Dissociative Identity Disorder

Dissociative Identity Disorder (formerly Multiple Personality Disorder) is characterized by a presence of multiple “selves” within a person that emerge at different times. This leads to memory impairment in that each “self” is not consciously aware of the actions of the other “selves”, with the end result being the individual feeling as if they have lost large chunks of time. Studies have shown that traumatic experiences in early childhood and continued emotional and/or social deprivation promote development of DID. Once a person develops DID, s/he may show symptoms of memory loss, hallucination and anxiety that may cause the development of further destructive symptoms such as night terror and urge to hurt him/herself. Marked differences in the structural and functional anatomical features of the brains between patients with D.I.D and healthy controls have been illustrated in recent literature. Studies conducted by various groups across the globe have shown a high degree of variance in DID prevalence within different test groups such as gender and ethnicity. Different diagnostic tests in addition to the fact that DID is comorbid with many other psychiatric diseases makes it difficult to properly assess and diagnose DID. The approach to treat dissociative identity disorder can be different among patients and their effectiveness also vary. The most used approach is a combination of medication and psychotherapies that target different symptoms and reunites the patient's identity. In most cases, patients with borderline personality disorder are also diagnosed with DID. Three genes - SLC6A4, monoamine oxidase A (MAO) and tryptophan hydroxylase 1 (TPH1) that are associated with BPD may become the candidate genes for DID in the further.

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Causes of Dissociative Identity Disorder

main article: Causes of Dissociative Identity Disorder
author: Ariane Rego

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source: http://2.bp.blogspot.com/_jvinTDh__2I/TNWw6PM-SWI/

The causes of Dissociative Identity Disorder are highly debated, but fall under two models. The first is the Posttraumatic model, which predicts that there is a correlation between the frequency of DID and childhood trauma, and that the incidence of dissociation is a means of coping with the trauma experienced[1] [2] The other is the Sociocognitive model, in which a number of factors, including social cues, influence from psychotherapists and personality type of the individual contribute to the diagnosis of Dissociative Identity Disorder, but does not include the possibility of conscious malingering. It also attributes the level exposure a certain culture receives to the idea of dissociation to incidences of DID (Spanos 1985)[1][2]. The continual revision of these two models is important in the detection and proper treatment of Dissociative Identity Disorder.

1. Xiao, Z et al. Trauma and Dissociation in China. American Journal of Psychiatry. 163(8): 1388-1391 (2006).
2. Ross, C et al. A Cross-Cultural Test of the Trauma Model of Dissociation. Journal of Trauma and Dissociation. 9(1): 35-49 (2008)

Epidemiology and Comorbidity of DID

main article: Epidemiology and Comorbidity of DID
author: Kiho Son

Dissociative Identity Disorder
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An artist's interpretation of dissociative identity disorder

Dissociative identity disorder (DID) is a mental disorder characterized by multiple persisting personalities or identities that emerge at different times to alter the person's behavior. Unfortunately, the high degree of comorbidity of DID with other various mental disorders such as post-traumatic stress disorder, major depression, obsessive compulsive disorder, and somatoform disorder makes proper diagnosis of DID is extremely difficult. [1]. As a result, patients are commonly misdiagnosed with schizophrenia due to common symptoms [1]. The prevalence of DID seems to heavily favor females over males according to several US studies performed in the last two decades [2]. In addition, clinical populations of psychiatric patients all seem to have varying levels of DID incidence depending on the country [3]. Distinct cultural backgrounds seem to have a strong influences on the diagnosis of DID, as countries perform different diagnostic tests and interpret symptoms in inconsistent manners [4].

1. International Society for the Study of Dissociation. (2005). Guidelines for treating Dissociative Identity Disorder in adults. Journal of Trauma & Dissociation, 6(4) pp. 69-149.
2. Lewis-Hall, F., Williams, T., Panetta, J., & Herrera, J. (2002). Psychiatric illnesses in women: Emerging treatments and research. Washington, DC: American Psychiatric Publishing.
3. Sar, V. (2011). Epidemiology of Dissociative Disorders: An Overview. Epidemiology Research International, vol. 2011, Article ID 404538, 8 pages, 2011. doi:10.1155/2011/404538
4. Friedl, M.C., Draijer, N., de Jonge, P. (2000). Prevalence of dissociative disorders in psychiatric in-patients: the impact of study characteristics. Acta Psychiatrica Scandinavica, 102, 423-428.

Neuroanatomy of Dissociative Identity Disorder

main article: Neuroanatomy of Dissociative Identity Disorder
author: Nathan Lai

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Neuroanatomy of dissociative identity disorder

Dissociative identity disorder (D.I.D) is very complex in nature, up until the last decade not much light has been shed on both the structural and functional differences in patients with D.I.D compared to healthy controls. Recent literature illustrating the structural and functional neuroanatomical differences between those with D.I.D and healthy controls could possibly lead to future research on the neural mechanisms of D.I.D. Such mechanisms may also be discovered by extrapolating conclusions from the neuroanatomical structures specifically related to the symptoms of D.I.D (i.e memory impairment common in patients with D.I.D so hippocampus may be involved in D.I.D’s mechanism[1]). It is important that we expand our currently limited knowledge on the neuroanatomical nature of D.I.D in order improve both pharmacological and behavioural treatment methods.

