PTSD FROM DSM III TO DSM 5: PROGRESS AND

CHALLENGES

Trauma:
Trauma is a deeply distressing or disturbing experience that overwhelms an
individual’s ability to cope, causing lasting negative effects on mental, emotional, and
physical well-being. It can result from a single event, a series of events, or chronic
circumstances that threaten safety or cause severe psychological shock.

Any disturbing experience that results in significant fear, helplessness, dissociation,

confusion, or other disruptive feelings intense enough to have a long-lasting negative
effect on a person’s attitudes, behavior, and other aspects of functioning.
Traumatic events include those caused by human behavior (e.g., rape, war, industrial
accidents) as well as by nature (e.g., earthquakes) and often challenge an individual’s
view of the world as a just, safe, and predictable place. any serious physical injury,
such as a widespread burn or a blow to the head.
Adapted from the APA Dictionary of Psychology

Types of trauma

Many experiences can be traumatic. And we all experience trauma in unique

ways. But some experiences or events that lead to trauma are sometimes grouped
together and given a name.
These terms normally describe how trauma affects people from certain groups, or in
specific situations. This section explains some of these terms:

1. Childhood trauma
You may have experienced trauma during your childhood. These experiences could
make you more likely to have mental health problems as an adult. This is especially if
you didn't have support to manage the trauma. Or if you experienced trauma
continuously, over a long period of time.
My high functioning depression and anxiety is a result of childhood trauma that lay
dormant from age 13 until it [was] triggered when I was 39.

2. Collective trauma

Collective trauma is when a traumatic event happens to a large number of people at

the same time.

This doesn't mean that everyone who experienced the event feels the same way about
it. Or that they all feel it was traumatic for them. Everyone still copes with it in their
own way.

Experiencing collective trauma can mean you experience personal symptoms and
'social symptoms'. Social symptoms can include how society has dealt with or reacted
to the trauma. For example:
  If it isn't socially acceptable to talk about the event, or only being able to talk
about it in certain ways
 If people avoid or discriminate against certain groups that might be unfairly
blamed for the trauma

The anniversaries of a collective trauma might lead to events such as memorials and
media coverage. You might find these events comforting ways of managing collective
trauma. Or you may find them very difficult. How you feel about these anniversaries
can also change over time.
Our information on coping with distressing events in the news might help if you're
struggling with media coverage of trauma.
Covid-19 has destroyed and remoulded me into someone I am still trying to figure out.
It has completely changed my outlook on life and it has broken a part of me which I
am still working hard to heal, with the help of my colleagues and loved ones.

3. Generational trauma

Generational or intergenerational trauma is a type of trauma that's experienced across

generations of a family, culture or group. For example, there's some evidence that
shows children and grandchildren of people who survived the Holocaust experience
higher rates of mental health problems.

Trauma that happened in the past has an impact on the mental health of current
generations. But it's not always clear how. Some researchers think trauma may affect
our genes. But it's more likely that trauma affects the environment we grow up in.
This can be through things like:

 Stories or warnings older generations have passed on about the trauma they
experienced. This could make you wary of the world around you.
 The legacy of trauma continuing to impact your wellbeing and safety, such as the
ongoing effects of colonialism on the health and wellbeing of people of colour.
 Trauma affecting how older generations have raised and looked after us. For
example, if your parent avoided certain places due to their experience of trauma,
you might also feel anxious in those places. This might be more likely to happen if
older generations haven't had support for their traumatic experiences when they
needed them.
As a second-generation South Asian woman, my lived experience has given me a
deep understanding of the impact of marginalisation, poor mental health, and racial
and intergenerational trauma, and how they intersect

4. Moral injury

Moral injury means how you feel when you're put in a situation that goes against your
morals, values or beliefs. It's often seen in people who have been in situations where
they need to make big decisions about other people's lives.

Moral injury might happen because of:

 Lack of resources provided by a workplace, government or ruling body to treat

everyone equally
  Poor safety practices
 Regulations or orders from people in charge that don’t seem to be in people’s
best interests
 Unsafe or immoral behaviour from others, particularly those in charge
 Working in a system you see as failing, but have no power to fix

This kind of trauma can impact your view of the world, your government, or the
organisation you work for. Along with other effects of trauma, you might:

 Feel a lack of purpose in your personal or professional life

 Feel disconnected from people around you
 Feel betrayed, alienated or ashamed
 Question your moral codes and ethics

If the moral injury happened in the workplace, you might also have difficult feelings
about continuing to work there. It can be difficult to seek help in the workplace in
these situations. This is because the people running the workplace can be part of the
cause of moral injury.
If you need to talk to someone about wrongdoing in your workplace, the
charity Protect provides confidential support.

5. Racial trauma

The impact racism can have on your mind and body is sometimes described as racial
trauma.
There's no universal definition of racial trauma. Some people use it to mean all the
effects that encountering racism can have on how we think, feel and behave. Others
use it to describe a specific set of symptoms. Find out more about racial trauma.

6. Secondary trauma

Secondary trauma is when you witness trauma or you're closely connected to it. But
you don't experience the trauma directly. It's sometimes called vicarious trauma.

For example, if you're a journalist who often reports on traumatic events. Or if you're
a medical professional working in an accident and emergency department.

Effects of secondary trauma are similar to general trauma. But you may find you also
begin to feel detached from the trauma. Or treat it as a very separate part of your life.
Experiencing secondary trauma is as valid as any other kind of trauma. It can impact
you just as much.

The concept of trauma is changing drastically in every publication or

revision of Diagnostic and Statistical Manual of Mental Disorders. The
underlying dimensions of trauma are also under constant [Link]-
traumatic stress disorder has been out there as back as human history.
However, the recognition of traumatic symptoms on people’s lives and
mental health has been recently recognized. Even though non-governmental
organizations and civic society drew attention of this issue for a long time,
the legal and administrative bodies were reluctant to take action and
recognize the effects of traumatic experiences on people’s life.

