WILLIAM M. STRUTHERS,
KERRYN ANSELL, AND
ADAM WILSON
While many counselors have extensive experience in treating individuals who have suffered from what is generally referred to as trauma, studying the neurobiological aspects of trauma may appear daunting. There is a growing consensus, however, that neuroscience will play an increasingly significant role in the research and practice of counseling (Gabbard & Kay, 2001; Goss, 2015) Thus, an understanding of the neurobiological systems involved in stress response is essential for any mental health professional (King & Anderson, 2004).
What we will attempt to do in this chapter is to provide an overview of neurological stress systems and address how a neuroscience-informed approach to trauma provides the clinician with additional layers of assessment and conceptualization (Goss, 2015). An additional goal will be to discuss how, as neuroscience increasingly informs clinical practice, it should inform psychoeducational dialogue with clients (Miller, 2016).
The subjective level of stress that an individual experiences may vary by stressor, situation, genetics (Yehuda & LeDoux, 2007), and preexisting trauma history (Frissa et al., 2016). And while experiencing acute versus chronic trauma may result in somewhat divergent consequences (Sperry, 2016), the physiological response to stress generally involves the same neurobiological systems, regardless of the nature of the traumatic event. An understanding of the nervous system, as well as the effect of trauma and trauma treatment within a neurobiological framework, is useful in the counseling process. Therefore, we will provide an overview of critical brain regions and their functions, along with a direct examination of the neurological effects of stress and trauma, before discussing the application of neuroscience to the counseling process.
When considering the neurobiological factors involved in trauma, it is important to first review and locate the brain within a biopsychosocial model (McRay, Yarhouse, & Butman, 2016). Because of its complexity, many counselors avoid including the brain as part of the counseling process. However, given the brain’s crucial role in processing stimuli, adapting to the environment, and coordinating responses to physical, psychological, and social stressors, an understanding of the major divisions of the brain is critical in developing a comprehensive understanding of trauma.
The brain and spinal cord are collectively referred to as the central nervous system (CNS). The remainder of the nervous system, a collection of neurons and nerve fibers that innervate other organ systems, is called the peripheral nervous system (PNS). The PNS has two major subdivisions: the somatic nervous system (SNS), which innervates muscles involved in voluntary movement, and the autonomic nervous system (ANS), which controls numerous involuntary systems such as endocrine glands, respiration, heartbeat, and digestion. The ANS has a sympathetic division involved in fight or flight responses and a parasympathetic division known as the rest and digest system.
As the brain develops in utero, it divides into three major subsections based on morphological landmarks (see Schneider, 2014, for further detail). An examination of the layers of tissue reveals that as the embryo grows, a unique tube begins to develop just under the surface. Called the neural tube, it will later become the nervous system. One end of this tube, which is hollow in the middle, will become the brain, and the other end, the posterior tip of the spinal cord. In the normal process of development, the tip of the neural tube, which is housed in the skull, develops three bumps that later form the forebrain, midbrain, and hindbrain. Within these three major subdivisions, a process of ongoing specialization and subdivision takes place throughout fetal development. This process leads to a key principle of brain function: the deeper and lower the brain region, the more primal the function; the higher up from the spinal cord, the more complex the function.
Hindbrain. Deep down in the brain, where it fuses with the spinal cord, lies the first bump on the neural tube. This region, referred to as the hindbrain, contains three components. The first, the medulla (or medulla oblongata), is the transition point between the spinal cord and the brain and serves as the deepest boundary of the brain. The medulla is responsible for regulating the internal processes that keep us alive, such as heart rate, breathing, and blood pressure. Its primary function is to keep involuntary systems vital for our continued survival. Because of its importance and deep position in the brain, the medulla develops early on and remains fairly unchanged. It should come as no surprise, then, that damage or disruption of this area can have life-threatening consequences.
As we move higher up into the brain, we find that the hindbrain contains two additional regions. The pons and cerebellum lie just above the medulla and form the remainder of the hindbrain. The pons assists the medulla in its life-support role, aiding in the regulation of breathing. It also takes on considerably more complex responsibilities. Involved in sleep and arousal, the pons also controls reflexive movements of the head and neck. It acts as a relay for incoming messages from the body as well as outgoing commands to the muscles. Adjacent to the pons is the cerebellum. Deriving its name from the Latin term meaning “little brain,” the cerebellum is involved in motor control as well as balance and coordination. It has also been implicated in some forms of learning, memory, and attention.
Midbrain. As we continue ascending into higher brain regions, we transition from the hindbrain into the next major bump on the neural tube, known as the midbrain. The midbrain is the smallest of the three developmental regions but is still quite important and complex. It is subdivided into two sections, the roof and the floor. The roof, or tectum, sits to the right and left sides of the midline. The tectum contains several bumps called the inferior and superior colliculi. The inferior colliculi are critical to hearing and responding to auditory information. As signals come into the ear, they are rapidly sent to the inferior colliculi, which then pass them along to higher brain regions. This coordination between lower and higher regions allows hearing to be coordinated with head and neck movements in order to determine the location of a sound.
