PFC Flashcards

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1
Q

PFC and personality

A

Link bw personality and PFC – esp. personality expression, moderating social behaviour.
Damage causes deficits in concentration, abstracting, judgement and problem solving.
Destruction of FL = inappropriate social behaviour

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2
Q

How did we come to know the PFC plays a role in personality?

A
  • Phineas Gage.
  • But PFC damage doesn’t always cause personality changes.
  • E.g. Welt’s case of man who fell out of window. Experienced big personality changes, which went back to normal after about a month.
    So Welt said personality change is more often absent than seen – examined 9 PFC cases and found significant orbitofrontal damage, and said this = personality change causation.
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3
Q

Why did people initially think the PFC was a silent area, and why did they then change their minds?

A

They initially thought it was silent bc lesion evidence was contradictory and not conclusive. However, studies of monkey lesions showed marked change in behaviour; PFC lesions caused aggression, impulsivity, sociality.

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4
Q

What does the PFC do?

A

Coordinates action, long-term planning and decisions, inhibition, determine consequences, social control.
HIGH LEVEL COGNITIVE PROCESSES GOVERNING WAYS OF BEHAVING OPTIMALLY AND APPROPRIATELY.

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5
Q

Does the PFC deal with routine or non-routine functioning?

A

PFC does not support routine functioning; these are things which are largely autonomic and well-rehearsed.
PFC deals with non-routine function, for instances mental operations which are poorly-rehearsed, or when there has been a behavioural impasse.

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6
Q

What is an example of this?

A

Reading is a low level process, which PFC has little executive function role in. However in the context of an exam hall, the PFC will inhibit the ‘reading aloud’ response that might otherwise go uninhibited in a more appropriate social context.

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7
Q

What is utilisation behaviour and why does it happen?

A

Utilization behaviour is the uncontrollable use of objects as they are seen in the environment: e.g. locking every door they come across with a key in it. It is social inappropriate, and makes you a ‘slave to the environment’.
Damage to the PFC causes this, as utilization cannot be inhibited. Normally, the PFC exerts top-down control over the rest of the brain, modulating other systems. (E.g. here, the motor system).

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8
Q

Is the PFC important for novel stimuli? What is the evidence?

A

Yes. When responding to unexpected novel stimuli, P300 is shown when the target is detected or when unexpected stimuli are.
Controls and PFC patients show no difference in P300 when target detection happens, but PFC patients show no P300 in response to novel stimuli, whereas controls do.

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9
Q

What is some evidence for the PFC’s role in working memory?

A

Monkeys with PFC lesions show STM deficits; they fail to retrieve food from a cup even if the food was only out of sight for a few seconds: they were unable to hold the information in mind.
This is backed up by other monkey studies, where non-lesioned monkeys showed enhanced PFC neural activity in the delay where the reward couldn’t be seen – suggesting the PFC is actively maintaining the representation of the reward.

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10
Q

Is the PFC involved in prospective memory?

A

Yes. Prospective memory = remembering to carry out an intention after a delay. PFC patients show deficits in long term planning, suggesting a prospective memory deficit.
However, in an experiment where PPs had to carry out an action after some stimuli but not others, there was bilateral FL activation, but different brain regions showed elevated activation too during specific sub-conditions, suggesting the role of other brain regions in prospective memory too.

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11
Q

Does the PFC have a role to play in delayed gratification?

A

Yes! PPs had to imagine spending certain amounts of money in a timeframe, OR just what the money could buy. When imagining spending the money in the timeframe, there was more rostral PFC activation when PPs chose to delay monetary gratification, suggesting the PFC was involved in the future planning/delayed gratification responses.

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12
Q

Are there deficits seen in these kind of decision making tasks in PFC patients?

A

Yep! Damage to the ventromedial PFC results in poor decision making (even when other intellectual functions are unimpaired). E.g. patient EVR – always made bad decisions, but had other normal functions (STM, WCST, IQ).
In tasks where you had to choose cards from low reward/punishment and high reward/punishment decks, healthy controls learned v quickly to go for the former, whereas EVR chose the latter.

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13
Q

Is there any difference in social behaviour depending on PFC damage onset?

A

Yes. Lesions before 16m result in severely impaired social behaviour, despite otherwise normal functioning.
Young onset PFC patients show more defective social/moral reasoning than adult-onset – psychopathy-like symptoms if onset is early.

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14
Q

Does the PFC have anything to do with humour?

A

Yep!
Damage to the right FL is associated with disrupted humour appreciation abilities – they react less to humour and have diminished responses to it emotionally.
Suggested that verbal humour is dependent on holding the details in working memory (and being able to pay attention to the details) and this might be why PFC patients show the deficit in humour appreciation.
Also, it is thought that the right FL is responsible for integrating cognitive and affective information, and this is needed to find jokes funny!

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15
Q

But is the PFC a singular system?

A

No, probably not. There is typically low correlation bw different PFC task performances, factor analysing symptoms shows they don’t load on to one factor. Different symptoms are related to impairments on different clinical PFC tasks.
Some symptoms are independent of all others in most cases (confabulation, e.g.)
NEUROIMAGINING DATA SUGGESTS FRACTIONATION OF THE PFC/EF SYSTEM.

