Course outline: 1. Methods and concepts in studying neuropsychology. 2. Theories and models of normal face processing. 3. Disorders of recognition: agnosia and prosopagnosia. 4. Agnosia and prosopagnosia (continued). 5. Neuropsychological studies of - PowerPoint PPT Presentation

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Course outline: 1. Methods and concepts in studying neuropsychology. 2. Theories and models of normal face processing. 3. Disorders of recognition: agnosia and prosopagnosia. 4. Agnosia and prosopagnosia (continued). 5. Neuropsychological studies of

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Title: Course outline: 1. Methods and concepts in studying neuropsychology. 2. Theories and models of normal face processing. 3. Disorders of recognition: agnosia and prosopagnosia. 4. Agnosia and prosopagnosia (continued). 5. Neuropsychological studies of


1
Course outline1. Methods and concepts in
studying neuropsychology.2. Theories and models
of normal face processing.3. Disorders of
recognition agnosia and prosopagnosia.4.
Agnosia and prosopagnosia (continued).5.
Neuropsychological studies of normal people ERP
and divided visual-field studies.6.
Neuropsychology of expression perception.7.
Student presentations (10 minutes each)8.
Student presentations (continued).
2
Methods for studying face processing
3
Behavioural studies on intact individuals
  • 1. Psychology experiments
  • Useful for finding out what people can do (as
    opposed to what they normally do).
  • Enable unambiguous identification of causal
    relationships.
  • Normally compare one or more groups.
  • Measure average difference in errors and/or RT's.

4
Typical measures taken in psychology experiments
  • Tests of explicit memory for faces
  • Latency and number correct for "famous" versus
    "not famous" responses, or for "old" (seen
    earlier in experiment) versus "new" (never seen
    before).
  • Identification (number correct, or latency to
    name using a voice key).
  • Tests of implicit memory for faces
  • Threshold exposure needed to identify a face.
  • Priming (reduction in RT due to previous
    exposure).

5
  • 2. Visual divided-field studies
  • Capitalise on quirks of organisation of the
    primary visual pathways.
  • Enable non-invasive study of lateralisation of
    visual processing in normal individuals.

6
Organisation of the visual pathways in normal
people Stimuli in extreme left visual field go
first to right hemisphere, and vice versa. With
brief exposures (lt200 msec), LH is more accurate
at perceiving words, and RH is better at
perceiving pictures (including faces).
7
  • 3. Adaptation studies
  • High-level "figural after-effects".
  • Prolonged exposure to a face temporarily affects
    its appearance, and sensitivity to it.
  • e.g. Leopold et al (2001), Webster and MacLin
    (1999).

8
3. Adaptation studies (cont.)
9
Neurophysiological studies of intact individuals
  • 1. Imaging techniques (PET, fMRI )
  • Useful for observing neural activity correlated
    with face processing.
  • Relatively poor temporal and spatial resolution.
  • Most cognitive functions involve a number of
    brain regions.
  • 2. Event-related potentials
  • Record electrical activity from various loci on
    scalp. Computer filters out noise.
    Millisecond-level precision, but limited to 2D.

(a) Single response to a 100 ms visual stimulus
at time 0, in monkey posterior parietal cortex
(b) Average of 888 responses (Bressler 2002).
10
Animal studies
  • Lesion studies surgical ablation of specific
    regions.
  • Single-cell recording techniques.
  • Less "messy" than naturally-occurring lesions.
  • Problems in generalising between species.
  • Ambiguities in interpreting increased cell
    activity levels - e.g. what are "face" cells
    actually responding to?

11
Studies of brain-damaged humans
  • Sometimes strikingly specific disorders,
    revealing the modularity of cognitive processing.
  • Messy seldom neatly confined to a single region.
  • Many disorders (e.g. agnosia, prosopagnosia) are
    very rare.
  • No two individuals have the same brain damage.
  • Patients are seldom in a stable condition -
    either recovering (to some extent) or
    deteriorating.
  • Need to select controls for comparisons very
    carefully.
  • Problem of establishing pre-morbid ability levels.

12
A brief history of neuropsychology 19th c.
localisationalists and faculty
psychology. Descriptive analysis of single
cases. Early 20th c. globalists and
associationism. Quantitative analysis of
groups. Modern modularity and rebirth of
faculty psychology. Quantitative analysis of
single cases.
13
Group study approach 1. Group studies (e.g.
"left frontal" vs. control). 2. Look for
syndromes - patterns of typical deficits. 3.
Focus on the typical association of deficits. 4.
Use syndromes as clue to the damage's location
confirm anatomically at post mortem.
14
Problems with group studies 1. May obscure
detection of subtle deficits because (a) Involve
averaging of data (b) Involve patients with
different types and extent of lesion. (c)
Time-consuming. (d) Difficult to define groups on
basis of symptoms. 2. Deficits may co-occur for
purely anatomical reasons (e.g. prosopagnosia and
cerebral achromatopsia).
15
Single case-study approach 1. Single case
studies (one patient vs. control gp.) 2. Look for
specific single deficits. 3. Focus on the
dissociation of deficits. 4. Anatomy is a
secondary consideration, since scans can locate
damage.
16
The concept of dissociation Single
dissociation If a patient can do task A but not
B, this implies that A and B are handled by
different brain systems. Problem - A might be
easier than B. Double dissociation One patient
can do A but not B another patient can do B but
not A. Strong evidence that A and B are dealt
with by separate systems.
17
Physiological changes after brain damage 1.
Anterograde (Wallerian) degeneration axon dies
once it has been severed from its cell body. 2.
Retrograde degeneration cell body and dendrites
die once the axon has been cut off. 3.Transneuron
al degeneration neurones connected to a
damaged/dead neurone also die. 4. Scarring
(invasion of damaged area by glial cells). 5.
Calcification. 6. Reduction in blood flow to
damaged tissue.
18
Physiological changes after brain damage
(continued) 7. Reduced metabolism in damaged
tissue. 8. Reduced production of
neurotransmitters. 9. Reduced blood-flow (due to
damage, stroke, ischaemic attack) - oxygen
deprivation - production of neurotransmitter
glutamate by hippocampal CA cells -
over-excitation of cells - cell death. 10.
Oedema (swelling) - increased intra-cranial
pressure. 11. Haemorrhage and alterations in
tissue fluids' salt concentrations.
19
Mechanisms underlying recovery 1. Regeneration
- in peripheral nervous system only. 2.
Re-routing of connections. 2. Collateral
sprouting. 3. Denervation hypersensitivity. 4.
Disinhibition of previously-inhibited regions.
20
Mechanisms underlying recovery (continued) 5.
Substitution of other brain regions. 6. Recovery
from diaschisis (shock). 7. Equipotentiality and
mass action. 8. Behavioural compensation and
alternative strategies.
21
Difficulties in interpreting lesion data
Y is solely responsible for face recognition
Y interferes with the region(s) which are
responsible.
Y disconnects the regions which are responsible.
Y is one of a number of regions which are
responsible.
22
Modern position on localisation
Regional equipotentiality, but also some
specialisation. Cognitive processes may be
functionally modular, without necessarily being
anatomically localised. Most cognitive processes
(including face processing!) involve a number of
brain regions acting in concert. e,g, Haxby
model (Gobbin and Haxby 2007) - "core" and
"extended" systems.
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