Just above the inferior colliculi are the superior colliculi, whose role is to unconsciously process visual information coming from the eyes in order to coordinate head, neck, and bodily movement. For example, reflexively moving your head out of the way of a softball or adjusting your gait as you reach the top of a set of stairs happens without much conscious thought, thanks to the superior colliculi.
Sitting under the roof of the tectum (the superior and inferior colliculi) is the floor of the midbrain. This floor is called the tegmentum and forms the second half of the midbrain. As noted, the brain increases in complexity in its higher regions. Thus, just as the tectum increases in its functional complexity by processing sensory signals that begin outside the organism (whereas the hindbrain is primarily involved in regulating the internal survival systems), so does the tegmentum focus on more complex tasks. For example, the tegmentum contains many specialized subsystems that are involved in arousal. It also contains regions that act as power generators for higher systems, such as voluntary movement and motivated behavior. In many ways, it acts like a manufacturing plant, where chemicals needed for complex behavior and thought are produced and then shipped up to higher brain regions.
While the tegmentum has a number of important subregions, an area especially relevant to understanding trauma is the ventral tegmental area (VTA). The VTA is perhaps one of the more critical regions of the midbrain because of its role in the production of the neurotransmitter dopamine. Dopamine is involved in a number of critical systems within the brain, including movement (Parkinson’s disease, a movement disorder, develops as a result of the death of dopamine-producing cells near the VTA). Dopamine has also become increasingly recognized for its fundamental role in the brain’s reward system.
Activation of cells within the VTA results in the release of dopamine into higher brain regions involved in the processing of significant stimuli. For example, VTA dopamine release has been linked to natural reinforcers such as food, water, and sex (Russo & Nestler, 2013). Many drugs of abuse and addiction hijack the VTA-dopamine system and cause it to activate the higher brain regions that receive this dopamine by triggering its release or mimicking dopamine (Volkow et al., 2001). This hijacking, and the resulting overuse of the reward system, ultimately results in diminished neurological functioning that may never be fully recovered.
Together the tectum and tegmentum have a considerable capability to respond to external stimuli and are able to respond with greater flexibility than a hindbrain region such as the medulla. Neurological issues involving the hindbrain or midbrain are typically life-threatening and would most likely be treated by a neurologist. Yet it is crucial for mental health professionals to understand the roles the hindbrain and midbrain play in the functioning of higher brain regions, where numerous mental health issues reside. For example, within the context of trauma, midbrain regions play a significant role in the detection of, processing of, and autonomic response to threatening cues.
Forebrain. Sitting atop the midbrain, and developing from the most anterior bump of the neural tube, lies the forebrain. Of the three developmental regions, the forebrain is the largest in mammals and displays a dazzling complexity. The forebrain is an especially plastic region of the brain. This neuroplasticity, or soft-wiring, is key to understanding the incredibly complex nature of human psychological experience. Numerous neurological processes, such as language, memory, creativity, abstract thought, and emotions, find their home in the forebrain.
As with the rest of the brain, we find that there are layers upon layers of interconnected subsections within the forebrain, each possessing a variety of functional capacities. The forebrain can be subdivided into two major subsections, the diencephalon and the telencephalon. The deepest subsection of the diencephalon is continuous with the midbrain and forms the hypothalamus. Connected to the pituitary gland, which sits outside the brain, the hypothalamus is involved in primary drives and motivation such as eating, drinking, temperature control, and reproduction.
The hypothalamus acts as the hormonal liaison between the body and the brain. It triggers release of its own hormones and stimulates release of pituitary hormones into the blood supply. It also detects hormones in the bloodstream released by other organs in the body. The hypothalamus and pituitary gland are critical in regulating reproductive cycles, growth hormones, and stress response. The hypothalamus detects what is going on inside the body and plays a critical role in the body’s response to stress and trauma. In connection with the VTA, the hypothalamus serves as a motivation center for the brain.
Above the hypothalamus, the midbrain’s tectum flows into the diencephalic region known as the thalamus. As the primary relay station for the senses, the thalamus takes input from the eyes, ears, mouth, and skin and sends these processed signals up to higher brain regions where our conscious perception is anchored. Sitting above the diencephalon is the telencephalon. The telencephalon expands outward from the midline of the brain in a symmetrical fashion. Because of this symmetrical nature, there are left and right hemispheres for each telencephalic subdivision. The telencephalon is made up of three major subregions: the limbic system and the basal ganglia, which are interconnected, and the outermost layer, the cerebral cortex.
Limbic system. The limbic system is a network of brain regions interconnected with other telencephalic sites, such as the cerebral cortex and diencephalon (i.e., the thalamus and hypothalamus). Yet three regions of this system are not part of the diencephalon or the cortex and deserve attention: the hippocampus, amygdala, and septum. While hardwired for certain prescribed responses, these three regions are remarkably flexible and thus have a greater ability to adapt to environmental changes and therefore therapeutic interventions. Here we will focus on the hippocampus and amygdala.
