This document discusses dissociative and somatic symptom disorders as outlined in Chapter 8 of the DSM-5. It provides an overview of dissociation and somatization, outlines the DSM-5 classification of dissociative disorders, somatic symptom and related disorders, and factitious disorders. It also summarizes key conditions including dissociative amnesia, depersonalization/derealization disorder, somatic symptom disorder, and factitious disorders.

1. Chapter 8
DISSOCIATIVE AND SOMATIC
SYMPTOM AND RELATED
DISORDERS

2. Chapter outline
• Introduction
• Dissociation, somatising, and stress
• Section 1: Dissociative disorders and their
comparative nosology
• Section 2: Somatic symptom and related
disorders and their comparative nosology
• Factitious disorders and Malingering
• Conclusion

3. *
DSM-5
Dissociative Disorders
Dissociative Disorder
Dissociative Amnesia
Depersonalization /
Derealization Disorder
Somatic Symptom and Related
Disorders
Somatic Symptom
Disorder
Illness Anxiety Disorder
Conversion Disorder
Psychological Factors
Affecting Other Medical
Conditions
Factitious Disorders

4. Introduction
• Somatoform and dissociative disorders together in this chapter –
neuroscientific and clinical similarities.
• 1800s – first attempts at systemic classification of these
conditions  repeated revisions since then.
• Limitations of existing DSM and ICD approaches.
• DSM-5 refined alignment, terminology, and diagnostic criteria.
• Overlap of categories between disorders characterised by
dissociation and somatising  discuss conditions without
assigning each to one or the other diagnostic category.
• Chapter covers related culture-specific conditions; range of
other conditions with dissociative or somatic symptoms; factitious
disorders and Malingering

5. *
What is dissociation?
•Common phenomenon in human experience,
NB when faced with a major threat.
•Feel detached from ourselves, experience
world as unreal or have little or no recall of a
trauma.
•Normal dissociation can also occur when
person is bored, engaged in monotonous
activities, when meditating, tired or sleepy.
•But, can also indicate pathology (see Table
8.1).

6. *
What causes dissociation?
•Cardeňa (1994): Dissociation has three distinct
features:
- suspended integration of mental modules
- altered state of consciousness
- a defence mechanism
•Recent insights into neural mechanisms support this.
•Cardeňa’s model broadened:
- genetically endowed trait
- partners ‘fight’ and ‘flight’
•Cardeňa: Dissociation involves two distinct
psychological processes (compartmentalisation and
detachment).

7. *
*Compartmentalisation
•Inability to control processes or take actions through acts
of volition.
•Inability to bring information usually accessible to
consciousness (i.e. susceptible to conscious influence) into
conscious awareness.
•Can manifest as amnesia, blindness, loss of tactile sensation
and paralysis.
•Anatomically and functionally, brain’s cortex is arranged
hierarchically.
•Primary cortical regions devoted to single operations;
subordinate to higher-order or association cortical regions.
•Compartmentalisation relies on this top-down regulation of
subordinate cortical regions.

8. *
Compartmentalisation, cont.
•If motor system involved, paralysis results (no
demonstrable pathology of apparatus of movement).
•‘Lesion’ responsible for this dissociation is not
anatomical, but functional.
•Evidence for this exists in functional brain
imaging.
•This process = one expression of fear response;
confers survival advantage (i.e. ‘playing dead’ or
‘freezing’ = ‘tonic immobility’).
•Sensory equivalent can  dampened experience of
pain.
•Freezing and anaesthesia + fight and flight are
characteristic of fear response.

9. *
*Figure 8.1: This diagram depicts the hierarchical
arrangement of motor integration and information flow in
the brain.

10. *
Figure 8.2: Depicts the same process as Figure 8.1.

11. *
Detachment
•Detachment corresponds to an altered state of
consciousness.
•Person experiences alienation of self or outside
world.
•Emotional experiences are numbed or blunted
(limbic system).
•Person may experience depersonalisation or
derealisation (parietal cortex).
•Altered state of consciousness interferes with
encoding of traumatic information, disturbing
the memory trace of the event.

