410 final Flashcards

1
Q

phrenology

A

observing bumps on the skull to infer something about the person

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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.
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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
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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?)
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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)
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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)
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7
Q

key principles of cognitive neuroscience

A
  • cognitions arise from the brain
  • application of interdisciplinary investigations
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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
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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)
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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
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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)
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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
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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
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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)
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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)
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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)
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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)
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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)
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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’)
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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
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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)
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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)
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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
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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
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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)
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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
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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
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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)
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29
Q

transcranial direct-current stimulation

A
  • stimulating specific brain areas
  • not good reliability
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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
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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
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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’)
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33
Q

other neuroimaging methods

A
  • mapping tracts for connections between brain regions
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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
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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
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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
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37
Q

paper and pencil tests

A
  • behavioural method
  • neuropsychological tools
  • often used in experimental work, but common in diagnosis
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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
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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
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40
Q

Anna O

A
  • hysteric case that inspired Freud’s research
  • disseminated widely
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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
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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
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43
Q

Patient Tan

A
  • Broca interested in functional specialization
  • lesion in left frontal lobe = specialized for language expression
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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’
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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)
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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)
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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
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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)
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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
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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
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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)
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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
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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)
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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)
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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)
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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
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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
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58
Q

neurology

A
  • linking cognitive processes to neural structures by selecting patients with circumscribed pathology
  • computed tomography
  • magnetic resonance imaging
  • diffusion tensor imaging
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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
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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
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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
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62
Q

angiography

A
  • imaging method to evaluate the circulatory system in the brain
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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72
Q

epilepsy

A
  • EEG: large-amplitude oscillations
  • having a seizure is not diagnostic of epilepsy
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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
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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
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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
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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)
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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
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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
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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
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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
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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)
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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)
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83
Q

irreversible lesions in humans

A
  • vascular disorder (strokes, aneurysms, hypoxia)
  • tumors (mass impeding on the brain)
  • degenerative disorders
  • head trauma
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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
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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
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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
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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
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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)
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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
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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
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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
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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)
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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
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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
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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
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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)
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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)
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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
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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
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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?)
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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
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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
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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”
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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
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105
Q

fractional anisotropy

A
  • a measure of axonal integrity and coherence
  • visual memory performance and visuospatial attention are correlated with FA
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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
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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
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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)
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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
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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
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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
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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
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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
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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)
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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)
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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
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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’
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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)
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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)
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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)
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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
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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)
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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)
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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
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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
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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?
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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137
Q

role of V1 in conscious perception

A
  • V1 could be required to feedforward
  • object substitution masking: rendering familiar objects invisible to us
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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?)
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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
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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.)
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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
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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)
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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)
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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)
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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
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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
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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
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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
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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
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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)
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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
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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
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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)
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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
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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)
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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)
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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
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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
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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)
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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)
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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
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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
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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
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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
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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
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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
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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
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168
Q

What is neurotheology?

A

Neurotheology is the scientific study of the neural correlates of religious or spiritual beliefs, experiences, and practices. It is also called spiritual neuroscience or neuroscience of religion.

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169
Q

What are the two main topics discussed in neurotheology?

A
  • whether a fundamental belief shared by many has a neural basis (similar to other processes such as perception)
    1. The role of the limbic system in mental experiences.
    2. Scientific methodology and inference in studying religious experiences.
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170
Q

What is the limbic system?

A

The limbic system is a cluster of cortical and subcortical structures that support a range of automatic and controlled functions, linking visceral states and emotions to cognition and behavior.

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171
Q

Is the limbic system a single, unified structure?

A

No, it is a cluster of areas rather than a single system, and its definition has evolved over time.

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172
Q

How did different researchers define the limbic system?

A

Willis: Included cortical regions around the brainstem.
Papez: Focused on structures around the corpus callosum, mammillary body, and thalamus.
Broca: Linked it to olfactory structures in the mammalian brain.

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173
Q

What are the three distinct but overlapping networks in the limbic system?

A
  1. Hippocampal-diencephalic & parahippocampal-retrosplenial (Yellow Network) → Memory & spatial orientation.
  2. Temporo-amygdala-orbitofrontal (Green Network) → Behavioral inhibition, memory for temporally complex visual information, olfactory-gustatory-visceral functions, multimodal sensory integration, object-reward association, outcome monitoring.
  3. Dorsomedial default network (Blue Network; mostly cortical) → Self-reflection, pain perception, attention, mentalizing, empathy, response selection, autobiographical memory, person perception, mind wandering.
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174
Q

What disorders are associated with the hippocampal-diencephalic and parahippocampal-retrosplenial networks?

A

Amnesias, Korsakoff’s syndrome, Mild Cognitive Impairment (MCI), Alzheimer’s, Balint syndrome.

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175
Q

What disorders are associated with the temporo-amygdala-orbitofrontal network?

A

Alzheimer’s, Kluver-Bucy syndrome, psychopathy, temporal lobe epilepsy (TLE), Geschwind syndrome, semantic dementia.

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176
Q

What disorders are associated with the dorsomedial default network?

A

Depression, autism, Alzheimer’s, anxiety, schizophrenia, OCD, ADHD, mild cognitive impairment.

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177
Q

What is the role of the temporal lobe in linking cognitive and emotional functions?

A

The temporal lobe is responsible for linking thoughts, behaviors, and emotions.

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178
Q

What is temporal lobe epilepsy (TLE)?

A

TLE is a form of epilepsy resulting from seizures within the temporal lobe, regardless of the specific location or underlying cause.

179
Q

What is mesial temporal lobe epilepsy (MTLE), and how does it differ from TLE?

A

MTLE (or limbic epilepsy) is a subtype of TLE where seizures originate in the hippocampus or amygdala (mesial = medial). It is not a single disorder but a cluster of syndromes with various causes and pathologies.

180
Q

What are common clinical features of TLE/MTLE?

A
  • Auras (indescribable rising abdominal sensations).
  • Sudden fear or anxiety.
  • Déjà vu or a sense of familiarity.
  • Less common: olfactory/gustatory hallucinations.
  • Arrest of behaviour (e.g., lip-smacking, chewing).
  • Convulsions are uncommon.
  • Amnesia post-seizure (lasting minutes to hours).
  • Seizures occur in specific brain regions and produce specific behavioral outcomes
181
Q

Why did Gloor et al. (1982) conduct intracranial EEG recordings on TLE patients?

A

Patients had intractable epilepsy with unclear seizure foci, requiring invasive EEG monitoring to identify spontaneous seizure origins.

182
Q

How was the Gloor et al. (1982) experiment conducted?

A
  • Intracerebral EEG was recorded continuously for 5 weeks to identify spontaneous seizures
  • On one day, electrodes were stimulated with an electric current.
  • Patients verbally reported experiences during stimulation.
183
Q

Front: What were the key experiential phenomena reported by patients?

A
  • Visual hallucinations (illusions, elementary and complex), not auditory or olfactory
  • Déjà vu, memory recall, fear, emotional distress.
  • Sensations of presence (rare).
  • Thirst, floating sensations.
  • Experiences clustered around visual hallucinations, memory, and fear.
184
Q

What did Patient 4 experience during a spontaneous seizure in Gloor et al. (1982)?

A
  • Déjà vu, illusion of precognition, a “weird feeling.”
  • Stopped speaking and showed posturing.
  • Different EEG frequencies were linked to specific experiences in different parts of the temporal lobe.
185
Q

What brain structures were most associated with experiential phenomena in TLE (Gloor et al., 1982)?

A

Amygdala, hippocampus, parahippocampus, and temporal neocortex.

186
Q

Front: What religious experiences did patients describe in Ramachandran’s video?

A
  • Following seizures:
  • Feelings of being God, omnipresence.
  • Extreme emotional highs and lows.
  • Religious/spiritual thoughts triggered by seizures (even in non-religious patients).
  • Sense of understanding the world on a cosmic level.
  • Feeling of floating, detachment from reality, heightened sensitivity to world suffering.
  • Religious/spiritual feelings resulted from seizure onset despite a lack of religiosity beforehand
187
Q

Front: How do TLE patients often describe their religious/spiritual experiences?

A

They report “feelings of God” or “sensed presence,” experiences of omnipresence, and deep philosophical thoughts, as seen in Ramachandran’s research.

188
Q

Front: How might the temporal lobe explain mystical or religious experiences?

A
  • The temporal lobe processes emotions and assigns salience to stimuli.
  • Seizures cause hyperconnectivity between sensory input and the amygdala.
  • This leads to increased emotional significance of all stimuli, making everything seem deeply meaningful.
  • This might explain mystical or religious experiences.
  • Activity in the temporal lobe may be conducive to religious experience
189
Q

Front: What evolutionary explanation is suggested for widespread religious beliefs?

A

Since religion provides stability in society, it may have evolved as a socially adaptive mechanism.

190
Q

Front: What is Persinger’s “God Helmet” experiment and how does it related to Rama’s MTLE hypotheses?

A
  • A device that applies weak electromagnetic fields across the temporal lobes to induce religious or sensed presence experiences.
  • Participants are placed in a silent room and blindfolded
  • These experiments were designed to test the “hardwired circuitry” hypothesis (ie. eliciting these feelings in all humans)
191
Q

Front: What experiences did participants report when wearing the God Helmet?

A
  • Fear, tingling, rushes of energy.
  • Sensed presence lurking behind them (this was associated with the right temporal lobe specifically)
  • Clammy hands, burping, malaise.
  • 80% of participants sensed “something.”
192
Q

What was the key finding in Persinger et al. about the right temporal lobe?

A

Stimulation of the right temporal lobe was most associated with feelings of sensed presence.

193
Q

How did Persinger explain spontaneous hallucinations in a patient who was having disrupted sleep?

A
  • The patient’s bedside clock emitted electromagnetic fields at the same frequency used in the experiment.
  • Those electromagnetic fields were overlapping with the patient’s brain (and the person’s brain was ‘sensitive’)
  • Removing the clock stopped the hallucinations.
194
Q

Front: What real-world phenomena might be explained by Persinger’s findings?

A
  • Ghost sightings near the Northern Lights (linked to electromagnetic fields).
  • Global increases in geomagnetic fields correlated with more seizures.
195
Q

Front: How did Richard Dawkins respond to the God Helmet?

A
  • Reported some tingling and twitching but no sensed presence (those could just be due to being relaxed in an isolation room)
  • He scored low on the temporal lobe sensitivity questionnaire.
  • This suggests individual differences in susceptibility to religious experiences (does one’s brain support these types of experiences?)
196
Q

Front: What criticism exists about Persinger’s research?

A
  • His findings are difficult to replicate.
  • This casts doubt on the “hardwired circuitry” hypothesis for religious experiences.
197
Q

Front: If religious experiences were “hardwired,” how could we test this?

A
  • We should be able to induce religious or sensed presence feelings in all humans, not just TLE patients.
  • God Helmet experiments (Persinger)
198
Q

Front: What studies attempted to test the “Hardwired Circuitry” hypothesis?

A

TMS (Transcranial Magnetic Stimulation) studies.
Persinger & Granqvist experiments.

199
Q

Front: How was the ‘heightened connections’ hypothesis tested?

A
  • Galvanic Skin Response (GSR) should be elevated to all stimuli for TLE patients vs. control
  • TLE patients vs. controls viewed neutral, unpleasant, and pleasant images.
  • TLE patients had higher GSR responses to all stimuli.
  • baseline GSR between groups was equal
200
Q

Front: What was a methodological issue in the GSR study?

