Session Nine (Executive Function and Neuro-Rehab) Flashcards

1
Q

What is Executive Function?

A
  • Abilities that enable a person to determine goals, work out ways of achieving them and then follow through with them in the face of competing demands and changing circumstances over long periods of time.
  • Allow the person to engage in independent, purposive, self-directed and self-serving behaviour.
  • So long as EF are intact, a person can sustain considerable cognitive loss and still continue to lead an independent and self-serving life.
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2
Q

How do you distinguish Cognitive from Executive functions?

A
  • EF relates to how a person goes about doing something (will they do it? how? when?)
  • CF relates to whether a person can do something (can they do this? how much of this can they do?)
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3
Q

What area of the brain has been historically associated with EF? Based on what evidence?

A
  • Frontal lobes
  • Believed to be somehow related to the programming, verification and regulation of human behaviours. Damage to the FL leads to complex behaviour being replaced by more basic and stereotypic behaviour.
  • As exampled by Phineas Gage, 19th century man who received substantial damage to the frontal lobe and displayed marked ‘animal’ and ‘instinctive’ behaviour’
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4
Q

How did Luria divide the brain?

A

Into 3 functional units:

  • Brain stem; maintains and regulates cortex arousal
  • Temporal, Parietal and Occipital lobes; encode, process, store information
  • Frontal lobes; Programme, verify and regulate human behaviour.

Therefore, damage to the frontal systems results in complex behaviour being replaced by basic/stereotyped behaviour.

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5
Q

Outline Shallice’s initial SAS model of executive function?

A
  • Supervisory Attentional System model
  • Multi-process model that improved on Luria by utilising two new components, the Supervisory Attentional System (SAS) and Contention Scheduling (CS)
  • Suggests that specific schemas triggered by environmental stimuli lead to a series of automatic actions without the need for conscious control.
  • CS is the step between schemas and actions that unconsciously decides which actions will be taken.
  • However, the SAS can exert top-down, supervisory control on the CS in cases where routine actions are not appropriate.
  • Leading to novel behaviour in certain circumstances.
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6
Q

What specifically does the SAS do in Shallice’s initial model of executive functioning?

A
  • Has control over CS
  • Monitors conscious, deliberate planning of action
  • Handles novel situations that cannot be solved by previously learned schemata
  • Creates new schemata as and when necesarry.

Shallice described 5 circumstances when the SAS becomes activated:

1) Planning or decision making
2) Error correction or trouble shooting
3) Novel or unlearned sequences of actions
4) When threatened
5) When trying to overcome habitual or automatic responses

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7
Q

How did Shallice build on his initial model of SAS?

A

Outlined the 3 procedures SAS is capable of:

  • Construction of temporary schema
  • Implement temporary new schema held in working memory
  • Assess and verify new schema (can lead to rejection, alteration or incorporation as new schema)

Essentially expanded upon it by delineating processes involved in SAS. Supported by lesion and computational modelling studies e.g. Hewitt (2006) and Fish (2007)

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8
Q

Outline Stuss and Benson’s Tripartite model of Executive Function?

A

3 systems interact to monitor attention and executive functions:

  • Anterior Reticular activating system
  • Diffuse Thalamic projection system
  • Fronto-Thalamic gating system
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9
Q

What is the role of the Anterior Reticular activating system in Stuss’ model of Executive functioning?

A
  • Maintains general arousal of individual

- Damage therefore results to loss of consciousness

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10
Q

What is the role of the Diffuse Thalamic projection system in Stuss’ model of Executive functioning?

A
  • Alertness to external stimuli over short periods

- Damage therefore leads to distraction by external stimuli

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11
Q

What is the role of the Fronto-thalamic gating system in Stuss’ model of Executive functioning?

A
  • Responsible for higher level cortical functioning

- Damage therefore results in inattention, lack of insight and goal-neglect

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12
Q

Outline Stuss’ detailed analysis of frontal lobe function?

A

Suggested the frontal lobe has 4 key functions:

  • Executive cognitive functions (e.g. task setting and monitoring)
  • Energisation
  • Behavioural and emotional self-regulation
  • Metacognition

Based this on highly detailed focal lesion studies, however emphasised how interconnected the frontal lobe is with other areas of the brain therefore we can’t be entirely sure which areas relate to what.

