Week 10 - delusions Flashcards
What is a delusion?
A false belief based on incorrect
inference about external reality that is firmly
sustained despite what almost everyone else
believes and despite what constitutes
incontrovertible and obvious proof or evidence to
the contrary (DSM-IV, 2000).
What are 4 delusions covered in this course?
- Fregoli delusion
- Cotard delusion
- Somoatoparaphrenia
- Capgras Delusion
What is Capgras Delusion (syndrome)? (CD)
Capgras delusion (CD) is the belief that someone
emotionally close to you has been replaced by an
imposter (Capgras & Reboul-Lachaux, 1924)
• Father, mother spouse, children, pets, objects
CD is a___________ delusion
monothematic
sufferers are delusional about a single issue
Other beliefs are normal
The false belief is often ______?
encapsulated
Sufferer doesn’t wonder why the family has been
replaced
• CD sufferer not aware their belief is a delusion but
often have a sense that what they believe is odd
• CD not that rare
Case Capgras (Alexander, Stuss & Benson, 1979)
44 yr old male, road accident victim
• bilateral lesions frontal lobe
• extensive right hemisphere damage
• Prior to accident – auditory hallucinations and
delusions following prolonged period of stress but
never acted on them
• Over 2 years after accident reported that he had
two families
Case Capgras (Alexander, Stuss & Benson, 1979) • In each family
• wife same name, similar appearance and manner
• 5 children same names, gender but thought original
family one year younger
• claimed change occurred in Dec 1975 (one month after
accident) when his new wife came to pick him up from
hospital (sig not told going home?)
• Reported he had not seen original family since then but
positive feelings towards both wives
• Although he believed this implausible was unable to
change beliefs
Another example
• Researchers at the Beheshti Hospital in Iran reported an
extremely rare variant of Capgras syndrome in which a
55-year-old woman with epilepsy believes her
possessions have all been replaced by substitute objects
that don’t belong to her.
• When she buys something new, she immediately feels
that it has been replaced.
• However, the authors reported there was no evidence of
dementia, her memory was intact, and her immediate,
recent, and remote memories were okay.
• She was oriented to time, place and person, and had
appropriate intelligence.
• She also had no history of head injury or migraine, and
brain scans revealed no gross abnormality.
Consistent features of Capgras
• Delusion often specific to one person or set of persons
• Patient is convinced that although the person is identical to
the original person in everyway they are different
• Belief resistant to criticism, however patients can recognise
the idea is absurd
• False person is never mistaken for someone else or given a
different name
• Patient cannot explicitly identify the differences between the
current and true person
• Delusion tends to occur in familiar contexts (home)
• Patients adapts well to imposter
When does Capgras delusion occur?
• Usually with a psychiatric illness • Organic illnesses • Neurological damage • Examples • 4% psychosis patients • Mostly paranoid schizophrenia • Schizoaffective and affective disorders • Alzheimer’s disease (20-30%) • Epilepsy, tumours, head injury, multiple sclerosis, Parkinson’s disease and so on
Explanations for CD: Psychodynamic
Oedipal interpretation - if one’s mother is not
actually one’s mother but an imposter then sexual
feelings towards her don’t allow you to feel guilty
(Capgras & Carrette, 1924)
• Feelings of hatred or aggression toward to a
spouse may make you feel guilty, and the
formation of a believe that the person at who
these feelings after directed it is not the spouse
but some stranger will remove this guilt (Enoch &
Trethowan, 1979).
• Defence against incestuous or hostility issues in
women
• Latent homosexuality in males
Explanations for CD: Neuropsychological
Joseph (1986): cerebral hemisphere disconnection
hypothesis
• Each hemisphere independently processes visual
information about faces
• Capgras delusion occurs when the two sets of
information fail to integrate
• Staton et al (1982): failure to update patient’s
mental representations
• Capgras due to mismatch between what is
currently seen and the memory representation
Explanations for CD: Neuropsychological
• Ellis et al. (1997)
• Normal participants view pictures of familiar faces
this generates a strong autonomic response
(SCR) compared to the autonomic response
generated for unfamiliar faces
• Capgras patients have weak autonomic
responses that do not depend on the familiarity of
the facial stimulus
• Capgras patients can recognise faces
• It appears that there is a disconnection between
the face recognition and the limbic system
Explanations for CD: Neuropsychological
• Ellis and Young (1990)
• Normal face processing – dual route (Bauer, 1984)
• Ventral route – seeing a face allows you to
recognise a familiar person
• Dorsal route – affective response to the face
• Prosopagnosia – damage to the ventral pathway
• Capgras delusion – damage to the dorsal
pathway
• Lack of affective response conflict within the
person they adopt a rationalization strategy
Explanations for CD: Neuropsychological
• Issue with Ellis et al (1997)
is the use of
famous faces in the familiar condition
• Does the same ↑ SCR occur for familiar but not
famous faces ?
