ASSESSMENT &

MANAGEMENT OF
DISSOCIATIVE
DISORDERS
CHAIRPERSON: Dr.SAFEEKH A.T.
PRESENTER : Dr.D.ARCHANAA
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Introduction:

In psychiatry there are forms of

illness, with names dating back
to two and a half millennia,
which had sentence of death
passed on them more than once,
yet they obstinately survive.
Paranoia is one such condition
and hysteria is another.
Aubrey Lewis (1975)
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What is dissociation?
Identity

Memory

AWARENESS
and
CONTROL

Movements

Sensations

Normally, all of
us are aware of,
and are able to
control various
functions
of
our
nervous
system,
as
shown in the
picture
opposite. your name

What is dissociation?
Memory

AWARENESS
and
CONTROL

Sensati
on

In certain people,
when faced with a
stressful situation,
one
of
these
functions
may
appear to split
away,
or
dissociate,
from
Movem
ent
voluntary control.

Identity

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Hypnosis, Dissociation & Suggestibility

~10% of population is profoundly
hypnotizable
Uses autohypnosis during stressor
Caused by & removed by forced
suggestion at least temporarily
Babinski Pithiatism (1908)
Loss of unitary state of self &
consciousness

Learning & Behavioral Theories:

Symptoms

of an illness experienced earlier

may appear again during a stressor Classical
conditioning
Development of the symptom is externally &
internally reinforced Operant conditning
Dollard & Miller (1950) 2 possible sources
of Symptoms: Organic & ModeL
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What is stress?
Stress
is any situation
involving a perturbation
(disturbance) to the normal
status of a living organism.
A stressful event is any
event that causes such a
disturbance for example,
loss of a job, failure in an
examination, or a dispute

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Normal responses to stress

This relationship between mind and body is
a common part of our daily life and
experience.
For example: headaches when tired, an
upset stomach when anxious, loss of
appetite when sad, increased sweating
when frightened.
All these physical changes are real, but
they occur in response to stress.
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Factors that increase the

risk of dissociation
1. Childhood abuse or neglect.
2. Presence of a severe physical illness
(that can serve as a model) in a family
member.
3. Personality disorders in which the
patient's coping skills may be poor.
4. Genetic factors family history of
depression, alcoholism or dissociative
disorder.
5. Somatization - presence of medically
unexplained symptoms related to stressors
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Initiation and maintenance

of dissociation
When dissociation initially occurs, it serves
the purpose of removing the patient from
a stressful situation or conflict. This is
known as primary gain.
However, later on, the patient's
symptoms may lead to certain benefits
or advantages, which can cause the
symptoms to persist. This is known as
secondary gain.

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Secondary Gain
Attention-seeking; Gain of Sympathy
Relief from duties & responsibilities
Manipulations of personal relationships
Symbolic expression of an emotionally
laden idea
Alleviation of guilt through suffering

Tertiary Gain
Significant others may derive gains
because of the patients illness; reinforce
the Symptoms

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Common stressors seen in

patients with dissociation
1. Bereavement loss of a loved one
2. Academic stressors particularly in
children and adolescents
3. Marital and family disputes
4. Financial loss or debt
5.
Stressors
related
to
romantic
relationships
6.
Work-related
stressors
and
unemployment
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Clinical features
Symptoms affecting voluntary motor/ sensory
fn that suggest a neurological condn/GMC
Initiation/exacerbation of Symptoms is
preceded by conflicts/ stressors
Not intentionally produced/ feigned
Cannot be fully explained by GMC, Substance
or culturally sanctioned behavior
Clinically significant distress or impairment
Not limited to pain/ sexual dysfunction; not
during Somatization or another mental illness
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Clinical features
Symptoms based on pts knowledge of
the CNS
Sudden, dramatic onset; Stressors
Look for normally preserved functions
underlying the superficial incapacity
Inconsistent findings/ Alteration of
findings with Suggestion
Astasia-Abasia (Paul Blocq 1888)
Camptocormia
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DISSOCIATIVE AMNESIA
Sudden amnesia
Concerning stressfull life events
Pt appears unconcerned about it
New learning is intact
Amnesia mostly limited to personnel
events
La belle indifference