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16
Q

Why is it sometimes hard to diagnoses PFC/dysexecutive syndrome?

A

Because there’s so many symptoms! Which are all involved in slightly different parts of the brain, and some can even be contradictory (euphoria/apathy). Shallice & Burgess thus put together the Multiple Errands Test to try and sort it all out.

17
Q

What is the Multiple Errands Test?

A

MET = task where given list of things to buy, list of rules, and then have to go shopping! People with PFC lesions simply can’t do it – even though they completely understand the list and the rules.

18
Q

Can PFC patients task-switch?

A

Not very well. This is tested in a task where PPs are given 4 booklets, each with six parts and are told to complete one part of each in 10m. YOU CANNOT COMPLETE ALL OF IT IN 10M. PFC patients fail this task, because they cannot task switch like typical controls.

19
Q

Does the specific place the lesion is in affect performance on the Brixton Spatial Anticipation Task?

A

Yeeeees indeed it does. Controls make 18 errors average, and so do posterior PFC damage PPs. Anterior PFC damage – 24 errors, and bifrontal PFC damage = 30 errors! Research like this could help us to pin down what bits of the PFC support what function.

20
Q

How do PFC patients perform on the Haylings sentence completion task?

A

PFC patients on the whole are slower to respond. Bifrontally damaged PFC patients show significantly more errors.
BUT annoyingly for us, there seems to be a dissociation bw performance on initiation tasks and suppression tasks - you tend to do well at one and bad at other, and patients all show different pattern of results.
SO: PFC can’t be a unitary executive system. Different lesions lead to different deficits, meaning the PFC must be made up of smaller sub-components.

21
Q

So what DO the different bits of the PFC do?!

A

Anterior = multitasking,
Dorsal = mentalising,
Lateral = episodic retrieval.
—- Ventrolateral = processes available environmental info. Storing of different forms of info? (controversial)
—- Dorsolateral = processing info NOT in environment (many bidirectional connections with ACC, which detects need for top down control)

22
Q

How does the PFC know when it needs to exert top-down control?

A

Might be a Dorso-lateral-ACC link? BUT this is not consistent with finding that pts w/ ACC damage have no problems with inhibition.
Might be coordinated by tothe ROSTRAL-PFC. Patients with rostral PFC damage don’t normally show deficits in EF, but MET shows they struggle to follow rules, multitask, imagine and retain episodic memory.
Thus, it is suggested that the rostral PFC is the gateway by which INCOMING info is integrated with INTERNALLY GENERATED info (e.g. HPC, diencephalons).

23
Q

What is Shallice’s Supervisory Attentional System model (SAS)? What are the first 3 components?

A

It is made up of 4 components. The first: action/cognitive units. These are the things we learn in life (walking/reading e.g.) which make up the building blocks of complex behaviour. They are triggered by the environment.

Second, there are schemas: collections of action/cognitive units. They become linked through rehearsal, and thus many schemas are also automatically triggered by the environment, like action/cognitive units are.

Third, is contention scheduling. This is the process of triggering schemas. Many schemas can be triggered in response to stimuli encountered in the environment.

24
Q

What parts of the brain are these these 3 components controlled by?

A

They are controlled by various brain regions, depending on what component and the environment. HOWEVER, these three components cannot explain everything, bc no two situations one might encounter are exactly the same: ESPECIALLY social situations, which the PFC plays a role in.

25
Q

So, what is the final component of the SAS model?

A

The supervisory attention system. This is synonymous with the functions the FLs support – they support the SAS and the SAS’s main task is to TWEAK contention scheduling to make it appropriate, or to inhibit it when it is not. SAS alters the valence of contention scheduling, so the person is acting optimally and appropriately.
And so PFC damage = inappropriate behaviour. SAS suppresses urges to act inappropriately/suboptimally.

26
Q

What is the Goal Management Training for PFC damage?

A

GMT is based on a simple principle of stopping the automatic pilot, and taking the time to state one’s goals periodically before and during a task. This intervention was formulated on the basis of the idea that the brain’s sustained attention network supports EF, and when there are lapses in sustained attention (as is common in PFC patients) there are also lapses in intention, thus failure to complete tasks. GMT avoids this, using periodic alerts to the sustained attention system (evidenced by neuroimaging) to ensure attention and intention are retained. It’s been shown to work in TBI, healthy ageing, stroke and post-critical care patients.

It is ‘metacognitive’.

27
Q

What are the 4 key aims of PFC rehabilitation?

A

(1) restoring or re-training executive functions;
(2) compensating for executive impairments through the use of internal or external strategies;
(3) promoting modIfication of the environment or behaviour by working with carers, family and friends and behaviour modification techniques; and
(4) pharmacological treatments

EVIDENCE FOR ANY OF THESE IS SCARCE.

28
Q

What is the attention and problem solving group approach?

A

People with PFC lesions meet in a group setting and work through a framework: e.g. ‘What do I need to do?’ – STOP/THINK to define goal – think of possible solutions – pros/cons of each – DECIDE – PLAN – carry out (adjust and monitor progress throughout) – EVALUATE.

29
Q

Does it work?

A

Some improvements shown, but not very impressive ones.