410 midterm 1 Flashcards
1
Q
phrenology
A
observing bumps on the skull to infer something about the person
2
Q
cognitive neuroscience
A
- field of study seeking to uncover links between cognitions and the brain using interdisciplinary methodologies
- looking at images of the brain to understand the person
- inference and assumption that the brain underlies behaviour and mental state (same assumption as phrenology)
- new understanding that cognitions may shift based on individuals, their group memberships, interests, etc.
3
Q
convergent methodology
A
- using different methods to give evidence for the links between brain and behaviour to ‘confirm’ them with more certainty
- but connecting a brain region with a function theoretically or experimentally doesn’t mean that link will always hold OR that this region drives a behaviour
4
Q
brain injuries as a method
A
- they result in some abnormal behaviour, so give insight into how regions are functionally related to behaviour
- but there are still atypical populations (comorbid problems, older people, more extensive damage) so may not be generalizable
- using neuropsychological syndromes to illustrate brain-behaviour links (how do we generalize from a patient group to a non-patient group?)
5
Q
inferences about how the mind works
A
- inputs into the mind (genes, environment, stimuli), then something happens in the black box, then there’s an output (thoughts, feelings, behaviour)
- what happens in the black box?
- neuropsychological syndromes lead to broken links between input and output due to missing parts of the brain (brain injuries are one of the only ways to achieve these causal links)
6
Q
what allowed for cognitive neuroscience to become a field
A
- rise of neuroimaging methods (1990s) allowing for imaging of live brains (fMRI and PET)
7
Q
key principles of cognitive neuroscience
A
- cognitions arise from the brain
- application of interdisciplinary investigations
8
Q
assumptions of cognitive neuroscience
A
- neural activity underlies behaviour
- cognitive functions can be localized in the brain
- mental representations and the system (the brain) are stable over time
9
Q
assumption: neural activity underlies behaviour
A
- how do mind and body connect?
- if this assumption were untrue, there would be no neural activity while a behaviour was occurring
- dualism and monism + four perspectives
- cog neurosci takes a monism perspective (cognitions arise from neural activity), but this view is perhaps challenged by certain syndromes (phantom limb)
10
Q
dualism and monism
A
- dualism: mind and body are separate
- monism: mind and brain (body) are linked, either one and the same, or mutually interactive
11
Q
perspectives on linking mind and body
A
- parallelism: two aspects of the same reality
- isomorphism: cognitions and brain share a ‘pattern’
- epiphenomenalism: mind is a byproduct of the brain
- emergent interactionism: cognitions are emergent properties of the brain (both exist on their own and modify the functional organization of the brain)
12
Q
parallelism
A
- mind and body are two aspects of the same reality (one-to-one correspondence between reality and brain states)
- whatever is ‘out there’ is also in the brain
- maybe computationally impossible
13
Q
isomorphism
A
- cognitions and the brain share a ‘pattern’ rather than being connected in one-to-one correspondence
- mental representations: brain representations of the external world (understandings of the external world)
- reality can be represented in multiple ways in the brain (unlike in parallelism) so the exact same stimulus is represented in many ways
- bistable representations that can flip sometimes spontaneously
14
Q
epiphenomenalism
A
- mind is a byproduct of the brain
- mental states are caused by physical states, but mental states do not influence physical states
- steam train metaphor: mind is like steam coming of the train (caused by the engine, but doesn’t affect anything)
15
Q
emergent interactionism
A
- cognitions are emergent properties of the brain, which both exist on their own and modify the underlying functional organization of the brain
- Roger Sperry and split-brain patients
- mental events are functional derivates from brain circuits and their connections (emergent)–we don’t know their shape or form, they are self-forming and emerging from the machinery (brain)
- something arises from the brain, exists on its own and exerts its own effect
- our representation of a bistable figure affects how we perceive this figure in the future
- thoughts arise from the brain and changes how the brain works (prior knowledge and expectations changing how the brain works)
16
Q
assumption: cognitive functions can be localized in the brain
A
- modularity: enough specialization in the system to allow for modularity and functional specialization (different areas are specialized, but collaborate to function as a whole)
- we need some assumption of modularity to start to look for brain-behaviour links (a function sits somewhere, and we can find it and connect it to behaviour)
- certain areas performing multiple contextually related functions (not necessarily one area per function)
17
Q
assumption: mental representations and the system are stable over time
A
- the way we represent the external world stays the same (our brain will invoke a similar representation of the bistable cube over time)
- similar functions making similar representations over time (i.e. functional specialization stays similar over time)
- the way we experience the world and ourselves in stable (except maybe in babies or neuropsychological patients)
18
Q
forward inference
A
- general way in which science is conducted
- modify the stimulus = changes the operations in the black box = different behaviour
- stimulus A activates process A and we see it in brain area A (face = face detection = FFA activity)
19
Q
reverse inference
A
- there could be many inputs that lead to the same behaviour
- brain area A leads to process A (FFA activation = we infer that they are thinking about faces)
- but this activation could be caused by many processes/stimuli
- default mode network (activated regions while at rest) = difficult to make reverse inferences by just looking at the brain (what are people thinking about when told to ‘do nothing’)
20
Q
brain fingerprinting
A
- reverse inference
- deciding if a person is innocent or guilty based on EEG waveform
- recognition waveform (P300) when presented with correct details about a crime
- P300 used for lack of novelty, something contradicting expectations
- but this can be elicited by many different things, so needs additional evidence to be credible
21
Q
why study methods
A
- we need to understand the methods to understand the validity of scientific articles
- we need to use the right methods to address certain questions
- understanding strengths and weaknesses of particular methods to ask certain questions and get certain conclusions
- methods are diverse and often complementary (different methods to answer the same questions, giving different insights)
22
Q
how can we use subjective reports
A
- since cognitions may differ based on individuals, use subjective reports to understand individual differences in cognitions and the brain
- we used to dislike subjective reports (not anymore)
23
Q
neuropsychology
A
- field of study concerned with understanding the structure and function of the brain and how they relate to cognitions and behaviour
- also concerned with understanding and describing neurological conditions, developing diagnostic, assessment, and rehabilitation methods
- it’s clinical practice and research (linking brain-behaviour links with clinical practice)
- includes single-case patient studies, lesion studies in humans and animals, recording of brain activity
24
Q
method: neuroanatomy
A
- postmortem analysis of the nervous system
- gross neuroanatomy (general structural divisions) like white matter v. grey matter, lobes and hemispheres
- fine neuroanatomy (cell structure and connections) like pyramidal cells in different areas v. granule cells so what are their functions and where do you find them
25
Q
method: neurophysiology
A
- in vivo technique for manipulating and measuring neuronal activity
- getting causal brain-behaviour links by manipulating cell activity to see how it affects behaviour
- generally done in animals, but some methods in humans
- microelectrodes (single cell recordings) and macroelectrodes (on the surface of the brain) can be stimulating (emitting electrical currents) or measuring (just listening)
