MODULE 2

Comprehensive Study Notes

Somatic Symptom & Related Disorders | Dissociative Disorders | Stress Disorders

SECTION 1: Somatic Symptom & Related Disorders

1.1 Overview & Definition

Somatic symptom and related disorders are conditions that involve physical (bodily) symptoms
combined with abnormal thoughts, feelings, and behaviours in response to those symptoms. People
with these disorders experience real bodily symptoms that cause significant psychological distress and
impairment in daily functioning.

Key Points to Remember

Previously called 'Somatoform Disorders' — fell under Anxiety Disorders
20–50% of physical symptoms that bring people to seek medical care are medically unexplained
Patients have NO control over their symptoms — they are NOT faking
DSM-5 recognises 4 main disorders in this category

The 4 main disorders in this category:

• Somatic Symptom Disorder (SSD)
• Illness Anxiety Disorder (IAD)
• Conversion Disorder (Functional Neurological Disorder)
• Factitious Disorder

1.2 Somatic Symptom Disorder (SSD)

SSD is the major diagnosis in this category. It combines and replaces three older DSM-IV diagnoses:
hypochondriasis, somatization disorder, and pain disorder.

DSM-5 Diagnostic Criteria

DSM-5 Criteria for Somatic Symptom Disorder
A. One or more somatic symptoms that are distressing or disrupt daily life
 B. Excessive thoughts, feelings, or behaviours related to the symptoms — shown by AT LEAST
ONE of:
1. Disproportionate & persistent thoughts about the seriousness of symptoms
2. Persistently high level of anxiety about health or symptoms
3. Excessive time & energy devoted to symptoms or health concerns
C. Symptoms must have persisted for at least 6 months (though any one symptom may come
and go)

Who is More Likely to Have SSD?

• More likely to be female
• More likely to be non-white and less educated
• Frequently seek additional medical procedures or tests even when doctors find nothing wrong

Key Psychological Features

• Hypervigilant — increased awareness and sensitivity to body changes
• Catastrophic thinking — they overestimate how medically serious their symptoms are
• Attentional bias towards illness-related information
• Discount reassurance — even good news does not reduce their fears
• They believe being healthy means being completely symptom-free
• They view themselves as physically weak and unable to tolerate physical effort

The Vicious Cycle in SSD

Anxiety about illness → physiological symptoms of anxiety → these symptoms give more 'evidence' of
being ill → more anxiety. This self-reinforcing loop is central to understanding SSD.

Additional Risk Traits

Trait Description
Negative Affect High negative emotionality is a major risk factor
Absorption Tendency to become deeply absorbed in one's
own experiences; often linked to high
hypnotizability
Alexithymia Difficulty identifying and describing one's own
feelings — emotions get 'converted' to physical
sensations

1.3 Causes of Somatic Symptom Disorders

A. Psychoanalytic (Freudian) View
• Concept of 'hysteria' — unresolved unconscious conflicts get 'converted' into physical symptoms
• Psychic energy from unacceptable inner conflicts is channelled into physical problems
 • This view is largely outdated but influenced later theories

B. Cognitive-Behavioural Model (Most Widely Accepted)

This 4-step model explains how SSD develops and persists:
• Step 1: Hypervigilance — person has an increased awareness of bodily changes
• Step 2: Misattribution — bodily sensations are interpreted as signs of illness
• Step 3: Catastrophising — person worries excessively and expects the worst
• Step 4: Medical seeking — distressed person repeatedly seeks medical attention

SSD is seen as a disorder of both perception (noticing benign sensations like a skipped heartbeat) and
cognition ('Does this mean I have serious heart disease?').

C. Secondary Reinforcement
Even though SSD brings misery, it can be accidentally reinforced. We learn from childhood that when
we're sick, we receive special attention, comfort, and are excused from responsibilities — this
inadvertently rewards sick-role behaviour.

