The Physiological Response to Trauma and its Implications for Counseling

Trauma is a bit of a buzz word these days, but the real deal is no joke. It’s often defined as an event or events that exceeds our perceived capacity to cope. Although there are vast individual differences in how we respond to #trauma, for those who are adversely impacted, unresolved trauma can profoundly disrupt psychological functioning. It can reorganize one's sense of self, shift our worldview, and cause considerable emotional distress both in the short and long term. It can manifest as intrusive flashbacks and hypervigilance or result in emotional numbing and a lingering sense of unreality. These pervasive psychological effects reflect the fact that when trauma overwhelms our innate defensive response, it fundamentally reorganizes our physiology.[[i], [ii], [iii]] These neurobiological adaptations not only have implications for health and well-being, but also can make counseling those who have experienced trauma particularly challenging. Therefore, a greater understanding of the physiological response to trauma can help to ensure we approach clients appropriately and provide more effective care.

Fight or Flight

What our nervous system flags as a stressor can vary widely, however, once it does, our physiological response to the stressor often follows a fairly set course, regardless of whether it is a physical threat (e.g., a hungry lion) or a psychological or emotional threat. There are two main players involved in the stress response, the #sympathetic branch of the #autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal #HPA-axis. Most bodily functions (heart rate, digestion) are coordinated by the ANS, which is composed of the more excitable sympathetic branch (SNS) and the generally calmer #parasympathetic branch (PNS). At rest, the PNS predominates and oversees restorative activity (e.g., slowing heart rate and facilitating digestion to conserve and replenish energy), but with ebbs and flow in control that allow for flexible responding to current needs. During times of stress, however, the SNS wrests majority control and, along with the HPA-axis, often initiates a variety of responses collectively referred to as “fight or flight”.[[iv]]

This shift to “action mode” is largely coordinated by the #brainstem and #hypothalamus. These highly intertwined regions of the brain continuously receive a wealth of information that can signal the presence of a threat, including input about the condition of our body, our external environment, and our emotional well-being. When a stressor is detected from any of these sources, the hypothalamus does two main things: 1) sends descending signals that shift the balance in ANS activity towards greater sympathetic control and 2) sends signals to the pituitary gland (an #endocrine gland located beneath the brain) that triggers the release of a hormone called adrenocorticotrophic hormone #ACTH into the blood stream.[[v]]

Activation of the SNS prompts the release of the neurotransmitter #norepinephrine from peripheral sympathetic fibers onto target organs (e.g., heart, lungs, smooth muscle) and increases the production and release of #adrenaline from the adrenal glands (an endocrine gland located above the kidneys). Meanwhile, the ACTH released into the blood stream by the pituitary makes its way to a different part of the adrenal glands where it triggers an increase in the production and release of #cortisol, the prototypical stress hormone. Together, the norepinephrine, adrenaline, and cortisol prepare the body for action – increasing heart rate, enhancing lung capacity, activating muscles (increasing blood flow and muscle tone), mobilizing energy stores, and diverting resources away from non-essential functions, like digestion.[[iv]; [vi]]

Stress also profoundly influences the mind. In response to a threat, there is an almost immediate surge in the release of key neurotransmitters in the brain, including norepinephrine, #dopamine, and corticotropin releasing hormone #CRH.[[vi]] Norepinephrine and CRH activity in areas of the brain like the locus coeruleus (arousal) and #amygdala (emotional salience) enhances focus and vigilance while dopamine activity in the ventral striatum (motivation) marks the stressor as important. The activity of these and other transmitters in the prefrontal cortex #PFC (executive functioning) and dorsal striatum (habitual responding) facilitates a shift from more cognitively driven, goal-directed behavior (“I wonder what I should do about that hungry lion?”) to automatic response patterns that allow for rapid action (lion = run!). And an increase in endogenous #opioids provides “stress-induced analgesia,” letting you act, at least temporarily, even in the face of injury. The net effect is to transfer energy and resources to the neural circuits most apt to keep you alive.[[iv]]