- knowledge about our visual system comes from microelectrode studies in monkeys (receptive fields of particular neurons)
26
Q
method: lesion studies
A
- how removal or alteration of a particular brain structure changes/affects resulting behaviour/cognitions
- in humans and animals
- irreversible and reversible (split-brain, HM are irreversible lesioning in humans)
- in humans, lesions result from brain injury or rare specialized surgery
- analysis of impaired performance after brain damage contributes to our understanding of the typical functional organization of the brain
- single and double dissociations
- brain damage usually doesn’t result in undifferentiated loss of function (relatively circumscribed) = functions need to be localizable and damage to same areas result in similar problems in different people
27
Q
single and double dissociations
A
- inferring functional independence of brain areas
- single: damage to FFA = disrupted face perception (this doesn’t tell us about the uniqueness of FFA for face perception)
- double: damage to another area than FFA disrupts another function, but spares face perception (object recognition v. object naming are doubly dissociated), this is the strongest neuropsychological evidence of a selective deficit
- triple: damage to frontal lobe spares face perception and face recognition but disrupts motor movements
28
Q
human reversible lesions
A
- transcranial magnetic stimulation leads to transient disruption of brain areas for a few seconds only
- MRI/fMRI to pinpoint brain areas you want to disrupt
- TMS can only affect cortical regions (cannot change subcortical activity)
- primary activation can be restricted to a small area, but there are downstream effects
- but a claim of causality requires showing that lesions of the area impair a function
- within-patient observations
- TMS has been used successfully in treatments for depression (but unclear by which mechanism)
29
Q
transcranial direct-current stimulation
A
- stimulating specific brain areas
- not good reliability
30
Q
other types of lesioning
A
- cooling the brain done in animals
- pharmacological manipulations in animals
- global pharmacological manipulations (like birth control changing brains) may have nonspecific effects
31
Q
method: neuroimaging
A
- typically of healthy brains
- anatomical: tissue spatial resolution
- connectivity analyses (not only functional connectivity, but also structural)
- MRI images show the average brain with statistical results plotted onto an MNI brain which tells us which brain regions are typically active relative to control condition (these are representations of our brain activity, but many other facts also go into this), so not showing brain activity but statistical tests
32
Q
fMRI
A
- measuring metabolic changes associated with brain function
- BOLD signal: blood-oxygen levels (oxygenated blood sent to active regions, contrast between oxygenated and deoxygenated blood provides BOLD)
- signal changes in fMRI require averaging over successive observations (getting a clear signal since metabolic changes to a single event may be hard to detect)
- key shortcoming: 2-3 second delay in activity (metabolic activity takes time to measure, so this isn’t a good method for timing)
- fMRI doesn’t tell us how activity occurs, just where (we don’t know where this activity comes from)
- key shortcoming: correlational only (activation is associated with manipulations, but not caused by manipulations, an activated region could just be ‘listening’)
33
Q
other neuroimaging methods
A
- mapping tracts for connections between brain regions
34
Q
electroencephalography
A
- data visualizations aren’t as intuitive as for MRI
- measures come from pyramidal neurons only
- real-time millisecond precision, but doesn’t tell us where things are happening (we can get a general idea of where things are more positive or negative)
- data from EEG is based on a contrast with control condition (average potentials)
- frequency component of the signal (as opposed to electrical component): high density of a particular frequency at a particular moment
- no insight into subcortical processes (MEG can measure subcortical activity)
- also a correlational method
35
Q
method: behavioural tests
A
- critical component of brain-behaviour links (this is the behaviour part)
- elicit a certain process (engage face perception by showing a picture of a face) and manipulate this process somehow
- then we measure behaviours (is the face familiar, do you like it, etc.)
- we can connect the behaviour with the other method we used: look at the brain when a certain process is engaged (look at constrasts in the brain between two conditions)
- chronometric investigations (response time, accuracy) as objective measures of performance for finer analysis of internal processes
- eye tracking investigations, paper and pencil tests (neuropsychological tools), subjective reports
- informing neuroimaging and neuropsychological investigations (this is the output part) but you need independent investigation to ensure that a process is activated, manipulated, and measured
36
Q
eye tracking investigations
A
- behavioural method
- movement and position
- what are people paying attention to (although people can pay attention to things they aren’t looking at)
- visual preferences
- which parts of the scene are informative for our judgments
- we can measure time, errors, how often, eye gaze path
37
Q
paper and pencil tests
A
- behavioural method
- neuropsychological tools
- often used in experimental work, but common in diagnosis
38
Q
subjective reports
A
- behavioural method
- questionnaires
- becoming more accepted, but still should be theoretically motivated
- can be difficult to use this and connect them to data
39
Q
Phineas Gage
A
- open head injury in frontal lobes for behaviour and impulse control
- behaviour was changed = conclusion that behaviour control is important in frontal areas
40
Q
Anna O
A
- hysteric case that inspired Freud’s research
- disseminated widely
41
Q
Little Hans
A
- Freud case study for sexual development in children
- had a fear of horses = Freud’s idea was that fear arose from deeper things
- Hans recovered from his phobia
42
Q
Patient HM
A
- medial temporal lobe excision to control epilepsy = anterograde amnesia
- not intellectually impaired, ability to learn new motor skills (so this is controlled by a different brain region)
- important for hippocampal contribution to memory
43
Q
Patient Tan
A
- Broca interested in functional specialization
- lesion in left frontal lobe = specialized for language expression
44
Q
single patient case studies viability
A
- historically important, very detailed, easy to digest
- but are they scientifically credible? especially the historical ones–are they accurate?
- are they representative? are all details relevant?
- contemporary view is that case studies have a place as ‘naturally occurring experiments’
45
Q
Caramazza & McCloskey (lecture material)
A
- we can use the pattern of impaired performance observed in neuropsychological patients to infer the structure and function of a normal cognitive system
- impaired and typical cognitive function results from the same underlying brain function
- brain damage doesn’t result in undifferentiated loss of function, but a selective loss of a particular ability
- single patient studies must NOT be group studies (avoid clumping patients into disorder categories)
- single patient study does provide a link to the general population
- damage that occurs in these patients is naturally occurring (so very diverse)
46
Q
four assumptions Caramazza & McCloskey
A
- fractionation: selective brain damage results in a selective not undifferentiated loss of ability
- modularity: complex function is represented in terms of more basic components of processing (memory can be broken into smaller components like procedural, working, long-term that all work together to produce memory)
- transparency: pathological (impaired) performance will provide a basis for inferring which module is affected (correspondence between behavioural impairment and module)
- universality: the model is true of normal human brains in general (showing this link in one person only generalizes to a model of the human brain, ie. taking out MTL region in other people will provide the same deficits as HM)
47
Q
statistical power
A
- probability of a test to detect the effect if it exists (80% is considered sufficient = 20% of not detecting an effect that exists)
- does a single patient case study have enough power to detect an effect?