12. *
Detachment, cont.
•Person also fails to integrate the emotional with
the contextual aspects of the experience.
•Memory is state-dependent  these weakly
integrated traces can be brought into conscious
experience when person is faced with new
stressful event.
•Thus, aspects of trauma can be re-experienced
(e.g. ‘flashbacks’ of PTSD).
•Like compartmentalisation, detachment may also
confer survival advantage – brain can remain
focussed on primary task of averting threat.

13. *
*Figure 8.3: This diagram illustrates the flow of
information when experiencing an event.

14. *
*Figure 8.4: This diagram illustrates the same neural
system as Figure 8.3.

15. *
Early adversity and future pathology
•How can an adaptive system  such disabling
pathology?
•Early adversity; when exposed to severe threat (e.g.
physical or sexual abuse), child may respond
defensively through compartmentalisation or
detachment.
•If repeated trauma, dissociative response is
strengthened through conditioning and becomes
established as preferential response to threat.
•Neural processes used more frequently  become more
efficient and more easily engaged.
•Also, sensory disturbances related to dissociation (e.g.
pain, dizziness, abdominal discomfort).

16. *
*Figure 8.5: A likely pathogenetic explanation for
pathological dissociation.

17. *
Section 2

18. *
•Somatising = key symptom of the somatoform
disorders.
•Refers to tendency to experience bodily (somatic)
distress in the face of psychological stress.
•Lack of robust evidence for causal link between
stress and somatising.
•DSM-IV-TR - somatic symptoms suggest medical
condition, but symptoms not fully explained by
the suggested medical condition.
•Onset, exacerbation, and maintenance of symptoms
correlate with stress.

19. *
•DSM-5 made multiple revisions to somatoform
and related disorders, including:
- Renamed category: ‘Somatic Symptom
Disorders’ (disorders with experience of physical
symptoms).
- Concern for associated psychological distress and
reduced quality of life.
- Complex and Simple Somatic Symptom
Disorders.
- Factitious disorders and Malingering to be
included under Somatic Symptom Disorders

20. *
•ICD-10 takes different approach:
- absence of Conversion Disorder (considered a
Dissociative Disorder)
- Body Dysmorphic Disorder (subsumed under
Hypochondriacal Disorder)
•Listed disorders:
- Somatisation Disorder
- Undifferentiated Somatoform Disorder
- Hypochondriacal Disorder
- Somatoform Autonomic Dysfunction
- Persistent Somatoform Pain Disorder
- Other Somatoform Disorders
- Somatoform Disorder, Unspecified

21. *
•Following slides describe individual conditions
included under dissociative and somatoform
disorders (using the DSM-IV-TR names).
•Conceptually related conditions are also
included:
- Acute Stress Disorder
- Posttraumatic Stress Disorder
- Borderline Personality Disorder
- Panic Attacks

22. *
•Like Conversion Disorder, Somatisation Disorder has
been known for millennia; considered a form of
hysteria.
•Also known as Briquet’s Syndrome.
•1950s - renewed interest in Feighner’s
comprehensive list (59) of diagnostic criteria.
•But, these are complex and unwieldy  not
commonly used in practice.
•DSM-III (1980) introduced ‘Somatisation Disorder’;
simpler criteria but still complex and off-putting 
practitioners avoid the diagnosis.
•DSM-5 has proposed much simplified criteria.

23. *
Epidemiology
•Common in primary health care and general
medical practice (± 10% of patients).
•Also, probably under diagnosed.
•Affects females with an incidence five-fold that
for males.
•Cultural factors.
•Mainly affects people of low socio-economic
standing and limited education.
•By definition, onset before age 30 (most
commonly in adolescence).

24. *
Aetiology and pathogenesis
•Psychoanalytic theories - symptoms are substitutes
for repressed unacceptable impulses.
•As a social communication, produces secondary gain
(avoid work and gain sympathy and support).
•Significant psychosocial trauma (NB in childhood).
•Frontal and non-dominant parietal lobes involved.
•Decreased blood flow in brain; also, reduced
metabolism and size of sub-cortical structures.
•Demonstrated neuropsychological abnormalities
(e.g. distractability).
•Role of cytokines?
•At least partly genetic; 29% concordance in
monozygotic twins.

