TASK 8 - LESION Flashcards

1
Q

lesion studies

A

= study brain lesion (caused by an injury or disease) induced behavioural impairments

  • brain activity as dependent variable
  • -> want to establish causal relationship between brain damage and impaired task performance
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2
Q

process

A
  1. injury/disease
  2. brain lesion (= brain area is impaired or non-existent)
  3. neuropsychological testing (e.g. reaction time)
  4. specific impairment in behaviour or cognition observed
  5. insights into original function of brain area revealed
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3
Q

dissociation

A

= performance on one task is impaired while performance on second isn’t

  • functions/processes are then dissociable/separable
  • -> cognitive neuropsychology: difficulty in one domain relative to an absence of difficulty in another domain can be used to infer independence of these domains (= separate neural resources)
  • might reflect two different populations of interspersed neurones
  • cannot conclude that it’s the only function of these neurones
  • always need a range of relevant tasks (not just 2) to properly interpret spared + impaired performance
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4
Q

dissociation

- single

A

= patient with lesion X shows severe impairment in task A but not in task B; patient with lesion Y does not show any impairment (neither A nor B)

  • -> non-reciprocal dissociation
  • or patient with lesion Y always impaired in both task
    a) classical single dissociation: patient performs entirely normal on one task
    b) strong single dissociation: impaired on both tasks, but significantly more impaired on one of them
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5
Q

single dissociation

- interpretation

A

A. hierarchal relationship: 2 functions are separate to some degree, but one of them is necessary for the other (e.g. blindness & inability to read visual material)
B. task A + B may use different cognitive processes with different neural resources (can’t conclude this)
C. task A + B may use same resources but one requires more of it than the other –> task-resource artefact (minimised by double dissociation)
D. single dissociation occurs because patient performs one of the tasks suboptimal –> task-demand artefact (control for IQ, instructions)

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6
Q

single dissociation

- localisation

A
  • lesion in region X produces impairment on task A, not B
  • lesion in region Y produces no impairment on either task
  • -> lesion X is not causing general deficit, but specific
  • because 2nd lesion in other location doesn’t produce the impairment
  • -> lesion in question doesn’t produce impairment in all tasks
  • because relatively good performance seen in 2nd task
  • leaves open the possibility that lesion has the effect because it is simply more important in some general sense (not because disrupted area is involved in the particular function)
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7
Q

dissociation

- double

A

= lesion X is impairing task A but not B, while lesion Y impairs B and not A

  • -> reciprocal dissociation
  • 2 single dissociations that have a complementary profile of abilities
  • each lesion-impairment serves as control for the other
  • different claims on how specific a particular lesion links to a specific function
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8
Q

double dissociation

- interpretation

A
  • evidence that 2 functions are relatively separate/independent
  • in each lesion we learn that it is involved in a particular function, but not another
  • -> e.g. Broca’s aphasia
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9
Q

doble dissociation

- localisation

A
  • lesion in region X produces impairment on task A, not B
  • lesion in region Y produces impairment on task B, not A
  • firmer grounds for localisation of function
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10
Q

association

A

= consistent co-occurrence of 2 or more impairments

- suggest one underlying process, but may be due to proximity

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11
Q

association

- localisation

A
  • single region is necessary for different functions
  • but functions may be separable but mediating brain areas in close proximity
  • when impairment in both functions usually but not always co-occurs (= sometimes dissociable)
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12
Q

single-case studies

A

=

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13
Q

single-case studies

- assumptions

A

1) fractionation assumption: damage to brain can produce selective cognitive lesions
- more likely if neurones performing a specific task are clustered rather than distributed
- partly met
2) transparency assumption: lesions affect one or more components within the pre-existing cognitive system but don’t result in the creation of a new cognitive system; intact regions continue to function in same matter as before
- if old function reinstated without creating a whole new way of performing the task
- more likely if brain lesioned in adulthood
3) universality assumption: all cognitive systems are basically identical; individual is representative of the population to make generalisations to normal cognition
- individual differences cannot be due to qualitative differences
- comparability between premorbid + postmorbid cognitive systems, not where they are located
- more likely if brain lesioned in adulthood + when studied soon after the injury (or if cognitive profile remains stable over time)

