task 8 Flashcards
LESION STUDIES:
a form of reverse engineering: observing what the rest of a cognitive system can and cannot do when a component or a region is removed
Patient-based neuropsychology consists of two broad forms/ lesion studies can improve our knowledge in two ways
- classical neuropsychology: infer the function of a given brain region by taking patients with lesions to that region and examining their pattern of impaired and spared abilities
- benefited from imaging methods that enables more accurate lesion localization and quantification
- favors group studies - cognitive neuropsychology: pattern of spared and impaired abilities due to a lesion is used to infer building blocks of cognition – irrespective where they are located in the brain
- informative for guiding the development of information processing models and provide cognitive frameworks that underpin imaging research
- favors single case studies
Virtual lesions
can be produced by TMS or tDCS, which are methods to temporarily disrupt cognitive function or boost cognitive functions
STATISTICAL ANALYSIS OF LESION DATA:
Statistics are estimated on a voxel-by-voxel basis, allowing fairly high spatial resolution
Can be compared to functional neuroimaging findings from healthy subjects, by aligning the images from different patients into a common stereotaxic space
PRODUCING LESIONS IN ANIMALS:
Aspiration: Aspirating brain regions using a suction device and applying a strong current at the end of an electrode tip to seal the wound
Transection Cutting of discrete white matter bundles such as the corpus callosum or the fornix
Neurochemical lesions Toxins are taken up by NTM systems and, once inside the cell, they create a chemical reaction that cill it
Reversible lesions Pharmacological manipulations
single dissociation
a situation in which a patient is impaired on a particular task (A) but relatively spared on another task (B). In general, there is no case in which impairment in function B without impairment in function A
Indicates that the two functions are separate to some degree but that one of them is necessary for the other (e.g., seeing words is necessary for reading)
Lesion in region X produces an impairment in task A but not B, while lesion in region Y produces impairments in both A and B
Leaves open the possibility of non-specific effect: the disrupted area is not specifically involved in the particular function but because that region of the brain is simply more important in a general sense
a) Classical single dissociation: patient performs entirely normal on task B compared to control group
b) Strong single dissociation: patient is impaired on both task but is significantly more impaired on one task
Task A and B utilize different cognitive processes with different neural resources
Dotted line on graph = control range
task resource artefact
If two tasks share the same neural cognitive resource but one task uses it more, then damage to this resource will affect one task more than the other
Task-demand artifact
when a single dissociation occurs because a patient performs one of the tasks sub-optimally
Double dissociation
two single dissociations that have a complementary profile of abilities (e.g., person lesion A writes vowels incorrectly while person with lesion B writes consonants incorrectly)
in some cases A is impaired and B isn’t, while in other cases B is impaired and A isn’t
Provides info on whether two functions are relatively separate or independent
Lesion in region X produces impairments in region A but not B, while lesions in region Y produces impairments in task B but not A
Use of double dissociations was criticized:
- Double dissociations imply an endorsement of the notion of modularity BUT it can also be that a non-modular system produces double dissociations, so this critic was rejected (other systems can also contain units that are functionally specialized for certain types of processes, even though the system is interactive)
- Reliance on double dissociation demands study of pure cases, BUT what is pure? (when a patient has Alzheimer’s, then studying the dysfunctions in isolation are feasible if memory and the dysfunctions are independent)
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Finding a double dissociation between two patients on two tasks is only part of the toolkit: to interpret the impaired performance, one requires evidence from a range of other relevant tasks (e.g., which types of errors are made?)