A critical feature of the HPA-axis stress response is that it is self-limiting. There is no doubt that it is an essential, protective process that helps us successfully cope with all manner of challenges, but it is also costly. It consumes energy stores and disrupts normal neural, endocrine, #immune, and metabolic functioning.[[viii]] To protect against extended activation, the stress response is a closed negative feedback loop - the cortisol produced in the adrenal glands in response to the ACTH ultimately travels back to the brain to “turn off” the HPA-axis. Therefore, once out of harm’s way the stress response terminates itself, cortisol and adrenaline levels normalize, and the PNS takes back some measure of control – slowing heart rate, decreasing blood pressure, turning back on digestion and immune activity, and just generally shifting the body out of panic mode back to normal functioning.

Overwhelming Stress

However, when an extreme or chronic stressor overwhelms the stress response, physiological adaptations can occur that can have long-term consequences.[[viii]] For example, sustained secretion of cortisol has many deleterious impacts on the body – among other things, it can suppress immune activity, impact insulin resistance, impair memory formation, dysregulate reproductive hormone functioning, and lead to hypertension and vascular disease.[[iv];[vi];[ix]] Moreover, because cortisol receptors in the brain are responsible for turning off the stress response, the wearing down of these receptors due to excess cortisol activity can cause this normal negative feedback loop to fail, leading to abnormal baseline cortisol activity and an impaired ability to cope with new stressors.[[v]]

In addition, chronic stress-related CRF activity in the extended amygdala (emotional salience) ultimately prompts the release of #dynorphin, and together the activity of these two neurotransmitters is routinely tied to hypervigilance, #anxiety, irritability, and dysphoria. [[x]; [xi]; [xii]; [viii]] Overactivation of the locus coeruleus-norepinephrine system inhibits critical parasympathetic activities like eating and sleeping, increases sympathetic activities (e.g., resting heart rate, blood pressure), impairs functioning of the prefrontal cortex (executive functioning), and is linked to chronic anxiety, heightened fear, and an increased startle response.[[v]; [vi]]

Freeze Response

However, fight or flight is not the only response to trauma. Often when faced with inescapable or chronic stressors, our body instead initiates a "freeze" response. As Peter Levine notes, “Trauma occurs when we are intensely frightened and are either physically restrained or perceive that we are trapped. We freeze in paralysis and/or collapse in overwhelming helplessness” [p. 48]. The freeze response is thought to be mediated, at least in part, by the unmyelinated #vagus nerve, a (cranial) nerve that innervates all the organs below the diaphragm (e.g., stomach, intestines) as well as the heart.[[ii]] It involves a dramatic drop in heart rate, a drastic reduction in metabolism, shallow breathing, numbing (likely due to a release of endogenous opioids) and sometimes collapse or fainting.[[xiii]] It is often accompanied by #dissociation, where the traumatized person feels as though they are watching the event from an outside vantage point [[i]; [xiv]]. This kind of dissociation and freeze also can occur in response to triggers that evoke past trauma, which causes the nervous system to try to escape the discomfort associated with reliving vivid traumatic memories.[[iii]] The end result can be a kind of dissociative fugue, often involving loss of time and flashbacks or vivid imagery.

Although the physiology underpinning the freeze response and dissociation is still being figured out by researchers, it's clear that when these defense mechanisms are chronically deployed, the end result can sometimes be a fundamental disconnect from one’s self, including a decreased awareness of one’s inner sensations (reduced #interoception), a decreased ability to experience and verbalize emotions (#alexithymia), an inability to focus, flattened affect, and a chronic sense of unreality (derealization). Dissociation also can prevent the traumatic experience from becoming integrated into one’s autobiographical memory. Indeed, brain imaging studies routinely show that those with #PTSD have abnormal activation of the #insula, the region of the brain responsible for integrating interoceptive input from the body and generating a sense of self. [[xv]; [xvi];[iii]]

Traumatic Memories

We often remember very specific details about what proceeds or accompanies a particularly terrifying or painful experience. This reflects a “conditioned fear response” which is sciencespeak for the fact that when something bad or stressful (e.g., mortal peril) is strongly or repeatedly paired with some preceding factor (e.g., loud noise) we form an association between the two and automatically anticipate the feared outcome when we encounter the "triggering" condition. Think Pavlov's dogs, only crueler and therefore extra memorable. This heightened memory for stressful events is biologically hardwired to ensure we learn from highly-aversive experiences so we can (ideally) avoid a repeat experience.

