Tutorial deck Flashcards
What is prosopagnosia?
• Prosopagnosia- failure to recognise faces
What is developmental prosopagnosia?
• Developmental prosopagnosia- individuals who either have CP or have sustained brain damage before birth or in early childhood resulting in prosopagnosia
What is acquired prosopagnosia?
• Acquired prosopagnosia- provided unique window into the psychological and neural substrate of face processing
What is congenital prosopagnosia?
• Congenital prosopagnosia (CP)- impairment in face processing that is apparent from birth in the absence of any brain damage, and occurs in the presence of intact sensory and intellectual fuctions
What is evidence of the properties of congenital prosopagnosia (its mechanism and proof that such people have difficulty recognising faces)
• Decreased reaction time in face matching tasks
• Impaired at discriminating between common objects and between novel objects, especially when the discrimination is at the individual level, even when the pair to be discriminated is visible to the subject for an unlimited duration
• Many CP individuals are also not adversely affected by inversion of faces and can also show the inversion superiority effect
o Less affected than normal people by inversion effect (inversion effect is when there is worse recognition for inverse faces than normal faces)
• BOLD-behavioural response in the fusiform gyrus is the same in CP people as normal people (fMRI)
• CP compensatory mechanisms
o CP subjects use prefrontal cortex more than normal people (fMRI), suggesting a working memory task and hence recruitment of compensatory mechanisms under taxing perceptual conditions by the CP subjects
• CP subjects have a smaller right anterior fusiform region and a larger right mid/posterior-fusiform gyrus
o But no differences observed in the hippocampus or parahippocampal region
o Structural difference could be a cause or a consequence of CP.
What are super recognisers?
• Super recognisers are people who are extremely adept at facial recognition
What does the existence of superrecognisers and prosopagnosia suggest about face recognition?
• Their existence, as well as that of the prosopagnosia syndrome, suggests that face recognition is on a spectrum
What are the advantages and limitations of treating people with deficiencies as a separate clinical groups?
Advantages:
- Less stigma to getting treatment
- Sense of community with others with condition
- More benefits and funding to help
- Easier to study these people as a discrete group
Disadvantages:
- More stigma as not considered “normal”
- Treatment may not be necessary
- Cut-off line: people who are around the cut-off line
- Less motivation to get better if categorised in discrete group
What are the advantages and limitations of treating people with deficiencies as part of the normal continuum?
Advantages:
- No stigma as seen more like normal
- Reduces possibility of not needing treatment
- Easier to personalise medicine: treat as a multidimensional problem
Disadvantages:
- Seen as viewing less treatment
- Hard to get special considerations
- Promise of improvement when the quantity may be discrete
Describe the procedure of EEG from scratch and the purpose of the steps when applicable
- Measure size of participants head (widest bit) to know the cap size
- Measure from nasium (nose) to base of skull
a. Cz should be halfway between nasium and base of skull - Attach the electrodes by matching their numbers to the number on the cap
a. More electrodes- takes longer to set up and increases the risk of bridging (electrodes record combined signal) but there is more accurate data - Put conductive gel to decrease natural resistance of the skull and allow for increased contact between electrodes and the scalp
a. Gel= salt solution
b. Use needles to move hair that is under the electrodes and put enough conductive gel under the electrodes
c. Electrodes have pre-amplifiers: boost signal before sending it to amplifier
i. These have less environmental electrical noise - Measure impedence from each electrode
a. Red= high impedance
b. Green= low impedance - Need participant to be still with muscles nice and relaxed (including eye movements) as these influence the EEG very strongly
- Record from electrode
a. Need neurons firing in concert with each other and arranged in a particular manner
b. Need numerous additive dipoles to create a bigger signal (such an example is pyramidal cells in the cerebral cortex)
c. Response specific to activity: e..g response to images of faces vs images of houses
What behaviour and symptoms are characteristic of REM sleeping disorders?Give an example of such a disorder
o Acting out dreams is common in dementia diseases
Rapid eye movement sleep behaviour disorder (RBD)
• Caused by degeneration within the brainstem- disables the mechanisms responsible for immobilizing muscles during REM sleep
• Connected to other neurodegenerative diseases
Can be hallmark of Parkinson’s
Clonazepam restored normal dreams and stopped RBD disorder
o Parasomnia- mixed states of sleep and wakefulness
Releases basic instincts in an inappropriate way during sleep
o Aspects of the brain being damaged/parts of the brain that are awake when they should be asleep
o Can often remember what they are dreaming about
What behaviour and symptoms are characteristic of REM sleeping disorders?Give an example of such a disorder
• Non-REM parasomnia-
o Sleepwalk
More common in children
o Genetic predisposition
o People prone to sleepwalking sleepwalk at times of stress
o Physiological and psychological factors
o Don’t always remember their episodes
How old is transcranial magnetic stimulation?
