2. 2
Introduction
Question 2
This short essay will be discussing how neurochemistry plays a role in posttraumatic
stress disorder, as well as discussing how cortisol can affect the brain’s neurotransmitters, and
how prolonged levels of glucocorticoids can negatively impact the brain and memory,
additionally this essay will discuss how neurochemistry can negative impact a person’s ability to
deal with reality.
Posttraumatic Stress Disorder
Posttraumatic Stress Disorder (PTSD) begins when a person experiences or witnesses a
traumatic event, and the affected person has a difficult time moderating the trauma as well as
gaining control of their own emotional regulation when memories arise or triggers are present
that remind the individual of the event that they experienced or witnessed (American Psychiatric
Association, 2013). Trauma can create a cycle where the individual begins to re-experience the
event in various forms including nightmares, rumination, flashbacks and dissociative episodes,
which then further increase cortisol within the body’s system by pushing the person to live
constantly in a state of stress. The process of flashbacks and dissociation will be discussed later
in this essay. It is important to discuss the process of how the brain and body first responds to the
activation of the stress cycle, and discuss how memory and emotion is affected later.
Neurochemistry of PTSD
The human response to stress is meant to be both a positive and a negative experience
and begins when the person experiences a stressful event and the hypothalamus-pituitary-adrenal
axis (HPA) is activated, this is a 3 step process that involves multiple locations within the body’s
system as a protective maneuver to ensure survival. This HPA cycle causes the brain to respond
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by releasing the corticotropin-releasing hormone (CRF) which then binds to special receptors in
your brain and activate the anterior pituitary gland which sits just in front of your brain. Once the
pituitary gland is activated then a signal by way of the adrenocorticotropic hormone (ACTH)
travels down your body to bind to receptor sites on your adrenal gland which stimulates the
adrenal cortex to activates the glucocorticoid hormone and your adrenal medulla which excretes
the stress hormone – cortisol, which can last for several hours post stressor.
Now, this process has a positive or beneficial function whereas the person experiences a
life-threatening scenario, for example, a hiker is traveling in the woods and due to not paying
attention to their surroundings they comes across a grizzly bear doing whatever bears do in the
woods. The hiker makes nanosecond evaluations of the situation via primary appraisal and
secondary appraisal to determine that the bear is a threat and harm can come to the person. The
HPA axis activates, also known as the fight or flight or freeze response, and the person goes
through the appraisal of threat and appraisal of challenge where the person either tries to fight off
the bear if they have the necessary means, or they try to run away which can cause the bear to
give chase and possibly maim and eat them, or they can freeze and become an uninteresting
object to the bear. After surviving the encounter with the bear from whichever method worked
the best, the person’s stress response then teaches this person the be hypervigilant of their
surroundings by paying greater attention to sights and sounds that may pose a threat. Beneficial
triggers could include the snapping of twigs or branches, the rustle of brush, maybe even the
presence of a tasty bush with wild raspberries or blackberries. Next time they return to the
woods, their fear of the bear has since been encoded in their brain as an important lesson or
experience since most individuals do not often visit the wilderness unless they live in that
environment on a daily basis.
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A negative or dysfunctional response to the stress process occurs when daily living
becomes a fearful or negative experience due to a situation that occurred within those
parameters. For example, a person who was in a horrific car accident that not only killed a friend
or relative but the entire accident involved multiple people where other unrelated individuals
died or were severely wounded as well. Add on top of that the person was trapped in their
vehicle with their dead or dying friend or family member, and could not escape until emergency
response teams could bring the “jaws-of-life” machine to pry open the vehicle and extract that
person. For this individual a daily event, driving in the car, became a traumatic environment and
the HPA axis turned the vehicle and various other situational experiences into negative triggers,
triggers that are seen and experienced on a daily basis such as the honking of car horns, car
alarms, shouting, the smell of smoke or the screech of tires on the ground, and even sitting within
the car itself can become a negative trigger. Now, because these are every day experiences, the
person who is affected can re-experience the horrific accident on a regular basis, which re-
excites or stimulates the HPA axis repeatedly, thus creating PTSD due to the constant re-
experiencing, intrusive thoughts, rumination, and fear associated with driving in a car, being on a
busy road, the sound of car horns, and the smell of smoke and burned tires, even emergency
response sirens and other sounds that are similar to sirens can become a trigger. This is where
PTSD becomes the disorder, and the HPA has a negative and detrimental effect on the human
brain and the neural system and can cause impaired memory and emotional regulation. More
specifically, PTSD is examined and explained as a “dysregulation of the hypothalamus-pituitary-
adrenal axis” (van Zuiden, et al., 2012).