25. *
Diagnosis, clinical presentation, and course
•Defining feature = occurrence of multiple bodily
symptoms from multiple organ systems; include
pseudo-neurological symptoms.
•Also, cognitive distortions and anxiety about
symptoms, and dysphoria.
•Early psychosocial adversity (mostly in childhood);
time of onset related to trauma.
•May also be histrionic or borderline personality
traits, conversion and dissociative phenomena,
sexual difficulties, menstrual irregularities, and
strained relationships.

26. *
Diagnosis, clinical presentation, and course, cont.
•ICD-10 approach differs from DSM-IV-TR.
•DSM-5 takes leaner approach; proposes collapse of
Somatisation Disorder, Hypochondriasis,
Undifferentiated Somatoform Disorder and Pain
Disorder into single new construct called Complex
Somatic Symptom Disorder.
•Although somatising is common in general medical and
primary care settings, diagnosis avoided due to
cumbersome diagnostic criteria.
•Hoped that simpler category will increase recognition
and treatment for many patients with substantial
disease burden.

27. *
Diagnosis, clinical presentation, and course, cont.
•Complaints presented in an exaggerated manner, with
colourful descriptions.
•Give vague accounts of multiple bodily complaints;
historical description of symptoms often faulty.
•Interpersonal conflict, chronic distress, anxiety, and
depression not uncommon.
•Self-harm and threats of suicide also not unusual.
•Female patients may be seductive or demure.
•Tend to be self-absorbed, external locus of control, seek
praise, behave dependently, and manipulate
interpersonal situations.
•Nature and occurrence rates of symptoms vary across
different cultures.

28. *
Diagnosis, clinical presentation, and course, cont.
•Chronic, disabling condition; symptoms worsen
with periods of heightened psychosocial stress.
•Symptoms come in spurts (last 6-9 months); rare to
be symptom free for more than a year.
•Common co-morbid psychiatric conditions are
Major Depressive Disorder, personality disorders,
substance-related disorders, Generalised Anxiety
Disorder and phobias.
•Most serious complications of Somatisation
Disorder are iatrogenic.

29. *
Differential diagnosis
•General medical and neurological illness, NB
conditions with non-specific, transient, and
fluctuating clinical manifestations (e.g. Multiple
Sclerosis and Myasthenia Gravis).
•Also, Porphyria, hyperthyroidism,
hyperparathyroidism, and haemochromatosis.
•Acquired Immune Deficiency Syndrome (AIDS).
•Psychiatric differentials include Hypochondriasis,
Conversion Disorder, and Pain Disorder.
•Also, Schizophrenia, Major Depressive Disorder
and Panic Attacks.

30. *
•Morbid preoccupation with a disease conviction
which involves the fear of contracting, or the
belief of having, a serious disease.
•Ancient Greece - Hypochondriasis referred to
unexplained conditions in the anatomical
hypochondrium.
•Validity as a separate condition long questioned.
•Hypochondriacal symptoms often occur in (or co-
morbid with) depressive and anxiety disorders.
•Better seen as a symptom dimension?

31. *
Epidemiology
•In general medical population, the six-month
prevalence ranges between 4% and 6% (but wide
range?).
•Very little info about prevalence in Africa.
•Sexes are equally affected.
•Age of onset is typically in the twenties (can be at
any age).
•Social class, education, and marital status appear
not to affect its expression.

32. *
Aetiology and pathogenesis
•Psychoanalytic theory:
- disturbed object relations
- displacement of repressed hostilities to the
body
- interplay between masochism, guilt, conflicted
dependency, and need for suffering and receiving
love.
•Defences against low self-esteem, inadequacy, and
conditioned reinforcement of the sick role have also
been considered causative.
•Most likely a variant expression of other mental
conditions (NB anxiety disorders and depression).
•These conditions establish a hyper-vigilant state.
•Neural substrate of fear implicated.

