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 normal people: ERP and divided visual-field studies. 6. Neuropsychology of expression perception. 7. Student presentations (10 minutes each) 8. Student presentations (continued).

Methods for studying face processing:

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.

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).

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.

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 (<200 msec), LH is more accurate at perceiving words, and RH is better at perceiving pictures (including faces).

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).

28% 36% 44% 52% 60% 68% Mainly Keanu Percentage of Brad in the morph: Mainly Brad 3. Adaptation studies (cont.):

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).

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?

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.

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.

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.

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).

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.

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.

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.Transneuronal 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.

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.

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.

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.

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. Difficulties in interpreting lesion data: XYZXYZ XYZ XYZ

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. Modern position on localisation: