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PSYC513 Exam One- brain,language, communication, memory and knowledge > dissociations and FMRI(L1) - matt roser > Flashcards

dissociations and FMRI(L1) - matt roser Flashcards

1
Q

what do patient studies provide?

A

provides a major source of knowledge about brain and mind, can tell a lot about trauma, stroke, tumour, epilepsy.

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2
Q

what are some neuropsycholgocial deficits?

A

agnosia
aphasia
apraxia
amnesia
ataxia

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3
Q

what is agnosia?

A

loss of ability to recognize objects, people, sounds, shapes, or smells; that is, the inability to attach appropriate meaning to objective sense-data (“The man who mistook his wife for a hat”)

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4
Q

what is aphasia?

A

general term relating to a loss of language ability

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5
Q

what is apraxia?

A

a general term for disorders of action

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6
Q

what is amnesia?

A

lack of mnemonic abilities

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7
Q

what is prosopagnosia?

A

faceblindness

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8
Q

why is behavioural testing useful?

A

existence of selective deficits tell us about the way function is organised in the brain

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9
Q

what are the goals of behavioural testing?

A

the goals are to relate brain anatomy to behaviour and to investigate mental processes

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10
Q

what do the behavioural tests aim to do?

A

tell us what functions are compromised and spared

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11
Q

what is the sagital section?

A

front to back of brain

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12
Q

what is the coronal section?

A

left to right view of the brain

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13
Q

what is the lateral section?

A

top and bottom of the brain

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14
Q

how can cognitive functions be dissociated?

A

through selective impairment
-same for brain regions

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15
Q

what do dissociation studies require?

A

require a minimum of two groups and two tasks
-the comparison between groups show deficits

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16
Q

what is the main function of dissociation studies?

A

determine whether a deficit is specific to a particular function or reflects a more general impairment

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17
Q

what are brodmann areas?

A

pre central gyrus, primary motor area - area 4
inferior frontal gyrus, brocas area - area 44

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18
Q

what happens in single dissociation studies?

A
  • two conditions: temporal lobe and controls
    -measured declarative and non declarative memory
    -found that in a single dissociation study that temporal lobes are involved in declarative memory
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19
Q

what are limitations of single dissociations?

A

-possible that poor performance was caused by another factor such as deficit in concentration - the test of declarative memory required more concentration than our test of non declarative memory

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20
Q

what happens in double dissociation studies?

A

two regions of the brain are monitored as well as a control condition
-found that temporal lobes involved in declarative memory and cerebellum involved in nondeclarative memory

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21
Q

why are studies of double dissociations good?

A

-provide strong evidence that there are cognitive processes critical for task x and not y, vice versa
-evidence that observed differences in performance reflect functional differences between the groups

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22
Q

what did Gazzaniga et al, find?

A

-hypothetical results showing single and double dissociations between cognitive processes
-temporal love in signal dissociation 90% correct in recency and 70% familiarity memory and the frontal lobe is better at familiarity memory than recency memory

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23
Q

what are limitations of patient studies?

A

modularity is assumed
lesions are extensive and varied
lesion anatomy inaccurate, as connections not considered
poor temporal resolution

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24
Q

who proposed phrenology and what is it?

A

Sir Franz Joseph Gall
-created the phrenomotor to measure and create maps of faculties within the brain

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25
Q

what is the modularity of function?

A

assumes that mental processes occur with a high degree of isolation from other mental processes and when one area is damaged other regions do not adapt their function
-brain plasticity and neglects dynamics

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26
Q

what is brain plasticity?

A

intact regions in the brain change their behaviour so it is difficult to infer function of damaged region

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27
Q

what is meant by lesions are extensive and varied?

A

-patients who are studied often have large lesions -> often damage to several functions centres, less patients with pure deficits
-lesion size and location variable, hard to find a group of similar patients and inferences from individuals are weak

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28
Q

what is meant by the lesions anatomy innacurate?

