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final exam Flashcards

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1
Q

Nuclear Magnetic Resonance

MRI

A

energy at specific radio frequencies is absorbed and reemitted by nuclei with non-zero spin
(electromagnetic energy but same concept as resonance)
w=yB
w=resonant (Larmor) frequency -> 85mHz typ.
y=gyromagnetic ratio
B=magnetic field strength

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2
Q

MRI signal

A

radio frequency pulse (at Larmor frequency to be absorbed by hydrogen in brain) goes into brain
excites atoms in brain and then energy is released

measures density of hydrogen atoms but pulse of certain freq. only absorbed by H atoms, measure how much is absorbed then released again

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3
Q

Gradients to encode space

A
  • parts of brain have slightly different magnetic field strengths s
  • resonance frequency for hydrogen will be different due to magnetic field

Encodes energy using frequency and phase (3 gradients to get separate measurements to create 3D image)

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4
Q

K space

A

represents density of hydrogen but changes timing to measure other things
records how much energy comes out of brain in each point in time during recording

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5
Q

convert k-space to real space

A

2D Fourier transformation (mathematical)
information needs to be decoded
different parts of brain represented by different frequencies and phases

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6
Q

Blood oxygenation level dependent (BOLD) contrast

A

key to fMRI
oxygenation of blood gives hint of how active areas of brain are
- cells require energy source when metabolically active so they use up oxygen and other resources provided by blood

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7
Q

Oxygenated hemoglobin

A

diamagnetic
zero magnetic moment
–> has iron in it, one of the more magnetically active elements

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8
Q

Deoxygenated hemoglobin

A

paramagnetic
significant magnetic moment
greater magnetic susceptibility
- causes faster T2 decay

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9
Q

timing from hemoglobin

A

spike of oxygenated blood rushes in to sweep away deoxygenated hemoglobin
(deoxygenated from active use)
this dip in deoxygenated blood (from replacement) takes about 6s and the response is much more spread out in time
*fMRI does not have very good temporal resolution (cannot see direct neural activity but slower smeared out response for circulatory system)

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10
Q

fMRI data

A

subjects –> run (sequence on trials and tasks) –> volume (allows to measure where changes happen) –> slices –> voxel

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11
Q

fMRI signal/data

A

in order to collect frames every 2 seconds, resolution is sacrificed
images are a lot blurrier for fMRI for quick image collection
doesn’t affect too much cause changes are what are being recorded (local areas serviced by certain blood vessels)
BOLD signal is really weak, most of signal is structure but BOLD changes sit on top of main structural signal

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12
Q

fMRI data preprocessing

A

1) slice timing correction
2) realignment
3) coregistration
4) normalization
5) smoothing

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13
Q

Slice timing correction

A

data collected slice by slice and it takes time to collect each slice so the time you collected data at the bottom is different from the top
takes 2 seconds to do whole brain
**data has to be interpolated

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14
Q

Realignment

A

cant assume a voxel equals same bit of brain across time (think small movements, few mms make a difference)
typical
- tries to correct for translations and rotations of the brain
uses 6 parameter rigid body transformation (3 translations 3 rotations)

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15
Q

Reslicing

A

after realignment, need to replace to match up voxels

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16
Q

Coregistration

A

align function images to structural image
- uses an affine transformation (translation, rotation, scale, shear)
collects functional and also clear structural images but using different techniques to make them comparable

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17
Q

Normalisation

A

warp each subject’s brain into a standard space using deformations by linear combination of smooth basis functions
- every brain is a snowflake but there is a standard brain other images are matched up with
segments into grey matter, white matter and CSF using tissue probability maps and Bayesian estimation

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18
Q

Smoothing

A

deals with remaining inconsistencies by smoothing/blurring images

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19
Q

Blocked design

A

trials are grouped into blocks
hemodynamic response is estimated per block
e.g. testing reactions to faces, first test response to fearful faces, then happy, then neutral

