Posttraumatic Stress Disorder (PTSD)

Overview

●​ PTSD is a severe, long-lasting emotional disorder that can develop after exposure
to traumatic events.​

●​ Common triggers include:​

○​ Wars (e.g., Iraq and Afghanistan)​

○​ Terrorist attacks (e.g., September 11, 2001)​

○​ Natural disasters (e.g., hurricanes like Sandy in 2012)​

○​ Physical assaults, particularly rape​

○​ Car accidents​

○​ Sudden death of a loved one​

Key Point

●​ PTSD is the most well-known trauma-related disorder, highlighting how trauma can
have enduring psychological effects.

Clinical Description of PTSD

Setting Event

●​ Exposure to a traumatic event including:​

○​ Experiencing or witnessing death or threatened death.​

○​ Experiencing or witnessing actual or threatened serious injury.​

 ○​ Experiencing or witnessing actual or threatened sexual violation.​

●​ Also includes:​

○​ Learning that the traumatic event happened to a close family member or

friend.​

○​ Repeated exposure to details of a traumatic event (e.g., first responders

handling human remains).​

Reexperiencing

●​ Victims relive the event through:​

○​ Memories.​

○​ Nightmares.​

●​ Flashbacks: Sudden memories with strong emotion, making victims feel as if they are
reliving the event.​

Victims’ Avoidance

●​ Avoidance of anything that reminds them of the trauma.​

●​ May display restriction or numbing of emotional responsiveness, disrupting relationships.​

●​ Sometimes unable to remember aspects of the event. → repression​

●​ Possible unconscious avoidance of emotion itself (similar to panic disorder) to prevent

recalling trauma.​

Victims Have Hyperarousal and Reactivity

●​ Chronically overaroused.​

●​ Easily startled.​

●​ Quick to anger.​

●​ DSM-5 addition: (PTSD E criteria) Reckless or self-destructive behavior.​

Dissociative Subtype (DSM-5)

●​ Individuals may show less arousal than typical PTSD patients.​

●​ Experiences include feelings of unreality (dissociation).​

●​ Respond differently to treatment compared to standard PTSD presentations.

DSM5 Diagnostic Criteria for Posttraumatic Stress Disorder

A.​ Exposure to actual or threatened death, serious injury, or sexual violence in one (or
more) of the following ways:
1.​ Directly experiencing the traumatic event(s).
2.​ Witnessing, in person, the event(s) occurred to others.
3.​ Learning that the event(s) occurred to a close relative or close friend. In cases of
actual or threatened death of a family member or friend, the event(s) must have
been violent or accident.
4.​ Experiencing repeated or extreme exposure to aversive details of the traumatic
event(s) (e/g/, first responders collecting human remains; police officers
repeatedly exposed details of child abuse).

Note: Criterion A4 does not apply to exposure through electronic media, television, movies. Or
pictures, unless this exposure is work related.

B.​ Presence of one (or more) of the following intrusion symptoms associated with the
traumatic event(s), beginning after the traumatic event(s) occured:
1.​ Recurrent, involuntary and intrusive distressing memories of the traumatic
event(s). Note: In young children, repetitive play may occur in which themes or
aspects of the traumatic event(s) are expressed.
2.​ Recurrent distressing dreams in which the content and/or affect of the dream are
related to the traumatic event(s). Note: In children, there may be frightening
dreams without recognizable content.
3.​ Dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if
the traumatic event were recurring. (Such reactions occur on a continuum, with
the most extreme expression being a complete loss of awareness of present
surroundings.) Note: In young children. Trauma-specific reenactment may occur
in play.
4.​ Intense or prolonged psychological distress at exposure to internal or external
cues that symbolize or resemble an aspect of the traumatic event.
5.​ Marked physiological reactions to internal or external cues that symbolize or
resemble an aspect of the traumatic event.
C.​ Persistent avoidance of stimuli associated with the traumatic event, beginning after the
traumatic event occurred, as evidenced by one or both of the following:
1.​ Avoidance of or efforts to avoid distressing memories, thoughts. Feelings, or
conversations about or closely associated with the traumatic event.
 2.​ Avoidance of or efforts to avoid external reminders (people, places,
conversations, activities, objects, situations) that arouse distressing memories,
thoughts, or feelings about or closely associated with the traumatic event.
3.​ Inability to recall an important aspect of the trauma
4.​ Markedly diminished interest or participation in significant activities
5.​ Feeling of detachment or estrangement from others
6.​ Restricted range of affect (e.g., unable to have loving feelings)
7.​ Sense of a foreshortened future (e.g., does not expect to have a career,
marriage, children, or a normal life span)
D.​ Negative alterations in cognitions and mood associated with the traumatic event,
beginning or worsening after traumatic event occurred, as evidenced by two (or more) of
the following:
1.​ Inability to remember an important aspect of the traumatic event (typically due to
dissociative amnesia and not to other factors such as head injury, alcohol, or
drugs).
2.​ Persistent and exaggerated negative beliefs or expectations about oneself,
others, or the world (e.g., “I am bad,” “no one can be trusted,” “the world is
completely dangerous,” “My whole nervous system is permanently ruined”).
3.​ Persistent distorted cognitions about the cause or consequences of the traumatic
event that lead the individual to blame himself/herself or others.
4.​ Persistent negative emotional state (e.g., fear, horror, anger, guilt, shame)
5.​ Markedly diminished interest or participation in significant activities.
6.​ Feelings of detachment or estrangement from others
7.​ Persistent inability to experience positive emotions (e.g., inability to experience
happiness, satisfaction, or loving feelings).
E.​ Duration of the disturbance (Criteria B, C, D and E) is more than one month
F.​ The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.

Specify if:

With delayed expression: If the diagnostic threshold is not exceeded until at least 6
months after the event (although it is understood that onset and expression of some
symptoms may be immediate.