• Case YY 20 yr old female with Capgras for her
father (Brighetti, Bonifacci, Borlimi & Ottaviani,
2007)
• YY - no SCR differences for pictures of family and
strangers but she could correctly identify the faces
as known/unknown to her
• Control showed greater SCR to familiar faces than
unfamiliar faces
• SCR (limbic) and face recognition disconnection
still holds
Explanations for CD: Neuropsychological
• Hirsten & Ramachandran (1997)
• Capgras due to a failure to process information
between the face-processing components of the
temporal lobe and limbic system
• Capgras – failure to integrate ongoing memories
of a person across episodes
• Damage prevents patient from integrating current
encounter with person to the stored “file” on that
person and so creates a new file
• Limbic activation (emotion) acts as a glow to help
link successive episodes with that person
Explanations for CD: Neuropsychological
• Breen et al (2000) – criticized Bauer’s account
• Structures within the dorsal route guide actions not the
recognition of objects
• Unlikely that this pathway has structures capable of
face recognition or a production of an affective
response in relation to familiar stimuli
• Face recognition occurs via the ventral pathway
and affective responses to faces are provided by
ventral limbic structures including the amygdala
• Model explains both Capgras delusion and
Prosopagnosia
• Model does not explain how a lack of affective
response to becomes a delusion
Explanations for CD: Neuropsychological
• To account the lack of autonomic response to the
a familiar face a Capgras patient may believe that
the person I am seeing is not my significant other
but is someone else which is why I no longer
have the same level of autonomic response that
used to occur
• Capgras not consciously aware of what is
different
• Patient readjusts their belief to match their
autonomic arousal level
Explanations for CD: Neuropsychological
• Coltheart et al
• Although the lack of arousal responses to faces is
necessary for Capgras it is not sufficient
• Patients with damage to ventromedial regions of
the frontal cortex show this lack of arousal to
familiar face but are not delusional (see Tranel,
Damasio & Damasio, 1995)
• A second deficit must be present to account for
the failure to reject the belief that results from the
SCR deficit (first deficit)
• Damage to the right hemisphere (second deficit)
Explanations for CD: Neuropsychological
• What is the role of the right-hemisphere (RH) in
Capgras delusion?
• Ellis and colleagues – damage to the RH impairs
face perception
• But Capgras delusion occurs for the voice of a
family member and for objects
• Coltheart et al. – RH damage impairs belief
evaluation
• Is there any evidence? Where is the lesion
located?
• Is there any evidence? Where is the lesion
located?
• Review of 22 cases of delusions – 18 cases
damage right frontal lobe, 2 cases diffuse bi-lateral
damage (Burgess, Baxter, Rose & Alderman (1996)
• ERP study of delusional patients, found that the
P300 component was reduced in the patients
compared to controls in the right frontal region
(Papageorgiou et al, 2003)
• Delusional and non-delusional patients with
Alzheimer’s disease – delusion patients had
reduced activity in the limbic and right frontal
regions compared to the non-delusional group (Staff
et al 1999)
Patient had tumour removed from right frontal
sagittal area Capgras delusion stopped (Fennig,
Naisberg-Fennig & Bromet, 1994)
• Evidence points to right frontal lobe playing a role
in belief evaluation
Explanations for CD: Neuropsychological
• Luccehlli & Spinnler (2007) – Capgras is a cross
modal disorder
Capgras occur with multi-modal interaction
• Capgras failure of person not face recognition
Organic evidence for Capgras
• Right hemisphere lesions
• Also bi-lateral damage in most patients
• Main areas of damage – frontal, temporal or
parietal lobes
• CT scans more extensive bi-lateral frontal and
temporal atrophy in schizophrenic patients with
Capgras than in those without Capgras
• PET abnormal brain glucose metabolism in
paralimbic structures and temporal lobes in
patients with Alzheimer’s and Capgras
• Neuropsychological tests show patients have
affected frontal lobe functioning
Treatment of Capgras delusion
• Capgras delusion can come and go
• See Coltheart (2007) for an example patient
• Evidence suggests that when a patient is directly
and explicitly analysing the evidence about their
delusion scepticism about the delusion
• But once the topic is changed the belief returns
• Cognitive behavioural therapy – Breen et al
• Other delusion patient cured with sufficient
evidence contrary to belief
• Brain damage must weaken the belief evaluation
system
Treatment of Capgras delusion: DRUGS
• Anti-psychotic drugs: olanzapine, sulpiride,
trifluoperazine
• Neuroleptic drugs: primozide
• Anti-depressant: mirtazapine
What is Fregoli Delusion?
case sort of thing
• People I know are following me around but in
disguise so I can never recognize them
• Courbon & Fail (1927) 27 year old single woman
had lifetime of menial job and lived in hostels.
• Believed that Robine and Sarah Bernhardt were
following her disguised as other people
• Aim to make her do things beyond her control
• Usually no similarity between person and disguise
Again what is it Fregoli Delusion??
