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PSYC211 > Machado > Flashcards

Machado Flashcards

1
Q

when talking abt brain scans (but Not gross anatomy)…

A

left + right r reversed

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2
Q

what makes up ur CNS (simple)?

A

spinal cord + brain

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3
Q

where does sensory info enter the CNS?

A

dorsal portion of the spinal cord

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4
Q

where do motor commands exit the CNS?

A

ventral portion of the spinal cord

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5
Q

what terms of orientation r used 4 reptiles thru-out the CNS?

A

dorsal, caudal, ventral, rostral

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6
Q

where do the terms of orientation (CNS) change 4 humans?

A

below the junction w the midbrain (diencephalic junction)

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7
Q

terms orientation above midbrain (human)?

A
  1. anterior = rostral (front of brain)
  2. posterior = caudal (tail/end of brain)
  3. superior = dorsal (top)
  4. inferior = ventral (bottom)
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8
Q

below midbrain terms of orientation (human):

A
  1. rostral (top)
  2. caudal (bottom)
  3. dorsal (towards back, like a fin)
  4. ventral (2wards stomach)
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9
Q

lateral def:

A

towards the side

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10
Q

medial def:

A

2wards the midline… get it.. med –> midline

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11
Q

ipsilateral

A

same side

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12
Q

contralateral

A

opposite side

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13
Q

where do most outgoing motor commands exit

A

on the opposite side!! contralaterally !!

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14
Q

terms 4 brain slices:

A
  1. horizontal (looking frm on top)
  2. coronal (straight thru the middle)
  3. sagittal (slice goes right thru midline of the brain, separates left n right hemispheres)
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15
Q

4 lobes of cerebral cortex (divided into 2 hemispheres):

A
  1. frontal
  2. parietal
  3. temporal
  4. occipital
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16
Q

insular cortex

A

situated between frontal + temporal lobes, revealed once you’ve removed cortex around the lateral sulcus

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17
Q

longitudinal fissure

A

separates left n right hemispheres, deeper than sulcus (but sometimes interchangeable)

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18
Q

lateral sulcus

A

separates frontal + parietal lobes frm temporal lobe

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19
Q

central sulcus

A

separates frontal lobe frm parietal lobe

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20
Q

major gyri:

A
  1. frontal lobe: superior, middle, inferior
  2. temporal: superior, middle, inferior
  3. parietal: postcentral gyrus, intraparietal sulcus (IPS) separates superior + inferior portions of lobe
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21
Q

which direction do the frontal lobe gyri run?

A

anterior –> posterior, meeting the pre-central gyrus at pre-central sulcus

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22
Q

what is the corpus callosum?

A

c-shaped bunch of axons crossing over n connecting the 2 hemispheres

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23
Q

where’s the cerebellum located

A

hangs off of the back/dorsal part of brainstem . looks like cauliflower

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24
Q

what r u Generally talking abt w cortical structures

A

hippocampus, cerebral cortex

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25
Q

what r u talking abt w subcortical structures

A

white matter, thalamus

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26
Q

what r the basal ganglia (in the broadest sense)?

A

lots of diff subcortical structures, main ones being: caudate nucleus, putamen, globus pallidus

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27
Q

what r the main structures in the basal ganglia generally made up of?

A

cell bodies, not axons

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28
Q

describe the shape of the caudate nucleus

A

c-shaped, head is the fattest bit n tail wraps around in2 the temporal lobe

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29
Q

brainstem structure overview

A

superior colliculus –> inferior colliculus –> pons –> medulla

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30
Q

where r the colliculi located?

A

hanging off back of midbrain, upper 2 bumps r superior; lower 2 r inferior

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31
Q

how many bumps 2 the colliculi?

A

4 :p

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32
Q

major divisions of the ventricular system:

A

lateral ventricles, 3rd ventricle, cerebral aqueduct, 4th ventricle

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33
Q

describe the ventricular system broadly

A

consists of interconnected cavities filled w CSF, helpful 4 orienting urself w brain scans

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34
Q

describe lateral ventricles

A
  1. largest of ventricles
  2. look like c-shaped horns, extend frm frontal lobe into parietal + temporal lobes . little end horns poke in2 occipital lobe
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35
Q

where do the lateral ventricles connect 2?

A

interconnected w the 3rd ventricle (which is the midline cavity)

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36
Q

where is the 3rd ventricle connected 2

A

connected w the cerebral aqueduct –> then connects 2 4th ventricle

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37
Q

where is ur 4th ventricle located

A

between cerebellum and brainstem

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38
Q

where does the 3rd ventricle sorta encircle?

A

thalamus

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39
Q

white vs. grey matter

A

white matter = axons, grey matter = cell bodies

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40
Q

what percentage do neurons make up of brain cells

A

abt 10% - glial cells account 4 abt 90% (mostly in supportive role)

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41
Q

basic structure of a neuron:

A

dendrites, soma (cell body), axon, axon terminals

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42
Q

what do dendrites do?

A

receive input frm other neurons, transmit message down neuron

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43
Q

purpose of neuron soma?

A

contains metallic machinery that maintains the neuron

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44
Q

what makes axons white

A

being covered in myelin yayy

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45
Q

how r long r axons

A

<1mm to over a metre wow….

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46
Q

what do u call it when axons branch out !