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14
Q

single-case studies

- reasons to use

A

• In non-damaged peeps it’s feasible to average group results bc. the only difference btw participants is noise
• In lesioned peeps, the differences in performance may be attributable to differences in lesions rather than btw patient noise
o Averaging across participants not possible
• Determining where in the cognitive system (not regionally) the lesion is can only be determined by empirically observing each case in turn
• Even if we were to find a group of identical patients, the study becomes a series of single case studies
• Provide valid data with which we can test, adapt & develop a cognitive theory
o Can generalise to a model of normal cognition, but not to another case

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15
Q

group studies

A

=

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16
Q

group studies

- reasons to use

A
  • establishing whether a given region is critical for performing a given task
  • when looking at fMRI: region of activity doesn’t apply its critical involvement in a task study –> solution: lesion method
  • lesions are rarely restricted to the region of interest –> to localise critical region, several patients may need to be considered
17
Q

group studies

- grouping

A

1) by syndrome (= cluster of symptoms; more rough analysis)
- more appropriate for understanding neural correlates of a given disease pathology rather than developing theories concerning the neural basis of cognition
2) by cognitive symptom (= one in particular; more fine-grained analysis)
- feasible by techniques that compare location of lesions from MRI voxel-by-voxel –> find likely lesion hot-spot
- reveal more than one region as being critically involved
3) by anatomical lesion (= anatomical region)
- when we have a specific testable prediction about what the region is critical for

18
Q

limits to interpretation

- localisation problems

A
  • localisation assumption: discrete anatomical modules deal with different cognitive functions
  • -> many brain functions carried out in distributed manner, with large portions of the brain working in a plastic fashion (rather than one region having a fixed function)
  • dissociation doesn’t tell us that the impaired function is localised in the area of the lesion
  • -> only tells us that lesioned area is necessary for the function in question + that other lesioned area isn’t
  • -> regions outside the area of either lesion may also be involved in the normal processing of the function
  • diaschisis: lesion may cause long-term disruptive effects in distant regions even if they otherwise function normally
  • -> due to disruption of connections (e.g. to earlier stages of information processing)
19
Q

limits to interpretation

- lesion localisation

A
  • difficulties of structural imaging techniques at identifying lesions
  • cannot pinpoint the exact location of the lesion + lesion may temporarily disrupt neighbouring tissue (e.g. due to swelling, bleeding + other short-term pathological processes)
  • -> distorts true size + may render neurones inoperative even when they aren’t destroyed
  • surviving arteries in surrounding area may show increased dilation to compensate for compromised arteries –> reduced task-related dilation –> region appears unresponsive on fMRI
  • -> solution: perfusion imaging
  • reliable lesion images best obtained 3 months after onset
20
Q

limits to interpretation

- differential vulnerability

A
  • some areas of the brain are more likely to be damaged by strokes –> location of brain damage not randomly distributed
  • difficult to interpret lesion overlay plots (are the highlighted damaged regions specifically involved with the effects or are they simply commonly damaged zones?)
  • -> solution: control group that with similar lesion + symptoms but no impairment
21
Q

limits to interpretation

- temporal resolution

A
  • doesn’t allow for assessing time course of information processing
  • need to have a good idea of the temporal sequence of information processing
  • -> crucial for determining stages of processing + role of feedback
22
Q

lesion studies

- advantages

A
  • higher level of inference than lesion method: determine necessity (not just correlation)
  • detect possible contribution of regions that are constantly active
23
Q

lesion studies

- diadvantages

A
  • if we test patients in the acute stage of their illness, we won’t be able to accurately identify all of the brain regions that are impaired
  • if we wait for the initial problems to resolve, problems with brain plasticity take over
  • -> patients can regain some function
  • you can only test lesions that you find –> cannot control lesions, difficult to have group of subjects with same lesion
24
Q

applications

- Balint’s syndrome

A

= bilateral damage to regions of posterior parietal and occipital cortex
- brain mechanisms involved in attending objects can be affected even with normal visual fields and no spatial biases

25
Q

applications

- neglect

A

= unilateral damage to parietal, temporal + frontal cortices (mostly right)
- despite normal vision, deficits in attending and acting in direction that is contralateral to brain damage