Specify if:

With Dissociative Symptom: The individual’s symptoms meet the criteria for
posttraumatic stress disorder, and in addition, in response to the stressor, the individual
experiences persistent or recurrent symptoms of depersonalization or derealization.

From American Psychiatric Association. (2013). Diagnostic and statistical manual of

mental disorders (5th ed.). Washington, DC
Historical Context (Samuel Pepys Case)
●​ PTSD first named in DSM-III (1980).​

●​ Historical accounts show the disorder existed long before formal recognition.​

●​ Example: Samuel Pepys, British diarist, witnessed the Great Fire of London (1666).​

Symptoms Observed in Pepys

●​ Sleep disturbance: Could not sleep at night without terror; insomnia lasted for months.​

●​ Intrusive thoughts/dreams: Recurrent distressing thoughts of the fire.​

●​ Guilt: Felt guilty for saving himself and his property while others perished.​

●​ Emotional numbing/detachment: Experienced reduced emotional response to the

event.​

Connection to DSM-5 Criteria

●​ Pepys’ experiences illustrate key PTSD features:​

○​ Difficulty sleeping.​

○​ Intrusive memories or dreams of the traumatic event.​

○​ Guilt and emotional numbing/detachment.

PTSD in the Jones Family Case

The Traumatic Event

●​ Family: Mrs. Betty Jones and her four children (Je, 8; Marcie, 6; Cathy, 4; Susan, 2).​

●​ Incident: Visiting a friend’s farm; a large German shepherd attacked Marcie, causing
severe facial injuries.​
 ●​ Immediate responses:​

○​ Je intervened to drive the dog away.​

○​ Mrs. Jones applied pressure to Marcie’s wounds.​

○​ Dog restrained later; Marcie taken to hospital.

Psychological Impact on Family Members

●​ Marcie (victim, 6 years old):​

○​ Developed PTSD.​

○​ Experienced developmental regression:

■​ nightmares
■​ bedwetting (nocturnal enuresis)
■​ fear of medical procedures
 ■​ avoidance of baths and nail trimming
■​ reluctance to be tucked in​

●​ Je (8 years old):​

○​ Developed PTSD and survivor guilt (“should have saved Marcie”).​

○​ Developmental regression:
■​ resumed finger-sucking
■​ nightmares
■​ separation fears.​

●​ Cathy (4 years old):​

○​ Displayed fear and avoidance in tests; did not verbally report problems.​

●​ Susan (2 years old):​

○​ Showed some symptoms (see Table 5.7).​

○​ Repeatedly verbalized trauma-related statements (“Doggy bit sister”).​

●​ Mrs. Jones (mother):​

○​ Also showed symptoms of PTSD following the event.​

Key Features of PTSD Observed

●​ Developmental regression common in young children post-trauma.​

●​ Symptoms can manifest differently depending on age and ability to verbalize

experiences.​

●​ Trauma affected multiple family members simultaneously, illustrating secondary trauma

effects.​

●​ PTSD symptoms included fear, avoidance, nightmares, regression in age-appropriate

behaviors, and somatic anxiety responses.
PTSD, Delayed Onset, and Acute Stress
Disorder
Timing of Diagnosis

●​ PTSD cannot be diagnosed until at least one month after a traumatic event.​

●​ Early stress reactions are common and often disappear within a month.​

Delayed Onset PTSD

●​ Some individuals show few or no symptoms immediately after trauma.​

●​ Full PTSD may develop 6 months or even years later.​

●​ The reason for delayed onset is not yet understood (O’Donnell et al., 2013).​

Acute Stress Disorder (ASD)

●​ Introduced in DSM-IV to capture severe reactions occurring within the first month
after trauma.​

●​ Essentially similar to PTSD but occurs immediately after the event.​

●​ Purpose:​

○​ Recognize severe early trauma reactions.​

○​ Allow insurance coverage and early treatment.​

Relationship Between ASD and PTSD

●​ Surveys show:​

○​ ~50% of people with ASD develop PTSD later (Bryant, 2010; Bryant et al.,
2011).​
 ○​ ~52% of trauma survivors who later develop PTSD did not meet criteria for
ASD initially.​

●​ Conclusion:​

○​ ASD or Early severe reactions are not reliable predictors of who will develop
PTSD.​

○​ People with ASD benefit from treatment, even if they may not develop full
PTSD later.

Statistics and Prevalence of PTSD

Prevalence After Trauma Exposure

●​ PTSD is not as common as might be expected after traumatic events.​

●​ Historical examples:​

○​ WWII air raids (London): Most people coped well; few developed persistent
psychiatric disorders (Rachman, 1991).​

○​ Natural disasters (fires, earthquakes, floods): Similar findings; short-lived fear

reactions were common, but chronic PTSD was rare (Green et al., 1983).​

●​ War and military exposure:​

○​ Beirut students (1980s Israeli invasion): Half experienced intense bombing; no

significant long-term differences in PTSD symptoms, except for those directly
exposed to danger (Saigh, 1984).​

○​ Iraq and Afghanistan veterans:​

■​ 4.3% of all personnel developed PTSD.​

■​ Combat-exposed: 7.6%​

■​ Non-combat: 1.4% (Smith et al., 2008).​

 ■​ Vietnam veterans: 18.7%, directly related to combat exposure.​

Lifetime and Annual Prevalence in General Population

●​ Lifetime prevalence: 6.8% (Kessler, Berglund, et al., 2005)​

●​ Past-year prevalence: 3.5% (Kessler, Chiu, et al., 2005)​

●​ Adolescents: 3.9% (Kessler et al., 2012)​

Prevalence by Type of Trauma

●​ Highest risk: Assaultive violence, e.g., rape, kidnapping, serious assault.​

●​ Women who experienced repeated sexual assaults:​

○​ 2.4–3.5 times higher PTSD risk after a single assault​

○​ 4.3–8.2 times higher after re-victimization (Walsh et al., 2012)​

Proximity to Trauma

●​ Close, direct exposure increases risk:​

○​ Hurricane Katrina victims: Severe mental illness doubled for those with high
direct exposure (Kessler et al., 2006).​