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Glucocorticoids and the Brain
Glucocorticoids are a naturally produced hormone that comes from the adrenal cortex,
and has two main functions, one is the metabolic response which has three main functions
including “stimulation of glucose production in cells, particularly the liver; stimulation of fat
breakdown in adipose (fat) tissues; and inhibition of glucose and fat storage in cells” and the
second is the anti-inflammatory response which occurs when the body experiences a threatening
substance under the protective skin layer, whereas the third function is to produce cortisol and
other related hormones (Liou, 2014). Studies have indicated that in utero exposure of
glucocorticoids can have a negative impact on the developing brain, and that exposure to
dexamethasone prenatally can damage the hippocampal neurons and reduce the size of the
hippocampus even after birth as well as showing changes in behavior and memory due to
hippocampal damage which was indicated in a study with rhesus monkeys (Seckl & Meaney,
2006).
When it comes to memory and emotional functioning, glucocorticoids in the role of
cortisol play a negative role within the human body. In a study conducted using mice and
corticosterone, researchers found that mice developed PTSD-like symptoms when exposed to a
tone followed by an electric shock felt through the foot after having corticosterone directly
infused into their dorsal hippocampus site which influenced memory impairments which can be
seen in PTSD (Kaouane, et al., 2012). At some point the proper consolidation of memory and
emotion is somehow overridden or damaged due to the intense influx of cortisol or cortisol
dysfunction, and this is where lapses in memory and flashbacks can occur. Furthermore, cortisol
stimulation paired with an emotional response from the amygdala could effect a person’s
emotions, particularly with emotional blunting which can also be known as blunted affect where
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a person’s expressed emotions, the emotions others would witness, are greatly reduced for
various reasons. Current studies cite that serotonin plays a role in PTSD and this could be the
connection between emotional blunting and cortisol. One article states that an individual would
develop learned helplessness after experiencing trauma multiple times, and the same article
discussed how researchers found a decrease in the 5-HT (serotonin) chemical, which in turn
would cause a person to appear depressed which then influences the presence of emotional
blunting or numbing which is often seen in individuals with depression and PTSD (Neumeister,
2006).
Furthermore, emotional blunting or numbing can be seen with depersonalization or where
an individual feel as if the event is not or did not happen directly to them but to someone else,
whereas depersonalization is influenced by serotonin which is influenced by trauma, heightening
anxiety, and negative emotional experiences (Blevins, Witte, & Weathers, 2013). Healthy
serotonin functioning plays an important role in assisting in emotional regulation and daily
functioning, which also can assist in whether or not developing PTSD is a risk factor where
higher levels of optimism as a healthy or positive coping mechanism can reduce the risk of
developing PTSD (Gil & Weinberg, 2015).
Conclusion
Neurochemistry is a complicated issue that can control a human being and their thoughts
and behaviors simply by producing too much or too little of a critical substance that balances our
moods, cognitions, and how we act towards ourselves and towards others. Serotonin balances
depression which can influence our optimism. Glucocorticoids, which assist us in breaking down
necessary fats and sugars for energy, can also influence the development of PTSD when
overproduced can impair both memory and emotional regulation in humans and animals alike.
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Reference
American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental
Disorders (5th ed.). Arlington, VA: American Psychiatric Association.
Blevins, C. A., Witte, T. K., & Weathers, F. W. (2013). Factor Structure of the Cambridge
Depersonalization Scale in Trauma-Exposed College Students. Journal of Trauma &
Dissociation, 289.