A

Anatomical scans show regions that are destroyed, but intact regions may not be functioning

Regions may be disconnected from other regions that provide input

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29
Q

what is meant by individual differences in functional anatomy?

A

We assume that an anatomical region of the brain does the same function in all individuals

Clearly violated assumption – e.g. Wada test indicates left hemisphere predominates in language processing in most, but not all, individuals

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30
Q

what is meant by poor temporal resolution and experimental control?

A
  • not possible to infer the stages of processing

-A memory deficit may arise from a failure of encoding, retention or recall

-There is no experimental control over lesion location, but animal studies using experimental ablation can provide this

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31
Q

what are benefits of patient studies?

A

-show which areas are necessary for particular cognitive function -> double dissociation
-show cognitive, emotional and social consequences of a deficit
-cost & time effective

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32
Q

why can’t speech be localised in the broca’s area?

A

-damage is not limited by functional boundaries
-lesion might be smaller than functional module
-interindividual differences in brain organization
result might reflect increased vulnerability of region to injury (e.g. because of vasculature)
-Area might just be interconnected with the actually relevant area

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33
Q

what are lesion studies?

A

-observing lesion maps of those with lesions to explain differences In abilities

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34
Q

why are control groups important in lesion studies?

A

-so we can control for the effect of RH damage caused by blood supply, and contrast across the factor of Visual Field Deficits presence

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35
Q

what does FMRI stand for?

A

functional magnetic resonance imaging

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36
Q

what do the darker parts in FMRI scans represent?

A

historically showed brain structure and brain function

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37
Q

what is Magnetic Resonance Imaging Physics (MRI)?

A

Uses a magnetic field (Bo) and radio energy to produce an image

A large magnet (50,000 x Earth) aligns nuclei that have a net magnetic moment (from odd number of protons/neutrons) e.g. H2O

Nuclei absorb and re-emit radio frequency energy

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38
Q

how are MRI images acquired?

A

nuclei spin around the magnetic field
RF pulse (oscillating magnetic field) tips M out of alignment with Bo and synchronises the phase of spins
M gradually returns to alignment and spins lose phase coherence -> change detected as MRI signal

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39
Q

what is mapping lesions?

A

extension of mapping structure to function using the lesion maps to make complex patterns of Data intelligible

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40
Q

how is normal variability in structure mapped?

A

-second order structures like sulcal asymmetry
-colour coded maps for statistical significance of gyro/sulcal variability
-large numbers of neurologically normal participants

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41
Q

what is the basis of FMRI?

A

Blood Oxygen Level Dependent response

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42
Q

what is the BOLD response?

A
  • levels of de/oxyhaemoglobin change from regional cortical activity

Momentary decrease in blood oxygenation immediately after neural activity increases, known as the “initial dip” in the haemodynamic response function (HRF).

  • blood flow increases to a level which overcompensates for the increased demand. Regional blood oxygenation actually increases following neural activation.

The blood flow peaks after around 6 seconds and then falls back to baseline, often accompanied by a “post-stimulus undershoot”.
De/oxyhaemoglobin have different magnetic properties

Local field strength is affected by relative levels

This affects the local signal in the image.

Increased signal is obtained from ‘active’ regions.

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43
Q

what composes of experimental logic?

A

-cognitive subtraction originated with reaction time experiments
-measures the time for a process to occur by comparing two reaction times,
-given tasks
-what is the assumption of pure insertion- can insert a component process into a task w/o disrupting the other components but task difficulty may differ between conditions

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44
Q

how does block design fmri be experimented with?

A

-tasks are given with a rest in between of 30 seconds

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45
Q

how is event related fmri experimented with?

A

-condition one event and condition two events are introduced after one another as a sequence
-allows random presentation of stimuli and retrospective coding of events

46
Q

what are FMRI preprocesses and analysis techniques?

A

image data, anatomical reference, kernel, design matrix, contrasts

47
Q

how is the data modelled?

A

regress our model of our experiment against the signal-change data.

