This chapter suggests neurobiological mechanisms to account for dissociative symptoms in general and structural dissociation in particular. Peritraumatic dissociation (PD) is associated with the release of endogenous opioids and other anesthetic neurochemicals that alter communication between lower and higher brain structures. MacLean's triune brain model provides a structure for the understanding of emotional functioning and dissociation. The integration of brain functioning both horizontally and vertically at different levels of the brain is at the core of information processing. The thalamus also plays a role in cortical oscillations, a phenomenon that has been related to cognitive-temporal binding and information processing, thus affecting cortical connectivity. The corpus callosum is the largest connective pathway in the human brain, constituted of nerve fibers that connect the left and right hemispheres, thus facilitating interhemispheric communication. Disruption of thalamocortical communication is a key component of anesthetic-induced unconsciousness.

This chapter highlights the neurobiology of the whole spectrum of defense responses to threats: near or distant, immediate or potential, physical or social. It focuses on vigilance, fight, flight, freeze, hide, cringe, submit, and avoid behaviors. When survival is threatened by physical injury, death, or social exclusion, the brain has well-established responses, immediate and sequential, to promote safety. These defense responses are based in the emotion-generating regions of the brainstem but are rapidly modified and modulated by the more developed and evolved cortical capacities. The chapter focuses on clinical observations, brain imaging studies in humans, and animal studies of responses to trauma to promote testable conclusions on the likely neurochemical mediators of the key components of posttraumatic stress disorders (PTSD). Chronic characterological changes arising from alterations in self-perception with guilt and shame, self-blame, feelings of ineffectiveness, and loss of trust are part of the long-term damage caused by early trauma.

This chapter describes two of the frequently occurring and important peritraumatic responses, namely, peritraumatic dissociation (PD) and tonic immobility (TI). It focuses on the definition of each phenomenon and their associations with posttraumatic psychopathology as it considers the relevant neurobiology. Dissociative reactions that may occur during trauma exposure include emotional numbing or detachment, reduced awareness, and distortions of reality. The main feature of TI is reversible physical immobility and muscular rigidity, which can last from a few seconds to many hours. Research regarding the basis, function, and mechanisms underlying the TI response has resulted in the acceptance of the fear hypothesis (FH), a multidimensional model of TI. Researchers have also examined the brain structures involved in the expression of TI, and three regions appear to be the most relevant to the induction and inhibition of this phenomenon: the frontal lobes, the limbic system, and the brainstem.

This chapter reviews the disturbances in self-referential processing and social cognition in posttraumatic stress disorder (PTSD) related to early-life trauma. It talks about the neural underpinnings of self-referential processing and examines how they may relate the integrity of the default mode network (DMN). The chapter describes the deficits in social cognition, with a particular focus on theory of mind in PTSD and the neural circuitry underlying direct versus avert eye contact. It then addresses the implications for assessment and treatment. Johnson demonstrated that self-referential processing is associated with the activation of cortical midline structures and therefore overlaps with key areas of the DMN in healthy individuals. Healthy individuals exhibited faster responses to the self-relevance of personal characteristics than to the accuracy of general facts. Less activation of the medial prefrontal cortex (PFC) was observed for the contrast of self-relevance of personal characteristics relative to general facts as compared to controls.

This chapter suggests that multiple animal models are relevant to our understanding of the phenomenology of traumatic dissociation. It includes the literature of learned helplessness (LH), stress-induced analgesia (SIA), as well as tonic immobility (TI). The opioid-mediated stress response is evident in all humans, though the extent and severity of it ultimately determines to what extent structural and pathological dissociation arises. The peritraumatic opioid activation is a probable functional mechanism for the development of phenomena related to pathological dissociation, structural dissociation, and somatoform dissociation. The endogenous opioid system is part of a stress-response mechanism that has its origins in the invertebrate nervous system. Prolonged stress appears to exacerbate the organism’s response to endogenous opioids. Catalepsy is a phenomenon related to immobilization that can be induced by emotional shock. The autonomic nervous system will respond to stress with both sympathetic and parasympathetic activation.

This chapter focuses on the modulatory role of the neuropetides in attachment as well as autonomic regulation, discussing sympathetic and parasympathetic arousal, particularly dorsal vagal and ventral vagal regulation as suggested by polyvagal theory. The probable role of the endogenous opioid system in the modulation of oxytocin and vasopressin release is discussed with a view toward the elicitation of both relational and active defensive responses are reviewed. Porges’ Polyvagal Theory delineates two parasympathetic medullary systems, the ventral and dorsal vagal. Brain circuits involved in the maintenance of affiliative behavior are precisely those most richly endowed with opioid receptors. Avoidant attachment is commonly associated with parental figures that have been rejecting or unavailable and refers to a pattern of attachment where the child avoids contact with the parent. The similarity of severe posttraumatic presentations to autism suggests that the research with regard to social affiliation in autism spectrum.

There is a range of immediate orienting and defense responses available when a threat is perceived, and a separate but overlapping system of vigilance when there is awareness of a potential threat. Vogt, Aston-Jones, and Vogt propose that the reduced anterior cingulate functioning repeatedly demonstrated in posttraumatic stress disorder (PTSD) during emotional tasks facilitates the firing of locus coeruleus (LC) neurons to create a state of hyperarousal. The noncognitive suppression of emotions in young trauma sufferers is based in the areas of the ventral prefrontal cortex (PFC), which has outputs to the defense response and threat evaluation regions of the amygdala, the periaqueductal gray (PAG), and the nucleus accumbens, among others. Deep brain stimulation can be used clinically without activation of a fearful freeze response, so ventral areas of the PAG are also involved in physiological states of relaxation, comfort, and soothing from pain.

A posttraumatic disruption of personal memory in dissociative amnesia has also been linked to underactivity in the right inferolateral prefrontal cortex (PFC), an area described by the authors as strongly interconnected with the amygdala and participating in the retrieval of negatively valenced autobiographical memories. The role of endocannabinoids in stress-induced analgesia (SIA) was confirmed by studies of brief, continuous electric foot shock applied to rats. Many trauma survivors have somatoform features that, by their subjective nature, are difficult to study in animal models. A severe pain etched in the mind/brain through the emotional memory system embodies a compartmentalization, which allows life to continue otherwise as apparently normal. The medically unexplained symptoms are the result of trauma-induced changes in pain and inflammation mediators at diverse parts of the interoceptive loops instantiated at different developmental stages. The memory system for emotionally charged uncompleted sequences of movements overlaps with procedural memory.

Conditioned emotional responses are generated by the actions of the hippocampus and septum on the amygdala, which induces physiological change through its midbrain projections. An emotional response to a social threat involves the appropriate sensory cortices, frontal cortex, hippocampus and septum, midbrain, and hypothalamus. The affective experience of abandonment can be followed by the separation distress sequence of protest and despair or it can initiate shame. Shame recruits circuits formed for hiding from physical danger for avoidant responses to the failure of social belonging. Attachment typically begins in the mother-infant dyad but broadens to promote and reward inclusion in a larger social group as the individual grows. The social attachments, fears of ostracism, and feelings of distress at loss of inclusion have their neurobiological bases in brain systems designed to ensure healthy attachment, learning of emotion regulation, and development of socialized behaviors, from infancy onwards.