- power curves for small, medium, large effects
- for small (0.2), the power is linearly related to number of observations (so it would be impossible to get to 0.8 power)
- for medium and large effects, there is a plateau in the number of observations so that any more will not result in greater power
- NOT # of participants, but # of observations (perhaps within a single patient)
- in a single patient, we reduce the amount of noise, and with the correct # of observations, we are able to reach the statistical power required
- so single patient studies are theoretically ok
- many observations from a diverse sample can reduce power by making it more difficult to find the effect
48
Q
cognitive psychology
A
- study of mental activity as an information-processing problem
- assumption that perceptions, thoughts, action depend on internal transformations or computations (sensation to perception to memory, but also attention and expectations and prior knowledge)
49
Q
what can reaction time data tell us (reading)
A
- whether a comparison is a parallel process (simultaneously for all items) so that RT is independent of # of items
- or a serial process (sequentially) so that RT slows as memory set becomes larger
50
Q
computers in cognitive science
A
- to simulate cognitive processes (artificial intelligence)
- computer is given input and must perform internal operations to create a behaviour (does this behaviour match that produced by a real mind?)
- but correct hypothesis about those mental operations are needed
51
Q
neural networks
A
- processing is distributed over innumerable units whose input and output can represent specific features (distributed like neurons)
- hidden units as intermediates to allow for the best mapping of input to output by changing the strength of connections between units
- learning rule: quantitative description of how processing within the model changes
- lesion techniques demonstrate how performance changes when parts are altered (graceful degradation because each unit plays a small part only)
52
Q
limitations of computational models
A
- always simplifications of the nervous system
- do elements correspond to single neurons or to ensembles of neurons?
- catastrophic interference (loss of old information when new material is presented)
- restricted to narrow problems
53
Q
single cell recording
A
- electrode inserted into animal brain
- typically extra-cellular (on the outside of the neuron)
- but the tip likely records from a small set of neurons (need to differentiate this pooled activity)
- correlating neuronal activity with a stimulus pattern or behaviour
- finding visual receptive fields = topographic representation (retinotopic maps and tonotopic maps in visual and auditory areas + cochlea)
- also multiunit recording (in many neurons at once)
54
Q
problems with lesion studies
A
- can force the animal to change its normal behaviour (a compensatory strategy) and alter the function of intact structures (deprived of input or axons cannot make normal connections)
55
Q
neurochemical lesions
A
- newer method with more control
- drug selectively destroys cells that use a certain transmitter
- kainic acid selectively destroys cell bodies (spares axons)
56
Q
neurochemical reversible lesions
A
- transient disruption in nerve conductivity (so the animal can serve as its own control)
- acetylcholine antagonist scopolamine for temporary amnesia
57
Q
genetic manipulations
A
- knockout procedures: specific genes are no longer present or expressed (lacking single types of postsynaptic receptors in specific brain regions)
- predicting who will develop a disorder via analysis of genetic codes (Huntington’s)
- we can use this to examine gene-environment interactions
58
Q
neurology
A
- linking cognitive processes to neural structures by selecting patients with circumscribed pathology
- computed tomography
- magnetic resonance imaging
- diffusion tensor imaging
59
Q
computed tomography
A
- like an x-ray, but you’re reconstructing 3D spaces from compressed 2D images
- absorption of x-ray radiations correlates with tissue density (high-density = bone = lots of radiation)
- high-density regions show up as light colour, low-density regions are dark
- it can be difficult to see the boundary between white and gray matter on a CT scan
60
Q
MRI
A
- magnetic properties of organic tissue (hydrogen in the brain and other organic tissue)
- protons become oriented parallel to the magnetic force, then radio waves pass through = protons absorb their energy so that their orientation is changes in a predictable direction
- when radio waves are turned off, the absorbed energy is dissipated so that protons rebound toward the magnetic field (MRI constructing an image of the distributions of protons)
- can resolve structures that are less than 1mm = good views of small and subcortical structures
61
Q
diffusion tensor imaging
A
- using MRI scanners to study axon tracts
- measures density and motion of water contained in axons (determining the boundaries that restrict water movement in the brain)
- diffusion of water is anisotropic (restricted) because of axon membranes
- regions are voxels (volumetric)
- detecting how far protons have moved in space in the specific direction being measured
62
Q
angiography
A
- imaging method to evaluate the circulatory system in the brain
63
Q
vasculatory system in the brain
A
- two internal carotid and two vertebral arteries
- each carotid artery branches into two major arteries (anterior cerebral and middle cerebral supply the anterior and middle portions of the brain with blood)
- vertebral arteries join into the basilar artery
- basilar artery inferior branches supply the cerebellum and posterior brainstem and into two posterior cerebral arteries to supply the occipital and medial temporal lobes
- major cerebral arteries partially overlap = border zones or watershed areas
64
Q
arteriosclerosis
A
- buildup of fatty tissue in arteries
- tissue can break free to become an embolus that is carried through the bloodstream
- embolus can easily pass through larger arteries but as their size decreases, the embolus gets stuck (infarcted) to block the flow of blood and preventing oxygen = cells eventually die
65
Q
ischemia
A
- partial occlusion of an artery or capillary due to an embolus or due to a sudden drop in blood pressure that prevents blood from reaching the brain
- a sudden rise in blood pressure can lead to cerebral hemorrhage
66
Q
cerebral arteriosclerosis
A
- chronic condition in which cerebral blood vessels become narrow due to thickening of arteries
- can result in persistent ischemia
- acute situation due to aneurysm (weak spot or distention in a blood vessel)–an aneurysm can burst = disruption of circulation (ischemic stroke)
67
Q
occlusive strokes
A
- occluded tissue is either completely infarcted, clot is too small to remove, or the embolus has been absorbed into tissue
- treated with drugs to dissolve the clot
68
Q
tumor/neoplasm
A
- mass of tissue that grows abnormally and has no physiological function
- benign if they do not recur after removal and remain where they originated
- malignant if they are likely to recur and are often distributed over many areas
- neurons can be destroyed by an infiltrating tumor or become dysfunctional due to displacement by a tumor
- gliomas: abnormal reproduction of glial cells
