Understanding Dissociative Identity Disorder

Abstract

Dissociative Identity Disorders (DID) has been thought to occur in individuals with trauma in their early developmental years. Many argue on the reason this happens, having some even question its reality. Although some think DID is a fictional disease, others believe it to be a form of developmental Post Traumatic Stress Disorder, having the alters carry the burden of the toxic memories. The purpose of this literature review is to collect past studies done on DID and evaluating its relationship with PTSD. The analysis will particularly be focused on the symptoms of DID, it’s diagnosis, treatment, and brain imaging. It will compare that of which we know about PTSD to what latest studies have shown about DID. Its result will show that these two disorders although linked by symptoms, diagnosis, and treatments, are not entirely the same. Because of three problematic questions with DID being PTSD in early developmental years, it concludes that those with DID are suffering from both PTSD and BPD. 

Understanding Dissociative Identity Disorder

And Its Relation to Other Disorders.

In its purest definition, Dissociative Identity Disorder (DID) is a separation of normal mental functions in one’s self (Farrell,2011). Suspected to affect 2% of the population, DID has an array of symptoms including a loss of memory and personal information, depersonalization, derealization, hypnotic trances, hallucinatory passive voices, and most exclusively personality alters. (Vermetten, Schmahl, Lindner, Loewenstein, and Bremner, 2006). These alters are known to have the abilities such as speaking in different accents, having different writing styles and in some very rare cases having allergies other alters don’t have. Additionally, alters may also differ in gender and age, leaving many wonderings if the inflicted are actually multiple persons stuck in a single body. This ideology is known as the Multiple Selves Thesis (MST). This theory takes form in many different arguments, but the basic idea is the same: because they have multiple different personalities, they are multiple different people. Besides the ethical implication involved, many questions are not answered using this theory. Maiese (2016) understands such a theory to be incorrect, proving because of semantical memory, consistent characteristic functions, and shared knowledge between alters, that all alters are in fact a single person decompartmentalizing metal states. This conclusion is commonly agreed upon one among researchers.  

  Diagnosis for DID is done by a licensed psychologist. According to the DSM-V (American Psychiatric Publishing, & American Psychiatric Association, 2013) criteria, the psychologist must (a) identify of two or more alters, (b) two of which are reoccurring, (c) find that patients are missing memories not only of traumatic events, and (d) asses that disturbance is not due to physiological effects. Similar to most psycho-determining checklist, this criterion is usually used as an affirmation on other tests. Such being the multidisciplinary and multi-technique approach which evaluates verbal and nonverbal cues during questioning, self-reported questionnaires by the patient, The Dissociative Experience Scale (DES), and The Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D) (Farrell, 2011). When conducting such tests, the administrator should be aware of exaggeration that might occur during the examination, along with other biases which can hinder the results.

Besides for psychological examinations, Vermetten et al. (2006) found by way of brain imaging it is also possible to make a diagnose for DID. Inspired by finding of smaller amygdala and hippocampus volumes in young children with post-traumatic stress disorder (PTSD) and those with borderline personality disorder (BPD), the study seeks to find the same correlation with DID. It reports that those with confirmed DID based on SCID-D and the DSM-IV criteria have significantly smaller volume in hippocampus and amygdala than those in a healthy patient. This conclusion implies that MRI scans may also be used to diagnose patients with DID.

In Sapolsky (2003) it was shown as a result of the stress, the brain of one with DID goes through Glucocorticoids- a steroid produced in the zona fasciculata- is released in the brain. Nijenhuis and Steele (2010) found that animals who are injected with a large dose of Glucocorticoids have by virtue decreased size in the hippocampus. Such an explanation can be applied to those with DID, using the Glucocorticoids as the reason those with DID have smaller hippocampus volume. (Soibelman, 2017)  

 When discussing treatments Putman & Loewenstein (1993) collected surveys from 305 clinicians. The survey found that most therapists use a long-term psychotherapy hypnosis. Reportedly, this was done twice a week. Other forms used include art therapy, family therapy, and behavioral modification therapy.

