Executive Function (and Schizophrenia) Flashcards
(40 cards)
What are ‘executive functions’?
Umbrella term for high level cognitive control functions necessary for complex behviours such as complex decision making and planning.. Can be assessed using neuropsychological tests.
Most commonly investigated are response inhibition, updating (requiring working memory) and set shifting (i.e. flexibility). Mediated in frontal lobe.
What is response inhibition? How can it be tested?
Ability to inhibit automatic proponent responses.
Test using:
* Stroop test: name the colour of the word not the word itself (automatic response is to read the word) (incongruent task)
* Stop-signal: have task e.g. say right or left when arrow presented. Then introduce a ‘stop’ signal during reaction time of a trial. Record time to inhibit
* Measuring transient β-bursts (EEG) of ~13-30Hz indicative of inhibition initiation (Wesel et al 2020)
What is working memory? How can it be tested?
Ability to temporarily hold information and update old irrelevant information with new, relevant information.
Test:
* N-back test: indicate whether the stimulus matches that two stimuli before
* Letter memory: letters are presented one-by-one. After each letter say the previous 3 letters.
What is cognitive flexibility? How can it be tested?
Ability to switch between tasks or mental sets.
Test:
* WCST: sort cards by colour, then shape, change according to feedback
* Tower of London: rearrange blocks in as few moves as possible.
* Learning reversal tasks
How can emotional processing be separated from executive functions when testing? Does this work?
Difference between hot and cold tasks.
* Cold tasks do not have emotional significance attached
* Hot tasks have an emotional element (e.g. performance determines punishment or reward)
* Emotion tends to slow down processing.
Problem: even ‘cold tasks’ can effect emotions - MDD patients perform significantly worse in a trial following -ve feedback (as more sensitive), meaning trials are no longer independent.
What is a major problem when interpreting results from an executive function test?
Task impurity: most tasks require a combination of functions (i.e. they are not isolated).
Therefore results need to be in context of several functions.
Give a possible network organisation used to explain working memory. What are the arguments for and against?
Baddeley model 1986: a central hub allocates information/tasks to specialised sub-areas (e.g. for each sensory system)
Later an ‘episodic buffer’ added to model to provide unified representation for long term memory.
Supporting arguments:
* Brain lesions and imaging studies show specific areas are heavily correlated with specific functions.
* Distinct functions can occur simultaneously (e.g. verbal + visual task much easier than verbal/verbal task)
Against arguments:
* The ‘central hub’ is not well specified and has not been found
* Doesn’t capture WM interaction with long term memory or other EFs well
What are the main theories for how different executive functions are achieved? (Give evidence)
Unity (‘single-factor’) model: all EFs are rely on a single cognitive ability (highly integrated)
* Stong correlations across tasks (e.g. tend to be good at all or bad at all)
* Particularly useful for assessing conditions like ADHD or frontal lobe damage
Segregated model: EFs are distinct but related skills mediated by different networks (or sub-networks).
* Some individuals are strong in one EF but weak in another
* Particular functions associated with particular brain regions
What theory did Freidman and Miyake present in 2007 for the network organisation of EFs?
‘Bi-factor’ model (Friedman and Miyake)
* There is a common ‘EF factor’ underlying all tasks
* Working memory and flexibility have their own ‘specific factors’
Used different tasks for each function and compared results to see the ‘correlation value’ - not ~1 (unity not complete)
Which parts of the brain are important for which executive functions?
Common: dlPFC, anterior CC, fronto parietal
Inhibition:
* Basal ganglia
* Conflict monitoring ACC
* dlPFC top-down control
Working memory:
* dlPFC more for spatial working memory
* vlPFC non-spatial WM
Flexibility:
* Rule-switching = lPFC (lesions allow learning of a rule but not switching)
* vlPFC = implemetation of switch (activity at point of switching)
* Reversal learning = OFC (monkeys with OFC damage struggle)
Why is it important to understand executive functions?
Implicated in many disorders (show different EF profiles):
* ADHD shows deficits in inhibition whereas reading disorder in WM
* Depression: deficient updating (Freidman et al 2018) but not flexibility (shifting)
How much are executive functions determined by genetics? (Present evidence)
Ability = genetics + environmental experience
Test using twin studies (Freidman et al): using Monozygotic twins share 100% genes, dizygotic twins share ~50% but grow up in similar environments (same household):
* Individual differences in EFs are strongly genetically influenced and stable across time (17-23yrs)
* Environmental differences account for the change across time seen
* Updating correlated with IQ more stongly and updating is influenced by genetics more strongly (caveat - IQ tests may bias towards WM?)
How has task impurity across EF investigation been tackled? (Freidman and Miyake)
Friedman and Miyake approached using 3 tasks to investigate each function (total 9) and comparing across. Having 3 for each allows diversity within each function to be seen (more reliable results)
- ‘Common factor’ is the shared function (accounts for approx. 19% of the variance seen)
- Inhibition can be used as a proxy to CF since it is correlated equally with updating and set-shifting
- The rest of the variance comes from updating and set-shifting specific factors for each individual.
