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
Normally, all of
Memory
us are aware of,
and are able to
AWARENESS
and
control various
CONTROL functions of
our nervous
Movements Sensations
system, as
shown in the
picture
opposite. your name
 What is dissociation?
Memory Identity In certain people,
when faced with a
stressful situation,
AWARENESS
and one of these
CONTROL functions may
appear to split
Sensati away, or
on dissociate, from
Movem
ent voluntary control.
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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 with one's
spouse.
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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. your name
 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 your name
 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 DISSOCIATIVE
GLOBAL AMNESIA EPILEPTIC AMNESIA
AMNESIA
AETIOLOGY UNKNOWN EPILEPTIC PSYCHIATRIC CAUSE
ACTIVITY
TRIGGERS Sudden onset often Sudden definite Mild head injury or an
ppt by exercise, onset, upon waking emotional event
immersion in water, from sleep
emotional stress,
etc
DURATION 4-10 hours <1 hr Several days atleast

CLINICAL Dense anterograde Persistent memory Extensive retrograde

FEATURES amnesia with deficits amnesia
repetitive May be asso. With Preserved new
questioning olfactory learning.
hallucinations or
automatisms
RESPONSE TO May not respond Responds well -
ANTICONVULSANT
S
RECURRENCE Rare Frequent your name
Frequent
 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 May be present Absent

MOVEMENTS

PROTECTIVE RESPONSE Absent Present

SYMPATHETIC Usually absent Usually present
OVERACTIVITY
RESISTANCE OF EYE Absent Usually present
MOVEMENTS
PRESERVATION OF Usually absent May be present
ABILITY TO HELP
FEEDING AND
ELIMINATION
MEANINGFUL POSTURE Absent May be present
AND FACIAL EXPRESSION

URINARY/ FECAL Usually present Unlikely

INCONTINENCE
FEATURES ORGANIC STUPOR DISSOCIATIVE STUPOR

ABNORMAL EEG Most likely Least likely

OCULOVESTIBULAR Absent Present

REFLEX

PENTOTHAL ( AMYTAL) Low dose increases High dose increases alertness and
INTERVIEW stupor and neurological mental status examination may
signs develop be possible

MORTALITY 35% 0-3%

Symptoms

Motor
Sensory
Convulsions
Mixed

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 Motor Sx Sensory Sx

Involuntary movemts Loss of touch/ pain

Tic-like/ Tremors sensation
Blepharospasm Midline anaesthesia
Torticollis Paraesthesia/
Aphonia Hyperaesthesia
Opisthotonus Blindness
Abnormal gait Deafness
Falls Tunnel vision
Paralysis Double vision
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Visceral Symptoms

Psychogenic
Vomiting
Diarrhoea
Swooning/ Syncope
Globus hystericus
Urinary retention
Pseudocyesis
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 Signs
SENSORY MOTOR
Map dermatomes Hoovers Sign
Midline splitting Arm-drop test
Splitting of Vibration Collapsing weakness
sense Co-contraction
Swinging flashlight Sternocleidomastoid test
test Pseudo-waxy flexibility
Visual fields Psychogenic Romberg
Tests in severe b/l test
blindness 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 your name
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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 Epileptic seizures
seizures
Preceding ictus Frequent evidence
Absence of of neurological
explanatory disease disease
or signs
Anxiety auras Wide range of
palpitations ,choking epileptic auras
present.
Induced or provoked Rarely induced your name
 During ictus
N.E.S E.S
Inconsistencies in Fit specific seizure
clinical presentation types
Seizures may differ Stereotypical seizure
from attack to attack pattern
When others are Night times ,in
present absence of people

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 Gradual onset Abrupt onset, short
prolonged duration(<2mins)
duration(>2mins) Tonic rigidity at onset
Rare whole body of GTCS
rigidity
Asymmetric out of Symmetrical clonic
phase movements, activity in GTCS
pelvic thrusts and
hyper arching

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

Vocalizations Single vocalization

throughout ictus if present at onset

Normal ictal EEG Abnormal

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Following ictus
No post ictal delirium Present
No increase in Increase for 10 -20
prolactin mins post ictally
Normal postictal Slowing post ictally
EEG
Subsequent recall of Fragmentary or nil
events during ictus recall
No relation of ictal Diminished
frequency to AED 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 your name
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
Therapy may be:
1. Supportive
2. Cognitive-behavioural
3. Psychodynamic
4. 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
/ problem-solving skills your name
 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
Reduce sick role
Behavioural diary
Medication
Physiotherapy
Cognitive
Sleep hygiene
restructuring
Activity structuring
Making links
Treating associated between thoughts,
problems where feelings and
appropriate (e.g. symptoms
anxiety)
Differential
reinforcement
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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
treatment your name
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
- INDIVIDUAL PSYCHOTHERAPY
- FAMILY COUNSELLING your name
 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
APPROACH SHOULD BE FLEXIBLE
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 10 skills
1. PSYCHOEDUCATION 6. TRAUMATIC
2. PACING & REENACTMENT
CONTAINMENT 7. SAFETY PLANNING
3. GROUNDING SKILLS 8. HEALING PLACE
4. `TALKING THROUGH 9. JOURNALING
` IN DID ( WRITING )
5. ` INTERNAL 10. ART - WORK
MEETINGS ` IN DID

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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 your name
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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