- meningiomas (meninges) produce pressure on the brain
- metastatic tumors originate in a non-cerebral structure and is carried to the brain
69
Q
Alzheimer’s
A
- genetic link is weaker (more environmental factors)
- hypothesis is the production of amyloid goes awry = plaques found in the brains of patients
70
Q
infectious diseases
A
- HIV causes acquired immunodeficiency syndrome (AIDS)-related dementia can lodge in subcortical regions of the brain causing diffuse lesions of white matter
- herpes simplex virus destroys neurons in cortical and limbic structures if it migrates to the brain
- suspected viral infection in multiple sclerosis
- CT and MRI can only confirm a diagnosis, but cannot reveal pathology early on
71
Q
head traum
A
- closed head injuries: skull intact, but the brain is damaged by mechanical forced generated by a blow to the head
- coup: site of the blow
- contrecoup: reactive forces bounce the brain against the skull on the opposite side of the head
- open head injuries: skull penetrated by an object (tissue can be directly damaged), can also produce coup and contrecoup
- trauma can disrupt blood flow by severing vessels or change intracranial pressure due to bleeding
- seizures can occur in scarred tissue
- trauma = extensive and diffuse damage = many neuropsychological conditions
72
Q
epilepsy
A
- EEG: large-amplitude oscillations
- having a seizure is not diagnostic of epilepsy
73
Q
functional neurosurgery
A
- extent of tissue removal is documents = correlation between lesion site and cognitive deficits (but we can’t attribute these deficits to the lesion)
- callosotomy (split-brain) providing insights into functions of both hemispheres
- eliminative (eliminating abnormal brain function) or restorative (return to normal function)
- deep-brain stimulation: electrodes in the basal ganglia to produce continuous electrical signals that trigger neural activity
74
Q
group vs. individual studies
A
- group as inappropriate for neuropsychology because of variability among patients assigned to the same groups (no two strokes are the same) but we can identify regions of overlap (common site of pathology can produce a pattern of deficits)
- case studies give powerful insight into functional components of cognition
75
Q
event-related potential
A
- the evoked response to a particular task which is a tiny signal embedded in the ongoing EEG
- obtained by averaging the traces to extract the ERP
- ERPs are better suited to addressing questions about the time course of cognition, not the brain structures that produce the events
- inverse problem: an infinite number of possible charge distributions can lead to the same pattern (all measurements are made at the scalp)
- dipole: create a spherical head and place a dipole within, then determine the distribution of voltages that this dipole could create at the surface, then compare this predicted pattern to actual data
76
Q
magnetoencephalography
A
- active neurons produce small magnetic fields, so MEG traces can be averaged over a series of trials to obtain event-related fields (ERFs)
- same temporal resolution as ERPs, but has an advantage in localizing the source of the signal
- the neurons that can be recorded with MEG are within sulci (where long axis of dendrite is parallel to skull)
77
Q
positron emission tomography
A
- more oxygen and glucose are made available by increased blood flow when the brain is engaged in cognitive tasks
- PET studies use radioactive elements (isotopes) as tracers in the blood
- PET scanner is a gamma ray detector to determine where there is more radiation (more blood flow)
- PET studies measure relative metabolic activity
- injection administered at least twice: at control and experiment and the results are reported in terms of a change in regional cerebral blood flow (rCBF) between the two conditions
78
Q
how does fMRI work
A
- same procedure as in traditional MRI (radio waves make the protons in hydrogen atoms oscillate and detector measures local energy fields that are emitted as protons return to the orientation of the external magnetic field)
- imaging is focused on the magnetic properties of hemoglobin
- deoxygenated hemoglobin is more sensitive (paramagnetic) than oxygenated hemoglobin–this ratio is the BOLD effect
79
Q
brain anatomy and function (Ramachandran)
A
- frontal lobe separated from the parietal by the central/rolandic fissure
- temporal lobe separated from the parietal by the lateral/sylvian fissure
- medulla oblongata connects the spinal cord to the brain and has clusters of cells that control blood pressure, heart rate, breathing
- medulla connects to the pons which connects to the cerebellum for coordinated movements
- hypothalamus (metabolic functions, hormone production, basic drives like aggression, fear, sexuality)
- hippocampus for forming new memory traces
- basal ganglia for natural smiles vs. motor cortex for forced smiles
- angular gyrus somehow necessary for numerical computational tasks but not for understanding concepts underlying computations
80
Q
holism
A
- overlaps with connectionism
- brain functions as a whole and any one part is just as good as another part
- many areas (cortical regions especially) can be recruited for many tasks
81
Q
right brain/left brain (Rama)
A
- stroke in the left brain = anxious, depressed, worried about recovery (the right brain takes over)
- stroke in the right brain = blissful indifference to their predicament (left hemisphere doesn’t care)
82
Q
Caramazza & McCloskey reading notes
A
- advocate for drawing inferences about normal cognitive systems from patterns of impaired performance consequent to brain damage
- brain damage doesn’t result in undifferentiated loss of cognitive abilities, but in the selective loss of some ability (but otherwise normal performance)
- assumption of universality: functional architecture of cognitive systems is invariant across normal individuals
- lesions are not in the control of the experimenter so cannot be assumed to be equivalent and cannot average their performance
- there are patterns of deficits that frequently co-occur, but these must be grouped only based on some theory (these deficits could be due to damage to distinct components)
- patient classification is useless and harmful (ie. only use single-patient studies)
83
Q
irreversible lesions in humans
A
- vascular disorder (strokes, aneurysms, hypoxia)
- tumors (mass impeding on the brain)
- degenerative disorders
- head trauma
84
Q
neural plasticity
A
- changes in typical neural organization (synapses, pathways, connections) as a function of behaviour, environment, injury
- umbrella term that covers many phenomena and changes (normal development, long and short-term changes in brain organization and chemistry)
- includes both functional and structural changes occurring in the brain as a result of reorganization
85
Q
May (2011) definition of neural plasticity
A
- environmentally driven constant rearrangement of network homeostasis balancing the integration of neuronal activity, neurotransmitter release, neuronal (and glial) morphogenesis and changes in network formation (including formation and elimination of synaptic structures)
- homeostasis: brain structures and functions attempting to find a balance where environmental demands push them out of balance (dynamic)
- unclear whether plasticity is always environmentally driven (could also be internal?)