33. *
Diagnosis, clinical presentation, and course
•Some differences in DSM and ICD criteria.
•These patients highly heterogenous:
- 25% of Hypochondriasis patients display ‘classical’
illness anxiety (fear of having serious medical
condition, but no somatic symptoms).
- 75% show mix of illness anxiety and somatic symptoms.
- DSM-5 proposes reclassifying these groups into two
separate disorders.
•Hypochondriacal concerns fluctuate and typically
intensify under increased psychosocial stress.
•Episodic course (episodes last months to years).
•One-third show significant long-term improvement.
•Good prognosis includes high socio-economic status,
absence of significant personality pathology, etc.

34. *
Differential diagnosis
•General medical conditions with ill-defined, transient, and
fluctuating phenomena (e.g. Multiple Sclerosis, Systemic
Lupus Erythematosus, etc.).
•Somatisation Disorder (but patient’s focus is on identified
symptoms, not disease entities).
•Conversion Disorder (but preponderance of female
patients; sudden and dramatic onset of pseudo-neurological
symptoms).
•Pain Disorder (but focus on pain symptom and pain
behaviour).
•Body Dysmorphic Disorder (but preoccupation with an
anatomical abnormality, not illness anxiety).
•Psychotic disorders – if concerns are of delusional
intensity.
•Co-existing anxiety and depressive disorders.

35. *
•Some neuroscientific evidence for dissociative neural
mechanism in Conversion Disorder.
•Dissociative or somatoform disorder?
•DSM-5 proposed to rename it Functional Neurological
Disorder.
History
•Long recognised; concept first introduced by Egyptian
physicians  symptoms result of ‘wandering uterus’
(Greek for uterus = ‘hyster’).
•Disorder revived in 1800s; thought cause was brain
dysfunction following stressful events.
•Charcot; thought vulnerability to disorder was
hereditary – precipitated by traumatic event.
•Janet viewed hysteria as a disturbance in selective
attention.

36. *
History, cont.
•Freud introduced term ‘conversion’; seen as result of
conflict between instinctual impulses, like aggression
or sexuality, and the prohibition of their expression.
•Resolution of intrapsychic conflict is considered the
primary gain, but may also be secondary gains (e.g.
special treatment, sympathy).
•Not supported by clinical experience.
•Other aetiological theories relate to social,
communication, and behavioural aspects.
•Rise of neuroscience in late 20th century  resurgence
of interest in underlying biological mechanisms.
•Neuropsychological evidence and advances in neuro-
imaging.

37. *
Epidemiology
•Conversion symptoms needing medical attention occur in up to
one-third of all people; in psychiatric patients, incidence
between 5% and 15%.
•Females outnumber males (up to 5 to 1); in men,
symptoms mainly relate to occupational accidents, military
service, being on trial, and serving a prison sentence.
•Onset can be at any age, but is most common in adolescence.
•Most common in youngest child in family; lower socio-
economic classes; sub-average intelligence; educational
underachievement; rural domicile; and exposure to war and
combat.
•Culturally universal but symptoms vary with socio-cultural
context (e.g. ‘brain fag’ in Nigeria and SA).

38. *
Aetiology and pathogenesis
•Conversion involves emergence of a single
symptom, or set of symptoms, referable to the
nervous system, i.e. ‘mono-symptomatic’
presentation.
•Can affect any aspect of neurological function,
including abnormal movements, paralysis, gait
disturbances, non-seizural convulsions, mutism,
urinary retention, etc.
•Many inconsistencies on neurological examination
(e.g. fluctuating weakness; sensory losses that do
not follow anatomical boundaries; and dramatic and
implausible movement and gait disturbances).

39. *
Aetiology and pathogenesis, cont.
•La belle indifférence; anosognosia.
•Alexithymia and anxiety also common.
•May also be concurrent or future neurological
disease.
•Likewise, actual neurological disease does not
exclude Conversion Disorder.
•Bi-frontal and right parietal dysfunctions; also,
left-dominant impairments and impaired inter-
hemispheric communication.
•Functional neuro-imaging provides support for
neurological basis of Conversion Disorder.

40. *
Aetiology and pathogenesis, cont.
•Long noted that early trauma predicts Conversion
Disorder.
•Earlier and longer trauma  more severe symptoms.
•Significant problems with attachment, impaired object
relations, and a dysfunctional family system.
•Disorder appears to be result of dynamic restructuring of
neural networks leading to disconnection of volition,
sensory experience, and movement.
•No identifiable anatomical lesion  disconnection is
considered ‘functional’.
•Result of dissociative compartmentalisation related to
early adverse experience.
•Specific conversion symptom related to level of
disruption of neural network.