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13
Q

Outline the Elephant and Rider theory of executive function?

A
  • Elephant represents 99% of our mind; our emotions and automatic thought processes
  • The elephant is powerful but not very sophisticated
  • The rider attempts to exert some control
  • Sometimes this is possible but the elephant is hard to control
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14
Q

How did Goldstein (2014) describe executive function?

A
  • As 33 different but over-lapping functions
  • Including planning, working memory, attention, self-monitoring and inhibition
  • Made the point that EF is an umbrella term used to describe a diverse range of cognitive processes associated with the frontal lobes.
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15
Q

How can you summarise the different models of executive function?

A
  • Different models emphasise different components, but share some overlapping themes e.g. organised representations of actions, goal neglect
  • Some evidence for localisation of different executive function in PFC
  • Role of emotions acknowledged, but less models representing mechanisms of influence.
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16
Q

Why do we test executive functioning?

A
  • To make inferences about neural basis of underlying function through lesion studies
  • Use test results to guide diagnosis, treatment and outcome measurement
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17
Q

How do we test executive functioning?

A
  • Verbal fluency
  • Stroop (inhibition)
  • Trails (switching or dividing attention)
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18
Q

What were Roca’s criticisms of measures of executive function?

A
  • Most of the differences in scores achieved by patients could be explained in terms of differences in fluid intelligence (therefore are inaccurate)
  • Others only measure deficits that arise from lesions to the most anterior regions of the right frontal lobe (therefore are incomplete)
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19
Q

What is the Stroop method of measuring executive function?

A
  • First asks patients to name the colour of a box (colour naming)
  • Then read a colour word in black and white (reading)
  • Then read a colour word in a different ink colour than the word itself (inhibition)
  • Then alternate between ink colour and word reading (inhibition and switching)
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20
Q

What is important to consider when interpreting executive functioning test results?

A
  • How do they compare to other individuals their age/ education/ intelligence…
  • At what level are they performing at a level below the general population?
  • Could other factors such as pain/ anxiety/ medication/ motivation have affected their performance on that day
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21
Q

What are some more general criticisms of neuro-psych measures of EF?

A
  • Lack ecological validity, the extent to which they predict an individual’s ability to drive/work is limited
  • This is obviously the most important thing from a medico-legal and treatment perspective
  • But these tests are mostly able to detect abnormalities, not predict function
  • And in fact many patients struggle with the novelty of the test but when presented with a familiar task can perform quite well
  • Absence/ presence of cues and distractions as well as degree of effort and emotional issues will be different between test and real life conditions
22
Q

What is an alternative to traditional measures of executive functioning believed to have greater ecological validity?

A

Performance based tests

  • = alternative approach that involves studying patient performance in real-world tasks
  • More in line with OT approach than clinical neuro-psych
23
Q

Give some examples of performance based tasks of EF?

A
  • Multiple errand test
  • Multi-level action task
  • Naturalistic action test
24
Q

What are some issues with performance based tests as a way of measuring EF?

A
  • Difficult to standardise as performance can vary according to the environment in which assessment carried out
  • Often lacks a norm to compare to, so almost entirely qualitative approach
25
Q

When do we use standardised and functional measures of EF and what are their fundamental differences?

A

S better prior to treatment, F better during treatment.

S = based on what a person has/is, diagnostic, indirectly related to treatment, only tests one situation

F = based on what a person really does, helps select treatment, tests a number of situations

26
Q

What are some issues with use of observational methods of measuring EF?

A
  • Limited experimental control
  • Time consuming
  • Expensive
  • Risky
  • Aversive
27
Q

What factors are important to consider when dealing with difficult behaviour in a brain injury/ neuro-rehab patient?

A
  • Effects of the Injury (e.g. decreased noise tolerance, communication difficulties, fatigue, poor impulse control, other ef difficulties)
  • Feelings caused by being Injured (e.g. frustration, anger, anxiety, intimidation)
  • Factors that can maintain these feelings (e.g. inability to verbalise discomfort, struggles making sense of environment, perception of others as confrontational)
  • Environmental triggers (tiredness, hunger, noise, other patients, memories)
28
Q

Which patients are typically put forward for NR?