  With regards to medication, Loewenstein (2005) found that medications can help alleviate agitation, anxiety, comorbid sleep disorders, and comorbid PTSD. Although not many studies were done on the exact effects, with proper monitoring and understanding of patient, medication will do more good than harm. A few cautionary problems which psychiatrist should look for is any sabotaging of the medical trial. Usually among the alters, one or more might have a phobia of medications. This is important to note before the medical trial, for during the trial the phobic alter will likely misuse the medications or report false symptoms to stop the trial completely. The best way of noting such a phobic alter would be by the consultation and permission stage. When asking the host if the medication trial would be permitted, the psychiatrist should ask the patient if any alters have a problem with the prescription.

With no specific gene predisposition, psychologists look for a connection between those that develop DID and those that don’t. Two models try to explain the phenomena. The commonly used states that trauma causes the DID, thus explaining the outstanding comorbid rate DID patients have with PTSD. While the other explains that those with DID are more prone to fantasy and suggestibility. Although the second model would explain why it isn’t so that all children who experience trauma are diagnosed with DID, when closely examined it falls short. When studying the suggestibility of those with DID and a healthy control group, the researchers found no significant difference between the two. (Vissia et al., 2016).

Because of the yearly decrease in male’s hippocampus size, those with DID are more commonly male than female (Vermetten et al., 2006). Also, a predisposition to having any sort of mood disorders is having an excessive amount of glucocorticoid being produced in the brain. For cases like those antidepressant drugs are recommended to be used (McEwen et al., 2015)

PTSD similarly is categorized as a dissociative disorder by the current DSM definition. It is thought to be the brain's inability to cope with a traumatic event that occurred to the patient. Patients with PTSD are thought be have symptoms like depersonalization, derealization, nightmares, avoidance behavior, loss of memory, and hypervigilance (American Psychiatric Publishing, & American Psychiatric Association, 2013).

Diagnosis is done using structured interviews, a criteria checklist, and self-reported questionnaire. Besides for clinical testing, Vermetten et al. (2006) cited a study that found a significant difference in the hippocampus and amygdala volume with those who had PTSD in early developmental years.

In regards to treatments, PTSD has been shown to have better results alleviating symptoms with a hypnotic therapeutic approach (Bryant, Moulds, Guthrie, & Nixon, 2005). Medical SSRIs have also been used for those suffering from PTSD. (Lowenstein, 2005).

Calling DID a type of developed PTSD for those who had the traumatic event in their early developmental years, is a logical conclusion. With its similar symptoms, tools of diagnosis, and even treatments, such a conclusion is well founded. And although most scientists agree, many issues have come up, making the once undoubtedly theory questionable. The concerns are as follows.

The first concern is the difference in volume of the brain’s hippocampus and amygdala. As written before, Vermetten et al. (2006) found that those with DID have smaller hippocampus and amygdala than those of a healthy person. If one wishes to say that both of these illnesses are identical, then it would be assumed that the brain that has said illnesses are equal. But when researched it was found that those with DID have hippocampus’s 19.2% smaller than average, while those with PTSD have no significant difference in their hippocampus size than those with a healthy brain (cited by Vermetten et al., 2006).

Many in the field of research disagree that this is a question at all. Seeing that the brain is formed when young, the brain of those with DID are likely to form smaller hippocampus and amygdala, while those who encountered the trauma later on with already formed hippocampus and amygdala size, would not be affected. Vermetten et al. (2006) also cited an earlier study that supports such an answer. The study claims to find in those with PTSD in early development to have 15% smaller amygdala volumes than those of an average brain.

