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dcyphr | Dissociation in Children and Adolescents as Reaction to Trauma--An Overview of Conceptual Issues and Neurobiological Factors

Abstract

Trauma is a known causal factor for dissociation (i.e., depersonalization). This overview updates the conception of dissociation as well as neurobiological findings. Research has illustrated neurochemical and structural and functional abnormalities of the brain resulting from trauma, especially childhood interpersonal trauma (i.e., sexual abuse). The authors begin to shed light on the neural underpinnings of dissociation present in childhood PTSD, somatoform disorder, and dissociative (or conversion) disorders. Dissociative symptoms among children and adolescents may thus be seen as complex developmental disorders prompted by environmental factors. 


Introduction 

Dissociation in the context of psychological disorders can be expressed as disturbances in memory, consciousness, and/or identity as well as disruptions in bodily sensations and feeling (i.e., feeling numb). The prevalence of dissociative symptoms is not well understood, but studies point to a range of 19-73%% among sexually abused or maltreated children. Child psychiatry has often misdiagnosed or been unaware of dissociative symptoms among children, resulting in disastrous implications for treatment. This unawareness or ignorance of dissociation can be attributed in part to Freudian psychoanalytic theory, which was repurposed to consider childhood trauma described by patients as imagined or desired, denying the alarming frequency of childhood interpersonal trauma. 


Interest in the importance of trauma was prompted in the 1970s after studies about the sufferings of veterans of World War II and the Vietnam War and concentration camp survivors came out. Also, active women’s movements that published works pointing to the occurrence of childhood sexual abuse helped push back psychoanalytic ideas of trauma being fantasies. Push back against dissociation, especially in debates surrounding multiple personality disorder (now known as dissociative identity disorder), involved memories of trauma being characterized as fake or imagined, perpetuated and reinforced by clinicians. New, more reliable and valid diagnostic instruments and neurobiological technologies have helped reinforce dissociative symptoms as resulting from severe trauma. 


Methods

Using a literature search on PubMed and PsychInfo, 309 relevant papers were rigorously studied. 


Concepts and terminology in the literature search

From a dimensional perspective, dissociation can manifest on the spectrum from the normative end of everyday daydreaming to the pathological end of depersonalization. Dissociation is a reaction to trauma, which is inherently overwhelming for both the mind and body. Thus, its defence functions to automatize behavior, compartmentalize painful memories or emotions, and/or alienate (or distance) oneself from the self (of the trauma). Dissociation protects the individual from trauma and can manifest as massive denial, identification with an (or the) aggressor, and numbing among. Dissociation can be delineated from repression in that repression involves enough processing of the repressed material (including its associated taboos), whereas completely averts any consideration of the trauma. From a categorical perspective, dissociation can only manifest as psychological symptoms (i.e., amnesia, derealization). Physical or somatoform symptoms (i.e., sensory loss) of dissociation are categorized under “conversion disorders”. 


Memory can broadly be categorized as implicit (non-declarative, procedural) or explicit (declarative, semantic) memory. Implicit memory involves the amygdala, basal ganglia, motor cortex, and sensory cortex. It can be seen as memory without conscious access (i.e., riding a bicycle, acquired habits). Explicit memory involves the hippocampus, parts of the medial temporal lobe, and the prefrontal cortex. It can be divided into episodic and semantic. Episodic (or autobiographical) memory refers to episodes in an individual’s life that s/he can recall and describe with a sense of self and time. It is mediated by the orbito-frontal cortex and related parts of the prefrontal cortex. Semantic memory refers to facts and other information one can recall. Implicit memory, in relation to trauma, is highly resistant to decay, and explicit memory is affected by traumatic events that result in disjointed recall. Van der Kolk proposes that the central nervous system fails to synthesize sensations related to the traumatic event into an integrated explicit memory, resulting in trauma-related sensations continuing to intrude after the traumatic event has passed. 


The criteria for dissociative (conversion) disorders used in this study involves severe impairment in memory, sense of self, immediate sensations, and control of bodily movements.


Results

Of the 932 articles from PubMed and 87 from PsychInfo, 237 described correlates of trauma and 72 the neurobiological correlates of dissociative disorders.


Traumatic correlates

Most research linking dissociation with traumatic events, address the strong association between early, chronic abuse, especially sexual abuse, and substantial dissociative symptoms. Some researchers argue that there is not enough evidence to suggest causality between early traumatic events and dissociative symptoms. Findings imply that there is likely a combination of genetic, neurological (i.e., post-concussion syndrome), and psychological vulnerability (i.e., tendency to self-blame) that lead to dissociation in the context of experiencing trauma. The most important predisposing factor to dissociative symptoms is early childhood traumatization. 