1.4 Treatments for SSD

1. Cognitive-Behavioural Therapy (CBT)
• Identify and challenge false beliefs about illness; correct misinterpretations of body
sensations
• Induce innocent symptoms deliberately (e.g., focus on heartbeat) to learn that attention
amplifies sensations
• Stop body-checking behaviours and constant reassurance-seeking
• Duration: brief — typically 6 to 16 sessions; can also be done in group format
• Also effective in reducing general anxiety and depression

2. Medical Management
• Identify one GP who integrates all care and sees the patient regularly
• Provides physical exams focused on new complaints (validates all symptoms as real)
• Avoids unnecessary diagnostic tests and minimal use of medication
• Studies show this reduces healthcare costs and sometimes improves physical functioning
• Best combined with CBT for optimal outcomes

1.5 Illness Anxiety Disorder (IAD)

In IAD, the person has very high anxiety about having or developing a serious illness, but has very few
(or very mild) somatic symptoms. This is the key difference from SSD.

Disorder Key Feature

Somatic Symptom Disorder Significant physical symptoms WITH excessive
 anxiety/thoughts about them
Illness Anxiety Disorder High anxiety about illness but LITTLE to NO
physical symptoms
Old Term: Hypochondriasis 75% → now SSD; 25% → now IAD

DSM-5 Criteria for IAD

Illness Anxiety Disorder — Diagnostic Criteria
A. Preoccupation with having or acquiring a serious illness
B. Somatic symptoms absent or only mildly present
C. High anxiety about health; easily alarmed about personal health status
D. Excessive health-related behaviours (e.g. repeatedly checking body) OR avoidance (e.g.
avoiding doctors)
E. Illness preoccupation present for at least 6 months (specific illness feared may change)
F. Not better explained by another mental disorder (e.g., panic disorder, OCD, GAD)

Two Types of IAD

• Constantly seeks medical reassurance; needs validation from doctors
• Reluctant to share fears or visit doctors due to anxiety about what they might find

The Vicious Cycle of IAD

Anxiety → Thoughts about being sick → Seeking reassurance → Temporary relief → Anxiety returns
(and often intensifies). This cycle perpetuates the disorder.

Risk Factors for IAD

• A time of major life stress
• History of childhood abuse
• Excessive internet use (self-diagnosis via health websites)
• A serious childhood illness

1.6 Conversion Disorder (Functional Neurological Symptom Disorder)

Conversion disorder is characterised by neurological symptoms (affecting senses or movement) in the
absence of a real neurological disease. The symptoms are REAL to the patient — they are not faking.

Key Features
The pattern of symptoms does NOT match how real neurological diseases present
Examples: partial paralysis, blindness, deafness, seizure-like episodes
 Diagnosed only after thorough medical and neurological workup rules out organic causes
Person is NOT intentionally producing symptoms
Psychological factors (stress, emotional conflict) often trigger or worsen symptoms

'La Belle Indifférence'

Freud observed that patients with conversion disorder often seemed surprisingly calm about dramatic
symptoms (e.g., a paralysed arm). He called this 'la belle indifférence' (the beautiful indifference).
However, this only occurs in about 20% of patients and is no longer emphasised in DSM diagnosis.

Four Categories of Conversion Disorder Symptoms

A. Sensory Symptoms
• 'Glove anesthesia' — loss of feeling in the hand (glove-shaped area) that doesn't match real
nerve pathways
• Conversion blindness — cannot see, yet can navigate a room without bumping into objects
• Conversion deafness — claims not to hear, yet responds when their own name is called
• The sensory input IS being registered but is blocked from conscious (explicit) awareness

B. Motor Symptoms
• Paralysis usually confined to one limb and selective in nature (e.g., can't write but can scratch)
• Aphonia — can only speak in a whisper, yet can cough normally
• Globus — sensation of a lump in the throat (common motor symptom)
• A person may not be able to walk normally but can walk in an emergency (e.g., during a fire)

C. Seizures
• Resemble epileptic seizures but are NOT true seizures
• No EEG abnormalities (brainwave differences) detected
• No post-seizure confusion or memory loss (unlike true epilepsy)
• Patients often show excessive thrashing and writhing
• Rarely injure themselves in falls or lose bowel/bladder control

D. Mixed Presentation
A combination of any of the above three categories.

Causes of Conversion Disorder

Concept Explanation
Primary Gain Escaping or avoiding a stressful situation
unconsciously through symptoms; symptoms
go away only when stress resolves
Secondary Gain External benefits like attention, sympathy, or
 financial compensation that reinforce the
disability
Negative Reinforcement Symptoms provide relief from an unbearable
situation — the person doesn't have to take
responsibility for escaping it
Positive Reinforcement Care, concern, and attention from others
reinforce the sick role

Treatment of Conversion Disorder

• Behavioural therapy with exercises and reinforcement — reward healthy behaviours, remove
reinforcement for abnormal motor behaviours
• CBT has been used successfully for psychogenic (conversion) seizures
• Hypnosis combined with problem-solving therapies shows some promise, especially for seizures

1.7 Factitious Disorder

In factitious disorder, the person intentionally produces or feigns psychological or physical symptoms —
but their goal is internal (playing the 'sick role' for attention/care), NOT external gain. This is the key
difference from malingering.

