Week 11 - Delusions part 2 Flashcards

1
Q

Delusion: (coltheart and davies definition)

A

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 and evidence
to the contrary (Coltheart & Davies, 2000)

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2
Q

Place Reduplication

A

Delusional Misidentification Syndrome
• Environmental reduplicative paramnesia
• Subjective belief that a place has been duplicated
• And the places exists in at least 2 locations
simultaneously
• Cause mainly neurological
– May occur in 8% of population
• Possibly the first case…
– Bonnet (1788) patient who believed they were dead
and
that her current location was in another place.

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3
Q

Place Reduplication

case

A

• Pick (1903) – patient with belief that there are two
or more places with the same name
• 67 yr old woman with possible neurodegenerative
disease
• Claimed there were two clinics each headed by
Professor Pick
• Maintained there were two clinics one in Prague
and another in her home town
• Patient claimed to be located/treated in the replica
clinic in her home town
• Patient resisted all attempts to explain that belief
was not correct

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4
Q

Place Reduplication

geschwind (82)

A

Geschwind (1982) patient in hospital in Boston
claim he was in hospital in Concord New
Hampshire

Knew he was in Beth Israel Hospital USA
maintained he was in branch in Concord (branch
non-existen

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5
Q
Place Reduplication (PR)
• Three variations of PR
A

1) place reduplication – place duplicated and exists
simultaneously (and identical in both cases) in
two or more locations that are geographically
separated
2) Chimeric assimilation – two places become
combined
3) Extravagant spatial localisation – patient believes
that the current location they are in in actually
somewhere else

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6
Q

Place Reduplication (PR)

foresight
confabulation
aetiology
delusion must…..

A

• Patient little concern for their condition and
decreased foresight
• Patient may initially display confabulation which
resolves shortly after injury
• Typically organic cause not psychiatric
– Head trauma, cerebral infarction,
– Patient does not have paranoia
• Delusion must persist after injury to be PR
• Must be resistant to reason

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7
Q

Place Reduplication (PR)

can they recognise landmarks and places?

A

• Patient can recognise familiar landmarks and
places
• May have issues orienting themselves in relation
to these landmarks

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8
Q

What are the 3 clusters of cognitive deficits for PR?

A

– Memory deficits
– Impaired geographical/visuospatial skills
– Executive skill dysfunctions

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9
Q

Place Reduplication (PR)

injuries

A

• PR – right hemisphere and/or bi-frontal injury
• Imaging studies and CT scans support this
• RH damage impairs visuospatial perception and
visual memory
• Damage to the RH frontal lobe – difficult to inhibit
the false impressions related to disorientation
– Also some evidence of parietal and temporal damage

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10
Q

• What does Right Hemisphere damage do that leads to Place Reduplication?

A

– Loss of self-related function monitoring of reality,
familiarity and memories OR
– Overactivity of the LH due to RH deficit

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11
Q

Place Reduplication (PR) TX

A
• May resolve after period of time
• Medications might be of use
• Not a lot on this
• May co-occur with deficits in
– memory
– Executive functions
– Attention
– Visuospatial and topographic functions
• But these deficit occur without PR so why does
PR occur?
– Patient has a false familiarity with place – mistaken
for somewhere more familiar
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12
Q

Invisible Doppelganger

A

• Person believes that
– They have a clone of their real self OR
– They are the clone of their real self
• Neurological cause (exact location unknown) but
it might be linked with the experience of owning
one’s own body.
• Might be within the thalamocortical and limbic
loops (widely distributed throughout the brain)
• DTI study showed small lesion fronto-opercular
region in otherwise health male

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13
Q

Mirrored-Self Misidentification

Case

A

• Patient FE (Breen et al., 2000) 87 year old make
• Brief hospitalisation for temporary stroke
• After discharge occasional nocturnal hallucinations
• 12 months after when they moved house
– FE could not recognise his own reflection in the mirror
– FE thought that his reflection was someone else
following him around
– Occurred in various places not just at home
• Tried to talk to this person and was not sure why
the person did not speak back to him
• Not paranoid about the person nor did he believe
the person had harmful intentions

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14
Q

Mirrored-Self Misidentification

Case
lh vs rh functioning

A

• FE’s family tried to explain the problems with his
belief
• FE listened and often agreed with them BUT
• Delusion persisted
• Left hemisphere functions OK
– Language and verbal memory
• Right hemisphere functions impaired
– Copying, drawing, visual memory
• Delusion continued for about 3 years
• FE’s cognitive function declined over 2-year
follow-up period
• Finally diagnosed with dementia (uncertain
aetiology)

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15
Q

Mirrored-Self Misidentification (case)

did not have mirror agnosia…

A

• Did not have mirror agnosia
• Semantic knowledge mirrors intact
• Object identification of mirrors OK too
• Used mirror to shave but this was an automatic
behaviour (not really looking)
• Covert behavioural evidence that is was himself in
the mirror
– Asked if the person was bald he tilted his own head to be
visible in the mirror image
• FE oriented to self, no depersonalisation
• Always the person in mirror, never a double or
imposter
• Good at indentifying his own things