A major function of the hippocampus is to take information that has been identified by the brain as important (whether we are consciously aware of it or not) and to store it for later use. The procedure of processing and storing memories is called “consolidation” and is the manner in which all learning occurs. Memories may be consolidated and retrieved intentionally, such as when you are studying for an exam. However, learning may also occur unintentionally. We often remember things that we did not intentionally try to store. Memories such as a funny thing our friend did when we were little, the smell of our grandmother’s house, or the details around a betrayal of a friend may have never been intentionally set to memory yet may be vividly recalled later in life. These memories may contain detailed information as well as powerful emotions and sensations. The hippocampus is directly involved in the consolidation of these unintentional, emotional, and episodic memories. As will be discussed more fully, the role of the hippocampus in memory consolidation is central to an understanding of the brain’s response to stress and trauma, as well as to the recovery process (Getz, 2014).
Some have argued that the reason we do not remember many things from our early childhood is due to an immature hippocampus. Yet while we may not remember details from our early years, it does not mean that there are not significant memories consolidated by the hippocampus that may have profound effects on us (Poulos et al., 2014). Thus, the hippocampus is involved in the formation of emotional bonds, attachments, and traumatic memories that lie beneath our consciousness. These unconscious memories are critical to psychological development and have far-reaching developmental impacts (e.g., healthy sexual attitudes and behaviors).
The amygdala is an almond-shaped structure situated in the limbic system that sits toward the tip of the hippocampus. The two amygdalae (one in the right and one in the left cerebral hemisphere) are located just under the surface of the cerebral cortex, near our temples. Long known to be involved in emotion and emotional learning, the amygdala is connected to the hypothalamus and the midbrain. Negative emotions such as fear and anxiety, as well as associations with emotional events, are connected to the amygdala. During the hippocampal process of consolidation, the amygdala influences and modulates how that memory is stored. If there is a high degree of emotion associated with an event, and thus increased involvement of the amygdala, there is an increase in the likelihood of that memory being stored. Given its connections to the hypothalamus, which is involved in regulating stress hormones and survival drives, and its connections with the midbrain, which is involved in detecting significant stimuli in the environment, it should come as no surprise that the amygdala is conveniently situated alongside the hippocampus to influence the formation of emotional memories (Shin & Liberzon, 2010).
Basal ganglia. Interlaced with the limbic system are the basal ganglia. Among the several subregions, the caudate nucleus, putamen, and globus pallidus are significant for their involvement in movement, motivation, and the integration of emotions. Of particular importance to the discussion of trauma is the fact that the basal ganglia are central in setting the body’s overall anxiety level (Getz, 2014). Extraordinarily intricate in their connections, these regions show a high level of plasticity compared to deeper brain regions. This plasticity allows them to learn complex goal-directed movements, as well as form nuanced layers of motivation that move beyond eating, drinking, and sex. For example, the willingness to put one’s own body in harm’s way in order to protect someone else requires complex levels of motivation that go well beyond basic survival instincts.
Because of their connection to the midbrain, the basal ganglia (along with the cortex) appear to be major target sites for midbrain VTA dopamine (Ikemoto, Yang, & Tan, 2015). Disruption of the basal ganglia, or their dopamine input, may result in movement disorders, motivational issues, and anxiety symptoms (Gunaydin & Kreitzer, 2016). A number of diseases are related to the basal ganglia. These diseases, such as Parkinson’s and Huntington’s disease, tend to display disruptions to movement. In addition, many drugs of abuse trigger the release of dopamine or activate dopamine receptors in the basal ganglia (Koob & Volkow, 2016).
Cerebral cortex. The outermost layer of the brain, which has a wrinkled and gray appearance, is the cortex. Neurologically, it is what sets humans apart from virtually every other species. The cortex enables our cognitive abilities and complex psychological experience. It is through the cortex that we exercise abstract thought, develop nuanced language, plan far into the future, and contemplate and solve complex problems. While the cortex contains numerous regions and systems, four primary cortical lobes can be identified: the frontal, parietal, temporal, and occipital lobes. These four lobes are made up of folded layers of tissue called gyri, which are composed of multiple layers of neurons and are involved in numerous tasks and functions. While there is a great degree of consistency between individuals in the way their gyri and lobes are formed, there is also a level of uniqueness from person to person.
While interconnected and complex in their roles, the four lobes of the brain also carry out discrete functions. For example, the occipital lobe is primarily involved in processing visual information. The temporal lobe is critical for hearing and language. The parietal lobe is involved in touch and space as well as integrating the senses. The frontal lobe is involved in higher-order thought and executive functioning. While all are important, each lobe appears to play its own part in helping us sense, integrate, process, and act on information from the world around us. It is here, in the cortex, that our conscious psychological experience emerges. The cortex is one of the last regions of the brain to finish its development and is one of the most flexible and plastic regions within the brain. Thus, it is also within the cortex that mental health interventions can have profound effects.
Additional trauma-related neurological subsystems. Early research in the physiology of stress has focused on the interconnection between the sympathetic division of the autonomic nervous system and the adrenal system located adjacent to the kidneys (Sapolsky, 2015). This sympathetic adrenomedullary (SAM) system is responsible for the release of the neurochemical epinephrine, also known as adrenaline. To initiate the SAM response, sympathetic neurons in the spinal cord communicate with the adrenal glands. This direct neural signal triggers the production and release of adrenaline into the bloodstream. Upon release, adrenaline binds to receptors on various target organs, causing elevated heart rate, increased blood flow to muscle tissue, and vasoconstriction in the skin and gastrointestinal area.