A

axon collaterals (cause they’re collateral… extra.. accidental)

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47
Q

what forms myelin

A

oligodendrocytes (type of glial cell)

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48
Q

multiple sclerosis + myelin. GO

A

its a demyelinating disease (destroys oligodendrocytes –> impacts myelination of axons –> disrupts normal communication)

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49
Q

what r the two sides of a synapse?

A

1/ pre- and post-synaptic
2. info flows frm presynaptic neuron 2 postsynaptic one (dendrites r postsynaptic cause they already have the info, positioned after the synapse)

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50
Q

what do synaptic vesicles contain

A

chemicals (e.g. dopamine), if a neuron communicates w dopamine NTs might say its dopaminergic

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51
Q

when is electrical signal in neurons translated in2 chem

A

@ axon terminal, then chem signal (NT) crosses synaptic cleft

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52
Q

when is chem signal translated back 2 chem

A

on post-synaptic membrane, chem signal converted back 2 electrical

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53
Q

what volume of brain do glial cells make up

A

a lil more than half of brain volume (smaller than neurons)

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54
Q

main types of glial cells in CNS:

A

astrocytes, oligodendrocytes, microglia

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55
Q

what do astrocytes do

A

form barrier between neuronal tissue n blood (BBB), protect CNS frm some molecules in bloodstream

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56
Q

how do oligodendrocytes form myelin

A
  1. by wrapping their cell membranes around axon during development
  2. myelinating 1 axon requires lots of oligos, but 1 oligo can myeline more than 1 axon –> both sluts
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57
Q

microglia function

A

eat n expel debris left by dead or degenerating brain cells

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58
Q

what triggers synaptic transmission (synaptic vesicles spill content in2 synaptic cleft, excite next neuron)

A

action potentials

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59
Q

what does ‘neuron has fired’ refer 2

A

when a neuron undergoes an AP

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60
Q

what might spikes refer 2

A

how many APs fired per second

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61
Q

what causes an AP

A

rapid change in the voltage of cell membrane

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62
Q

how might an AP b elicited artificially

A

having an electrode inject current –> neuron goes woww guess i better fire

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63
Q

a rat moves 1 whisker. how many APs will somatosensory neuron fire per second?

A

abt 100

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64
Q

what’s a single cell recording in theory

A

picking up electrical activity frm one neuron

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65
Q

cell’s receptive field def:

A

all visually sensitive cells only respond 2 stimuli in a region specific 2 them - that’s their receptive field

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66
Q

background firing rate

A

how many times neuron wld fire without stimulation

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67
Q

maps of neural activity: monkey study (M1)

A
  1. while monkey viewing left stimulus, inject it w radioactive agent
  2. metabolically active cells in V1 absorbed agent –> showed that organisation of cells represented the visual field (like an image of what was being seen)
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68
Q

what tool do u use 2 look @ how many neurons r involved in the rep of 1 image?

A
  1. fMRI: records changes in metabolic activity, producing functional view of brain
  2. signal frm fMRI is roughly proportional 2 neuronal activity –> can use it 2 estimate no. of neurons involved in specific cognitive process
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69
Q

fMRI study (Levy et al., 2004)

A
  1. visual cortex scanned while participant viewed image (e.g. house)
  2. found: @ leats 2 mil neurons involved in rep of one image
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70
Q

somatosensation

A

sensation frm the body

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71
Q

what defines tonotopic map in primary auditory cortex?

A

frequenting tuning (e.g. neurons tuned 2 higher frequencies stick 2gether)

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72
Q

describe brain lesion analysis

A
  1. look @ how brain normally functions by investigating behaviour of patient w lesion in region of interest (ROI)
  2. compares patients w ROI lesion vs. no lesion in ROI
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73
Q

which has higher resolution - CT (computed tomography) or MRI?

A

MRI, cause its more modern

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74
Q

describe EEG

A

electrodes attached 2 scalp, signal detected by each electrode amplified n recorded –> provides recording of brain’s electrical activity

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75
Q

describe ERPs (event-related potentials)

A
  1. signature of brain’s electrical activity in response 2 certain event –> ERPs r averaged across trials (removes background noise) –> true ERP found
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76
Q

ERP research looks @ electrical activity in response 2 an event in terms of:

A
  1. latency (earlier electrical activity = brain responding faster)
  2. amplitude (e.g. if looking @ Jen Aniston cells + present her face, wld have higher amplitude response/higher magnitude of electrical activity)
  3. polarity: positive vs. negative activity (up or down on graph)
  4. scalp topography: where activity is - but Not v precise
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77
Q

strengths n weaknesses of ERPs

A

poor spatial resolution, great temporal resolution (when activity occurred)

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78
Q

structural imaging types:

A

CT, MRI, DTI

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79
Q

functional imaging types:

A

PET + fMRI

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80
Q

describe CT

A

uses x-ray 2 produce series of brain images (old but common), helpful 4 determining damage 2 brain tissue

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81
Q

describe DTI (diffusion tensor imaging)

A

provides view of white matter tracts (i.e. axons) using MRI scanner

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82
Q

describe PET

A
  1. radioactive material enters bloodstream, goes 2 metabolically active areas of brain (firing the most)
  2. PET scanner provides image of concentration + distribution of radioactive agent (functional view of brain)

note: hot colours = lots of radioactive material; blue colours colours = none
note 2: bc just provides functional view, must b overlaid on2 structural image

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83
Q

fMRI description

A
  1. records metabolic-activity related changes in successive images –> functional view of brain
  2. better spatial resolution than PET
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84
Q

Neuroanatomical Correlates of Single + Dual-Language Picture Naming in Spanish-English Bilinguals study (fMRI):

A
  1. compared brain activity when engaged in bilingual or unilingual task
  2. found more activation (Broca’s Area) in bilingual condition
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85
Q

TMS (transcranial magnetic stimulation) description

A
  1. brief magnetic pulse causes brief disruption 2 brain activity
  2. disruption can b excitatory (e.g. when TMS coil held over right hemisphere + left hand moves) or inhibitory (e.g. when TMS coil held over right hemisphere + there’s difficulty moving left hand)
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86
Q

where do neurons in primary motor cortex control?