A
  • Control group was hospital employees and students.
  • Their GSR did not respond to unpleasant stimuli (e.g., burned man).
  • This questions the validity of the findings, though the heightened GSR effect remained.
201
Q

What is developmental prosopagnosia (DP)?

A

DP is a neurological condition where individuals have lifelong difficulty recognizing faces, despite normal vision and intelligence. It is not caused by brain injury but is present from early development.

202
Q

How common is DP?

A

DP has a similar prevalence to autism, affecting approximately 2-2.5% of the population.

203
Q

Front: Why is early identification of DP important?

A

Identifying DP in childhood allows for better treatment and coping strategies compared to diagnosis in adulthood.

204
Q

What are Rama’s possible explanations for MTLE being linked to religiosity?

A
  1. God really exists
  2. Patients seek tranquility in religious feelings given their medical condition
  3. Heightened connections between sensory systems and the amygdala so that every objects becomes emotionally salient = sense of “special”
  4. Humans have hard-wired circuitry for the purpose of religious experiences which have evolved with human culture.
205
Q

What characterizes mystical experiences, and how do they function according to Persinger et al.?

A

Mystical experiences involve an altered state of consciousness, characterized by an expansiveness of space or time and an enhanced meaningfulness related to the self. They are generally positive and help reduce anxiety related to self-dissolution (death).

206
Q

What are the two forms of mystical experiences (Persinger)

A

1) The experience of another Sentient Being near the experient. 2) Perceived localization of the self in a different frame of reference, at significantly different times or distances.

207
Q

How do the left and right hemispheres differ in their roles during wakefulness and dreaming?

A

The left hemisphere dominates wakefulness with sequential verbal processing and categorical organization, while the right hemisphere dominates dreaming with spatial imagery organized by emotional meaning.

208
Q

What are the primary functions of the left and right hemispheres (Persinger et al.)

A

The left hemisphere is primarily responsible for sequential linguistic processes, while the right hemisphere handles spatial, affective, and vigilance-related functions.
The right hemisphere can perform syntax at the level of a six-year-old and semantics of a pre-adolescent. The left hemisphere has some visual-spatial processing ability, but neither can fully substitute the other.

209
Q

What are the two types of associative learning, and how are they optimized?

A

1) Sequential/serial learning, optimized for hearing. 2) Simultaneous/parallel learning, optimized for visual processing.

210
Q

How are experiences and their organization mapped onto different brain regions (Persinger)?

A

Experiences are processed in caudal cerebral regions, while their organization in relation to expectations, social norms, and morality occurs in the prefrontal regions.

211
Q

What is the right hemispheric equivalent of the ‘sense of self’?

A

It is dominated by affect, spatial references, and minimal verbal imagery. When weak magnetic fields are applied to the right hemisphere, people report a ‘sensed presence’ beyond the self but personally significant.

212
Q

What is the hypothesis linking the ‘sensed presence’ to brain function?

A

The sensed presence might be the left hemisphere becoming aware of the right hemisphere’s self, which could be the neurological basis for gods and deities.

213
Q

What gender differences exist in mystical experiences?

A

Women report sensed presences, vestibular sensations, fear, out-of-body experiences, and feeling of being ‘in another place’ more frequently than men. This may be linked to greater EEG coherence between the temporoparietal regions in women.

214
Q

What is the vectorial hemisphericity hypothesis?

A

This hypothesis states that for one hemisphere’s processes to intrude into the other, either the active hemisphere must be hyperactivated, or the passive hemisphere must be hypoactivated.

215
Q

What structures interconnect the two hemispheres, and how many neurons cross over?

A

The Anterior Commissure and Corpus Callosum interconnect the hemispheres, but only a small proportion of neurons directly cross via these routes.

216
Q

How does the vectorial hemisphericity hypothesis relate to psychological depression?

A

Depression might involve diminished left temporal lobe activity, allowing intrusion of right hemispheric equivalents, leading to personality transformations.

217
Q

What conditions promote hemispheric intercalation?

A

Life-threatening distress, epilepsy (especially temporal lobe epilepsy), and minor closed head injuries can promote intercalation between left and right hemispheric processes.

218
Q

How do the locations of sensed presences relate to emotion and gender perception?

A

Left-side presences are usually unpleasant; right-side presences are more positive and may involve hearing a voice. The perceived gender of the presence is typically the opposite of the experient’s.

219
Q

What brain regions are critical for mystical states?

A
  • The temporal lobes, particularly the right hemisphere. The hippocampal-amygdaloid region is especially important.
  • Electrical stimulation of the amygdala produces complex mental states, including déjà vu, Nirvana-like pleasantness, fear, and out-of-body-like experiences.
  • Disrupting activity in the right temporoparietal junction reduces the role of beliefs in moral judgments, suggesting a link between right temporoparietal activity and moral cognition.
  • Activation in the STS resulted in dreamy states in epileptic patients
  • cortical and mesiobasal temporal lobe structure stimulation = expected visceral sensations, déjà vu and the incorporation of memories into current contexts
220
Q

According to Persinger et al., what role do magnetic fields play in inducing mystical experiences?

A

Weak magnetic fields interact with electromagnetic substrates mediating consciousness. Specific configurations can induce out-of-body experiences and sensed presences.

221
Q

What experimental conditions increase the likelihood of mystical experiences?

A

Sensory deprivation, sitting in an acoustic chamber, being blindfolded, and exposure to dim red light increase the probability of sensed presences when exposed to appropriate magnetic fields.

222
Q

What effect does electrical stimulation of the right inferior parietal region have on movement perception?

A

It triggers strong intention and desire to move the homunculus-related portion of the contralateral body. With increased stimulation, patients believe they have actually performed the movements, even though they haven’t.

223
Q

What is associated with the sensed presence during an epileptic aura with religious overtones?

A

Bilateral hypoperfusion within the temporal lobes.

224
Q

Which brain regions show increased activation during religious recitation?

A

The frontal-parietal pathways, including the dorsolateral prefrontal, dorsomedial frontal, and medial parietal cortices.

225
Q

How do temporal and frontal lobe functions contribute to religious experiences?

A

The temporal lobe is involved in religious experiences, while frontal alterations may increase religious interests as a personality trait, influencing religious-related vocations.

226
Q

How do weak magnetic fields interact with the electromagnetic substrates of consciousness?

A

They mediate consciousness and mystical states (e.g., sensed presence, out-of-body experiences) through field-to-field interactions rather than direct current induction.

227
Q

What type of magnetic field patterns are most effective (Persinger)?

A
  • Irregular-shaped patterns with intrinsic burst-firing and frequency modulation, rather than sine waves.
  • 64 solenoids distributed evenly around the head
  • 3ms duration most effective
  • takes 15 minutes for the EEG to change under magnetic exposure
228
Q

How does expectancy influence sensed presence?

A
  • expectancy determines the verbal label that the person gives, and those verbal labels are reconstructed as memories after the experience
  • so it’s important that participants be blinded (and double-blind also important)
229
Q

What was the aim of the Granqvist paper?

A
  • The study aimed to replicate and extend previous research using a double-blind protocol. It also assessed personality traits indicative of suggestibility to determine if they predict the experience of a sensed presence and related phenomena.
  • Undergraduates were blinded and not informed about the sham condition; they were told they would be exposed to weak magnetic fields comparable to cell phones while exploring feeling states.
230
Q

Mechanism of Weak Complex Magnetic Fields

A
  • Weak magnetic fields are likely too weak to induce currents strong enough to depolarize neurons, making their mechanism of action unclear. However, the waveform of the field has been suggested to be crucial.
  • They may disrupt electromagnetic activity between hemispheres, causing right hemispheric activity to intrude into left hemisphere awareness, potentially leading to a sense of a non-self presence.
231
Q

What indirect evidence suggests a link between temporal lobe activity and paranormal experiences?

A

Studies show that individuals with partial epileptic signs (e.g., sensory enhancement, affective dissociation) report more paranormal and mystical experiences, including sensed presence. However, this remains correlational.

232
Q

What methodological weaknesses exist in Persinger’s studies?

A
  • Lack of clear randomization and blinding procedures, raising concerns that experiences may be artifactual due to expectancy effects or differential experimenter interactions.
  • EXIT scale was constructed inductively and has unknown reliability and construct validity.
233
Q

What is Tellegen’s Absorption Scale, and why is it relevant?

A
  • It is a widely used measure of suggestibility, assessing openness to self-altering experiences. It predicts hypnotic susceptibility and has been linked to paranormal and mystical experiences.
  • absorption correlates with scores on the Temporal Lobe Signs Inventory (TLSI), which assesses complex partial epileptic signs.
  • personality traits of High absorption, a new-age lifestyle orientation, and signs of anomalous temporal lobe activity associated with mystical and somatosensory experiences—together explaining 10–25% of variance in outcomes.
234
Q

What is the Temporal Lobe Signs Inventory (TLSI) used for?

A

It assesses psychological experiences indicative of temporal lobe activity, including déjà vu, paranormal experiences, formed visual hallucinations, unusual smells, and stereotyped thinking.

235
Q

What does the EXIT Scale measure?

A

It captures somatosensory sensations that may follow weak magnetic field exposure, including dizziness, sensed presence, tingling, vibrations, odd smells/tastes, and emotional states.

236
Q

What were the effects of weak complex magnetic fields on reported experiences in Granqvist et al.?

A
  • No statistically significant effects were found on any outcome measures, contradicting previous claims.
  • Higher temporal lobe signs, absorption, and new-age orientation were associated with higher EXIT and mysticism scores, but these effects were independent of magnetic field exposure.
  • did not find evidence that weak magnetic fields induced the sensed presence of a sentient being, mystical experiences, or other somatosensory effects.
237
Q

If magnetic fields did not cause the effects in Persinger’s studies, what alternative explanations exist?

A
  • Highly suggestible participants may have responded to experimenter effects, expectancy biases, or the priming effects of filling out pre-test questionnaires on anomalous experiences.
  • Individuals high in openness to unusual experiences may simply have more unusual experiences when placed in a sensory deprivation context.
238
Q

What does research suggest about the neurophysiological basis of religious experiences?

A
  • Rather than temporo-limbic emotional processes, religious experiences may be more related to attentional and higher cognitive functions associated with prefrontal cortical activation.
  • magnetic fields closer to those used in TMS might induce effects, but religious experiences are likely complex and involve multiple motivational, cognitive, and environmental factors.
239
Q

What is change blindness?

A

Change blindness occurs when we fail to notice changes in our environment because we are not paying attention to them. This affects our subjective experience by causing us to miss significant alterations.

240
Q

How does an attentional set affect change blindness?

A

If our attentional set is focused on a particular feature (e.g., all red cards on a red background), we may miss even large changes because they do not stand out as expected alterations.

241
Q

What role do transients play in detecting change?

A

Transients (sudden visual changes, like a person changing their shirt) typically cue attention. However, a mask can remove these transients, making it harder to detect changes without environmental support.

242
Q

What is William James’ definition of attention?

A

“Taking possession of the mind, in clear/vivid form, of one out of what seem several simultaneously possible objects or trains of thought… It implies withdrawal from some things in order to deal effectively with others.” This contrasts attention with distraction.

243
Q

What does Pashler say about defining attention?

A

Pashler (1998) argues that “no one knows what attention is, and… there may not even be an ‘it’ there to be known about,” emphasizing the challenge of defining attention as a single mechanism.

244
Q

How do researchers study attention?

A

Attention is studied in different components, such as spatial attention, selective attention, and inattention, rather than as a whole mechanism.

245
Q

What are the different states of arousal in attention?