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20
Q

Event-related design

A

mix different trial types together and show them in random sequence
uses jittering between conditions
neural activity to each one of the trials will highly overlap with response to other trials (try to control for with jittering)

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21
Q

Mixed design

A

blocks of separated conditions within which there are separated temporally jittered events of interest

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22
Q

Mass-univariate general linear model (GLM) analysis

A

univariate analysis of each voxel but for every voxel

  • data collected from each voxel in brain over time
  • predicted time course for activity related to each event/condition of interest (try to explain data in terms of what’s going on in the experiment)
  • look at what was recorded in brain for each voxel and look at pattern of activity for what voxels respond to
  • estimates are made for how much each event contributes to signal in each voxel
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23
Q

Familywise error rate (FWE)

correction for multiple comparisons

A

family-wise error correction gets rid of false positives but also gets rid of most of the signal

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24
Q

False discovery rate (FDR)

correction for multiple comparisons

A

still has a pretty good job of detecting signal and getting rid of false positives (compromise)
e.g. 5% of active voxels are false positives instead of each test being 5% wrong

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25
Q

Long term memory (LTM)

A

processes by which information is encoded, stored and retrieved

  • encoded within connections between neurons, affected by how many connections, frequency, neurotransmitters, etc.
  • massive timescale (minutes, hours, days, years)
  • massive capacity (words, faces, events, skills, etc.)
  • common underlying representation (# and strength of synaptic connections)
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26
Q

Types of LTM

A

semantic
episodic
procedural

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27
Q

LTM processes

A

1) encoding
2) consolidation
3) storage
4) retrieval
5) ~~ reconsolidation?

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28
Q

Encoding LTM

A

initial creation of memory traces in brain from incoming information

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29
Q

Consolidation LTM

A

continued organization and stabilization of memory traces over time

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30
Q

Storage LTM

A

retention of memory traces over time

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31
Q

Retrieval LTM

A

accessing/using stored information from memory traces

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32
Q

Reconsolidation LTM

A

possible reorganization and re-stabilization of memory traces after retrieval

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33
Q

Episodic memory

A

events
specific personal experiences from a particular time and place
- medial temporal love, middle diencephalon, neocortex

subset of declarative/explicit memory (LTM)

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34
Q

Semantic memory

A 
facts
world knowledge
object knowledge
language knowledge
conceptual priming
middle temporal lobe, middle diencephalon, neocortex

subset of declarative/explicit memory (LTM)

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35
Q

Procedural memory

A

skills (motor and cognitive)
basal ganglia
skeletal muscle
subset of non declarative (implicit) memory

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36
Q

Recognition memory paradigm

A

Study phase presents words, images, pairs, etc.
Delay is active or passive
test phase presents test items and response = “old” or “new” item
sometimes asks for confidence, “remember vs. know” etc.

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37
Q

Recollection (remember)

A

conscious memory for seeing the item during study phase

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38
Q

familiarity (know)

A

intuitive feeling of having recently encountered the item

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39
Q

DRM paradigm

A

Deese, Roediger, McDermott
present list of semantically related words
recognition memory test
- words on list
- unrelated distractors
- semantically-related distractors (lures)
lures are not on the list but similar in meaning which are the ones we incorrectly remember as being on the list

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40
Q

DRM paradigm

false memories for lures

A

lures affirmed almost as often as words actually on the list
high confidence in accuracy if assessed
high level of “remembering”
happens even if informed about effect

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41
Q

Implications from DRM

A

memory is not replayed like a video but reconstructed based on multiple pieces of information

  • what actually happened
  • one’s knowledge, experience and expectations

*false memories are possible, likely and vivid in right circumstances

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42
Q

Cabeza et al. 2001 study

A

18 thematic and categorical 14 word lists
thematic: water, ice, dark, wet, freeze
categorial: cucumber, pea, potato, onion, corn
words presented every 2s with interval of several seconds between lists
participants instructed to remember words and who presented them

