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Neuroscience and behaviour > Neuroscience methods > Flashcards

Neuroscience methods Flashcards

1
Q

neuroscience techniques

A
  • Serving for study of relationship between brain & beh
    Ideal methods?
  • Spatial resolution: cellular level
  • Temporal resolution: millisecond scale
  • Whole brain studied simultaneously?
  • Non-invasive
  • No such method
  • Match existing methods, all with certain limitations, to the research question
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2
Q

microscopic anatomy: Brodmann areas

A
  • Brain segmented according to appearance in microscope (cytoarchitectonics)
  • 6 layers correlating to function
  • Combined with comparative neuroanatomy
  • Appearance reflects type of cells e.g. inputs vs outputs
  • Type of cell sometimes correlates with function
  • Studies restricted to small num of brains
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3
Q

6 layers of Brodmann areas

A
  • 1: closest to cortical surface
  • Not equally wide
  • Layer 5 wider than 4
  • Layer 5: contains mostly cells sending signals from brain –> periphery (output levels)
  • Layer 4: cells receiving input from periphery (output layer)
  • Relatively wide output layers typical of brain areas e.g. primary moto
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4
Q

transcarnial magnetic stimulation (TMS)

A
  • Stimulator placed above scalp, contains a coil of wire
  • Brief pulse of high electrical current fed through the coil
  • Result: magnetic field with flux lines perpendicular to plane of coil
  • Magnetic field induces electrical field perpendicular to magnetic field
  • Electric field leads to neuronal excitation within the brain (trans-cranial)
  • non-invasive, painless, safe stimulation of human brain cortex
  • effects depend on stimulation site
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5
Q

how to measure effects of TMS

A
  • Spatial resolution? - TMS to neighbouring sites of neighbouring sites of motor homunculus activates diff lower arm muscles (thumb vs little finger twitches)
  • Motor cortex stimulation
  • occipital cortex stimulation
  • somatosensory cortex stimulation
  • auditory cortex stimulation
  • frontal cortex stimulation
  • effects measured as peripheral responses, as impaired/altered perception task performance, or as brain’s direct response
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6
Q

motor cortex stimulation

how to measure effects of TMS

A
  • Activates corticospinal neurons trans-synaptically
  • Example: TMS coil 5cm lateral from vertex > often contralateral thumb twitches (20ms post TMS)
  • Small change in coil position would result in little finger twitches instead of thumb twitches
  • Record motor Eps (surface EMG, target muscle relaxed) - relaxed target muscle: motor evoked potential start from 20ms post TMS
  • Record silent period in contracted target muscles ~150ms after motor cortex stim’, cortical mechanisms
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7
Q

occipital cortex stimulation

how to measure TMS

A
  • Excitatory effects: e.g. phosphenes; inhibitory effects: suppression of motion perception & letter identification
  • Phosphenes: ppt reports perception of light in the absence of light input to the eye
  • Inhibitory effects can occur as ppt-reported suppression of motion perception or as decreased performance in a latter identification task
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8
Q

somatosensory cortex stimulation

how to measure TMS

A
  • May elicit tingling, block the detection of peripheral stim (tactile, pain)
  • Detection of tactile or painful stim may decline
  • Can modify somatosensory evoked potentials (SEPs)
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9
Q

auditory cortex stimulation

how to measure TMS

A

interpretation of results challenging: loud coil click

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10
Q

frontal cortex stimulation

how to measure TMS

A
  • Effects on subject’s mood? Potential for therapeutic use?
  • Ongoing studies about this
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11
Q

example application TMS

A
  • Study crossmodal plasticity in the brain
  • Braille
  • Superior tactile perception (compared with sighted ppl)
  • Underlying changes in the brain?
  • Blind persons’ visual cortex is known to be activated during Braille reading - Example of crossmodal plasticity
  • Functional sig of this activation? = research question for TMS studies - Unclear if this activation is functionally sig
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12
Q

chronometry as an example of TMS

A
  • Single-pulse TMS for mental chronometry
  • Early blind subjects
  • Tactile stim in shape of Braille letters applied to tip of right middle finger (peripheral stim) in a grid that display wither meaningful or nonsense characters
  • Real & nonsensical Braille stim presented via tactile stimulator
  • 2 TMS conditions in separate blocks: TMS coil either placed over left somatosensory cortex, Over left occipital cortex
  • Interval between tactile stim & TMS systematically varied
  • Subjects’ task - Detect stim, Identify stim as real vs nonsensical
  • DV: num of correctly detected/identified stim
  • Conclusion: visual cortex contributes to tactile info processing in early blind subjects = crossmodal plasticity
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13
Q