41. *
Diagnosis, clinical presentation, and course
•Four categories of symptoms: sensory, motor, seizure,
and mixed.
•Diagnosis of exclusion, but nature of conversion
symptoms raises suspicion.
•Symptoms do not conform to neurological facts; show
incongruence and internal inconsistencies.
•Sometimes, history of physical or sexual abuse.
•MSE often reveals psychologically unsophisticated
person of low intellect; poor insight.
•May come across as depressed or anxious; also,
alexithymia; ± 50% display la belle indifférence.
•Associated personality styles - passive-aggressive,
dependent, antisocial, and histrionic.
•Risk of suicide and self-harm.

42. *
Sensory symptoms
•Anaesthesia (loss of sensation) and paraesthesia
(abnormal sensations like ‘pins-and-needles’) of
extremities are common.
•‘Glove-and-stocking’ distribution of anaesthesia;
hemi-anaesthesia.
•May include any sensory modality.
•Neurological examination usually uncovers normal
sense organs and intact pathways.

43. *
Motor symptoms
•Weakness, paralysis, abnormal movements, and
gait disturbances.
•In paralysed limb, muscle tone and reflexes
remain normal; no wasting.
•Movement disturbances often grotesque and
involve the extremities, trunk, head, and face.
•Swaying, rhythmical tremors, tic-like and
choreiform (dance-like) movements occur; also
bobbing of the head.
•Weakness and abnormalities tend to fluctuate
between visits.

44. *
Pseudo-seizures
•Convulsive events resembling true seizures (but
one-third have confirmed epilepsy).
•‘Seizure response’ becomes the preferential
response to trauma.
•Behaviour looks like true seizure, but no
indicators on EEG.

45. *
Other symptoms
•Communication disturbances (e.g. mutism,
aphonia, etc.).
•Globus hystericus common in anxiety states;
probably a mixed sensory and motor conversion
phenomenon.
•Non-physiological and fanciful symptoms tend to
occur in least educated patients.
•May include false memories of childhood physical
and sexual abuse.
•Pseudo-hallucinations (differ from psychotic or
other hallucinations); may have useful, supportive
quality.

46. *
Course
•In 90% to 100% of cases, conversion symptoms
resolve within a few days.
•25% experience recurrence of conversion during
periods of psychosocial stress.
•Prognosis improved by:
- good pre-morbid psychosocial adjustment
- sudden onset of symptoms following a clearly
identifiable stressor
- no co-morbid psychiatric or medical conditions
- absence of civil or criminal litigation
- shorter duration of symptoms
•Beware delayed emergence of a neurological

47. *
Differential diagnosis
•Neurological conditions (e.g. cerebral neoplasia,
infection, epilepsies, dementias, etc.).
•Myasthenia Gravis and other muscle diseases.
•Multiple Sclerosis can mimic conversion symptoms.
•Optic Neuritis.
•Guillain-Barre Syndrome.
•Schizophrenia, depression and anxiety may have bodily
phenomena.
•Somatisation Disorder can have pseudo-neurological
symptoms.
•Hypochondriasis (but preoccupation with disease rather
than specific symptoms).
•Malingering and factitious disorders (diagnostic

48. *
•International Association for the Study of Pain
defines pain as ‘an unpleasant sensory and
emotional experience associated with actual or
potential tissue damage, or described in terms of
such damage’.
•Note subjective nature of pain.
•Acute pain is a cardinal adaptive response to
tissue damage, initiated by nociception
(stimulation of nerves conducting pain) and
accompanied by behaviours that limit tissue
damage.
•Chronic pain is ‘pain that persists beyond the
normal time of healing’ - involves pain experience,
suffering, and pain behaviour; dysfunctional

49. *
•Pain behaviour = patient’s efforts to avoid factors that
may precipitate or aggravate pain.
•Pain maintained through peripheral and central nervous
system mechanisms; also, emotional and motivational
aspects.
•Pain in Pain Disorder may have had definite nociceptive
origin; persistence related to psychological factors.
•Validity of Pain Disorder long questioned.
•Pain without nociceptive origin is unusual.
•Separating psychological and physical aspects of
chronic pain is nearly impossible.
•DSM-5 highlights similarities between Pain Disorder,
Hypochondriasis, and Somatisation Disorder; and includes
Pain Disorder as a subtype of Complex Somatic Symptom
Disorder.