Gil, S., & Weinberg, M. (2015). Coping Strategies and Internal Resources of Dispositional
Optimism and Mastery as Predictors of Traumatic Exposure and of PTSD Symptoms: A
Prospective Study. Psychological Trauma: Theory, Research, Practice, and Policy, 7(4),
405. doi:http://dx.doi.org.libproxy1.usc.edu/10.1037/tra0000032
Kaouane, N., Porte, Y., Vallee, M., Brayda-Bruno, L., Mons, N., Calandreau, L., . . . Desmedt,
A. (2012). Glucocorticoids can induce ptsd-like memory impairments in mice. Science.
doi:10.1126/science.1207615
Liou, S. (2014). Glucocorticoids. Retrieved October 25, 2015, from Hopes:
http://web.stanford.edu/group/hopes/cgi-bin/hopes_test/glucocorticoids/
Neumeister, A. (2006, Spril). What Role Does Serotonin Play in PTSD? Psychiatric Times,
23(4), p. 50. Retrieved from
http://search.proquest.com.libproxy1.usc.edu/docview/204569669?accountid=14749
Seckl, J. R., & Meaney, M. J. (2006). Glucocorticoid "Programming" and PTSD Risk. Annals of
the New York Academy of Sciences, 360. doi:10.1196/annals.1364.027
van Zuiden, M., Heijnen, C. J., Maas, M., Amarouchi, K., Vermetten, E., Geuze, E., &
Kavelaars, A. (2012). Glucocorticoid sensitivity of leukocytes predicts PTSD, depressive
and fatigue symptoms after military deployment: A prospective study.
Psychoneuroendocrinology, 1832.
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Introduction
Question 5
The discussion of this portion of the short essay is evaluating how normal memories are
stored within the brain compared to how traumatic memories are stored in the brain and how
traumatic memories can actually alter and negatively impact an individual’s mental health. The
essay will also discuss the indications of traumatic memories via behavioral and cognitive
alterations.
Normal Memory
When a person is in the process of creating a new memory several things must occur.
First, the person must witness or experience an event that has an impact on them and that event
then goes into their brain and sifts through their thalamus, which is in charge of sensory
perception (The Human Memory, 2010). If the event has a strong emotion for the person
attached to it, then the chances are even higher that the event will be encoded as a stronger and
more retainable memory, and that happens when the amygdala is activated and stimulated by
either anger, fear, or happiness. Fear is the emotion that tends to create a stronger or vivid and
longer lasting memory. After the amygdala has been activated and the brain has been able to
decode the experience per how the individual is understanding the situation (perception), then the
event is funneled into one single moment or experience via the activation of the hippocampus
which then evaluates the experience and determines if it is worthy of short-term or long term
commitment or storage (Applegate & Shapiro, 2005). The purpose of the hippocampus is to sort
experiences and dedicate them to long or short term memory caches, additionally, the
hippocampus also as a giant filing center where similar memories and experiences can be easily
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retrieved later for various reasons. How this happens is the hippocampus stimulates the brain
with the formation of a memory or similar memories and creates a neural pathway that then
makes electrical signals easier to travel for quicker memory retrieval. When normal memories
are created, a person can retrieve the information and often go about their day without any ill
effects that put them at risk. However, when a traumatic memory is created it can cause a cycle
that tends to involve maladaptive behaviors and unhealthy coping mechanisms that tend to
strengthen the traumatic memory.
Traumatic Memory
In the case of traumatic memory the brain wires a neural pathway in a way that creates a
negative loop between the amygdala and memory, which then strengths the neural pathways in
order to make it easier for the person to access those traumatic memories and emotions. During
periods of extreme or severe stress, glucocorticoids have been shown to reduce the healthy
function of the hippocampus because it is impaired due to cell atrophy and death from
corticosteroids like cortisol (Pannu Hayes, et al., 2010). When this happens, and the
hippocampus and the amygdala are overwhelmed with cortisol to the point of dysfunction, then
the way an individual recalls memories can become overwhelming as well in the sense that there
is no distinction between what is considered an appropriate threat and what is a benign threat or a
threat that could cause harm but is currently not a serious issue because the threat is neutral.
Additionally, researchers have found that the consolidation and storage of the traumatic
memories, as well as normal memories, occurs even during sleep and can exacerbate the
traumatic memories by keeping the neural pathways ‘alive’ and further damage the brain by
reducing quality of sleep which further damages the hippocampus’ ability to properly encode
memories (van Liempt, Vermetten, Lentjes, Arends, & Westenberg, 2011).