• Transcranial magnetic stimulation
o Been around for 30-45 years
What are the physics involved in TMS and how old are they?
o Physics involved in TMS has been known for 200 years (Farraday)
Electromagnetic induction
• Electrical current will induce a magnetic field
• Showed that changing magnetic field will induce an electrical current
What is the biology involved in TMS and how old is it?
o Biology back in 250 years (Galvani)
Muscle/nervous tissue will create electrical currents and can be activated by electrical currents
Who failed to perform elementary TMS and why?
o Thompson (1910) and Magnusson+ Stevens (1911) tried to use magnetic fields to stimulate the brain Failures as magnetic fields generated were too weak and too slow
Who was the first person to invent working TMS and when?
o Barker (1985)- effective stimulation with TMS Invented the first usable TMS
Describe the procedure of TMS and its design
2000-3000 amps of current at 2000-3000 volts to generate strong enough magnetic field
Device has capacitors that stores up charge which is then released
Current passes through heavily insulated coil and ring
• As electrical current passes around coil, generates a magnetic field strong enough to pass through bone/scalp into the brain
• Machines deliver current as short pulse (50-100 us long) in order to induce changing magnetic field
o Electrical current is passed through the coil-> coil generates a very brief magnetic field-> onset and offset in magnetic field induces electrical field in brain tissue-> depolarises neuronal membrane
How invasive is TMS?
TMS is minimally invasive
What are the uses of TMS? Give examples
Can be used for mapping of brain
• Fairly focal interference
o TMS to motor cortex induces muscle contractions
o TMS to visual cortex induces phosphenes
What are the limitations of TMS?
Generally limited to surface of brain
• Decays with square of distance from surface of coil
-TMS can induce epileptic seizures
In TMS, what coils can be used? Why?
o Size of coil affects size of magnetic field
Figure 8 coil- magnetic fields summate in the middle
• Focal- limits area of stimulation
Big ring coil- broader magnetic field and deeper in the brain
• But also stimulates everything above target deep in brain
Describe the four stimulation protocols of TMS
Online single pulses (spTMS)
Paired pulses (3 ms vs 10 ms vs 200 ms)
Online repetitive trains (rTMS)
Offline rTMS
What are online single pulses for in TMS?
• Localised interference
What are paired pulses for in TMS?
• 3 ms before main pulse-First weaker pulse can preferentially stimulate GABAergic inhibitory interneurons- can see effects of inhibition on certain pathways
• 10 ms before main pulse- first pulse can sensitize effects of second pulse
• 200 ms before main pulse- first pulse can diminish impact of second pulse
• Depends on timing
o Study excitatory vs inhibitory pathways interactions
What are online repetitive trains for in TMS?
- 4-5 pulses in a row that extends out effect: more time to study task
- Effect of stimulation is no longer than the pulse itself
What are offline rTMS for in TMS?
• Repeated stimulation over extended amount of time
o Has effects that outlast duration of stimulation itself
• Low frequency rTMS
• Theta burst
o Trains of pulses in a particular pattern (theta frequency pattern)
Where and what method of TMS is the safest?
• Have set safety controls
o Regulate frequency of stimulation and brain location of stimulation
Paired and single pulses of TMS are safest
What are the questions in the TMS safety screening?
• Safety screening-TMS can induce epileptic seizures
o Do you suffer from epilepsy?
o Do you have any first degree relatives who suffer from epilepsy?
o Have you ever been diagnosed with hydrocephalus or increased intracranial pressure?
o Have you ever suffered a serious head injury or a stroke?
o Do you suffer from migraines or severe and frequent headaches?
o Are you taking any drugs for a neurological or psychiatric condition?
o Do you have a pacemaker?
o Do you have metal clips or any other metal in your head other than dental fillings?
o Do you have a heart condition?
o Is there a chance you might be pregnant?
o Have you ever had a fainting spell or syncope?
