The man who mistook his wife for a hat Flashcards

1
Q

what is Acquired prosopagnosia?

A
- individuals who
have acquired the
disorder after
neurological illness or
injury
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2
Q

Developmental

prosopagnosia

A
Lifelong face
recognition
impairment in the
absence of
neurological injury
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3
Q

benefits of studying prosopagnosia?

A

1) Tells us the kind of visual cues they can or
cannot use and may give us clues to normal
face recognition (VanBelle et al., 2010)

2) Can help us better understand the location
and critical role of brain areas involved in
face recognition (see Rossion et al., 2003)

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4
Q

Acquired prosopagnosia

A

Defined as a specific inability to recognise
familiar faces. (Bodamer 1947)
• Severe impairment
• Unable to recognise friends, family &
sometimes even self!
• Recognition triggered by alternative means:
voice, paraphernalia, gait
• Appropriate semantic information about
familiar people
• Good visual acuity
• Disorder of visual perception

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5
Q

history of AP

A

First report of AP in 1844 by Wigan (see
Grusser & Landis, 1991 review)
• Assumed to be part of generalised visual
agnosia
• Landmark case in 1937 by Hoff & Potzl of
patient who was unable to recognise faces but
could recognise objects
• Term ‘prosopagnosia’ adopted by Bodamer
(1947) who described three wounded WWI
soldiers
Prospon = Greek word for face
Agnosia = non-knowledge

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6
Q

double dissociation in AP?

A

The fact that some patients show a deficit
for recognizing objects, while others show a
selective deficit for recognising faces
• This suggests that objects and faces may be
processed by separate perceptual
mechanisms/brain areas

lots of example papers on slides.

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7
Q

prevalence of AP

A

Very rare especially in ‘pure’ form, most people who can’t identify faces can’t identify objects.
e.g. Zihl & von Cramon (1986) of 258 patients with
posterior lesions none with prosopagnosia

• Riddoch et al. (2008). Patient FB. Unilateral
right hemisphere lesion
- fine with naming other categories of complex
novel objects
- recognition deficit confined to faces
- pure prosopagnosic.

Increased prevalence if prosopagnosia
considered a symptom rather than a disorder in
own right
e.g. Valentine, Powell et al. (2006) screened 91
patients with brain injury in previous 6 months.
50% reported everyday problems with face
recognition.

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8
Q

Aetiology of AP

A

Many causes of the lesions that bring about AP
– CO poisoning, encephalitus, temporal
lobectomy, tumour, head trauma
• Cases of AP alongside frontotemporal and
semantic dementia (Josephs et al., 2009)
• Traditionally thought due to unilateral damage
to right hemisphere, particularly right
occipitotemporal area (DeRenzi et al., 1994)
• Others argued that bilateral lessions. Damasio
et al., (1982) – 8 cases with bilateral lesions

Some reports that AP can also result from left
hemisphere lesions (Barton, 2008).
• Farah (1990): 65% of 81 prosopagnosics had
bilateral damage, 29% RH only, 6% LH only.
• Unilateral lesions lead to impairments in face
processing. Bilateral lesions cause more
extensive disruption (?; Boeri & Salmaggi, 1994)
• When bilateral lesions there is no possibility of
compensation from un-lesioned hemisphere.

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9
Q

other common impairments with AP

A

Other visual impairments are common:
• Can be low level visual impairments – difficulties
discriminating luminance, spatial resolution,
curvature etc
• Poor contrast sensitivity at higher frequencies
– affects ability to extract fine-grained
information from the face (?; Caldara et al.,
2005)
• Visual field defects

Impairment in colour vision
• Navigational difficulties and problems with
memory for places
• Most have problems recognising shapes and
objects
• Problems with other aspects of faces such as
gender or age. Also problems determining
emotional expression

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10
Q

apperceptive difficulties

A

visual difficulties that prevent person from creating a correct percept of a face

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11
Q

Associative difficulties

A

can create a normal percept of a face but cannot associate percept with stored visual representations
of known faces

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12
Q

bruce and young model of face processing

A

1986

two routes.
structural encoding occurs - this is a face, followed by either:

1: expression, facial speec, age, gender.

  1. recognition.
    face recognition units: stored faces.
    person identity nodes: access to semantic information.
    name generation.
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13
Q

prosopangosia in relation to bruce and young model

A

Prosopagnosia in relation to the Bruce and Young model:
In theory, face recognition could break down at any stage:
encoding, FRU or PIN - net result would be some form of prosopagnosia.

“Apperceptive” prosopagnosia:
Problems at the structural encoding stage?

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