A
  • Brain injury
  • Spine injury
  • Peripheral neurology
  • Progressive conditions

Normally caused by; stroke, inflammatory conditions, trauma, anoxic injuries…

29
Q

What are some stroke risk factors?

A
  • Male
  • Age
  • Ethinicity (south asian, African)
  • High BP
  • AF
  • Cholesterol
  • Smoking
  • Alcohol
  • Diet
  • Weight
  • Fitness
30
Q

What are the most common causes of TBI?

A

Traumatic Brain Injury:

  • RTAs
  • Falls
  • Assaults
31
Q

What are the risk factors for TBIs?

A
  • Male (3x)
  • Age (tri-modal distribution; below 4, 15-29, above 65)
  • Risk taking behaviour (mainly alcohol)
32
Q

What are the two types of TBI?

A
  • Primary = mechanical effects of applied force e.g. skull fracture, haemorrhage, acceleration-deceleration forces and diffuse axonal injury
  • Secondary = resulting from a compromised oxygen supply, swelling, raised ICP
33
Q

What are the initial management steps involved in brain injuries?

A

1) Minimise factors likely to lead to secondary BIs e.g. with neurosurgery, medications, ventilation…
2) Stabilise other injuries and manage other needs e.g. seizure, physiotherapy, nutrition
3) Examine and monitor neurological status e.g. GCS

34
Q

What is the ICF model and how does it relate to Neuro-Rehab?

A

Tate (2010), model for explaining how a condition affects what a patient can and can’t do.

Health condition (e.g. stroke) affects…

  • Body function and structure
  • Activity
  • Participation

Also bares in mind that all 3 of these factors are influenced by contextual factors such as personal factors and environmental factors

35
Q

What are the two main principles of NR and the three processes used to achieve them?

A

Principles:

  • Restoration
  • Compensation

Processes:

  • Direct retraining (e.g. motor aphasia post-stroke)
  • Substitution (the building of a new method of response to replace one damaged irreparably by a cerebral lesion e.g. reading by letter tracing)
  • Compensation (reorganisation of psychological function so as to minimise or circumvent a particular disability e.g. alternative communication strategies such as writing on a slate)
36
Q

What is neuro-rehabilitation?

A

Neuro-rehab can be described as any intervention strategy or technique which enables patients/clients and their families or carers to live with, manage, by-pass, reduce or come to terms with cognitive deficits precipitated by injury to the brain.

It is concerned with the amelioration of cognitive, emotional, psychosocial and behavioural deficits caused by an insult to the brain. Focuses on the cognitive, emotional and psychosocial factors.

37
Q

How did Robertson and Murre (1999) describe functional losses seen in NR patients?

A

Triad of post-lesion states characterised by loss of connectivity:

  • Small loss- autonomous recovery
  • Large loss- permanent loss of function so need for external support
  • Middle loss- this is the difficult group to manage, potentially rescuable lesioned circuits but guided recovery depends on precisely targeted bottom-up and top-down inputs
38
Q

What are the different routes to recovery in NER in terms of neuro-plasticity?

A
  • Repairing the damaged area (restoration)
  • Having the remaining cells work harder (restoration)
  • Re-tunning cells (compensation and restoration)
  • Have another area or network take over (compensation and restoration)
  • use a different behavioural strategy (compensation)

Animal and human studies support the existence of neural plasticity in functional recovery, both spontaneously and in response to treatment.

39
Q

What are the 3 natural recovery mechanisms seen post brain injury that make up the idea of neuro-plasticity?

A

1) Synaptic plasticity, changing synaptic strengths
2) Micro-structural changes (increased synaptic density, remyelination, axonal and dendritic growth and sprouting)
3) Making new neutrons (neurogenesis)

40
Q

What does the recovery curve look like after a brain injury?

A
  • Rapid improvement followed by a slow improvement and plateau
  • Some skills more likely to return than others but many will stop short of premorbid level
  • Reason for slow recovery is processes such as oedema, perfusion changes, inflammation and oxidative stress continue to occur during the period immediately after injury
  • As these slow off and plasticity processes steps in, recovery occurs.
  • N.B. Curve can also dip back down e.g. through learned disuse of a limb
41
Q

What drives recovery post brain injury in the weeks, months and years following the injury?

