TASK 8 - LESION Flashcards
lesion studies
= 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
process
- injury/disease
- brain lesion (= brain area is impaired or non-existent)
- neuropsychological testing (e.g. reaction time)
- specific impairment in behaviour or cognition observed
- insights into original function of brain area revealed
dissociation
= 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
dissociation
- single
= 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
single dissociation
- interpretation
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)
single dissociation
- localisation
- 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)
dissociation
- double
= 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
double dissociation
- interpretation
- 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
doble dissociation
- localisation
- 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
association
= consistent co-occurrence of 2 or more impairments
- suggest one underlying process, but may be due to proximity
association
- localisation
- 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)
single-case studies
=
single-case studies
- assumptions
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)
single-case studies
- reasons to use
• 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
group studies
=
group studies
- reasons to use
- 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
group studies
- grouping
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
limits to interpretation
- localisation problems
- 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)
limits to interpretation
- lesion localisation
- 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
limits to interpretation
- differential vulnerability
- 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
limits to interpretation
- temporal resolution
- 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
lesion studies
- advantages
- higher level of inference than lesion method: determine necessity (not just correlation)
- detect possible contribution of regions that are constantly active
lesion studies
- diadvantages
- 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
applications
- Balint’s syndrome
= 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
applications
- neglect
= 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