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FEATURES

TRANSIENT
TRANSIENT
GLOBAL AMNESIA EPILEPTIC
AMNESIA

DISSOCIATIVE
AMNESIA

AETIOLOGY

UNKNOWN

EPILEPTIC
ACTIVITY

PSYCHIATRIC CAUSE

TRIGGERS

Sudden onset often

ppt by exercise,
immersion in water,
emotional stress,
etc

Sudden definite
onset, upon waking
from sleep

Mild head injury or an

emotional event

DURATION

4-10 hours

<1 hr

Several days atleast

CLINICAL
FEATURES

Dense anterograde
amnesia with
repetitive
questioning

Persistent memory
deficits
May be asso. With
olfactory
hallucinations or
automatisms

Extensive retrograde
amnesia
Preserved new learning

RESPONSE TO
May not respond
ANTICONVULSANT
S

Responds well

RECURRENCE

Frequent

Frequentyour name

Rare

DISSOCIATIVE FUGUE
Sudden unexpected wandering away
Complete amnesia for earlier life
Assumption of purposeful new identity
Abrupt termination with amnesia for the
episode
D/D : Epileptic fugue, Mania,
Depression, Schizophrenia

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DISSOCIATIVE
PERSONALTY DISORDER
Person being dominated by 2 or
more personalities of which ONLY
ONE is being manifest at a time
One personality not aware of the
other amnestic barriers
h/o losing periods of time or does
not recall events
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FEATURES

ORGANIC STUPOR

DISSOCIATIVE STUPOR

PAST PSY ILLNESS

Usually absent

Usually present

PAST EPISODES OF STUPOR

Usually present

Usually absent

PRECIPITATING STRESSOR

10%

24-33%

COURSE

Longer

Usually present, shorter.

Generally recover within 7
days

FREQUENCY

Most common

Uncommon (3.5% of all

stupor cases)

BLEPHAROSPASM

Absent

May be present

MENACE REFLEX

Absent

Present

DOLLS EYE MOVEMENTS

Present

Absent

FEATURES

ORGANIC STUPOR

DISSOCIATIVE STUPOR

ROVING, EYE
MOVEMENTS

May be present

Absent

PROTECTIVE RESPONSE

Absent

Present

SYMPATHETIC
OVERACTIVITY

Usually absent

Usually present

RESISTANCE OF EYE
MOVEMENTS

Absent

Usually present

PRESERVATION OF
ABILITY TO HELP
FEEDING AND
ELIMINATION

Usually absent

May be present

MEANINGFUL POSTURE
AND FACIAL EXPRESSION

Absent

May be present

URINARY/ FECAL
INCONTINENCE

Usually present

Unlikely

FEATURES

ORGANIC STUPOR

DISSOCIATIVE STUPOR

ABNORMAL EEG

Most likely

Least likely

OCULOVESTIBULAR
REFLEX

Absent

Present

PENTOTHAL ( AMYTAL)
INTERVIEW

Low dose increases

stupor and neurological
signs develop

High dose increases alertness and

mental status examination may
be possible

MORTALITY

35%

0-3%

Symptoms

Motor
Sensory
Convulsions
Mixed
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Motor Sx
Involuntary movemts
Tic-like/ Tremors
Blepharospasm
Torticollis
Aphonia
Opisthotonus
Abnormal gait
Falls
Paralysis

Sensory Sx
Loss of touch/ pain
sensation
Midline anaesthesia
Paraesthesia/
Hyperaesthesia
Blindness
Deafness
Tunnel vision
Double vision
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Visceral Symptoms
Psychogenic
Vomiting
Diarrhoea
Swooning/ Syncope
Globus hystericus
Urinary retention
Pseudocyesis
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Signs

SENSORY
Map dermatomes
Midline splitting
Splitting of Vibration
sense
Swinging flashlight
test
Visual fields
Tests in severe b/l
blindness

MOTOR
Hoovers Sign
Arm-drop test
Collapsing weakness
Co-contraction
Sternocleidomastoid test
Pseudo-waxy flexibility
Psychogenic Romberg
test
Preserved cough in
aphonia
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ATASIA & ABASIA

Lempert and colleagues found 6 key features
were identified in 97% of 37 patients through a
videotape analysis. These included
momentary fluctuation of gait and stance
excessive slowness,
psychogenic Rhomberg,
uneconomic postures,
walking on ice, and
sudden buckling of knees without falls.
In another study by Baik and Lang 279
videotapes were analyzed also showed similar
results
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Screening instruments
Perceptual Alterations Scale
Questionnaire on Experiences of Dissociation
(Riley 1998)
Dissociative disorders interview schedule( DDIS based on DSM
IV)

Dissociation Questionnaire (DISQ ; Vanderlinden et al.1991)