Association of deficits
theoretically, two symptoms can occur together because they are reflected closely together in the brain or because they are a manifestation of an underlying process
It is important to know how common a particular dissociation is in order to rule out that it has been observed by chance
Syndromes: associations between symptoms (can also be the focus of research rather than dissociation)
Limitations on the interpretation of dissociations
Dissociations don’t tell us that the impaired region is localized in an area, it tells us only that it is necessary for the function in question and that the other lesioned area which did not produce impairment is not
- Perhaps, the entire rest of the brain is also involved in the function, but we don’t know
- Diaschisis: even a very discrete brain lesion can disrupt the functioning of distant brain regions that are structurally intact
Technical problem of identifying the site of a lesion – rarely possible to precisely designate the location of a lesion in the living brain
- Ability of current structural imaging techniques to identify lesions is limited
- Reliable images are best obtained 3 months after onset when neuropsychology testing is carried out
fMRI
look at brain activity in healthy people – eliminate the problem of differential vulnerability, plasticity and disconnection that are associated with lesion method
better temporal resolution than can be achieved by examining permanent injury
Limitations:
more sensitive in younger than in older people
brain damage can disrupt blood flow reduced metabolism; surrounding intact areas receiving blood flow in excess of their demands (luxury perfusion)
surviving arteries can show sustained dilation, compensating from compromised arteries: a region might be functioning perfectly well, but appear to be unresponsive to standard fMRI analysis
Mri
emphasize different tissues and physical properties
a) T1-weighted images: good contrast between grey and white matter and superior spatial precision
b) T2 weighted scans: highly regions of damage, giving good pathological information
Both scan types have limitations:
Often fail to detect acute strokes
Sequences do not necessarily show where a function is acting normally
Diffusion-weighted imaging (DWI):
enables strokes to be visualized at an early stage
Identify brain lesions more accurately than T1 and T2-weighted images
Diffusion tensor imaging (DTI):
takes advantage of the fact that water motion in the brain is constrained perpendicular to fiber tracts, but much else constrained in the direction of the fiber tracts
Help to identify whether regions are disconnected after stroke
limitations-Lesion method
only post-mortem
lesions assume that discrete anatomical modules deal with different cognitive functions, but often brain functions are carried out in a distributed manner
presents a limitation for most tools that are used, but especially for the lesion method, as the extent of strokes are constrained by the blood supply of the brain resulting in wide range of deficits in several areas
small lesions that only partially damage a brain area might not lead to any obvious behavioral problems
Superimposing individual lesions to identify the crucial area for a certain function assumes that these functional modules are in the same location across individuals
Some areas of the cortex are particularly likely to be damaged by stroke (– locations of brain damage are not randomly distributed in the brain
difficult to interpret lesion overlay plots (e.g., are the regions highlighted specifically involved in the dysfunction, or are they simply commonly damaged zones)
To assess how different regions of the healthy brain function, we need to have good idea of the temporal sequence, which is not possible with lesion methods
Brain regions can be disabled but intact after injury, which can be shown by structural CT and MRI
Functional imaging: show every part of a neural network that is involved in a task or behavior – cannot be done with lesioning methods but with modern imaging
Modern imaging: limitations
limitations:
task correlates with activation, but we don’t know whether this region is crucial to perform the task (lesion data tell us which areas are necessary for controlling a cognitive function)
- some activated areas may not have a direct role in information processing but are activated because of their connections to regions that are required for the task
not possible to interpret regions where no activity is detected: fMRI cannot detect the possible contribution of regions that are constantly active, regardless of the task (regions may be crucially involved in the task, but since they are always active, their activity is cancelled out as the blood flow does not significantly changes)
only weaker inferences can be drawn compared to lesion data
Caramazza’s assumptions for theorizing in cognitive neuropsychology: three assumptions underpinned almost all neuropsychological studies
- Fractionation assumption: damage to the brain can produce selective cognitive lesions within a cognitive model (doesn’t refer to a lesion to a particular brain part)
- Transparency assumptions: lesions affect one or more components within the cognitive system but don’t result in completely new cognitive systems being created
- Universality assumption: all cognitive systems are basically identical
Assumptions do not hold under some situations:
Fractionation assumption: whether selective cognitive impairments will be observed depends on the neural architecture. BUT they can be observed, even if there are some processes that may be hard to uncover
Transparency assumption: most problematic: examples of neural plasticity and rehabilitation and recovery after brain damage might be an argument against this assumption, BUT it could still be that preexisting cognitive models have just been reinstated and not newly created
- More likely to hold true for brain damage acquired during adulthood than childhood and when studies soon after injury relative to later in time
- Refers to the cognitive organization of the cognitive system, not to its location (not necessarily)
Universality assumption: one needs to assume that an individual is representative of the population at large in order to make generalizations to normal cognition. Individual variability must then be attributable to noise only, and not reflect qualitative differences in the way a task is performed
PRO SINGLE-CASE STUDIES
Researchers have been suggested that the single case study is the only acceptable method in cognitive neuropsychology
1. Experiment with non-brain damaged population: sample of participants make an experiment, and it is assumed that all pp have broadly equivalent cognitive system and carry out the experimental task in equivalent ways.
