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
1Course 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).
2Methods for studying face processing
3Behavioural 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.
4Typical 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.
6Organisation 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).
83. Adaptation studies (cont.)
9Neurophysiological 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).
10Animal 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?
11Studies 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.
12A 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.
13Group 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.
14Problems 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).
15Single 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.
16The 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.
17Physiological 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.
18Physiological 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.
19Mechanisms 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.
20Mechanisms 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.
21Difficulties 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.
22Modern 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.