A

left hemisphere innervates left side of body; right hemisphere - vice versa

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87
Q

outer ear structure

A
  1. pinna: prominent fold of cartilage-supported skin, captures sound + focuses it into the auditory canal
  2. auditory canal ends @ eardrum
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88
Q

middle ear structure

A
  1. ear drum/tympanic membrane
  2. ossicles - middle ear bones
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89
Q

middle ear process

A
  1. when sound wave reaches middle ear, series of differing pressure regions impinge on eardrum (high pressure pushes eardrum inward, low pulls eardrum outward)
  2. continuous arrival of differing pressures causes eardrum 2 vibrate –> vibrate ossicles 2
  3. ossicle vibrations transmitted 2 inner ear fluid via vibration of membrane @ the oval window
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90
Q

inner ear structure n function explained

A
  1. cochlea (spiral-shaped, fluid-filled tube) contains hair/receptor cells
  2. vibrations in the cochlea produce waves in the fluid –> hair cells move –>
  3. convert mechanical signal into electrical, synapse on2 spiral ganglion cells in cochlea
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91
Q

describe spiral ganglion cells

A

cells r tuned 2 specific frequencies, cells that prefer same/similar sound usually clustered 2gether

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92
Q

tinnitus cause/s

A

disease processes affecting cochlea or auditory nerve OR spontaneous activity (transient, e.g. cause of loud gig)

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93
Q

inner ear + balance

A
  1. spiral ganglion axons exit cochlea + converge w vestibular axons –>
  2. form vestibulocochlear nerve, which carries nerve impulses 4 balance + hearing frm ear 2 brain
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94
Q

where do spiral ganglion cells in vestibulocochlear nerve synapse on2?

A

once @ brain stem, spiral ganglion cells synapse on2 neurons in the cochlear nuclei (located @ level of lower pons/upper medulla)

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95
Q

auditory pathways described

A
  1. frm cochlear nuclei, auditory info ascends bilaterally 2 inferior colliculi
  2. neurons in inferior colliculi synapse on2 neurons in the medial geniculate nucleus (MGN) of thalamus
  3. MGN neurons synapse on neurons in primary auditory cortex (A1)
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96
Q

thalamus described

A

large structure connected 2 top of brain stem, contains MGN

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97
Q

A1/Heschl’s gyri

A
  1. 1st region of cortex 2 process sound, located in superior temporal lobe n buried w/in lateral sulcus
  2. A1 organised by tonotopic map (maintained frm cochlea)
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98
Q

interaural time def

A

difference in arrival time of a sound @ each ear, can b used 2 determine location

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99
Q

sound localisation along the vertical plane is… ?

A

Newt as good in humans

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100
Q

cochlear implants vs. regular hearing aids

A
  1. regular hearing aids amplify sound, cochlear implants have implanted electrodes (directly stimulate any functioning spiral ganglion cells w/in cochlea)
  2. cochlear implants have only abt 24 electrodes to replace 16k hair cells (not Great hearing experience)
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101
Q

do ur ears project auditory info in2 one or 2 hemispheres?

A

both, so still receive info even w damage to one ear

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102
Q

success of vision depends on which factors (broad)?

A
  1. localisation of light reflected off of distant objects
  2. object identification based on size, shape, colour, past experience
  3. movement detection
  4. compensation 4 changes in lighting conditions
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103
Q

pupil

A

opening that allows light 2 enter eye + reach retina (focuses light)

104
Q

iris

A

circular muscle that controls size of pupil

105
Q

cornea

A

transparent surface covering pupil + iris

106
Q

sclera

A

eye white, continuous w cornea

107
Q

lens

A

helps focus rays of light on2 retina

108
Q

retina (basic overview + flow of visual info within it)

A
  1. rear 2/3s of eye, converts images into electrical impulses (then sent 2 brain)
  2. Flow of visual info in the retina: photoreceptors → bipolar cells → retinal ganglion cells (their axons carry info frm eye 2 brain)
109
Q

macula

A

central area of retina around fovea specialised 4 central vision

110
Q

fovea

A

midpoint of retina, visual info received by fovea is the least distorted

111
Q

optic nerve

A

consists of retinal ganglion axons, carries impulses 4 vision frm retina 2 brain

112
Q

muscle of the eye - describe

A

have 3 pairs of extra ocular muscles inserted in2 sclera, enable eye 2 move

113
Q

what light waves can humans see

A

between 400-700nm

114
Q

receptors of vision (broad)

A
  1. millions of photoreceptors in back of retina, two types: rods + cones
  2. on one end of both rods n cones is photopigment that absorbs light energy –> excites cell –> cell transmits info on2 bipolar cells
115
Q

rods (properly)

A
  1. 4 low light levels (approx. 1k x more sensitive to light than cones)
  2. no colour vision
  3. rod-shaped
116
Q

what do we primarily rely on 4 vision + why

A

centre of vision - has higher concentration of cones

117
Q

does the peripheral retina have more rods or cones

A

more rods

118
Q

cones (properly)

A

better for higher light levels, gives colour vision

119
Q

what determines cone type

A

photopigment sensitivity 2 certain wavelengths

120
Q

what r the 3 types of cones

A

blue, red, n green

121
Q

structure of a cone

A

photopigment –> cell body –> synaptic terminals

122
Q

what abt the photopigment in rods?