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43
Q

Cabeza et al. 2001 study

task/test phase

A

Recognition tested
- each word presented for 3s
- old vs. new judgment with button press
- 9.5 second pause before next trial (SLOW EVENT RELATED DESIGN)
-for each list: 1 old, 1 lure (often answered as old but should be new), 1 unrelated word
6 blocks of 6 lists each –> 36 old words, 36 lures, 36 unrelated new words

Asked whether female or male presented the word

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44
Q

Cabeza

Bilateral (anterior) hippocampal regions

A

activation for lures is almost the same as activation for true words
the brain gets fooled by lures

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45
Q

Cabeza study

Left posterior parahippocampal region

A

in this brain region, lures do not look like true memories but new items

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46
Q

Cabeza conclusions

A

Left posterior parahippocampal region
- memory for sensory information (new items, thinking at a lower level and more sensory focused)
Bilateral hippocampal regions
- memory for semantic information = incorrectly thinking lures were on list

True memories activate both
false activate hippocampal but not parahippocampal
new memories activated neither
Lure items = no memory for sensory information but for semantic

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47
Q

Broca

A

1861

  • patient w/ lesion of Inferior frontal gyrus
  • deficit of speech production
  • damage to Broca’s area leads to Broca’s aphasia
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48
Q

Wernicke

A

1874

  • patients w/ damage to superior temporal gyrus
  • deficit of speech comprehension
  • damage to Wernicke’s area leads to Wernicke’s aphasia
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49
Q

Aims of cognitive neuroscience

A

1) identify processes that underlie normal condition
2) to localize these processes to particular neural structures/systems

often uses brain damage and breakdown of function/behaviour

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50
Q

Lesion method

A

infer what mental process a brain area implements by observing what behavioural deficit a patient shows when that brain area is damaged

51
Q

Localization of function/modularity

A

each mental process is carried out by a particular part of the brain

52
Q

single case studies pros and cons

A

Pros:

  • one patient can be studied in great detail
  • allows the study of extremely rare conditions

Cons:
- the pattern observed for one individual may not be representative of people in general (e.g. can have an atypical brain)

53
Q

group studies pros and cons

A

Pros:

  • avoids conclusions based on a single patient
  • more generalizable to the population at large

Cons:

  • the group average may not reflect any particular patient
  • when it comes to brain damage, very particular so are you really studying multiple copies of the same thing or different brain damage
54
Q

Sources of brain damage

A

1) deprivation of oxygen and nutrients
2) damage mechanically (through or on skull)
3) subarachnoid hemorrhage (Leakage of blood from circ. system into brain)

55
Q

Deprivation of oxygen and nutrients

A

Ischemia: blood flow is cut off or restricted/tissues become oxygen and nutrient deprived (e.g. glucose)

  • deprivation +10 minutes = cell death
  • areas of dead tissue = lesion or infarct
56
Q

mechanical damage

A
  • blow to head or penetrating object (direct damage)
  • increase intracranial pressure (squashes cells)
  • surgical removal of brain tissue
57
Q

Subarachnoid hemorrhage

A

rupture of cerebral artery

  • can lead to ischemia
  • can result in subdural hematoma (blood clot on surface of brain which increase intracranial pressure)
  • blood can block drainage of CSF from the ventricles (increased intracranial pressure)
58
Q

Major causes of brain damage

A
  • head injuries
  • cerebrovascular causes
  • brain tumours
  • neurotoxins
  • neurological diseases
59
Q

Cerebral edema

A

Swelling

  • collection of fluid around damaged tissue
  • increased intracranial pressure (squashing)
60
Q

Thromobosis

A

Thrombosis is the formation of a blood clot, known as a thrombus, within a blood vessel. It prevents blood from flowing normally through the circulatory system

61
Q

Embolism

A

a blockage-causing piece of material formed, inside a blood vessel. Is formed elsewhere and moves through vessels and then gets blocked. The embolus may be a blood clot (thrombus), a fat globule (fat embolism), a bubble of air or other gas (gas embolism), or foreign material.