virtual lesions as an example of TMS

A
  • Repetitive TMS for temporary inhibition of brain areas, fully reversible: virtual lesion (for a few mins, ppts behave as if after a brain lesion)
  • repetitive TMS can induce temporary inhibition of brain areas in a fully reversible way, meaning that lesions can arise
  • During these few mins, a behavioural tasks can be carried out
  • Errors during Braille reading, early blind vs sighted subjects
  • Error rates depend on sight of virtual lesions
  • Crossmodal plasticiaty in early blind subjects: occipital cortex supports Braille reading
  • With certain TMS protocols virtual lesion can outlast TMS stimulation by several mins - During these mins a behavioural task can be carried out
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14
Q

TMS advantages

A
  • Temporal resolution in ms range
  • Virtual lesion in subject may be better defined than lesion in patient
  • Short duration of experiment minimizes risk of plasticity
  • Repeated studies in same subject
  • Group studies with standardised experimental setup
  • Study double dissociations: stimulate or temporarily disrupt diff cortical regions during 1 task, 1 region during diff tasks
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15
Q

TMS disadvantages

A
  • Spatial under-sampling (only 1 area at a time) - Notice paired-pulse TMS with 2 diff coils, assessing the effect of a conditioning stim from coil 1 on the response to a later test stim from coil 2
  • Only cortical areas accessible
  • Auditory cortex areas accessible
  • Auditory cortex stimulation problematic (muscles)
  • Loud coil click, need “sham stimulation”
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16
Q

EEG

measuring electrical activity of the brain

A
  • Neurons aligned perpendicular to cortical surface, dendrites closer to the surface & axons closer to the white matter
  • Synchronous firing of large neuron populations can be recorded non-invasively - Electrodes placed on scalp - evenly spaced to cover whole scalp
  • EEG generated by postsynaptic potentials
  • Under the influence of postsynaptic potentials, cortical neurons create surface-negative electrical dipoles
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17
Q

non-invasive neurophysiology

EEG

A
  • Occipital rhythm of ~10 cycles/second or 10Hz = alpha rhythm: typically blocked by opening the eyes = Berger effect
  • Oscillatory waveform
  • Rhythms (oscillations) that can be observed in “spontaneous” (“continuous”)
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18
Q

EEG rhythms

A
  • beta
  • alpha
  • theta
  • delta
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19
Q

beta rhythms

EEG

A
  • most evident frontally
  • dominant rhythms when subject is alert
  • eyes open
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20
Q

alpha rhythms

EEG

A
  • occipital maximum
  • dominant when subject is relaxed with eyes closed
  • blocked by opening the eyes or by onset of mental effort (Berger effect)
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21
Q

theta rhythms

EEG

A
  • ‘slow’ activity
  • rare in adults when awake but perfectly normal inn children and sleep
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22
Q

delta rhythms

EEG

A

dominant rhythm in infants and stages 3 and 4 of sleep

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23
Q

spontaneous EEG without experimentally controlled sensory stim & without task

A

Ongoing oscillations in multiple freq bands e.g. varying with sleep stage

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24
Q

EEG-based parameters for bio psych

A
  • Event-related oscillations: stimulus- or task- related changes in EEG oscillations, in terms of freq/amplitude
  • Event-related potentials: waveforms defined in terms of latency relative to an event such as a sensory stim
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25
Q

event-related EEG oscillations

A
  • Example: lateralised occipito-parietal alpha (~10 Hz) oscillations during visual spatial attention
  • Regionally specific change to ongoing alpha oscillations
  • After cue for right (left) hemifield, suppression of alpha oscillations in left (right) occipito-parietal region of interest (ROI)
  • A brain correlate of lateralised attention towards subsequent target
  • Processed signal: momentary amplitude of EEG alpha oscillations as a function of time - Relative to cue = 0ms
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26
Q