A
  • Weeks; recovery driven by resolution of pathological processes (oedema, inflammation)
  • Months; recovery driven by spontaneous recovery of neural circuits (possibly caused by resolution of path processes)
  • Years; recovery driven by learning and rehabilitation
42
Q

What does the recovery curve look like for a degenerative condition?

A
  • In neurodegenerative diseases plasticity mechanisms act to maintain function against an overall decline
  • Primary disease processes cause decline
  • Secondary processes such as inflammation, reduced perfusion and oxidative stress all contribute
  • Interventions such as cholinesterase inhibitors may lead to an uptick or slow the decline process
43
Q

What does the body of evidence suggest about the success of “restoration” interventions?

A

Some evidence of effectiveness at training specific cognitive functions e.g.

  • Goal management (executive function)
  • Attention (visual attention therapy)
  • Working memory

But current clinical data is overall disappointing, suggests that training can provide short term benefits on tasks that are trained, or similar tasks, but with very little generalisability.

Melby-Lervag et al (2016) however showed that there might be some transferability in patients trained on a working memory task, but only to very similar tasks not distant tasks like reading.

44
Q

What is INCOG and what did they decide about Cognitive Rehabilitation?

A

International Congress of researchers and clinicians that tried to evaluate the mixed evidence about the efficacy of NR.

Confirmed that certain patients will benefit from it and therefore should be offered. Produced guidelines that provide clinicians with evidence based options.

45
Q

What evidence is there in favour of “Compensation” neuro-rehab training?

A

Waldron et al (2012):

  • 5 participants with ABI trained to use digital PDAs
  • Tasks were set up for them across the week
  • Compared how well they were able to perform these tasks in comparison to those relying on memory alone
  • All 5 did significantly better during the two weeks in which they used the PDA
46
Q

Why is it important to measure the outcomes of NR?

A
  • Determine whether they lead to better outcomes compared to natural recovery
  • If they do, by what mechanism
  • Justify the cost of the service
  • Obtain information needed to modify programmes
  • Obtain information necessary to guide NHS prioritisation
  • Medicolegal reasons e.g. how much compensation is owed to an accident victim
  • Patient centred reasons such as preventing early death, enhancing QoL, helping people recover from episodes of ill health, provision of a safe environment
  • Allows us to set goals for patients, which can then provide them with motivation
47
Q

What psychological changes are common post brain injury or illness?

A
  • Adjustment and loss of our sense of self (i.e. our role at home, ability to work and do the things we enjoy, loss of hopes and dreams, loss of agency)
  • Stress, anxiety and depression coming from major life changes e.g. marital/ sexual/ change of home/ loss of job/ loss of friends/ unable to do things they enjoy/ difficulties in making new friends.
48
Q

What biopsychosocial changes are common post brain injury or illness?

A
  • Physical changes: movement, communication, speech, bowel control, eating
  • Lifestyle changes: independence, choices, self-care skills, where living, who living with
  • Social network: reduces to people who are committed to you, close family and friends
  • Life role may become destabilised
  • Social role and personality can be affected (e.g. may be harder to be as funny or insightful)
49
Q

What evidence exists about the effectiveness of Neuro-Rehabilitation?

A

Cochrane review of 16 RCTs of multidisciplinary rehabilitation programmes for brain injuries performed by Turner-Stokes in 2011:

  • Mild BI = Good recovery when given appropriate info
  • Moderate-Severe BI = Benefits from formal intervention, more intensive programmes associated with earlier functional gains
  • Continued outpatient rehab helps sustain early gains
  • Severe BI = Limited evidence for benefit from specialist care, but no other real options
50
Q

What did Zeiler et al (2015) suggest about neuro-rehab?

A
  • Mouse study
  • Induced strokes
  • Showed that early implementation of training lead to better outcomes
  • Suggests that in the period immediately following a stroke the brain enters a period of heightened responsiveness to training and mediates full recovery from a stroke.
  • Also suggests early rehab should focus on IMPAIRMENT, later rehab should focus on COMPENSATION
51
Q

What was UKROC?

A
  • Study that compared complexity and cost of rehab needs, necessary input from services and patient outcome
  • Basically sought to identify which patients it was cost-effective to provide long term support for (in terms of drop in necessary care later in life) and which it wasn’t.