62
Q

Arteriosclerosis

A

thickening and hardening of artery walls (which can lead to blockages)

63
Q

Aneurysms

A

vascular dilations resulting from local defects in blood vessel elasticity

64
Q

Stroke

A

cerebral vascular accident

- sudden appearance of neurological symptoms as a result of sever interruption of blood flow

65
Q

Infarct

A

area of dead tissue resulting from an obstruction of blood vessels normally supplying the area (can be caused by a stroke)

66
Q

Tumour

A

mass of new tissue that persists and grows independently of its surrounding structures and has no physiological use

67
Q

Gliomas

A

arise from glial cells
brain tumour
typically an infiltrating tumour

68
Q

Meningiomas

A

growths attached to the meninges

brain tumour

69
Q

metastatic tumours

A

established by a transfer of tumour cells from elsewhere in the body

70
Q

Neurotoxins

A

often result in diffuse brain damage
some cause specific:
Alcohol - mammillary bodies (Korsakoff’s Amnesia)
MPTP (heroin related) - substantiated migra (Drug-Induced Parkinsonism)

71
Q

Single dissociation

A

Single: have 1 patient with some type of damage
Dissociation: perfomance differs (dissociates) across two tasks

72
Q

Double dissociation

A

Made of two single dissociations
Double: two patients with some type of damage
Dissociation: their performance differs (dissociates) across two tasks

73
Q

Issues with lesion method

A 
- preexisting patient variability
(age, Education, intelligence)
- variability of lesion
(location, size, etiology, accidents of nature not controlled experiments --> measurement not manipulation)
- poor temporal & spatial resolution
(permanent so part of task affected cant be determined, cant turn lesion on or off, compensation & cant measure single neuron  cause damage usually widespread)
- compensatory strategies
- fibres of passage could be damaged
74
Q

Wernicke-Lichteim-Geschwind model

A

theory/model of how language is implemented in the brain

- primarily based on lesion studies of aphasia

75
Q

Wernicke’s area

A

language perception (speech sounds)

76
Q

Arcuate fasciculus

A

fibre tract from wernicke’s area to Broca’s area

77
Q

Broca’s area

A

language production (speech actions)

78
Q

Angular gyrus

A

converts written words to spoken words

  • when we read text, there’s sort of an internal conversion and comprehension
  • links visual form to spoken form (internal dialogue)
79
Q

Spoken language perception

A
  • auditory sensory pathway
  • primary auditory cortex
  • Wernicke’s area
  • Higher-level cortex
80
Q

Written language perception

A
  • visual sensory pathway
  • primary visual cortex
  • secondary visual cortex
  • angular gyrus
  • Wernicke’s area
  • higher-level cortex
81
Q

Spontaneous spoken language production

A
  • higher level cortex
  • Wernicke’s area
  • arcuate fascicles
  • Broca’s area
  • primary motor cortex
82
Q

Repetition of speech

A
  • auditory sensory pathway
  • primary auditory cortex
  • Wernicke’s area
  • Arcuate fascicles
  • Broca’s area
  • Primary motor cortex
83
Q

APHASIA

A 
- impairment of language
Tested using multiple communication modalities --> not simply input/output pathway, must affect core aspects of language and is somewhat independent of solely motor or sensory pathways
- spoken language perception
- spoken language production
- written language perception
- written language production

**often caused by stoke, typically left side of brain (where language area usually located)

84
Q

Broca’s aphasia

A

Expressive aphasia, motor aphasia
*motor apparatus is fine but expression of words is difficult