- plasticity can refer to functional changes in brain activity
- experience, learning, and damage can all cause structural and/or functional reorganization
86
Q
examples of plasticity
A
- typical development: brain reorganizes itself in the first few years of life, also in adult life, and especially while aging (inverse-U shaped)
- expertise: brain dedicates more real estate to the fingers that play an instrument in musicians (motor cortex, corpus callosum for integrating hands, planum temporale), in experts listening and moving fingers were very similar (ie. integrated)
- injury (loss of vision): brain rededicating visual processing areas to other modalities (tactile)
- posterior hippocampal gray matter volume correlates positively with spatial representation skills (depends on detail and duration of use of these spatial representations)
- juggling training led to a transient gray matter increase in area MT and left inferior parietal sulcus (and these changes degraded when training stopped), altered gray matter in occipitotemporal cortex
- learning a new language = structural changes in left IFG
87
Q
loss of vision plasticity
A
- braille starts to activate previously visual areas
- age of loss of vision is critical
- sighted control P has no activity while reading braille but visual cortex of blind P activates
- after 1yr training in braille, more areas in sensory, motor, occipital cortices activated while reading
88
Q
TMS study braille
A
- TMS to examine the effects of visual and somatosensory cortex disruptions to Braille reading in blind people
- rTMS applied over the visual cortical area disrupts braille reading in blind people (visual cortex representing tactile information)
- TMS can induce tactile sensations in fingers of braille readers
- P having somatosensory disrupted = disruption of responses in detection and identification 10-15ms after
- P having occipital cortex disrupted = stimulus detection is spared, but identification is disrupted 40-70ms during processing
- so somatosensory cortex involved earlier in detection and identification, and occipital involved later for identification–this is reversed typical processing (usually visual would come first, then somatosensory)
89
Q
May (2011) lecture notes
A
- is plasticity due to internal reorganization of the brain or does learning influence plastic changes
- studies of brain morphology have found learning-related changes
90
Q
maladaptive plasticity (May, 2011)
A
- plasticity occurring, but the change is not helpful to us
- PTSD, depression, anxiety are changes in the brain
- aging brain changes
91
Q
cross-sectional v. longitudinal comparison
A
- comparing two different groups of people (blind and sighted) that could have individual differences
- comparing the endpoints; we don’t know how the changes arose, what caused them, were the patients atypical in some way
- longitudinal are more methodologically sound, but often impossible
92
Q
somatosensory cortex and phantom limb
A
- person moves their phantom limb which elicits activity in the brain (an experience becomes real in the brain–a perception)
- maps change after amputation (what happens to the cells that aren’t in use anymore)
- maybe the cells get reassigned to neighbouring areas (remapping)
- the amount of the shift to neighbouring cells directly relates to the degree of phantom limb pain (more remapping = more pain)
- our brain represents our body in both motor and somatosensory cortices on either side of the central sulcus (disproportional maps–the penfield homunculus)
93
Q
phantom limb
A
- a lingering feeling (representation) of a missing limb
- the representation of a limb remains (may even change) when a limb is lost
- the part of the brain that usually gets input from the limb no longer gets any input = neighbouring area invades that region = touching the body part that corresponds to the neighbouring area will activate sensations for the missing limb
94
Q
pain from phantom limb
A
- usually, when your brain asks to clench your hand, you get sensory feedback from the limb to stop clenching or that you’re clenching too hard, so you stop
- in phantom limb, there are no signals from the limb that no longer exists to stop clenching, resulting in pain
- a mirror helps provide those feedback signals by visual means, so you can ‘stop’ clenching which diminishes the pain
- Rama explanation: slight error in the remapping process so that touch input gets attached to pain centers so that when face is brushed = pain
95
Q
possible explanations for phantom limb
A
- sprouting new neurons (jumping from one area to the next)
- redundancy in the connections (so connections come alive if other ones are lost), but this isn’t feasible because we can’t prepare for every possible accident and have extra connections ready to take over
- frayed nerve endings in the stump (neuromas) that originally supplied the limb become inflamed, so fool the brain into thinking that the limb is still there
- neuronal scar tissue innervates the neighbouring areas (Rama explanation)
- subcortical reorganization
96
Q
Pons et al. (1991) phantom limb study
A
- studied the effects of nerve de-afferentation (removing all inputs) on somatosensory cortex representations in monkeys (recorded from the areas pre and post the deafferentation)
- mapped the somatosensory cortex, then deafferented (this is similar to what happens in patients–nerves getting removed from the spinal cord)
- so the area doesn’t receive any inputs
- post-deafferentation recordings indicated that this region now represented the face (expanded face map)
- in patients, touching the face = sensation in phantom hand
- the entire affected area (10-14mm) responded to stimulation of the small part of the face area (but other studies found reorganization at the scale of 1-2mm)
- no evidence for sprouting or redundant connections hypotheses
- favoured explanation is that reorganization occurs subcortically, and this is relayed to the cortex (unclear why it’s the neighbouring areas or whether it’s always the neighbouring area)
97
Q
representations of space and our body are dynamic
A
- we can acquire representations of external objects and perceive them as our own body parts
- this can occur in neurologically intact individuals very quickly
- our body image can be ‘overriden’ by visual input, the brain’s plasticity allows us to ‘adopt’ a fake hand into our representations
- this process is broken in phantom limb; visual input of the lack of limb is not overriding the somatosensory representation of the limb (but the mirror box works visually to alleviate pain)
- representations of our body parts are changing
- implications for robotic surgery (probes could be extensions of our body parts)
98
Q
how is the mirror box used
A
- as a therapeutic tool for arthritis and carpal tunnel as well as phantom limb
- a process of recreating connections, so this needs to be practiced on multiple occasions and in different contexts
- not as miraculous as initially assumed
- right parietal lobe presented with conflicting signals: visual feedback saying that arm is moving and muscles saying the arm is not there = conclusion that there is no arm = loss of phantom pain
99
Q
Rama study for phantom limb and somatosensory representations
A
- used magnetoencephalography to touch different body parts and see where the localized activity arises in the penfield map
- found that brain maps can change, sometimes very quickly (the Penfield map is not innate and unchangeable)
- the phantom doesn’t emerge from the stump (contrary to the neuromas explanations) but from the face because every time a patient moves their face, this activates the ‘hand’ area of the cortex = illusion of phantom limb
100
Q
atypical cases of phantom limb (Rama)
A
- Mirabelle who was born without a limb but still experienced phantom limb (this suggests that neural circuitry for body image is at least partly laid down by genes)
- John’s telescoped phantom hand (hand directly attached to stump without an arm in between)
- lack of phantom limb syndrome in loss of limb due to leprosy (progressive nerve damage allowing more time to readjust body image?)