Incorporating hormones produced by the hypothalamus and the pituitary gland, a second hormonal stress-response system, the hypothalamic-pituitary-adrenocortical (HPA) axis, activates the adrenal glands via hormones released into the bloodstream. The HPA is often associated with chronic stress and the hormones cortisol and glucocorticoids (GCs; Gądek-Michalska, Spyrka, Rachwalska, Tadeusz, & Bugajski, 2013). The HPA response originates in the hypothalamus, from which neurons secrete corticotropin-releasing hormone (CRH) to stimulate the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH is released into the bloodstream and elicits a release of GCs from the adrenal glands as long as the stressor (and ACTH) persist, affecting various organ systems throughout the body. During the HPA stress response, cortisol is released as a protective measure to manage organ damage and to promote adaptive behavior (Bale & Epperson, 2016). While the SAM and HPA systems are often understood as independent, they are in fact interconnected. The fight/flight/freeze response, originating from the SAM, functions to increase vigilance and arousal, which can activate the HPA stress response. In addition to the hypothalamus, several other brain areas show a sensitivity to these stress hormones. Neural pathways connected to the limbic system involve regions such as the amygdala, the hippocampus, and portions of the prefrontal cortex. The involvement of numerous systems allows for psychological and social stimuli to be involved in both the initiation and perpetuation of the stress response (McEwen, 2012).
Now that we have completed our primer on brain regions, we can move on to a more detailed description of how the brain responds to trauma and stress. This partial overview of the brain was necessary to help the reader understand the complexity of the interrelated systems that make up the central nervous system and to help the reader more fully understand the nature and impact of trauma on the integrated neurobiological system. As with any discussion of the brain, it must be noted that, while growing rapidly, our understanding of the brain remains limited. The sheer complexity and interrelated nature of the nervous system makes a comprehensive understanding of the brain problematic. Thus, the reader will recognize that the following discussion is intended to be a summative clinical guideline that undoubtedly will be developed over time.
The neurodevelopmental impact of trauma. Trauma results when stress overwhelms an individual’s existing stress-response systems, inhibiting recovery from the stressor. Often this loss of neurological equilibrium results in physical, psychological, and functional declines (Getz, 2014). In cases of severe or chronic stress, a healthy baseline may never be fully recovered, particularly without intervention. An individual who has been exposed to chronic stress may remain hindered from recovery on a neurological level, even after the cessation of the stressor (Gray, Rubin, Hunter, & McEwen, 2014). Thus, long after a traumatic experience, an individual must operate from a compromised physiological and psychological baseline. This disrupted baseline can have a severely disruptive effect on an individual’s overall behavior, self-regulation, and mental health (Carr, Martins, Stingel, Lemgruber, & Juruena, 2013). And while trauma at any age can lead to mental health issues, the brain appears to be especially vulnerable to the effects of trauma during particular developmental stages (Dunn, Nishimi, Powers, & Bradley, 2017).
It will be of no surprise to most clinicians that many instances of trauma occur during childhood. This is particularly unfortunate neurologically, as childhood contains several psychologically and neurologically critical windows. The earlier an individual experiences trauma in the lifespan, the more likely it is that he or she will suffer long-term negative effects (Ogle, Rubin, & Siegler, 2013). One of the key development periods occurs during infancy.
Trauma during these early years can pose a particularly serious threat to long-term neurobiological function. Trauma, with its neurological ramifications, is experienced differently depending on the age when the trauma occurs (Perry, 2009). This is largely due to the hierarchical nature of neural development discussed above. As in stage theories of development (e.g., Erikson, Freud), early dysregulation will be built on as development progresses, leading to subsequent dysfunction. This type of neurological dysregulation is detrimental as it significantly increases the sensitivity and duration of the stress response. This oversensitivity results in excessive use of the infant’s physiological stress systems and an overexposure to excess cortisol released by the HPA axis. Researchers have found that trauma in infancy can promote long-term dysregulation of the HPA axis (Kindsvatter & Geroski, 2014; Kuhlman, Vargas, Geiss, & Lopez-Duran, 2015).
Similarly, within the first five years of life, trauma can significantly decrease brain volume, inhibit the downregulation of cortisol, and slow general recovery from acute stress (Kuhlman et al., 2015). This difficulty in regulation can lead to serious disruption in a child’s overall behavior as well as his or her ability to function in social and academic settings (Kisiel et al., 2014). This developmental period of sensitivity may differ between male and female children because of the effects of gonadal hormones on HPA organization and functioning. Thus, the timing of trauma within childhood may have a significant impact on later symptomology (Bale & Epperson, 2016; Kuhlman et al., 2015).