How are EFs investigated?
Mainly correlation studies:
* Behavioural tasks for ability (e.g. CNTRICS tests)
* Imaging studies (fMRI) activity for brain region
* Neurophysiological findings (e.g.
* Measuring transient β-bursts (EEG) of ~13-30Hz in right FC indicative of inhibition initiation (Wesel et al 2020)
* Neurochemical findings
Causal studies:
* Lesion observation in humans
* Lesion studies in non-human primates.
Give an example of neurochemical dissociation for flexibility:
Neurochemical dissociation between flexibility.
* In Lat PFC, DA (not 5-HT) necessary for flexibility
* Whereas in OFC, 5-HT not DA required
* Slightly differenct tasks used to target specific area (both flexibility but rule switching task for LPFC and reversal for OFC)
* Therefore was difference due to task or area?
Why is it difficult to measure executive functions in patients with severe ADHD?
Attention deficit hyperactivity disorder.
* Deficient attentional processing makes it difficutl to perform cognitive tasks
* E.g. Stop signal reaction time (SSRT) for inhibition requires high attention to notice and attend to stop signal.
* E.g. WM tasks (such as 2-back task) requires a significant attentional period for several trials.
Is there a way to test these functions independently?
Are questionnaires useful?
Can be a useful measure of concious elements of processing.
However:
* Very subjective
* Confirmation bias difficult to avoid
E.g. In a study on PFC contribution to visual memory: learn association between objects and choose correct pair in FCT
* Then had to report if they ‘knew’, ‘remembered’ or ‘guessed’ - very difficult to answer that (can be interpreted differently)
Which brain areas are involved during the Stroop task?
- ACC highly active during incongruent tasks (e.g. Stroop) i.e. when there is conflicting information
- Signals to dlPFC (high level control) which implements top-down control to solve conflict
What is the evidence for β-burst involvement in inhibition processing?
Correlation:
* Wesel et al 2020: Transient β-burst activity (13-30Hz) (as opposed to sustained activity) is strongly apparent just preceding successful inhibitory response.
* Does show significant variation amongst individuals
* Choo et al 2020: loss of β-burst activity (due to frontotemporal damage) seen with inhibitory control deficits (SSRT) (failure rate x5 compared to healthy participants)
* Choo et al: when β-burst activity did occur in right frontotemporal area, stimulates activity in SMA allowing effective implementation of inhibition.
What is the distributed parallel network model for executive functions?
Gratton, Ladwig and Perez et al 2024: there are 6 major networks with different ‘connectivity fingerprints’ which have weighted responsibilities. These overlap in some regions and are distinct in others:
- Fronto-parietal: central executive network (sensory map)
- Default mode: for internal control and social cognition (least activity when core function occuring)
- Salience: responding/noticing to an environmental stimulus (active during attention)
- Cingulo-opercular: regulates motivation and pain
- Doral and ventral attentional networks: DAN for top-down control (OFC & dlPFC) and VAN for bottom up stimulation (e.g. ACC)
Provide evidence for a cause of OCD due to reduced connectivity:
Functional connectivity study (Vaghi et al 2017):
* Poor attentional set-shifting (Flexibility) correlated with reduced vlPFC - Caudate connectivity.
* Poor goal-oriented decision making associated with reduced dlPFC-Putamen connectivity
Striatum has a role in habit formation, therefore reduced connectivity may disrupt habit control and learning.
What are the difficulties in producing a uniform concensus for distributed parallel networks in the brain?
Generally agreed that there are networks of distributed activity in particular brain regions for particular executive functions (e.g. attention, inhibition, default mode…). These overlap somewhat (conducive with bi-factor/unity-diversity model).
Difficulting in agreement of each network definition (which function and brain regions in each network?)
* Mostly correlational imaging studies while performing tasks - task impurity (i.e. tasks supposedly testing same function may in fact activate different areas
* Different naming systems (require anatomical map)
* Inter-personal variation: averaging activity across many participants reduces accuracy of a single map (but there are feasibility and cost constraints) (Dworetsky 2021 - mapped ROIs of particularly high variability)
Provide evidence of ephaptic communication being necessary for spatial working memory:
Wilson & Jones 2005:
* Mice trained in a maze (control maze has only route)
Correlation evidence:
* Hippocampal CA1 shows θ ~10Hz activity approx. 40ms before same pattern in mPFC during encoding phase of spatial WM
* Coherence not seen in error trials
Causal evidence:
* Blocking synchrony impairs spatial WM (Spellman et al 2015)
* Optogenetic inhibition used.
Give examples of ephaptic activity being involved in EFs
- Hippocampal CA1 → mPFC information during encoding phase of spatial working memory: coherent θ ~10Hz activity which is causally involved in spatial working memory.
- Between CA1 and OFC when encoding contextual information (e.g. make a particular decision only when in one environment) - high coherence during decision point (Elston & Wallis)
- β-burst activity correlated with inhibitory control initiation and loss associated with deficits in inhibition (e.g. SSRT trials)