ERP types

A
  • exogenous
  • endogenous
  • mesogenous
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27
Q

exogenous ERPs

A
  • automatic responses of the brain, controlled by physical props of the stim
  • sensory evoked potentials (<100ms post stim)
  • Elicited whenever modality-specific sensory pathway (auditory, somatosensory…) is intact
  • Influenced by intensity/freq of stim
  • Highly important for neurological diagnosis, less so for psych research
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28
Q

endogenous ERPs

A
  • reflect interaction between subject & event (attention, task-relevance, expectation)
  • Response to omitted stim
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29
Q

mesogenous ERPs

A
  • semi-automatic but modulated by cog processes
  • effect of attention: subject responses to standard tones in attended ear
  • effect of selective attention emerges as early as 100ms after
  • mismatch negativity (MMN) passive auditory oddball paradigm
  • subject not attending to auditory stim but reading a book the more discriminable the stim, the shorter the MMN latency and the larger the MMN amplitude frontal/central maximum MMN may reflect
  • preattentive processing of deviant features
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30
Q

source localisation for ERPs

A
  • ‘determine neural generator(s) whose activity results in scalp-recorded potential’ = inverse problem: no unique solution
  • further difficulty: scalp distorts and ‘smears’ electrical fields

2nd bullet point: can be overcome by recording magnetic instead of electric fields as skull is transparent to the former: MEG

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31
Q

applications of MMN

A
  • MMN in patients with SZ
  • MMN in children with dyslexia
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32
Q

MMN in patients with SZ

A
  • Decrease in MMN amplitude (compared with healthy control group)
  • Attenuation stronger for duration deviants than for freq deviants
  • Attenuated MMN also in first-degree relatives of SZ patients who are at increased risk for SZ, reflecting genetic vulnerability
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33
Q

MMN in children with dyslexia

A
  • Reduction in amplitude (freq-deviant MMN)
  • Reduction correlated with the severity of dyslexia
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34
Q

P300/P3

A

+ve deflection with ~300ms latency which can be observed under several conditions

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35
Q

endogenous ERPs, P300

A
  • classic P3, P3b
  • novelty P3, P3a
  • omitted stim P3
  • endogenous ERPs elicited by infrequently occuring targets, equally infrequent novel, environmental sounds
  • during an actively attended novelty oddball task
  • diff topographic distributions
  • surface potential maps
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36
Q

classic P3, P3b

endogenous ERPs

A
  • Response to task-relevant oddball stim, parietal maximum
  • Sensitive to stim probability
  • May reflect categorisation of stim (longer latency when stim are difficult to categorise)
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37
Q

novelty P3, P3a

endogenous ERPs

A
  • response to unexpected deviant stim, frontal max orienting to stim for which no mem template available
  • Amplitude maximum over frontal electrodes
  • Auditory oddball paradigm may elicit MMN & P3a
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38
Q

omitted stim P3

endogenous ERPs, P300

A

when expected stim dont occur of definition of endogenous ERPs

39
Q

application of P300

A
  • P300 in patients with SZ
  • Reduced auditory P300 amplitude (compared with healthy control group)
  • Reflecting impairment in sustained attention?
  • Attenuated P300 also in first-degree relatives of SZ patients, suggesting increased genetic risk of SZ
40
Q

endogenous ERPs, N400

A
  • Semantically incongruent (but syntactically correct) sentence endings
  • Amplitude proportional to the degree of incongruence
41
Q

endogenous ERPs, movement-related potential

A
  • Preceding voluntary movement RP, readiness potential
  • Maximum contralateral to responding limb
  • Cz recording negativity upwards
  • onset of voluntary movement = 0ms (detected in EMG)
42
Q

endogenous ERPs, contingent negative variation

A
  • CNV in S1-S2 paradigm: warning stim –> tone, tone unpleasantly loud, played until ppt presses response button
  • Orientating wave
  • Expectancy wave (could be same as readiness potential)
43
Q

magnetencephalogram

MEG

A
  • Electrical activity in the brain generates magnetic fields
  • Skull doesn’t distort magnetic fields before they are detected by MEG sensors
  • Better spatial resolution than EEG/ERP ~5mm in optimal cases
  • Same ms temporal resolution as ERPs
  • Highly sensitive to electromagnetic noise: requires magnetic shielding
  • MEG responses to stim through averaging
  • Cryogenic MEG using SQUID sensors: sensors cooled in liquid helium
  • Recent development: wearable MEG at room temperature
44
Q

goals of structural imaging with non-invasive methods

A
  • to study anatomy
  • to identify abnormalities (as in brain disease)
  • To follow dev (childhood to old age)
  • to show plasticity
45
Q

CT & structural MRI rely on?