Allostasis. One of the primary functions of the brain is to identify stressors and threats, recall and select appropriate responses to them, and then execute those responses. These functions ultimately facilitate adaptation based on the physiological and psychological consequences of past experience and allow the brain and body to return to a state of homeostasis. In the case of normal stressors, this process is adaptive and efficient. The process of seeking homeostasis in the face of stress is commonly referred to as allostasis (McEwen & Wingfield, 2003; McEwen et al., 2016). Regardless of whether the brain categorizes stress as good, tolerable, or toxic, stressors may alter neurobiological structure and function. As noted, this is especially true if the stress is experienced early in life (Shonkoff, Boyce, & McEwen, 2009).
Good stress, or eustress, can be understood as positive arousal and excitement. Eustress triggers hormonal responses but generally does not produce lasting negative physiological consequences. Tolerable stress may be caused by a stressor that contains a negative or potentially harmful component that requires an adaptive response in order to reduce potential damage to the system. An adaptive level of stress response, also known as allostatic load, generally occurs within a specific time-limited window and serves to protect the organism. Toxic stress, however, may be understood as the result of a massive, unmanageable stressor or the chronic presence of a stressor that cannot be properly dealt with or avoided. Toxic stressors are likely to overload an organism’s ability to cope with the threat and to result in physiological, neurological, and psychological damage (Grant et al., 2014; McEwen et al., 2016).
Trauma may be understood, then, as an overwhelming of the allostatic system, which may result in long-lasting and maladaptive neurophysiological, psychological, and social outcomes. Exposure to multiple or repeated toxic stressors can result in a cumulative impact and overload and erode the protective allostatic response, causing psychological trauma and physiological damage to the brain and other organ systems (McEwen, 2013). As noted above, stressors evoke physiological, psychological, and behavioral responses. In the event of a tolerable allostatic response to stress, physiological and neurological systems will gradually return to homeostasis, whereas toxic stress is likely to result in dysregulation of these systems. This neurophysiological dysregulation is correlated with maladaptive patterns of self-regulation of emotions, thoughts, and behavior (i.e., trauma, complex trauma, posttraumatic stress disorder; Bergen-Cico, Wolf-Stanton, Filipovic, & Weisberg, 2016).
Resilience. The allostatic response and the subsequent ability to respond to stressful events may often be understood by counselors as resilience. Defined by Rutten et al. (2013) as “successful adaptation and swift recovery after experiencing severe adversity” (p. 4), resilience plays a central role in the clinical treatment of trauma. The impact and role of resilience in trauma can be seen throughout four phases: the initial trauma or stressor, a consequent decline in either mental or physical health, a period of recovery, and finally the establishment of a new baseline from which the individual will operate moving forward. This process of decline, recovery, and establishment of a new baseline may vary by stressor and the individual’s unique susceptibility, but the general sequelae tend to follow this model. Resiliency involves the epigenetic interactions between genetics, neural functioning, and the environment (Gillespie, Phifer, Bradley, & Ressler, 2009; Rutten et al., 2013). Regarding specific neural pathways, brain systems involving both stress response and reward pathways are critically important to resilience. Systems such as the HPA axis, the sympathetic nervous system, and the mesolimbic reward pathway utilize various hormones throughout the body to activate long-term stress adaptation (Gillespie et al., 2009; Kasanova et al., 2016). While stress and trauma affect everyone, the genetic predisposition of the individual plays a significant role in the brain’s baseline ability to adapt to stress and trauma.
Secure attachment is considered a significant component of resiliency (Karreman & Vingerhoets, 2012). Throughout childhood and adolescence, it is critical for an individual to develop a secure bond with his or her primary caregiver (Tost, Champagne, & Meyer-Lindenberg, 2016). This bond is first achieved through proximity and responsiveness, ultimately leading to trust. Trust allows the child to develop cognitive schemas that can adaptively integrate affective experiences. As the individual grows, this bond plays a significant role in resilience formation. Through his or her experiences with attachment in adolescence, the individual may develop emotion-regulation competencies and create an internal working model through which he or she may effectively understand and interact with the world (Rutten et al., 2013).
Similar to healthy attachment, positive emotion has also been found to provide an important source of resilience, as it may decrease pain experience and assist in psychological health recovery (Rutten et al., 2013). Researchers suggest that the presence of positive emotions may buffer against the negative effects of stress, resulting in improved physiological functioning. Positive emotion may seem a rather elusive construct, yet researchers have found tangible evidence regarding its role in resilience (Gloria & Steinhardt, 2016). Positive emotion has even been found to have a modest degree of heritability and provides a critical window during which emotional reactivity is largely determined (Roth, 2012; Straussner & Calnan, 2014). Chronic stressors often serve to decrease positive emotion during the time the stress is being experienced, yet chronic stressors such as malnutrition, adverse environmental conditions, and poverty may have a lasting impact on an individual’s stress systems over time, resulting in an inability to manage stress or fear and to experience positive emotions. For example, animal studies have found that poverty negatively altered brain plasticity, reduced cortical gray matter, and impaired amygdala and hippocampal functioning (Lipina & Posner, 2012).