A

they have one type of photopigment w one sensitivity

123
Q

how does light cum thru eye - not frm fovea

A

light cums thru pupil, projects 2 retina
–> light has 2 make its way thru other cells to get 2 photopigment (visual info gets a lil distorted)

124
Q

how does light cum thru eye (fovea n macular region)

A

cellular processes (like RG cells) r pushed aside, light arrives 2 photoreceptors less distorted

125
Q

organisation of like, the internal eye (photoreceptors etc)

A

nerve fibres –> ganglion cells –> bipolar cells –> photoreceptors

126
Q

blind spot … explained…..

A

where axons of RG cells exit the retina, there r no photoreceptors (no visual experience) - but we dont notice cause brain fills in visual info

127
Q

what is the optic nerve (simple)

A

RG axons sending info 2 brain, located @ optic disk

128
Q

what does a lack of blood vessels in macular region mean 4 vision there

A

better vision (less clutter?)

129
Q

nasal vs. temporal hemiretina

A
  1. nasal = closer 2 ur nose
  2. temporal = other hemiretina/closer to ur Temple
130
Q

why does blind spot affect temporal hemifield

A

cause optic nerve fibres exit eye via nasal hemiretina

131
Q

when do RG axons in the nasal hemiretinas cross over

A

@ the optic chiasm

132
Q

do RG axons frm the temporal hemiretinas cross over

A

they do Nawt,,, so after optic chiasm, u end up w everything frm left hemifield on right side of brain n everything frm the right hemifield on the left

133
Q

when does optic nerve become optic tract (now in CNS)

A

after optic chiasm….

134
Q

what happens 2 vision if left optic nerve is cut

A

vision frm left eye will b lost completely, resulting in loss of left peripheral vision

135
Q

what happens if optic chiasm cut/transected (affecting nasal hemiretinas)

A

peripheral vision lost bilaterally

136
Q

what happens if left optic tract cut

A

lose all right hemifield vision

137
Q

what is superior colliculus called in non-mammalian vertebrates

A

optic tectum

138
Q

what is the subcortical visual pathway

A

the retinotectal pathway…. tectum = superior colliculus

139
Q

describe retinotectal pathway (simple)

A

retina projects 2 superior colliculus

140
Q

describe the retinotopic map of superior colliculi in the retinotectal pathway

A
  1. each superior colliculus has a map of opposite/contralateral hemifield
  2. retinotopic map is distorted, w more neurons devoted 2 analysis of central visual field
141
Q

what percentage of RG axons project via the retinotectal pathway

A

abt 10%

142
Q

what is the cortical vision pathway (simple)

A

retinogeniculostriate pathway… retina –> thalamus (lateral geniculate nucleus) –> V1/striate

143
Q

what percentage of RG axons project via retinogeniculostriate pathway

A

abt 90%

144
Q

overview of V1/striate cortex/area 17

A
  1. receives visual input thru thalamus
  2. 1st region of cortex 2 process visual info, has complete map of retina
  3. located in medial part of occipital lobe + buried w/ in the calcarine fissure
145
Q

describe the retinogeniculostriate pathway (more in-depth)

A

each LGN receives info abt contralateral hemifield, contains visual maps –> project axons (optic radiation) 2 V1 (where there’s another retinotopic map of contralateral hemifield)

146
Q

describe: study revealing V1 topography

A

injected monkey w radioactive agent while looking @ display (V1 cells firing wld be stained by agent) –> showed that display was in fact preserved

147
Q

what happens when TMS placed over occipital cortex (broad)

A

light sensations elicited (phosphenes) even when no visual stimuli
2. When placed over the occipital cortex, TMS elicits light sensations (phosphenes) in the absence of any visual stimuli
Minimum TMS intensity 2 evoke phosphenes is referred to as the ‘phosphene threshold’
Reduced phosphene threshold reflects increased visual cortex excitability; increased phosphene threshold reflects reduced visual cortex excitability

148
Q

phosphene threshold explained

A
  1. minimum TMS intensity 2 evoke phosphenes referred 2 as phosphene threshold
  2. reduced phosphene threshold = increased V1 excitability; increased = reduced V1 excitability
149
Q

ecstasy + V1 excitability (study)

A
  1. using excitatory TMs on ecstasy users
  2. comparing excitability of V1 4 users + non-users, hallucinators + non-hallucinators (w/ in ecstasy users)
    results: users had significantly lower phosphene threshold than controls, hallucinators also had lower threshold
150
Q

is sensory info integrated immediately or later

A

later- initially transmitted 2 unimodal areas of cortex, then goes 2 hetero/multi-modal regions of cortex for sensory integration

151
Q

give an example of where sensory integration might take place

A

for auditory info, inferior colliculi send info not only 2 MGN but Also superior colliculi (where visual n auditory info can b integrated)

152
Q

ventriloquist illusion explained

A

when speech appears t2 come frm puppet’s mouth this is due 2 the sound source being mislocalized 2wards a synchronous but spatially discrepant visual event

153
Q

where is Most sensory info relayed frm to the cortex

A

thalamus (LGN, MGN) –> cortex

154
Q

what side of ur body wld right hemisphere neurons in primary motor cortex represent

A

the left side !!