INTRODUCTION
Obviously wars have adversarial effects on everybody’s life whether they
have been in combat or not. Vietnam war is the hallmark for the recognition
of traumatic stress on public and civic sphere. Many veterans have
adjustment, marital, drug and alcohol, and occupational problems after the
war. Thus, following WW-II, the American Psychiatric Association (APA)
published the first of the series of Diagnostic and Statistical Manual of
Mental Disorders (DSM) in 1952.
The DSM-I used the name “Gross Stress Reactions” in reference to stress-
related experiences. Gross Stress Reactions referred to a reaction to extreme
stress, such as war, disasters, fires, earthquakes or explosions (Berthold
and Carlier, 1992). By definition, the disorder was described as acute stress,
and in the absence of stress it was suggested to look for another diagnosis.
In DSM-I and DSM-II, the categories of gross stress reaction and transient
situational disturbance, respectively, were used to describe acute
symptomatic distress following adversity; whereas more prolonged
disorders were conceptualized as being anxiety or depressive symptoms
(Yehuda and McFarlane, 1995).

The APA published the second DSM in 1968. DSM-II

did not include a specific category for stress related reactions.
However, it recognized that extreme stress could be followed by mental
health problems in that it included the diagnostic category of “Temporary
Situational Disorder” (O’Brien, 1998). This category was intended to define
reactions to unusual stress caused by anything from unwanted pregnancy to
a death sentence (Berthold and Carlier, 1992). However, such stress was
seen as a self-limiting condition. It was felt that chronic problems occurred
only in those with severe premorbid personality disturbances. In those cases,
the condition was solidified into a recognizable psychiatric disorder.

VIETNAM ERA AND CONTRIBUTIONS OF WAR

The Vietnam War was definitely a turning point in the history of
posttraumatic stress disorder. Post-traumatic Stress Disorder (PTSD) was
not a particularly popular topic before Vietnam. Even though the APA had
published two DSM manuals and did some modification in the definition of
extreme stress and traumatic experiences, literature provides very few
studies concerning traumatic stress. In early studies, it was reported that
Vietnam had low rates of psychiatric casualties (Jones, 1967). However,
later studies suggested that 300,000 to 700,000 or more of the 3,000,000
who served in Vietnam had PTSD (O’Brien, 1998). Some studies had
focused on Holocaust survivors and women who had suffered violent sexual
crimes, but the Vietnam War was the essential element in the development
of the diagnosis of PTSD.

The Vietnam War is said to have been different from other wars. It was
unpopular, prolonged, low intensity, distant, a guerilla conflict, and lost by
Americans. Moreover, during the era, peace was socially more accepted
than war. Thus, Vietnam veterans were not welcomed as heroes. Gradually,
a database was developed and small-scale studies were conducted,
especially single case studies, which were done in many hospitals and
research centers. Then, Vietnam began to be associated with social problems,
poor integration in society, criminal behavior, mental health problems,
divorce, and substance and alcohol abuse (O’Brien, 1998). Despite the much
lower rates of acute illness, there were apparently much higher rates of
chronic illness such as PTSD in veterans after they left the army. In line
with that, a series of books, films, television programs, and newspaper
articles, emphasized the plight of veterans who had been marginalized and
socially handicapped. There were some attempts to get government
involvement in this new issue.

However, Congress constantly refused to fund any rehabilitation,

intervention or prevention programs for Vietnam veterans. Nonetheless,
finally in 1979 Congress agreed to subsidize services for Vietnam veterans
with readjustment problems (Kelly, 1985). These adjustment problems were
described as “a low-grade motivational and behavioral impairment with a
victim’s overall ability to cope reasonably with his daily life.” A
readjustment problem does not usually amount to a definable psychiatric
illness. However, with new funding, new hospital and treatment centers
opened, more professionals were hired, and large scale data were collected.
Therefore, most of today’s current knowledge about the etiology, prevalence,
and treatment is based widely on Vietnam War veteran studies. The
Vietnam phenomenon led the way to defining a new classification in 1980,
when PTSD was officially identified for the first time (APA, 1980).

Historical, political, and social forces have played a major role in the
acceptance of the idea of trauma as a cause of the specific symptoms of
PTSD (Yehuda and McFarlane, 1995). Political turbulence, atrocities, and
ethnic genocide as well as civil and guerilla wars in different parts of the
world in the late 70’s and early 80’s, (for example, communist oppression in
Cambodia, Vietnam, guerilla wars in Latin America, and civil war in
Lebanon, and Revolution in Iran) caused many to be persecuted, tortured
and exiled from their own homeland and millions of refugees sought a safe
haven in Western Europe and North America. Studies of political
persecution and big tides of exodus shed more light on our understanding of
the dynamics of trauma and its long-term effects. Thus, the formulation of
PTSD as a normative and adaptive response to trauma in the DSM-III
addressed social and political issues as well as mental health issues. From a
social and political perspective, PTSD as a concept has done much to assist
in the recognition of the rights and needs of victims who have been
stigmatized, misunderstood, or ignored by the mental health field.

The APA acknowledged the role of trauma in the etiology of certain

psychological symptoms in 1980. Before that time, traumatic symptoms
(hysteria) were seen as an individual pathology, rather than caused by
external factors. In 1980, the construct of PTSD was incorporated into the
DSM-III, Diagnostic and Statistical Manual of Mental Disorders, and there
was a move away from looking at premorbid vulnerability as the
contributing factor. At the same time, the construct of “hysteria”
disappeared from the DSM system, and was divided into several different
mental disorders (van der Kolk et al., 1996b).

The introduction of the new diagnosis PTSD was the recognition of the
psychic consequences of war, especially as experienced by Vietnam
veterans (Berthold and Carlier, 1992). The early studies reported a lot of
similar symptoms and emotional and behavioral reactions to disaster, war,
and trauma experience. However, it was not until 1980 that the diagnostic
category of PTSD was officially introduced in the DSM-III American
Psychiatric Association (APA) because evidence gained from empirical
studies suggested that the impairment following extreme adversity is
etiologically and phenomenologicaly
different from what it was originally thought to be.