Stating that those with smaller hippocampus and amygdala must have had an early exposure to trauma is still difficult. Vermetten et al. (2006) also cited studies on those with BPD. While each study brought different percentages, they all agreed that those with BPD have smaller hippocampus and amygdala volumes than those in healthy brains. While it is true that those who had BPD had a larger percentage of a discrepancy to those with healthy brains, nevertheless the outcome proves that those with a developed brain can also have a smaller hippocampus and amygdala volume.

The second issue with such a comparison is based on a study done in Asia about DID. The study was driven by the question of why there were so few cases of DID reported in Asia. It collected the two cases in Korea of young adults who developed DID (Kim, Kim, & Jung, 2016). If DID is simply PTSD in younger children, why is it not as common in Asia?

The third and last problem with such a comparison is the co-morbidity with BPD. Horevitz and Braun, (cited by Gillig, 2009) found that 70% of those with DID meet the criteria for BPD. Although the same can be said with PTSD, having Vermetten et al. (2006) state the co-morbid rate for those with DID having PTSD is 80-100%, the question of why BPD is so highly attached to DID still should be entertained. Horevitz and Braun discovery allowed Coons et al. (cited by Gillig, 2009) to conclude that those with DID are suffering from an extreme case of BPD.

This collective study would like to bring a solution to all of these problems. As of this far, all research topics only mentioned either PTSD or BPD as a possible cause for DID. But in truth, maybe both are need to allow such a condition to exist. This theory allows all three questions to be resolved.

First, by stating that the smaller hippocampus and amygdala are caused by the BPD part of the disease. This explains why those with BPD have smaller hippocampus and amygdala, even if the illness developed after childhood. It also explains why those with PTSD as adults don’t have a discrepancy in their hippocampus and amygdala size.

Although some might wonder why those with PTSD as children have smaller amygdala levels, this theory would not dispute that childhood harshens the ability of the brain to correctly form.

The second issue is answered as well. Although BPD and PTSD are both found in Asia, because both are present in DID, many doctors might diagnose the illness incorrectly, mistakenly thinking it is either BPD or PTSD (Kim, Kim, & Jung, 2016).

Lastly, the third question is obviously answered. BPD has a 70% co-morbidity with DID because DID is essentially made up of both BPD and PTSD. It too explains why PTSD had such a high reported comorbid rate with DID.

Such a theory can also be affirmed by Chlebowski and Gregory (2012), who found DID patients using Dynamic Deconstructive Psychotherapy (DDP), a therapy developed for those with BPD, had a 34%-79% reduction in their Dissociative Experience Scale.

To conclude, those with DID suffer from a dissociation in their mental cognitive process. This causes them to create alters which have their own personality and thought process. Both the diagnosis and treatments have been known to alleviate symptoms with those who have PTSD. This has lead to many stating that DID is a form of developmental PTSD. Various studies have come to support such an idea, using PTSD as a criterion for DID. A few problems were found with this the theory, having doubt if the theory is in fact correct. This paper has concluded that PTSD, although a part of DID, is not completely the same. Rather DID is made up of two components, PTSD and BPD. This allows for understanding on why co-morbidity between DID is high with both PTSD and BPD, as well as explaining why those with DID have a smaller amygdala volume than those found in adults suffering from PTSD.

 

References

American Psychiatric Publishing, & American Psychiatric Association. DSM-5 Task Force. (2013). Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Arlington, VA: American Psychiatric Association.

Bryant, R. A., Moulds, M. L., Guthrie, R. M., & Nixon, R. D. (2005). The additive benefit of hypnosis and cognitive-behavioral therapy in treating acute stress disorder. Journal of Consulting and Clinical Psychology, 73(2), 334-340.

Chlebowski, S. M., & Gregory, R. J. (2012). Three cases of dissociative identity disorder and co-occurring borderline personality disorder treated with dynamic deconstructive psychotherapy. American Journal of Psychotherapy, 66(2), 165-180.

Farrell, H. M. (2011). Dissociative identity disorder: Medicolegal challenges. Journal of the American Academy of Psychiatry and the Law Online, 39(3), 402-406.