155
Q

response properties

A

what stimuli excite certain cells or neurons

156
Q

area MT in monkeys is what in humans..?

A

area V5

157
Q

pt.2 Macque monkey study: what did they do next?

A

once they discovered what direction of motion area MT neuron preferred, went w that + varied speed –> realised neurons also had speed preference

158
Q

single-cell recording in area MT (pt.1 study on Macaque monkeys)

A
  1. single-cell recording done while white bar passed thru neuron’s receptive field in varying directions (trying 2 understand motion/direction sensitivity)
    results: neuron fired more when bar moved downward 2wards the left, opposite movement elicited least activity
    –> area MT neurons sensitive 2 direction of motion
159
Q

how might u use PETs 2 investigate specialisation of function in V1

A

since PET measures regional cerebral blood flow, can identify which paths of brain r involved in the perception of certain visual stimuli

160
Q

using PETs 2 look @ which part of human brain is involved in colour processing (study)

A
  1. used abstract coloured scenes
  2. to remove background noise, activity elicited by abstract scene (grey) was subtracted by abstract scene (coloured)
    results: ventral area of extra striate cortex involved in colour processing
161
Q

subtraction method

A

results frm experimental condition - results frm control condition

162
Q

study: PET activation during visual stimulation (motion processing)
Participants shown moving display (black + white square patterns), 2 subtract noise showed stimuli not moving

A
  1. participants shown moving display (black n white square patterns)
  2. to remove noise showed stimuli not moving (subtraction method)
    results: dorsal area of extra striate cortex involved in motion processing
163
Q

what r the 2 main projection routes frm V1 to extrastriate visual cortex?

A
  1. dorsal (motion + location; ‘where’)
  2. ventral (processes detailed stimulus features + object identity; ‘what’)
164
Q

do the visual areas w/in extrastriate cortex contain maps of contralateral or ipsilateral hemifield?

A

contralateral !!!

165
Q

where is V4 located, what does it do

A

located along ventral stream, once thought 2 only b important 4 colour processing but actually important 4 form/shape processing 2

166
Q

where is V5 located, function

A

located along dorsal stream, selective 4 direction + speed of motion

167
Q

how much brain power goes in2 cortical vs. subcortical visual processing?

A

LOTS more 4 cortical

168
Q

r subcortical pathways colour blind yes or no . AND did they evolve earlier than cortical

A

YES !! and yes (phylogenetically older)

169
Q

where r neurons that receive info frm RG cells located in the superior colliculi

A

superficial layers of superior colliculi

170
Q

what did Goldberg & Wurtz (1972) do/find

A
  1. mapped receptive fields of neurons in superficial layers of superior colliculi (monkeys)
  2. used single-cell recording
  3. found: superficial layers of superior colliculi provide retinotopic map, each representing contralateral hemifield
171
Q

what prompted the unilateral removal of visual cortex study

A

damaged cortical visual system in cat → cat cld no longer see contralaterally (cortically blind, specific 2 opposite hemifield)

172
Q

what did unilateral removal of visual cortex study do/find

A
  1. by removing contralesional superior colliculus OR cutting fibres connecting superior colliculi, inhibitory fibres of superior colliculus wiped out → visual orienting returns
  2. known as Sprague Effect
173
Q

why were subcortical visual pathways initially unable 2 compensate 4 damaged cortical visual system ?

A

bc ipsilateral superior colliculus needed 2 b released frm normal inhibition - which wld disinhibit subcortical pathway on side of cortical damage

174
Q

explain Sprague Effect- why does it happen

A

results frm cutting inhibitory fibres that originate in another nearby structure + project 2 the ipsilateral (2 the cortical lesion) superior colliculus

175
Q

study comparing effects of disrupting cortical vs. subcortical vision (rodents)

A
  1. group 1: bilateral removal of visual cortex
    group 2: bilateral disruption of retinotectal pathway
  2. findings (localisation): rodents w cortical damage unimpaired, subcortical damage impaired
  3. soooo subcortical visual system important 4 base visual orienting + cortical more useful 4 complex stuff
176
Q

define double dissociation

A

groups have opposite pattern of results 4 same set of tasks

177
Q

how might u assess the contribution subcortical visual pathways (in the absence of cortical pathways) in humans?