1. Vermetten, E., Schmahl, C., Lindner, S., Loewenstein, R., & Bremner, J. (2006).
Hippocampal and amygdalar volumes in dissociative identity disorder. American Journal of Psychiatry, 163(4), 630-636
2. Brunson, K.L, Chen, Y., Avishai-Eliner, S., & Baram, T. (2003). Stress and the developing hippocampus a double edged sword?. Molecular Neurobiology 27(2): 121-136
3. Packard, M. G., Cahill, L., & McGaugh, J. L. (1994). Amygdala modulation of hippocampal-dependent and caudate nucleus-dependent memory processes. Proceedings of the National Academy of Sciences, 91(18), 8477-8481.
4. Yang, R. J., Mozhui, K., Karlsson, R. M., Cameron, H. A., Williams, R. W., & Holmes, A. (2008). Variation in mouse basolateral amygdala volume is associated with differences in stress reactivity and fear learning. Neuropsychopharmacology, 33(11), 2595-2604.
5. Forrest, K. A. (2001). Toward an etiology of dissociative identity disorder: A neurodevelopmental approach. Consciousness and Cognition, 10(3), 259-293.
6. Sar, V., Unal, S. N., & Ozturk, E. (2007). Frontal and occipital perfusion changes in dissociative identity disorder. Psychiatry Research: Neuroimaging, 156(3), 217-223.
7. Reinders, A. A. T. S., Nijenhuis, E. R. S., Paans, A. M. J., Korf, J., Willemsen, A. T. M., & Den Boer, J. A. (2003). One brain, two selves. Neuroimage, 20(4), 2119-2125.
8. Reinders, A. A. T., Nijenhuis, E. R., Quak, J., Korf, J., Haaksma, J., Paans, A. M., … & den Boer, J. A. (2006). Psychobiological characteristics of dissociative identity disorder: A symptom provocation study. Biological psychiatry, 60(7), 730-740.

Potential Genetic Factors of DID

main article: Potential Genetic Factors of DID
author: Chenlu Wang
DID is a type of mental disorder characterized by enduring at least two different identities and suffering from memory lost due to switching between identities [1]. No gene has been suggested to own a direct link with DID throughout the literature. The genetic factor is not the only thing that remains unclear about this disorder, so does its diagnosis. In most cases, patients with borderline personality disorder are also diagnosed with DID. Although no evidence shows that genes causing BPD will cause DID as well, these genes may become candidate genes for DID in the future. This part of the Neurowiki will introduce three genes - SLC6A4, monoamine oxidase A (MAO) and tryptophan hydroxylase 1 (TPH1), and their connections with mental disorders based on literature [2]. Instead of relating single genes to disease condition recent studies started to attribute disease condition to complex forms of mechanism which include gene-gene interaction and gene-environment interaction. Two examples from serotonin system will be given to help our understanding of these mechanisms.

1. Ross, C. A., Ferrell, L. & Schroeder, E. Co-Occurrence of Dissociative Identity Disorder and Borderline Personality Disorder. Journal of Trauma & Dissociative 15, 79-90 (2014).
2. Reichborn-Kjennerud, T. et al. The genetic epidemiology of personality disorder. Dialogues in Clinical Neuroscience 12, 103-114 (2010).

Treatments of DID

main article: Treatments of DID
author: Jun Liu

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Dissociative Identity Disorder

Treatments of Dissociative Identity Disorder
Patients with DID often possess multiple distinct personalities and each personality has its own memory and it is not interconnected within the patient. These memory lapses are the main target of DID treatment. However, patients with DID are often comorbid with other psychological disorders such as schizophrenia that make it difficult to diagnose and treat. It is now believed traumatic stress is the primary factor that causes DID[1]. Current treatments not only use psychotherapies but also involve medications in side-symptom reduction. Although treatments vary among each patient; but in general, they follow a common guide-lined approach, a three staged treatment by International Society for the Study of Dissociation[2]. This phasic treatment aims for the building of connection between memories and unification to the “host” personality. Numerous reports conducted on the recoveries of patients after receiving such treatment have shown that the combination of medication and long-term, periodic psychotherapies could be an effective way of treating DID[3].

1. Foote, B.; Park, J. (2008). "Dissociative identity disorder and schizophrenia: Differential diagnosis and theoretical issues". Current psychiatry reports 10 (3): 217–222. doi:10.1007/s11920-008-0036-z
2. International Society for The Study (2011). "Guidelines for Treating Dissociative Identity Disorder in Adults, Third Revision"Journal of Trauma & Dissociation 12 (2): 188–212. doi:10.1080/15299732.2011.537248
3. Brand, B.; Loewenstein, R. J. (2014). “Does Phasic Trauma Treatment Make Patients With Dissociative Identity Disorder Treatment More Dissociative?” Journal of Trauma & Dissociation 15(1): 52-65. doi:10.1080/15299732.2013.828150

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