A

Awake:
1. Inattentive: Drowsy, relaxed.
2. Attentive: Focusing on specific information (e.g., exam material).
3. Automatic: Unexpected events (e.g., fire alarm) capture attention reflexively.
Asleep: Attention persists in sleep (e.g., dreams), but is difficult to study due to lack of reportability.

246
Q

What is the flanker task?

A

A test that measures how peripheral distractions affect target judgments. Participants identify arrow directions while ignoring surrounding distractions.

247
Q

What is the Stroop task?

A

A test where people must name the color of a word, which is easier when congruent (word matches color) and harder when incongruent (word and color differ).

248
Q

What is the visual search task?

A

A task that measures how quickly a target is found among distractors. Simple targets (one feature) are easy to find, while conjunction targets (multiple features) are harder.

249
Q

What are the two types of attention in Posner’s model?

A

Voluntary (goal-driven): Slow to engage (300-500ms), long-lasting. Example: Studying.
Involuntary (stimulus-driven): Fast to engage, short-lived. Example: A phone ringing.

250
Q

what is the attentional network task (ANT)?

A
  • merging flanker + cuing
  • adding visual noise to the target
251
Q

what is a hierarchical processing task?

A
  • navon figures congruent and incongruent conditions
252
Q

What does Posner’s cuing task tap into?

A
  • when attentional cue (arrow) tells us that the target will be here 80% of the time, the other 20% of the time, the target is in the unattended location
  • faster response to the attended target
  • very little difference between cued and uncued when time is short, response time decreases as cue-target time increases, but response time is roughly the same for uncued even as cue-target time increases
  • when cue is in the periphery (instead of central) AND the cue is irrelevant to the target (50% correct), so any benefit to this location is automatic attention benefit
  • crossover interaction: in early cue-target time (0-300ms), there are response time benefits to the target location
  • in later cue-target times (300-1000ms), there is an inhibition response time effect
253
Q

What is inhibition of return?

A

In automatic attention, after an initial benefit of attending to a stimulus, attention shifts away over time, making it harder to return to the same location.

254
Q

What brain networks are involved in attention?

A

Dorsolateral frontoparietal (blue network; frontal eye fields, inferior parietal sulcus, visual areas): Voluntary attention, bilateral representation, controls attention orienting,
Ventrolateral frontoparietal (orange network; ventral frontal cortex, temporoparietal junction, middle frontal gyrus, FEF): Reflexive attention, responds to behaviourally relevant stimuli, lateralized to right hemisphere

255
Q

What is the role of the middle frontal gyrus (MFG) in attention?

A

The MFG acts as a “circuit breaker,” switching between voluntary and reflexive attention based on task demands.

256
Q

What is the relationship between mind-wandering and attention?

A
  • dorsolateral frontoparietal network (attention) and default mode network (inattention) operate in opposition
  • Mind-wandering (inattention) opposes attention, engaging the default mode network (DMN), which is active when attention lapses.
  • for short periods of time, you can do both (and this activated the overlapping areas)
257
Q

what processes is attention involved in?

A
  • sensory processing/perception: change blindness, visual searches
  • action/motor control: behaviours, movements
  • awareness (experience of life—if we don’t attend to them, we don’t experience them)
  • memory (how is material that we pay attention to remembered—better or worse? differently?)
  • social communication: informational cues given to people about other people, what are other people attending to, etc.
258
Q

What are the key properties of attention?

A
  1. Selective: Filters information, allowing focus on only a subset of inputs.
  2. Limited Capacity: Can only process a small amount of information at once.
    * dual tasks reduce performance due to the switch cost (because of both these properties)
259
Q

What are early and late selection theories of attention?

A
  • Early selection: Filtering occurs before semantic processing (e.g., ignored sounds in a dichotic listening task).
  • early filter at the perception stage—what isn’t attended to in the perceptual stage doesn’t move on to cognitive systems, no semantics, so no behaviour
  • Late selection: All stimuli are processed perceptually, but only meaningful information is consciously attended to.
  • late filter at the semantic analysis stage—all stimuli are processed perceptually until analyzed for their meanings, then only those that are semantically processed go on to be experienced and influence behaviour
260
Q

Which attentional filter theory is correct?

A
  • both
  • cocktail party effect: dichotic listening task playing different messages into different ears
  • people cannot report what is happening in the ignored stream (no comprehension) which supports the early filter theory
  • BUT personally relevant and survival relevant information (names, children crying) can break through the early filter to be processed semantically
261
Q

what are switch costs?

A
  • limited capacity property: limited set of items one can pay attention to at the same time (usually we can only do one thing at once)
  • we cannot perform dual tasks without costs (reading and copying words, driving and talking on the cell phone,)
  • there appears to be a single pool for available attentional resources (cannot be divided, we can switch but there are always switch costs (we can try to minimize these, but there are always costs))
262
Q

Sana et al., 2013 Computers and Education study

A
  • people are better at remembering information when we write rather than type (we need to reformulate information to write it down succinctly)
  • group 1 used a laptop as they normally would (researchers could track what people were doing on the laptop), group 2 could not use a laptop
  • group 1 (multi-tasking group) had 10% less memory for class content
  • E2: laptop users were placed in front of non-laptop users = the people who didn’t have the laptop were distracted by the people who were using the laptop in front of them (less retention for class content attributed to distraction by laptop use in front of them)
  • so attention cannot be held on two things at once
263
Q

What is hemispatial neglect?

A
  • A condition where patients ignore one side of space, usually due to right parietal damage (may be seen due to damage to either hemisphere). It affects multiple sensory modalities and is not due to visual deficits.
  • Tests include:
    Line cancellation: Patients fail to mark items on the neglected side.
    Line bisection: Patients bisect lines too far to the right.
    Object copying/drawing: Patients omit the left side of images.
  • brain damage associated with neglect correspond with brain areas involved in attention (frontoparietal network of attention)
264
Q

What is extinction in hemispatial neglect?

A

A phenomenon where patients can detect contralesional stimuli only when presented alone, but fail to notice them when an ipsilesional stimulus is also present.

265
Q

theoretical accounts of neglect

A
  • sensory deficit: patients do not respond to contralesional stimuli/sensations because they are functionally blind (this isn’t the case because patients can perceive stimuli)
  • motor deficit: patients have deficits in initiating motor actions towards the contralesional space (patients do tend to have a sluggish left side)
  • representational deficit (most correct): neglect is not externally mediated, but affects mental representations
  • Bizzi et al.: neglected space depended on a mental vantage point (so it has to do with the representation, not a sensory deficit)
266
Q

What is Balint’s syndrome?

A
  • A rare neurological condition caused by bilateral damage to the occipital and parietal lobes, leading to severe visuospatial deficits, impaired eye movement control, and difficulty perceiving multiple objects simultaneously.
  • patients’ experience of space disappears, can only see/engage with one object at a time, cannot locate the object that they report seeing, cannot report whether it’s moving toward or awar from them
    1. Simultanagnosia: Inability to perceive multiple objects at once.
    2. Optic apraxia: Difficulty shifting gaze to new objects.
    3. Optic ataxia: Problems coordinating visually guided movements.
  • these three symptoms may occur at the same time, but don’t have to
  • No formal imaging criteria, but bilateral parieto-occipital atrophy on CT/MRI and decreased cerebral perfusion on SPECT scans are suggestive.
267
Q

What is the complete form of Balint’s Syndrome?

A

The full syndrome occurs when there is involvement of:

Bilateral posterolateral occipital lobes (visual association area)
Parieto-occipital junction
Posterior aspects of both parietal lobes

268
Q

What is the most common cause (and other causes) of Balint’s Syndrome?

A
  • Bilateral watershed infarctions due to sudden hypotension, leading to damage in the parieto-occipital regions.
  • Traumatic brain injury (TBI)
  • Pre-eclampsia
  • Embolic stroke
  • Infections
  • Posterior cortical atrophy (PCA): A progressive dementia with predominant visual-spatial deficits that eventually leads to full dementia.
  • Atypical Alzheimer’s disease: Rare cases affect posterior brain regions, impacting visual processing.
269
Q

Ghoneim et al. case study

A
  • patient saw numbers and letters reversed, couldn’t perform tasks requiring complex visual orientation (e.g., pouring water from a kettle), unable to navigate spaces despite recognizing objects and knowing where to go, repeatedly fell due to poor visual-spatial awareness
  • Failed to copy a complex figure, Showed no organization in performing visual-motor tasks, Struggled with forming movements to visual stimuli, simultanagnosia
  • patient could not read (skipping letters/words)
  • Bilateral posterior parietal and occipital atrophy, more on the right side
  • Moderate to marked decreased perfusion in the same areas (right > left)
  • No perfusion abnormalities in temporal or frontal lobes, ruling out Alzheimer’s disease
  • The disease course was nonprogressive (no change 4yrs later)
  • NO APPARENT CAUSE
270
Q

How much does the brain grow from birth to teenage years?

A
  • The brain undergoes a fourfold increase in volume, leading to improvements in cognition and perception as different brain regions become specialized.
  • Development is the process of becoming biologically mature, involving changes in brain structures, pathways, emotions, behaviors, and cognition as a function of age.
271
Q

Why is brain development important to study?

A
  1. Understand the relationship between anatomical and functional changes.
  2. Examine how social interaction, cognition, and behavior develop.
  3. Identify atypical development in neurological disorders.
272
Q

What are some key anatomical changes around birth?

A

Most neurons have migrated to their respective locations.
Subcortical structures are largely intact.

273
Q

What is synaptogenesis?

A

The formation of new synapses (connections between neurons) in the brain. It increases synaptic density (the number of synapses per unit of brain tissue).

274
Q

How does synaptogenesis vary by brain region?

A

Occurs until around age 2 (varies by region).
Primary visual (V1) and auditory (A1) cortices peak around 1 year and decline.
Prefrontal cortex (PFC) peaks later (~3.5 years), with prolonged synaptogenesis.

275
Q

What happens after peak synaptic density?

A

Synaptic pruning eliminates excess synapses (~60% decrease), making the brain more efficient by refining connections.

276
Q

How does grey matter change between childhood and adulthood?

A

grey-matter maturation: Grey matter volume decreases as the brain becomes more efficient.
This loss starts in sensory/motor areas, then spreads to parietal, occipital, temporal, and prefrontal cortex (PFC) last.

277
Q

How does cognitive development progress in early childhood?

A
  • Rapid development in: Language acquisition, Object recognition, Motor actions
  • 3 models for how anatomical changes facilitate cognitive development
    1. maturational model
    2. skill learning model
    3. interactive specialization model
278
Q

What does the maturational model propose?

A

A brain region matures, enabling a new behavioral ability (like a light switch turning on). Development is sequential and stage-like.

279
Q

Johnson (1990) visual pursuit study and the maturational model

A

Newborns: Saccadic (jerky) eye pursuit, lagging behind objects.
2 months: Smooth pursuit but still lags.
3+ months: Anticipatory saccades (predictive eye movements).
* passive viewing task
* condition 1: predictable (slides alternate between left and right (if the baby has anticipatory saccades, they should be visible in this condition)
* condition 2: unpredictable (slides don’t follow a pattern), unable to make anticipatory saccades
* anticipatory saccades only in the predictable condition
* sticky gaze in 1 month old babies mimics adults with Balint syndrome (parietal damage), so 1 mo old babies have immature parietal cortices
* 2 month old babies no longer have sticky gaze issues because their parietal cortex has matured

280
Q

Assumptions of the maturational model

A
  1. Mature = adult-like function (otherwise immature).
  2. Development is one-off (once a region matures, it stays functional).
  3. Intrinsic, genetic, biological factors drive development.
281
Q

What does the skill-learning model propose?