○​ 9/11 Manhattan residents:​

■​ General south-of-110th-Street residents: 7.5% PTSD​

■​ Residents south of Canal Street (closest): 20% PTSD (Galea et al., 2002)​

○​ NYC schoolchildren grades 4–12: ~10.5% developed PTSD after 9/11; 155
developed agoraphobia.​

Chronicity and Risk

●​ PTSD tends to run a chronic course (Breslau, 2012; Perkonigg et al., 2005).​
 ●​ Predicts suicide attempts independently of other disorders (Wilcox et al., 2009).​

Key Insight

●​ Not everyone exposed to severe trauma develops PTSD.​

●​ Conversely, some individuals develop full-blown PTSD after relatively mild stressors.​

●​ Understanding these discrepancies requires examining etiology, not just exposure.​

Causes of Post-Traumatic Stress Disorder

(PTSD)
Direct Precipitating Event

●​ PTSD is unique in that the cause is known: personal exposure to a trauma.​

●​ Trauma types include assaultive violence, severe accidents, burns, war experiences, or
torture.​

Complexity Beyond the Trauma

●​ Not everyone exposed to trauma develops PTSD.​

●​ Example: Vietnam POWs​

○​ ~67% developed PTSD after long-term deprivation and torture.​

○​ 33% did not, including notable cases like Senator John McCain.​

●​ Example: Severe burns in children​

○​ Likelihood of PTSD rises with burn severity and associated pain.​

Contributing Factors
 ●​ Biological, psychological, and social factors interact with trauma exposure to
determine risk.​

●​ Intensity of exposure matters but does not fully account for why some develop PTSD
and others do not.​

Key Question

●​ What explains individual differences in PTSD development despite similar traumatic

experiences?​

●​ Suggests that predispositions (genetic, cognitive, social support, coping skills) play an
important role.​

Biological and Psychological

Vulnerabilities in PTSD
General Concept

●​ Like other disorders, PTSD risk is influenced by generalized biological and

psychological vulnerabilities.​

●​ Greater vulnerability → higher likelihood of developing PTSD.​

Genetic and Family Influences

●​ Family history of anxiety suggests a generalized biological vulnerability.​

●​ Twin studies:​

○​ Monozygotic (identical) twins: symptom correlation 0.28–0.41.​

○​ Dizygotic (fraternal) twins: symptom correlation 0.11–0.24.​

○​ Suggests genetic influence, but no direct causation.​

Diathesis-Stress Model
 ●​ Genetic factors predispose individuals to heightened stress reactivity and anxiety,
increasing susceptibility to PTSD after trauma.​

Evidence from Traumatic Events

●​ Northern Illinois University shooting (2008):​

○​ Female undergraduates experienced the same traumatic event.​

○​ Those with two short alleles (SS) of the serotonin transporter gene were
more likely to develop acute stress symptoms.​

○​ Demonstrates gene-environment interaction in PTSD risk.​

●​ Combat veterans: similar genetic risk factors identified (Wang et al., 2011).​

This shows how PTSD risk arises from the interplay of biological predispositions and
environmental trauma, consistent with the diathesis-stress model.

Predisposing Factors for PTSD

Vulnerability Traits

●​ Certain personality characteristics increase the likelihood of trauma exposure and later
PTSD:​

○​ Tendency to be anxious.​

○​ Minimal education (less awareness or resources to avoid risky situations).​

Evidence from Longitudinal Studies

●​ Breslau, Davis, and Andreski (1995; Breslau, 2012):​

○​ Random sample of 1,200 individuals.​

 ○​ Showed that pre-existing traits predicted both exposure to trauma and increased
PTSD risk.​

●​ Breslau, Lucia, and Alvarado (2006):​

○​ 6-year-old children with externalizing behaviors (acting out) more likely to

encounter trauma.​

○​ Higher intelligence predicted lower exposure to trauma.​

Interpretation

●​ Personality and heritable characteristics can predispose individuals to environments

where trauma is more likely.​

●​ This reflects a reciprocal gene–environment interaction:​

○​ Existing vulnerabilities influence the environment a person is exposed to.​

○​ The environment, in turn, affects the type of psychological disorder that may
develop (e.g., PTSD).​

Generalized Psychological Vulnerability

Definition and Context

●​ Described in multiple disorders, including anxiety and trauma-related disorders.​

●​ Based on early experiences with unpredictable or uncontrollable events.​

●​ Makes individuals more prone to develop disorders when stressors are moderate.​

Trauma and Stress Interaction

●​ High levels of trauma: vulnerability matters less.

○​ MAKE SENSE BECAUSE IT’S BEYOND OUR CAPACITY ALREADY. IT CAN
WRECK OUR SYSTEM SINCE IT’S HIGH, EVEN IF YOU ARE VULNERABLE
PSYCHOLOGICALLY OR NOT, WE CANNOT TOLERATE ENOUGH. IT WILL
BYPASS THE SYSTEM.​
 ○​ Example: 67% of prisoners of war studied by Foy et al. (1987) developed PTSD,
regardless of preexisting vulnerability. ​

●​ Low levels of trauma/stress: vulnerability plays a significant role in disorder

development.
○​ MAKE SENSE BECAUSE IT’S LOW LEVEL OF TRAUMA BUT WHY DO SOME
INDIVIDUAL DEVELOP DISORDER? SIMPLY BECAUSE GENERALIZED
PSYCHOLOGICAL VULNERABILITY IS AT PLAY. TOLERANCE BECOMES
LESSER.​

Family Instability as a Risk Factor

●​ Early family instability can create a sense that the world is uncontrollable or
dangerous (Chorpita & Barlow, 1998; Suárez et al., 2009).​

●​ Individuals from unstable families are at higher risk of PTSD after trauma.​

●​ Supported by studies on Vietnam veterans: family instability was a pre-war predictor of

PTSD in a sample of over 1,600 men and women (King et al., 1996, 2012).​

This highlights how generalized psychological vulnerability interacts with environmental

stressors to influence the likelihood of developing anxiety or trauma-related disorders.