Gillig, P. M. (2009). Dissociative identity disorder: A controversial diagnosis. Psychiatry (Edgmont), 6(3), 24-28.

Kihlstrom, J. F. (2005). Dissociative disorders. Annu. Rev. Clin. Psychol., 1, 227-253.

Kim, I., Kim, D., & Jung, H. J. (2016). Dissociative Identity Disorders in Korea: Two Recent Cases. Psychiatry investigation, 13(2), 250-252.

Loewenstein, R. J. (2005). Psychopharmacologic treatments for dissociative identity disorder. Psychiatric Annals, 35(8), 666-673.

Maiese, M. (2016). Dissociative Identity Disorder, Ambivalence, and Responsibility. Philosophical Explorations,19(3), 223-237.

McEwen, B. S., Bowles, N. P., Gray, J. D., Hill, M. N., Hunter, R. G., Karatsoreos, I. N., & Nasca, C. (2015). Mechanisms of stress in the brain. Nature Neuroscience, 18(10), 1353.

Nijenhuis, E., van der Hart, O., & Steele, K. (2010). Trauma-related structural dissociation of the personality. Activitas Nervosa Superior, 52(1), 1-23

Putnam, F. W., & Loewenstein, R. J. (1993). Treatment of multiple personality disorder: a survey of current practices. The American journal of psychiatry, 150(7), 1048-1052.

Sapolsky, R. M. (2003). Stress and plasticity in the limbic system. Neurochemical Research, 28(11), 1735-1742.

Soibelman, A. (2017). The correlation between stress and the development of Dissociative Identity Disorder. The Science Journal, Lander College of Arts & Science, 6(1), 56-62.

Vermetten, E. (2006). Hippocampal and Amygdalar Volumes in Dissociative Identity Disorder. American Journal of Psychiatry,163(4), 630-636.

Vissia, E. M., Giesen, M. E., Chalavi, S., Nijenhuis, E. R., Draijer, N., Brand, B. L., & Reinders, A. A. (2016). Is it Trauma‐or Fantasy‐based? Comparing dissociative identity disorder, post‐traumatic stress disorder, simulators, and controls. Acta Psychiatrica Scandinavica, 134(2), 111-128.

Abstract

Understanding Dissociative Identity Disorder

And Its Relation to Other Disorders.

In its purest definition, Dissociative Identity Disorder (DID) is a separation of normal mental functions in one’s self (Farrell,2011). Suspected to affect 2% of the population, DID has an array of symptoms including a loss of memory and personal information, depersonalization, derealization, hypnotic trances, hallucinatory passive voices, and most exclusively personality alters. (Vermetten, Schmahl, Lindner, Loewenstein, and Bremner, 2006). These alters are known to have the abilities such as speaking in different accents, having different writing styles and in some very rare cases having allergies other alters don’t have. Additionally, alters may also differ in gender and age, leaving many wonderings if the inflicted are actually multiple persons stuck in a single body. This ideology is known as the Multiple Selves Thesis (MST). This theory takes form in many different arguments, but the basic idea is the same: because they have multiple different personalities, they are multiple different people. Besides the ethical implication involved, many questions are not answered using this theory. Maiese (2016) understands such a theory to be incorrect, proving because of semantical memory, consistent characteristic functions, and shared knowledge between alters, that all alters are in fact a single person decompartmentalizing metal states. This conclusion is commonly agreed upon one among researchers.  