A

by looking @ victims of stroke involving V1

178
Q

perimetry testing

A

have patient fixate on centre, present light in diff positions + position says ‘yes’ until they can no longer see it
–>
maps out blind spot (scotoma)

179
Q

what causes contralesional hemianopia

A

unilateral v1 damage

180
Q

residual vision w/out V1? (Weiskrantz, 1986)

A
  1. used task that (unlike perimetry testing) didn’t require explicit report - instead tapped in2 patient’s implicit knowledge of their hemianopia field
  2. had patients w right V1 damage (left hemifield blindness)
  3. spot of light presented (don’t see it), then instructed 2 look 2ward where light was when tone sounds
  4. found: when spot of light appeared up to 20 degrees in2 blind field, responses were highly correlated w position of light (blindsight)
181
Q

what might b responsible 4 blindsight Weiskrantz’s study

A

since V1 wiped out, subcortical visual pathways may have been responsible 4 blindsight

182
Q

residual vision w/out V1 (2nd experiment, Rafal 1990)

A
  1. measured how quickly hemianopia patients patients cld look @ stimulus presented in their intact hemifield, depending on presence of irrelevant stimulus (distractor) in their blind spot
  2. results: eyes moved slower w presence of distractor in blind spot → can b explained by competing activation frm the distractor via the retinotectal pathway (subcortical visual system)
183
Q

what is electromyography (EMG) + when might it pick up smth

A

picks up electrical activity associated w muscle activity (e.g. when eyes moved)

184
Q

what is electrooculography (EOG) + when might it pick up smth

A

picks up electrical activity w moving eyes (finds neurons firing prior 2 + during eye movement)

185
Q

what is the implication of being able 2 move ur eyes in pure darkness

A

since ur without visual stimulation in this situation, means u have some pure motor cells here (in the deeper superior colliculus layers)

186
Q

do neurons in deeper layers of SC have a movement field (part of visual field that the eyes move 2 in response 2 cell activity; ‘motor map’)

A

yes, they have large movement fields
–> meaning each cell fires b4 a wide range of saccades (altho most intensely b4 saccades of their most preferred direction + amplitude)

187
Q

movement fields of SC neurons code 4 eye movements in2 the contralateral hemifield. yes or no?

A

yes

188
Q

movement fields tend 2 code 4 eye movements in2 the same area of visual field represented by the retinotopically organised visual receptive field of the neurons in the superficial SC layers. T or F?

A

True

189
Q

how might u determine the movement field of a neutron in deeper SC layers?

A

thru electrical stimulation- wld evoke saccade in2 the movement field of the stimulated neurons

190
Q

@ upper part of SC, have 0 amplitude movement (eyes dont move) → as u move down (rostral to caudal), get higher + higher amplitude. T or F?

A

True

191
Q

reflexive saccade

A

rlly fast eye movement

192
Q

effects of unilateral (right, in this case) SC damage on reflexive saccades in humans (study)

A
  1. latencies of reflexive eye movements were recorded
  2. found: contralesional saccades were delayed (when stimulus appeared opposite damaged SC) → SC helps 2 generate reflexive saccades 2wards stimuli that appear in the contralateral hemifield
193
Q

how does a sudden change in visual periphery trigger a reflexive saccade?

A

visual info projects thru the retinotectal pathway to the SC → motor related activity in the SC then causes the eyes 2 rotate until the location of the visual change projects onto fovea

194
Q

what r reflexive eye movements also referred to/why

A

exogenous eye movements - driven by external stimuli

195
Q

where r the smallest saccades represented in the SC

A

smallest = rostral SC; largest = caudal SC

196
Q

explain what fixation cells r

A
  1. when stimulus is present @ fixation point, cells in rostral portion of the superior colliculus r activated
  2. when fixation point disappears, firing rate of these cells declines –> they r fixation cells (underlie fixation reflex)
197
Q

fixation reflex (simple def)

A

triggered by external visual stimulus projecting on2 central vision

198
Q

difference between reflexive saccades + fixation reflex

A
  1. reflexive saccades help our eyes move in order 2 foveate a sudden change in the visual periphery, while fixation reflex helps eyes maintain their position
  2. ALSO, rostral cells + saccade cells inhibit each other (opponent processes)
199
Q

how might u look @ the opponent process nature of the reflexive saccades + the fixation reflex

A

fixation offset effect paradigm

200
Q

fixation offset effect paradigm (study)

A
  1. 2 conditions: fixation overlap (fixation dot + peripheral stimulus present @ same time), fixation offset (fixation stimulus disappears when peripheral stimulus appears)
  2. looking @ which condition will result in faster eye movement 2ward peripheral stimulus
  3. results: fixation offset faster
201
Q

why is the fixation offset condition faster 4 eye movement 2ward peripheral stimulus?

A

cause when fixation stimulus disappears, fixation cell activity drops –> increased activity of saccade cells (less inhibition)

202
Q

what’s the fixation offset effect formula

A

RT on overlap trials - RT on offset trials

203
Q

what does FOE give measure of

A

how responsive ur fixation reflex is
–> large FOE indicates strong fixation reflex, small FOE = weak fixation reflex

204
Q

FOE in young adults (result of 1 study)

A

20ms

205
Q

what r endogenous eye movements

A

voluntary eye movements ! u don’t need external prompting

206
Q

endogenous eye movement task

A
  1. fixate on centre until arrowhead appears
  2. move eyes 2 direction that arrowhead points
  3. after each response, turn eyes 2 centre + wait 4 next arrowhead
207
Q

what were Ro et al. (1997) looking @

A

looking @ the contribution of the superior prefrontal cortex (SPFC) + superior parietal lobule (SPL) in generating voluntary + visually guided (exogenous) saccades

208
Q

Ro et al. (1997): method + findings

A
  1. each ‘go’ signal presented w a TMS pulse (inhibitory - slowing down eye movements)
  2. TMS coil placed over either SPFC or SPL
  3. results: no effects, except when TMS was over SPFC 4 endogenous eye movements directed contralaterally
209
Q

what was hypothesised frm the results of Ro et al. (1997)