Disorder Motivation
Somatoform (SSD/IAD) Unintentional symptoms — no faking involved
Malingering Intentional faking for EXTERNAL incentives
(money, avoid military, avoid prison)
Factitious Disorder Intentional faking for INTERNAL gain (attention,
sympathy, sick role — no external reward)

DSM-5 Criteria — Factitious Disorder Imposed on Self

A. Falsification of physical or psychological signs/symptoms OR induction of injury/disease, with
deception
B. Person presents themselves to others as ill, impaired, or injured
C. The deceptive behaviour is evident even in the ABSENCE of obvious external rewards
D. Not better explained by another mental disorder (e.g., delusional disorder)

Key Facts about Factitious Disorder

• Patients may secretly alter their physiology (e.g., take drugs) to simulate real illnesses
• More common in women than men
• Prevalence: approximately 0.5–0.8% of general hospital patients
• Patients may be at serious risk for injury or death from self-inflicted symptoms
Factitious Disorder Imposed on Another (Munchausen's Syndrome by Proxy)
• Person intentionally produces illness (or its appearance) in ANOTHER person under their care
(usually a child)
• Typically: a mother presents her child for treatment of symptoms she has fabricated or induced
• This is a form of child abuse and is a serious clinical and legal concern

SECTION 2: Dissociative Disorders

2.1 Overview of Dissociation

Dissociation is the human mind's capacity to engage in complex mental activity in channels split off
from, or independent of, conscious awareness. The concept was first introduced by French neurologist
Pierre Janet.

Mild dissociation is NORMAL — it includes daydreaming, losing track of time, or missing part of a
conversation. It only becomes pathological when it is perceived as disruptive, causes loss of needed
information, creates discontinuity of experience, or involves recurrent involuntary intrusions into one's
sense of self.

DSM-5 Types of Pathological Dissociation

1. Depersonalisation/Derealisation Disorder
2. Dissociative Amnesia
3. Dissociative Fugue (subtype of Dissociative Amnesia)
4. Dissociative Identity Disorder (DID)

2.2 Depersonalisation/Derealisation Disorder

Term Definition
Depersonalisation One's sense of one's OWN self/reality is
temporarily lost — feeling detached from your
own body, thoughts, feelings
Derealisation The EXTERNAL world seems unreal,
dreamlike, foggy, or visually distorted

Clinical Features
• Persistent or recurrent episodes of feeling like an outside observer of one's own body or mind
• May feel as if floating above one's body
• Reality testing remains INTACT during episodes (unlike in psychosis — person knows it's not
real)
• People often describe it as living in a dream or movie
• Can occur alone or alongside depression, anxiety, or schizophrenia
Epidemiology
• Worldwide lifetime prevalence: 0.8% to 2.8%
• Equally common in men and women
• Average age of onset: approximately 23 years
• 79% report impaired social or work functioning
• Most patients have at least one other psychiatric diagnosis (most commonly depression)
• History of childhood emotional, physical, or sexual abuse is common

DSM-5 Criteria — Depersonalisation/Derealisation Disorder

A. Persistent or recurrent experiences of depersonalisation, derealisation, or both
B. Reality testing remains intact during the experiences
C. Symptoms cause significant distress or impairment in social/occupational functioning
D. Not attributable to substance use or another medical condition
E. Not better explained by another mental disorder

2.3 Dissociative Amnesia

Dissociative amnesia involves an inability to recall important autobiographical (personal) information,
usually of a traumatic or stressful nature, that is too extensive to be ordinary forgetting.

