Neurobiological and Chemical aspects of Dissociative Identity Disorder
Abstract:
Early childhood chronic stress induces a neurotoxic effect on the anatomy and chemistry of the brain. Elevated glucocorticoids triggers premature apoptosis in regions such as the hippocampus, modifying its functions. Variations in neurotoxicity has been paired with mental illnesses ranging from mood and personality disorders to stress-related disorders. Dissociative identity disorder (D.I.D), formerly known as multiple personalities, has been neglected by prior researchers in investigating neurobiological developmental differences. Examining the structural neurological distinctions in patients who suffer from D.I.D, primarily within the limbic system, may elucidate more effective future treatment plans. Expand, state your hypothesis…
Introduction:
Dissociative identity disorder (D.I.D), remains one of the most controversial dissociative disorder. Depicted by an emergence of amnesia, depersonalization, and compromised sense of self. The criteria listed for diagnosis by the Diagnostic and Statistical Manual of Mental Disorder-IV includes the existence of two or more distinct identities. Due to the inability to integrate a traumatic experiences as a whole, dissociating into an altered identity is used to cope and encompass the events. D.I.D patients “switch” between numerous identities, the original person is considered the “host”. Often times there is an alter referred to as the “protector”, which represents a neuroprotective entity from their surroundings (Gentile et al., 2013). The childlike alter is the age that the patient was at the time of the trauma (Soibelman, 2017). Each identity is portrayed to have its own name, age, gender, race, and physiological characteristics. Individuals who suffer from D.I.D often speak in third person, referring to their identities as different people, rather than alters. Patients must also experience amnesia, which is elucidated as gaps in recalling, not only the traumatic effect, but also everyday events and personal information. Experiences may feel completely foreign to the individual, with a lack of recollection of specific events or memories. Mental illnesses become a diagnoses once symptoms inhibit normal everyday functions, such as when distress, depression and/or anxiety are hyperstimulated. Therefore, D.I.D patients must experiences distress that interferes with their day to day functions. To eliminate any attributes to culture, religion, medical conditions or substance such as intoxications, D.I.D must not be apart of these circumstances. D.I.D is better understood as fragments of a personae that the brain fails to amalgamate.
The prevalence of this disorder is approximately 1% to 3% of the general population and 6% of inner-city outpatient psychiatric population (Foote et al., 2006). An estimated 99% of individuals who develop a dissociative disorder have experienced chronic traumatic events before the age of nine. Traumatic events in early childhood have shown to play an important role in neurological alterations, such as neuroanatomy and the homeostasis of neurological chemicals. For several years, researchers have been investigating the effects childhood traumas have on the development of the brain. As a child represses and attempts to cope with the trauma, if the trauma or the memory remains, it becomes pernicious. Exposure to threatening simulations, triggers the hypothalamic-pituitary-adrenal (HPA) axis.
Hypothalamic-Pituitary-Adrenal axis:
The neuroendocrine system, hypothalamic-pituitary-adrenal (HPA) axis is the stress response system. The hypothalamus controls the release of corticotropin-releasing hormone (CRH) signaling the pituitary gland to make adrenocorticotropic hormone (ACTH), which in turn stimulates the adrenal glands to release glucocorticoids. Glucocorticoids, such as cortisone and cortisol, stimulate the release of neurotransmitter glutamate. Glutamate plays an important role in storing declarative long term memory. The hippocampus is known for storing long term declarative memory of two kinds; episodic which are events and semantic which are facts. Stronger recollection of episodic memories correlate with high levels of glutamate (Thielen et al., 2018). High levels of glutamate are responsible for long term potentiation, which are due to strong signaling processes. When a memory is rarely recalled, the synapses decreases and weaken. Repeated stimulation strengthens synaptic connections causing long term potentiation.
Hippocampal Neurons and Cortisol:
In the hippocampus, glutamatergic neurons release glutamate which binds to its receptors AMPA and NMDA. AMPA is activated when small amounts of glutamate are present, allowing sodium to enter the postsynaptic cell. Whereas NMDA contains magnesium ions in the center of the receptor, a high concentration of glutamate is required to continuously activate AMPA to allow a greater influx of sodium. A higher sodium concentration inside the cell will repel the magnesium ions. In turn activating NMDA allows calcium to enter the postsynaptic cell, which is vital for long term potential induction (Luscher and Malenka 2012). Hippocampal neurons have a great concentration of glucocorticoid receptors, thus being more susceptible to the effects of cortisol. Thus, the HPA axis is regulated via negative feedback by the hippocampus and hypothalamus (Roozendaal et al., 2001). Cortisol binds to receptors on the hippocampus and reduces the length the dendrites. In response, electrical signals diminish, therefore it is unable to inhibit the HPA axis, resulting in the inability to control stress (Kim et al., 2015). Patients with D.I.D often experience amnesia, a result from reducing hippocampal functions, such as the ability to create or recall declarative memories. Removable of hippocampal neuron CA3 has been identified as a causative for diminished memory retrieval. The inability for hippocampal neurons to act as a negative feedback regulator also increases blood cortisol levels (Roozendaal et al., 2001).
