Developmental Neurobiology

Research Summaries

The Biological Psychology of Dissociative Identity Disorder Developmental Neurobiology of DID

	THE FOLLOWING IS A SUMMARY OF SOME KEY POINTS FROM: Teicher, Martin H. M.D., Andersen, Susan L. PhD, Polcari, Ann PhD, Anderson, Carl M. PhD, & Navalta, Carryl P. PhD. (2002). Developmental neurobiology of childhood stress and trauma. Psychiatric Clinics of North America, 25, 397-426.

Developmental Neurobiology of Dissociative Identity Disorder

Teicher et al developed a theory of developmental neurobiology to explain the etiology of dissociative identity disorder. Their theory posits a "cascade effect" of childhood abuse and neglect on the developing brain.

Overview of postnatal brain development

Before birth, the human brain develops many more neurons than it needs. These neurons migrate to their appropriate positions, and develop dendrites and axons in order to establish needed connections. Through a program of apoptosis, or "programmed suicide", approximately 50% of these neurons are eliminated before birth. From birth to 5 years old, the brain triples in size, largely due to myelination, which increases speed of information processing.

Critical motor systems develop first, and the maturation process is much slower in the prefrontal cortex, which is responsible for executive functions. During childhood, axons and dendrites proliferate for the purpose of developing synaptic connections, and are "pruned back" during the transition to adulthood to reduce redundancy. The final configuration is determined by cell interactions in the process of gaining new information and developing skills. Because of this process of development, the human brain is shaped by early experiences, and the consequences of childhood abuse may be long lasting and not easily reversed.

The cascade model

Early exposure to stressors activates stress-response systems and changes their molecular organization, altering their sensitivity and response bias.
The developing brain is modified by exposure to stress hormones, changing its myelination, programmed cell death, and genesis of new neurons and synapses.
Different brain regions have different sensitivity, partly due to genetics, gender, timing, rate of development and density of glucocorticoid receptors.
Lasting results of early stress exposure include reduction in left hemisphere development, decreased right/left hemisphere integration, increased limbic system irritability and reduced activity of the cerebellar vermis.
These changes increase vulnerability to neuropsychiatric consequences, including dissociative identity disorder.

Molecular consequences

Three stress-related feedback systems are involved: (1) the hippocampus and the hypothalamic-pituitary-adrenal axis, which regulate cortisol, an important stress hormone; (2) the amygdala, locus coeruleus, adrenal gland and sympathetic nervous system, which produces the noradrenergic and adrenaline stress response, producing a fight-or-flight response; and (3) the vasopressin-oxytocin peptide prohormone group, which cause pituitary gland to release adrenocorticotropin hormone. These systems are "programmed by experience", leading to a net effect of increased fearfulness and anxiety and enhanced hormonal response to stress.

Effects of stress hormones on the developing brain

Corticosteroids have a particularly profound effect on the process of brain development, resulting in behavioral consequences of changes in social behavior, insufficiency of active avoidance learning, and "delays the maturation of auditory-, visual-, and somatosensory-evoked potentials."

Neurobiological effects of early abuse Some studies show a decrease in left hippocampal volume when adults who have experienced childhood trauma have a diagnosis of dissociative identity disorder. Studies also found maternal separation stress increased dopamine and reduced serotonin in the amygdala and nucleus accumbens, increasing vulnerability to EEG abnormalities associated with violent or self-destructive behaviors. Another study found a reduction in amygdala volume correlated with self-reports of depression and irritability.
	Stress hormones also suppress glial cell division critical for myelination. This may lead to decreased size of the corpus collosum and attenuation of hemispheric integration and communication. In one study, adults with no history of abuse showed bilateral involvement in memory of both neutral and traumatic memories, while adults with a childhood trauma history showed activation of the left hemisphere during neutral memories with a marked shift to right hemisphere activation with disturbing memories.
Another study of effects of early exposure to stress hormones showed a decrease in perfusion of the cerebellar vermis in patients with repeated sexual abuse, leading to increased limbic irritability. Studies of glucocorticoid exposure on the development of the prefrontal cortex have found precocial maturation ("parentified child"), possibly arresting development and preventing it from reaching its full adult capacity. Other studies of children with documented histories of abuse have found right hemispheric dominance, even though the children were right handed. The right hemisphere was at the same stage as controls who had no history of abuse, but left hemisphere development was behind. Studies indicate that early abuse changes cortical neuronal development.

Functional effects of early maltreatment

The hippocampus is theorized to be the area of generation of dissociative states, generalized anxiety and panic disorders. Alterations in its development are associated with anxiogenic, dissociative, amnesic and disinhibitory aspects.

Excessive amygdaloid activation by stress hormones has been related to triggering fight-or-flight responses. The amygdala is also involved in formulating and remembering emotional memories.

Temporolimbic EEG abnormalities have been associated with episodic violence in patients with significant histories of childhood deprivation or parental violence. These EEG abnormalities are also correlated with risk of suicidal ideation and attempts.

Imbalances in right-left hemispheric asymmetries in serotonin and dopamine in the amygdala and prefrontal cortex are more correlated with anxiety than actual levels of the neurotransmitters.

DISSOCIATIVE IDENTITY DISORDER Dissociative identity disorder may be a result of an extreme of reduced hemispheric integration. One study indicated that patients diagnosed with DID had a much greater degree of left hemisphere activation. It is theorized that switches between identities may be related to transition to a right hemisphere dominant mode.
Atypical development of the hippocampus may make possible the production of dissociative states, which may be associated with abnormal temporolimbic EEG activity or limbic irritability. In one study, patients diagnosed with DID had 5-10 times the rate of EEG abnormality with paroxysmal spike and sharp waves than that reported in studies of patients with other psychiatric abnormalities.
Source: Teicher, Martin H., MD et al. (2002). Developmental neurobiology of childhood stress and trauma. Psychiatric Clinics of North America, 25, 397-426.

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