Type of Amnesia Description

Retrograde Amnesia Unable to recall PAST information or events —
this is the type seen in dissociative amnesia
Anterograde Amnesia Unable to form or retain NEW memories after
an event — this does NOT occur in dissociative
amnesia

Key Features
• Memory gaps most often follow severely stressful events — combat, serious accidents, suicide
attempts, violent outbursts
• Forgotten information is NOT permanently lost — it remains in the unconscious
• Can sometimes be retrieved through hypnosis or drug-assisted interviews (sodium amytal / 'truth
serum')
• Basic habit patterns (skills, reading, job abilities) remain intact
• Only episodic and autobiographical memory is affected
• Episodes typically last days to years; many people have only one episode in their lifetime

DSM-5 Criteria — Dissociative Amnesia

A. Inability to recall important autobiographical information (traumatic/stressful) — inconsistent
 with ordinary forgetting
Note: Usually localised/selective amnesia for specific events, or generalised amnesia for
identity and life history
B. Causes significant distress or impairment in functioning
C. Not attributable to substances or a medical/neurological condition
D. Not better explained by DID, PTSD, ASD, somatic symptom disorder, or neurocognitive
disorder

2.4 Dissociative Fugue

Dissociative fugue is a subtype of dissociative amnesia. The person not only loses their memory but
also travels to a new location and may assume an entirely new identity, with no memory of their
previous life.

Key Features
• Person travels to a new place, behaves normally there, and does not find the memory loss
unusual
• May return to their previous life suddenly, resuming it as if nothing happened
• The memory loss is especially long-lasting and resistant to recovery
• Fugue can last days, months, or years
• Diagnosed as extremely rare
• The pattern mirrors conversion disorder: instead of physical dysfunction, the person avoids an
unbearable situation by literally leaving the scene and forgetting it

2.5 Dissociative Identity Disorder (DID)

Formerly known as Multiple Personality Disorder, DID involves the presence of two or more distinct
identities (alters) that alternately take control of the person's behaviour, along with memory gaps that
cannot be explained by ordinary forgetting.

Key Concepts
• The identity encountered most often; carries the person's real name — but is NOT
necessarily the original identity or the best-adjusted one
• May differ in gender, age, handedness, sexual orientation, handwriting, prescription for
glasses, predominant emotions, and even languages spoken
• Alters take control rapidly (often within seconds); more gradual switches can also occur
• Alters are often completely amnesic for what other alters did; sometimes one-way
amnesia (one knows what the other did, but not vice versa)

Types of Alter Personalities

Alter Type Role & Behaviour
Child Alter Created during trauma to take on the victim
 role; when 'out', the adult may speak and
behave like a child
Persecutor Alter Inflicts pain on other alters — self-mutilation,
self-burning, suicide attempts; may believe it
can harm others without harming itself
Protector/Helper Alter Offers advice, performs functions the host can't
(e.g., sexual relations), controls switching
between alters, acts as observer

Associated Features & Comorbidities

• PTSD is frequently comorbid with DID — both involve severe trauma histories
• Self-injurious behaviour is common — wrist slashing, burns, drug overdoses
• About 75% have a history of suicide attempts; over 90% report recurrent suicidal thoughts
• Children: erratic school performance, antisocial behaviour (theft, fire-setting, aggression), early
substance use
• Childhood trauma (especially repeated sexual/physical abuse) is strongly associated with DID

Causal Controversies in DID

There are four major controversies researchers and clinicians debate:

1. Is DID Real or Faked?

• Some cases may be fully fabricated (especially in criminal contexts to avoid prosecution)
• However, most researchers believe genuine faking of DID is relatively rare

2. How Does DID Develop?

Theory A — Posttraumatic Theory:
• DID develops as a coping response to overwhelming, repeated childhood trauma
• Child dissociates through a process like self-hypnosis, escaping into a fantasy or 'becoming'
someone else
• If this relieves pain, it is reinforced and happens again
• Over time, different 'selves' are created at different points — laying the foundation for DID
• Diathesis-stress model: children who are fantasy-prone and highly hypnotisable have a diathesis;
severe abuse is the stress
• DID may be a complex, chronic variant of PTSD (trauma is central to both)

Theory B — Sociocognitive Theory:

• DID develops when a highly suggestible person LEARNS to adopt multiple identities, often
unintentionally encouraged by therapists
• Therapists using hypnosis or other suggestive techniques may inadvertently create or reinforce
alters
• Evidence: Most DID patients show no unambiguous signs BEFORE entering therapy; number of
alters often increases with time in therapy
 • This does NOT mean the person is consciously faking — it happens spontaneously without
awareness

