Cognitive, Damage to brain, WEEK 4 Flashcards

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1
Q

Bálint’s syndrome: Simultanagnosia

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  • Patient RM > had two strokes damaging large areas of bilateral occipito-parietal cortex > essentially damage to the “where” stream (covers occipital + parietal lobe)
  • Primary impairment of Bálint’s syndrome is SIMULTANAGNOSIA > impairment where patient reports not being aware of more than one object at a time
  • Also requires a lot of effort for them to shift their attention to another part of space to allow them to perceive the other object
  • People with this syndrome make conjunction errors (combined features of different objects to perceive something not there - illusory conjunction) > happens even when stimuli is shown for 10 secs whereas in typical people, it only tends to happen when shown for around 100ms as well as not actively paying attention to it > significant attention impairment
  • Parietal lobe appears important for feature binding (hence why people with Bálint make more conjunction errors) > damage to “where” pathway is a specific
    impairment in visual attention
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2
Q

Parietal Cortex and Feature Binding

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  • Evidence from cog neuropsychology: Corbetta et Al (1995) finds that, during conjunction search, posterior temporal cortex and parietal cortex show increased activation over baseline control conditions
  • Conjunction search tasks require attention, when ppts complete these tasks, they are using their parietal lobe
  • Links parietal cortex to binding of features to visual attention
  • Evidence from cog neuroscience: Walsh et Al (1995) looked at TMS (brain stimulation) to the parietal lobe. > TMS to parietal lobe specifically disrupts conjunction search but not feature search
  • Supports that the “where” stream in the parietal lobe is important for visual attention because it is the part helping bind features which is what you need to accurately perform conjunction search but feature search doesn’t need this so it is not impaired
  • Esterman et Al (2007), stimulating part of the parietal lobe (the intraparietal sulcus > towards back of the parietal lobe), this reduces the amount of illusory conjunctions the person experiences > somehow boosts visual attention + makes it easier for their brain to bind features + perceive objects
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3
Q

Hemispatial Neglect

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  • Evidence for the role of parietal cortex in visual attention is supported by patients w/ hemispatial neglect
  • People w/ hemispatial neglect have a complete lack of awareness of stimuli which happen in the opposite side of space to where the brain damage is (contralesional = opposite side of damage)
    This is typical to the right parietal cortex > here they would have problems being aware of items in the left side of space
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4
Q

Symptoms of Hemispatial Neglect

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  • Can look for hemispatial neglect is w/ a cancellation task > present patient w/ paper with lines all over and ask them to put a cross through all the lines they see > people w/ this damage tend to only cross through lines on the right side of the page (cannot see the left)
  • Another way is by doing a line bisection, present a line and ask the patient to put a line through the very middle of the first line. Results in patients tend to show them putting a line more towards the right, it seems as though they don’t see the line as continuing on the left hand side
  • Can also look at people w/ this by asking them to copy drawings > results show that it is as if they are ignoring the left hand side and only drawing the right but this is what they are paying attention to. Interestingly, the drawing of the clock by the patient continues on in terms of the circle > perception and expectations? If we see half a circle it is easier to assume there is a whole circle
  • Struggle to perceive objects in the left side but perhaps not whole things experienced?
  • Patients also have neglect for bodily space, some patients only shave half of their beard (what they see) + neglect to shave the other side, or put one one sock and neglect the other side
  • Hemispatial neglect is a complicated neglect for information on the left hand side of the external world, for information in the “mind’s eye” and for bodily space.
  • Unilateral neglect (neglect to one side) seems to be object-based rather than space based > patient didn’t ignore the tree + fence but ignored the left hand side of all of the objects > the neglect is not necessarily about what is on the left hand side of space but more about what is on the left hand side of objects
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5
Q

Bisiach & Luzzatti (1978): Representational neglect

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  • had 2 patients who normally spent time in the square, after their damage, the researchers asked the patients to imagine they were sitting at the steps outside the cathedral in the square > the patients generally didn’t describe anything on the contralesional side of space.
  • To ensure what they were imagining is nothing interesting on the right side only, they asked them to sit on the opposite side of where they were + imagine, but they were able to describe the things on the right hand side from their view
  • As if they have neglect for things in their minds eye, they neglect things they imagine on the left as well > not just external info
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6
Q