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16
Q

Mirrored-Self Misidentification

FE’s face recognition

A

• FE did have some deficits in face recognition for
famous faces
– Did have semantic knowledge of these people
• FE good at face recognition of family members
including himself
• Months after delusion onset FE developed another
delusion
– Wife was 2 people and his son had a brother (he had
son and daughter)
• General intellectual function occurred after this so
no further investigation possible

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17
Q

Mirrored-Self Misidentification

• Explanation via Coltheart’s two factor approach

A

1) Patient some impairment of face recognition
2) RH damage or impaired function in frontal
region weakened belief evaluation system

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18
Q

Auditory Word Recognition

• Auditory phonological analysis

A

– Identification of speech sounds

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19
Q

auditory word recognition

• Phonological Input Lexicon

A

– Store auditory word recognition units

– Sounds of familiar words

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20
Q

auditory word recognition

• Semantic system

A

– Store of word meaning and concept meaning

21
Q

Auditory Word Processing Disorders

• Word sound deafness

A

– deficit in auditory
phonological analysis

– Problem with comprehension of auditorily presented
words
– Ok for non-speech sounds
– Can match pictures to non-speech sounds
– Cannot repeat real words : cannot access
phonological input lexicon
– Cannot decide if letter strings have same sounds

22
Q

Auditory Word Processing Disorders

Word form deafness –

A

problem within
phonological input lexicon (spoken word stores)
or problem gaining access to this store
– Cannot do an auditory lexical decision test
– Problem matching spoken word to picture

23
Q

Auditory Word Processing Disorders

• Word meaning deafness

A

– impairment in
accessing semantics from the phonological input
lexicon

– Auditory lexical decision performance OK
– Understanding an auditorily presented word is
impaired
– Access to semantic via picture or printed word – OK

24
Q

Auditory word processing disorder: • Central semantic deficit

A

impaired written and
spoken word comprehension
– Typically degradation in semantic system rather than
complete impairment

• Central semantic deficit – impaired written and
spoken word comprehension
– Typically degradation in semantic system rather than
complete impairment
– Imagability effects should be evident
– Category specific deficits possible
– Errors for written and verbal presentation will be
semantic in nature
– Spoken word – picture matching
– Written word - picture matching
– Written or spoken synonym judgments
– Written or spoken association matching task

25
Q

Auditory Processing Disorders

Auditory agnosia –

A

– problem with the recognition of
auditorily presented information
– Behave like deaf people (not deaf) and can read, write
and speak

26
Q

• Verbal auditory agnosia -

A

speech problems

27
Q

• Nonverbal auditory agnosia –

A

nonspeech problems

28
Q

Phonagnosia -

A
  • inability to recognize familiar voices
    or to discriminate between unfamiliar ones
    – Ok auditory speech comprehension
29
Q

Auditory Processing Disorder

• Music agnosia

A

– failure to recognise familiar music

– Ok for other non-speech sounds

30
Q

Amusia

A

– deficit music processing

– Congenital or acquired deficit

31
Q

Receptive amusia

A

– problem reading or
understanding music
– Problem with pitch or rhythm

32
Q

Expressive amusia

A

– problem singing, writing
music or playing an instrument
– Vocal expressive amusia
– Instrumental motor amusia

33
Q

Synaesthesia

A

Synaesthesia – sensory activation in one
modality causes (or is linked to) sensory
activation in another modality
• Can also cause additional activation in the same
sensory modality
• Experiences occur at the same time as the
actual stimulus is experienced

34
Q

• Synaesthestes report that

A
their experiences are
very real and occur without conscious control 
automatic process(es)
• Acquired and developmental skills
• Hypnosis may induce synaesthesia like
experiences
• May inform normal models of perception and
cognition
35
Q

Synaesthesia Prevalence

A
• More prevalent in females ratio 5:1(maybe)
• Tendency for family clusters
• Prevalence differs across reports
– 4% of population
– 0.05% of population
– 1 in 2000 people
• Consistency in associations of stimuli and
perceptions
• Use Stroop task – consistency
36
Q

Synaesthesia Associations

A

• Each synaesthete has a unique scheme of
associations
• Associations for one person are always the same
pairings
• Synaesthetic images usually simple and come
and go as the stimulus does
• Induction of sensation usually unidirectional
• Synaesthetes have normal cognitive function
• Imaging studies show activation of “perceptual
areas” but normal activation/inactivation
elsewhere
• Might be due to “extra” neural connections
– Differences in axon guidance, disruption border
information, failure of normal synaptic pruning

37
Q

Developmental Synaesthesia

A

• Runs in families
• Not the exact same stimuli-perception pairings
• Children less consistent with stimuli-perception
pairings than adults
• Better than controls for consistency
• Tested later in adulthood consistency stabilized
• New synaesthesia characteristics can be
developed in adulthood