3. Are Recovered Memories of Abuse Real or False?

• Many trauma memories in DID emerge during therapy — critics warn these may be false
memories created by suggestive questioning
• Determining real vs. false memories is extremely difficult
• Independent verification (medical, hospital, police records) is the most reliable way to confirm
memories
• Researchers are working on neuroimaging tools to distinguish true from false memories

4. If Abuse Occurred, Does It Cause DID?

• Child abuse often occurs alongside other adversities (neglect, poverty, parental psychopathology)
— hard to isolate the causal factor
• People who experienced abuse AND DID symptoms may be more likely to seek treatment —
creating a sampling bias
• Childhood abuse is claimed to lead to many different disorders, not just DID

2.6 Treatment of Dissociative Disorders

Depersonalisation/Derealisation
• Generally resistant to treatment; often treated for associated conditions (depression, anxiety)
• Hypnosis/self-hypnosis — patients learn to dissociate and 're-associate', gaining control over
experiences
• Antidepressants, antianxiety, and antipsychotic drugs have modest effects
• Randomised controlled study: Prozac showed NO difference from placebo
• rTMS (repetitive transcranial magnetic stimulation) to the temporo-parietal junction shows
promise — half of subjects showed significant improvement after 3 weeks

Dissociative Amnesia & Fugue

• Removing the person from the perceived threatening situation sometimes allows spontaneous
memory recovery
• Hypnosis helps facilitate recall of repressed/dissociated memories
• Drugs such as benzodiazepines, barbiturates, sodium pentobarbital, and sodium amobarbital can
assist memory recall

Dissociative Identity Disorder (DID)

• Main goal of treatment: INTEGRATION — merging all alters into the host personality into a
unified whole
• Patients often resist integration as they view dissociation as protective
• Partial integration is common; symptom improvement is more realistic than full integration
• Treatment approach: psychodynamic and insight-oriented — uncovering and processing
traumatic memories
 • Hypnosis is a primary tool: patients recover unconscious traumatic memories, which are then
processed
• DID does NOT spontaneously remit with time; must be actively treated
• Key findings about DID treatment:
◦ (1) Treatment must be prolonged, often lasting many years
◦ (2) More severe cases require longer treatment

SECTION 3: Stress Disorders

3.1 Stress & Stressors — Definitions

Stress (APA definition): The physiological or psychological response to internal or external stressors. It
involves changes affecting nearly every system of the body, influencing how people feel and behave.

Term Meaning
Stressor The external demand or trigger (e.g., job loss,
exam, death of loved one)
Stress The internal effect or response that the stressor
creates in the organism
Coping Strategies The efforts made to deal with and manage
stress

3.2 Types of Stress

• Negative form of stress from being overwhelmed by demands, losses, or perceived
threats
• Positive stress that keeps a person motivated and goal-directed
• Short-term stress encountered in day-to-day activities
• Ongoing, long-lasting stress that can lead to biological and psychological problems

3.3 Factors That Predispose a Person to Stress

1. Perception & Coping Skills
The same stressor affects different people differently. How you perceive a stressor (as a threat vs. a
challenge) and what coping resources you have greatly shapes your response.

2. Individual Characteristics
• Optimism — positive outlook buffers against stress
• Greater psychological control and sense of mastery
• Higher self-esteem
• Better social support
3. Genetic Factors
• The 5HTTLPR gene (serotonin transporter gene) plays a role in stress reactivity
• Caspi et al. (2003): People with two 'short' forms (s/s genotype) were more likely to develop
depression after 4+ stressful life events compared to those with two 'long' forms (l/l genotype)

4. Early Life Stress

• Effects of stress may be cumulative — each stressor makes the system MORE reactive over time
• Stress tolerance refers to a person's ability to withstand stress without significant impairment

5. Self-Perpetuating Cognitive Cycle

• People with a history of depression perceive negative events as MORE stressful than others do
• This can worsen and maintain stress — a self-reinforcing cognitive cycle

3.4 Characteristics of Stressors

Characteristic Details
Severity Some stressors have greater
pathophysiological impact; severity is context-
dependent and can change over time
Chronicity Short-term vs. long-term; neurochemical
changes diminish with chronic predictable
stress; chronic/unpredictable/uncontrollable
stressors are hardest to cope with
Timing/Frequency Continuous vs. intermittent; stressors have a
cumulative effect over time
Impact on Life Stressors affecting important life domains are
more severe; intensity increases with personal
closeness to the traumatic situation
Predictability Unpredictable and unanticipated stressors are
more severe (e.g., study on hip-replacement
patients)
Controllability Perceived control over stressor occurrence and
termination is psychologically and physically
protective; uncontrollable stressors are the
most damaging

3.5 Resilience
Resilience is the ability to adapt successfully even in the face of very difficult circumstances. It is the
MOST COMMON reaction to loss or trauma — most people do bounce back.