A
  • Brain activation in infants is similar to adults learning a new skill. Activation shifts from frontal (learning phase) to posterior (expert phase).
  • infants with frontal damage show long-lasting deficits in visual orienting tasks, while infants with damage in other brain areas do not
  • this model assumes the involvement of experience (not just nature, also nurture)
282
Q

How does the skill-learning model explain eye movement planning?

A
  • ERP study time-locked to eye saccades
  • Adults: Eye movements planned in the posterior parietal cortex (pre-saccadic spike potential 8-20ms before the saccade)
  • the SP is posterior, in the parietal cortex, represents eye movement planning
  • 12-month-olds: Some posterior SP activation (learning phase).
  • 6-month-olds: No SP, but some FEF activation (early learning).
    *
283
Q

What does the interactive specialization model propose?

A
  • Brain regions start with broad, overlapping functions.
  • Over time, regions compete and specialize for specific tasks.
  • Specialization is driven by experience and environmental factors (reorganization can occur at different ages, not linear)
  • Emphasizes networks: collaboration between brain regions (work together to produce function)
284
Q

How does the interactive specialization model explain face processing?

A
  • task: passive viewing of natural and manufactured faces
  • Younger children: More activation in the left middle temporal cortex (among other regions) for faces.
  • Older children: Some areas increase specialization, others decrease (face specialization index for middle temporal decreases, so is becoming responsible for something else)
  • Adults: Fusiform face area (FFA) becomes highly specialized for face processing.
285
Q

What evidence supports the interactive specialization model?

A

Progressive changes: Some brain areas increase specialization.
Regressive changes: Other areas lose specialization.
Challenges the maturational model (development isn’t a one-time event; the maturational model doesn’t allow for regressive changes).
Emphasizes network collaboration—multiple regions interact to support behavior.

286
Q

What are the key differences between the three models of brain development?

A

Maturational: Regions mature → new abilities emerge, Sequential, stage-like development
Skill-Learning: Infants learn like adults acquiring skills, Frontal to posterior shift in activation
Interactive Specialization: Regions start broadly, then specialize, Progressive & regressive changes, network collaboration

287
Q

What are the two perspectives on how the adult functionally specialized brain develops?

A

Functional specialization arises through intrinsic genetic and molecular mechanisms, with experience only fine-tuning the system.

Functional brain development involves a prolonged specialization process shaped by postnatal experience.

288
Q

What are two contrasting views on infant cognitive development?

A

Infants are born with ‘innate modules’ and ‘core knowledge’ about the physical and social world.

Many behavioral changes during infancy result from general mechanisms of learning and plasticity.

289
Q

What does the developmental model predict regarding species with delayed development?

A
  • The more delayed the development, the larger the relative volume of later-developing structures, such as the cerebral and frontal cortex.
  • allows for extended postnatal interaction with the environment, shaping brain circuitry.
290
Q

How is developmental neuroanatomy studied?

A

postmortem analysis, developmental PET, and MRI (mostly on children with suspected clinical problems).

291
Q

What are key findings from PET scans of infants?

A
  • At under 5 weeks, glucose uptake is highest in the sensorimotor cortex, thalamus, brainstem, and cerebellar vermis.
  • By 3 months, activity rises in parietal, temporal, occipital cortices, basal ganglia, and cerebellar cortex.
  • The frontal cortex and dorsolateral occipital cortex mature around 6–8 months.
  • By the end of the first year, the brain shows adult-like resting activity.
  • Resting brain metabolism peaks at 4–5 years (150% of adult levels in some areas).
292
Q

How does myelination progress postnatally?

A
  • Most fibers myelinate postnatally, allowing structural MRI studies.
  • By 2 years, brain structures resemble adult forms; by 3 years, major fiber tracts are visible.
  • After rapid gray matter growth up to 4 years, a slight decline occurs due to pruning.
  • White matter increases through adolescence, especially in frontal regions.
293
Q

What methods are used to test infant cognition and perception?

A

Habituation: Infants get bored with repeated stimuli; looking longer at new stimuli suggests perception of novelty.

Preferential looking: Measures time spent looking at different stimuli.

Heart and sucking rate monitoring: Measures interest and recognition.

294
Q

What object-processing abilities do infants have?

A
  • During the first year, infants understand object solidity, object permanence, and gravity.
  • Until 9 months, infants struggle to reach for occluded objects or detect changes when objects move behind an occluder.
  • They may not be surprised if two distinct objects move as one.
  • By 4 months, they perceive the two ends of a moving rod as continuous behind an occluder and expect objects to be solid.
  • Infants possess innate principles of object perception, such as solidity and spatiotemporal continuity.
295
Q

Q: What are two extreme views on how infants develop social processing skills?

A
  1. Infants have prespecified modules for processing socially relevant information.
  2. Social brain development results from early social interactions shaping experience-sensitive circuits.
    * Middle ground: Infants are born with biases toward social stimuli, which shape learning and plasticity.
296
Q

What early social behaviors do infants display?

A

Preferential looking at face-like stimuli (possibly for bonding and neural specialization).

By 3 months, they follow gaze direction and respond to interactive objects.

By 12 months, they interpret adult actions in terms of goals or intentions.

297
Q

What evidence supports the maturational view from the reading?

A

Early behaviors rely on subcortical structures, later replaced by cortical control.

Parietal cortex maturation at 2–3 months allows disengagement from stimuli.

Frontal cortex maturation at 4–6 months enables inhibition of reflexive saccades.

298
Q

What are limitations of the maturational view?

A

It cannot fully explain dynamic changes in cortical activation or the role of postnatal experience.

Studies of pre-term vs. full-term infants suggest postnatal environment plays a critical role.

299
Q

What evidence supports the importance of early experience (sensitive periods)?

A

Infants with congenital cataracts show persistent deficits in face processing even after early treatment.

Rapid visual acuity improvements post-surgery suggest a ‘triggered’ neural development process.

this supports the skill-learning model: need input to trigger the development of these circuits

300
Q

What is spina bifida?

A

A congenital condition where the spinal column fails to fuse completely, leaving nerve tissue exposed.
The majority of individuals with spina bifida also suffer from hydrocephalus.

301
Q

What is hydrocephalus?

A

A disturbance in the circulation of cerebrospinal fluid (CSF) through the brain’s ventricles.
Causes back pressure that can enlarge the ventricles, compressing the brain against the cranium.
In young children with malleable skulls, this can lead to a grossly enlarged head.
Prolonged pressure results in brain matter loss.

302
Q

What are the four categories of ventricular expansion in hydrocephalus according to Lorber?

A
  1. Minimally enlarged ventricles.
  2. Ventricles filling 50-70% of the cranium.
  3. Ventricles filling 70-90% of the cranium.
  4. Severe cases: Ventricles fill 95% of the cranium. This group makes up less than 10% of the total sample. Many are severely disabled, yet half have IQs greater than 100.
303
Q

What does Lorber suggest about brain function and the cortex?

A

Neurologists have long assumed the cortex is responsible for all higher functions.
Lorber suggests deep brain structures may perform many functions typically attributed to the cortex.
He compares the cortex to a “reference library” that is consulted as needed.

304
Q

How do rat brain lesions inform our understanding of hydrocephalus?

A

Large surgical brain lesions cause severe dysfunction.
However, gradual damage over time leads to minimal dysfunction.
This suggests the human brain can adapt to a slow reduction in available neural structures, as seen in hydrocephalus.

305
Q

What are the effects of asymmetrical hydrocephalus?

A

In cases where only one side of the brain is affected, a minority of patients show contralateral paralysis or spasticity.

306
Q

How does hydrocephalus primarily affect brain tissue?

A
  • Principally a disease of white matter.
  • Enlarging ventricles stretch and disrupt white matter fibers.
  • Axons and their myelin sheaths break down.
  • Gray matter is remarkably spared, though prolonged hydrocephalus eventually causes some gray matter loss.
  • This sparing may explain why some hydrocephalus patients retain function.
307
Q

How does the brain recover following the implantation of a shunt?

A

Releasing fluid pressure allows the brain to rebound.
Stretched fibers shorten, reducing ventricular space.
Scar tissue forms from glial cells.
Challenges the neurobiological idea that central nervous system cells cannot repair themselves.

308
Q

Does the brain function in a disjointed left vs. right manner as pop psychology suggests?

A
  • No, the idea originates from misinterpretations of split-brain studies, leading to pseudoscience.
  • No scientific evidence supports the idea that humans rely on only one hemisphere for processing.
  • Both hemispheres work together as a unified system, not as isolated modules.
  • While they process information with subtle differences in processing styles, they do not function as “spares” for each other.
  • The split-brain patient data only applies to individuals with severed corpus callosum (CC), not typical brains.
309
Q

Why is the left-right brain myth problematic in applied settings like education?

A
  • It has led to misguided educational approaches, such as tailoring instruction based on “hemisphere dominance.”
  • This influences how people perceive themselves, despite no correlation with actual performance.
  • Featured in This Idea Must Die: Scientific Ideas That Are Blocking Progress.
  • Misinterprets Gazzaniga’s split-brain studies, falsely suggesting that all people have a “dominant hemisphere.”
  • In reality, for those with an intact CC, both hemispheres work together at all times
310
Q

Where does most of our knowledge about hemispheric specialization come from?

A
  • Primarily from a single patient, J.W., studied by Michael Gazzaniga.
  • Split-brain research has its roots in Roger Sperry’s work on animals.
  • Early findings showed that when the CC was severed, the two hemispheres had no knowledge of each other’s learning.
  • Later applied to humans, confirming independent processing in disconnected hemispheres.
311
Q

How do the left and right hemispheres communicate?

A
  • Via the corpus callosum (CC), the largest white matter fiber bundle (200 million axons).
  • Most connections are homotopic (linking corresponding regions across hemispheres). Posterior: Connects visual areas, Midline: Connects motor areas, Anterior: Connects frontal areas.
  • Heterotopic connections link non-corresponding areas across hemispheres.
  • Ipsilateral connections stay within the same hemisphere.
312
Q

How are some brain functions lateralized?

A
  • Each hemisphere processes sensory and motor information from the opposite side (contralateral representation).
  • SUBCORTICAL structures are NOT LATERALIZED
  • Some functions, like language, are highly lateralized:
  • Left hemisphere (LH): Language processing.
  • Right hemisphere (RH): Higher lateralization for face processing.
  • Both hemispheres contain similar architecture for V1 (visual cortex), indicating shared processing capacities.
313
Q

How is language represented in the brain?

A
  • Uses Broca’s and Wernicke’s areas for speech production and comprehension.
  • Usually lateralized to the left hemisphere, but individual variability exists.
  • Some individuals have bilateral representation of language.
  • Grammatical functions are more left-lateralized, while contextual and other processing involves the right hemisphere.
  • both hemispheres show the word superiority effect (recognize words faster when they’re in words vs. non-words)
  • RH cannot understand verbs, pluralizations, possessive or active-passive verb differences
  • but some patients’ RH can correctly judge sentences as ‘grammatical’ vs. ‘non-grammatical’
314
Q

Why have lateralized specialization?

A
  1. speech is lateralized to enable speed of processing as transcortical projections and transfer take time
  2. advantages in having nonidentical forms of representation between the hemispheres, with each having certain advantages for tasks and both hemisphere containing essential machinery for computation
  3. efficiency in processing due to limited cortical real-estate?
315
Q

Are there structural differences between LH and RH that explain their functional specializations?