Dissociative Processes Scale (DPS;Watson 2003)
Mini-SCIDD (Steinberg et al. 1992).
Stanford Acute Stress Reaction Questionnaire
Peritraumatic Dissociative Experiences Questionnaire
(Marmar et al., 1994)
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Comparison between epileptic and

non epileptic seizures
Non epileptic
seizures
Preceding ictus
Absence of
explanatory disease
or signs
Anxiety auras
palpitations ,choking
present.
Induced or provoked

Epileptic seizures
Frequent evidence of
neurological disease
Wide range of epileptic
auras
Rarely induced
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 During ictus
N.E.S
Inconsistencies in
clinical presentation
Seizures may differ
from attack to attack
When others are
present

E.S
Fit specific seizure
types
Stereotypical seizure
pattern
Night times ,in absence
of people

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 Gradual onset
prolonged
duration(>2mins)
Rare whole body
rigidity
Asymmetric out of
phase movements,
pelvic thrusts and
hyper arching

Abrupt onset, short

duration(<2mins)
Tonic rigidity at onset of
GTCS
Symmetrical clonic
activity in GTCS

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Common
Rare incontinence,
tongue bite, self injury.
Corneal reflex,
Disturbed
autonomic
hyperactivity,pupillary
responses intact
Can not avoid
Avoids noxious stimuli
or eye opening
Vocalizations
throughout ictus

Single vocalization
if present at onset

Normal ictal EEG

Abnormal
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Following ictus
No post ictal delirium
No increase in
prolactin
Normal postictal
EEG
Subsequent recall of
events during ictus
No relation of ictal
frequency to AED

Present
Increase for 10 -20
mins post ictally
Slowing post ictally
Fragmentary or nil
recall
Diminished frequency
with AED
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Comorbidity
Depression
Anxiety disorders
PTSD
Borderline PD
Adjustment disorder with brief
depressive reaction
Childhood emotional disorder
unspecified

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 Adjustment disorder mixed and

anxiety and depressive reaction
A.D. mixed disturbance of emotion
and conduct

Unsocialized conduct disorder

Sibling rivalry disorder
Non organic eneuresis
Other childhood emotional disorder
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Evaluation of the patient

Careful history-taking, keeping in
mind the other medical conditions
Assessment of duration, premorbid
personality, psychosocial conditions
(not only stressors), past history,
family history and comorbidities
most important.
PHYSICAL EXAMINATION
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INVESTIGATIONS

Blood investigations
Hormonal assay
EMG
Video telemetric EEG / EEG
NCS
CT Scan
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Investigations
Recent studies using modern
diagnostic criteria and investigations
show a low rate of conversion to
organicity
Investigate and refer where
appropriate, but avoid providing
gains sick role
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Management of acute dissociation

Rule out any organic causes where
possible
Rule out other psychiatric disorders
Reassurance
Suggestion
Removal of gains
Identifying any acute stressors and
dealing with them
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Once symptoms are stable

Normalization involvement in
physical or other forms of
rehabilitation
Build a therapeutic alliance with the
patient
Education regarding the nature of
illness, without being confrontational
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Psychotherapy

1.
2.
3.
4.

Therapy may be:

Supportive
Cognitive-behavioural
Psychodynamic
Others

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Supportive therapy
For patients who are unwilling or
unable to engage in other therapies
Patients with severe personality
disorders, poor coping skills
Use of techniques such as empathic
validation, reinforcement, suggestion,
advice
Strengthen patients defences and
improve problem-solving skills your name

Cognitive-behavioural
therapy
In the acute stage:
1. Therapeutic alliance
2. Explanation of diagnosis, avoid
elaborate models
3. Behavioural techniques
physiotherapy
4. Positive reinforcement
5. Social skills / assertiveness training
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/ problem-solving skills

CBT continued
In chronic dissociation:
Regular sessions (e.g. once in 2
weeks)
Relate physiological, behavioural and
cognitive changes Langs model
Structured treatment
Homework assignments
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Types of interventions used

Behavioural diary
Physiotherapy
Sleep hygiene
Activity structuring
Treating associated
problems where
appropriate (e.g.
anxiety)
Differential
reinforcement

Reduce sick role

Medication
Cognitive restructuring
Making links between
thoughts, feelings
and symptoms

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Steps in CBT
1) Behavioural analysis
2) Developing a therapeutic alliance
3) Generating the willingness to
change
4) Giving the patient a rationale for
treatment
5) Conducting treatment
6) Generalizing progress and ending
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treatment