Psychological Factors in Trauma

Response (Psychological Preparedness)
Study Overview

●​ Conducted by Basoglu et al., 1997 in Turkey.​

●​ Participants: Torture survivors divided into two groups:​

○​ Non-activists (34 survivors):​

■​ No history of political activity or expectations of arrest/torture.​

○​ Political activists (55 survivors):​

■​ Engaged in political causes; anticipated potential arrest/torture.​

Key Findings

●​ Abuse Severity: Non-activists experienced less severe torture than activists.​

●​ Psychopathology: Non-activists showed higher levels of psychological symptoms after

torture.​

●​ Psychological Preparedness:​

○​ Political activists were more psychologically prepared.​

○​ Anticipation and predictability of torture appeared to buffer them from severe

psychological symptoms.​

Implication

●​ Psychological factors (expectation, preparedness, mindset) can protect against or

increase the risk of developing PTSD following trauma.​

Social Factors in PTSD Development

Protective Role of Social Support

●​ Strong, supportive social networks reduce the likelihood of developing PTSD after
trauma.​

●​ This pattern is observed across cultures (e.g., American and Russian adolescents;
Ruchkin et al., 2005).​

Evidence from Research

●​ Hurricane Andrew Study (Vernberg et al., 1996):​

○​ Sample: 568 elementary school children, 3 months after the hurricane.​

○​ Findings: Over 55% reported moderate to severe PTSD symptoms.​

○​ Protective factors:​
 ■​ Support from parents, friends, classmates, teachers.​

■​ Positive coping strategies (active problem solving).​

○​ Risk factors:​

■​ Anger and placing blame on others.​

●​ Hurricane Charley Follow-up (La Greca et al., 2010):​

○​ Longer-term data (9 and 21 months post-trauma).​

○​ Strong social support reduced persistence of PTSD symptoms.​

Key Takeaways

●​ Social support is consistently protective against PTSD.​

●​ Broader and deeper social networks correlate with lower PTSD risk and symptom
persistence.​

●​ Coping style interacts with social support to influence outcomes.

Social Support and Stress Response

Human Social Nature

●​ Humans are inherently social animals.​

●​ Being surrounded by a loving, caring group influences biological and psychological

responses to stress.​

Evidence from Research

●​ Studies in children show that support from loved ones:​

○​ Reduces cortisol secretion.​

○​ Lowers hypothalamic–pituitary–adrenocortical (HPA) axis activity during

stress.
○​ Reference: Nachmias, Gunnar, Mangelsdorf, Parritz, & Buss (1996).​

ADDITIONAL INFORMATION!

1. The HPA axis

HPA = Hypothalamus → Pituitary → Adrenal cortex​
It’s a major stress-response system in the body:

1.​ Hypothalamus senses stress and releases CRH

(corticotropin-releasing hormone).​

2.​ Pituitary gland responds to CRH by secreting ACTH

(adrenocorticotropic hormone) into the bloodstream.​

3.​ Adrenal cortex (on top of the kidneys) releases cortisol, the main
stress hormone.​

2. What “HPA axis activity during stress” means

●​ When someone experiences stress, the HPA axis activates to mobilize
energy and prepare the body for “fight or flight.”​

●​ Measures of HPA activity:​

○​ Cortisol levels in blood, saliva, or urine​

○​ ACTH levels in blood​

○​ CRH activity in some research settings​

●​ Effects of cortisol:​

○​ Increases blood sugar​

○​ Suppresses non-essential systems (like digestion and some

immune functions)​
 ○​ Heightens alertness​

3. Why this matters in psychology

●​ Chronic HPA activation → linked to anxiety, depression, PTSD.​

●​ Support from loved ones can reduce HPA activity, lowering cortisol
responses to stress.​

✅“HPAIn short:​
axis activity during stress” = how strongly the body’s core
stress-response system (hypothalamus → pituitary → adrenal → cortisol) is
Diagram of the HPA axis and its role in stress:

STRESS

Hypothalamus

── releases CRH ──►

(Corticotropin-Releasing Hormone: signals the pituitary to produce ACTH)

Pituitary Gland

── releases ACTH ──►

(Adrenocorticotropic Hormone: signals the adrenal cortex to release

cortisol)

Adrenal Cortex

── releases Cortisol ──►

(Primary stress hormone: increases blood sugar, heightens alertness,

suppresses non-essential systems like digestion & immune response)

 │

Body Effects

• ↑ Blood sugar (energy for fight-or-flight)

• ↑ Alertness

• ↓ Non-essential functions (digestion, immunity)

Summary:

●​ CRH = signals the pituitary​

●​ ACTH = signals the adrenal cortex​

●​ Cortisol = carries out stress-response effects on the body

Key points to remember:

●​ CRH = Corticotropin-Releasing Hormone​

●​ ACTH = Adrenocorticotropic Hormone​

●​ Cortisol = primary stress hormone​

●​ Chronic overactivation → anxiety, depression, PTSD risk​

●​ Supportive social relationships can reduce HPA activity and cortisol

release

Real-World Implication

●​ High prevalence of PTSD in Vietnam veterans compared to Iraq/Afghanistan veterans

may be partially explained by lack of social support when returning home.​
Neurobiological Factors in PTSD
HPA Axis and CRF

●​ PTSD involves multiple neurobiological systems.​

●​ Corticotropin-releasing factor (CRF): Elevated or restricted in PTSD, reflecting

abnormal HPA (hypothalamic–pituitary–adrenal) axis activity.​

●​ Chronic arousal in PTSD may be directly linked to HPA axis dysregulation.​

Brain Structure Changes

●​ Evidence of hippocampal damage in PTSD populations:​

○​ War-related PTSD (Gurvits et al., 1996; Wang et al., 2010).​

○​ Adult survivors of childhood sexual abuse (Bremner et al., 1995).​

○​ Firefighters exposed to extreme trauma (Shin et al., 2004).​

●​ Hippocampus functions: Regulates HPA axis, learning, and memory.​

Functional Consequences

●​ Hippocampal damage may lead to:​

○​ Persistent and chronic arousal.​

○​ Memory deficits, evident in:​

■​ Gulf War veterans (Vasterling et al., 1998).​

 ■​ Holocaust survivors with PTSD vs. survivors without PTSD (Golier et al.,
2002).​

Reversibility of Damage

●​ Some hippocampal damage may be reversible:​

○​ Example: Cushing’s disease patients showed up to 10% hippocampal volume

increase after successful treatment (Starkman et al., 1999).​

●​ Suggests potential for trauma-induced changes in hippocampus to be partially

reversed with treatment.​

TO UNDERSTAND MORE:

Got it! Let’s integrate that into the explanation so it’s clear what HPA dysregulation means
for someone with PTSD vs. a normal stress response, and why some people develop
PTSD.

1. Normal HPA Axis Response

●​ Normal reaction to stress:​

1.​ Hypothalamus releases CRF → activates HPA axis.​

2.​ Pituitary releases ACTH → adrenal cortex releases cortisol.​

3.​ Cortisol helps body cope with stress (↑ energy, alertness) and feeds back to
turn off the stress response once the threat ends.​

●​ Outcome: Stress is acute, adaptive, and temporary.​

2. PTSD & HPA Axis Dysregulation

●​ In PTSD, the HPA axis may become overactive or underactive, often due to
trauma:​

HPA axis What happens Examples / Symptoms

state
Overactive Too much Hyperarousal, irritability, exaggerated startle,
CRF/cortisol insomnia, anxiety

Underactive Blunted cortisol Impaired stress regulation, fatigue, emotional

response numbing, difficulty responding to new stressors

●​ ​
Effect on hippocampus: Chronic dysregulation → hippocampal shrinkage → poor
memory, difficulty distinguishing safe vs. dangerous contexts.​

3. What makes someone develop PTSD

●​ Trauma exposure is necessary, but not sufficient. Risk factors include:​

○​ Genetic vulnerability (some people have more reactive HPA axes).​

○​ Prior trauma or childhood adversity.​

○​ Poor social support.​

○​ Pre-existing anxiety or mood disorders.​

○​ Brain factors: smaller hippocampus may increase risk; amygdala

hyperreactivity increases fear learning.​

✅ Key concept: PTSD arises from an interaction of trauma, HPA axis dysregulation, and
brain vulnerability, not just the traumatic event itself.

SUPPLEMENTAL:

🔬 Biological Core of PTSD

1.​ HPA Axis Dysregulation (starter problem)​

○​ Trauma → abnormal cortisol release (either too high or too low).​

○​ This dysregulation floods the brain with stress signals.​

2.​ Hippocampal Shrinkage (structural consequence)​

○​ The hippocampus is sensitive to cortisol.​

○​ Chronic exposure damages neurons → reduces hippocampal volume.​

 ○​ A smaller hippocampus can’t effectively inhibit the HPA axis or contextualize
fear memories.​

○​ This is why PTSD patients have trouble distinguishing “safe” vs. “dangerous”
situations.​

3.​ Amygdala Hyperactivity (functional driver)​

○​ Amygdala does not shrink; instead, it becomes overactive.​

○​ Overactive amygdala = exaggerated fear and emotional responses.​

4.​ Vicious Cycle​

○​ Hippocampal shrinkage = weak stress “brakes.”​

○​ Amygdala hyperactivity = strong fear “accelerator.”​

○​ HPA axis remains dysregulated → cycle continues → chronic PTSD

symptoms.​

✅ Bottom line in biology terms:

●​ HPA dysregulation starts the process.​

●​ Hippocampal shrinkage is the key structural damage that maintains PTSD.​

●​ Amygdala hyperactivity fuels symptoms.​

SUPPLEMENTAL 2:

Exactly — the hippocampus is central for long-term memory, especially episodic memory
(personal experiences situated in time and place). But there’s a subtlety here:

●​ The hippocampus isn’t just a “memory warehouse.” It acts more like a memory
organizer and contextualizer — binding together details of experiences and
distinguishing between similar contexts (“this noise was fireworks at a party, not
gunfire in a war zone”).​

●​ In PTSD, hippocampal shrinkage (or dysfunction) weakens this contextualization. That

can cause overgeneralization: harmless cues (a car backfiring) trigger the same fear
as the original trauma (gunfire).​

●​ Meanwhile, the amygdala—the brain’s alarm system—becomes hyperactive. Without

the hippocampus reigning it in, the amygdala drives exaggerated fear responses.​

●​ The prefrontal cortex (which normally regulates both the hippocampus and
 amygdala) also tends to be underactive in PTSD, so top-down control weakens
further.​

So yes, the hippocampus is essential for long-term memory, but in PTSD its reduced size and
function don’t erase memories; instead, they make traumatic ones harder to contextualize
and regulate, so they intrude more forcefully and seem inescapable.

FINAL REVISION:

Stress, the HPA Axis, and PTSD (Integrated Overview)

When the body encounters stress, it activates the hypothalamic–pituitary–adrenocortical
(HPA) axis:

1.​ Hypothalamus releases CRH (corticotropin-releasing hormone).​

2.​ CRH signals the pituitary gland to release ACTH (adrenocorticotropic hormone).​

3.​ ACTH stimulates the adrenal glands to release cortisol, the main stress hormone.​

Cortisol prepares the body for survival (increasing energy, sharpening alertness).