Least-squares best-fit analysis of the data that best estimates the amplitudes of the predictors (minimize residuals)

A T-test tests whether the slope of the function differs from 0 (i.e. flat)
This analysis is done independently at every voxel (3D pixel/volume)
- i.e. thousands of times!

Contrasts allow one to test for voxels where activation in one condition is greater than another.

Voxels with significant T statistics can then be coloured in according to the size of T

48
Q

what do the blobs on scans represent?

A

clusters of significant statistics for either a main effect or a contrast between two sets of regressors at each voxel
-shows areas where the signal chance was predicted by the model
-change in signal is due to regional hemodynamics and activations are distantly related to the underlying neurological events

49
Q

what has functional brain imaging told us?

A

Identified functional areas – e.g. Fusiform face area – stimuli; Anterior Cingulate - attention

Corroborated findings from other methods (e.g. hippocampal involvement in memory)

Allowed the localization of function from undamaged brains

Meta-analyses bring some order to the flood of data, but are these maps from
multiple different studies any more useful than the 1957 electrophysiology map (slide 10)?

50
Q

what are the new directions of brain imaging?

A

-Functional-connectivity analyses: calculate correlations between activations in different areas

-Dynamic causal modelling: explicit models of distributed networks are tested to see which best fits the observed data

51
Q

what does bistability allow for?

A

allows for dissociation of low level stimulation and awareness - the pattern itself does not change, but your awareness of it does!

52
Q

what did Goodale 1991 test?

A

Goodale et al 1991 tested an apperceptive agnostic patient, DF, who had difficulty reporting the orientation of simple lines or real objects

53
Q

what did Goodale 1991, conclude about DF?

A
  • asked her the orientation of narrow slot cut into face of a drum → unable to report angle and made errors but when asked to post a card through the slot she did it with accuracy
  • she struggle to hold the letter by her side and rotate it to match the angle of the slot → slot seemed less clear
  • strong evidence to suggest there are separate pathways for processing “what” and “where” a stimulus is to provide a visually guided action
  • DF has damage to the ventral visual pathway but intact processing in dorsal pathway
54
Q

how does James et al 2003 support goodale, 1991?

A

->supports the Goodale et alt claim of DF damage to ventral visual pathway: they propose that the dorsal system is not only responsible for processing “ where ” objects are but also “ how ” actions can be performed toward a particular object, such as pointing or reaching for that object.
-> visual processing in the dorsal system is not accessible to consciousness - the patient cannot report the orientation of the slot - yet the dorsal system can guide the right action.

55
Q

what are some exceptions to the pathway?

A

Patients with prosopagnosia are still able to recognize objects well but have great difficulty in recognizing or telling apart faces (Bodamer, 1947; Meadows, 1974b). Deficits can be severe; some prosopagnosic patients can no longer recognize close family members or friends and, instead, must rely on other cues such as the person ’s voice or clothing to recognize that person.

56
Q

what can prosopagnosia result from?

A

Prosopagnosia can result from bilateral damage around the regions of the lateral occipital cortex, the inferior temporal cortex, and the fusiform gyrus (Bouvier & Engel, 2006; Meadows, 1974b).
->In some cases, unilateral damage to the right hemisphere may lead to this impairment. Because lesions are usually quite large and might damage fiber tracts leading to a critical brain region, it is difficult to identify a precise site.

57
Q

what may hypnosis involve?

A

a dissociation between voluntary control (dorsolateral prefrontal cortexDL-PFC) and the ability to monitor errors(the ACC).

58
Q

what did Egner et al 2005 report?

A

an fMRI-EEG study of hypnosis in the Stroop task –> showing that “ hypnosis decouples cognitive control from confict monitoring processes of the frontal lobe.

59
Q

what have lesion studies of animals and human show us?

A

have provided a wealth of information about which visual areas are required to be intact for visual consciousness to arise

60
Q

what do different visual defects result from?

A

result from neural damage at different levels of the visual processing heirarchy, for example, damage to the retina or optic nerve of one eye can result in monocular blindness, the loss of sight from one eye

61
Q

what is achromatopsia associated with?