Memory. Any approach to trauma treatment must address not only the resulting symptomology of the trauma (e.g., anxiety, depression, maladaptive behaviors) but the memories of the trauma as well. This is evidenced by the multiple diagnostic criteria for posttraumatic stress disorder (PTSD) that address symptoms related to traumatic memories (American Psychiatric Association [APA], 2013). Thus, in order to understand and effectively treat the effects of trauma, it is necessary to further explore the manner in which traumatic memories are stored and subsequently utilized within the brain.
As mentioned, the amygdala is central to the processing of episodic memory. Yet it is also critical to the overall stress response and is often considered the primary fear-processing region of the brain. A primary functional goal of the amygdala is to assess potential threats and subsequently store those experiences for future threat assessment. These memories affect how the individual remembers and responds to similar stressors in the future (Parsons & Ressler, 2013; van der Kolk, 2002). The hippocampus, a neighboring region of the limbic system, is similarly connected to fear and threat conditioning. As the hippocampus is also involved in long-term memory processing, it too plays a crucial role in the formation and storage of traumatic memories (Tallot, Doyère, & Sullivan, 2016).
Both the amygdala and hippocampus are adept at responding to daily stressors. Yet in the face of extreme stress or trauma, the responses of and changes to these regions may diminish an individual’s ability to manage future stress of any type (Bergen-Cico et al., 2016; Nalloor, Bunting & Vazdarjanova, 2014). For example, GCs in the hippocampus affect spatial and episodic memory as well as mood regulation. GCs released as a result of chronic stressors may atrophy hippocampal cells and reduce their connectivity, ultimately affecting memory storage and recall. In fact, those suffering from dissociative PTSD symptoms have been shown to have reduced gray matter volume in the hippocampus (Nardo et al., 2013).
In addition to these two fear-processing regions, the prefrontal cortex (PFC) plays a central role in managing stressors (Lanius, Bluhm, & Frewen, 2011; Lanius et al., 2001; Rinne-Albers, van der Wee, Lamers-Winkelman, & Vermeiren, 2013; Tyler, 2012). As previously discussed, this region is the center for rational thought, decision making, and higher-order cognitive processing. Yet the PFC shares connection with and is significantly affected by both the SAM and HPA. Thus the impact of stress on the SAM and the HPA can also have a significant impact on the PFC and can affect the way traumatized individuals consciously process traumatic experiences (Parsons & Ressler, 2013). Chronic stress has been shown to atrophy and reduce connections in the PFC, resulting in cognitive rigidity and increased vigilance (McEwen et al., 2016). Cognitive distortions frequently seen with PTSD (e.g., magnification and minimization) become quite understandable in light of the mediating effect fear plays on memory consolidation and cognitive functioning. Similarly, stress responses may impair a traumatized individual’s ability to determine steps forward subsequent to the trauma. This impairment often leaves those suffering from PTSD with a sense of hopelessness about their future in addition to the hopelessness they may have experienced as a part of the traumatic stressor.
As stated at the beginning of this discussion, exploring the neurobiological dimensions of trauma may appear overwhelming to some. Indeed, any description of the brain’s role in psychological functioning should carry with it a recognition of the limitations of our current knowledge about neurobiological processes. The sheer complexity of the brain displays the wonder of God’s creation (Ps 139; Rom 1:20). Yet we may increasingly glean insights from scientific observation that can guide our understanding of creation and suggest how best to intervene within that system. This is particularly true in regard to the clinical applications of neuroscience.
As noted, one of the primary roles of the brain is to sense, process, and store experience in order to develop homeostatic patterns that guide future functioning. These templates manage most common threats that present themselves in daily life (e.g., stopping quickly at a red light). Trauma occurs when the events of life move outside those homeostatic patterns and thus the brain’s ability to manage the circumstance. Therefore, trauma ultimately disrupts the brain and body’s ability to maintain, or return to, homeostasis. This neurophysiological dysregulation and resulting psychological distress may lead to numerous negative outcomes for the individual.
As anyone who has been in an auto accident can attest, the driver experiences an immediate loss of equilibrium (e.g., increased heart rate, shaking hands, sensation of heightened senses). Yet ideally the neurological system quickly determines that the threat has passed, and the sympathetic and parasympathetic systems begin to return to a more balanced state. However, for many, and particularly for those who seek treatment for symptoms related to trauma, an initial loss of neurological equilibrium may lead to longer-term consequences. In the case of extreme or chronic stress, the initial responses of the brain’s stress-response systems (e.g., HPA, SAM) may become neurologically hardwired. In other words, what is designed to be a temporary response to threat may become established as the new homeostatic level of functioning.
While the hippocampus and amygdala are designed to determine the nature and severity of threats, they do so based on past experiences. Thus, through the overwhelming of the brain’s allostatic system, a sense of threat may be sustained well after a stressful event or life circumstance has passed. Knowledge of this process is imperative for clinicians and their clients, as it displays a central tenet of neurology that informs trauma treatment: the brain changes through experience. Trauma symptoms develop through experience, and so treatment must seek to facilitate neurological change through experience. A client can no more easily “get over” their trauma than they can forget how to walk. Both were learned through experience and thus are a part of a homeostatic system.