Although still not entirely understood, the notable strength of these associations is thought to be a result of stress-related norepinephrine and cortisol in the extended amygdala helping to facilitate particularly strong neural connections linking the contextual trigger with the emotional and physiological response it evoked.[viii; v] This strong association may be further amplified by input from the vagus nerve, which (as noted) is constantly monitoring the state of the body. This means it can detect when circulating adrenaline and cortisol levels are particularly high and alert the brain that something notable must be happening and therefore it better REALLY remember it. Unfortunately, once this strong link is made, whenever the trigger is encountered again, the amygdala prompts the hypothalamus and brainstem areas to initiate our innate fear and stress response as if we were back in the trauma.[vi] How this manifests – whether it results in a #panic attack, a #flashback, a dissociative fugue, a freeze or collapse response, or the automatic use of an (adaptive or maladaptive) coping strategy –  depends a great deal on the client’s past experiences and current resources. 

The term “conditioned fear” typically makes it into (somewhat) common parlance in the context of PTSD. For example, when a soldier returning from combat panics in response to a loud noise, it is likely because loud bangs have threatened very real imminent danger in the past, and that learned association is (understandably) taking some time to fade. In most cases, as the soldier continues to encounter the triggers without the resulting mortal peril, this conditioned fear will dissipate in a process called "extinction learning." However, for reasons that can be contextual (e.g., severity, controllability of stressor) or individual (e.g., genetic or acquired susceptibility), sometimes extreme, repeated or unpredictable stressors results in wiring that refuses to be modified despite outlasting its usefulness.[[xvii]]

In addition to being overly strong, often these traumatic memories do not get integrated and stored in the same way as other memories. While not fully understood, high levels of arousal seem to enhance the vividness of emotional details of a memory, but at the exclusion of contextual details.[[xviii]; [xvii]] This phenomenon, which may be related to hypoactivity in the #hippocampus (contextual/spatial memory) can result in the “flashbulb” type memories typical of trauma, but also can prevent these memories from being integrated into a cohesive narrative.[[xvi]] In fact, recent research suggests that at the brain level, activation of traumatic memories often looks far more like present moment experiencing than it does recalling non-traumatic autobiographical memories.[[x]] Further complicating matters, activation of these flashbulb memories also seems to be tied to deactivation of much of the left side of the brain, which is critically involved in language, linear time, and analytical thinking.[[iii]]

Counseling Implications & Challenges

The physiological changes that can occur due to trauma can make counseling difficult in a variety of ways. As described above, trauma often is not integrated into memory like ordinary events, and activation of traumatic memories is tied to deactivation of the areas of the brain responsible for language and sequential thinking, meaning that some clients may find it challenging to effectively verbalize their experience even as they are forced to relive the emotions and sensations that accompanied it. For these clients, simply talking about trauma is unlikely to be particularly beneficial and may not even be possible.

Trauma also generally results in hyperactivity in the areas of the brain responsible for evaluating the salience of novel stimuli (e.g., amygdala, locus coeruleus) and hypoactivation of the areas of the brain typically responsible for top-down regulation of autonomic responses (e.g., the anterior cingulate cortex #ACC, medial prefrontal cortex #mPFC).[[vi](); [xvii]; [xvi]] The overall result is often hypervigilance and/or abnormal autonomic activity. This means those who have experienced trauma often have difficulty regulating affect and arousal due to dysregulated physiology,[[xix]] and some may turn to substance abuse or self-harm in attempts to quell excess sympathetic activation. This heightened arousal also can make developing a therapeutic alliance particularly challenging. When a client perceives threats everywhere, it can be difficult to establish the kind of trust necessary for a healing relationship. Because our nervous system frequently detects threats and activates our stress response even before we have time to consciously assess the danger,[[ii]] rational discourse may not be enough to counteract this overzealous harm alarm system.