Neurobiological correlates

The human brain is equipped with a stress-response system. This system involves the activation of the hypothalamic-pituitary-adrenal (HPA) axis, which broadly results in the fight-flight-freeze response from the release of epinephrine, norepinephrine, and cortisol. Brain endorphins are also released, affecting the way the stressful event is perceived. This may explain the physical and emotional sensations that accompany response to stress. High levels of cortisol are toxic for the brain, especially early in life. Impairments in memory and synaptic connections (i.e., early neuronal degeneration) are implicated here. Secure attachment with a primary caregiver (i.e., support and comfort from a parent) acts to cushion the neurotoxic effects of cortisol in infants and children. 


Effects of trauma on the developing brain

Severe neglect, seeing violence between parents, emotional and physical abuse during childhood are powerful sources of prolonged stress-response that can result in subsequent permanent neurochemical abnormalities as well as functional and structural abnormalities. 


Neurochemical abnormalities

Severe childhood trauma can result in a permanently altered HPA-axis response in which the hypothalamus down-regulates the stress response, resulting in lowered cortisol levels in response to stress. New threats or dangerous situations no longer evoke a normal response. 

Traumatized children can have an overactive sympathetic nervous system from continued stress responses. This is indicated by high secretion of dopamine and norepinephrine in combination with decreased platelet adrenergic receptors and increased resting heart rate. Hyperarousal and hypersensitivity to stress and reminders of trauma result. 

   Children can dissociate and essentially “shut down” in response to a traumatic experience in which there is no escape. The vagus nerve gets activated by circulating norepinephrine, resulting in slowed heart rate and falling blood pressure. Brain endorphins from the dopamine system in the prefrontal cortex may be released as well. 


Functional abnormalities

EEG studies involving recall of traumatic events reveal the left and right hemispheres function independently:

  • There is striking hemispheric lateralization (brain functions specific to one side). Traumatic memories may be stored in the right hemisphere and expressed as nonverbal emotional experiences. There is increased activity in areas of emotional arousal. Dissociative patients may re-experience traumatic memories as physical and visual rather than verbal (Broca’s area is turned off). The limbic system is dysfunctional in traumatized children, with decreased activity in the left prefrontal cortex. This helps explain why traumatized children may function emotionally (increased right hemisphere activity) rather than in a problem-solving manner (decreased left hemisphere activity). 


Structural abnormalities

Elevated cortisol secretion may be implicated in reported reductions of brain size among traumatized children:

  • There is reduced total cerebellar volume and corpus callosum size that are correlated with the duration and age of trauma. There are mixed results about trauma resulting in reduced hippocampal volume, so further research is needed. Reduced corpus callosum size is implicated in reported depersonalization and derealization as children are not able to function in a problem-solving manner. 


Dysfunctions in the developing limbic and neocortical systems 

Dissociation from trauma may be the result of over-stimulation of the limbic and neocortical systems, which are the last parts of the brain to mature and thus are especially vulnerable to the effects of trauma. 

  • Overstimulation of the amygdala can result in hyperarousal and poor behavioral control of anxiety, aggression, impulsivity, and sexual behavior. The neurotoxicity of cortisol (producing cell death) in the context of the hippocampus may lead to amnesia and dissociative symptoms. A reduced hippocampus can also result in misinterpretation of stimuli and hypersensitivity to threats. It may also contribute to the fragmentation of experience into an incoherent isolation of sensory information (i.e., sounds, bodily sensations). Altering the maturation of the prefrontal cortex can result in an inability to gain full adult capacities (i.e., in the dimensions of planning, judgement, and impulse control).      


Conclusions 

There is a high proportion of dissociative symptoms among patients of child and adolescent psychiatry. Many of them have been misdiagnosed with ADHD and bipolar affective disorder, among others, leading to mistreatment and long-term suffering. Recent innovations in brain-imaging technologies have allowed for a bridging between developmental psychology and neurobiology. The central nervous system, HPA-axis, and many other brian regions are implicated in dissociation and the relationship it has with childhood trauma. Cortisol neurotoxicity offers only one explanation for some of this relationship. The study of neurobiological correlates with dissociation is still preliminary, and as most research relies on adults, more research among child populations is necessary for a better understanding of dissociation. It is worth noting that trauma is necessary for a diagnosis of a dissociative disorder, but not all traumas result in dissociation. Protective factors in children and other vulnerabilities (i.e., genetic) for dissociation in the context of trauma should be researched.