Extinction vs Neglect

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  • Similar deficit we see w/ patients of neglect but not always is symptom of extinction
  • Blue cross is where patients eye fixates > first condition flash the frog very quickly, patients w/ extinction will say they see a frog while patients of neglect say they see nothing (as it is on the contralesional side)
  • Second condition, sun is flashed = same reaction for extinction + neglect patients
  • Third condition flash frog AND sun (something is on both sides of space), patient’s with extinction only report seeing things on the ipsilesional side of space (same side as damage), only report the sun + do not report the frog > this happens even though extinction patients CAN experience things of the LEFT side of space
  • They can only experience things on the contralesional side if they are presented alone > is because if there is competition (2 objects on either side) then the ipsilesional side wins
  • Suggests how visual attention works > maybe visual attention is not unitary (not a spotlight), perhaps attention may just appear
  • Attention might be the outcome of the fact there are multiple representations in the visual world + they are all competing, some will win (due to different bottom-up + top-down reasons) and the thing that wins, is what we pay attention to
  • Attention is not necessarily one single concept, may be the outcome of a result of other processes of competition between representations in our visual system > the one that wins is the one we say we are paying attention to.
    Hemispatial neglect is not blindness or damage to the primary sensory cortex
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7
Q

Rehabilitating people with neglect

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  • can rehabilitate neglect patients using motivation > found in task where they have to circle pound coins on paper, they did better when told they get £1 for each one they get right rather than the control condition where they got no reward > patients only realise something is wrong when it keeps getting pointed out to them
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8
Q

Di Russo (2008): How much is neglected in hemispatial neglect patients

A
  • at what point is the visual processing hierarchy do people w/ hemispatial neglect stop being aware of things in the contralesional side? How much is neglected + at what point does it become neglected?
  • Di Russo measured amplitudes of ERPs in microvolts for control ppts (healthy) and neglect patients > ERPs elicited by visual stimuli in the left visual field (i.e. the neglected side)
  • Results show amplitude of processing up to 120ms was relatively the same in controls + neglect, suggests that processing up to this point was similar
  • From around 130ms to 200ms, control ppts ERP amplitude starts becoming negative (esp around 140-200mw) whilst neglect patients don’t have this or is considerably smaller for them
  • Early ERPs (in first few hundred ms) are generated within visual cortices (V1,V2,V3 etc) > is similar between neglect + control ppts
    Whereas ERPS generated from after 130ms, in this case are those generated in the dorsal part of the parietal lobe (“where” pathway)
  • For neglect patients there is still basic visual processing happening in the first few hundred ms > from this point onwards things change in perceptual processing > there is still the processing happening, it just doesn’t get sent along the brain in the same way as healthy controls
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9
Q

McGlinchey-Berroth et Al (1993): How much is processed in hemispatial neglect patients?

A
  • studied this by asking patients to look at the fixation point for 500ms so that we know objects presented is in their left or right visual field.
  • flash an apple in the LVF and lines (not an object) in the RVF for 200ms (has to be quick so we know which side of the brain is processing it + eyes can’t move that quick). Have a 400ms gap then are presented w/ an apple and a bed + asked what object did you see?
  • Behavioural evidence of neglect: shows patients w/ neglect show that their discrimination accuracy (being able to tell is an apple) in the LVF is very low + 50% likely due to chance (50% because they had two possibilities to choose from)
  • There better than chance so there is some processing available to them when they make decisions but their performance is very poor > Little to no conscious access of what happened in the LVF whilst its much better in the RVF (worse than healthy control but still good)
  • Can use priming tasks > ask ppts to look at fixation point + present a priming stimuli in LVF or contralesional side of space + lines on the RVF or ipsilesional side. Wait 400ms then present them with a word + ask them to answer as quick as possible is this a real word?
  • The bat in LVF primes the target because “baseball bat” is related to the word presented “ball” > the priming stimulus will be related to the word presented > baseball bat primes the word ball
  • If you understand the bat is a baseball bat then your brain accesses the meaning of a baseball bat > baseball bats are linked conceptually + semantically in your brain to balls > hand in hand
  • RT’s show that patients of neglect respond faster to primed stimuli than to unprimed stimuli
  • This suggests that patients w/ neglect have on some level processed the bat because, if they didn’t process the bat, why would they be quicker to respond to ball?
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10
Q