A

contrast between tissue types

white matter vs gray matter vs cerebrospinal fluid

46
Q

example application of brain plasticity after motor learning

structural MRI

A
  • juggling requires expert visual motion perception
  • learning to juggle = changes to the brain?
  • clusters of stat sig expansion of gray matter
  • Not to be confused with fMRI
  • Observed in volunteers who have learned to juggle
  • Correspond to area hMT/V5, a visual motion area
  • Increase in gray matter as an anatomical change over months irrespective of activation
47
Q

extrastriate visual areas

structual MRI

A
  • Process input from geniculostriate system
  • The anatomical location of human MT/V5 as a lateral occipito-temporal area & part of extrastriate visual cortex, separate from primary visual cortex
  • 2 pathways of extrastriate visual processing, ventral pathway for object recog & dorsal pathway for visually guided action
48
Q

how to generate structural MR contrast

A
  • ppt’s/patient’s position in scanner bore
  • Key components of the scanner: magnet surrounding the bore & radiofrequency coil both of which essential to processes
  • Gradient coils equally essential
  • Because of high water content of soft tissue, there are abundant protons which are in rotatory motion & axis of rotation is randomly oriented rotation axes become aligned to magnetic field within scanner bore
  • Spin of protons when subject/patient outside magnetic field
  • Spin of protons when subject/patient inside magnetic field - vertical external magnetic field
49
Q

role of radiofrequency coil in an armchair experiment

structural MRI

A
  • Compass needle pointing north: due to earth’s magnetic field
  • Once magnet removed, needle will return pointing northwards, the lowest energy state in the Earth’s magnetic field
  • Magnetic field in scanner bore corresponds to the Earth’s magnetic field
  • Sequence in MR scanner
  • Protons in diff tissue types require diff time to realign
50
Q

sequence in MR scanner

A
  • Net magnetisation vector parallel to the external magnetic field in the scanner bore: 100% of net magnetisation is in the direction of the external magnetic field
  • When the radiofrequency coil emits a radiofrequency pulse, the net magnetisation vector is turned into an orientation perpendicular to the external magnetic field, so at this moment 0% of net magnetisation is in the direction of the external magnetic field
  • After the radiofrequency pulse, the vector of net magnetisation returns to the direction of the external magnetic field, or net magnetisation recovers to 100% of pre-RF value. During this phase of recovery, an MR signal is measured
  • Net magnetisation returns to the value before the radiofrequency pulse, so the process can be run as cycle with multiple repeats
  • Sequences of radiofrequency pulses & readout to as MR protocols
51
Q

How structural contrast in MRI can be generated on the basis of increasing longitudinal magnetisation after the radiofrequency pulse

A
  • Radiofrequency coil first emits radiofrequency pulse, then same coil detects change in longitudinal magnetisation
  • Increase of vertical component = increase of magnetisation that is parallel with external magnetic field = increase in longitudinal magnetisation = spin-lattice relaxation (T1)
  • Structure-specific time courses of spin-lattice relaxation - structural contrast: in brain tissue faster relaxation than in ventricles
  • T1 signal (brain) > T1 signal (CSF)
  • MR signal measured at time T is tissue-specific, establishing contrast
52
Q

functional imaging

A
  • Goal: identify brain areas that support sensory & cog processes, derive models of brain function
  • Blood flow (PET/SPECT/fMRI)
  • Need contrast that separates non-activated vs activated tissue (in a stimulus- or task-specific way)
53
Q

problems with fMRI

A
  • how to measure neural activity in functional contrast?
  • how to generate measurable functional contrast in exp?
  • how to identify functional contrast in fMRI raw data?
54
Q

how to measure neural activity in functional contrast: BOLD effect

A
  • T2 contrast
  • during local neuronal activation
  • BOLD signal as an indirect measure of neural activity
55
Q

T2 contrast

how to measure neural activity in functional contrast - BOLD

A
  • Depends on balance of deoxygenated to oxygenated haemoglobin (Hb) within blood in a voxel
  • Depends on local regulation of arterial width
56
Q

during local neural activation

how to measure neural activity in functional contrast: BOLD

A
  • Flow is increased, more oxy-Hb in capillaries
  • Oxy-Hb is diamagnetic (does not affect local magnetic fields)
  • Deoxy-Hb is paramagnetic - making field inhomogeneous
  • In inhomogeneous field, horizontal magnetisation decays faster (T2 decay)
  • Slower T2 decay: increased MR signal intensity = blood oxygen level dependent (BOLD) effect
  • BOLD effect: diff signal intensities forming the basis of a contrast
57
Q