A
  • we haven’t found any large differences anatomically to indicate specialization (areas specialized for different functions look anatomically similar)
  • Sylvian fissure (planum temporale): Larger in 65% of right-handers according to postmortem analysis (not neuroimaging), but 95%+ of people have language in LH, showing it is not a strong predictor.
  • Micro-anatomy differences:
    1. Cortical column spacing in LH’s Wernicke’s area is wider, allowing more connections.
    2. Larger pyramidal cells in LH, suggesting structural specialization for language.
316
Q

What happens when the corpus callosum is severed?

A
  • Split-brain syndrome: Hemispheres function semi-independently.
  • Language-dominant hemisphere (usually LH) speaks.
  • Sensory, motor, and visual functions remain within their respective hemispheres.
  • Used as a treatment for severe epilepsy when no other options remain.
  • quite successful, as seizures become localized to one hemisphere and then often fully subside within weeks of the operation
317
Q

Roger Sperry’s CC studies

A
  • original work on perceptual learning in cats with severed CC
  • found that each hemisphere had no idea what the other learned when CC was severed
  • later developed tests of hemispheric function on humans with Michael Gazzaniga (his graduate student)
318
Q

methodological issues with split-brain patients

A

only a few suitable for experimental investigations due to:
* most patients aren’t neurologically intact prior and after operation (long history of seizures)
* most show abnormal performance on standard neurological tests, tests of language, and intellectual function
* only a few patients have an ability to comprehend and/or train RH for simple language commands, so testing usually confined to visual stimuli due to good experimental control afforded by lateralized hemispheric projections in the visual areas

319
Q

How do split-brain patients behave differently in lab studies?

A
  • LVF (Right Hemisphere) → Left Hand Response (Nonverbal).
  • RVF (Left Hemisphere) → Right Hand Response + Speech.
  • When shown a word in LVF, patients cannot verbally report it but can draw it with the left hand.
  • JW (split-brain patient) confabulates explanations when his left hand (RH) performs an action.
  • present a word to LVF + complete CC split = info goes to RH = person cannot verbally report what they saw “I didn’t see anything”
  • present a word to LVF + partial CC split = info to RH = incomplete report of what they say, like images
  • very important to control for eye movements to keep images stabilized on the retina so that info doesn’t get presented to both hemispheres
320
Q

most famous split-brain patients/studies

A
  • JW had a full CC resection, but couldn’t be scanned using fMRI due to anxiety and seizures
  • VP has a partial resection, but still does not integrate visual information, which is transmitted by the posterior part of the CC
  • JW unable to verbally report info in LVF, but able to draw it with left hand, and confabulates when left hand points to an image that the left hemisphere didn’t see
  • letter priming task: identify “H” primed with either “t” (incompatible) or “h” compatible
  • JW did a lateralized version of this task: showed priming in RVF (LH) but not LVF (RH), ie. faster for compatible only in LVF
  • JW also impaired in judging word meaning categories (furniture being superordinate to chair) and in judging antonyms (love-hate)
321
Q

How is visual processing lateralized?

A
  • RH is specialized for processing of faces (but VJ had face processing in LH)
  • LH is better at recognizing the self
  • face morph spectrum between JW and Gazzaniga —is it me or is it Gazzaniga?
  • self-recognition bias in LH (starts recognizing self at 40-50% morph)
  • familiar other recognition bias in RH (only starts recognizing self at 70% morph)
322
Q

Is attention lateralized?

A
  • Attention is not strongly lateralized; JW could pay attention using both hemispheres.
  • but only with RH when cued by faces
  • RH follows gaze direction, LH does not.
  • When cueing is social (faces), RH dominates.
  • When cueing is non-social (arrows), both hemispheres perform equally.
323
Q

What is the Left Hemisphere Interpreter Hypothesis?

A
  • speaking LH constructs a narrative of the information it perceives and ‘interprets’ our reality and provides a narrative of experiences (we contextualize things, interpret circumstances and feelings)
  • Gazzaniga suggests that the LH interpreter is a basis for our conscious experiences
  • JW draws a telephone with the left hand = LH doesn’t know why, so it makes up a story
324
Q

How do we test the LH interpreter hypothesis in split-brain patients?

A
  • decision making experiments: arrow indicated visual field of target, either LVF or RVF (80% upper, 20% lower), participants asked to guess where the target will be presented (upper or lower)
  • frequency matching: try to guess on each trial correctly where the square will appear (we don’t do this well, we usually get it at chance levels (50%))
  • maximizing: choosing upper 100% of the time (this would allow us to get 80% correct)
  • for JW: RH eventually learns to maximize (goes above the line), LH doesn’t learn to maximize, keeps frequency matching
  • for VP: RH maximizing from the start, LH frequency matching the whole time = not the best possible outcomes
  • so interpreting as narratives doesn’t always lead to best outcomes
  • RH maximizes, LH frequency matches, even though this is not the optimal response (LH looking for patterns and causal interpretations)
325
Q

What was observed in a case of callosal agenesis in the laboratory?

A
  • Callosal agenesis is a birth defect where the corpus callosum is completely or partially absent.
  • Despite this structural anomaly, the individual exhibited no obvious cognitive or behavioral deficits.
  • Raises questions about neural plasticity and alternative interhemispheric communication pathways.
326
Q

How did W.J.’s right hemisphere respond to visual stimuli after callosotomy?

A
  • A picture flashed to the left of fixation was transmitted exclusively to the right hemisphere.
  • Since the right hemisphere lacks language production, W.J. was unable to verbally report what he saw.
  • The severed corpus callosum prevented communication between hemispheres.
  • Demonstrated the independence of each hemisphere when disconnected.
327
Q

How do split-brain patients respond to visual stimuli in different visual fields?

A
  1. When a circle appears in the right visual field:
    The right hand (controlled by the left hemisphere) points to it.
    The left hemisphere can verbally describe it.
  2. When a circle appears in the left visual field:
    The left hand (controlled by the right hemisphere) points to it.
    The right hemisphere perceives it but cannot verbally report it.
328
Q

What additional insights did further split-brain studies provide?

A
  • Confirmed the original findings across multiple patients.
  • Showed that not just the visual system, but also the somatosensory and motor systems, were functionally split.
  • More strikingly, cognitive and perceptual systems were also divided between hemispheres.
  • Despite these divisions, patients maintained a subjective sense of psychological unity.
  • Highlighted the brain’s parallel and distributed organization.
329
Q

The operation of callosotomy might create a person with the ultimate split personality, but early studies suggested no observable split in consciousness or personality. Why?

A

Consciousness may be housed entirely in one hemisphere.

Consciousness could be tied to language, which is lateralized.

The hemispheres may divide labor so that consciousness shifts depending on task demands.

330
Q

What does the split-brain surgery involve?

A

Severing all or part of the corpus callosum, the major fiber tract connecting the cerebral hemispheres.

Sometimes includes severing additional forebrain commissures.

The corpus callosum contains ~200 million axons from layer 2/3 pyramidal neurons.

331
Q

Why are split-brain patients ideal for studying hemispheric independence, yet not always suitable for behavioral studies?

A

Theoretically ideal due to full separation of hemispheres.

Practically limited because: Many have only partial callosotomies + Most have long histories of severe epilepsy and cognitive impairments

332
Q

What did early split-brain studies confirm about hemispheric specialization?

A

Language is usually lateralized to the left hemisphere.

Right hemisphere excels in spatial processing.

Right hemisphere processing is more literal, while left hemisphere is more constructive.

333
Q

Are all perceptual processes superior in the right hemisphere?

A
  • No, asymmetries depend on stimuli and task type.
  • Example: Two patients discriminated objects equally well, but the right hemisphere was better at spatial location discrimination.
  • Right hemisphere excels in: Line orientation and vernier acuity + Amodal completion (visual grouping), while modal completion is equal in both hemispheres.
  • Left hemisphere was indifferent to color cues in line motion perception; right hemisphere showed strong effects.
334
Q

what is the ‘right hemisphere interpreter’ (Wolford)?

A
  • lateralization of visual grouping to the right hem
  • in JW: left hemisphere indifferent to the manipulation of the magnitude of the gap in temporality that would affect whether we interpret events as being causally related, but the RH was correctly affected by this temporal gap
335
Q

What are the differences in spatial cognition between the hemispheres?

A

Right hemisphere is superior in mental rotation.

Left hemisphere excels at perspective-taking (imagining oneself in a different spatial perspective).

Neuroimaging confirms parietal and frontal activations in both hemispheres but with different emphases.

336
Q

How does hemispheric specialization affect attention?

A

Right hemisphere (but not left) showed faster response to targets aligned with eye gaze direction.

Effect disappeared with inverted faces, suggesting lateralized cortical processing.

Gaze cueing is tied to the hemisphere specialized for face processing (typically right hemisphere).

So, for higher-order processes like attention, specialization appears driven by stimulus properties

337
Q

How does hemispheric specialization affect memory encoding and retrieval?

A

Encoding is more lateralized than retrieval

Left prefrontal cortex dominant in episodic encoding, particularly for verbal material.

Right prefrontal cortex more involved in encoding nonverbal stimuli (faces, textures).

Split-brain patients show little episodic memory impairment, implying material-specific rather than process-specific encoding/retrieval (ie. encoding processes available in both hemispheres)

338
Q

How does self-referential processing differ between hemispheres?

A

Self-relevant processing enhances memory beyond semantic processing.

Medial prefrontal cortex is more active during self-referential judgments.

Split-brain study found: Right hemisphere more likely to recognize others in face morphs + Left hemisphere biased toward recognizing self.

339
Q

How might the left hemisphere interpreter be linked to the perception of self?

A
  • Consciousness, the self, and the LH interpreter intimately connected.
  • Two-stage signal detection model
  • Left hemisphere has a general bias toward saying “yes” to recognition tasks.
  • Split-brain patients show deference to the specialized hemisphere for certain tasks, so that responses from the unfavoured hemisphere seem random
  • example: patient may believe that face recognition is the responsibility of the right hemisphere and may not try very hard on faces presented to the left.
  • [When the probability guessing paradigm was to guess whether a face would have facial hair or not] the patient frequency matched with the right hemisphere and responded randomly with the left hemisphere. Our interpretation was as above. Faces were seen as the purview of the right hemisphere, so only that hemisphere took the task seriously.
  • but for most other stimuli that are seen as being the purview of LH, the RH doesn’t try = inconsistent and random responses
340
Q

What is the two-stage signal detection model?

A
  • Subjects first decide to respond (should I bother trying), and once they have decided to respond, the traditional signal detection model would apply.
  • unwillingness to respond could present as not trying when you need to respond (50/50 responses or perseveration on a response, for instance)
341
Q

How does hemispheric specialization relate to consciousness and awareness of deficits?

A

Modular specialization extends to awareness of one’s own deficits.

When a hemisphere assumes responsibility for a task, it also assumes awareness of that task.

Some responses from the “unfavored” hemisphere may reflect an unwillingness to try rather than true incompetence.

Consciousness may be modular and tied to the regions performing specific cognitive tasks.

342
Q

What is the connection between temporal lobe epilepsy and religious experiences (Rama)

A

Temporal lobe epilepsy patients often report intense spiritual experiences.
The left temporal lobe is particularly implicated.
Even when not having seizures, these individuals may show an increased focus on religious and moral concerns.

343
Q

Why are religious hallucinations commonly associated with temporal lobe activity?

A

Religious and moral concepts may be deeply embedded in the neural architecture of the temporal lobes.
This suggests that mystical experiences have a specific neurological basis rather than being purely cultural or psychological.

344
Q

Explain Rama’s perspective on our experience of emotions.