Lesions underlying neglect

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  • Parietal lobe is where lesions primarily need to be for patients with hemispatial neglect > typically right inferior parietal lobe (towards bottom of parietal lobe)
  • Cog neuroscience studies show performing TMS on the same regions, you can induce neglect + extinction like symptoms in healthy controls w/o neglect (TMS is where you can reduce neurons firing temporarily)
  • Supports parietal lobe’s role in neglect
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11
Q

Explaining neglect and extinction

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  • Neglect + extinction are NOT deficits of perception > they ARE deficits of attention > we can make patients perceive things on the contralesional side of space, deficit comes from ability to pay attention
  • If we can get a patient to effortfully move their attention to an object, they WILL see it is there
  • They just do not automatically pay attention to things on that side of space
  • This diagram shows that the same areas damaged in neglect patients coincide with the exogenous attention system which is bottom-up driven (things which pull our attention)
  • Perhaps neglect is specifically an impairment to the bottom up system + not the top down
  • Can look at this using a Posner task in patients (tests endogenous + exogenous attention)
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12
Q

Results of Posner task

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  • Smania et al (1998): Neglect patients benefit from valid endogenous cues in both visual fields (left + right)
    -The patients can choose to pay attention to one side of space over another > primarily when the cue is valid (points to right + target comes up on right) > if the cue says pay attention to the left, patients generally can
  • Bartolomeu et Al (2001): similarly if you put a cue in the ipsilesional side which predict or points to the contralesional side, attention is given to the left side
  • Patients benefit as much as healthy controls from a valid cue > Both studies suggests that endogenous orienting system is relatively intact in neglect patients > they can pay attention but only if they consciously do so
  • Supports there may be a problem with the exogenous system
  • Invalid cue where patients are told to pay attention to the right but then the target appears on the left, then there is a significant impairment in comparison to controls > an exogenous response is expected as it pulls your attention but in patients this doesn’t happen, they ignore it
  • patient has to consciously move their attention in order to perceive things in the left space
    Neglect/extinction is related to disengagement of the attentional spotlight from the ipsilesional side of space > if neglect happens from damage to the right parietal lobe
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13
Q

ADHD

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  • Most common neurodevelopmental disorder diagnosis in children > 5% of children have this
  • Behaviour is characterised by hyperactivity, impulsivity and inattention beginning in childhood
  • 3x more likely in boys than girls > but this includes prescribing bias (males are seen as impulsive and not paying attention more so than females) > difference may not be quite as large as it appears to be
  • 4x more likely in children living in socio-economic deprivation than those who don’t > social influence on ADHD
  • Increases likelihood that children w/ ADHD are more likely to engage in risk-taking as adolescence (teenage pregnancy, drug-abuse etc)
  • Still has a prevalence of 2.5% in adulthood > significant proportion of people fail to pay attention for long periods of time
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14
Q

ADHD Subtypes

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  • Predominantly Inattentive: people who struggle to finish tasks, especially if it is a long task, problems w/ following instructions + easily distracted > primarily inattentive
  • Predominantly hyperactive/impulsive: Difficulty in sitting still for long periods; fidgeting; speaks or acts at inappropriate times.
  • Combined inattentive and hyperactive/impulsive: The most common subtype - the above mixed
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15
Q

DSM V - Diagnostic Criteria for ADHD

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  • Difficulty with sustaining attention, to be diagnosed at least 6 inattention symptoms need to be met
  • Hyperactivity/Impulsivity symptoms, people who struggle to sit still e.g. > need 6 symptoms to be diagnosed
  • These symptoms need to be present before the age of 12 to get diagnosed with ADHD
  • The symptoms need to cause a significant impairment in the functioning of the child (in their social, academic or occupational life)
  • Symptoms causing impairment has to be present in 2 or more settings (e.g. at school and home) to rule out if it is associated with one context or many
  • Cannot be due to another disorder such as autism or a anxiety disorder
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16
Q

ADHD - Aetiology

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  • Aetiology = what is the cause of ADHD
  • There is a heritability component > Parents/siblings of a child with a diagnosis of ADHD are 4-5 times more likely to have a diagnosis of ADHD > other components may also be present
  • Pre-natal exposure to alcohol and nicotine > premature birth, low birth weight, perinatal brain injury
  • Social environmental factors such as exposure to lead and pesticides are linked to propensity of developing ADHD
17
Q

ADHD - Neural Dysfunction

What is different in the brain of people w/ADHD and people without it?