101
Q
pre-amputation paralysis in phantom limb
A
- arms paralyzed or held in a sling, so the parietal lobe doesn’t receive visual feedback of the limb moving when commanded to = ‘learned paralysis’ so that when the limb is amputated, the body image is stuck in this revised form as a paralyzed phantom
102
Q
how is our body image created
A
- internal image and memory of one’s body in space and time
- parietal lobes combine information from muscles, joints, eyes, and motor command centers
103
Q
motor cortex and initiating movements (Rama)
A
- movement originates in the frontal lobe (just in front of the central sulcus)
- contains an upside-down map of the body and sends signals to muscles
- supplementary motor area is in charge of giving specific instructions about the sequence of required movements to the motor cortex
- identical copies of the command signal are sent to the cerebellum and parietal lobes which help compare your intended action with actual performance (feedback loop to modify movements as needed and coordinate)
- in phantom limb, the parietal lobe constructs a body image of the phantom limb “moving”
104
Q
experience-dependent plasticity in the mature cortex (May)
A
- axonal remodeling, growth of new dendritic spines, synapse turnover as structural mechanisms for experience-dependent plasticity
- enrichment is associated with increased learning and memory and reduction in age-related memory decline AND hippocampal cell proliferation, angiogenesis, microglia activation
105
Q
fractional anisotropy
A
- a measure of axonal integrity and coherence
- visual memory performance and visuospatial attention are correlated with FA
106
Q
voxel-based morphometry
A
- whole-brain method to analyze MRI images
- can be used for intrasubject analysis of different time points to look at individual differences which can’t be done in cross-sectional studies
- useful for patterns of learning-induced structural plasticity
107
Q
underlying plasticity processes (May)
A
- physical exercise-induced changes in the hippocampus confirmed that angiogenesis/neurogenesis may underlie plasticity
- changes in brain morphometry are not restricted to gray matter (increased FA measures of fiber tracts) so maybe increased myelination after training
108
Q
older age plasticity
A
- hypothesis of a reserve against physiological brain atrophy and decline in cognitive functions because no relation between degree of atrophy and clinical manifestation of that damage
- improvements in cognitive function are due to improvements in cardiovascular fitness (so exercise is important)
109
Q
brain alterations in pain areas
A
- plasticity in pain structures in people with phantom limb, chronic pain, etc.
- cingulate cortex, OFC, insula, dorsal pons, thalamus, BG, parahippocampus (damage or loss of gray matter)
- these changes are a consequence of pain
110
Q
correlates of morphometric changes
A
- change in cell size
- growth or atrophy of neurons or glia
- changes in intracortical axonal architecture (synaptogenesis)
- increase in gray matter due to increase in cell size, neural or glial genesis, spine and synaptic densities, changes in blood flow or interstitial fluid
- synaptic contacts are the substrate of long-term potentiation
- gene expression, protein synthesis, dendritic density, astrocytic proliferation
111
Q
sensation vs. perception
A
- senses: receptors sensitive to a particular input (light, sound waves, etc.)
- perceptions: interpretations of that sensation
- unclear how sensations translate to human perceptions of stimuli
- perception is very personal and subjective (ie. variable), generated by individual brains
- oddities in perception may not be immediately noticed because they’re the norm to the person (this is the difference from sensation)
- vision is a percept because it’s so subjective
112
Q
synesthesia
A
- cross-wiring between the senses so you could head colours, associate colours with numbers
- people with this believe that everyone perceives in this way
- an oddity in perception that shows perception isn’t the same as sensation
113
Q
right/left visual field pathway
A
- temporal retinas stay ipsilateral
- nasal retinas cross contralaterally
- results in the left and right visual fields getting separated contralaterally
114
Q
visual pathways
A
- LGN to V1
- to the superior colliculi (this is a colour blind tract with few fibers, so it’s primitive)
115
Q
LGN visual pathway
A
- LGN has topographical maps similar to V1
- cortical magnification: small foveal area is represented by a larger cortical area proportionally to the larger peripheral areas of the visual field
- foveal items are represented on the outer surface of the brain, then toward the periphery of the visual field, representations are moved further into the calcarine sulcus
- representations of the world are top-bottom and left-right reversed
- somehow the brain flips the image in the brain (perception)
116
Q
cortical hierarchy
A
- V1 to V2, V3, V4 (colour), V5 (motion)
- dorsal pathway is where/how: the unconscious pathway for visually guided movements
- ventral pathway is what: conscious pathway for naming and identification
117
Q
myth #1: the eye sees
A
- this implies that perceptions occur in the eye, but only sensations occur there
- truth: the brain sees
- we can close our eyes and ‘see’ things via mental imagery
- migraine auras: percepts generated in various modalities in the brain, but the sensation isn’t ‘out there’
118
Q
myth #2: vision is a faithful record
A
- we think of vision as very detailed, but it’s actually more of a gist that the visual system generates
- vision operated on top-down ideas of what the world should be (the bottom-up system is pretty slow)
- vision is active and reconstructive (not an active percept) to compensate for the sluggishness of the visual system (so what we see is largely an illusion)
119
Q
myth #3: vision is detailed
A
- limits of the visual and attentional system
- inattentional blindness occurs where two different pictures separated by a mask yields an inability to see the difference between the two pictures (big changes can occur in foveal vision without us noticing)
120
Q
blindsight
A
- an ability of cortically blind people (damage to V1) to respond to stimuli that they do not consciously perceive
- vision without awareness
- ‘blind’ refers to people’s claim not to see the stimuli
- ‘sight’ refers to the residual or recovered ability to localize, detect, and discriminate between those unseen stimuli (changing gaze to look at it)
121
Q
Rama blindsight
A
- older pathway goes to the brainstem for reflexive behaviour, directing gaze, orienting, then to extrastriate areas of the visual system
- this older pathway is used to guess the movement of stimuli they can’t consciously see
- Rama arguing that we use blindsight all the time to orient ourselves in the world without conscious awareness (autopilot vision that occurs without us knowing it)
- the expression of this ‘zombie’ happens when people have damage to V1
122
Q
perimetry
A
- testing blindsight by mapping the visual field (how far does the blindsight extend)
- patients respond to flickers of light in various parts of the visual field to see where the blindness is (this allows us to infer where the damage in the visual system is)
- disrupted light sensitivity in the lower right quadrant of the visual field = damage to upper left side of the visual system (quadrantanopia)
- hemianopia = damage to the contralateral visual cortex (upper and lower areas around the fissure)
123
Q
testing within a blind field
A
- direct: present a stimulus to the blind field, ask whether the patient can see it (they say no), then ask them to guess = if they guess above chance, it’s blindsight
- indirect: patient engaged to respond to stimuli in blind field (saccades: looking at the stimulus even if they say they can’t see it)
124
Q
why is the zombie metaphor misguided
A
- assumes blindsight is just like normal vision but without conscious awareness, but it’s not
- patient with blindsight may perform poorly on some tasks like stimulus discrimination and perform normally on others like localization
- not like vision ‘at threshold’ because a small increase in threshold (increasing salience) will render the stimulus visible for sighted people, but not for blindsight patients
125
Q
Weiskrantz et al. blindsight original studies
A
- blindsight arises because of the subcortical visual connections that feed directly into the how pathway
- this explains spared visuomotor function and spared eye movements
- bypassing LGN-V1 but going directly to superior colliculi and directly upward
126
Q
Fendrich et al.
A
- blindsight arises because of cortical sparing (residual islands of V1 function)
- using perimetry with image stabilization; Purkinje eye trackers move the visual field with the retina to keep eyes at the fixation point
- this perimetry revealed islands of V1 tissue sparing (hemianopia patient had a small area of preserved function but we can’t say if this is preserved tissue or residual function)
- is this small island of residual function enough to generate conscious perception or not?