With the DSM-III (1980), PTSD was classified as an anxiety disorder with
social, emotional and behavioral dimensions (Foy et al., 1987). When the
diagnosis of PTSD was first introduced in 1980, 12 symptoms were
specified, clustered into three groups:
Criterion: Set B (3 re-experiencing symptoms; that is, recurrent and
intrusive recollections of the traumatic event, such as flashbacks and
nightmares),
Set C (3 symptoms representing numbing of responsiveness;
restricted affect) and
Set D (6 other symptoms, including symptoms of hyperarousal,
avoidance of trauma-related stimuli, and guilt about surviving the trauma).

An individual must present at least one re-experiencing, three avoidance,

and two arousal symptoms to be diagnosed with PTSD (Taylor et al., 1998).
DSM-III is the first classification which considered the role of external
environmental elements as triggering factors.
Challenges: However, some important issues remained unresolved
(McFarlane, 1988b). The first problem was that the reliability of DSM-III
was established in outpatient settings. This led to some problems in
discriminating between war and disaster-related experiences. Even though
the DSM-III was published sometime after the Vietnam War, the initial
reports showed a very low prevalence of psychiatric disorders during the
war. In the following years, thousands of veterans flooded into hospitals and
became involved in many social, marital, and criminal behaviors, drug
addiction, and other psychiatric disorders. Then the delayed recognition of
substantial psychiatric morbidity gained more attention and changed the
clinician’s understanding of the early phenomenology of PTSD and other
disorders. On the other hand, many veterans demonstrated significant
achievements and adaptations in their private as well as social life (Breslau
and Brenner, 1987).
Secondly, other studies (Saigh, 1991; Solomon and Canino, 1990; Yehuda
and McFarlane, 1995) reported that a majority of patients with PTSD
diagnosis had some other concurrent psychiatric diagnosis. These
comorbidity issues had been cited in many resources and gave way to
consider a new classification. Most studies assess PTSD reports either in
terms of rates of full-blown diagnosis, or else in terms of undefined partial
or subclinical levels (Solomon et al., 1989).
Criteria C and D are misplaced and, in fact, are symptoms of other disorders
such as depression or anxiety, and therefore resulted in artificially high rates
of co-morbidity diagnoses. Breslau and Brenner (1987) argued that the
DSM-III diagnosis was based on face validity (expert consensus). They
further claimed that PTSD overlaps with other disorders, especially with
generalized anxiety disorders, phobia, and depression. In defining the
symptoms of PTSD, there is a clear overlap with psychoanalytically defined
anxiety neurotic symptoms, such as depersonalization, de-realization,
obsession and compulsions, histrionic behavior, and mood disturbance. Both
the theoretical connection with neurosis through the re-experiencing of
the trauma and the phenomenological similarity in clinical symptoms make
it clear that DSM-III PTSD is in fact a special case of the psychoanalytic
construct of neurosis in which affective components are especially intense
(Breslau and Brenner, 1987).

The suggested new criteria included a) existence of a severe stressor, and b)

the re-experiencing of the trauma. Re-experiencing of the trauma does not
occur with other disorders. Similarly, a connection was seen between the
stressor and an adjustment disorder. However, adjustment disorder was not
defined in DSM-III as a distinctive category. Common significant distress or
the stress “outside of usual human experience” did not provide a definitive
rule in determining PTSD. For example, common stressful experiences did
not qualify a person for PTSD, but chronic illness, man-made disasters, and
natural disasters did quality an individual for PTSD diagnosis.

Solomon and Canino (1990) provided empirical findings and argued that
common stressful events such as moving, money problems, breaking-up
with a best friend, involuntarily taking someone into the home, and similar
incidents are more closely related to PTSD than life events are. Their results
suggested that the definition of trauma as “outside the range of usual human
experience” is inappropriate. Because some problems attached to DSM-III
criteria and children’s reactions were not specifically addressed, some
researchers (Galante and Foa, 1986; McFarlane et al., 1987) continued to
use instruments that measure aggression, school problems, depression etc. in
order to identify emotional problems. Rutter Behavioral Questionnaires and
Beck Depression Inventories (both instruments had parents’ and teachers’
forms available) were commonly used to assess “posttraumatic phenomena”
(McFarlane et al., 1987) reactions in children.

Then in the following years the DSM-III was revised again (APA, 1987) and
the symptom list was modified again and expanded to 17 symptoms. Set B
was increased to 5 re-experiencing symptoms. Set C was increased to 7
symptoms by including avoidance and numbing symptoms, and set D was
refined to include 5 symptoms of hyperarousal. The symptom regarding
survivor guilt was dropped from the list. Moreover, the DSM –III-R
classification did not distinguish between acute and chronic PTSD (Foy et
al., 1987).

Thus far, it is clear how often emphasis was put on the temporary or reactive
aspects of PTSD while extending the stressor group to include a much
broader spectrum of undesired experiences. Discussion about the reactive
and temporary nature of the “stress reaction” became a major argument after
1980. The duration of time of a reaction to a stress was being argued.

Finally, in DSM-III-R, duration of the emotional state of discomfort of at

least one month was required, but the general opinion was that the one
month stipulation was purely arbitrary (Berthold and Carlier, 1992). The
symptoms in the DSM-III-R were retained in the DSM-IV (American
Psychiatric Association, 1994), with the only exception being that one of the
symptoms from Set D was reallocated to set B. One of the most significant
changes was to acknowledge that children might react to a traumatic event
with disorganized and agitated behavior (APA, 1994). Previous classical
studies cited some regressive behavioral patterns as symptoms of stress.
Conversely, the DSM-IV discarded the criterion of “loss of newly learned
skills.” Palmer (2001) brought up another criticism, saying that although the
DSM-IV is being used extensively by mental health professionals as a basis
for diagnostic and treatment purposes, the construct of disorders within the
DSM-IV has not been empirically validated.

