Purpose: This paper discusses the most current research regarding the structural alterations in

the brain as a result of Post Traumatic Stress Disorder, and how those affect the symptoms or
behaviors of the individuals. I will also examine the treatments most effective to

Thesis: The main structural alterations in the brain of those with PTSD lie in the hyperactivated
amygdala, decreases hippocampal volume, and thinner prefrontal cortex. These alterations
translate, in order, to the hyperarousal, failures in working memory, attention, and cognitive
flexibility, and increased numbing and avoidance experienced by affected patients.

Introduction
1. What is PTSD?
a. Video definition: reordering of your neural networks and
pathways and your sensory pathways so that you can survive in a really dangerous
situation (4)
b. DSM V qualifications: the occurrence of distressing or disabling
perceptual, emotional, and behavioral changes that persist after an experience in
which the sufferer has witnessed or been threatened with death or severe injury
(5)
i. Re-experiencing: the emotional or perceptual
reliving of traumatic events either spontaneously or in response to triggers
Avoidance and numbing: tendency to social isolation and reduced ability
to experience positive emotions in relationships
Hyperarousal: hypervigilance (overly aware) of ones surroundings, sleep
disturbance, anxiety, anger dyscontrol, violence, reckless and self
destructive behavior
Negative alterations in cognitions and mood: similar to avoidance and
numbing but in addition distorted blame of self or others, persistent
negative emotional state
ii. All of these symptoms are a result of brain
functions, but what specific functions make their brains different than the
normal population?

2. High prevalence of PTSD in overall population and soldiers

a. Between 5-10% of the population (2, 5) and 15-20% military (15)
i. Vietnam 1990 survey: 15.2-30.9% men, 8.1-26.9%
women
Gulf War: 12% of 30,000 sampled
Among Operation Iraqi Freedom/Operation Enduring Freedom: 13.8-14%
2008 study: $6.2 billion is spent by government on PTSD and depression
in troops (5)
b. For a disease so prevalent, we know too little about it. Education is
key to making advancements in this field.
 3. Neurobiology, specifically, is important to study for any Cognitive Behavioral
therapist or clinical psychologist administering treatment for PTSD.
a. 3 reasons (10): First off, it provides a more complete
understanding on the disorder in general. Secondly, it increases understanding of
how treatments (psychosocial and pharmacological) will affect the patients at a
biological level. Finally, the most important benefit lays in the ability to answer
the many questions of patients stemming from the fear of not understanding what
is actually wrong with them.
b. Exploration of the relationship between different symptom
presentations and potential neurobiological markers may assist in identifying
pharmacological treatments that more effectively target dimensional PTSD
symptoms. (18)

Manifestation of Symptoms in Those With PTSD (4, 10)

1. In the symptom category of Re-experiencing
a. Recurring and intrusive distressing recollections OR dreams of the
event (images, thoughts, perceptions)
b. Feeling or acting as if the event is recurring through illusions,
hallucinations, flashbacks, when awake or intoxicated
i. Janet Seahorns husband on the roller coaster at the
amusement park (3)
c. Intense psychological distress OR physiological reactivity at the
exposure to cues that resemble as aspect of the trauma
2. Avoidance and Numbing
a. Efforts to avoid thoughts, feelings, conversations, activities, places,
or people that remind of trauma
b. Inability to recall pieces of trauma
c. Less interest in participating in activities and feeling detached
d. Sense of a shortened future (not have a career, children, etc.)
3. Hyperarousal
a. Difficulty falling or staying asleep
b. irritability/outburst of anger
i. Janet Seahorns husband when they were late (4)
c. Difficulty concentrating
d. Hypervigilance or high sensitivity and intensity of behavior with
the purpose of detecting threats (high anxiety)
e. Exaggerated startle response
i. Fireworks (3)
4. How do all these symptoms occur? We know that PTSD is an invisible wound
because it manifests itself silently into the body, but where? The most basic beginnings to
the problem come from the response to fear.
Normal Responses to Fear
1. Reactions of the cortical versus subcortical brain (3)
a. Cortical brain: the cortexes that hold personality and
thought/decision processes
b. Subcortical brain: the more primitive limbic structures that control
basic instincts such as food, survival, and sex drive
c. When soldiers are deployed they face extreme conditions that keep
their bodies and minds (subcortical brain) in constant fight or flight to survive
d. The problem occurs when soldiers return home, because the
subcortical brain cannot process the geographical shift back to the US like the
cortical brain can
2. Explain diagram of how fear travels through both the cortical and subcortical