Spontaneous speech: slow, laboured, nonfluent
- most difficult verbs, articles, pronouns
- makes sense but ungrammatical
- better fluency for memorized phrases, singing
Repetition: slow, laboured, nonfluent
Comprehension: relatively spared (aware of struggle/inability to articulate knowledge and aware of gap between what they want to say and what is being said
Writing: shows same errors as speech (production problem)

Impairment of grammar and hierarchy of language than production

85
Q

Wernicke’s aphasia

A

Receptive aphasia, sensory aphasia
Spontaneous speech: fluent, unlabored, prosodic, but relatively meaningless (and unaware of errors)
- words used inappropriately
- nonsense words (neologisms)
- roundabout expression of meaning (circumlocution)
Repetition: fluent, unlabored but w/ neologisms
Comprehension: severely impaired
Writing: shows same errors as speech
Impairment of comprehension rather than perception
–> problem is linking speech sounds to meaning, not perceiving the words

86
Q

Global aphasia

A 
Spontaneous speech: severely impaired
Repetition: severely impaired
Comprehension: severely impaired
Writing: severely impaired
Associated with damage to both areas
87
Q

Transcortical motor aphasia

A

Broca’s aphasia with intact sentence repetition

turning sounds into speech without needing to know what its about, then those pathways still intact

88
Q

Transcortical sensory aphasia

A

Wernicke’s aphasia w/ intact sentence repetition

89
Q

Mixed transcortical aphasia

A

global aphasia w/ intact sentence repetition

90
Q

Conduction aphasia

A

Spontaneous speech: relatively intact
- phonemic paraphasia–> (e.g. pants = splant, plants, plant, pants” or pretzel = trep, tretzle, trethle, tredfles) & conduit d’approche
Repetition: severely impaired
Comprehension: relatively intact
Writing: relatively intact
Associated with damage to ARCUATE FASCICULUS
* disputed cause fibres of passage damaged or something else?

91
Q

Anarthria/dysarthria

A

impaired speech production

- specific to speech and not local (control of vocal apparatus)

92
Q

Auditory verbal agnosia/pure word deafness

A

impaired speech perception

can still hear in general but have a specific problem hearing and recognizing spoken words

93
Q

Alexia/dyslexia

A

impaired reading

- visual comprehension

94
Q

agraphia/dysgraphia

A

impaired writing

95
Q

anomia/dysnomia

A

impaired naming

- not being able to name vs. difficulty naming but really just used interchangeably

96
Q

Apraxia of speech

A

motor difficulties with formation of words due to brain damage

Disorder in programming the speech musculature to produce correct sounds of words in the proper sequence with the appropriate timing

  • inconsistent articulatory errors
  • articulatory groping
  • disruption in prosody
  • disruption in rate of speech
  • *Not a perceptual problem
  • -> no difficulty perceiving or recognizing speech sounds, including their own articulatory errors
97
Q

Localization of speech articulation planning

A

the pre-central gyrus of the left insulated is necessary for the preliminary planning and initiation of articulatory movements

  • because left hemisphere stroke and for most right handed people have language on the left
  • insula mediates motor aspects of speech production (articulatory control)
98
Q

Goals of cognitive neuroscience

A
  • determine how the brain mediates cognition and behaviour

- relate neural structures to mental functions and behavioural acts

99
Q

Challenges of cog. neuro

A 
brain is massively complex
~100 billion neurons
~100 trillion synapses
The mind is not directly observable
behaviour is noisy, inconsistent, individualized, diverse
100
Q

Diffusor tensor imaging (DTI)

A

measuring fibre tracts between brain areas

101
Q

Positron emission tomography (PET)

A

e.g. using radio tracers to track dopamine distribution in the brain

102
Q

Magnetoencephalography (MEG)

A

imaging magnetic fields due to neural activity

103
Q

Functional near-infrared spectroscopy (fNIRS)

A

imaging hemodynamic response non-invasively

104
Q

Brainbow

A

imaging of individual neurons using genetic manipulation and fluorescent proteins