The most current version of the DSM is the Fourth Edition, Text Revision
(DSM-IV-TR; 2000), published in June 2000 by the American Psychiatric
Association. Similar symptoms are employed in their revised edition as well.
PTSD is officially classified as an anxiety disorder, but some have argued
that it fits more closely with the dissociative disorders, and others feel it
belongs by itself. While some consider PTSD the pure and only result of
trauma, some studies present various symptoms as related to this theme.
Depression, anxiety, and dissociation are three disorders that may
sometimes arise after the traumatic experience. Dissociation is a fairly
normal coping strategy in the face of overwhelming stress, but extreme
dissociative tendencies may be pathological. The current understanding of
dissociation with regard to PTSD is very close to Janet (1911)’s
explanations. In addition, some researchers have also reported somatoform
reactions. There has also been discussion over differential diagnoses for
simple vs. chronic traumatic histories. Classification issues such as these
will continue through field trials for the DSM-V (Magritte, 2000).

In 2013, American Psychiatric Association revised the criteria for PTSD,

which requires the following criteria: re-experiencing the event, alterations
in arousal, avoidance, negative alterations in cognition and mood (APA,
2013). It also requires a clinically significant distress or impairment in social,
occupational or other important areas of human functioning. This should last
at least one month or longer and the disturbance should not be caused by
substance or medical condition.

CONCLUSIONS
As the time progress and the clinical and theoretical experiences grow, new
information would accumulate and help us to understand better the
phenomenon of traumatic experiences. By itself, PTSD is very complex and
heterogeneous set of symptoms that may resemble anxiety or affective
disorder. Psychiatrist, psychologist and mental health workers are making
bit-by-bit progress to fully understand this phenomenon. Especially,
neurological sciences and cognitive sciences are discovering new advances
to help us to fully understand this mysterious experience.

PTSD FROM DSM III TO DSM 5: PROGRESS

1. The Shift in Nosological Classification

In earlier editions, PTSD was categorized as an Anxiety Disorder. This implied that
the primary pathology was a malfunction of the fear circuit (the amygdala-
hippocampal axis). DSM-5 moved it to Trauma- and Stressor-Related Disorders.
This is a significant theoretical shift: it acknowledges that while anxiety is common,
the core of PTSD often involves dissociation, shame, anger, and moral injury,
which are not captured by traditional anxiety models.

2. The Transition from a 3-Cluster to 4-Cluster Model

DSM-IV used a tripartite model: Re-experiencing, Avoidance/Numbing, and Arousal.
However, Factor Analytic Studies demonstrated that "Avoidance" and "Numbing" are
distinct constructs. Consequently, DSM-5 split them. Cluster C (Avoidance) now
focuses on behavioral efforts to avoid triggers, while Cluster D (Negative
Alterations in Cognitions and Mood) captures the internal cognitive shifts, such as
persistent distorted blame of self or others.

3. Refining the Definition of "Trauma" (Criterion A)

DSM-III defined trauma as an event "outside the range of usual human experience,"
which proved too vague. DSM-IV added Criterion A2 (requiring an emotional
response of fear/horror). DSM-5 eliminated A2 entirely because it was not an accurate
predictor of PTSD development—particularly in "high-stakes" professions like the
military or police where emotional blunting is a trained response.

4. Inclusion of Internalizing and Externalizing Symptoms

Earlier versions focused heavily on internalizing symptoms (nightmares, fear). DSM-
5 added externalizing behaviors to the Arousal Cluster (Cluster E), specifically
"irritable behavior and angry outbursts" and "reckless or self-destructive behavior."
This allows for a better diagnosis of veterans and survivors of childhood trauma who
may present with aggression or substance abuse rather than just "fear."

5. Recognition of the Dissociative Subtype

A major advancement in DSM-5 was the formalization of the Dissociative Subtype.
High-trauma individuals often experience depersonalization (feeling detached from
one's body) or derealization (feeling the world is unreal). For an [Link]. student, this
is critical because these patients often require different therapeutic approaches, as
standard prolonged exposure might lead to severe flooding or dissociation.

PTSD FROM DSM III TO DSM 5: CHALLENGES

1. Psychometric Complexity and Heterogeneity

The "Polythetic" nature of the DSM-5 (where a patient only needs a subset of
 symptoms) means there are 636,120 different ways to meet the criteria for PTSD. For
researchers, this "heterogeneity" is a nightmare; two people can share the same
diagnosis while having zero symptoms in common. This complicates the search for
biological markers (biomarkers) for the disorder.

2. Overlap with Major Depressive Disorder (MDD)

The expansion of Cluster D (negative mood and cognitions) has brought PTSD closer
to MDD. Symptoms like "anhedonia" (loss of interest) and "negative emotional state"
are core features of depression. This raises the question of Comorbidity vs. Concept
Overlap: are we seeing two different disorders, or is the DSM-5 definition of PTSD
simply absorbing depression?

3. The "Bracket Creep" and Criterion A Expansion

There is a constant tension regarding what counts as a "traumatic event." While DSM-
5 tried to limit this to life-threatening events, clinicians often see PTSD-like
symptoms from non-Criterion A events (e.g., painful divorce, emotional abuse). This
creates a challenge for Forensic Psychology, where a PTSD diagnosis can have
massive legal weight in personal injury or criminal cases.

4. Cultural Validity and the "Western" Bias

Critics argue that the DSM-5 framework is heavily based on Western populations. In
many non-Western cultures, trauma is expressed through somatization (physical pain)
rather than the "internalized cognitions" emphasized in Cluster D. This remains a
significant barrier to global clinical application.

5. Divergence from ICD-11 (The "Complexity" Challenge)

While the DSM-5 became more complex, the WHO ICD-11 did the opposite—it
simplified PTSD to just 6 symptoms. This creates a global rift: a patient in the US
might be "disordered" under DSM rules but "healthy" under ICD rules. Furthermore,
ICD-11 introduced Complex PTSD (C-PTSD), a category the DSM-5 chose to omit,
leading to ongoing debate about whether "personality changes" following chronic
trauma should be a separate diagnosis.