A
  1. was hypothesised 2 b a consequence of disrupting the normal operation of the frontal eye field (FEF)
  2. however, still cannot b certain that TMS pulse disrupted FEF activity → need more experimentation
210
Q

effects of a lesion involving the FEF on voluntary saccades (Henik et al., 1994)

A
  1. experimental group all had damage to one FEF
  2. results: patients w a FEF lesion had delayed voluntary saccades 2ward contralesional hemifield
    –> FEF normally involved in generating voluntary saccades
211
Q

do Henik et al. (1994)’s findings support Ro et al. (1997)’s theory

A

yes, they support his theory that delayed contralateral endogenous saccades caused by TMS over SPFC were a consequence of disrupting the normal FEF operation

212
Q

exogenous vs. endogenous eye movements

A
  1. exogenous eye movements depend more on subcortical structures, endogenous eye movements depend more on cortical structures
    –>
    FEF (cortical) receives info indirectly, has less direct projections down → so, reflexive faster (require fewer neural connections since less processing required)
213
Q

what sort of structures r babies believed 2 have @ birth?

A
  1. mature subcortical structures, but not fully developed cerebral cortex (cortical systems)
214
Q

FOE experiment (Hood & Atkinson, 1993) - most important findings

A
  1. results: compared 2 older infants, 1.5-month-olds have slower responses on fixation overlap trials
    → fixation reflex stronger in 1.5-month-olds
  2. so: maturation of cortex in older babies may have given them more control over fixation reflex
    –> more specifically, maturation of cortico-subcortical pathways might b behind shift frm predominantly exogenously controlled orienting (in 1.5mos) 2 increasing endogenous control (in older babies)
215
Q

@ how many months of age did Hood & Atkinson (1993) find infants 2 exhibit prolonged periods of fixation w some apparent difficulty in looking away frm fixated stimuli

A

abt 1-2 months of age

216
Q

why might newborns exhibit a poverty of strategic behaviours (instead controlled largely by external stimuli)

A

immaturity of the frontal cortex -
frontal lobe not developed until 15-20yrs, performance on tasks requiring strategic control may continue 2 develop thru 20s

217
Q

anti-saccade task

A
  1. fixate on centre, when stimulus appears look away frm it (this requires inhibition of a reflexive saccade, followed by execution of a voluntary saccade)
  2. performance assessed by: errors in the direction of the saccade (i.e. erroneous reflexive eye movements) + RTs (4 correct responses only)
  3. abnormally slow RTs suggest struggle imposing voluntary control (including over reflexive behaviours), high percentage of reflexive eye movements also suggest difficulty imposing voluntary control over them
218
Q

age-related performance on anti-saccade task (Fischer et al., 1997)

A
  1. participants aged 9-20
  2. youngest children making Lots of reflexive errors (more than half of trials)
    –> between 9-15, rapid decrease in frequency of direction errors (60 → 22%)
    –>
    RTs also decreased
219
Q

age-related performance on anti-saccade task (Munoz et al., 1998)

A
  1. starting frm 5 years old
  2. results:
    -dramatic improvement in the performance of anti-saccades between the ages of 5-15 years
    -children aged 5-8 had most direction errors (erroneous reflexive saccades)
220
Q

effects of lesion involving the FEF on anti-saccades (Machado et al., 2004)

A
  1. damage 2 one FEF
  2. anti-saccade task, measured variable was percentage direction errors
  3. results: had most difficulty when contralateral damage 2 stimulus presentation
    (difficulty imposing voluntary control over reflexive eye movements)
221
Q

what hypothesis do Machado et al. (2004)’s results support? n what does this mean

A

hypothesis that the FEF normally imposes inhibitory control over ipsilesional circuitry that generates reflexive saccades
–> so:
difficulty in inhibiting contralesional reflexive eye movements in patients w unilateral lesion involving the FEF cld reflect impaired modulation of activity in ipsilesional SC

222
Q

which hemifield does each SC control reflexive eye movements towards

A

each SC controls reflexive eye movements 2ward contralateral (opposite) hemifield

223
Q

after receiving info frm the retina, where does the SC project to?

A

projects 2 the saccade generators (SGs) in brain stem

224
Q

how does the FEF receive info + where does it project 2

A

receives info indirectly, also projects down 2 SGs

225
Q

where is FEF located

A

@ intersection of the superior frontal sulcus + precentral sulcus

226
Q

do younger or older adults have less anti-saccade direction errors

A

young adults have less direction errors, smaller RTs too

227
Q

frog brain has high proportion of subcortical neurons . is it more reflexive or endogenous in eye movements

A

reflexivee

228
Q

what is an example of an exogenous attention task (hint: suns)

A

find the red sun amongst the green ones !

229
Q

example of endogenous attention task (hint: also suns)

A

find red sun- but amongst not only green colours, but also red (have to use strategy, not reacting reflexively)

230
Q

overt vs. covert shifts in attention

A
  1. overt - movement of eyes 2 shift attention
  2. covert - eyes dont move, but attention still shifts
231
Q

ERP experiment in healthy adults

A
  1. looking @ activity in occipital lobe when stimulus appears in place participant is paying covert attention 2 (attention is directed voluntarily here) vs. in place where they r Not
  2. results: stronger neuronal signal occurred in response 2 stimulus when attention was directed there
    →
    selective attention 2 one part of visual field means neglect of other parts
232
Q

r SC important 4 exogenous or endogenous shifts in attention

A

exogenous !!