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Implications for Mental Health
Currently, the issues that one would see when investigating an individual who is dealing
with traumatic memories and reduced quality of sleep would be the presence of either acute
stress disorder or posttraumatic stress disorder. Granted, there would be other physical and
mental behaviors also associated with traumatic memories besides the reduced quality of sleep,
but also things such as emotional dysregulation, According to the DSM-5, the individual must
meet the criteria in order to be diagnosed with either acute stress disorder (ASD), which has
symptoms lasting between 3 to 30 days, or posttraumatic stress disorder (PTSD) which has many
similar diagnostic criteria but present for more than 30 days (American Psychiatric Association,
2013).
Should an individual meet the criteria for PTSD, then a myriad of issues can arise just
from the presence of such a disorder. Individuals suffering from PTSD can have sleep
disturbances, flashbacks, difficulty in mood regulation, difficulty with concentration, difficulty
with memory, ruminating about the traumatic experience(s), and avoiding future situations that
cause stress which was discussed in an article about PTSD symptoms, traumatic experiences, and
delinquent youth (Kerig, Vanderzee, Becker, & Ward, 2012). This can cause a disruption in
many areas of a person’s life which can further impair their ability to do necessary and daily
functions such as attend work or school, interact with individuals in society or with their own
family, the ability to regulate their emotions, as well as understand and regulate intense events
such as anxiety and depression. Anxiety and depression, in conjunction with PTSD symptoms,
can further reduce the effectiveness and functionality of the hippocampus as well as the
amygdala due to the increase in stress (cortisol) which researchers suggest actually affects the
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size of the hippocampus during chronic stress which can have a negative impact on the
hypothalamus-pituitary-adrenal axis which helps regulate stress (Hannibal & Bishop, 2014).
Conclusion
If a person is unable to properly regulate their emotions due to some kind of damage to
their hippocampus and amygdala, it inhibits their ability to consolidate, process, and encode their
experiences as well as evaluate the level of intensity of their experiences in order to reduce
things like PTSD. Teaching individuals healthy coping skills in order to manage their stress can
help them in retraining their minds to encode experiences and not continue to fuel the cycle of
traumatic memories which can later turn into PTSD if left unmanaged. The current studies
suggest that chronic stress actually can shrink the size of the hippocampus, thus further reducing
its ability to encode and process memory, whether it is a normal memory or traumatic memory.
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References
American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental
Disorders (Fifth ed.). Arlington, VA, American Psychiatric Association.
Applegate, J. S., & Shapiro, J. R. (2005). Neurobiology for Clinical Social Work. New York,
NY: W.W. Norton & Company, Inc.
Hannibal, K. E., & Bishop, M. D. (2014). Chronic Stress, Cortisol Dysfunction, and Pain: A
Psychoneuroendocrine Rationale for Stress Management in Pain Rehabilitation. Physical
Therapy, 94(12), 1820.
Kerig, P. K., Vanderzee, K. L., Becker, S. P., & Ward, R. M. (2012). Deconstructing PTSD:
Traumatic Experiences, Posttraumatic Symptom Clusters, and Mental Health Problems
among Delinquent Youth. Journal of Child & Adolescent Trauma, 130.
Pannu Hayes, J., LaBar, K. S., McCarthy, G., Selgrade, E., Nasser, J., Dolcos, F., . . . Morey, R.
A. (2010). Reduced hippocampal and amygdala activity predicts memory distortions for
trauma reminders in combat-related PTSD. Journal of Psychiatric Research, 45(2011),
661.
The Human Memory. (2010). Parts of the Brain. Retrieved from The Human Memory:
http://www.human-memory.net/brain_parts.html
van Liempt, S., Vermetten, E., Lentjes, E., Arends, J., & Westenberg, H. (2011). Decreased
nocturnal growth hormone secretion and sleep fragmentation in combat-related
posttraumatic stress disorder; potential predictors of imparied memory consolidation.
Psychoneuroendrocrinology, 36, 1362.