●​ Once the stress is over, the hippocampus (which monitors context and memory)
helps shut down the HPA axis through negative feedback, preventing prolonged
stress exposure.​

What Happens in PTSD

In people with post-traumatic stress disorder (PTSD), this system becomes dysregulated:

●​ Hippocampus:​

○​ Often smaller in volume (hippocampal shrinkage).​

○​ Weaker at distinguishing past vs. present → traumatic memories feel like they
are happening right now.​

○​ Because it normally helps shut down the HPA axis, its shrinkage means stress
regulation breaks down.​

●​ Amygdala:​

○​ Becomes overactive, exaggerating fear and threat detection.​

 ○​ This drives hypervigilance, exaggerated startle responses, and intrusive
emotional memories.​

●​ Prefrontal Cortex:​

○​ Becomes underactive, meaning it fails to regulate or “brake” the amygdala.​

○​ Result: less rational control over overwhelming fear.​

●​ HPA Axis:​

○​ Stress response may be overreactive (excess cortisol release → damage to

neurons, including hippocampus)​

○​ Or underreactive (blunted cortisol response → inability to adapt to stress).​

○​ Either imbalance worsens vulnerability to PTSD.​

Core Idea
It’s not just the HPA fluctuation itself that “causes” PTSD.

●​ The biological cascade is:​

1.​ Trauma + chronic stress → abnormal cortisol activity.​

2.​ This contributes to hippocampal shrinkage.​

3.​ Smaller hippocampus = poor memory contextualization + poor HPA shut-off.​

4.​ Combined with overactive amygdala + underactive prefrontal cortex → PTSD

symptoms (intrusive memories, hyperarousal, flashbacks).​

👉 Shortcut to remember:
●​ Amygdala alarms too loud.​

●​ Prefrontal brakes too weak.​

●​ Hippocampus too small (can’t add context, can’t shut stress off).​

●​ HPA axis out of tune.​

 That’s the biological “triangle” of PTSD.

Panic Attacks, PTSD, and the Alarm

Reaction
Panic Attack as an Adaptive Alarm

●​ Panic attacks = normal fear/alarm response occurring at the wrong time.​

●​ In both Panic Disorder and PTSD, the “alarm reaction” looks similar
physiologically.​

False (Panic Disorder) vs. True Alarm (PTSD)

●​ Panic Disorder: Alarm is false (triggered without real danger).​

●​ PTSD: Initial alarm is true (real danger present, e.g., trauma exposure).​

Conditioned/ Learned Alarms in PTSD

●​ Severe trauma can lead to conditioned alarm reactions:​

○​ Neutral cues become linked with trauma.​

○​ Example: Marcie → being tucked into bed reminded her of the emergency room
board.​

●​ These reminders later trigger intense fear and panic, even when no real danger exists.​

Anxiety About Future Experiences (Fear of Flashbacks)

 ●​ PTSD can also produce anticipatory anxiety “about losing control over emotions”.​

●​ Example: fear of flashbacks (common symptom in PTSD).​

●​ This adds a secondary layer of anxiety beyond the original trauma response.​

Role of Vulnerabilities

●​ Whether anxiety develops depends on individual vulnerabilities (biological,

psychological, social).​

●​ This aligns with the broader triple vulnerability model.​

Etiology Model

●​ The described framework is summarized in Figure 5.12 (below).​

​
Treatment of PTSD
Core Principle (Psychological Perspective)

●​ Most clinicians agree:​

○​ Patients must face the original trauma.​

○​ Process the intense emotions associated with it.​

 ○​ Develop effective coping procedures to reduce debilitating effects (Beck &
Sloan, 2012; Najavits, 2007; Monson, Resick, & Rizvi, in press).​

Catharsis (Psychoanalytic View)

●​ Definition: Reliving emotional trauma to relieve emotional suffering.​

●​ Challenge: Re-exposure must be therapeutic rather than retraumatizing.​

Practical Limits of Re-Exposure

●​ Unlike phobias (where feared object can be recreated), traumatic events are:​

○​ Difficult to recreate safely.​

○​ Risky for therapists to attempt directly.​

Imaginal Exposure (Solution for Exposure That Is Safe)

●​ Solution: Trauma and its emotions are worked through systematically in

imagination.​

●​ Has been used for decades under different labels.​

●​ Common strategy with adolescents and adults:​

○​ Develop a narrative of the traumatic experience.​

○​ Review it extensively in therapy.​

Cognitive Therapy Component

●​ Targets negative assumptions about trauma:​

○​ Self-blame.​

○​ Guilt.​

●​ Goal: Reshape maladaptive thoughts as part of healing.​

Trauma Memory and Early Intervention in
PTSD
Memory Repression and Return

●​ Trauma victims often:​

○​ Repress emotional aspects of the trauma.​

○​ Sometimes repress the memory itself.​

○​ This process is automatic and unconscious.​

●​ With treatment:​

○​ Memories may “flood back.”​

○​ Patients can dramatically relive the trauma.​

○​ Though frightening, this reliving can be therapeutic if managed properly.​

Preventive Interventions After Trauma

●​ Evidence shows that early, structured interventions right after trauma can prevent
PTSD development (Bryant et al., 2003; Ehlers et al., 2003; Kearns et al., 2012).​

●​ Preventive psychological approaches are more effective than medications (Shalev et

al., 2012).​

Example: Ehlers et al. (2003) Car Accident Study

●​ Participants: trauma victims at high risk for PTSD after car accidents.​

●​ Intervention: 12 sessions of cognitive therapy.​

●​ Outcomes:​

○​ 11% developed PTSD (with cognitive therapy).​

 ○​ 61% developed PTSD (with detailed self-help booklet).​

○​ 55% developed PTSD (with repeated assessments only).​

●​ Afterward, patients who needed it received cognitive therapy, confirming its

effectiveness.​

Debriefing Risks (WAG PILITIN MAG CHIKA ANG VICTIMS AFTER

TRAUMA!!!)