A
  • mediated by back-and-forth connections with the frontal lobes
  • outward expression of emotions depends on the hypothalamus, which has 3 main outputs
    1. hypothalamic nuclei send hormonal and neural signals to the pituitary gland, which is often described as the “conductor” of the endocrine system (those hormones affect the entire body)
    2. hypothalamus sends commands to the autonomic nervous system, which controls various vegetative or bodily functions, including the production of tears, saliva and sweat and the control of blood pressure, heart rate, body temperature, respiration, bladder function, defecation and so on
    3. 4 Fs (the actual behaviour)
345
Q

Temporal lobe personality (Rama)

A
  • repeated electrical bursts inside the patient’s brain (the frequent passage of massive volleys of nerve impulses within the limbic system) permanently “facilitate” certain pathways or may even open new channels
  • heightened emotions and see cosmic significance in trivial events, humorless, full of self-importance, and maintain elaborate diaries that record quotidian events in elaborate detail (hypergraphia), loss of libido and a preoccupation with sexual rituals
346
Q

Evolutionary psychology perspective on religion (Rama)

A
  • many human traits and propensities, even ones we might ordinarily be tempted to attribute to “culture,” may have been specifically chosen by the guiding hand of natural selection because of their adaptive value (but not genetically predetermined)
  • human tendency to seek authority figures—giving rise to an organized priesthood, the participation in rituals, chanting and dancing, sacrificial rites and adherence to a moral code—encourages conformist behavior and contributes to the stability of one’s own social group
  • those conformist traits multiply with evolution, while people without them are ostracized and
347
Q

Rama’s GSR testing of ‘heightened connections’ hypothesis

A
  • heightened response mainly to religious images and words, and blunted response to other, normally arousing stimuli
  • eliminates the ‘heightened connections’ hypothesis
348
Q

3 components of Darwinism (Rama)

A
  1. constant struggle for existence
  2. random variations in body type that arise from the random shuffling of genes that takes place during cell division
  3. fortuitous combinations of genes that cause individuals to be slightly better adapted to a given local environment tend to multiply and propagate within a population since they increase the survival and reproduction of those individuals
349
Q

Savant syndrome (Rama)

A
  • General intelligence evolved, the argument goes, so that one can do the myriad things that humans enjoy and that help them survive. But once this intelligence was in place, you could use it for all sorts of other things, like calculus, music, etc.
  • savant: mental capacity or general intelligence is abysmally low, yet who have islands of astonishing talent
  • refutation of the argument that specialized talents are merely clever deployments of general intelligence
  • one part of the brain may for some obscure reason receive a greater than average input or some other equivalent impetus to become denser and larger—a huge angular gyrus = better math ability
350
Q

hemineglect brain circuits according to Rama

A
  • reticular activating system activates the entire cerebral cortex, leading to arousal and wakefulness, or a small portion of the cortex, leading to selective attention
  • limbic system for emotional behaviour and emotional salience and values of the external world
  • frontal lobes for abstract processes: judgment, foresight, planning
  • three areas connected in a positive feedback loop that takes a stimulus from the outside world, extracts its salient features and then bounces it from region to region, before eventually figuring out what it is and how to respond to it.
  • when that loop is interrupted = hemineglect
  • RH has a broad searchlight for both halves of visual field, while LH is confined to RVF (so if LH fails, the RH can take over, but if RH fails, LH cannot)
351
Q

mirror agnosia or looking glass syndrome (Rama)

A
  • hemineglect patient (Ellen) tried to reach for an object that was being reflected from the left side as though it was inside the mirror, even checking behind it as though it was hiding
  • because of her neglect: “Since the reflection is in the mirror, the object must be on my left. But the left does not exist on my planet—therefore, the object must be inside the mirror.”
  • not a consequence, but accompanies neglect: right parietal lobe is damaged, patients have all kinds of difficulties with spatial tasks (and mirrors take a lot of spatial processing to understand)
352
Q

anosognosia

A
  • the tendency to ignore or sometimes even to deny the fact that one’s left arm or leg is paralyzed, despite being mentally lucid in all other respects
  • vision is fine, yet the patient insists that their paralyzed body parts are working perfectly, confabulate (almost hallucinate) that they are working as expected, and rationalize reasons that they are not producing the movement required
  • somatoparaphrenia—the denial of ownership of one’s own body parts
353
Q

Rama explanations for anosognosia

A
  • Freudian: patient simply doesn’t want to confront the unpleasantness of his or her paralysis (problem: difference in magnitude of psychological defense mechanisms between patients with anosognosia and what is seen in normal people, problem: asymmetry of this syndrome because denial associated with RH damage, not LH)
  • consequence of neglect (problem: neglect and denial can occur independently, problem: why denial usually persists even when the patient’s attention is drawn to the paralysis)
  • division of labor between our two cerebral hemispheres and in our need to create a sense of coherence and continuity in our lives
354
Q

Anosognosia Rama favoured explanation

A
  • LH sifts through information to build a coherent and consistent belief system
  • when confronted with information that threatens this worldview, LH either ignores it or tries to squeeze it into your existing framework (this is the basis of Freudian defense mechanisms)
  • RH is the “Devil’s advocate” (explains why defense mechanisms are so exaggerated in stroke/denial patients) because at a certain threshold of unbelievability, it forces LH to revise its belief system
  • What is damaged in these patients is the manner in which the brain deals with a discrepancy in sensory inputs concerning the body image; it’s not critical whether the discrepancy arises from the left or right side of the body
  • able to locate the center in the brain that monitors discrepancies; it is a small region of the right hemisphere that receives information from the right parietal lobe
  • denial type/severity depends on the brain region that is damaged
355
Q

Freudian defense mechanisms (Rama)

A
  • denial, rationalization (and confabulation), humor
  • repression: patient will sometimes admit with repeated questioning that she is in fact paralyzed, only to revert soon afterward to denial—apparently “repressing” the memory of the confession she made just a few minutes earlier
  • reaction formation: a subconscious attempt to disguise something that is threatening to your self-esteem by asserting the opposite (“I tried with both my hands”)
  • projection: to avoid confronting a malady or disability, we conveniently attribute it to someone else
356
Q

cold water in vestibular system experiment (Rama)

A
  • cold water acted as a “truth serum” that brought her repressed memories about her paralysis to the surface
  • admitted she was paralyzed
  • after it wears off, patient denies their earlier admission of paralysis
    1. connections from the vestibular nerve projecting to the vestibular cortex in the right parietal lobe as well as to other parts of the right hemisphere. Activation of these circuits in the right hemisphere makes the patient pay attention to the left side and notice that her left arm is lying lifeless
    2. During these dreams we are often confronted with unpleasant, disturbing facts about ourselves. Thus in both the cold − water state and REM sleep there are noticeable eye movements and unpleasant, forbidden memories come to the surface. Stimulation of vestibular system activates same REM sleep circuit (patients should dream that they are paralyzed)
357
Q

can you “cure” his denial by simply tampering with the structure of his beliefs? (Rama)

A
  • experimental epistemology
  • [fake injection to ‘paralyze’ the left arm] Apparently my mock injection had worked, for she was now able to accept the fact that her left arm was indeed paralyzed. [this experiment doesn’t work on the non-paralyzed right arm]
358
Q

anosognosia and anorexia

A
  • Is the disorder of appetite (linked to feeding and satiety centers in the hypothalamus) primary, or does the body image distortion cause the appetite problem?
  • certain parts of the limbic system such as the insular cortex are connected to the hypothalamic “appetite” centers and also to parts of the parietal lobes concerned with body image
  • intellectual beliefs about whether you are too fat or thin, your perception of your body image and your appetite are all more closely linked in your brain than you realize—so that a distortion of one of these systems can lead to a pervasive disturbance in the others as well
359
Q

experimental tractability

A
  • wanting to study something objectively from a third-person POV
  • when something is experimentally tractable, it affords itself to objectivity (studying memory for faces vs. words = use recall to study this objectively)
  • when something is not experimentally tractable, we reduce it to something we can study or find domain-adjacent realms
360
Q

is consciousness experimentally tractable?

A
  • it is inherently subjective and cannot be known by another person (first-person)
  • to study it scientifically, we reduce it to something else (certain aspects of consciousness are more amenable to scientific study) or find consciousness-adjacents concepts to be studied
361
Q

definition of consciousness

A
  • vast and multifaceted area of investigation (cognitive scientists, physicists, neuroscientists, philosophers, etc.)
  • little theoretical unity in understanding within and across fields (physicists study it differently than neuroscientists) which contributes to multifaceted and complex nature of the phenomenon
  • unity of the concept remains at an intuitive level
  • despite tractability problems, understanding human consciousness remains one of the end goals of science (biological bases of consciousness)
362
Q

two approaches to studying consciousness (in terms of cognition)

A
  • unity of consciousness: refers to a unity of experience that most humans experience on a daily basis (low experimental tractability, this approach is theoretical)
  • divide & conquer: study aspects/functions of conscious behaviours—consciousness is seen as an umbrella term that includes executive functions, metacognitive processes, awareness and self-awareness, and unconscious processes (higher experimental tractability, mostly used by cognitive scientists)
363
Q

problem with divide & conquer approach to consciousness

A
  • once you’ve broken consciousness into parts, have you lost the unity of the concept?
364
Q

Block (1995) division of consciousness

A
  1. Access: cognitive aspects of consciousness and its representational content
  2. Phenomenal: qualitative experience of consciousness (that may not be reducible to aspects, it’s more of a feeling)
365
Q

Access consciousness

A
  • conscious information is available for report, reasoning, and behaviour (we can name something, reason about it, act on something)
    1. implicit: affects our behaviour without us necessarily knowing about it or being able to talk about it
    2. explicit: verbalization, declarative, being able to talk about it
366
Q

Phenomenal consciousness

A
  • raw experience of sensations, forms, feelings
  • this is subjective—we can’t understand how other people experience rain, sound, colour
  • people experience the world differently; people who are colour-blind don’t experience the world in terms of colour and may not know their experience is different
  • consciousness is irreducible to mechanistic, physiological, physical explanations
367
Q

implicit access consciousness

A
  • no verbal or declarative output
  • example: priming, split-brain (RH/LH cannot report on the other hemisphere’s knowledge), blindsight
368
Q

explicit access consciousness

A
  • verbal or declarative output is available
  • examples: conscious identification of stimuli, ability to report mental content
369
Q

priming levels

A
  • perceptual priming: presentation of a perceptually degraded image facilitates recognition later on (based on sensory form)
  • semantic priming: priming meaning (doctor-nurse, bread-butter, table-chair)
  • conceptual priming: prime with context, bias, stereotype
370
Q

perceptual priming example

A
  • word-stem completion task (more likely to complete a word with an unusual ending if you are primed with it rather than an everyday word)
371
Q

conceptual priming example

A
  • voter behaviour (Berger et al., 2008): assigned polling locations (church, school, etc.) influence how people vote
  • school = supporting school-funding initiative
  • even when controlling for voters’ political views, demographics, unobservable characteristics of individuals living near schools
  • priming occurring outside conscious awareness affecting behaviour
372
Q

qualia

A
  • phenomenal consciousness: feeling of experience
  • experience, experiential properties
  • p-conscious states when we see, hear, smell, taste, have pains
  • totality of experiential properties of a state are “what it is like” to have it
  • fully depends on subjective reports, may be irreducible to brain functions
373
Q

linking access and phenomenal consciousness

A
  • the problem of integrating first-person & third-person data (Chalmers article)
  • easy and hard problems of consciousness
  • will an accumulation of first-person data lead to emergence of an understanding of consciousness? sum of parts = whole?
374
Q

measures of consciousness

A

consciousness remains mostly assessed using subjective verbal reports (first-person data)