Comparison of PTSD Criteria: DSM-III to DSM-5

Feature DSM-III (1980) DSM-IV (1994) DSM-5 (2013)
Classification Anxiety Disorder Anxiety Disorder Trauma- and Stressor-Related Disorders

Number of Clusters 3 Clusters 3 Clusters 4 Clusters (Avoidance & Negative Mood

split)

Total Symptoms 12 Symptoms 17 Symptoms 20 Symptoms

Criterion A (Stressor) "Outside the range of Split into A1 (Event) A2 removed. Stricter focus on direct or
usual human experience." and A2 (Emotional professional exposure.
Response).

Cluster Structure Re-experiencing, (B) Re-experiencing, (C) (B) Intrusion, (C) Avoidance,
Numbing, & Avoidance/Numbing, (D) (D) Negative Alterations (NACM), (E)
Miscellaneous. Arousal. Arousal.

Thresholds 1 (B), 1 (C), 2 (D). 1 (B), 3 (C), 2 (D). 1 (B), 1 (C), 2 (D), 2 (E).

Externalizing Signs Not emphasized. Anger/Irritability. Added Reckless or Self-Destructive

behavior (Cluster E).

New Symptoms N/A N/A Distorted blame, Persistent negative

emotions, Self-destructive acts.

Specifiers Acute vs. Chronic. Acute vs. Chronic vs. Dissociative

Delayed Onset. Subtype (Depersonalization/Derealization
).

Pediatric focus Minimal. Adult criteria applied to Specific Preschool Subtype (age 6 and
kids. younger).

DSM-5 Diagnostic Criteria for PTSD

Note: The following criteria apply to adults, adolescents, and children older than 6
years. For children 6 years and younger, see the DSM-5 section titled “Posttraumatic
Stress Disorder for Children 6 Years and Younger” (APA, 2013a).
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) as it occurred to others.
3. Learning that the traumatic event(s) occurred to a close family member or close
friend. In cases of actual or threatened death of a family member or friend, the event(s)
must have been violent or accidental.
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 to 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) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic
event(s). Note: In children older than 6 years, 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(s) were recurring. (Such reactions may occur on a continuum,
with the most extreme expression being a complete loss of awareness of present
surroundings.) Note: In 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(s).
5. Marked physiological reactions to internal or external cues that symbolize or
resemble an aspect of the traumatic event(s).
C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning
after the traumatic event(s) occurred, as evidenced by one or both of the following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about
or closely associated with the traumatic event(s).
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(s).
D. Negative alterations in
cognitions and mood associated with the traumatic
event(s), beginning or worsening after the traumatic event(s) occurred, as
evidenced by two (or more) of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically due to
dissociative amnesia, and not to other factors such as head injury, alcohol, or drugs).
2. Persistentand 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(s) that lead the individual to blame himself/herself or others.
4. Persistent negative emotional state (e.g., fear, horror, anger, guilt, or 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. Marked alterations in arousal and reactivity associated with the traumatic
event(s), beginning or worsening after the traumatic event(s) occurred, as
evidenced by two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no provocation), typically
expressed as verbal or physical aggression toward people or objects.
2. Reckless or self-destructive behavior.
3. Hypervigilance.
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disturbance (e.g., difficulty falling or staying asleep or restless sleep).
F. Duration of the disturbance (Criteria B, C, D and E) is more than 1 month.
G. The disturbance causes clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance
(e.g., medication, alcohol) or another medical condition.
Specify whether:
With dissociative symptoms: 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 either of the following:
1. Depersonalization: Persistent or recurrent experiences of feeling detached from,
and as if one were an outside observer of, one’s mental processes or body (e.g.,
feeling as though one were in a dream; feeling a sense of unreality of self or body or
of time moving slowly).
2. Derealization: Persistent or recurrent experiences of unreality of surroundings (e.g.,
the world around the individual is experienced as unreal, dreamlike, distant, or
distorted). Note: To use this subtype, the dissociative symptoms must not be
attributable to the physiological effects of a substance (e.g., blackouts, behavior
during alcohol intoxication) or another medical condition (e.g., complex partial
seizures).
Specify whether:
With delayed expression: If the full diagnostic criteria are not met until at least 6
months after the event (although the onset and expression of some symptoms may be
immediate).
Source: APA, 2013a, pp. 271–272.
 PSYCHOLOGICAL THEORIES OF PTSD
Schema‐based and social cognitive models of PTSD
1. THE SHATTERED ASSUMPTIONS THEORY

The Shattered Assumptions Theory, developed by Ronnie Janoff-Bulman, is a

psychological framework that explores the impact of traumatic experiences on an
individual's core beliefs and assumptions about the world. This theory suggests that
when individuals experience a traumatic event, it can shatter their fundamental
assumptions, leading to psychological distress and the need to reconstruct their
worldview. In this article, we will delve into the key concepts of the Shattered
Assumptions Theory and its implications for understanding the psychological
aftermath of trauma.

1. Assumptions about the World:

According to the Shattered Assumptions Theory, individuals hold certain assumptions

about the world that provide a sense of stability, predictability, and meaning. These
assumptions typically include beliefs about personal invulnerability, the benevolence
of the world, and the meaningfulness of one's life. Trauma disrupts these assumptions
and challenges individuals' beliefs about themselves and the world.

2. Shattered Assumptions:

The experience of a traumatic event can shatter an individual's assumptions in various

ways. For example, a traumatic event can destroy the belief in personal invulnerability,
making individuals confront their own vulnerability and mortality. It can also
challenge the belief in the benevolence of the world, as individuals may question why
such a traumatic event occurred. Additionally, trauma can disrupt the belief in the
meaningfulness of life, causing individuals to question the purpose and value of their
existence.

3. Psychological Impact:

When assumptions are shattered, individuals may experience psychological distress,

such as anxiety, depression, and post-traumatic stress disorder (PTSD). The shattered
assumptions can lead to a loss of trust, a sense of betrayal, and a feeling of being
disconnected from others and the world. The individual's sense of identity and self-
worth may also be shaken, as they struggle to make sense of the traumatic event and
its implications for their lives.

