Neuropsychology Flashcards

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1
Q

what does neuropsychology study?

A

studies the link between brain and behaviour. fundamentally about studying impairments in individuals who have suffered brain damage

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2
Q

what is the aim of clinical neuropsychology?

A

understanding the condition (diagnoses, assess)

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3
Q

what is the aim of cognitive neuropsychology?

A

understand normal functions in the brain by studying patterns of impairment after brain damage

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4
Q

what is the difference between ‘strong’ and ‘weak’ cognitive neuropsychology?

A

strong= use patient data to construct a theory
weak= use patient data to refine a theory

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5
Q

list seven causes of brain damage:

A

-traumatic injury
-stroke
-lack of oxygen (hypoxia)
-tumours
-brain infections or inflammation
-nutritional deficiencies
-chronic alcohol abuse
-surgery

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6
Q

Name the four assumptions in neuropsychology:

A

1- universality
2- modularity
3- fractionation
4- transparency

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7
Q

Explain the assumption ‘universality’ and how justified it is:

A

-cognitive processes are the same in all individuals. there is still scope for differences but average group of individuals is reflection of any individual in wider population

-everyone has the same structure of the brain but there are little differences in individual gross anatomy. brains are not symmetrical and some brains show different proportions of matter in different places

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8
Q

Explain the assumption ‘modularity’ and how justified it is:

A

complex cognitive processes can be broken down into simpler processing units

-there is very little actual evidence because it is difficult to prove

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9
Q

Explain the assumption ‘fractionation’ and how justified it is:

A

brain damage can result in the selective impairment of a particular process

-there is an abundance of evidence

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10
Q

Explain the assumption ‘transparency’ and how justified it is:

A

the cognitive system of brain damaged patient is fundamentally the same as that of a normal subject except for a local modification of the system- all other processes are in tact

-there can often be disruption to other cognitive processes, behavioural compensation, and natural re organisation

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11
Q

how do split brain patients complicate neuropsychology assumptions?

A

surgery is done in some epilepsy patients where they cut connection between the two hemispheres which stops the connections involved in epilepsy. for these split brain patients, once the fibre is cut the brain is deemed as acting ‘normal’ which means their original brain was abnormal. is it a fair assumption that their brain is representative of everyone?

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12
Q

What post morbid damage was found in patient HM that was resulted from surgery?

A

there was evidence of an undetected stroke as a result of brain trauma from the surgery, also there were metal chips left in the brain which had corroded over time and began to damage tissue around them

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13
Q

What is the group study approach?

A

patient group vs control group. inferences are drawn from between group comparisons, looking for associations of common deficits or common sites of damage

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14
Q

what are some problems with the group study method ?

A

-relies on the assumption of universality
-similar behavioural symptoms may arise from different underlying patterns of damage
-similar sites of damage may be associated with very different symptoms
-specific behavioural impairments within a syndrome may vary
-it is time consuming to find patients
-there is a risk of over interpreting associations

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15
Q

what is the Case Study approach?

A

looking for specific single deficits in a patient. mainly concerning dissociations between behaviour patients can or can’t do

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16
Q

Explain Single and Double dissociations:

A

Single Dissociation: if patient can do A but not B, A and B are likely to be independent processes in the brain and may involve different brain regions

Double Dissociation: one patient can do A but not B, another can do B but not A. strong evidence of involving different cognitive processes and brain regions

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17
Q

What is an alternative explanation for a single dissociation?

A

may simply be that B is harder than A, so damage to the process that controls A and B results in a more noticeable problem in B than in A

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18
Q

How was double dissociation used to distinguish Broca’s and Wernicke’s aphasias?

A

patient had spared word order and meaning (A), but impaired fluency (B).
other patients had impaired word order and meaning (A), but spared fluency of speech (B)

= different lesion sites for the aphasias

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19
Q

Why are double dissociations difficult to replicate?

A

it is difficult to find patients with purely damage to one cognitive process, and that are complementary to each other

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20
Q

what are the methods in Cognitive Neuropsychology?

A

-studies of individuals with localised brain damage
-studies of individuals who have been surgically operated on
-behavioural studies of healthy individuals
-imaging studies of both healthy and brain damaged individuals
-inducing temporary lesions in healthy patients

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21
Q

how can neuropsychologists confirm links from functions to structure?

A

-post mortem; confirm deficits in anatomy after death

-imaging techniques

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22
Q

Name four functional imaging techniques and a disadvantage of them:

A

-fMRI; slow time course
-PET; involves radioactive materials
-EEG; bad spatial resolution
-MEG; few machines in the world

23
Q

What is a famous example of fMRI potential for error?

