As a result, the survivor may be unable to process the beginning, middle, and end of an event, which explains why in PTSD the State-Dependent Memory and Triggers State-dependent memory refers to the process in which events encoded in the brain during particular emotional states of mind will be more likely to be recalled if the person is in a similar state of mind in the future (Siegel, 2012). The environment itself can be responsible for triggering the state-dependent memory. The activation of the trauma neurocircuitry responses during state- dependent memory can occur in seemingly neutral or benign situations. This happens when the necessary healthy flexibility of response differentiation is unavailable because the conditions of the original or subsequent trauma trigger the individual in this state-dependent mode. The higher cortical modes of thinking, such as rational thought and self-reflection, are temporarily shut down and replaced by lower limbic modes of reflexive and impulsive response. Because much of traumatic memory is state-dependent, subsequent internal or external triggers that remind the survivor of the original traumatic event can serve to cascade the emotional and behavioral responses. To the survivor, it seems as though they are still experiencing the event, based on the connective neurocircuitry that was laid down when the event occurred. Examples of external triggers include the backfiring of a car engine that elicits the same response in a war veteran as the original sound of a bomb being dropped and the smell of beer on someone’s breath at a party or in a moment of intimacy that brings out the same physiologic or emotional response as the smell of beer on an alcoholic parent’s breath, before and during an assault. Internal triggers may include a particular physical posture or sensation of discomfort in a particular part of the Neuroplasticity Neuroplasticity describes the dynamic ability of the human brain to make and remove synaptic connections and remap itself based on experiences. There are sensitive periods, in early childhood, when the brain is most malleable, but the brain remains plastic throughout life (Gray et al., 2013). On the positive side, neuroplasticity means that the brain has the ability to repair itself. The downside is that neuroplasticity leaves the brain susceptible to remapping in a way that may be counterproductive in the long term (Cicchetti, 2015). Research has also demonstrated that trauma can reduce brain volume by limiting the production of brain-derived neurotrophic factor Psychoneuroimmunology The field of psychoneuroimmunology (PNI) has identified the role of trauma in inflammatory and autoimmune disease. PNI refers to the mind–body connection between the brain and the immune system and the way that psychological suffering (i.e., trauma) can induce deleterious physical consequences (Douthit & Russotti, 2017). Acute stress, such as trauma, initiates the inflammatory response of the immune system, and overactivation of this system is commonly observed in individuals with trauma histories (Bind & Pariante, 2018; Danese & Lewis, 2016). The impact of trauma on the immune system in childhood can lead to a chronic compromised immune system in adulthood (Bind & Pariante, 2018). Trauma can cause a reduction in the number Epigenetics Trauma can affect the individual at the genetic level. Although genes are stable, research has shown that they are not necessarily destiny. Epigenetics refers to chemical modifications that attach to DNA and have the ability to turn genes on or off, affecting their expression but not altering the underlying DNA itself (Binder, 2016). Epigenetic changes occur in response to environmental signals and experiences, such as trauma. Research has shown that traumatic experiences can act to “turn off” genes involved with the stress response system, potentially contributing
survivor senses that the trauma is still ongoing and has not yet ended.
body that implicitly triggers the cascade of neurochemical responses that are reminiscent of the traumatic events. It has been suggested that due to this state-dependent learning, when engaging in treatment, it may be useful to engage in efforts to more closely approximate the state in which the trauma was encoded (Maddox et al., 2019). This again supports the integration of “bottom-up” sensory processing into more traditional “top-down” cognitive and exposure-based interventions to more fully address all aspects of the trauma system. Case Example Alana reported that she began to feel anxiety as a sensation in her chest and gut when she even thought about driving on the highway. If she actually approached a highway, she had a full-blown panic attack and had to pull over, switch seats to let her passenger drive, and close her eyes until the ride was over. This behavioral reaction followed the combination of the external trigger of the highway and the internal trigger of the sensations of a rapid heartbeat and shortness of breath that she had experienced during a serious car accident several years previously. These sensations became exacerbated during a stressful period in her life when she felt chronically overwhelmed. She described this time period as one in which she felt she would “crash and burn. ” Effective trauma treatment will help clients to recognize and then disconnect this neurocircuitry pattern through various methodologies and replace it with present-day responses and associations that are not state-dependent on previous events (van der Kolk, 2014). (BDNF; Notaras et al., 2020). Brain-derived neurotrophic factor is a protein that works to stimulate brain growth by acting as a kind of fertilizer for neuronal production (Russell-Chapin, 2016). Reduced BDNF can also be genetic and increase one’s sensitivity to stress, highlighting the importance of the gene–environment interaction (Notaras et al., 2020). Though trauma can damage the brain, the effects are potentially reversible. Professionals can recommend interventions, such as exercise, that can stimulate the production of BDNF and promote new growth in place of the previous deficits (Gray et al., 2013; Russell-Chapin, 2016). of natural killer cells—a type of cell that regulates cancerous cell production—as well as increased production of C-reactive protein and other proinflammatory cytokines (Bind & Pariante, 2018; Cicchetti et al., 2015) that contribute to dementia, arthritis, and various autoimmune diseases. When treating trauma, professionals should consider PNI-related treatments, such as anti-inflammatory medications or healthy behaviors (e.g., exercise and improvement in diet) that counteract inflammation. Muscatell (2021) proposes that our social experiences play an even larger direct role in immune function than has been considered thus far and suggests social psychoneuroimmunology as an emerging area for further research. to a dysfunctional or dysregulated stress response (Binder, 2016). Thus, trauma can reach down to the core blueprint of human development. Epigenetic changes are, however, flexible and dynamic, suggesting that negative consequences can be reversed with positive inputs, such as therapy (van der Kolk, 2014).
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