BOLD signal as an indirect measure of neural activity

how to measure neural activity in functional contrast: BOLD

A

during local neuronal activation, the blood flow is increased, leading to more oxy-Hb in capillaries

58
Q

how to generate functional contrast

A
  • Main components: magnet, gradient coils & radiofrequency coil
  • 100% = summed prestimulation signal intensity over 10 voxels in visual cortex
  • Huge temporal delay: fMRI has poor temporal resolution
  • 24s per trial
  • 2% signal change is tiny
  • How to increase signal? > experimental design
59
Q

experimental design for functional contrast

how to generate functional contrast

A
  • Spaced event-related design
  • How to increase (improve) (functional contrast)/noise: more complex designs increase the functional contrast to noise ratio without unduly extending the duration of experiment
  • Design types differ in temporal sequence of stim
  • Block design
  • rapid event-related design
60
Q

block design

experimental design for functional contrast

A
  • slow BOLD responses to ind stim overlap
  • Responses are enhanced
  • Inflexible: with a block there are only stim of 1 class
61
Q

rapid event-related design

experimental design for functional contrast

A
  • stim of 2 classes occur in a mixed sequence, without a regular pattern
  • When sequences of each stim class are plotted separately, it is evident that the stim-onset asynchronies (SOAs) are variable, including occasionally long intervals
  • Due to random SOAs, MR signal recorded during stim presentation can be separated into responses to each of the stim classes
62
Q

functional contrast: block design

how to generate functional contrast

A
  • BOLD effect is additive: More stim = more signal
  • Good stat power
  • Stim predictable - Making the block design unsuitable for many tasks in experimental psych
  • MR signal intensity coded as gray level
63
Q

block design strengths

A
  • good stat power
  • robust
  • continuous activation
64
Q

block design weaknesses

A
  • inflexible
  • limited num of conditions
65
Q

event-related design strengths

A
  • avoids habituation
  • analyse subtypes of responses such as correct/incorrect
66
Q

event-related weakness

A

reduced sensitivity to neural events

67
Q

aims of experimental design for fMRI

A
  • Optimise ratio of functional contrast to noise
  • Ensure that experiment measures contrast of interest: baseline well-controlled, attentional effects
  • Duration of experiment
68
Q

stages of fMRI data analysis, images undergo….

how to identify areas that show functional contrast

A
  • spatial preprocessing
  • fMRI stats
69
Q

spatial preprocessing

stages of fMRI data analysis

A
  • motion correction
  • coregisteration between subject’s fMRI & anatomical scans
  • normalisation: warp scans from diff inds
  • spatial smoothing
70
Q

fMRI statistics

stages of fMRI data analysis

A
  • statistical analysis on each voxel (per subjects)
  • statistical anaysis across subjects (random effects)
71
Q

preprocessing: motion correction

A
  • registration/transformation of time series
  • align each volume of the brain to a target volume
  • detect (and correct for) subject’s movement

for easier spatial interpretation of the activation map, it is possible to co-register the functional images with the spatial image from the same ppt

72
Q

preprocessing: normalisation

how to identify areas that show functional contrast

A
  • subject 1&2 –> template –> average activation
  • Activation map from multiple ppts can be aligned & warped to a common template for 2 purposes
  • To allow further analysis at group level –> average patterns of activation
  • To label the location of activation by comparison with a brain atlas
73
Q

preprocessing: normalisation for comparison with anatomical template

how to identify areas that show functional contrast

A
  • image has to be in same co-ordinate system as the atlas: the Talairach-Tournoux atlas uses the anterior commissure as reference point
  • Relative to the origin of co-ordinate system a location can have x, y & z coordinates: correspond to a cortical area
  • Procedure not particularly precise
  • Procedure highly standardised and can therefore facilitate comparison of results from multiple studies (meta-analysis)
74
Q

limitations of Talairach-Tournous atlas

normalisation for comparison with anatomical template

A
  • only 1 brain
  • only 1 hemisphere
  • fixation likely changed shape of brain
75
Q

fMRI statistics: evaluate block design data

how to identify areas that show functional contrast

A
  • Predicted timecourse for a voxel activated during ‘light on’
  • Occipital voxel timecourse follows predicted timecourse: ‘voxel activated’
  • Frontal voxel timecourse doesn’t follow predicted timecourse: ‘voxel not activated’
  • How to test if voxel follows predicted timecourse - General linear model
76
Q

