relational pattern called disorganized attachment.¹⁶ Attachment theory notes that:

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.

Empathic treatment of dissociation, therefore, is based on appreciating the difficulties that arose from an individual’s experience of being alone with overwhelming distress. The relation of dissociation to attachment theory has specific therapeutic implications, including a focus on constructing a safe therapeutic relationship for patients.

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.

Screening tools. To identify at-risk patients, consider screening with a validated questionnaire such as the Childhood Trauma Questionnaire (CTQ),¹⁹ particularly for patients with psychiatric comorbidity (Table 2). Using the CTQ—which assesses physical, emotional, and sexual abuse and neglect—is a high-yield procedure, given the role of early trauma in brain development and future mental health.²⁰

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