Neuropsychological Factors

Psychological Causes

One common psychological factor leading to Dissociative Identity Disorder is when one experiences overwhelming childhood experiences, usually severe abuse or trauma as a child.

How does childhood trauma/ abuse lead to dissociation?

Research has found a strong association between DID and childhood trauma/ abuse where dissociation is used as a defense mechanism to cope with the overwhelmingly intense emotions during the traumatic experience. When a child experiences a form of traumatic experience, he/ she detaches oneself from what is happening to the extent that it may seem more like a movie or a show rather than reality. Alters or various personalities then arise from the roles the child took on during his/ her dissociation episodes (Gleaves, 1996).

Some reported forms of childhood trauma include:

(Coons et al., 1988; Kluft, 1984; Putnam, 1989; Ross, Norton, & Wozney, 1989 as cited in Gleaves, 1996)

•       Physical abuse, sexual abuse (Abuse can be severe, brutal and for extensive periods of time)
•        Neglect
•        Abandonment
•        Wartime experiences
•        Witnessing parent/sibling being killed
•        Near-death experiences
•        Painful medical procedures

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Neurological Causes

In this section, we will be exploring the various neurological factors related to brain activity which contribute or are found to be different in people who have DID. This is divided into 3 sections:

A. Memory

B. Chronic Stress

C. Bio-structural differences

A. Memory

Compartmentalisation of memory in people with DID

Research has found that biological reasons may also play a part in abused children developing DID. Studies show that when an extremely traumatic experience occurs, chemicals in the brain may be released in excessive amounts. This influences the part of the brain which is accountable for memory to store the memory into separate compartments (Science Encyclopedia, 2012).

This is supported by a study by Nissen et al (as cited in Gillig, 2009), conducted on subjects who were diagnosed with DID. It was found that the degree of compartmentalisation was based on the extent to which the information was interpreted and stored in ways that had a unique meaning to the alternative personality. Furthermore, depending on an individual’s brain chemistry, some people are able to better dissociate than others (Science Encyclopedia, 2012).

Encoding of traumatic experiences in memory

Memories of traumatic experiences are encoded in a unique way in people with DID. Pierre Janet (n.d.) suggested that the emotional impact of the trauma prevents the victim from translating the experience into the words and symbols necessary for storage in the semantic memory. Instead, the experience gets stored in a sensory form which makes it easier for lucid and clear  recall of the event (Kaplan, 2008).

Studies of images of brain activity when stimulated by memories of traumatic events show reduced activity in the Broca’s area (the part of the brain which is highly related to translation of experiences into words) and increased activity in the right hemisphere of the brain (parts which are responsible for processing emotional and visual stimulus) (Rauch et al., 1995, as cited in Kaplan, 2008). Thus, a person with DID stores these emotional and visual symbols of the traumatic events in a whole separate identity that is as underdeveloped as the traumatic memories themselves. When recalled, memories are subject to distortion because they are recalled in a different context (Kaplan 2008).

       

Memory and brain activity when personality is triggered

Generally, while physiological stimulus can trigger memories related to a traumatic event, these trauma-related memories may also lead to physiological arousal. This phenomenon might explain why the presence of a stimulus triggering a traumatic memory may cause a switching of personality. The memory may produce a stress reaction which would eventually bring about a different physiological state. Given that different personality states may have different physiologies and functioning, it may be possible that a specific physiological state corresponds with a specific personality state (Kaplan, 2008).

The reason why personality states differ in their physiological profile can be explained by an article from New Scientist (Adler, 1999) which studied the functional magnetic resonance imaging (fMRI) of a patient with DID conducted by Tsai, Condie, Wu, and Chang (1999). In the study, one DID patient was guided into switching from her adult personality, Marnie, into her 8-year-old child personality state, Guardian while fMRIs of the brain were recorded. The images showed that when Marnie was in control, hippocampal activity was relatively normal, but as she switched to Guardian, hippocampal activity decreased (the hippocampus is partly responsible for memory) (Merckelbach, Devilly, & Rassin, 2002).

This implies that when an individual with DID switches personality states, hippocampal activity in the brain may decrease, resulting in lesser memory storage of the situation they are in. Research also shows that memory retrieval is dependent on the state of one’s personality (Kaplan, 2008). This then links back to the notion that different personalities states take on specific physiological states. Therefore, not all personalities remember the same information.

MRI scan indicating the location 

of the Hippocampus in the brain


B. Chronic Stress

Researchers have yet to find clear evidence that links biological factors with dissociative identity disorder (DID). However, many researchers have hypothesized that chronic stress is one factor that triggers DID in a person. Bio-structural differences of the brain of DID patients have also been studied in efforts to explain the disorder biologically.

In the following paragraphs, the biology of stress (processes that occur in the brain under stress) and bio-structural differences of the brain in relation to DID will be explained.

How the Biological Process of Stress can Contribute to Triggering DID


Kaplan (2008) wrote an article on the effects stress and chronic stress has on a person, that may trigger DID. When experiencing extreme stress, certain substances are released. These include:

• Endogenous, stress-responsive neurohormones
• Cortisol

• Norepinephrine & Epinephrine

• Vasopressin

• Oxytocin

• Endogenous opioids

The release of these substances stimulate the release of glucose and trigger the immune system, allowing a person to deal effectively with stress.