A

Emotional processing of faces by dead salmon

24
Q

Explain fMRI:

A

-measures changes in oxygenation levels in the blood supply to the brain, not brain activity

-compares activity during task to a control group for tasks vs rest groups or difference between tasks

25
Q

Explain TMS:

A

-Transcranial Magnetic Stimulation
-temporary damage to the brain to understand the link between structure and function
-sends electric pulse to temporarily disrupt activity in a localised function

26
Q

Who established the term ‘Agnosia’?

A

Freud, 1891

27
Q

What is visual object agnosia sensitive to?

A

specific to visual modality but can also be category specific e.g. recognising man made objects or natural things

28
Q

how would a person with associative agnosia perform in the Matching by Appearance Task?

A

they could tell if the tow object items are the same, but they could not explain what the object is

29
Q

Describe apperceptive agnosia:

A

can tell things about an object such as colour, shiny ness etc. but cannot understand how the individual components fit to make one object

30
Q

how would a person with associative agnosia perform in a matching by function task?

A

they could make a match based on what object has the closest three dimensional structure

31
Q

How much of a three dimensional understanding do associative agnosia patients have?

A

they can piece together pieces into three dimensional understanding of an object but they can’t name it

32
Q

describe how associative and apperceptive agnosia patients perform when they are told to copy a drawing:

A

associative: can copy drawing but don’t know what they’re drawing

apperceptive: struggle to copy a drawing but can produce some of the correct elements

33
Q

describe how associative and apperceptive agnosia patients perform when drawing from memory:

A

associative: could not draw from memory

apperceptive: could draw an object from memory

34
Q

what are the damage sites of patients with associative and apperceptive agnosia?

A

apperceptive: unilateral right hemisphere damage in the right inferior parietal lobe

associative: usually bilateral. crucial area thought to be left hemisphere, more ventral than apperceptive

35
Q

According to Warrington’s anatomical model, how does normal visual processing happen?

A

initial visual processing in occipital lobes, info passed to right hemisphere where perceptual categorisation happens, once the three dimensional model is complete info is passed to left hemisphere where semantic processing happens

36
Q

How is perceptual categorisation disrupted according to Warrington’s Anatomical Model?

A

the three dimensional model can’t be made and the information cannot be passed on to semantic categorisation. but if they can access semantic categorisation by memory individually, info can be accessed.

37
Q

In associative agnosia what part of the anatomical model is damaged?

A

semantic categorisation

38
Q

What did progressive cerebral atrophy suggest about there being two distinctive types of agnosia?

A

there may be a continuum of agnosia with apperceptive on a more severe end than associative (De Renzi 1986)

39
Q

describe pareidolia:

A

our facial recognition is so powerful that we can even see faces in cars, inanimate objects, food etc.

40
Q

What might severe prosopagnosia look like?

A

patients can’t tell what is a face and what isn’t i.e. may think a clock is a person

41
Q

What strategies can people with prosopagnosia use?

A

they can recognise people on the basis of other features like hair colour and clothing

42
Q

What damage is associated with specific failure of face recognition?

A

damage to right fusiform gyrus

43
Q

True or False: imaging face and object processing are the same process?

A

false, they are different processes

44
Q

what is the inversion effect?

A

happens to recognition abilities when things are turned upside down.

45
Q

why are faces harder to recognise when turned upside down?

A

inversion effect. we use the fact eyes are above nose and mouth, and also spacing between them. turning faces upside down upsets that configuration.

46
Q

how do patients with prosopagnosia perform better in upside down face recognition?

A

inverted images release the pressure of the process of estimating nose and mouth spacing, and patients can use the other characteristics such as hair colour instead

47
Q

how did patient WJ recognise his sheep after three strokes resulting in prosopagnosia?

A

found that he was able to recognise his sheep really well. categories of stimuli other than faces are in tact

48
Q

what happened to Patient RM after he suffered an aneurism and was unable to recognise faces?

A

he was a car enthusiast and although he couldn’t recognise faces he was exceptionally able to recognise different cars

49
Q

is right fusiform gyrus key for recognising and processing faces?

A

no, some patients have other damage. right fusiform gyrus also shows activity for non face stimuli and so is not specifically tuned to human faces

50
Q

how does the right fusiform gyrus work for patients with congenital prosopagnosia?

A

there is brain activity when looking at faces like normal

51
Q

how did dog breeders perform in the dog inversion tasks?

A

found dogs much harder to recognise upside down

52
Q

how was Greeble Inversion consistent with ‘expertise’ recognition bias?

A

by the end of a special ‘training’ on made up creatures the participants started to show inversion effect but less so than for faces

53
Q

why is expertise recognition probably untrue?

A

if right fusiform gyrus is process for recognising expertise, people with damage to this should not be able to become experts on recognising anything that’s new. this is not true i.e. farmer able to recognise sheep again after time