Dysregulation of Hypothalamic-Pituitary-Adrenal axis:
The effects of chronic childhood trauma, and elevated stress has been proven to alter neurological regulations. Researchers found that mice injected with CRH in their early life, had a reduced number of hippocampal neurons later in life. (Brunson et al., 2001). Suicide victims with a history of childhood abuse in comparison to suicide victims with no history of child abuse, had increased methylation in hippocampal neurons. Thus, was attributed as a factor to the dysregulation in HPA axis (McGowan et al., 2009). Dysregulation in the HPA also causes hormones, like catecholamines, synergistically works with CRH by enhancing its function. Thus, any minor reminder that triggers a “fight or flight” response, will cause an exaggerated response in the HPA, increasing secretion of cortisol and ACTH (De Bellis and Zisk, 2014). Additionally, as the brain develops, elevated stress leads to a delay in myelination and inhibits neurogenesis by inducing apoptosis (De Bellis et al., 2014; Grogan et al., 2011). The HPA axis becomes extremely sensitive through ceaseless stimulations, increasing cortisol which alters declarative memory (Grogan et al., 2011). Symptoms D.I.D are commonly due to dismantled fragments of a memory, where the misperception of a neutral stimuli as a threatening one can trigger symptoms.
Hippocampus and Amygdala:
The amygdala is anterior to the hippocampus and is the fear response system. Responsible for implicit, sensory and emotion memory, recollection of certain memories are enhanced by an emotion. Chronic stress increases activation in the amygdala stimulating an increase in fear and the recurrence of vivid memories (Kinner et al., 2018). Further studies were done utilizing an MRI to investigate the volumes of both the hippocampus and the amygdala in D.I.D patients. Researchers used 15 female patients with D.I.D and 23 healthy female controls. Results showed that the patients with D.I.D had a 19.2% decrease in the hippocampal volume, and a 31.6% decrease in the amygdala (Vermetten et al., 2006). Post-traumatic stress disorder (PTSD) also commonly occurs due to a traumatic experience that modify neurological functions, such as altering declarative memory (Samuelson, 2011). PTSD and D.I.D patients, often co-morbid, have overlapping symptoms in relation to vivid erratic memories and amnesia. Researchers have also noted that PTSD patients show a decrease in both the hippocampus and the amygdala (Morey et al., 2012; Zhang et al., 2014).
Theory of Structural Dissociation of the Personality:
D.I.D has been thought to be merely an act, or a more intense form of dissociation of PTSD, which is called The Theory of Structural Dissociation of the Personality (TSDP). According to TSDP, dissociation is thought to be classified under two main parts; The Emotional Part (EP) which is present during trauma and the Apparently Normal Part (ANP) which detaches to function daily. Researchers tested if there were any scientific evidence to support this theory. The participants included females with D.I.D and matched healthy female actors, which were the controls. In both parts, EP and ANP, they were shown neural and angry faces, utilizing an fMRI machine to detect any heightened neural activities. The data concluded a difference between DID patients in both parts, and that the female actors were different than the patients with DID. Results showed that brain activity in D.I.D Emotional Part was overactivated and ANP was underactivated. EP showed an increased blood flow in the parahippocampal gyrus, which plays a role in visuospatial memories indicating a fixation on the traumatic memory. PTSD patients have shown a heightened activation in the parahippocampal gyrus when exposed to a stimulus that reminds them of the trauma (Bremner., 2007). EP, D.I.D participants also had greater activation in the precentral gyrus, which is the motor area. Activation in the precentral gyrus could be a defensive response to a stimuli. In contrast, D.I.D, ANP overall decreased activation in the brain is conveyed as a detachment under all circumstances to trauma. EP, D.I.D patients had a slower reaction time to the neutral faces, indicating neutral faces were perceived as threatening (Schlumpf et al., 2013). Likewise, this was also seen another study done with borderline personality disorder participants perceiving neutral faces as menacing (Donegan et al., 2003). Controversial assertions that claim D.I.D patients are actors, has been negated by several studies where the actors failed to successfully mimic both behavioral and neural activity response to a stimulus (Schlumpf et al., 2013;Vermetten et al., 2006).