Factors That Increase Resilience

• Being male, older, and more educated
 • Having more economic resources
• Ability to show genuine positive emotions even while grieving
• Optimism and high positive affect (combined with low negative affect)
• Self-confidence and overly positive self-view (surprisingly adaptive in trauma)

Factors That Decrease Resilience

• High negative affect / tendency to ruminate
• Trying to find meaning in what happened is linked to WORSE outcomes
• Lack of social support

3.6 Biological Response to Stress

Allostatic Load
The biological cost of adapting to stress. When relaxed, allostatic load is low; under stress, it is higher.
Chronic high allostatic load damages the body and brain.

Stress increases susceptibility to colds, raises blood pressure, increases epinephrine, reduces oxygen
supply to the heart, and dramatically increases risk of heart attack. Most heart attacks occur on
Mondays — linked to the stress of returning to work.

A. The SAM System (Sympathetic-Adreno-Medullary)

• Purpose: mobilise resources for fight-or-flight response
• Pathway: Stressor → Sympathetic Nervous System → Adrenal gland medulla → releases
epinephrine & norepinephrine
• Effect: increases heart rate, accelerates glucose metabolism, prepares body for immediate action

B. The HPA Axis (Hypothalamus-Pituitary-Adrenal)

• Hypothalamus releases CRH (Corticotropin Releasing Hormone)
• CRH travels to pituitary gland → releases ACTH (Adrenocorticotropic Hormone)
• ACTH travels to adrenal cortex → releases CORTISOL (a glucocorticoid)
• Cortisol prepares the body for fight-or-flight AND inhibits the innate immune system (delays
inflammatory response)
• DANGER: If the stress response doesn't shut off, prolonged cortisol can damage brain cells —
especially in the HIPPOCAMPUS (memory centre)

C. Psychoneuroimmunology
The study of interactions between the nervous system and the immune system. Key insight: the brain
influences the immune system AND the immune system influences the brain through circulating
neurochemicals that modify brain states.
3.7 Trauma-Related Disorders
Disorder Key Feature
Adjustment Disorder Response to COMMON stressor; symptoms <
6 months after stressor ends
Acute Stress Disorder (ASD) Response to TRAUMATIC stressor; symptoms
last 3 days to 1 month after trauma
PTSD Response to TRAUMATIC stressor; symptoms
persist MORE than 1 month after trauma

3.8 Adjustment Disorder

An adjustment disorder is a psychological response to a COMMON stressor (e.g., divorce, job loss,
death) resulting in clinically significant emotional or behavioural symptoms.

Diagnostic Criteria — Adjustment Disorder

A. Emotional or behavioural symptoms develop within 3 months of onset of identifiable
stressor(s)
B. Symptoms are clinically significant: either (1) distress out of proportion to stressor severity, OR
(2) significant impairment in functioning
C. Does not meet criteria for another mental disorder
D. Symptoms do not represent normal bereavement
E. Once stressor ends, symptoms do not persist more than an additional 6 months

3.9 Post-Traumatic Stress Disorder (PTSD)

PTSD entered DSM in 1980. It was initially viewed as a normal response to an ABNORMAL stressor. In
PTSD, the stress symptoms fail to decrease even when the traumatic event has passed — this is what
makes it a disorder.

Traumatic stressors include: combat, rape, concentration camps, natural disasters (earthquakes,
tsunamis, tornadoes), serious accidents.