in this case it is feasible to average the observations of the group because it is assumed that the difference between pp is noise only
2. experiment with brain damaged population: each participant has different lesions to the cognitive system and so differences in observed performance are not noise but could also be attributable to the lesion
averaging across participants is not possible
Conclusion: establishing cognitive impairments requires cognitive testing of individual patients
I a group of patients had identical lesions, one could still not average across patients and instead the study would become a series of single-case studies:
to be sure that all have the same lesion, each pp would need to be tested individually and as such, one would not learn more from averaging a set of patients than one could learn from a single case itself
Conclusion: Averaging across patients that are possibly not equivalent is not good, so use single studies
CONS SINGLE CASE STUDIES
one cannot create a theory based on observations from only a single case, or generalize from a single case
counterargument: single-case data constitute valid data that can be used to develop a theory
counterargument: it is plausible to generalize from a single case to a model of normal cognition, but less plausible to generalize from a single case to another single case
GROUPING PATIENTS
Grouping by syndrome Patients with the same clustering of different symptoms are grouped together
appropriate for understanding the neural correlates of a given disease
Grouping by cognitive symptoms Patients are grouped when they possess one particular symptom – locate the lesion of the pp
may also possess other symptoms, but they may differ compared to the other patients in the group
made feasible by new techniques that compare the location of lesion from MRI scans of different patients (map of the likely lesion can be produced)
Grouping by anatomical lesion: Patients are selected based on having a lesion to a particular anatomical region
doesn’t require that patients have damage exclusively to the region of interest
There is no right or wrong way to do that
One advantage of working from a symptom to a lesion location is that it could potentially reveal more as one doesn’t specify on a specific brain region (syndrome and cognitive symptom grouping)
Limitations of group studies:
Limitations of group studies: individual brains differ in brain size, shape and structure, so individual brains need to be transformed to a standard stereotaxic space to make such comparisons
Superimpose individual lesions in an overlap plot and find the location that is commonly lesioned among patients that show the same disorder
group studies need control patients
Simply overlaying plots for patients who have a disorder can be misleading, because the region that they highlight might reflect increased vulnerability of certain regions to injury rather than any direct involvement with the disorder of interest
Example: if we are interest in brain regions responsible for speech production and we look at a large group of pp who have problems with speech production, we will find that they have damage to several brain regions
Problem: it could be that these regions are typically damaged by strokes
Solution: we need to compare it to pp with brain lesions in the same hemisphere that do not have speech problems
Subtracting them = brain regions that are involved in speech production
UNILATERAL SPATIAL NEGLECT/NEGLECT:
UNILATERAL SPATIAL NEGLECT/NEGLECT: attention network is damaged in only one hemisphere, usually due to a stroke
TESTING NEGLECT:
a) Line cancellation test: participants are given a sheet of paper containing many horizontal lines and are asked to bisect the lines in the middle
Patients with lesions to RH bisect the lines to the right of the midline, or even completely miss lines on the left side of the paper
b) Copying objects or scenes: patient shows an inability to draw the entire object and tends to neglect the left side
c) Effect on imagination and memory: imagine standing at Milan cathedral and describe the piazza from memory patient s neglects the side of the piazza contralateral to their lesion. When researchers asked pp to image standing at the other side, looking at the cathedral, pp suddenly reported only the side that was neglected before
d) Extinction: neglect patients detect stimuli normally when those stimuli are salient and presented in isolation, even when in the neglected field (sensory inputs are competitive)
Neglect becomes obvious, when participants are presented with two stimuli, one in each hemifield. The patient then doesn’t perceive or act on the contralesional stimuli
Can be overcome when attention of pp is directed towards the neglected field
BALINT’S SYNDROME: demonstrate three main deficits:
- Simultanagnosia – difficulty perceiving the visual field as a whole scene (see only a spoon, but not the plate)