However, chronic stress (repeated exposure to stress such as repeated sexual abuse) decreases the immune system’s effectiveness. Since people with DID are thought to have undergone intense psychological trauma, the repeated exposure to stress could have decreased their system’s effectiveness, making them deal with stress ineffectively.

Researchers have hypothesized that when the immune system is overloaded, there will be a malfunction in the negative feedback loop.

How does the negative feedback loop work on a normal basis?

On a normal basis, the negative feedback loop is a system that is in charge of self-regulation where “increased output from the system inhibits future production by the system” (Boskey, 2009). 

For example, if there is a high amount of hormone X in the system, it will stop itself from producing any more of that particular hormone in an effort to regulate. Thus, the negative feedback loop controls the level of production by halting manufacturing of the hormone, in the event that hormone levels get too high.

What happens when the negative feedback loop malfunctions?

However, when the negative feedback loop malfunctions due to a system overload, the system operates in positive feedback mode, where the increase in the amount of hormones leads to an even higher production of the hormone.

This results in an unbalanced system that fails to achieve regulation, ultimately causing desensitisation of the system and making a person react very intensely to stress in the presence of the smallest trigger.

The desensitization of the system also aggravates the dissociative process.  The more frequent the abuse, the more their system gets overloaded, causing the system to become more desensitised and the person more dissociated.

Thus, after a while, the coping method of dissociation gets embedded in a person, resulting in impaired functioning.

C. Bio-Structural Differences

To biologically account for DID, a study by Vermetten, Schmahl, Lindner, Loewenstein and Bremner (2006) has revealed that there is indeed a difference in the volumes of the hippocampus and amygdala. Female patients suffering from DID were found to have a 19.2% smaller hippocampal volume and a 31.6% smaller amygdalar volume than healthy females. Due to this structural difference, patients were said to have a larger hippocampal to amygdalar ratio.

Literature by Durand and Barlow (2010) found that patients of DID are frequently exposed to repeated stressful conditions in their early life. Glucocorticoids are released in response to stress, causing the hippocampus to be affected. Researchers have hypothesised that a lot of contact to glucocorticoids could result in progressive deterioration of the hippocampus.

Thus, this research shows that there may be a link between stress exposure and the small hippocampal volume of patients.

Due to differences in the brain structure, patients with DID were also found to have decreased regional cerebral blood flow (rCBF) in the orbitofrontal cortex regions bilaterally (similar to  in people with attention deficit disorder) and increased flow in the superior frontal regions, median and occipital regions bilaterally (Gillig, 2009).

The difference in blood flow in the brain for people with and without DID might also be an underlying biological factor that contributes to the disorder.










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References

Bosky, E. (2009). Negative Feedback Loop – Menstrual Cycle. Retrieved from http://std.about.com/od/glossary/g/negfeedgloss.htm


Broca’s area picture [Image] (2008). Retrieved from http://editthis.info/psy3242/Broca's_area

Child abuse picture [Image] (2011). Retrieved from http://thequietvoice18.wordpress.com/2011/08/07/child-abuse-and-depression/

Durand, V. M., & Barlow, D. H. (2010). Essentials of abnormal psychology. Wadsworth: Cengage Learning. Retrieved from http://books.google.com.sg/books?id=L7BZTtO5rh8C&pg=PA189&dq=dissociative+identity+disorder&hl=en&sa=X&ei=R4KfT4_xLIPrrQe687XqAQ&ved=0CF4Q6AEwCA#v=onepage&q=dissociative%20identity%20disorder&f=false

Gillig, P. M. (2009). Dissociative identity disorder – A controversial diagnosis. Psychiatry Matrix Medical Communications (Edgmont), 6(3), 24-29. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719457/


Gleaves, D. H. (1996). The sociocognitive model of dissociative identity disorder: A reexamination of the evidence. Psychological Bulletin, 120(1), 42-59. doi: 10.1037/0033-2909.120.1.42

Kaplan, R. (2008, January 9). Dissociative Identity Disorder [Web log message]. Retrieved from http://serendip.brynmawr.edu/exchange/node/1780


Merckelbach, H., Devilly, G. J., & Rassin, E. (2002). Alters in dissociative identity disorder: Metaphors or genuine entities?. Clinical Psychology Review, 22(4), 481-497. Retrieved from http://www.sciencedirect.com/science/article/pii/S0272735801001155

MRI scan indicating hippocampus location picture [Image] (2011). Retrieved from http://en.wikipedia.org/wiki/File:MRI_Location_Hippocampus_up..png

Right brain and left brain picture [Image] (n.d.). Retrieved from http://mc3336.aisites.com/brainSite/right.htm

Science Encyclopedia. (2012). Multiple personality disorder- Causes of multiple personality disorder. Retrieved from http://science.jrank.org/pages/4496/Multiple-Personality-Disorder-Causes-multiple-personality-disorder.html

The hippocampus and the brain picture [Image] (2008). Retrieved from http://www.paulhazel.com/tag/brain/

Vermetten, E., Schmahl, C., Lindner, S., Loewenstein, R. J., & Bremner, J. D. (2006). Hippocampal and amygdalar volumes in dissociative identity disorder. The American Journal Of Psychiatry, 163(4), 630-636. Retrieved from http://ajp.psychiatryonline.org/article.aspx?articleid=96513