Unfortunately, because of a lack of understanding on the part of individuals and society, trauma symptoms are often overlooked after the traumatic event. Yet as the individual continues to struggle in a state of disequilibrium, they will frequently seek some form of neurological, physiological, and psychological equilibrium. These attempts may lead to maladaptive behaviors such as substance abuse, social isolation, and avoidance (Hammack, Cooper, & Lezak, 2012). Thus, clients presenting with a history of trauma may well display symptoms of chronic substance use as well as relational and professional difficulties.
As discussed, the brain’s ability to accurately form new memories can be disrupted following trauma (Nardo et al., 2013). This is especially true in regard to memories of the traumatic event itself (Dekel & Bonanno, 2013). Thus, clinicians should avoid seeking to determine the accuracy of a traumatic memory. The subjectivity of trauma (Yehuda & LeDoux, 2007), as well as the brain’s disrupted ability to process and store memories related to the stress, makes the exact details of the events less crucial than the neurological and physiological processes that maintain the traumatic state.
In addition to deficits in memory, traumatized individuals may display significant disruptions in overall cognitive functioning. Trauma has been shown to disrupt attention as well as general executive functioning (Getz, 2014). This is in large part due to the communication that takes place between the PFC and midbrain structures such as the limbic system. Ideally, the PFC maintains regulation of the limbic system and other midbrain structures. Within the typical allostatic system, the PFC becomes less active as the midbrain assesses and responds to basic threats. In the case of trauma, however, the midbrain can become dominant, limiting the individual’s ability to effectively carry out executive functions such as planning or logic. Thus, clients who present with symptoms of poor executive functioning (e.g., inattention, poor decision making) should be assessed for trauma history to determine appropriate treatment.
Additional trauma symptoms described in the Diagnostic and Statistical Manual of Mental Disorders (APA, 2013) can also be understood in light of the neurological impact of trauma. For example, while not fully understood, the amygdala appears to play a central role in the presence of flashbacks, due to its connections to memory storage and retrieval as well as the infusion of emotion into memory (Storm, Engberg, & Balkenius, 2013). It is also important to note that the midbrain, and thus the amygdala, is not directly, or consciously, controlled by the individual. This helps to explain the intrusive nature of flashbacks and is also relevant to other common trauma symptoms such as dissociation. Research indicates that dissociation occurs in part because of the effect of trauma on the hippocampus (Ross, Goode, & Schroeder, 2015). Thus, the core symptoms of trauma generally function outside the individual’s volition. While this may appear somewhat obvious to clinicians who have treated traumatized individuals, it may not be as clear to clients, who may be bewildered by the apparent hijacking of their behaviors and emotions.
Neurological impact of psychotherapy. Considerable space in this chapter has been devoted to discussing the neurological basis for trauma symptoms. Yet it is also important to discuss the manner in which the brain recovers, or is hindered from recovery, and how treatment can aid the healing process. Fortunately, research has repeatedly shown treatment to be effective in reducing trauma symptoms (Bradley, Greene, Russ, Dutra, & Westen, 2005). And while numerous treatment modalities have been used to address trauma, it is beyond the scope of this chapter to cover the various options in depth. Extensive bodies of literature explore the effectiveness of approaches such as trauma-focused cognitive behavioral therapy (Ehring et al., 2014), neurofeedback (Reiter, Andersen, & Carlsson, 2016), and eye movement desensitization and reprocessing (Watts et al., 2013).
Common to the various approaches to treatment, however, is the facilitation of the client addressing the various cognitive, behavioral, and physiological aspects of the trauma in a safe and gradual manner. This commonality begins to make sense in light of the key neurological realities discussed earlier, specifically that the brain must change through experience. In order for any treatment modality to be successful in changing the brain’s homeostatic functioning, it must allow the individual to activate, and then regulate, the very neurophysiological networks underlying the trauma symptoms. Each of the above-mentioned modalities requires the client to identify, monitor, and regulate their cognitive and physiological symptoms.
For example, exposure therapy, a form of cognitive behavioral therapy, requires a client to gradually face fear-inducing stimuli while maintaining a state of relaxation. By facing the fearful stimuli, the areas of the brain affected by the trauma are activated. Yet instead of allowing himself or herself to become enveloped by their trauma response, the client learns to increase his or her own regulation, thus bringing the brain back to a more ideal state of homeostasis. This repeated process ultimately leads to lasting neurological changes.
Helpman et al. (2016) found that prolonged exposure therapy led to an overall reduction in the volume of the anterior cingulate cortex (ACC) within the midbrain as well as an overall reduction in PTSD symptoms. Similar to a reduction in the ACC, psychotherapy has been shown to reduce the overall activation of the amygdala while increasing the activation of the PFC and hippocampus (Thomaes et al., 2014). This implies that, with therapy, there is a gradual reduction in the emotional content associated with the trauma (in the amygdala) as well as increases in cognitive processing (in the PFC) and an increased ability to process and store new memories (in the hippocampus).