375
Q

examples of first-person data

A
  1. necker cube bistable image—participants tell us when they experience the image ‘flips’
    * fundamental different experiences of reality, measure how many spontaneous flips each person experiences
    * perhaps supplement this first-person report with objective measures like MRI data, participants’ response time, or accuracy (which may converge or diverge)
  2. mental imagery
376
Q

problems with subjective reports

A
  • cannot assess consciousness in non-verbal populations (infants, animals)
  • subjective reports are subjective—even if we’re measuring it in an objective way, it’s still subjective and may or may not be true
  • subjective reports may influence objective measurements
377
Q

third-person data

A
  • experimental tasks often used to assess consciousness
  • continuous flash suppression, binocular rivalry
  • these two methods afford experimental manipulation and control of conscious awareness by capitalizing on well-known properties of the visual processing system
  • rendering things visible or invisible—see how long it takes for things to become visible or invisible to participants
  • measure access consciousness mostly
378
Q

continuous flash suppression

A
  • exploits retinotopic mapping in the visual cortex to experimentally render stimulus consciously reportable
  • flash a competing stimulus on the exact same retinotopic location but on the other side of the brain = the person will report the flashing stimulus and stop reporting the stimulus that they initially saw (flashing stimulus replacing conscious perception of the static stimulus in the other visual field)
  • but both stimuli are represented in the brain/visual areas
  • how long does something have to flash? what happens with the other stimulus? what parameters does the flashing have to use for the effect to occur?
379
Q

binocular rivalry

A
  • percepts alternate between two different images presented to each eye simultaneously
  • images gets fused or unfused based on how they are presented to the eyes, then eventually the images alternate in our conscious perception (even though the stimuli stay the same)
380
Q

attention and consciousness

A
  • links between attention and consciousness are intuitive (explicit attention and access consciousness)
  • attending to a stimulus most often leads to a conscious perception of that stimulus (but not always)–change blindness
  • are the two processes dissociable? if not, which process is superordinate—attention or consciousness?
  • to dissociate: one would need to demonstrate attention without consciousness AND consciousness without attention
381
Q

Does attention exist without consciousness?

A
  • yes—habitual tasks without paying effortful attention to them, attention gets pulled without conscious effort (bottom-up)
  • example: blindsight patients (Kentridge et al., 1999)
382
Q

Kentridge et al., 1999

A
  • right field hemianopia confirmed with MRI and computerized perimetry, resulting from a car accident
  • attention was cued to targets presented in a blind field using a cuing task (auditory tone + central cue 70% informative (directing towards blind hemifield))
  • target occurs when the cue informed, or uncued target, or no target
  • required response: (1) press a key if a target accompanied a tone (2) report any experience relating to the tone
  • patient had a reaction time advantage for the cued target (that they’re unable to consciously report)
  • valid discrimination around 70-80% (able to discriminate whether tone accompanied target)
  • no reduction in discrimination accuracy of target presence
  • so dissociation of attention without consciousness—attending to something they’re not consciously aware of
  • attention can exist without awareness, and potentially may facilitate awareness
383
Q

is there consciousness without attention?

A
  • unclear
  • pop out visual search: a salient target does not require attention, but it is consciously reportable (may provide evidence of consciousness without attention), but not strong evidence that perception of a salient target requires no attention whatsoever (in other paradigms, salient targets don’t pop out as readily (faces, other complex stimuli))
  • whole report vs. partial report (Sperling, 1960): content in consciousness is reportable (more reportable when directed by attention)
  • in whole-report, people can report a lot of the letters in the array but not 100% of them
  • in partial report, when people are cued to a particular line, they are nearly 100% accurate in reporting the letters (attention mediates consciousness toward reportable content)
384
Q

model 1: attention gates consciousness/awareness

A
  • inputs = sensory analysis, some parts are attended = awareness = conscious report
  • this is the partial report condition
  • the other parts are unattended
385
Q

model 2: consciousness gates attention

A
  • inputs = sensory analysis, some parts are conscious = attended or unattended = only attended is consciously reported
  • some parts are unconscious
  • this is the whole report condition
386
Q

disorders of consciousness

A
  • altered states of consciousness resulting from brain injury
  • umbrella term for several different states of consciousness
  • this definition does not include altered states of consciousness due to medication, drugs, etc.
  • has stratified into 7 states of consciousness and how responses change through these states
  • assessment and diagnosis is ambiguous and difficult
  • recent advances in neuroimaging are being used to examine altered states of consciousness without a need for overt response
  • understanding altered consciousness is problematic since we still don’t know what consciousness is—many investigations equate consciousness with awareness
387
Q

vegetative state

A
  • a diagnosis is made only when repeated examinations have yielded no evidence of sustained, reproducible, purposeful response to sensory stimulation (visual, auditory, tactile). There must also be no evidence of language comprehension of expression
  • unlike patients in come, patients in vegetative states display cycles of eye closure and eye opening, appearing as if they show a wake/sleep pattern
  • show a wide range of reflexive behaviours which could also be misinterpreted as volitional actions
388
Q

minimally conscious state

A
  • new diagnostic category
  • like vegetative patients, cycles of eye opening and closing are seen, but unlike vegetative patients, at least one of the following bx must be observed and reproducible:
    1. simple command following (move your hand)
    2. verbal or gestural yes/no responses
    3. intelligible speech
    4. non-reflexive purposeful movements
389
Q

coma

A

a complete lack of arousal, no responses or cycles of sleep/wakefulness, stimulation does not lead to arousal, it is assumed that these patients have no awareness of their surrounding or themselves (this is the most severe in the taxonomy)

390
Q

neuroimaging approaches to consciousness

A
  • hierarchical approach: suggestion to study consciousness disorders by understanding brain processing for simple functions first followed by more higher order processing
  • two patients in vegetative state were presented with spoken words:
  • normal controls have temporal lobe activation, patients have reduced activation, but in similar brain areas as control
  • little evidence for differential patterns of processing in disordered consciousness
391
Q

differential brain activation in disorders of consciousness

A
  • in general, little evidence for differences in brain activity in typical and disordered consciousness
  • similar activity in the same brain areas
  • imagining playing tennis = motor cortex activity in both control and vegetative patient
  • no overt language of language comprehension in these patients, but we get the same brain activation as in a control, so this is a backward inference
  • it would be impossible to tell just from the MRI scans that the vegetative patient doesn’t have consciousness
  • so what is the significance/utility of the brain imaging approach to studying disorders of consciousness? the patient cannot confirm that they are thinking about playing tennis
  • how useful is knowledge of brain activity without the behavioural output?
  • interpretive issues regarding neuroimaging methods
392
Q

Rama: Is the notion of a unified self inhabiting the brain an illusion?

A

The concept of a single, unified “self” may be an illusion.

Brain functions are distributed; many unconscious systems (“zombies”) perform complex tasks without awareness.

These systems coexist in harmony, creating the illusion of a central “you.”

What you call reality is assembled from fragmentary information.

You are unaware of most brain activity driving perception and behavior.

393
Q

Rama: How do we create our own reality according to brain studies?

A

Normal and brain-damaged patients show we piece together reality from incomplete data.

What we see is reliable but not always accurate.

Most actions are performed unconsciously.

Consciousness is a narrative layered on top of unconscious processes.

The brain constructs a seamless story—this is not direct perception but a construction.

394
Q

Rama: Where in the brain does consciousness seem to arise?

A

Main regions involved:

Temporal lobes: amygdala, septum, hypothalamus, insular cortex.

Frontal lobe: cingulate gyrus.

These areas are associated with qualia—the raw feel of experience.

Must meet three laws of qualia (inspired by Newton): Richness, Integration, Irrevocability

395
Q

Rama: What are “qualia” and why are they a philosophical challenge?

A

Qualia = subjective, raw sensations (e.g., red, pain, taste).

Challenge: how does brain matter (neurons, ions) produce experiences?

Philosophers call this the riddle of qualia.

Scientific descriptions seem incomplete without accounting for subjective experience.

396
Q

Rama: Why are qualia considered private and not necessarily scientific?

A

Science gives a third-person view; qualia are first-person phenomena.

The problem is epistemological, not necessarily ontological.

Language creates a barrier—experience can’t be fully conveyed verbally.

Philosophers argue this is a permanent barrier, but maybe it’s just apparent and due to translation limits between languages (e.g., neural to spoken).

397
Q

Rama: What is the “language barrier” problem in communicating qualia?

A

Example: color-blind superscientist can’t experience red.

Explaining red verbally does not transmit the actual experience.

The “redness” of red is lost in translation.

Could be overcome by direct brain-to-brain links, bypassing language.

398
Q

Rama: What happens if we stimulate a blind person’s visual cortex directly?

A

Magnetic pulses could simulate vision without functioning eyes.

Outcomes:

If they feel novel sensations tied to external space, it’s vision-like.

Topographic mapping in visual cortex could confirm this.

Suggests consciousness of seeing could arise without eyes—only brain processing is required.

399
Q

Rama: What do Crick and Koch suggest about the origin of qualia?

A

Qualia may originate in lower layers of sensory areas.

These project to the frontal lobes, where higher-order processing happens.

Suggests conscious experience begins early in the sensory hierarchy but gains meaning through projection.

400
Q

Rama: How might neural synchronization relate to consciousness?

A

Conscious awareness might come from synchronized neural firing.

Widely separated brain areas fire in sync when we pay attention.

Still speculative, but offers a temporal basis for consciousness.

No direct proof yet—remains a promising hypothesis.

401
Q

Rama: What is reductionism, and how does it apply to consciousness?

A

Reductionism: explaining wholes as functions of parts and their interactions.

Challenge: unclear which level of reduction (neural, systems, experiential) is appropriate.

Consciousness may require multi-level explanations, not just neuron-level.

402
Q

Rama: What is the epiphenomenon view of consciousness?

A

Some philosophers say consciousness is causally inert.

Like a train’s whistle or a horse’s shadow—present but doesn’t do anything.

This view denies a functional role for qualia in behavior or decision-making.

403
Q

Rama: What is “filling in” and how does it relate to qualia?

A

Brain “fills in” gaps (e.g., blind spot) with fabricated perception.

Not just deduction—you literally see the filled-in region.

Demonstrates that qualia can exist even in absence of external input.

Filled-in qualia provide actual sensory support.

404
Q

Rama: What makes qualia-laden perceptions “tamper-resistant”?

A

You can imagine a hidden object behind your finger (imaginative flexibility).

But you can’t change what you perceive in the blind spot (e.g., yellow).

This rigidity = hallmark of qualia-laden perceptions.

Indicates these perceptions resist higher-level override.

405
Q

Rama: How does seeing the dog in a bistable image change your brain?

A

Once seen, you cannot unsee the dog (in a bistable image)

Neurons permanently rewire after recognition.

Suggests perception alters brain circuits irreversibly.

Shows plasticity of consciousness and visual awareness.

406
Q

Rama: What are the three functional features of qualia?

A

Irrevocability (Input side): Once a qualia-laden sensation is perceived, it cannot be “taken back” or questioned.

Flexibility (Output side): Allows for a range of behavioral choices or responses.

Persistence in memory: Must be held long enough in an intermediate buffer or immediate memory to enable decision-making.

407
Q

Rama: How do qualia relate to Denise’s (blindsight) visual processing and memory systems?

A

Denise’s “how” pathway (unconscious action system) is: Devoid of qualia & Lacks short-term memory

Her “what” pathway (conscious recognition system) is: Normally conscious and qualia-laden & Involves memory

Damage to the “what” pathway leaves her with only the zombie “how” system, limiting conscious visual processing and memory.