38
Q

Acquired Synaesthesia

A

• Results from sensory loss (vision) or LSD
• Inducers (stimuli) tend to be simple sensory
stimuli rather than learned and meaningful
stimuli
• Matches differences in neural reorganisation
• Blindness – auditory-vision or tactile-vision
synaesthesia
• Onset –days to one or two years after deficit
occurs
• Not clear why only some people have this
experience after deficit onset

39
Q

Nature of specific associations between

stimuli and perception

A

• Consistency in synaesthesia experiences
• Audio-visual associations: high pitch sounds
brighter, smaller and higher in space than low
pitch sounds
• Letter-colour associations: A- red, B-blue, Cyellow
– Common letters have common colours, uncommon
letters less common colours
• Number-colour associations: single digits (light to
dark, saturated to unsaturated as magnitude
increases)

40
Q

Consequences of synaesthesia

A

• Causal nature of these effects?
• Perception: S better perception than nonsynaesthetes
(NS)
– But is this causal?
• Imagery: more vivid in grapheme-colour S and
spatial S
• Memory: Some S exceptional memories
– Link between type of S and type of memory affected
• Art & Creativity: greater proportion of S involved
in this area
• Numeracy: S can lead to better or worse
performance, may depend on type of S

41
Q

Case of colour-taste synaesthesia

A

• Nikolinakos et al. (2013) - case colour-taste
synaesthesia
• Colour is inducer
• Taste is concurrent
• TK 72 year-old right handed male
• artist,-painter, print maker and art teacher
• Unidirectional synaesthesia for 3 of 4 basic tastes
– Green  bitterness
– Red  sweetness
– Yellow  sourness
– No colour  saltiness
– Colours not resulting in taste qualities = neutral taste

42
Q

Case of colour-taste synaesthesia 2

A

• TK became vividly aware of colour –tastes when he
started arts school in his 20s
• Prior to this no memory of synaesthesia experiences
• TK painted since early childhood
• Synaesthesia experiences occur when painting,
looking at art and from colours in environment
• TK’s synaesthesia experiences vary with the purity,
amount and intensity of the perceived hue
• Experiences taste on his tongue but it differs from
the taste of food (less strong)
• No experiences when forming mental images of
colours or when dreaming

43
Q

Multimodal synaesthesias & thalamic

stroke

A

• Fornazzari et al. (2012)
• 45 year old male who developed acquired
multimodal synaesthesia 9 months after stroke
in thalamic region
• Developed sound  colour, sounds  tactile
(touch), grapheme  taste synaesthesia
– Blue print meant chicken tasted bad
– Black print chicken OK
• During 3 years of study his experiences were
consistent (Synaesthesia Battery)

44
Q

Multimodal synaesthesias & thalamic
stroke

Patient could

A

• Patient could voluntarily suppress all of his
synaesthesia experiences
• Patient could elicit his experiences just by thinking
about the stimuli
– Letters on shopping list  chicken task
• Conceptual synaesthesia
• Lesion left posterior part of thalamus, relay station
for
– posterior parietal cortex
– Multimodal integrative areas – posterior insula to
orbitofrontal cortex
– Input into other visual areas

45
Q

Super-recognisers of Faces

A

• Study by Russell, Duchaine & Nakayama (2009)
• Tested face recognition abilities of 4 participants who
never forget a face (Super-recognisers)
• Tests included
– Before They Were Famous test
– Cambridge Face Memory test
– Cambridge Face Perception Test
• Super recognisers out performed controls on before
they were famous and memory task
• Super recognisers had better face perception than
controls and were about as good as prosopagnosics
were bad
• Continuum of face recognition skills?

46
Q

Face Processing Patient JS (Neuroscase 2012)

A

• Patient JS had a stroke, reported problems in
recognising family members visiting her in hospital
• While in hospital
– JH did not recognise the daughter she sees
regularly
– no problem recognising the daughter she had not
seen for 8 yrs
– Would not allow grand kids to sit on her lap
because they looked repulsive

47
Q

Face Processing Patient JS

impaired percept

A

• Impaired perception of facial expression
• Impairment on Benton Facial Recognition test
• Face processing tested using photos of faces of
family, celebrities and unfamiliar people
• problem identifying family and friends but not
celebrities (RT data)
• JS could identify pictures of celebrity look alikes
• Reported the pictures of family members had
distorted facial proportions and she could not tell
which way the proportions were distorted

48
Q

Face Processing Patient JS

compared to controls

A

• Compared to controls JS was slower and less
accurate at indentifying celebrity faces and even
more so for family members
• JS SCR indicated lower psychological arousal to
faces than controls but her SCR for familiar was
higher then non-familiar faces
• JS problems
– Impaired recognition of basic emotional expressions
– Poor recognition of familiar faces in general but this is
worse for family members
– Face of family members appear distorted

49
Q

Face Processing Patient JS

does not have but might have…

A

• JS does not have Prosopagnosia
• JS does not gave Capgras Delusion
• JS might have mild Metamorphopsia
(Prosometamorphopsia)
• Could be due to poor integration between
identity and emotion related processing of faces