127
Q
Stoerig response
A
- no topographical links between islands of tissue and islands of blindsight
- Fendrich assumes that preserved tissue is visually responsive
- cannot be a general explanation because blindsight occurs after surgical ablation of V1 in primates and in humans after surgery (no sparing)
- lack of converging evidence from manual and computerized perimetry
128
Q
Weiskrantz response
A
- problems with Fendrich’s perimetry because no one has used it so far
- is this patchiness a general property of blindsight?
- vascular issues could result in patchiness, but how is this residual function in V1 playing into blindsight
129
Q
Fendrich response
A
- PET evidence for spared tissue functionality
- defends the utility of the perimetry procedure as small islands could be missed with gross procedures
- small changes in eye movement position can and do change retinal image position so they must be controlled
130
Q
functional explanations for blindsight
A
- result of subcortical function (SC/LGN direct connections to dorsal stream) (Rama, Stoerig, etc.)
- result of cortical sparing within V1 (Fendrich)
- may not be mutually exclusive
131
Q
behavioural implications of blindsight
A
- role of V1 in visual awareness; most people put V1 at the epicentre of visual awareness (the only way we have conscious perception) but V1 doesn’t really do that much in the visual system
- role of feedforward and feedback connections
132
Q
Leopold et al. (2010) blindsight
A
- before LGM inactive, stimuli presented in the blind field activated extrastriate areas and produced blindsight type behaviour
- in monkeys, ablated V1 then presented stimuli outside scotoma (control), within scotoma, and catch (no stimulus)
- as contrast % increased = blindsight behaviour (more salient stimulus = getting better at detecting within scotoma but still not comparable to control
- after LGN inactivation, no more activity or blindsight behaviour (the whole visual cortex lacks activity)
- so blindsight responses are driven by direct connections between LGN and dorsal visual stream (not SC connections)
- the area of LGN they inactivated is one that receives input from SC, so SC inactivation would also disable blindsight, but this is actually due to LGN lack of input not direct connections b/w SC-dorsal stream
133
Q
Boyer et al. (2005) blindsight
A
- used TMS to temporarily deactivate V1 in typical participants (to produce blindsight)
- procedure produced transient blindsight for visual targets (orientation and colour) presented within the ‘scotoma’
- TMS presented with the target stimulus, asked to guess orientation and a confidence ratine
- as people were better at discriminating orientation, higher confidence
- most people were above chance despite not seeing the orientation of the stimulu
- typical participants with all the normal connections = still able to disrupt conscious vision via V1 TMS
134
Q
feedforward connections
A
- slow and laborious
- early sensory system = late sensory systems = cognitive systems (from LGN to occipital to frontal)
- bottom-up takes time as light becomes edges, then colour, motion, etc.
- info reaches V1 at 100ms after stimulus
135
Q
feedback connections
A
- quick and dirty, top-down
- cognitive systems = late sensory systems = early sensory systems (from frontal back to occipital)
- feedback loop doesn’t follow the same pathway as feedforward
- feedback loops provide biasing context rather than acting on information received from feedforward
- multiplexing neurons
136
Q
multiplexing neurons
A
- assume different functional roles depending on the nature of the top-down signal, including changing their visual preferences and visual field properties
- doing different things based on what they expect to see or your motivations
- feedback loop influencing what the feedforward system is doing before it even starts
- same neuron will process colour, shape, luminance based on what you expect, what is wanted, what the task is
137
Q
role of V1 in conscious perception
A
- V1 could be required to feedforward
- object substitution masking: rendering familiar objects invisible to us
138
Q
object substitution masking
A
- put four dots on the objects (the mask) at careful titrating of time = we only see the dots and we don’t see the underlying objects
- this effect only happens with a trailing mask, not a leading mask
- dots are replacing the visual experience of the object
- visual input of the original display is unconscious at 40ms, but as time of processing increases (100ms) and feedback loops come back to V1, the original display is gone and all we see is four dots
- the feedback loop checking in on what V1 is doing (what did you see?)
139
Q
feedback loop in blindsight
A
- LGN/SC connections are trying to go back to V1, but are unable to get there
- V1 providing early input which can be checking in with feedback and feedforward loops
- feedforward loop is unconscious and feedback loop is providing conscious experience
140
Q
Kluver-Bucy syndrome
A
- widespread damage to both temporal lobes (ie. what pathway)
- putting everything in their mouths, indiscriminate sexual behaviour (due to not knowing what a mate is, what food is, etc.)
141
Q
Balint syndrome
A
- bilateral damage to the parietal lobes (ie. how pathway)
- patient’s eyes stay focused on any object that is in foveal vision and ignores other objects
142
Q
what pathway anatomy
A
- V1 for orientation, luminence, then V2, etc.
- receptive fields of neurons coding for different properties get larger as you move forward in the stream (small in V1, until whole objects in TE)
- specializations vary by hemisphere (right is engaged by faces, left by other stimuli such as words)
- for houses, activation in both hemispheres
- for faces, more activity in right hemisphere and widespread in frontal (FFA is a central hub, but involves other areas too)
- double dissociations of processing in patients with damage to parts of the ventral visual stream (unable to name tools, able to name vegetables and vice versa)
143
Q
face processing
A
- all exemplars of the same object, but many different iterations (and we can automatically tell them apart even if they’re strangers)
- object category that is relevant for everyday life and also very unique
- upright and holistic biases (we’re better and faster at processing upright faces AND we see them as wholes not collections of parts)
- inverted faces often used as visual controls because they contain the same visual information but not social information (they tend to be processed as parts, not holistically = bottom-up)
144
Q
specialized face cells
A
- in the superior temporal sulcus in monkeys
- sensitive to many different features of the face (social rank, species, friendship status, face orientation, facial expressions) to process face social value
- as the relevance of the stimulus drops, the number of spikes also diminishes (different latencies of spikes for different faces)
- receptive fields extend both contralaterally and ipsilaterally (not only contralateral representation)
145
Q
specialized neural signal markers for faces
A
- N170: negative wave observed when stimuli are faces (face detection, not discrimination)
- face vs. scrambled face vs. car = N170 largest for face, slightly less for cars, smallest for scrambled
- inverted Archibaldo (vegetables) vs. face = larger N170 amplitude for face Archibaldo
- but some recent evidence questioning this neural marker
146
Q
specialized area for face processing
A
- fusiform face area
- presentation of faces to humans activate the right FFA and occipital face area
- when the stimulus is a face = high activity in this area (same for human and cat faces), very low activity for objects, schematic faces in between
147
Q
FFA details
A
- only for faces, not facial features
- face detection (not as clear in face discrimination)
- early studies used passive viewing
- more activity in right hemisphere (left has some, but not as much)
- well defined functionally (not anatomically defined), so you define its location based on which voxels are most activated when viewing faces
148
Q
domain-specific view of face perception
A
- FFA is a module that is specialized for face processing only