The opposite physiological response also poses a challenge. Clients whose nervous system has dealt with trauma through emotional numbing and disassociation can be hard to reach at times. If they cannot access their emotions or engage in the present moment, talk therapy may be virtually useless. Numbing or intellectualizing also can prevent clients from truly engaging with the past trauma and therefore integrating it into their experience. This is why it is important for counselors to manage the level of emotional stimulation - too little prevents the traumatic material from being integrated, while too much can overwhelm the client and retraumatize them. Emotional numbing and feeling disconnected from one’s self (depersonalization) also can make it challenging for clients to envision a future and make plans to change and can result in self-harming and other risky behaviors as clients attempt to feel something. Moreover, although physiologically hardwired, the freeze response often causes a great deal of shame, as those who freeze berate themselves for not fighting back. Dealing with this shame can be a particular challenge for trauma survivors. 

In his Polyvagal Theory #PVT, Stephen Porges also describes how both the freeze and the fight or flight responses actively suppress the area of the brainstem that controls what he calls the “social engagement system.”[[ii]] This system includes the nerves essential for social communication - the ones that control the muscles of the ear that direct auditory attention (e.g., to focus on the high frequencies associated with human speech or instead block them out and only scan for predators), the muscles in the mouth and throat that can modify verbal intonation and prosody (tone and pitch), the muscles in the neck and around the eyes that help to direct gaze, and the muscles of the face that can produce the wide variety of expressions necessary for effective non-verbal communication. This too has implications for successful collaboration between a client and therapist and may negatively impact the client’s ability to maintain relationships and mobilize their social support networks when needed. As Bessel van der Kolk notes, “in order to feel emotionally close to another human being, our defensive system must temporarily shut down” ([iii], p. 84), but this can be exceptionally difficult for those who have experienced trauma. (Conveying a need for emotional closeness also becomes a whole hell of a lot trickier when it’s physiologically more difficult for you to listen to others and/or express the kind of non-verbal behaviors that typically encourage intimacy.)

Current Treatment Approaches

Given the heightened vigilance, perhaps the most fundamental need for treating trauma is to make sure clients feel safe. While this is true in the immediate aftermath of any crisis, it remains true long after the fact for those who have experienced trauma. One way of establishing this safety is for counselors to find and project calm. Our nervous system can be greatly influenced by others, especially those with whom we feel emotionally attuned. [[i]; [xx]] Therefore, it is essential that a counselor be able to convey empathy and caring through mirroring and reciprocity and be able to regulate their own physiological response to traumatic material. [[xxi]; [xxii]; [iii]]

Techniques that help to ground clients in the present also can be useful, especially for trauma survivors who are having difficulty accessing or regulating their emotions. For example, #mindfulness techniques can help to increase trauma survivors’ awareness of their bottom-up physical sensations (which, as noted, frequently get numbed-out post-trauma) and can help to strengthen top-down regulation of autonomic nervous system activity. Because trauma survivors, especially those who engage in emotional numbing, often have a hard time feeling safe within their own bodies, it is important to titrate these somatic experiences so as to limit the risk of being retraumatized.[i]

Therapists working with trauma also often attempt to directly engage the autonomic nervous system through breathing and movement. Inhalation activates the sympathetic nervous system and exhalation activates the parasympathetic nervous system, therefore breathing exercises can directly modify our  “automatic” physiology. More broadly, somatic approaches help clients gain knowledge of their internal experiences with the goal of increasing their ability to feel safe in their body and comfortable with their emotions. Meanwhile, cognitive approaches can help clients to identify and replace unhelpful relationship schema or negative thought or behavioral patterns and begin to challenge the pervasive feelings of brokenness and fragmentation that often accompany trauma. Beyond these foundational steps, therapists have a variety of approaches to choose from when working with trauma, all with varying levels of empirical support. The approach that works best for a given client depends on many factors, and is typically of FAR less importance than the strength and quality of the therapeutic bond between therapist and client.