• People I know are following me around but in
disguise so I can never recognize them
• Strong autonomic response to faces
• Believe faces belong to known people
• But people do not look familiar
• People must be disguised
• Explanation offered by Ellis and colleagues
Fregoli Delusion
• Coltheart et al
Although the hyper- arousal responses to faces is
necessary for Fregoli delusion it is not sufficient
• A second deficit must be present to account for
the failure to reject the belief that results from the
SCR over-activity (first deficit)
• Damage to the right hemisphere (second deficit)
What is Cotard Delusion?
Case
• I am dead
• Patient WI 28 year old male injured in motorbike
accident (Young et al, 1992)
• CT scan damage to temporo-parietal region RH
and some bi-lateral damage frontal lobes.
• WI convinced he was dead
• Problems recognising familiar faces, buildings
and places and feelings of derealisation (feeling
dead)
What is Cotard Delusion?
• I am dead
• Person has autonomic underactivity not just for
faces but all stimuli
• GSR evidence from Ramachandran & Blakesee
(1998) to support this
• Disconnection of all sensory areas from limbic system
• How does this fit with the Ellis and Lewis model?
• Patients with pure autonomic failure
• progressive decline in feedback from ANS
• Patients show no autonomic response to emotional
stimuli for all sensory modalities
• Do not show Cotard delusion
Cotard Delusion
• Coltheart et al
• Although the under-arousal for emotional stimuli
is necessary for Cotard delusion it is not sufficient
• A second deficit must be present to account for
the failure to reject the belief that results from the
ANS under-activity (first deficit)
• Damage to the right hemisphere (second deficit)
Somatoparaphrenia (case)
• Two patients with anosognosia for motor and
somatosensory neurological deficits had delusions
for ownership of their left limbs (Gerstmann, 1942)
• Patients delusions side of their body contralateral
to brain damage
• Brain damage =>paralysis on contralateral side of
body
• Body parts belong to someone else
• Deny ownership of body parts
• Frontal lobe damage, Associated with right
hemisphere damage
Somatoparaphrenia
• Assessed by verbal interview
• Might be sensory motor deficit or not
• May have visual field deficit or not
• Can recognise their own objects on the
disowned limbs
• May improve if disowned limb is moved to
attended right hand side of space
• May co-occur with unilateral spatial neglect
• Delusion due to limb paralysis and damage to
right frontal region
Somatoparaphrenia
• Explanation via Coltheart’s two factor approach
1) Paralysis in limb creates disconnection,
therefore not mine
2) RH damage or impaired function in frontal
region weakened belief evaluation system
Delusion of Alien Control
• Action
• Construct a motor program to execute
• During action get sensory feedback about
movement
• Usually movement and feedback match
• Impaired self-monitoring
• Expected feedback not understood
• Expected feedback not generated or
• Comparison of movement and feedback didn’t
happen
• Therefore how did this movement occur?
- Not me who executed the movement
* Control from someone else - Aliens !
Alien control:
• Coltheart two factor model
• 1) impaired self-monitoring action and sensory
feedback link
• Not all cases lead to delusion of Alien control
(Foruneret et al 2002).
• 2) impaired right frontal lobe function =>
weakens belief evaluation system => delusion
Reverse Intermetamorphosis (case)
• Patient RZ (Breen et al. 2000).
• 40 yr old woman who believed she was her
father or grandfather
• Only responded to father’s name, gave his
history, was his age etc.
• Schizophrenia at 23 but was well until 12 months
before hospitalisation
• When looking at herself in the mirror reported
seeing her father
• Reported physical characteristics that were
consistent with seeing her father
• Unexplained hirsutism (unidentified cause)
• Elaborated her delusion – Drs gave her
injections
• Cognitive function – fine
• Flattened affect, monotonic speech, reduced
social responsiveness
Reverse Intermetamorphosis
• Explanation via Coltheart’s two factor approach
1) Patient deluded about who she was
2) RH damage or impaired function in frontal
region weakened belief evaluation system
Reduplicative Paramnesia of Person
• Breen et al (2000) patient DB, 76 year old female
• No history of psychiatric illness
• No dementia or amnesia
• Had right hemisphere damage
• Right parietal stroke => Reduplicative Paramnesia
• She was disoriented for time and place
• Husband died 4 years ago and was cremated and
that he was also a patient in the same hospital as
her.
Reduplicative Paramnesia 2
• Acknowledge husband had passed away
• In same conversation reported he was a patient in
the hospital
• Reduplicated other family members
• daughters, grandson
• All family members worked or were patients at
hospital
• 19 months later while in a nursing home she still
insisted her husband was alive
• Reduplicated places – nursing home taken over
her house
Reduplicative Paramnesia
• Explanation via Coltheart’s two factor approach
1) Right parietal stroke she was disoriented for
time and place
2) RH damage in frontal region weakened belief
evaluation system