- Ocular apraxia – deficit in making eye movements to scan the visual field, resulting in an inability to guide eye movements voluntarily
- Optic ataxia – problem in making visually guided hand movements
NEGLECT VS. BALINT’S SYNDROME
Similar disturbances in perception, but different patterns of perceptual deficits because different brain regions are damaged
- Neglect: unilateral lesion of parietal, posteriorly temporal and frontal cortex, or subcortical areas
- Balint’s syndrome: bilateral occipitoparietal lesion
Neglect:
None of the deficits are the result of damage to the visual system per se, because the patient is not simply blind
SINGLE CASE STUDY: INTACT VISUAL IMAGERY AND IMPAIRED VISUAL PERCEPTION IN A PATIENT WITH VISUAL AGNOSIA
Topic of the study: It is unclear to what extent visual perception and mental imagery use common mechanisms
a) Visual perception and imagery are associated
in support
-Common neural substrates for perception and imagery
-Common representations for perception and imagery:
b) Visual perception and imagery are dissociated:
- Imagery deficits with intact visual
Patient RM: unable to draw from memory, lost dream imagery, unable to describe objects from memory but could perfectly recognize objects in control conditions deficits affected only image generation
perception/recognition
-Perception/recognition deficits with preserved imagery:
results exp 1
Overall results:
- impaired object recognition (3-dimensional and 2-dimensional)
- impaired object recognition is not attributable to a loss of knowledge or a failure to retrieve the verbal label for visually presented items instead the appropriate semantic information cannot be accessed for items presented in visual modalities
exp 2
Overall results:
impaired in letter recognition; alexic
ability to recognize faces, while he cannot recognize other visual stimuli
recognition deficits cannot be attributed to a loss of knowledge
exp3
Overall results:
Able to produce a reasonable copy of visually presented figure, but unable to derive a coherent and full structural description of the image
Performed poorly on tasks require segmentation or parsing of stimuli but not on tasks that did not require grouping
Agnosia type = functional deficit intermediate stage of visual processing
exp 4
Overall results: provide compelling but not definite evidence for the dissociation between imagery and perception
CK performed normally on all these tasks:
4a: imagery for object color:
4b: Imagery for object shape:
4c: imagery for object size
4d: verification of high and low imagery:
Experiment 5: Comparison of perception and imagery
Overall results: despite propound object recognition deficit, visual mental imagery remains intact
Experiment 6: mechanisms for perceiving the internal visual image
C.K can recognize items from internal, but not from external input suggests that they are mediated by different mechanisms
6b: identification of recreated letters in imagery:
Method: letters were the target stimulus same procedure as before
Results: perfect performance when imagining letters BUT when letters were presented visually, he performed poorly
faze
How to integrate evidence of dissociated mental imagery and perception with the evidence supporting a common underlying mechanism between these processes?
A scheme that doesn’t isolate imagery and recognition completely but also doesn’t integrate them completely. Instead, it should reflect a partial overlap but also some unique processes
a) Unique component view
b) Unique pathways of access to the shared long-term representations:
Damaged feedforward projections in which the intact representations cannot be accessed may impair object recognition, whereas damaged back projection or ‘top-down’ pathways from the stored representations may selectively impair imagery C.K.’s feedforward projections are affected
o Not an adequate solution, as in the mental imagery task described before, C.K. described and transformed an item and then, through feedforward mechanisms accessed the long-term store to assign an identity to the item same ‘impaired’ feedforward mechanisms would be implicated
c) Shared system in which imagery and recognition are associated. There are a series of component stages through which an object is passed prior to recognition: (proposed by the authors)
Early stages: primitive features are registered
Intermediate stages: processes involve figure-ground segregation and feature grouping
Late stages: activation of stored knowledge
C.K.’s deficits affect intermediate stages of processing, disrupting the access to higher level processes that are in themselves fully functional
He can recognize an internally generated object even when the deficit affects bottom-up processes because the internally generated image is maybe not reliant on intermediate processes