Conclusions

Trauma can fundamentally disrupt a person’s sense of self and have long-lasting impacts on their relationships with others and their emotional well-being. Understanding the physiological changes that occur in response to overwhelming or repeated stress can help counselors to more effectively engage with traumatized clients. It can help counselors appreciate that those who have experienced trauma often have a nervous system that is constantly vigilant and may perceive threats where none exist. It underscores the importance of counselor emotional attunement, awareness, and self-regulation. It begs patience for those clients who are unable to verbalize their trauma. It clarifies why breathing exercises can be so crucially important. It elucidates why feeling “stuck” can be such a hallmark of trauma. It helps to explain why some clients may seem detached and emotionally numb, or why others may turn to self-harm and substance use. Although there is no one-size-fits-all approach to treating trauma, understanding the physiological adaptations that can occur provides a critical base from which counselors can more confidently explore effective treatment options that might best fit their clients’ unique needs.

References

[i] Levine, P. A. (2010). In an unspoken voice: How the body releases trauma and restores goodness. North Atlantic Books.

[ii] Porges, S. W. (2011). The polyvagal theory: Neurophysiological foundations of emotions, attachment, communication, and self regulation. W.W. Norton & Company.

[iii] van der Kolk, B. (2014). The body keeps the score: Brain, mid, and body in the healing of trauma. Viking.

[iv] Chrousos, G. P. (2009). Stress and disorders of the stress system. Nature Reviews: Endocrinology, 5, 374-381. https://doi.org/10.1038/nrendo.2009.106

[v] Zoladz, P. R., & Diamond, D. M. (2013). Current status on behavioral and biological markers of PTSD: A search for clarity in a conflicting literature. Neuroscience & Biobehavioral Reviews, 37, 860-895. https://doi.org/10.1016/j.neubiorev.2013.03.024

[vi] Charney, D. S. (2004). Psychobiological mechanisms of resilience and vulnerability: Implications for successful adaptation to extreme stress. American Journal of Psychiatry, 161, 195-216. https://doi.org/10.1176/appi.ajp.161.2.195

[vii] Charmandari, E., Tsigos, C., & Chrousos, G. (2005). Endocrinology of the stress response. Annual Review of Physiology, 67, 259-284. https://doi.org/10.1146/annurev.physiol.67.040403.120816

[viii] McEwen, B. S. (2000). Allostasis and allostatic load: Implications for neuropsychopharmacology. Neuropsychopharmacology, 22(2), 108-122. https://doi.org/10.1016/s0893-133x(99)00129-3

[ix] Sapolsky, R. M. (1996). Why stress is bad for your brain. Science, 273, 749-750. https://doi.org/10.1126/science.273.5276.749

[x] Henkens, M. J., Deussing, J. M., & Chen, A. (2016). Region-specific roles of the corticotropin-releasing factor-urocortin system in stress. Nature Reviews: Neuroscience, 17(10), 636-651. https://doi.org/10.1038/nrn.2016.94

[xi] Knoll, A. T., & Carlezon, W. A. (2010). Dynorphin, stress, and depression. Brain Research, 1314, 56-73. https://doi.org/10.1016/j.brainres.2009.09.074

[xii] Land, B. B., Bruchas, M. R., Lemos, J. C., Xu, M., Melief, E. J., & Chavkin, C. (2008). The dysphoric component of stress is encoded by activation of the dynorphin k-opioid system. Journal of Neuroscience, 28(2), 407-414. https://doi.org/10.1523/jneurosci.4458-07.2008

[xiii] Hagenaars, M., Oitzl, M., & Roelofs, K. (2014). Updating freeze: Aligning animal and human research. Neuroscience & Biobehavioral Reviews, 47, 165-176. https://doi.org/10.1016/j.neubiorev.2014.07.021