4. Reconstructing Assumptions:

In order to cope and recover from trauma, individuals engage in a process of

reconstructing their shattered assumptions. This process involves integrating the
traumatic experience into their worldview, developing new beliefs and meanings, and
 restoring a sense of coherence and purpose. Reconstruction may involve seeking
support from others, finding new sources of meaning and values, and developing a
sense of resilience and post-traumatic growth.

5. Challenges and Coping Strategies:

Reconstructing assumptions is not a linear or easy process. Individuals may encounter

various challenges, such as intrusive thoughts, emotional numbing, and difficulty
trusting others. Coping strategies can play a vital role in this process. Seeking
professional help, engaging in therapy, practicing self-care, and participating in
support groups can provide individuals with the necessary tools and resources to
navigate the challenges and facilitate the reconstruction of their shattered assumptions.

6. Post-Traumatic Growth:

While trauma can be a devastating experience, the Shattered Assumptions Theory also
recognizes the potential for post-traumatic growth. Through the process of
reconstructing assumptions, individuals may develop new strengths, increased
resilience, and a deeper understanding of themselves and the world. They may find
new sources of meaning and purpose, and their worldview may become more nuanced
and compassionate.

Conclusion:
The Shattered Assumptions Theory provides a valuable framework for understanding
the psychological impact of trauma on an individual's core beliefs and assumptions
about the world. By recognizing the shattering of assumptions and the subsequent
process of reconstruction, individuals can find ways to cope, heal, and grow in the
aftermath of traumatic experiences. Therapy, support, and self-reflection can play
crucial roles in facilitating this process and restoring a sense of coherence, meaning,
and well-being.

2. Stress Response Theory

Mardi Horowitz proposed that the mind has an inherent "completion tendency"—an
automatic drive to integrate new, distressing information into existing mental
schemas.
 Oscillation: Because traumatic information is overwhelming, the mind fluctuates
between two states:

 Intrusion: Flashbacks and nightmares force the trauma back into awareness to be
processed.

 Denial/Numbing: Psychological defense mechanisms shut down emotions to prevent

mental overload.

 The Goal: Healing occurs when the individual can eventually process the event
enough to integrate it without being overwhelmed by these cycles.
Schema theorists (see Rafaeli et al., 2011; Young, 2006) suggest that
information, knowledge, and beliefs about oneself, others, and the world
is organized in the mind as units of knowledge called schemas, and that
people make meaning of new information using their schemas, which
influence their emotional, cognitive, and behavioural responses to such
information. Horowitz (1983, 1986, 2011) explains PTSD symptoms
using two general “response modes” to stress. First, intrusion symptoms
are the result of a failure to integrate traumatic experiences into one's
pre‐existing schematic network. Horowitz (1983) proposes that people
have a completion tendency, which involves a propensity to assimilate
new information (e.g., trauma), as well as the meaning of such
information, into pre‐existing schemas, and that people possess a bias
toward preserving existing schematic structures. Should the trauma or the
meanings that individuals assign to the trauma conflict with existing
schemas, the person may experience completion failure, which results in
a normative stress response. Furthermore, the individual will continue to
experience intrusion symptoms until they successfully integrate the
trauma information into their schematic network.

The individual may engage in a second response mode to defend against

distressing intrusions. This response mode involves defence mechanisms,
such as numbing, denial, repression, and avoidance that reduce the stress
response by keeping the traumatic information out of conscious
awareness. Horowitz (1983) describes PTSD symptoms as an oscillation
between these two response modes whilst the individual processes the
trauma information. Processing of trauma involves slow schematic
change and PTSD symptoms resolve once traumatic experience is
integrated within the schematic network.

3. Social cognitive theory

Benight and Bandura's (2004) social cognitive theory states that unhelpful
self‐schemas, specifically in relation to perceived self‐efficacy, underlie
PTSD symptoms. Self‐efficacy describes one's perceived ability to
manage their own functioning, but when considered in the context of
traumatic experiences, describes an individual's ability to cope with the
trauma and its sequelae, which shapes their cognitive, affective, and
behavioural responses to trauma. Benight and Bandura (2004) propose
several ways in which self‐efficacy shapes trauma responses. First,
self‐efficacy can impact attentional and evaluative processes; those who
have lower self‐efficacy are likely to be vigilant toward potential threats
and amplify the severity of risk associated with those threats. Second,
self‐efficacy can affect how people respond to perceived threats; people
with low self‐efficacy are less likely to try to control their environment to
reduce their distress and are more likely to experience heightened
emotional reactivity or attempt to avoid and/or escape threatening stimuli.
Third, individuals with low self‐efficacy may struggle to control their
thoughts, emotions, and behaviours in response to threatening stimuli. As
such, people with low self‐efficacy are more likely to have intrusion
symptoms and re‐experience the emotional and behavioural aspects of
trauma.

Behavioural models of PTSD

1. Theories of associative fear‐learning

Classical conditioning is a key process in associative fear‐learning

theories. The unconditioned feared stimulus that is central to the person's
trauma experience (e.g., being assaulted by a tall man at night) is paired
with neutral stimuli (e.g., tall men and dark environments). As a result,
previously neutral stimuli become conditioned stimuli that produce
conditioned responses that are similar to those produced by the
unconditioned stimulus (e.g., fear; Lissek & van Meurs, 2015). Fear
conditioning can be altered via extinction, whereby an individual acquires
new learning; conditioned responses decline with repeated exposure to
conditioned stimuli in the absence of the unconditioned stimuli and/or
aversive outcomes (Lissek & van Meurs, 2015).

The main tenet of associative fear‐learning models is that PTSD is the

result of extinction failure, whereby conditioned fear responses to
non‐threatening stimuli do not decline with repeated non‐aversive
exposures to conditioned stimuli (Lissek & van Meurs, 2015).
Competition theory (for a review, see Bouton, 2004) suggests that
extinction learning does not erase original fear conditioning but
outcompetes the original fear‐acquisition learning; extinction is only
successful if the extinction learning is stronger than the fear‐acquisition
learning (see Figure 1). Some have suggested that individuals with PTSD
may have (a) hyper‐conditionability, which results in strongly acquired
fear‐based learning (Orr et al., 2000), and/or (b) inhibitory learning
deficits that impair their ability to inhibit fear‐based learning in favour of
extinction learning (Jovanovic & Ressler, 2010). Others have suggested
that some conditioned responses are distressing enough to serve as
unconditioned stimuli, which causes normal extinction processes to be
inhibited and repeated fear responses during extinction learning to
strengthen reactivity to conditioned stimuli (Eysenck, 1979).