●​ Single-session debriefing, where victims are forced to discuss feelings right after
trauma:​

○​ Can be harmful (Ehlers & Clark, 2003).​

○​ Increases distress rather than prevents PTSD.​

⚖️ Key Tension:
●​ Early structured cognitive therapy → helpful, preventive.​

●​ Forced single-session debriefing → potentially harmful.

Case Example: Marcie and Her Brother

Background

●​ Patient: Marcie, a young girl who developed PTSD after being bitten by a dog.​

●​ Primary difficulty: Fear of doctors and medical procedures.​

●​ Context: Treated simultaneously with her brother at the clinic.​

Treatment Approach

●​ Graduated Exposure (least to most intense):​

○​ Mild tasks: having her pulse taken, lying on an exam table, taking a bath after
cutting herself.​

○​ Most intense task: being strapped to a restraining board.​

●​ Observational Learning:​

○​ Marcie first watched her brother undergo these tasks with minimal fear.​

○​ This modeling reduced her anticipatory anxiety.​

●​ Active Participation:​

○​ After observing, Marcie attempted each task herself in sequence.​

○​ Reinforcement included:​

■​ Instant photographs of her success.​

■​ Drawing pictures of the situations.​

■​ Praise and encouragement from therapist and family.​

Special Considerations

●​ Because of her young age, Marcie could not effectively use imaginal exposure
(recreating traumatic memories in imagination).​

●​ Instead, therapy focused on altering current perceptions of medical procedures

through direct experiences.​

Outcome
 ●​ Marcie’s PTSD symptoms were successfully reduced.​

●​ Her brother’s guilt (about being involved in the traumatic incident) also decreased
because he played a supportive role in treatment.​

This is essentially an application of exposure therapy adapted for children, with extra reliance
on modeling, reinforcement, and concrete activities (photos, drawings) because young
children lack the same imaginative and cognitive capacities as adults.

PTSD: Evidence on Treatment Outcomes

Long-Term Effects of Evidence-Based Psychological Treatments

●​ Study of 144 female rape survivors:​

○​ Treated with evidence-based psychological interventions.​

○​ Follow-up: 5–10 years post-treatment.​

○​ Findings: Substantial decreases in symptoms were maintained with very little

change (Resick et al., 2012).​

○​ Implication: These treatments produce lasting change.​

Couple-Based PTSD Treatment

●​ Study of 40 heterosexual and same-sex couples:​

○​ One partner met criteria for PTSD.​

○​ Partner was directly included in treatment.​

○​ Purpose: Address severe disruptions in intimate relationships, which can lead to

relapse.​

○​ Outcomes (Monson et al., 2012):​

■​ Significant improvement in PTSD symptoms.​

 ■​ Increased relationship satisfaction → may contribute to long-term
adjustment.​

Pharmacological Treatments

●​ SSRIs (e.g., Prozac, Paxil):​

○​ Effective for anxiety disorders in general.​

○​ Also helpful for PTSD (Dent & Bremner, 2009; Schneier et al., 2012).​

○​ Likely mechanism: Reduction of severe anxiety and panic attacks prominent in

PTSD.

Adjustment Disorders – Clinical

Description
Core Features

●​ Definition: Anxious or depressive reactions to identifiable life stress.​

●​ Severity:​

○​ Milder than acute stress disorder or PTSD.​

○​ Still impairing — disrupts work, school, relationships, or daily life.​

●​ Onset context: Triggered by stressful life events that are not severe enough to be
classified as traumatic (unlike PTSD triggers).​

Special Patterns

●​ Adolescence: Life stress may lead to conduct problems (e.g., acting out).​
 ●​ Chronic Course: If symptoms persist longer than 6 months after stress is removed,
the adjustment disorder is considered chronic.​

Diagnostic Use and Limitations

●​ Historically, often used as a residual diagnosis:​

○​ For individuals with significant anxiety or depression tied to life stress.​

○​ When symptoms don’t meet full criteria for another anxiety or mood
disorder.​

●​ Because of this broad “leftover” usage, little systematic research exists on adjustment
disorders.​

Underlying Vulnerabilities

●​ Likely reflects individuals who already have:​

○​ Biological vulnerability: inherited tendency toward heightened stress reactivity.​

○​ Psychological vulnerability: trait anxiety that “flares up” when under stress.​

●​ But not severe enough to cross the diagnostic threshold for more serious conditions (like
PTSD or major depression).​

This section shows how adjustment disorders occupy a middle ground: not as intense as
PTSD, but still clinically significant and often requiring intervention.
Attachment Disorders (mostly children)
General Description

●​ Definition: Disturbed and developmentally inappropriate behaviors in children.​

●​ Age of Onset: Emerge before 5 years of age.​

●​ Core Feature: Child is unable or unwilling to form normal attachment relationships

with caregiving adults.​

●​ Cause: Inadequate or abusive child-rearing practices, such as:​

○​ Frequent changes in primary caregiver (e.g., multiple foster placements).​

○​ Neglect at home.​

●​ Impact: Basic emotional needs (affection, comfort, nurturance) and even basic daily
necessities are not met.​

●​ Etiology: Considered pathological reactions to early extreme stress (Kay & Green,
2013).​

DSM Shift

●​ DSM-IV: Both patterns were grouped under Reactive Attachment Disorder (RAD).​

●​ DSM-5: Now split into two separate disorders (Zeanah & Gleason, 2010; Gleason et
al., 2011):​

1.​ Reactive Attachment Disorder (RAD) – inhibited type.​

2.​ Disinhibited Social Engagement Disorder (DSED) – disinhibited type.​

 1.​ Reactive Attachment Disorder (RAD) – Emotionally
Withdrawn/Inhibited Type
●​ Behavioral Features:​