statistical analysis of fMRI data using quant method

A
  1. a predicted timecourse of activation is defined, based on the known durations of rest & stimuli
  2. fMRI data from each location is compared with the predicted activation
  3. quant & stats steps
77
Q

fMRI data from each location being compared with the predicted activation

A
  • The observed time course of MR signal from an occipital location (blue dots) follows the predicted time course
  • Voxel therefore labelled as activated
  • MR signal from locations outside occipital cortex e.g. from a frontal location don’t follow the predicted timecourse
  • Frontal voxel therefore labelled as no activated
78
Q

quant & stats steps

stat analysis of fMRI data

A
  • How closely an observed MR signal follows the predicted timecourse can be quantified as correlation between observed & predicted timecourses
  • A statistical voxel-by-voxel test of activation can be run through GLM analysis with observed and predicted timecourses as input
79
Q

fMRI analysis having low power

A
  • e.g. 32 slices (3mm each, no gap) x 64x64 voxels (3mmx3mm) cover the whole brain: 131072 voxels
  • Chance of one of these voxels being active at the 0.05 level is very high
  • By chance, we expect 0.05x131072=6553 voxels (at 0.05)
80
Q

neuropsychology aim

A

relate brain anatomy to beh

81
Q

albert task

A
  • asked to fixate on dot, cross out all lines patient sees
  • patients with brain lesions - Only lines to right of fixation mark have been cancelled
82
Q

line bisection task

A
  • fixate on dot then place a marker that would divide lines into halves of equal length
  • Patient with brain lesion makes a bisection point far to the right of actual half of each line
83
Q

hemineglect syndrome

A
  • typically lesions at border between right temporal lobe & right parietal lobe
  • Temporo-parietal junction
84
Q

goals of neuropsychology

A
  • localise impaired beh to damaged regions BUT lesion may affect a relay station rather than the originally functional region
  • exclude localisation of preserved skills to damaged regions BUT other regions may have may have re-organised to perform functions that were originally localised to damaged region
85
Q

association

A

damage to a single brain region, but multiple deficits (in typical combination, as a syndrome)

86
Q

dissociation

A

damage leads to impaired performance in task A but performance in task B is normal

87
Q

studying associations

A
  • balint’s syndrome
  • Damage to a single brain region, but multiple deficits (in typical combination, as a syndrome)
  • Damage to region X –> deficits in function A,B,C
  • Inference: tasks A,B,C require same neural circuit
  • Alternative: A,B,C may be processed by separate functional regions that are anatomical neighbours
  • Alternative 2: X is a common relay station for anatomically and functionally distinct regions A,B,C
88
Q

balint’s syndrome

A
  • simultagnosia: perceive 1 item at a time
  • oculomotor apraxia: failure to make predicted eye movements
  • optic ataxia: inability to reach see target

parieto-occipital cortex

89
Q

studying dissociations

A
  • visual form agnosia
  • Definition: patient is impaired in 1 task but performs normally in a diff task
  • Inference: tasks rely on separate networks
  • Alternative 1: impaired task simply more difficult?
  • Alternative 2: performance on ‘unimpaired’ task at ceiling?
  • Stronger inference can be drawn from double dissociations
90
Q

visual form agnosia

studying dissociations

A
  • One of the tasks given to the patient was to match the orientation of a hand-held card to the orientation of the slot in a disc
  • 2nd task given to patient DF was perceptual matching
  • patient’s lesion in ventrolateral occipital cortex impairs vision for recognition but not vision for action, a pattern of dissociation
91
Q

extrastriate visual areas

process input ffrom geniculostriate system

A
  • example of double dissociations: background info for the juggling task
  • in the extrastriate visual areas there is functional and anatomical separation between an occipito-temporal pathway of vision for recognition and an occipito-parietal pathway of vision for action
92
Q

visual pathways: lesions to the ventral stream

A
  • functional & anatomical separation between vision for action and vision for recognition can also be found at earlier stages of visual processing, from retinal to cortical level
  • Main input to the dorsal stream is from retinal M-ganglion cells of the magnocellular system
  • Main input to the ventral stream is from retinal P-ganglion cells
93
Q

studying double dissociations confirms…

A

a functional & anatomical dissociation in extrastriate visual cortex, with separate pathways supporting vision for action and vision for recognition

Neuroscience and behaviour (17 decks)

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