NIMHANS MODEL (FOR DD IN

CHILDREN: SRINATH et al 1993)
STRUCTURED AND INTENSIVE
TREATMENT PACKAGE
FOLLOWING A SET OF
STEPWISE AND OFTEN
OVERLAPPING MODELS.
COMPONENTS:
- NORMALISATION
FAMILY CRISIS INTERVENTION

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NORMALISATION
GOALS :
- to counter illness behavior and sick role
TECHNIQUES :

- encouraging
and insisting on adherence ward routine as well
as ful filling personal & social task demands
- removal of
secondary gains
- behavior
modification techniques like contracting,
rewards , differential reinforcement
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FAMILY CRISIS RESOLUTION

GOALS :
- alleviation or reduction of stress
- enhancing parental competence and
empowerment
TECHNIQUES :
- individual and group parent education
- supportive techniques like ventilation ,
exploration of feelings , anxieties and
reassurance
- teaching appropriate handling of symptoms
through instructions ,modeling , monitering ,
rehearsal
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INDIVIDUAL PSYCHOTHERAPY
GOALS :

- to uncover underlying sources of

stress / conflict /maladaptive coping
- resolution of stress / reaction to
stress and improve coping
TECHNIQUES :
- rapport , ventilation , exploration ,
suggestion,reassurance, environmental
manipulation
- dynamic interpretation and others methods of
insight
- cognitive self - control
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FAMILY COUNSELING
GOALS :
- to resolve intra familial issues which have
played role in determining / maintaining role in
the disorder
TECHNIQUES :
- attending psychopathology / disorder in
family members
- optimization of child parent interaction
(inconsistent disciplining ,inadequate parent
control ,overinvolvement and overexpectation )
- management of deeper family pathology
such as scape goating and intrafamilial discord
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PSYCHODYNAMIC
PSYCHOTHERAPY ( TURKUS &
KAHLER 2006)
EGO STRENGTHENING SKILLS
AND PRINCIPLES TAUGHT TO THE
PT. EARLY IN THERAPY
PT. TAUGHT SYMPTOM
MANAGEMENT AND COPING
SKILLS
10 KEY SKILLS AND TECHNIQUES
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APPROACH SHOULD BE FLEXIBLE

10 skills
1. PSYCHOEDUCATION
2. PACING &
CONTAINMENT
3. GROUNDING SKILLS
4. `TALKING THROUGH
` IN DID
5. ` INTERNAL
MEETINGS ` IN DID

6. TRAUMATIC
REENACTMENT
7. SAFETY PLANNING
8. HEALING PLACE
9. JOURNALING
( WRITING )
10. ART - WORK

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PHARMACOTHERAPY
Antidepressants comorbid MDD /
Dysthymia
BZD to control anxiety symptoms
and to facilitate retrieval of traumatic
memories
Anti convulsants seizure disorder
m/c co morbidity
Treat other comorbid
psychiatric/medical illness
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DIFFERENTIAL DIAGNOSIS

MALINGERING
FACTITIOUS DISORDER
DEMENTIA
DELIRIUM
EPILEPSY
METABOLIC DISORDER
PTSD
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 POST CONCUSSIONAL
POST OP AMNESIA
CEREBRAL INFECTIONS OR
NEOPLASMS
WERNICKE -KORSAKOFF `S SYND.
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Physical disorders which can be

misdiagnosed as dissociation
Idiopathic dystonia
DOPA responsive dystonia
Lambert eaton myasthenic
syndrome
Blepharospasm
Primary orthostatic tremor
Multiple sclerosis
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Paroxysmal choreo athetosis

Reflex epilepsy
Porphyrias
Subdural hematomas
Early manifestations of AIDS
Paroxysmal hemicrania
Thoracic outlet syndrome
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PROGNOSTIC FACTORS
GOOD PROGNOSIS :
acuteness and recent onset
definite precipitation by stressful event
good premorbid health
absence of organic illness or concomitant
major psychiatric illness
CARTER showed 70 % of 90 pt.s seen for
acute conditions followed up for 4 6 yrs were
well adjusted .only 7 pt.s could not work
POOR PROGNOSIS : in pt,s wth longer
lasting symptoms and comorbidity

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CONCLUSION
DD CONSTITUTE A CHALLENGING AND
FASCINATING SPECTRUM OF PSY.
ILLNESSES
DD ARE GENERALLY TREATABLE
DOMAIN IN WHICH PSYCHOTHERAPY IS A
PRIMARY MODALITY
ALTHOUGH PHARMACOLOGICAL
TREATMENT FOR COMORBID CONDITIONS
LIKE DEPRESSION CAN BE QUITE
HELPFUL.
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THANK U
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