  Diagnosis for DID is done by a licensed psychologist. According to the DSM-V (American Psychiatric Publishing, & American Psychiatric Association, 2013) criteria, the psychologist must (a) identify of two or more alters, (b) two of which are reoccurring, (c) find that patients are missing memories not only of traumatic events, and (d) asses that disturbance is not due to physiological effects. Similar to most psycho-determining checklist, this criterion is usually used as an affirmation on other tests. Such being the multidisciplinary and multi-technique approach which evaluates verbal and nonverbal cues during questioning, self-reported questionnaires by the patient, The Dissociative Experience Scale (DES), and The Structured Clinical Interview for DSM-IV Dissociative Disorder (SCID-D) (Farrell, 2011). When conducting such tests, the administrator should be aware of exaggeration that might occur during the examination, along with other biases which can hinder the results.

Besides for psychological examinations, Vermetten et al. (2006) found by way of brain imaging it is also possible to make a diagnose for DID. Inspired by finding of smaller amygdala and hippocampus volumes in young children with post-traumatic stress disorder (PTSD) and those with borderline personality disorder (BPD), the study seeks to find the same correlation with DID. It reports that those with confirmed DID based on SCID-D and the DSM-IV criteria have significantly smaller volume in hippocampus and amygdala than those in a healthy patient. This conclusion implies that MRI scans may also be used to diagnose patients with DID.

In Sapolsky (2003) it was shown as a result of the stress, the brain of one with DID goes through Glucocorticoids- a steroid produced in the zona fasciculata- is released in the brain. Nijenhuis and Steele (2010) found that animals who are injected with a large dose of Glucocorticoids have by virtue decreased size in the hippocampus. Such an explanation can be applied to those with DID, using the Glucocorticoids as the reason those with DID have smaller hippocampus volume. (Soibelman, 2017)  

 When discussing treatments Putman & Loewenstein (1993) collected surveys from 305 clinicians. The survey found that most therapists use a long-term psychotherapy hypnosis. Reportedly, this was done twice a week. Other forms used include art therapy, family therapy, and behavioral modification therapy.

  With regards to medication, Loewenstein (2005) found that medications can help alleviate agitation, anxiety, comorbid sleep disorders, and comorbid PTSD. Although not many studies were done on the exact effects, with proper monitoring and understanding of patient, medication will do more good than harm. A few cautionary problems which psychiatrist should look for is any sabotaging of the medical trial. Usually among the alters, one or more might have a phobia of medications. This is important to note before the medical trial, for during the trial the phobic alter will likely misuse the medications or report false symptoms to stop the trial completely. The best way of noting such a phobic alter would be by the consultation and permission stage. When asking the host if the medication trial would be permitted, the psychiatrist should ask the patient if any alters have a problem with the prescription.

With no specific gene predisposition, psychologists look for a connection between those that develop DID and those that don’t. Two models try to explain the phenomena. The commonly used states that trauma causes the DID, thus explaining the outstanding comorbid rate DID patients have with PTSD. While the other explains that those with DID are more prone to fantasy and suggestibility. Although the second model would explain why it isn’t so that all children who experience trauma are diagnosed with DID, when closely examined it falls short. When studying the suggestibility of those with DID and a healthy control group, the researchers found no significant difference between the two. (Vissia et al., 2016).

Because of the yearly decrease in male’s hippocampus size, those with DID are more commonly male than female (Vermetten et al., 2006). Also, a predisposition to having any sort of mood disorders is having an excessive amount of glucocorticoid being produced in the brain. For cases like those antidepressant drugs are recommended to be used (McEwen et al., 2015)

PTSD similarly is categorized as a dissociative disorder by the current DSM definition. It is thought to be the brain's inability to cope with a traumatic event that occurred to the patient. Patients with PTSD are thought be have symptoms like depersonalization, derealization, nightmares, avoidance behavior, loss of memory, and hypervigilance (American Psychiatric Publishing, & American Psychiatric Association, 2013).

Diagnosis is done using structured interviews, a criteria checklist, and self-reported questionnaire. Besides for clinical testing, Vermetten et al. (2006) cited a study that found a significant difference in the hippocampus and amygdala volume with those who had PTSD in early developmental years.

