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Kayton Sanchez

Neurobiology Behind Emotional Trauma


    Structural, functional, and neurochemical development in the brain during adolescence is slow and focused. Significant developmentally-based changes are concentrated on strengthening neural connections and advancing emotional regulation, risk-reward assessment, problem solving, and planning. Communication between emotional and thinking centers becomes efficient to provide a greater capacity of thinking before acting and provide multiple solutions to emotionally-charged situations. This period of development, however, is also vulnerable to the emergence of mental health disorders as well as intensifying childhood emotional and behavioral issues. Children subjected to physical or emotional abuse, including moderate psychosocial stress, and neglect have deregulated developing neurobiological systems and reduced resistance to stressors. In fact, meta-analysis has revealed structural brain abnormalities associated with emotional trauma with overall global brain volume reductions. 


    Physically and emotionally exhausting psychological trauma is a type of prolonged traumatic stress that alters brain circuitry, particularly the stress response system. The development stage, the severity of the trauma, and the involvement of interpersonal interactions are important psychological trauma risk factors. Emotional trauma, particularly childhood traumatic experiences, poses a significant risk factor for the development of serious mental illnesses in the future, such as major depression, and it is highly comorbid with mood and anxiety disorders. Emotional trauma has serious implications on a brain’s executive functionality resulting in development of falsifications, distortions, and deregulations of cognitive functions. Children who have experienced abuse become hyper-vigilant to potential dangers, have trouble controlling their emotions, and have trouble enduring negative emotions or experiencing positive ones. Early abuse and neglect disrupt a child's developing nervous system by lowering its capacity to cope with stressful situations, which exacerbates emotional dysregulation. Cases of posttraumatic stress disorder (PTSD), an anxiety and memory disorder characterized by a person's inability to integrate the traumatic event into consciousness, can be found in environments that place them at increased risk of adversity into adulthood. PTSD manifests with systems of hyperarousal, intrusive memorial recollections, nightmares, and somatosensory flashbacks.


The qualities of a functioning “integrated brain” include: body awareness, ability to attune to others, balanced emotions, ability to calm fears and pause before acting, capability of insight and reflection, and the capacity to feel morality, fairness, and the common good. All of these functions are compromised by emotional trauma. The limbic system, which is located in the midbrain, helps the brain perceive danger. The limbic system signals the adrenal glands to release stress hormones and serves as an internal alarm system. These hormones sharpen the senses for quick responses and boost blood flow to the major muscles, but in the event of persistent stress or trauma, the limbic system remains on alert. The prefrontal cortex, considered the thinking or reasoning part of the brain, finds difficulty in calming the limbic system. Depression and pessimism cause people to dwell on their painful pasts, which in turn keeps the hyperarousal of the limbic system. Stress hormones are no longer needed after becoming chronically activated from trauma and become toxic to the brain, interfering with the ability to learn and explicit memory. 


Neuroimaging studies of PTSD patients have found hypoactivity in the frontal lobe, anterior cingulate, and thalamic areas, which all indicate the disorder’s impact on executive function, attention, memory, and somatosensory integration. The right amygdale, orbitofrontal cortex, and anterior cingulate gyrus all activate during the narration of a traumatic event. The medial and anterior temporal cortex, which are linked to the physical effects of negative emotions, as well as the anterior insula, which is connected to negative emotions, all become active as well. Repeated emotional stresses result in dendritic retraction in the hippocampus, increased synapse development in the basolateral amygdala, and anxiety-like behavior in response to certain triggers. Damage to the hippocampus's ability to encode cognitive and autobiographical memory can interfere with neural circuits that fragment stress in ways that lead to dissociation. Additionally, the sympathetic nervous system's activity following trauma causes anger or fear, along with related aggressive behavior and cognitive processing.  It may also lead to dissociate detachment response as it focuses more on emotional numbing and intense derealization, depersonalization, and interpersonal passivity that may be manifestations of parasympathetic nervous system activity.



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