Mowrer (1947) suggests that PTSD involves a two‐stage learning process,

and that the second stage is primarily responsible for extinction failure.
The first stage involves classical conditioning. The second stage involves
the person actively avoiding and escaping conditioned stimuli to alleviate
distress, which leads to negative reinforcement; the reduction in distress
increases the likelihood of future avoidance, which thwarts opportunities
for extinction learning. Others have suggested that people with PTSD
have an inability to suppress fear when presented with safety cues, and as
extinction relies on fear‐inhibition, people who fall into this category
experience extinction failure (Jovanovic & Ressler, 2010).

Contrary to the theory of hyper‐conditionability, the associative‐learning

deficits model suggests that people with PTSD have difficulty identifying
realistic associations between unconditioned and associated stimuli,
which leads to difficulties identifying real danger cues (Grillon, 2002).
Consequently, these people may associate the unconditioned trauma
stimulus with the general environment in which the trauma occurred,
which may lead to generalized contextual anxiety and a chronic state of
arousal. Furthermore, people with PTSD may overgeneralize, whereby
they readily associate neutral stimuli to conditioned stimuli, which results
in fear responses to safe stimuli that are seemingly unrelated to the
traumatic event (Grillon, 2002).

2. Theories of non‐associative fear learning

Non‐associative fear‐learning theories conceptualize PTSD as changes in
a person's reactivity to fear‐relevant stimuli due to problematic
habituation and sensitization processes (for a review, see Lissek & van
Meurs, 2015). Habituation describes a gradual decline in autonomic and
psychological arousal after repeated exposure to fear‐inducing stimuli
(Groves & Thompson, 1970). Failure to habituate, whereby individuals
experience persistent startle responses to non‐threatening stimuli, may
maintain hyperarousal symptoms of PTSD. In contrast to habituation,
sensitization describes the process of a person experiencing increasing
autonomic and psychological reactivity with repeated exposure to
fear‐related stimuli (Groves & Thompson, 1970). Sensitization is
suggested to result from previous activation of a person's fear system,
which results in the fear system becoming hypersensitive to new, unusual,
or fear‐relevant stimuli (Lissek & van Meurs, 2015).
Information processing models of PTSD
1. Dual representation theory

According to the dual representation theory of PTSD (Brewin et al., 1996;

Brewin & Holmes, 2003), trauma is processed emotionally within two
memory systems. The first system involves conscious processing,
whereby a traumatic event is integrated into long‐term autobiographical
memory. These memories were originally called “verbally accessible
memories” because they can be both voluntarily and involuntarily
retrieved, verbalized, and updated. However, Brewin et al.'s (2010)
revised model, which integrates the original model with neurobiological
models of memory and imagery, refers to these memories as
“contextual‐based representations” (C‐Reps). C‐Reps contain information
about the context and events that occurred prior to, during, and following
trauma, as well as the individual's appraisal of the meaning of a trauma
(Brewin et al., 2010; Brewin & Holmes, 2003). C‐Reps may include
primary emotions that occurred during the event (e.g., fear), as well as
secondary emotions about the perceived meaning of a trauma that are
retrospectively generated (e.g., guilt or shame; Brewin & Holmes, 2003).
Heightened arousal during trauma limits an individual's capacity to
process large amounts of information (Brewin & Holmes, 2003), which,
combined with attentional biases toward highly threatening aspects of the
trauma, can result in fragmented and poorly contextualized C‐Reps
(Brewin et al., 1996; Brewin & Holmes, 2003). The second system
involves unconscious processing of the physiological, motor, and sensory
information associated with the trauma (Brewin et al., 1996). These
memories are inflexible and cannot be retrieved intentionally. Instead,
these memories are involuntarily accessed when the individual is exposed
to internal (thoughts or bodily sensations) or external stimuli that match
elements of the trauma (Brewin & Holmes, 2003). As they are comprised
of mental representations of sensory information, they are difficult to
verbalize (Brewin & Holmes, 2003) and, therefore, were labelled
“situationally accessible memories” and later, in the revised model,
“sensation‐based representations” (S‐Reps).

According to Brewin et al. (1996, 2010), PTSD is the result of a lack of

integration between C‐Reps and S‐Reps (see Figure 2). When an
individual is exposed to situational reminders of a trauma, highly detailed
sensory, motor, physiological, and emotional features (S‐Reps) are
automatically activated in the absence of temporal and contextual
information (C‐Reps). Consequently, rather than recollecting a trauma
memory, the individual re‐experiences the memory as if it were occurring
in real time along with the distressing affective, motor, physiological, and
sensory experiences associated with the original memory (i.e., flashbacks
or nightmares).
2. Fear network account of emotional processing

The fear network account of emotional processing (Foa et al., 1989; Foa
& Kozak, 1986) suggests that feared stimuli are embedded in long‐term
memory within a “fear network” (Foa & Kozak, 1986). Fear networks
contains information about (a) feared and associated stimuli; (b) cognitive,
behavioural, and physiological reactions to feared stimuli; and (c) the
associations between feared stimuli and responses (i.e., meanings about
trauma and trauma responses). Foa and Kozak (1986) suggest that PTSD
symptoms result from a pathological, change‐resistant fear network
comprised of excessive stimuli and response information, and heightened
associations between elements that do not accurately reflect reality. When
a person encounters an element of their fear network (e.g., dark outside)
within their environment, the entire fear network becomes activated and
triggers the survival response prescribed by that network (see Figure 3).
Consequently, pathological fear networks produce strong emotional and
behavioural responses to non‐threatening stimuli (i.e., re‐experiencing).
Furthermore, avoidance and numbing symptoms are conceptualized as
coping strategies that reduce the likelihood the fear network will be
activated and, therefore, prevent re‐experiencing symptoms (Foa et
al., 1989). Additionally, hyperarousal symptoms may reflect lower‐level
activation of the fear network (Foa et al., 1989).
Integrated models of PTSD
1. Emotional processing theory