408
Q

Rama: Why does the “what” pathway need memory, and the “how” pathway does not?

A

What Pathway: Involves making choices from perceptual representations.
Choice requires time → requires memory.

How Pathway: Engages in continuous, real-time sensorimotor loops.
Functions like a thermostat—automatic, no choice → no memory needed

409
Q

Rama: What is needed for qualia to exist in terms of memory and representation?

A

Must begin with a stable, finite, irrevocable representation in short-term memory (e.g., yellow).

This representation can carry infinite implications (e.g., bananas, jaundice).

Revocable or inferred representations (e.g., cat under a sofa) lack strong, vivid qualia

410
Q

Rama: Why must perceptions have vivid qualia, and beliefs not?

A

Perceptions: Drive real-world decisions, Need to be irrevocable for swift action.

Beliefs/Internal images: Should remain tentative and revisable, Flexibility prevents error from overcommitment to uncertainty

411
Q

Rama: How does irrevocability of qualia aid in decision-making?

A

Helps avoid indecision: If you say, “Maybe it’s not yellow,” you can’t act.

Perceptions must be treated as certain even if they’re 90% accurate.

Irrevocability confers decisiveness, avoiding paralysis in action

412
Q

Rama: What’s the distinction between perception and conception in relation to qualia?

A

Seeing (perception): Involves vivid qualia, irrevocable representations.

Knowing (conception): Tentative, flexible, open to revision.

There may be a gray area, but they’re possibly mediated by different brain circuits

413
Q

Rama: How does the brain treat qualia differently in blind spots vs. inferred regions?

A

Blind spot: Filled in automatically and irrevocably; no qualia distinction.

Behind the head (inferred space): Remains revocable and open to possibilities (e.g., an elephant could be there).

Level of danger or importance dictates the certainty threshold for qualia

414
Q

Rama: Why don’t bees have qualia despite intelligent behavior?

A

Bees show complex behavior (e.g., waggle dance), but: Actions are hardwired and inflexible, Lacking symbolic representation and choice.

Qualia emerge from systems that: Allow multiple behavioral options, Require memory and decision-making, Have irrevocable representations to base decisions on

415
Q

Rama: What are the computational preconditions for qualia?

A

A system with:

Choice among multiple responses (not just stimulus-response).

Intermediate representations held in short-term memory.

Irrevocable perceptual units for stability in decision-making.

These conditions are rare in evolution → qualia are rare

416
Q

Rama: What does the split-brain phenomenon reveal about the self?

A

In split-brain patients:

Each hemisphere can act independently.

Left hemisphere often creates confabulatory narratives.

Suggests:

The sense of a unified self is an illusion.

The self is likely distributed, not centralized

417
Q

Rama: What happens to the self during temporal lobe seizures?

A

Patients may feel: Merged with the cosmos, loss of ego boundaries, Timelessness, infinite significance.

Suggests that the self is:

Constructed by temporal lobe circuits.

Fragile and easily altered by brain activity

418
Q

Rama: What role does memory play in the construction of the self?

A

Personal identity relies on autobiographical memory.

Damage (e.g., in amnesia) can disrupt the continuity of self.

Suggests self is:

A narrative built from remembered experiences.

Dependent on brain systems that can be damaged or lost.

419
Q

Rama: Why might the unity of self be an evolutionary “trick”?

A

Brain may create a fictional narrative for coherence.

Helps in: Social communication, Long-term planning, Stable identity

But actually, mental functions are modular and distributed.

The “self” may be a post-hoc interpretation

420
Q

Rama: How is the temporal lobe implicated in the generation of qualia?

A

Temporal lobe: Involved in symbolic representation and memory, Supports semantic knowledge and self-related processing.

Seizures here often produce: Hyper-qualia (e.g., intense emotional meaning), Mystical experiences or strong sense of presence.

Suggests it plays a central role in qualia and self-awareness

421
Q

What components are needed for a sense of self to emerge?

A

Memory: for continuity and autobiographical narrative.

Language: to express and frame the self.

Attention and perception: to anchor the self in the present.

Emotion and motivation: to give the self personal relevance.

Brain structures: including temporal lobe, prefrontal cortex, default mode network

422
Q

🔹 What is the distinction between third-person data and first-person data in consciousness science?

A

Third-person data: Concern the behavior and brain processes of conscious systems, Includes data from cognitive psychology, neuroscience, etc., Gathered through objective observation

First-person data: Concern subjective experiences (qualia), Gathered by introspection or verbal reports of conscious individuals, Data are private and available only to the subject

423
Q

🔹 Why can’t first-person data be reduced to third-person data?

A

Third-person data explain objective functions (e.g., perception, report)

Even a full account of these functions leaves open the question: “Why is this functioning associated with subjective experience?”

First-person and third-person data are irreducible to each other

A complete theory must admit and connect both kinds of data

424
Q

🔹 What is the goal of explaining third-person data?

A

To explain the objective functioning of the system

Requires specifying a mechanism (usually neural/computational)

Leads to a reductive explanation

Explains high-level phenomena (e.g., memory) via lower-level ones (e.g., neurons)

Still leaves open the “hard problem”—explaining experience itself

425
Q

🔹 How can a science of consciousness handle both types of data?

A

Must articulate systematic connections between subjective experience and objective function

Through bridging principles: Explain how specific brain functions relate to specific experiences

Not necessarily reductive, but systematic

426
Q

🔹 What are some views on reducing first-person data to third-person?

A

Dennett: Only objective functioning needs explaining

Churchland: First-person data may be reducible in future neuroscience

Correlational view: Correlations count as reductive explanation

427
Q

🔹 What are examples of third-person projects in consciousness research?

A

Explaining functioning differences (e.g., sleep vs. wakefulness)

Studying voluntary behavior

Understanding synchronized neural firing for integration

Investigating the global workspace (Baars, 1988): Shared info across cognitive systems, Access to verbal report

428
Q

🔹 How do conscious and unconscious processes differ in data?

A

From the third-person view: Both may involve perceptual registration, But differ in behavioral capacities and neural substrates

From the first-person view: One involves experience, the other doesn’t

Example Milner & Goodale: Ventral stream = conscious perception, Dorsal stream = unconscious motor control

429
Q

🔹 What are neural correlates of consciousness (NCC)?

A

Minimal neural systems directly associated with conscious experience

Aim: isolate specific regions/processes that track experience

Not all of the brain is equally involved

Different NCCs may exist for different types of experience

e.g., Inferior temporal cortex for visual consciousness, Primary visual cortex: less predictive of subjective visual change

430
Q

🔹 What are the six major projects in the science of consciousness?

A

Explain third-person data

Contrast conscious vs. unconscious processes

Investigate the contents of consciousness

Identify neural correlates of consciousness (NCC)

Systematize connections between 1st- and 3rd-person data

Infer general principles linking brain processes to experiences

431
Q

🔹 What are the obstacles in gathering first-person data?

A

Privacy: Only the subject has direct access

Verbal reports: Can’t use with infants/animals, Some experiences (e.g., emotions/music) hard to describe

Methodological limits: Introspection is difficult and may alter the experience, Especially hard for non-attended experiences

Lack of formalism: Need tools to structure and represent experiences

432
Q

🔹 What formal systems are being developed to study first-person data?

A

Parametric: isolate and measure experience features (e.g., color)

Geometric/topological: formalize experience structure (e.g., visual space)

Informational: represent experience as informational states

Representational: link experience to what it represents in the world

433
Q

🔹 How can researchers deal with first-person data in nonverbal subjects?

A

Use behavioral indicators (e.g., primate responses)

Assume a degree of similarity in conscious experience

Combine verbal reports from humans with behavioral data

Example: neurophenomenology (Varela) combines introspection with EEG/fMRI

434
Q

🔹 What is the ideal aim of a science of consciousness?

A

Derive general, simple principles linking neural states to conscious experience

Ideally: Applies to all conscious systems, Predicts features of subjective experience from neurophysiology

Can remain neutral on metaphysics (e.g., dualism vs. materialism)

435
Q

“A convincing illusion can leave behavior unaffected”: What does this suggest about the relationship between perception and action?

A

Observers do not adjust finger distance despite being deceived by an illusion.

Indicates that overt behavior can proceed independently from perceptual experience.

Suggests the existence of isolated visuomotor processes that operate without conscious perception.

Supports the idea that action and perception are handled by separate neural systems.

436
Q

Can unconscious stimuli affect behavior?

A

Yes, behavior can be influenced by stimuli that are not consciously perceived.

Robust perceptual aftereffects have been shown even when stimuli are not consciously seen (Rees, Kreiman, & Koch, 2002).

Implies much of brain function occurs outside of conscious awareness and control.

Automatic, domain-specific processing happens without the need for awareness

437
Q

What does neglect reveal about the relationship between consciousness and brain function?

A

Patients with neglect often deny their deficits, lacking awareness of both space and their condition.

Lesions can destroy not only processing of certain stimuli but also the consciousness of those stimuli.

Early visual areas may remain intact, showing that higher-level integration is critical for awareness.

Demonstrates dissociation between intact sensory processing and conscious experience

438
Q

Is the activity of the brain strictly continuous with our conscious experience?

A

No, neural activity can occur without entering consciousness.

Conscious experience represents only a fraction of total brain activity.

Much processing is unconscious and does not necessarily result in subjective awareness

439
Q

What is binocular rivalry and what does it reveal about consciousness?

A

Different images shown to each eye lead to alternating conscious percepts.

Subjects report changes in perception despite static stimuli.

Neural activity correlates with what is consciously seen, not what is shown.

Brain areas specific to a stimulus type are more active when that type is consciously perceived.

Unperceived stimuli still activate category-specific areas (e.g., face areas), but less intensely.

Supports a graded or threshold model of consciousness—only sufficiently integrated processing becomes conscious

440
Q

How does binocular fusion inform our understanding of unconscious processing?

A

When colors are fused (e.g., red + green = yellow), the original images (like faces) disappear from consciousness.

However, brain areas for faces still activate, suggesting unconscious processing.

Conscious perception requires more intense and widespread activation.

Reinforces the idea of a threshold for conscious experience

441
Q

What is the Global Neuronal Workspace hypothesis? (Dehaene & Naccache, 2001)

A

Proposes that consciousness arises when localized, modular processes are integrated into a global system.

Requires amplification via attentional gating to enter awareness.

Consciousness = dynamic integration of activity across brain regions.

Explains neglect: local processing occurs, but lack of integration prevents awareness of deficits.

Wild confabulations may arise due to partial or fragmented integration of conscious contents

442
Q

What is the role of confabulation and the left-hemisphere interpreter in consciousness?

A

Patients create rationalizations to resolve conflicts between hemispheres or explain deficits.

Left hemisphere generates hypotheses, even if incorrect, to maintain a coherent narrative.

Drives the construction of a unified conscious experience.

The constructive, interpretive nature of consciousness is typically not accessible to introspection.

Confabulations in split-brain and brain-damaged patients show how fragmented awareness can be stitched into a seamless story.

443
Q

How can fMRI and statistical analysis of brain data help investigate consciousness?

A

Correlations between neural activations yield maps of cerebral interactivity.

Consciousness is associated with the activation of large-scale networks.

These maps help identify which brain processes correlate with subjective experience.

Integration with anatomical data strengthens these findings.

444
Q

What role does diffusion-tensor imaging (DTI) play in studying consciousness?

A

DTI tracks neural pathways and models brain connectivity.

Allows mapping of structural connections that underlie functional activation patterns.

Helps determine which brain areas are wired to support integrated, conscious processing.

Expected to significantly enhance our understanding of the neural correlates of consciousness