In regards to treatments, PTSD has been shown to have better results alleviating symptoms with a hypnotic therapeutic approach (Bryant, Moulds, Guthrie, & Nixon, 2005). Medical SSRIs have also been used for those suffering from PTSD. (Lowenstein, 2005).

Calling DID a type of developed PTSD for those who had the traumatic event in their early developmental years, is a logical conclusion. With its similar symptoms, tools of diagnosis, and even treatments, such a conclusion is well founded. And although most scientists agree, many issues have come up, making the once undoubtedly theory questionable. The concerns are as follows.

The first concern is the difference in volume of the brain’s hippocampus and amygdala. As written before, Vermetten et al. (2006) found that those with DID have smaller hippocampus and amygdala than those of a healthy person. If one wishes to say that both of these illnesses are identical, then it would be assumed that the brain that has said illnesses are equal. But when researched it was found that those with DID have hippocampus’s 19.2% smaller than average, while those with PTSD have no significant difference in their hippocampus size than those with a healthy brain (cited by Vermetten et al., 2006).

Many in the field of research disagree that this is a question at all. Seeing that the brain is formed when young, the brain of those with DID are likely to form smaller hippocampus and amygdala, while those who encountered the trauma later on with already formed hippocampus and amygdala size, would not be affected. Vermetten et al. (2006) also cited an earlier study that supports such an answer. The study claims to find in those with PTSD in early development to have 15% smaller amygdala volumes than those of an average brain.

Stating that those with smaller hippocampus and amygdala must have had an early exposure to trauma is still difficult. Vermetten et al. (2006) also cited studies on those with BPD. While each study brought different percentages, they all agreed that those with BPD have smaller hippocampus and amygdala volumes than those in healthy brains. While it is true that those who had BPD had a larger percentage of a discrepancy to those with healthy brains, nevertheless the outcome proves that those with a developed brain can also have a smaller hippocampus and amygdala volume.

The second issue with such a comparison is based on a study done in Asia about DID. The study was driven by the question of why there were so few cases of DID reported in Asia. It collected the two cases in Korea of young adults who developed DID (Kim, Kim, & Jung, 2016). If DID is simply PTSD in younger children, why is it not as common in Asia?

The third and last problem with such a comparison is the co-morbidity with BPD. Horevitz and Braun, (cited by Gillig, 2009) found that 70% of those with DID meet the criteria for BPD. Although the same can be said with PTSD, having Vermetten et al. (2006) state the co-morbid rate for those with DID having PTSD is 80-100%, the question of why BPD is so highly attached to DID still should be entertained. Horevitz and Braun discovery allowed Coons et al. (cited by Gillig, 2009) to conclude that those with DID are suffering from an extreme case of BPD.

This collective study would like to bring a solution to all of these problems. As of this far, all research topics only mentioned either PTSD or BPD as a possible cause for DID. But in truth, maybe both are need to allow such a condition to exist. This theory allows all three questions to be resolved.

First, by stating that the smaller hippocampus and amygdala are caused by the BPD part of the disease. This explains why those with BPD have smaller hippocampus and amygdala, even if the illness developed after childhood. It also explains why those with PTSD as adults don’t have a discrepancy in their hippocampus and amygdala size.

Although some might wonder why those with PTSD as children have smaller amygdala levels, this theory would not dispute that childhood harshens the ability of the brain to correctly form.

The second issue is answered as well. Although BPD and PTSD are both found in Asia, because both are present in DID, many doctors might diagnose the illness incorrectly, mistakenly thinking it is either BPD or PTSD (Kim, Kim, & Jung, 2016).

Lastly, the third question is obviously answered. BPD has a 70% co-morbidity with DID because DID is essentially made up of both BPD and PTSD. It too explains why PTSD had such a high reported comorbid rate with DID.

Such a theory can also be affirmed by Chlebowski and Gregory (2012), who found DID patients using Dynamic Deconstructive Psychotherapy (DDP), a therapy developed for those with BPD, had a 34%-79% reduction in their Dissociative Experience Scale.