brain (10)
3. Explain the purposes behind these structures in the fear response:
a. Amygdala: assesses threat related stimuli, receives information
from all senses and projects to subcortical structures signs of fear/anxiety
Hippocampus: memory formation and emotional regulation by putting events in
proper context, putting together multiple events, and converting short to long term
memory; encodes context of fear
mPFC (medial prefrontal cortex): inhibits activation of the amygdala
ACC (anterior cingulate cortex): implicated in evaluating emotional significance
of stimuli and attentional function (8)
Main Structural Changes
1. Overall: main disturbances from PTSD have been found in the functioning of the
neural network located in the medial prefrontal and medial temporal lobe structures (6),
as well as in limbic structures (1)
2. Hippocampus is smaller (2)
a. Hippocampus: long term stress causes - decreased formation of
new nerve
cells in the dentate gyrus (a subregion of the hippocampus), decreased
hippocampal cell survival, and increased programmed cell death (8)
3. Amygdala is hyperactivated (1, 2, 5, 6)
a. when viewing negative emotional valence (intrinsic averseness)
images researchers found that subjects who developed PTSD had a higher
reactivity in the limbic brain regions, more specifically the insula and amygdala.
This activation in the presence of negative stimuli could cause subjects to enact
protective coping strategies. There was also less response in the prefrontal and
frontal cortex. When you combine these two it suggests an immediate reaction to
emotional stimuli without more complex information processing.
b. Found to have dendritic hypertrophy (overgrowth) (8)
4. Prefrontal cortex is thinner
a. Medial PFC: atrophy of dendrites (8)
i. Dendrites are the structures at the end of neurons
that receive stimuli or action potentials
b. Ventrolateral and Dorsolateral PFC, among other brain regions,
showed significant reductions with increasing trauma related symptom severity
(18)
5. Insula and Anterior Cingulate Cortex is reduced (1)
a. ACC- extinguishes fear in brain (6, 8) and is implicated in
evaluating emotional significance of stimuli and attentional function (8)
b. left dorsal ACC, and right posterior cingulate both reduced (18)
6. Looking forward
a. Reversible in hippocampus and mPFC but hypertrophy in
amygdala is not as plastic (could be a reason why symptoms talk a long time and
sometimes dont go away) (8)
b. The brain is what keeps the body regulated and functioning, so
when noticeable and large changes appear, there is no reason to doubt that there
will be changes in the functioning of the human being as a result. In the case of
PTSD, most of these major structures affected link to memory and cognition and
primitive, subcortical brain in charge of responding to stimuli such as fear.
Hypothesized Areas of Change
1. The several categories of brain changes listed above cannot account for the entire
complexity of symptoms
a. Eckart et al. in 2011 tentatively found that patients with PTSD
were found to have reduced brain volumes in several lateral prefrontal regions,
the right inferior parietal cortex, and the bilateral isthmus of the cingulate (6)
b. This addition to the emotional processing network suggests that
these structural changes might explain memory disturbances, or fragmentation of
traumatic memories, worse autobiographical memories, or high occurrence of
recurrent, intrusive recollection of traumatic memories.
c. Building block effect - volume loss correlates with extent of
traumatization (6, )

Impact on Behavior
1. avoidance / emotional numbing:
a. decreased activity in the cortexes could possibly be the basis of
avoidance and numbing symptoms that are commonly found in subjects with
PTSD (1)
b. This prefrontal cortex recognizes emotions, increases self-
awareness, and controls the experience of pleasure. Problems with the prefrontal
cortex, such as those which occur with PTSD, can result in insensitivity or
inability to focus - two common reactions to a traumatic war experience. The
emotional numbing experienced by soldiers could also be a result of the prefrontal
cortexs ability to experience pleasure. (2, 3, 6)
c. Consistent with our study hypothesis, we found that cortical
thickness negatively correlated with total PTSD symptom severity in a number of
brain regions relevant to emotional inhibition and emotion-cognition interactions.
Secondary analyses of the relationship between cortical thickness and
dimensional symptoms of PTSD also lent support to the hypothesis that different
symptom dimensions
would map onto different cortical regions. (18)
i. These brain regions overlap with networks that
broadly support emotion processing, emotion regulation, and executive
control, all of which are impacted in PTSD (18)
d. the reduction in dACC thickness was associated with the numbing
dimension (symptoms comparable to depression), but not arousal or
reexperiencing (symptoms related to anxiety and fear expression). This
observation is intriguing considering that activation of the dACC has been
previously related to arousal and expression of conditioned fear (Fonzo et al.,
2010; Mechias et al., 2010).... the study results raise the question for future
longitudinal investigations to determine whether the structural deficit in dACC
 contributes to a pathological behavioral shift from arousal and reexperiencing
dimensions to depressive numbing and perhaps dissociative symptomatology
(18)
2. Hyperarousal
a. Amygdala causes irritability / hyperarousal / avoidance (5, 19)
b. Intrusive memories and hyperarousal are consistent with either a
more responsive amygdala and a less active mPFC (8)
3. Cognitive tasks
a. Hippocampus reduction (6, 8)
i. memory formation and emotional regulation by
putting events in proper context, putting together multiple events, and
converting short to long term memory; encodes context of fear (8)
b. When hyperaroused, increase cortisol which inhibits memory (3)
c. Loss of dendrites and spines in pyramidal cells of the prefrontal
cortex, which relate to working memory, attention, and cognitive flexibility (18)

What This Means for Treatment