- module’s function is highly specific, often innate, and all-or-none
- humans and primates tend to show specialized responses to faces from birth
- FFA shouldn’t respond to anything other than faces
- Kanwisher’s view, though she doesn’t say it’s innate
149
Q
flexible fusiform area
A
- domain-general view of face perception: face processing is just an example of perceptual expertise
- FFA is involved in making distinctions between highly similar exemplars of objects (not specific to faces), so it’s because we interact with faces all the time that we’re better at this
- area for distinguishing objects of expertise
- people are better at distinguishing faces that belong to their own race than other races (due to visual expertise) and with increased exposure to faces of other races, people get better
- evidence from bird and car experts
150
Q
bird and car expertise
A
- faces showed the highest activity in FFA for bird and car experts
- for birds, bird experts showed more activity than car experts
- for cars, car experts showed slightly more activity than for bird experts in the center of right FFA
- but these are between-subjects experiments (could be individual differences)
151
Q
greebles
A
- test of visual expertise hypothesis
- within-subject before and after training
- for novices, activity in right FFA for faces, but not for greebles
- for experts in greebles, activity in right FFA starts appearing for greebles
152
Q
prosopagnosia
A
- an inability to recognize familiar faces that typically results from an injury to FFA
- recent studies have identified a congenital type that runs in families
- report seeing faces as objects, as stones, formations that don’t radiate identity
- blunted FFA response to faces for upright Archibaldo faces
153
Q
evidence for domain-specific
A
- Patient CK (object visual agnosia): preserved facial recognition, impaired object recognition
- CK cannot distinguish between tin soldiers and airplanes (his area of expertise, which became impaired)
- Patient WJ (prosopagnosia): cannot recognize familiar faces but learned to distinguish between familiar and unfamiliar sheep after stroke
- CK and WJ = double dissociation to object and face perception
- electors delivering current to FFA = distorted face perception (causal evidence)
154
Q
evidence for domain-general
A
- although FFA is typically lesioned in prosopagnosia, face detection is spared (know it’s a face, but cannot identify it–FFA is supposed to be a detector, not a recognizer)
- prosopagnosic patients are impaired most when they have to make distinctions between similar objects and whether or not they’re faces
- CK cannot recognize greebles (even when told to see them as faces) so it’s unclear to what extent he has preserved facial recognition (deficits to acquiring visual expertise)
- there is space in FFA to code for both faces and objects with visual expertise
155
Q
Capgras delusion
A
- a belief that close family members have been replaces by imposters or robots
- often accompanies psychiatric disorders, but in 25% of cases is caused by injury to the brain
- the patient recognizes their loved ones, but lacks a feeling of emotional connection to them
- most patients also have deficits in face-processing tasks (very likely to also have deficits of overt system, but these are more variable than the lack of SCR)
156
Q
Capgras (Rama)
A
- the appropriate emotion needs to be evoked by the visual input
- temporal lobe pathway links with the amygdala for emotional experience
- separate pathway from auditory cortex to amygdala (so unaffected in Capgras)
- emotion overrides intellectual understanding
- able to remember instances, but failing to link them emotionally via familiarity (maybe creating a new category every time)
157
Q
explanation of Capgras
A
- disconnection between emotional processing centers (limbic system, amygdala) and the face perception centers in the visual cortex
- typical controls show normal SCR for familiar vs. unfamiliar faces (same for psychiatric controls)
- Capgras patients show blunted response for familiar faces (becomes equivalent to unfamiliar faces)
- dual-route model
158
Q
dual-route model
A
- covert system (emotional recognition) which is broken in Capgras (so a lack of emotional connection)
- overt system (visual recognition) which is spared in Capgras
- face perception and affective evaluation involve extrastriate visual processing and limbic system
159
Q
Capgras as a mirror of prosopagnosia
A
- prosopagnosia: disconnection of overt face perception from the limbic system (patients do not recognize people but maintain the covert emotional response)
- capgras: disconnection of covert face perception from the limbic system (patients recognize people but lack covert emotional response)
160
Q
delusion of imposters?
A
- limbic and visual face perception data have to be compared and integrated somewhere
- bilateral vmPFC damage = similar emotional disconnection like Capgras patients (so this is a candidate area for where this integration occurs)
- reduced activity in the extended face-processing system that deals with processing of mental states
- Thiel et al. (2014)
161
Q
Thiel et al. (2014) Capgras
A
- 70yr woman with a right frontal intracerebral hemorrhage
- recovered in most aspects, but still maintains the imposter delusion
- relatively normal activity in FFA to faces
- when asked to compare faces of husband v. stranger = no differences in activation when trying to differentiate
- overall reduced activity may contribute to this interpretation of loved ones as imposter
162
Q
galvanic skin response
A
- autonomic nervous system controls involuntary activities of organs, blood vessels, glands
- hypothalamus helps prepare your body to take appropriate action in response to a stimulus
- this is the basis of the galvanic skin response, which we can measure by placing electrodes on your palm, recording electrical resistance of the skin
163
Q
Cotard’s syndrome
A
- patient asserts they are dead
- perhaps all sensory areas are disconnected from the limbic system, leading to a complete lack of emotional contact with the world
164
Q
eye gaze and Capgras
A
- cells in the amygdala respond to facial expression and emotion and to direction of eye gaze
- patients with Capgras impaired in judging the direction of gaze
- a change in gaze direction can be sufficient to provoke Capgras’ delusion
165
Q
Fregoli syndrome
A
- patient keeps seeing the same person everywhere
- confusions about general categories and specific exemplars
- a single episode with one exemplar of a category sets up a limbic connection that is generalized to include all members of that class and is impervious to intellectual correction
166
Q
Kanwisher
A
- greebles too similar to faces (animate figures, subjects identify them using proper names, face-like arrangement)
- magnitude of expertise and categorization-level effects are small and response to faces are twice as strong
- within-category discrimination isn’t sufficient to strongly engage the FFA
- bird and car expertise results could be due to greater interest and engagement in their categories (FFA strongly modulated by visual attention)
- patient MT (prosopagnosia) is normal at discriminating between brands of cars and fruits and veggies
- argues for a degree of modularity and domain specificity, not that FFA can only handle faces
167
Q
Tarr & Gauthier
A
- face inversion only minimally influences activity in FFA despite its strong effect on performance (this inversion effect has been replicated with non-face experts)
- geometric similarity model: similar shapes and image features activating the same areas (not supported)
- flexible process map (their preferred model): particular geometries that define object categories are associated with recognition strategies (domain-general view)
- flexible fusiform area for plasticity based on task demands and experience
- FFA automatically processes expertise objects at the subordinate level (but efficacy of this system modulated by attention)
- patients with prosopagnosia impaired with more than faces (speed-accuracy tradeoff to achieve good performance with greebles)
- interaction of homogeneity, categorization level, and expertise