A

with lesions that include area V4 and possibly regions just anterior to area V4.
-> Damage to one hemisphere can even lead to selective loss of color perception in the contralateral visual field.

62
Q

what have monkey brain lesion studies implicated?

A

implicated the PFC, and the DLPFC, in particular, in WM function. With very precise techniques for localizing experimentally induced lesions, it has been shown that damage isolated specifically to the DLPFC is sufficient to impair performance on WM tasks (Fuster, 1997).

63
Q

how can lesions change over time?

A

brains can compensate for damage as lesions change over time as cells die and adaptation occurs → post mortem exams don’t reflect the injury at the time of diagnosis

64
Q

how can brain lesions be stimulated in healthy subjects?

A

by using magnetic pulses over the scalp can inhibit or excite a region of cortex.

65
Q

how did savoy, 2001 define brain mapping?

A

the attempt to specify in as much detail as possible the localisation of function in the human brain

66
Q

how did savoy 2001 define neuropsychology?

A

the science that attempts to understand the interactions between the nervous system and behaviour

67
Q

what did sperrys 1960 work reveal?

A

split-brain patients revealed that the left
hemisphere has superior language and arith-
metic skills, whereas the right hemisphere has
better spatial skills

68
Q

how has neuropsychology research refined understanding of how emotions are processed?

A

damage to the amygdala resulting in difficulty
in recognizing whether faces are expressing
fear
-> damage to the left insula and basal
ganglia leading to a selective difficulty in iden-
tifying disgust

69
Q

what are two types of MRIs?

A

T1 - weighted scans offer good contrast between grey and white matter and have superior spatial precision, T2 - weighted scans which highlight regions of damage, giving good pathological information

70
Q

what are limitations of MRIS?

A

fail to detect acute strokes, don’t show whether an area is functioning normally.

71
Q
A
72
Q

What is bistability in visual perception?

A

Bistability allows for dissociation of low level stimulation and awareness; the pattern itself does not change, but your awareness of it does.

73
Q

What is the phenomenon of multi-stable perception valued for?

A

It enables scientists to study changes in visual awareness of any changes in the visual stimulus.

74
Q

What does bistable patterns refer to?

A

Any pattern that primarily has only two primary interpretations.

75
Q

What occurs even when eyes are fixed on a certain point of a stimulus?

A

The image on retinas is constant over time but perception fluctuates.

76
Q

What did Goodale et al. (1991) discover about the patient DF?

A

DF had difficulty reporting the orientation of simple lines or real objects but could perform actions accurately.

77
Q

What was DF unable to do when asked about the orientation of a narrow slot?

A

She was unable to report the angle and made errors.

78
Q

What ability did DF demonstrate when asked to post a card through a slot?

A

She did it with accuracy.

79
Q

What strong evidence is suggested by DF’s case?

A

There are separate pathways for processing ‘what’ and ‘where’ a stimulus is to provide a visually guided action.

80
Q

What damage did DF have in her visual pathways?

A

DF had damage to the ventral visual pathway but intact processing in the dorsal pathway.

81
Q

What do James et al. (2003) propose about the dorsal system?

A

The dorsal system is responsible for processing ‘where’ objects are and ‘how’ actions can be performed toward a particular object.

82
Q

Is visual processing in the dorsal system accessible to consciousness?

A

No, it is not accessible to consciousness.

83
Q

What ability do patients with prosopagnosia retain despite their condition?

A

They can still recognize objects well but have great difficulty in recognizing faces.

84
Q

What brain regions are associated with prosopagnosia?

A

Bilateral damage around the lateral occipital cortex, inferior temporal cortex, and fusiform gyrus.

85
Q

What may unilateral damage to the right hemisphere lead to?

A

It may lead to prosopagnosia.

86
Q

What is hypnosis thought to involve regarding brain function?

A

A dissociation between voluntary control (dorsolateral prefrontal cortex) and the ability to monitor errors (ACC).