Not excluded on this category
Describe Kanwisher (1997)’s study, what was found and why it is such a cited study
• Kanwisher 1997
o Compared brain activation for faces to a range of other categories (objects, houses, body parts, scrambled objects)
Looked for region of brain responding preferentially to faces
o A small region in ventral temporal cortex consistently showed high activation for faces
o Cited so much because early paper that looked for modalities in the brain
Perspective that we should be looking for little modules in the brain that do specialised function
Precursor to widespread approach of localising brain regions
o fMRI experiment
Describe Haxby’s 2001 study, what was found and the impact of the study in the field. Describe limitations of the study
o Used patterns of activation to predict the category of picture subjects were viewing
o Took activation patterns of even runs (cross-validation) and made pattern template
Computes correlation for patterns between runs
Similarity of patterns measured using correlation between voxel response patterns
o Did not look at specialised regions- look at activations around specialised regions
o Birth of decoding approach
Try to patterns of activation in brain and predict what a person is looking at
o About pattern of activation amongst multiple regions that tells us what the brain is looking at
If removed major area postulated to be responsible for particular object, could still infer what object the person was looking at
o fMRI experiment
o Challenge to assumption of modularity
o Thought patterns of activation more important than modules
o Used machine learning
o However, limitation:
If the entire pattern of activity across IT cortex determines what we’re going to see, idea falls down with downstream perspective
• The distributed pattern of activation could just be due to downstream communication to other brain parts
Compare Kanwisher’s 1997 study and Haxby’s 2001 study
o Their approaches are not mutually exclusive
o However, their two perspectives cannot be resolved due to the process of selection of controlled stimulus
Modular and distributed are not easily detangled
Kanwisher-
-Modular
—Modules responsible for specific functions
-Activation
-Finds area that responds strongest to stimulus, which is what she labels as the function
Haxby-
-Distributed representations
—Patterns of activation that determine what the brain is seeing
-Information
Describe the approach of representational geometry (kriegeskorte 2013)
- How brain activity is measured
- What the information can be used for
- What categories are the most prominently separated
• Representational geometry (Kriegeskorte 2013)
o Information based approach
Measure brain activity using recordings (e.g. fMRI, EEG)
• Compute correlation distance between stimuli in activation patterns (like Haxby)
Measure brain using behaviour
• Collect behavioural ratings for stimuli
• Compute distance between ratings
Also, can construct computational models
The collective set of distances (from brain, behaviour or models) define representational geometry
Compare geometry between brain representations, behaviour and models
Correlation tells you how far things are in representational space
• Can make similarity matrices
Brain cares a lot about separation of animate vs inanimate object
• We have to react to animate objects more dynamically than inanimate objects
Describe Maguire et al.’s 2000 study on taxi drivers and what it found
• Found that taxi drivers in right posterior hippocampus showed slightly thicker/more volume but found that taxi drivers had a smaller right anterior hippocampus compared to controls
o Posterior hippocampus-affected by intense training
• Volume of right posterior hippocampus increases as the time the participant spent as a taxi driver increases
• Volume of right anterior hippocampus decreases as the time the participant spent as a taxi driver decreases
How did Maguire et al. 2000 control for experimental bias?
• To control for experimenter bias in the MRI data, used blind observers to do the pixel counting (verify that the results had real effects)
Describe the process of measuring cortical thickness with MRI?
• MRI-cortical thickness
o Original structural image
o Image with skull removed
o Determine borders of cortical gray matter
o Measure thickness of cortical gray thickness
Describe the two measures of Gieed and Rapoport’s 2010 study and the point of the study
• Diffusion Tensor Imaging (DTI) • MRI-cortical thickness and volume o Grey matter o White matter • Development trajectories
What is the development trajectory of white matter and how did Giedd and Rapoport 2010 visualise this? What influences white matter during development and can these changes always be seen?
o White matter increases as a function of age
Visualised by DTI
Connections between brain areas are being fortified at different times- its not just a matter of simple growth
• Sequence of events could affect higher order cognition and connections
o Deficits can either be reflected or not reflected (if they are reformed) in adults
By studying patient groups as adults and ignoring developmental trajectory in children, could miss some part of the story
What is the development trajectory of grey matter and why?
o Grey matter increases until the age of around 10 and then decreases as a function of age (U shape trajectory)
Associated with higher order cognition
Increase may be due to synaptic formation, decrease may be due to synaptic pruning
What is the difference between synaptic formation and synaptic pruning?
• Synaptic formation-> potential connections that could be used for a specific function
• Synaptic pruning-> for memory and knowledge. Prunes the irrelevant neurons
o The extra formations are noise
What is the subplate in the brain and what is it used for? What is its developmental role?
• Crucial structure for vision
• Special group of cells that are present in development that just disappear from the brain in adults
o Crucial for setting up connections in vision and preparing the brain to see and perceive, but once their job is done they’re gone
• Special category of cells that disappear after trajectory
What is the development trajectory of total cerebral volume?
o Total cerebral volume
Hit a peak at adolescence (girls- 10, boys- 14)
U shaped trajectory
However, size of brain doesn’t really determine intelligence
What is developmentally needed to make a good brain?
o If you want to make a good brain, need perfect sequence of changes/activity throughout development
Describe the developmental changes of child onset schizophrenia and why it is important to look at this developmentally
o E.g. child onset schizophrenia
Schizophrenia affects cortical thickness
First stages- affect some parts of the brain, but over time, damage changes and spreads all over the brain
Cannot look at a single timepoint at a trajectory-> could miss a lot of important conclusions