The role of medication in trauma treatment. While the brain can and does change, it does not change quickly or easily. The neurological effects of trauma are often hardwired. Thus, clinicians and clients must be prepared to gradually work through the treatment process, allowing the brain the time it needs to change. This patience will be all the more necessary in those who have suffered trauma early in life. As discussed, early trauma can have a far more significant impact on later neurological and psychological functioning (Kuhlman et al., 2015).
In cases of early trauma, but also with trauma experienced later in life, clients may need to determine whether medication should be incorporated into their overall treatment plan. As with other areas of mental health treatment, there is increasing evidence that the incorporation of psychotropic medication with psychotherapy can prove beneficial (Thomaes et al., 2014). In fact, the combination of psychotherapy and psychotropic medications is now considered an industry standard for the treatment of many mental health issues (Gabbard & Kay, 2001; King & Anderson, 2004). Common classes of medications used in the treatment of trauma include antidepressants (e.g., SSRIs) and anxiolytics (e.g., benzodiazepines). These medications are generally utilized to address trauma symptoms of anxiety and depression.
More recent studies show the potential benefit of pairing anxiety-reducing medication with exposure to fearful stimuli (i.e., reminders of the trauma) in order to weaken the overall neurological patterns associated with that stimuli (Parsons & Ressler, 2013). Compounds such as ecstasy, psilocybin, and other nontraditional forms of medication have also been explored as potential treatments for trauma (Mithoefer, Grob, & Brewerton, 2016). These compounds decrease amygdaloid over-excitation, resulting in decreased anxiety (Johansen & Krebs, 2009; Oehen, Traber, Widmer, & Schnyder, 2013).
The scope of the current chapter does not allow for an in-depth analysis of these or more mainstream psychopharmacological treatments of trauma. For more information, see Preston, O’Neal, and Talaga (2013). Prescription medications have become increasingly common in the treatment of mental health issues, including trauma (Olfson, Blanco, Wang, Laje, & Correll, 2014). Thus, in order to ethically carry out clinical tasks such as referring clients for medication evaluations or coordinating treatment with prescribing physicians, counselors must be able to understand and confidently utilize basic neuroscientific information in the clinical context. This is especially true in regard to the treatment of trauma.
Trauma and psychoeducation. Much of the current chapter has focused on the usefulness of neuroscientific knowledge to the counselor’s conceptualization of trauma. Yet, as Miller (2016) posits, not only must counselors be educated and competent in the utilization of neuroscience in the assessment and conceptualization of cases, but they must also be able to educate their clients about treatment-relevant neuroscientific information. She explains that psychoeducation has long been an essential component of mental health treatment, and thus as neuroscience increasingly informs clinical practice, so should it inform psychoeducational dialogue with clients.
Many trauma victims struggle with their response at the time of the trauma. For example, instead of fighting back or calling for help, sexual assault victims may find themselves frozen. This freezing, otherwise known as tonic immobility, is a temporary state of physiological immobility brought on by an overwhelming of the allostatic system. Learning about this involuntary/reflexive response to trauma can help trauma survivors understand why they were unable to respond when the trauma was first experienced and why they continue to find themselves unable to move when they become afraid. This response is rooted in the autonomic nervous system and, as a result, is difficult to extinguish long after the traumatic event has passed. This state can become a learned response in trauma survivors that may be reexperienced when they subsequently encounter situations involving extreme fear (Abrams, Carleton, Taylor, & Asmundson, 2009). Explaining the neurological basis of this response may allow the client to view his or her reaction more accurately, rather than seeing it as a personal failure.
Psychoeducation can play a similarly normalizing role in trauma treatment in regard to explaining why clients cannot merely get over the traumatic events of the past. Explaining the hardwired nature of the neurological response to trauma not only frees clients from the shame of their ongoing symptoms but also prepares them for the long-term nature of treatment and recovery. The counselor can serve as a guide to assist clients in understanding how their brains were changed by trauma, how those changes relate to the symptoms that daily affect them, and how treatment can reduce the effect of trauma on their lives.
Scripture describes a call “to bind up the brokenhearted, to proclaim freedom for the captives and release from darkness for the prisoners” (Is 61:1). It is difficult to imagine a group more in need of this freedom and release than those who have been traumatized. Trauma is a condition of extreme complexity and severity. Stemming from a vast spectrum of acute or chronic stressors, trauma affects many facets of emotional and physical functioning, yielding serious short- and long-term neurobiological consequences for affected individuals. Having an understanding of the neurobiological systems that underlie trauma is of great importance to the mental health professional and those called on to provide support, understanding, and a framework for recovery.
While research remains somewhat limited regarding the neurobiology of stress, trauma, attachment, and resiliency, there is a growing body of literature describing the neurological impact that severe stressors, trauma, and complex trauma have on individuals. With an understanding of both the neurobiological processes involved in the formation of traumatic memories and the difficulty in managing the neurological, emotional, and psychological consequences of trauma, counselors will be better able to help clients understand their particular symptoms and to develop strategies for helping them manage and potentially overcome their traumas. By taking advantage of the plasticity of cortical systems and by understanding the more difficult-to-access subcortical regions where the emotional responses are housed, mental health professionals can be empowered to help their clients develop compensatory responses and to provide the scaffolding necessary for their clients to begin the process of recovery.
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