105
Q

optogenetics

A

genetic manipulation to allow use of light to switch neurons on and off

106
Q

Independent epistemic support

Benefits of converging methods

A

converging results support each of the converging techniques since its unlikely that by chance two different techniques that make different assumptions would produce convergent results

  • redundancy
  • replication
107
Q

Complementation

benefits of converging methods

A

“to obtain complementary information about the phenomenon under investigation”
integrating results from multiple techniques can give a better understanding of the relationship between neural structures and cognitive operations
- different perspectives
- new insight

108
Q

Decision making

A

selection of a brief or action (choice) among alternatives possibilities (options)
Choice = make a response or withhold a response (can be selecting from multiple options or not making a selection)
- requires integration and evaluation of multiple factors

109
Q

Decisions under certainty

A

each option has a sure known outcome

110
Q

Uncertainty

A 
lacking knowledge about what outcome will follow from a decision 
3 types:
- under risk
- under ambiguity
- under ignorance

*most decisions in life are more focused on ignorance and ambiguity and are made under partial ignorance

111
Q

Decision under risk

A

options are probabilistic, but all information (value and probability) is known

112
Q

Decision making under ambiguity

A

options are probabilistic, and either values or probabilities of an option are unknown

113
Q

Decision under ignorance

A

one of more options is unknown

114
Q

Preferences (stated vs. revealed)

A 
Stated = what they would prefer if given these options
Revealed = what do they prefer when given those options
115
Q

Normative/prescriptive model of decision making

A
  • describes how people “should” decide (in order to maximize wealth)
  • grounded in economic and statistical theory
Expected value (option I with j possible outcomes)
*people should make decisions based on expected values
116
Q

Prospect theory

A

Descriptive model of choice
- describes how people “do” decide
- grounded in observed behaviour
~relative decisions are not absolute

Key features:

  • objective values are transformed into subjective values (what would be the value or utility of outcome)
  • objective probabilities are transformed into subjective decision weights
  • options are evaluated based on a common reference point (e.g. what I have rn, what I want, need, etc.)
117
Q

Aversive stimuli

A

options involved increased risk or punishment

  • insular cortex (INS)
  • ventrolateral prefrontal cortex (vlPFC)
118
Q

Unexpected rewards

A

outcomes are better than expected

  • ventral striatum (STR)
  • medial prefrontal cortex (mPFC)
119
Q

Executive control

A

Top-down processed required for evaluation of uncertain choice options

  • dorsolateral prefrontal cortex (dLPFC)
  • posterior parietal cortex (PPC)
120
Q

Behavioural inhibition system

carver & white, 1994

A
  • sensitive to signals of punishment, non reward, and novelty
  • inhibits behaviour that may lead to negative or painful outcomes
  • responsible for experience of negative feelings such as fear, anxiety, frustration and sadness
121
Q

Behavioural approach/activation system (BAS)

A
  • sensitive to signals of reward, non punishment and escape from punishment
  • causes person to begin (or to increase) movements towards goals
  • responsible for experience of positive feelings such as hope, elation and happiness
122
Q

Stroop task model

Cohen, Dunbar & McClelland, 1990

A

neural network model

  • name ink colour or word
  • hard/slow: two competing responses

Requires top-down cognitive control to inhibit word reading/facilitate colour naming (or vice versa)

123
Q

Top down control

A
  • goal representations in dorsolateral prefrontal cortex (DLPFC) provide top-down biasing of perceptual-motor mappings
  • working memory provides the representation
  • inhibition is the resulting process

Cognitive control is not a set of independent faculties but an integrated system

124
Q

DLPFC

A

online maintenance and manipulation of information needed to guide goal-oriented
- top down influence of information on decision making behaviour

**right DLPFC needed for active suppression of option that appears seductive because of higher payoff (role in value based decision making)
direct evidence that free choice is implemented physically in the brain

Psych 351C (1 decks)

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