○​ Rarely seeks caregiver for protection, support, or nurturance.​

○​ Rarely responds to caregiver offers of comfort.​

○​ Lack of responsiveness to social interactions.​

○​ Limited positive affect (few signs of joy/pleasure).​

○​ Heightened emotionality: fearfulness, intense sadness.​

2.​ Disinhibited Social Engagement Disorder (DSED) –

Indiscriminate/Disinhibited Type
●​ Cause: Often linked to same inadequate child-rearing, possibly including harsh
punishment.​

●​ Behavioral Features:​

○​ No inhibitions in approaching unfamiliar adults.​

○​ Overly familiar or inappropriately intimate behaviors.​

○​ Willingness to go off with strangers without checking back with the caregiver.​

Key Distinction

●​ RAD (Inhibited): Child withdraws emotionally, avoids/ignores caregivers.​

●​ DSED (Disinhibited): Child is overly social, lacks normal caution with strangers.​

●​ Reason for DSM-5 Separation: Presentations are markedly different, so now classified
as distinct disorders (Gleason et al., 2011).​
IN A NUTSHELl

Differentiation
Feature Adjustment Disorder Attachment PTSD
Disorders (RAD /
DSED)

Trigger Any identifiable life Pathological Trauma: actual or

stressor (divorce, job caregiving threatened death,
loss, moving, breakup, environment in early serious injury, or
illness). Does not need childhood (severe sexual violence.
to be trauma. neglect, abuse,
repeated caregiver
changes).

Age of Onset Any age Must occur before Any age

age 5

Symptoms Emotional/behavioral - RAD: emotionally Intrusion

reaction out of proportion withdrawn, limited (flashbacks,
to stressor (e.g., affect, doesn’t seek nightmares),
depression, anxiety, or respond to avoidance, negative
conduct issues). comfort. - DSED: mood/cognition,
indiscriminate hyperarousal
sociability, overly (startle,
familiar with hypervigilance).
strangers.

Course/Duratio Starts within 3 months of Persistent if Can be acute or

n stressor; resolves within caregiving chronic; may last
6 months after stressor environment remains years if untreated.
ends. inadequate; chronic
developmental
impact.

Core Stress response that is Attachment failure Direct traumatic

Mechanism out of proportion but due to neglect/abuse stress response
triggered by disrupting normal with re-experiencing
non-traumatic stressors. bonding. and avoidance.
 Example Teen becomes severely - RAD: Child doesn’t Survivor of assault
depressed after parents’ seek comfort when has nightmares,
divorce and grades drop. hurt and shows flat avoids reminders,
affect.- DSED: Child and is hypervigilant.
hugs strangers and
leaves with them
without hesitation.

Why All Are in the Same DSM-5 Section

They’re grouped together because exposure to stress or trauma is central, but the nature
of the stressor and the developmental timing differ:

●​ Adjustment disorder → everyday life stressors​

●​ Attachment disorders → early caregiving neglect/abuse​

●​ PTSD → trauma meeting Criterion A​

Good push here — you’re asking about the boundary lines between adjustment disorder,
attachment disorders, and PTSD. These often get blurred because they all sit in the
Trauma- and Stressor-Related Disorders section of the DSM-5, but they aren’t the same
thing. Let’s break them down.

Why They’re Grouped Under PTSD’s Category

●​ In DSM-5, PTSD, Acute Stress Disorder, Adjustment Disorder, Reactive
Attachment Disorder, and Disinhibited Social Engagement Disorder are all in the
Trauma- and Stressor-Related Disorders chapter.​

●​ The unifying theme is that exposure to a stressor/trauma is central to the diagnosis.​

●​ They differ in type of stressor, timing, age of onset, and symptom pattern.​

Differentiation
1. Adjustment Disorder

●​ Trigger: A clearly identifiable stressor (breakup, job loss, moving to new country,
 illness).​

●​ Timing: Symptoms begin within 3 months of the stressor.​

●​ Symptoms: Emotional/behavioral reaction that is out of proportion to the stressor

(depression, anxiety, conduct issues, etc.).​

●​ Duration: Does not persist beyond 6 months after the stressor ends. BUT
SOMETIMES COULD BE CHRONIC.​

●​ Example: A college student becomes so anxious and depressed after failing classes
that they withdraw from social life and drinking increases.​

👉 Key point: Stressor can be “everyday life” stress, not trauma-level.

2. Attachment Disorders (RAD and DSED)

●​ Trigger: Pathological caregiving environment — severe neglect, abuse, or multiple

caregiver disruptions before age 5.​

●​ Age: Must occur in early childhood.​

●​ Types:​

○​ Reactive Attachment Disorder (RAD): Child is emotionally withdrawn,

doesn’t seek comfort from caregivers, minimal emotional responsiveness.​

○​ Disinhibited Social Engagement Disorder (DSED): Child is overly familiar

with strangers, lacks appropriate boundaries.​

●​ Example:​

○​ RAD: A 4-year-old in foster care doesn’t cry when hurt, doesn’t go to adults for
comfort, and shows flat affect.​

○​ DSED: A child eagerly hugs strangers at the park and goes with them without
hesitation.​

👉 Key point: Rooted in early attachment failure, not a later stressful event.
3. PTSD

●​ Trigger: Actual or threatened death, serious injury, or sexual violence (not just stress).​
 ●​ Symptoms: Intrusive memories/flashbacks, avoidance, negative mood/cognition,
hyperarousal.​

●​ Timing: Can emerge soon after trauma (ASD) or delayed (Delayed Onset Disorder).​

●​ Example: Car accident survivor relives the crash at night, avoids highways, and is
hypervigilant around traffic.​

👉 Key point: Always requires trauma that meets the DSM-5 “Criterion A” definition.
Why It Matters
●​ Adjustment disorder = stress response gone wrong, but doesn’t need trauma.​

●​ Attachment disorder = early caregiving failure, developmental problem.​

●​ PTSD = trauma-related disorder with hallmark re-experiencing and avoidance.​

●​ Grouped together because the trigger is central, but they differ in severity of stressor,
developmental timing, and symptom expression.​