50. *
*Epidemiology
•Pain is commonest complaint in all of medicine
(NB lower back pain, joint pains, and headaches).
•In the developed world, chronic pain range
estimated at between 25% and 30% of general
population.
•Thousands get disability benefits annually.
•Diagnosed twice as commonly in women.
•Onset is usually in fourth or fifth decades of life.
•Associated with lower educational achievement
and lower socio-economic standing.

51. *
Aetiology and pathogenesis
•Chronic pain has multifactorial origins (constitutional
predisposition is likely).
•Inherited risk of developing Pain Disorder.
•Developmental risks include childhood adversity (e.g.
parental separation, lack of physical affection towards
the child, etc.).
•Association between chronic pain and depressive
conditions.
•Conscious experience of pain modulated by the
cerebral cortex using serotonin as neurotransmitter.
•Endorphins (naturally occurring opioid-like molecules)
also modulate expression and experience of pain.

52. *
Aetiology and pathogenesis, cont.
•Kindling = systematic amplification of a nerve’s
responsiveness following repeated sub-threshold
stimulation of post-synaptic nerve.
•Occurs through taking over non-nociceptive nerves
to mediate pain.
•Sensitisation and amplification can also maintain
pain in absence of tissue damage.
•Psychodynamic theories - patients symbolically
express intrapsychic conflicts through the body.
•Others may regard emotional suffering as
weakness.
•Secondary gains (pain functions as way of obtaining
love and nurturance, and averting responsibilities).

53. *
Diagnosis, clinical presentation, and course
•ICD-10 criteria note all-consuming nature of disorder.
•DSM-5 considers pain as a somatic symptom, regardless
of origin.
•Chronic nociceptive pain (e.g. chronic cancer pain) is
not a mental disorder.
•Patients can become utterly preoccupied with pain;
may deny any other causes of distress.
•Evidence of depression present in nearly all patients.
•Pain Disorder often complicated by substance abuse.
•Common co-morbid conditions are Major Depressive
Disorder and Dysthymic Disorder.
•Chronic, unremitting, and disabling course.
•Outcome influenced by antecedent personality
pathology, marked passivity, substance abuse, and a
long pain history.

54. *
Differential diagnosis
•Nociceptive pain (but physical pain fluctuates and is
sensitive to emotions and contextual factors;
distraction is usually possible and analgesics provide
relief).
•Somatisation Disorder (but multiple systems are
involved and non-pain symptoms are present).
•Hypochondriasis (but preoccupation about being ill,
as opposed to the presence of pain).
•Conversion Disorder (but typically short-lived and
symptoms limited to single pseudo-neurological set).
•Factitious disorders and Malingering (look for
external motivations) – BUT Pain Disorder patients may
also be motivated to malinger for disability
compensation or payment of damages.

55. *
•Included in this chapter for sake of completeness.
•DSM-5 proposes subtle name change -
Psychological Factors affecting Medical Condition.
•Reflects de-emphasis of mind-body dualism.
•Proposed to go under Somatic Symptom Disorder
category.
•Psychological factors adversely affect expression
of established physical illness.
•Psychological factors are considered ways of
responding to stress, interpersonal style,
maladaptive coping, denial, and non-compliance.
•By contrast, a psychological reaction to a
physical condition is best considered an
Adjustment Disorder.

56. *
•Illness-endorsing behaviours involving intentional and
untruthful presentation of phenomena suggestive of
illness or impairment.
•Any symptom, or combination of physical or
psychological symptoms, can be presented.
•In Malingering, deceit involves falsely claiming illness to
avert threat or receive unfair advantage (e.g. obtain
disability grant).
•In Malingering, motivation is external and the
malingerer is aware of it.
•In factitious disorders, motivation is internal, or
intrapsychic, and the patient unaware of it.
•In both Malingering and factitious disorders, the
deception is volitional and occurs with full awareness.