87
Q

What did Egner et al. (2005) report about hypnosis in the Stroop task?

A

Hypnosis decouples cognitive control from conflict monitoring processes of the frontal lobe.

88
Q

What do lesion studies in animals and humans reveal about visual consciousness?

A

They provide information about which visual areas are required to be intact for visual consciousness to arise.

89
Q

What visual deficit can result from damage to the retina or optic nerve?

A

Monocular blindness, the loss of sight from one eye.

90
Q

What is achromatopsia typically associated with?

A

Lesions that include area V4 and possibly regions just anterior to area V4.

91
Q

What can damage to one hemisphere lead to in terms of color perception?

A

Selective loss of color perception in the contralateral visual field.

92
Q

What role does the DLPFC play in working memory (WM) function?

A

Damage to the DLPFC is sufficient to impair performance on WM tasks.

93
Q

What happens to performance on WM tasks as the length of the delay increases?

A

The impairment gets worse, suggesting more rapid forgetting.

94
Q

How do brains adapt to damage over time?

A

Lesions change over time as cells die and adaptation occurs.

95
Q

What can be done to stimulate brain lesions in healthy subjects?

A

Using magnetic pulses over the scalp can inhibit or excite a region of cortex.

96
Q

What did Sperry’s work with split-brain patients reveal about the left hemisphere?

A

The left hemisphere has superior language and arithmetic skills

Sperry’s research began in the 1960s.

97
Q

What are the spatial skills associated with in Sperry’s findings?

A

The right hemisphere

Sperry’s work highlighted the different cognitive functions of the brain’s hemispheres.

98
Q

What is the result of damage to the amygdala?

A

Difficulty in recognizing whether faces are expressing fear

This reflects the amygdala’s role in emotional processing.

99
Q

Which brain areas are associated with difficulty in identifying disgust?

A

Left insula and basal ganglia

These areas are linked to processing specific emotions.

100
Q

What is one assumption of lesion studies?

A

Discrete anatomical modules deal with different cognitive functions

This assumption can lead to oversimplifications in understanding brain function.

101
Q

What does superimposing individual lesions assume?

A

Functional modules are in the same locations in different individuals

This may not hold true due to individual anatomical differences.

102
Q

What is a limitation of the lesion method regarding brain function after a focal lesion?

A

Intact regions of the brain continue to function in the same manner as before the lesion

This does not account for the brain’s ability to reconfigure after damage.

103
Q

What is the impact of brain plasticity on cognitive functions after damage?

A

Different regions can change their function in response to damage

This adaptability complicates the interpretation of lesion studies.

104
Q

What is a common issue with the areas of the cortex affected by stroke?

A

Some areas are particularly likely to be damaged

This can affect the overall assessment of brain damage.

105
Q

What advantages do single-photon emission computed tomography and positron emission tomography offer?

A

They can look at brain activity of healthy people and eliminate problems associated with the lesion method

These techniques provide more dynamic insights into brain function.

106
Q

What do T1-weighted MRI scans offer?

A

Good contrast between grey and white matter with superior spatial precision

This helps in differentiating brain structures.

107
Q

What is the advantage of T2-weighted MRI scans?

A

They highlight regions of damage and provide good pathological information

However, they have limitations in detecting acute strokes.

108
Q

What do T2-weighted fluid-attenuated inversion-recovery (FLAIR) imaging sequences detect?

A

Acute cerebral infarcts

This imaging technique is sensitive to early signs of stroke.

109
Q

What is the sensitivity of DWI imaging for detecting infarcts?

A

Particularly sensitive for the detection of hyperacute infarcts

This technique can accurately predict the final infarct size.

110
Q

How do modern imaging techniques compare to conventional T1- and T2-weighted images?

A

They can often identify the extent of brain lesions more accurately

This enhances diagnostic capabilities in clinical settings.

PSYC513 Exam One- brain,language, communication, memory and knowledge (5 decks)

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