A

Structural Impairments
- 3-4% of the brain has reduced cortical volume especially in the prefrontal cortex > by volume we mean size (how many brain cells are taking up space) > there are fewer brain cells in the cortex of people w/ ADHD
- Reduced grey matter specifically in fronto-parietal attention network (grey matter = dendrites in neurons) > there are less dendrites in the neurones of the brain within the fronto-parietal network (connection between parietal to frontal lobe)
- Reduced cortical connectivity (white matter tracts where there are a lot of axons connecting parts of the brain) between 2 hemispheres and within fronto-parietal attention networks >
Functional Impairments
- Hypoactivity (less activity) in the prefrontal cortex (especially dorsal pfc) when performing tasks + at rest > less resting baseline activity in the prefrontal cortex of people with ADHD
Molecular neuroscience + impairments
-There is an imbalance in dopamine and noradrenaline circuits > these are neurotransmitters which travel in certain pathways
- Dopamine is primarily linked to the reward system which is in subcortical parts of the brain (below the cortex + basal ganglia)
- Noradrenaline has networks across the brain
-These neurotransmitters like certain pathways which overlap with frontal-parietal network +
Overlap with Endogenous system
-Highlighted areas of deficit in ADHD seems to overlap with the endogenous system > we have reduced volume, reduced activity + connectivity in areas which overlap with the endogenous attention system (top-down)
- Is ADHD deficit linked to the endogenous system > but there is also a significant pre-frontal impairment as well. The prefrontal cortex is primarily linked to executive function > is EF associated with ADHD?

18
Q

ADHD treatment

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  • Most commonly prescribed treatment is Methylphenidate (e.g. Ritalin) and Dextroamphetamine (e.g. Attentin) are effective and commonly prescribed
  • The chemicals in this focus on molecular pathways (dopamine + noradrenaline circuits which are impaired) > circuits connecting frontal parietal attention regions + lower level subcortical reward pathways
  • Methylphenidate and Dextroamphetamine inhibit the re-uptake of norepinephrine and dopamine or facilitate their release > more noradrenaline + dopamine is left present when taking this medication
  • This reduces symptoms of ADHD by targeting the fact that it seems that resting brain of a person with ADHD has low noradrenaline + dopamine compared to a healthy control > by increasing it, they will function more like healthy controls
  • Effective treatment + can improve quality of life
19
Q

Societal view + impact on psychological disorders

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  • Karistad et Al (2017) looked at 500,000 boys in Scandinavia and how likely it was for any given child to be diagnosed with ADHD relative to the month they were born
  • January is reference point, e.g. chance of a boy born in February being diagnosed w/ ADHD is higher than for January
  • HR at the bottom = hazard ratio so how many times more likely than January
  • Shows the probability of having ADHD increases across the year relative to children who are born in January > up to a point of being more than 1.5x likely
  • Children born in December are 50% more likely to have ADHD than those in January
  • Is not a cycle > e.g. doesn’t go up in summer then go back down for winter > goes up until December than right back down for January
  • May be because, people who are born in January in Scandinavia would be oldest in their class while people born in December would be youngest > so the youngest people in the class are more likely to be diagnosed w/ ADHD than the oldest
  • Raises the issue that, in classes there are a range of children where there are some who are younger than others > because they are younger they don’t sit still or pay attention as much + because they behave in those ways relative to the other children, they are more likely to be referred to get diagnosed with ADHD
  • Shows a societal influence because the youngest children, possibly the children causing most trouble in class are most likely to get diagnosed
  • Do they actually fulfil the ADHD criteria? Or do they not fulfil requirements of sitting still e.g. for the required time for the year they are in at school
  • Also important to consider who makes the diagnostic criteria? E.g. by American Psychiatric Association > classed using DSM V, there were only 137 doctors who contributed to writing DSM V
  • Over half of the 137 doctors have ties to industries like pharmaceutical companies > major conflict of interest as over half of them stand to make money from selling methylphenidate + ritalin
  • For them, having more diagnoses of ADHD = more money for them possibly
  • When looking at psychological diagnoses, we have to see it from a societal standpoint > look at whole picture > psychological problems are influenced from different angles