233
Q

what is true 4 results of both endogenous + exogenous attention tasks?

A

attention facilitates response (can respond more quickly)

234
Q

what happens when u have an exogenous cue followed by a long delay?

A

after abt a second, actually respond slower - disadvantageous to have had attention drawn there
–>
a.k.a. inhibition of return = if ur attention is drawn somewhere + nothing happens, ur visual system inhibits attention in the future

235
Q

is stronger or weaker inhibition of return (IOR) associated w better driving performance

A

stronger!!

236
Q

when does the formation of CNS occur

A

during prenatal development

237
Q

purpose of Flanker Task ?

A

2 assess efficacy of strategic control over attention (i.e., how easily distracted the participant is)

238
Q

describe what happens during Flanker Task

A
  1. maintain fixation on screen centre
  2. when stimulus appears @ centre, indicate its identity by pressing the appropriate button ASAP
  3. 2 conditions: incongruent (participant is supposed 2 click ‘k’, but there’s an ‘s’ where ur not supposed 2 b paying attention; congruent (distractor is of the same letter as stimulus u shld b focusing on)
239
Q

what is the Flanker Effect

A

RTs on incongruent trials minus RTs on congruent trials

240
Q

what does the Flanker Task find 4 young vs. older adults

A
  1. younger adults slowed down by 23ms w distractor
  2. older adults slowed down much more (larger Flanker Effect), ageing associated w worse driving performance
    →
    according 2 these findings, cld b bc more easily distracted
241
Q

what r the 3 main steps of brain development (just naming, not describing)

A
  1. cell division
  2. cell migration
  3. cell differentiation
242
Q

outline cell division

A
  1. stem cells in CNS divide in2 two cells
  2. after dividing, newly divided cell migrates 2 take up position in cortex + stem cell remains 2 undergo more divisions
  3. stem cells divide until all the neurons of the cortex have been generated
243
Q

outline cell migration

A
  1. new cell migrates by slithering along thin fibres that radiate 2ward brain surface
  2. cortical layers formed frm the inside out
244
Q

once cells r in proper place, differentiation occurs. describe this .

A

process by which the newly divided cells take on the appearance + characteristics of a neuron or glial cell

245
Q

what does neural plasticity refer 2

A

ability of nervous system 2 change

246
Q

how does the level of overlap in the neural projections frm the eyes progress frm birth 2 some months of sensory experience

A

@ birth projections r quite overlapped, but later become more separated

247
Q

ocular dominance columns def:

A

stripes of neurons in the visual cortex that respond preferentially 2 input frm a certain eye

248
Q

describe formation of ocular dominance columns in V1

A
  1. @ birth, input frm the LGN representing both eyes r mixed in V1
  2. w early postnatal development, the input frm the eyes segregates in2 ocular dominance columns
249
Q

what happens if you surgically rewire the brain 2 direct visual input 2 the auditory system? (von Melchner et al., 2000)

A
  1. looking @ newborn ferrets
  2. rewired hemisphere so that it went: retina → medial geniculate nucleus (MGN) → A1
  3. results: once adults, A1 neurons in the rewired hemisphere behaved like visual neurons in response 2 visual stimuli (e.g. had retinotopic organisation) AND when they disrupted cortical visual pathway thru lesioning, ferrets cld still see !!
250
Q

effects of stimulating visual cortex in adults w impaired vision (study)

A
  1. all participants had visual impaired due 2 damage b4 LGN
  2. measure: self-reported experience of phosphenes elicited by TMS over visual cortex (did u experience light flash)
  3. results: ppl w least impairment all experienced light flash, 60% who had poor residual vision, 20% w no residual vision
251
Q

what do the results of the ‘stimulating visual cortex in adults w impaired vision’ study indicate

A

effect of activating visual cortex is altered in ppl w severe visual impairment

252
Q

which brain structure is activated during mental imagery in sighted versus congenitally-blind adults? (study)

A
  1. participants either blind frm birth or sighted + blindfolded
  2. measures: looked @ brain activity using fMRI during passive listening 2 abstract words + subtracted that frm brain activity during mental imagery task
  3. results: both groups showed V1 activation
253
Q

what is an example of functional plasticity in A1 (monkeys)

A

training monkeys 2 discriminate specific tone frequencies leads 2 enlargement of the cortical regions where the trained frequencies r represented

254
Q

describe a study that demonstrates the plasticity of human primary motor cortex (M1)

A
  1. participants used non-dominant hand 2 perform finger to thumb tapping sequence
  2. two conditions: practised vs. unpractised sequences
  3. fMRI used 2 measure M1 blood flow under the respective conditions
  4. results:
    - 3 wks practise: there were greater changes in blood flow in the contralateral M1 4 practised sequences (as compared 2 unpractised)
    - 8 wks after final training: greater changes persisted in the contralateral M1 4 practised sequences
255
Q

what happens when u have less plasticity of brain + atrophy

A

ur memory function declines! which has been connected 2 age-related reductions in size of hippocampus

256
Q

ageing brain + aerobic exercise (study)

A
  1. lasted over 1 yr, assigned 2 aerobic exercise or stretching
  2. results: engagement in aerobic exercise can increase hippocampus size, improve accuracy of spatial memory

PSYC211 (5 decks)

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