57. *
•Success of deceit rests on two pillars:
- familiarity with the subject of deceit
- style of communication that avoids raising
suspicion
•Deceitful communication succeeds if it appears
natural and targets an unsuspecting audience.
•Suspicion more often raised by nature of the
communication than by factual errors about the
illness.
•Recognising presence of deceit rests on keen
observation and familiarity with human nature.
•In both factitious disorders and Malingering,
untruthfulness of a claim exists on a continuum.

58. *
•DSM-IV-TR - intentional production or feigning of
physical or psychological symptoms in order to
assume the sick role.
•Deceive in reporting of symptoms; misrepresent
medical and personal histories.
•DSM-5:
- proposes to relocate factitious disorders to
Somatic Symptom Disorder category
- draws attention to objective identification of
deceit
•Factitious Disorder by Proxy is where caregiver
intentionally produces or feigns signs and symptoms
in a person entrusted to their care, usually a child.

59. *
Aetiology, pathogenesis, and epidemiology
•Aetiology unknown.
•Men more often affected than women.
•History of childhood abuse, poor attachment, etc.
•Frequent contact with medical system seen as
source of care and nurturance and escape from
harsh familial environments.
•This reinforces the illness-endorsing behaviour.
•But, patients provoke repeated rejection 
repeated cycle.
•Patients often have first-hand experience with
relative with mental disorder and/or above-average
medical or psychological knowledge.

60. *
Diagnosis, clinical presentation, and course
•Challenge doctor-patient relationship:
- deceive and break trust
- retaliation tempting but NB to avoid confrontation
•Popularly known as Münchhausen Syndrome.
•Present with pathological lying; patient appears to
believe own stories.
•Present with bewildering array of signs and symptoms;
adept at manipulating laboratory tests.
•Submit themselves to repeated dangerous diagnostic
procedures.
•Co-morbid conditions (e.g. Borderline PD; depression).
•Chronic course; high morbidity.
•Patients with factitious disorders are distressed and
dysfunctional.

61. *
Differential diagnosis
•Differential diagnosis involves any conceivable
condition.
•Psychiatric differentials include Somatisation
Disorder, Hypochondriasis, and Pain Disorder,
Borderline, Antisocial, and Histrionic Personality
Disorder, Schizophrenia, and Malingering.
•Ganser’s Syndrome (similarities in response style).

62. *
•Malingering is not a mental disorder.
•Cunnien (1997): Malingering is:
- conscious and deliberate behaviour
- that constitutes a form of pretence, fabrication, or
feigning
- in the presence of an objectively identifiable goal
•Can coexist with true illness.
•Neither symptom nor illness, but behaviour.
•Malingering by Proxy involves reporting untruthful
symptoms in another and is motivated by an identifiable
external incentive (e.g. securing a child support grant).
•Extended Malingering involves co-opting others to
endorse the index malingerer’s deceitful claims.
•Dysfunctional Malingering Syndrome involves
continuation of Malingering despite lack of success.

63. *
Epidemiology, clinical presentation, and
assessment
•Surprisingly common; incidence in general
psychiatric population = 50% (damage claims) and
21% (court assessments).
•Confusing clinical picture.
•Differential diagnoses embrace all of medicine
and psychology.
•Detection requires alertness to inconsistency and
a healthy dose of scepticism, all without
sacrificing compassion.

64. *
Assessment, cont.
•Many psychological tests to detect Malingering.
•Most clinicians rely on their pattern-recognition ability;
however, this needs experience.
•Du Plessis (2003) – three-step ‘Expert Model’ for
detection of Malingering (Table 8.31):
- suspicion – formation of the initial Malingering-
hypothesis
- iterative hypothesis testing – the deductive stage
- clinical confirmation
•Malingering detectable along two dimensions:
- errors of fact
- errors of communication

65. *
Assessment, cont.
•Errors of fact concern symptomatology; amenable
to clinical assessment.
•Special investigations, neuropsychological measures,
and information from third parties may assist in
detecting false symptoms.
•Errors of communication concern how malingerer
communicates the deception; also amenable to
clinical appraisal.
•In Expert Model, both error dimensions composed
of domains designed to assist practitioner detect
Malingering (see Table 8.32 and Table 8.33).
•Very difficult to strike balance between trusting
patients and naively believing what patient reports.