To conclude, those with DID suffer from a dissociation in their mental cognitive process. This causes them to create alters which have their own personality and thought process. Both the diagnosis and treatments have been known to alleviate symptoms with those who have PTSD. This has lead to many stating that DID is a form of developmental PTSD. Various studies have come to support such an idea, using PTSD as a criterion for DID. A few problems were found with this the theory, having doubt if the theory is in fact correct. This paper has concluded that PTSD, although a part of DID, is not completely the same. Rather DID is made up of two components, PTSD and BPD. This allows for understanding on why co-morbidity between DID is high with both PTSD and BPD, as well as explaining why those with DID have a smaller amygdala volume than those found in adults suffering from PTSD.

 

References

American Psychiatric Publishing, & American Psychiatric Association. DSM-5 Task Force. (2013). Diagnostic and statistical manual of mental disorders: DSM-5 (5th ed.). Arlington, VA: American Psychiatric Association.

Bryant, R. A., Moulds, M. L., Guthrie, R. M., & Nixon, R. D. (2005). The additive benefit of hypnosis and cognitive-behavioral therapy in treating acute stress disorder. Journal of Consulting and Clinical Psychology, 73(2), 334-340.

Chlebowski, S. M., & Gregory, R. J. (2012). Three cases of dissociative identity disorder and co-occurring borderline personality disorder treated with dynamic deconstructive psychotherapy. American Journal of Psychotherapy, 66(2), 165-180.

Farrell, H. M. (2011). Dissociative identity disorder: Medicolegal challenges. Journal of the American Academy of Psychiatry and the Law Online, 39(3), 402-406.

Gillig, P. M. (2009). Dissociative identity disorder: A controversial diagnosis. Psychiatry (Edgmont), 6(3), 24-28.

Kihlstrom, J. F. (2005). Dissociative disorders. Annu. Rev. Clin. Psychol., 1, 227-253.

Kim, I., Kim, D., & Jung, H. J. (2016). Dissociative Identity Disorders in Korea: Two Recent Cases. Psychiatry investigation, 13(2), 250-252.

Loewenstein, R. J. (2005). Psychopharmacologic treatments for dissociative identity disorder. Psychiatric Annals, 35(8), 666-673.

Maiese, M. (2016). Dissociative Identity Disorder, Ambivalence, and Responsibility. Philosophical Explorations,19(3), 223-237.

McEwen, B. S., Bowles, N. P., Gray, J. D., Hill, M. N., Hunter, R. G., Karatsoreos, I. N., & Nasca, C. (2015). Mechanisms of stress in the brain. Nature Neuroscience, 18(10), 1353.

Nijenhuis, E., van der Hart, O., & Steele, K. (2010). Trauma-related structural dissociation of the personality. Activitas Nervosa Superior, 52(1), 1-23

Putnam, F. W., & Loewenstein, R. J. (1993). Treatment of multiple personality disorder: a survey of current practices. The American journal of psychiatry, 150(7), 1048-1052.

Sapolsky, R. M. (2003). Stress and plasticity in the limbic system. Neurochemical Research, 28(11), 1735-1742.

Soibelman, A. (2017). The correlation between stress and the development of Dissociative Identity Disorder. The Science Journal, Lander College of Arts & Science, 6(1), 56-62.

Vermetten, E. (2006). Hippocampal and Amygdalar Volumes in Dissociative Identity Disorder. American Journal of Psychiatry,163(4), 630-636.

Vissia, E. M., Giesen, M. E., Chalavi, S., Nijenhuis, E. R., Draijer, N., Brand, B. L., & Reinders, A. A. (2016). Is it Trauma‐or Fantasy‐based? Comparing dissociative identity disorder, post‐traumatic stress disorder, simulators, and controls. Acta Psychiatrica Scandinavica, 134(2), 111-128.