Emotional processing theory extends on the fear network account of

emotional processing in several ways (Brewin & Holmes, 2003;
Dalgleish, 2004). The revised theory incorporates additional information
about pre‐trauma beliefs and information available prior to, during, and
after the trauma, as well as negative appraisals of one's responses during
and after trauma (see Figure 4; Brewin & Holmes, 2003). There are three
key components to emotional processing theory that interact to produce
PTSD symptoms. Two of these components involve mental
representations, and one involves post‐traumatic reactions.
The first component involves memory records, which include pre‐trauma
memories, the trauma memory itself, and post‐trauma memories
(Dalgleish, 2004). Memory records are akin to “fear networks”; however,
they have several extensions. First, biased information processing during
encoding is acknowledged as producing disorganized memory records
(Foa & Riggs, 1993, as cited in Dalgleish, 2004). Second, it is
acknowledged that numerous, erroneous, and vague associations between
trauma and non‐trauma stimuli are recorded within memory records,
which accounts for the widespread perception of danger amongst
traumatized individuals (Foa & Rothbaum, 1998). Finally, memory
records include physiological and behavioural survival response elements
(e.g., dissociation) that may have been unsuccessful in preventing the
trauma, which have led the individual to develop a sense of incompetence
(Foa & Rothbaum, 1998).

Like earlier schema‐based models of PTSD (Horowitz, 1986;

Janoff‐Bulman, 1989), the second component of emotion processing
theory suggests that traumatic events violate pre‐existing positive
schemas, which results in intrusion and avoidance symptoms
(Dalgleish, 2004). However, whilst the shattered assumptions theory did
not explain why people with a trauma history have increased vulnerability
to PTSD (Dalgleish, 2004), emotional processing theory suggests that
when people with a trauma history experience a new trauma, their
negative schemas, which were shaped by past trauma, become activated,
leading to distress and survival responses (Foa & Rothbaum, 1998).

The third component of emotional processing theory involves a variety of

post‐traumatic reactions to the self and others, and subsequent negative
appraisals of such reactions (Dalgleish, 2004). Heightened emotional
responses may lead to maladaptive appraisals such as “I am weak”,
particularly if the person's pre‐existing self‐schemas reflect incompetence.
In turn, appraisals of post‐traumatic responses may develop new, or
strengthen existing, negative schemas about the world and the self (Rauch
& Foa, 2006).

NEUROBIOLOGICAL MECHANISMS UNDERLYING PTSD

Critical evaluation of the neurobiological mechanisms underlying Post-Traumatic
Stress Disorder (PTSD) reveals a complex, interdependent system of structural,
neurochemical, and endocrine dysfunctions. While the "amygdalo-centric" model of
hyper-reactivity remains foundational, current research emphasizes a broader failure
of contextual processing and top-down emotional regulation.
 1. Neuroanatomical Circuitry: The Regulatory Triad
PTSD is characterized by a "triad" of dysfunction in the Amygdala, Hippocampus,
and Prefrontal Cortex (PFC).
 Amygdala (Hyperactivity): Serves as the "threat detector." In PTSD, it is
hypersensitized to both trauma-related and generic emotional stimuli, driving
hyperarousal and exaggerated startle responses.

 Prefrontal Cortex (Hypoactivity): Specifically the ventromedial PFC

(vmPFC) and anterior cingulate cortex (ACC). These regions normally act as a
"brake" on the amygdala. Their diminished volume and activation lead to a failure in
inhibiting fear and a deficit in fear extinction—the ability to learn that a previously
threatening cue is now safe.

 Hippocampus (Volume Reduction): Involved in contextualization. Smaller

hippocampal volume is one of the most replicated findings in chronic PTSD, though
debate persists on whether this is an acquired result of toxic stress (via high
glutamate/cortisol) or a pre-existing vulnerability factor.

2. Neuroendocrine Dysregulation: The HPA Axis Paradox

Unlike the typical chronic stress response (hypercortisolism), PTSD often manifests a
unique paradox involving the Hypothalamic-Pituitary-Adrenal (HPA) axis:
 Hypocortisolism: Many patients exhibit low baseline cortisol levels despite high
stress.

 Glucocorticoid Hypersensitivity: The system becomes hypersensitive to negative

feedback. This lack of "cortisol brake" may leave central stress systems (like
norepinephrine) unopposed, facilitating the over-consolidation of traumatic
memories.

3. Neurochemical Imbalances
 Norepinephrine (NE): Elevated levels in the Locus Coeruleus contribute directly to
hypervigilance, flashbacks, and nightmares.

 GABA and Glutamate: A reduction in GABA (the brain's primary inhibitor) and an
excess of Glutamate (the primary excitor) creates a state of excitotoxicity that may
damage the hippocampus and impair cognitive control.

 Serotonin (5-HT): Dysregulation in the raphé nuclei compromises anxiolytic effects

and contributes to impulsivity and memory intrusions.

4. Critical Evaluation & Emerging Perspectives

 Heterogeneity: Research increasingly suggests PTSD is not a monolithic entity but a
collection of subtypes (e.g., dissociative vs. non-dissociative), each with distinct
neurobiological signatures.

 Beyond the Brain: New evidence highlights the role

of neuroinflammation (elevated pro-inflammatory cytokines like IL-6) and the gut-
microbiome in programming the HPA axis.

 Vulnerability vs. Consequence: It remains difficult to distinguish whether structural

changes (like smaller ACC volume) are a pre-existing risk or a result of living with
the disorder.

Feature Biological Change Behavioral Symptom

Amygdala Hyper-responsiveness Hypervigilance, Flashbacks

vmPFC / ACC Hypo-responsiveness Failure to extinguish fear

Hippocampus Reduced volume Contextual overgeneralization

HPA Axis Hypocortisolism Sensitization to future stress