66. *
•Dissociative and somatoform disorders appear
very complex.
•Unsettled classification and often difficult
diagnostic criteria.
•Management is frequently difficult  strained
therapist-patient relationship not uncommon.
•No unitary biopsychosocial explanatory model.
•Summary of features of dissociative and
somatoform disorders…

67. *
Pathogenesis
•Dissociative and somatoform disorders mostly follow
a similar pathogenic process:
- Early adversity or trauma: child-abuse, trauma, serious
illness, and poor attachment.
- Constitutional predisposition exists.
- Dissociation is expressed as a defensive response to
trauma and partners fight and flight.
- Detachment and compartmentalisation are neural
information processes at play.
- Dissociative compartmentalisation and detachment
operate to produce predictable disturbances in:
•memory
•sensory experience
•motor behaviour
•representation of the self and the external world

68. *
Symptom expression
•Emergence, exacerbation, or maintenance of symptoms
follows, or is related to exposure to trauma or adversity.
•Symptoms consist of a variable mix of dissociative
phenomena and somatising.
•A mix of mental and bodily symptoms is the norm.
•Somatic symptoms can occur in almost any bodily system or
affect almost any function.
•Negative affects and limited capacity to describe
experienced feelings are common co-occurrences.
•Somatic symptoms do not yield to medical explanation.
•Course is often chronic.
•See Table 8.34 for guide to recognise and differentiate
conditions.

69. *
Dissociation and somatising as symptom dimensions
•Dissociation occurs across a wide spectrum of psychiatric and
medical conditions:
- Acute Stress Disorder and Posttraumatic Stress Disorder
- Panic Attacks and other Anxiety Disorders
- Schizophrenia and other Psychotic Disorders
- Depressive Disorders
- Borderline Personality Disorder
•Somatising and somatic phenomena also occur across a wide
spectrum of mental conditions:
- Depressive Disorders
- Schizophrenia and other Psychotic Disorders
- Panic Attacks
- Generalised Anxiety Disorder and other Anxiety Disorders
•In these instances, dissociation and somatising occur as fairly
predictable symptom clusters but do not define the
conditions.

70. *
Psychosomatic conditions
•Phenomenology appears not unlike dissociative and
somatoform disorders.
•A primary bodily locus of disease is recognised. Expression of
the condition is influenced by psychological factors.
•Differentiation from dissociative and somatoform disorders is
often difficult.

71. *
Malingering and factitious disorders
•Presentation is deceitful.
•Symptoms are deliberately feigned or exaggerated.
•Presentation can involve mental and bodily symptoms.
•May resemble dissociative and somatoform disorders.
Malingering
•Recognition of external motivation essential for Malingering.
•Malingering is not a disorder, but can coexist with true mental
or bodily illness.
•Patients with confirmed psychiatric of medical conditions can
also malinger.
Factitious disorders
•Risks are not unlike those for dissociative and somatoform
disorders.
•Morbidity in factitious disorders can be severe.
•Course is mostly chronic and patients may abscond from
therapy.

72. *
Disease burden
•Symptoms are real.
•Distress and dysfunction are real and can be severe.
•Somatoform and factitious conditions often present a
greater burden of disease than the conditions
suggested by their primary presentation.
•Psychiatric co-morbidity and medical complications
are common and add to disease burden.
•Presentations can tax the doctor/psychologist-
patient relationship and add to a sense of therapeutic
nihilism.

73. *
Final word
•Symptoms, distress, and dysfunction of
dissociative and somatoform disorders are real.
•Diagnosis and management require a rigorous and
empathic approach.
•Diagnosis is often one of exclusion.
•Treatment is mostly a long-term undertaking.
•Treatments are modestly successful.
•Factitious disorders are likewise real, with real
distress and dysfunction.
•Although a blatant act of deceit, Malingering can
co-exist with true illness