Four Symptom Clusters of PTSD

1. INTRUSION — Recurrent re-experiencing: flashbacks, nightmares, intrusive images,
physiological reactivity to trauma reminders
2. AVOIDANCE — Efforts to avoid trauma-related thoughts, feelings, or external reminders
3. NEGATIVE ALTERATIONS IN COGNITION & MOOD — Detachment, negative emotional
states (shame, anger), distorted self-blame or blame of others
4. AROUSAL & REACTIVITY — Hypervigilance, exaggerated startle response, aggression,
reckless behaviour
Diagnosis requires: symptoms lasting at least 1 MONTH.

Risk Factors for PTSD

Individual Risk Factors
• Certain occupations (soldiers, firefighters) — higher exposure to trauma
• Being male, having conduct problems in childhood
• Less than a college education
• Family history of psychiatric disorder or substance abuse
• High scores on extraversion and neuroticism
• Lower levels of social support
• Pre-existing depression and anxiety
• Negative appraisals of stress symptoms immediately after trauma

Sociocultural Risk Factors

• Being a member of a minority group increases risk
• Returning to a negative, unsupportive social environment increases vulnerability
• Stigma around seeking help
• War's justification and clarity of goals affects soldiers' adjustment

Biological Risk Factors

• High levels of cortisol in PTSD patients
• Smaller hippocampal volume (memory centre) — may be a vulnerability factor
• 5HTTLPR gene (serotonin transporter): 's/s' genotype + low social support = highest risk for
PTSD
• PTSD and depression are highly comorbid, making it hard to isolate PTSD-specific brain changes

3.10 Prevention & Treatment of Stress Disorders

Prevention
• Reduce frequency of traumatic events
• Prepare people in advance with information and coping skills
• Prepares people to tolerate anticipated threats by changing self-talk before/during
stressful events (a type of self-instructional training)

Treatment Methods
1. Telephone Hotlines
• National and local hotlines for severe stress, suicidal thoughts, rape/sexual assault victims
• Often staffed by trained volunteers
2. Crisis Intervention
• Central assumption: the person was functioning well BEFORE the trauma
• Focus is on helping through the immediate crisis — NOT remaking the personality
• Therapist is active: clarifies the problem, suggests action plans, provides reassurance and
support
• Single-session behavioural treatment has lowered fear and increased sense of control in
earthquake victims

3. Psychological Debriefing
• Provides emotional support and encourages discussion of experiences shortly after a disaster
• Common reactions to trauma are normalised
• 3–4 hour group session, usually 2–10 days after trauma
• Participants often report satisfaction, but no well-controlled study has proven CISD reduces PTSD
or speeds recovery in civilians

4. Medications
• Antidepressants: help with PTSD symptoms of depression, intrusion, and avoidance
• Antipsychotic medications: sometimes used (similar to those used in schizophrenia)
• Effectiveness of medications is still debated — not fully established

5. Cognitive-Behavioural Therapy (CBT)

• Patient vividly and repeatedly recounts the traumatic event until emotional response
decreases; also involves facing avoided (objectively safe) trauma-related situations in real
life or imagination
• Prolonged Exposure is evidence-based and highly effective for PTSD
• Modifies excessively negative appraisals of the trauma or its consequences; decreases
the threat felt when trauma memories are triggered; removes maladaptive cognitive and
behavioural strategies

QUICK REFERENCE SUMMARY TABLE

Disorder Core Feature Key Point

Somatic Symptom Physical symptoms + Symptoms > 6 months; not faking
Disorder excessive health anxiety
Illness Anxiety Health anxiety with LITTLE/NO 25% of old hypochondriasis cases
Disorder physical symptoms
Conversion Disorder Neurological symptoms NOT intentional; la belle indifférence
without neurological cause (20%)
Factitious Disorder Intentional faking for No external reward; different from
INTERNAL gain (sick role) malingering
Malingering Intentional faking for Not a mental disorder
 EXTERNAL gain
Depersonalisation/ Detachment from self or Prevalence: 0.8–2.8%
Derealisation reality; reality testing INTACT
Dissociative Amnesia Inability to recall Only retrograde; skills preserved
autobiographical info after
trauma
Dissociative Fugue Memory loss + travel + new Very rare; subtype of amnesia
identity
DID 2+ distinct identities; amnesia Linked to childhood trauma; PTSD
between alters comorbid
Adjustment Disorder Response to COMMON Onset within 3 months of stressor
stressor; symptoms < 6
months
PTSD Intrusion, avoidance, negative Symptoms > 1 month; traumatic stressor
mood, hyperarousal

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