1
Q
food can be rewarding, why is this dangerous?
A
food is very enjoyable but we cant constantly indulge in it
2
Q
what % of adults in the US are either overweight or obese?
A
68% (Alonso-Alonso et al., 2015)
3
Q
Are people getting bigger over time? why?
A
Yes, the average American adult in 2015 weighed 24 pounds heavier that in 1960
- Cant be due to biology/genetics factors hasn’t been a major genetic change in our genes to account for this
- one major component contributing to this - food reward
- bombarded with food ads/ mcdonalds everywhere you look/ food cues for energy-dense delicious unhealthy foods
- just become very acessible
4
Q
ohw can we use neuroscience to help with weight gain/obesity increases
A
we can use neuroscience to
- understand what is going on in the brain when n are perceiving these food rewards
- help n self-regulate their responses to food rewards (eating behaviour)
5
Q
how can reward cue research help us with drug addiction epidemic?
A
also involves problematic responding to (now drug) cues
drug addiction can be understood as a compulsive and exessive seeking of drug reward
drug reward is what driving the behaviour - we want to use neuroscience to help people change their responses to these cues. reward cue reactivity.
6
Q
does treatment for addiction work?
A
does it fuck!
lack of efficacy of available treatment options for substance abuse disorders (Dutra et al., 2008)
- high drop out rate
- poor sustainability of treatment sucess: only 31% achieve long term abstinence
7
Q
what is a reward
A
Anything that can that is positive reinforcer - so element of subjectivity - do n find this rewarding
8
Q
do you have to enjoy the reward to keep chasing it if you have a problem e.g., heroin addiction
A
- no, a reward involves coming back for more despite not enjoying the reward
- heroin addicts continue to take the substance despite not enjoying it
- Almost like they are a slave to their addiction.
9
Q
are humans the only animals capable of experiencing reward?
A
reward is also seen in any animal that is capable of instrumental learning → changes its behaviour based on a reinforcer. It is capable of experiencing something as rewarding.
All vertebrates, all animals with a CNS. also operant learning is seen in invertebrates - aplysia (Brembs et al., 2002)
10
Q
definition of a reward
A
any stimulus, object, event or situation that is a positive reinforcer because of its incentive properties, it:
- produces pleasure
- OR produces the desire to approach/consume. so a reward could be something that you desire but just dont enjoy it
- this is an important distinction - between wanting and liking we see this in the literature a lot too
11
Q
some rewards are in-born while others we learn trough a form of classical conditioning: unconditioned vs conditioned reward
describe this
A
classify the wards based on their acquisition
- rise in blood sugar levels is an example of an unconditioned reward
- chocolate is an example of a conditioned reward
- juicy bit - all learned rewards are linked to an unconditioned reward → thats what makes them so powerful
12
Q
different ways to classify rewards
A
- based on their acquisition - conditioned vs unconditioned reward
- the way they satiate the hunger - primary vs secondary
- the thing itself - natural rewards (all non-drug rewards that change our physiology) and drug rewards (drugs)
13
Q
classifying rewards in terms of the way they satiate the hunger
A
primary vs secondary
- primary reward - those with evolutionary benefit - serve homeostasis or help us with reproduction. So food, sex are examples of primary rewards.
- secondary rewards - only a means to obtain a primary reward
14
Q
why does it make sense to look at food and drug rewards together
anatomical reasons
A
both rewards engage the same neuroanatomical reward circuits
- the reward circuit is whoring about
- cortical regions - orbitofrontal cortex and insula - representations of reward
- subcortical regions - mainly nucleus accumbens and ventral palladium -representation AND causation of a reward. so in animal study if you stimulate these areas that causes pleasure/wanting reactions
all areas in circuit shown below
15
Q
why does it make sense to look at food and drug rewards together
psychological reasons
A
both food and drug reward categories can be differentiated by
wanting (motivational component)
- often triggered by a cue
- state of anticipation for something in the future
- unconscious and conscious urges, desires, craving elicited by reward cues
- wanting it even if you dont enjoy it anymore
- neurochemical difference: mainly dopamine based
liking (affective component)
- experience of pleasure during reward consumption
- neurochemical difference: mainly opioid based
16
Q
how can we dissociate liking from wanting behaviour in humans/animals
A
animals: liking
- orofacial reactions
- licking behaivour
animals wanting:
- hard work for foor/drugs
- effort
Humans
It’s difficult to measure liking in adults because they always suppress it e.g., the urge to lick their fingers (problem with social norms). Subjective ratings of liking and wanting are often mistaken for each other (problem with definitions). when you ask participants whether they like or enjoy something you will often find its highly correlated with one another
17
Q
dissociating liking from wanting is difficult in humans. can brain imaging help?
A
18
Q
fmri studies on rewards - which type of response do they normally look at - wanting or liking?
A
focus on wanting response
- present pictures of rewards in the scanner
- then look at brain responses
- always seems to be a pavlovian learned response to that e.g., food → cognitive response measurable
19
Q
what is the difference between an exterosceptive and interosceptive cue
A
- exterosceptive means its an external stimulus - e.g., a picure of food//sound of a sizzling pan// olfactory cues // haptic e.g., touching a cig
- interosceptive means its an internal stimulus e.g., tiredness could be a cue to have a coffee// knowing the time of day is 1 can elicit food wanting
20
Q
what are 3 type of ways we can respond to a drug/food cue
A
firstly, there is always an interaction between these cues and our physiology, e.g., if you are starving you will have a different reaction to a food cue if you were full
if its been a while since your last meal - will strengthen your responses to food cues
but in general there are 3 ways we can respond to a cue
- behavioural level - actually moving towards X
- cognitive level - the wanting/craving of X
- physiological level - heart rate/skin conductance/temperature inside
21
Q
what 2 models have been used to look at cue reactivity in alcohol addicted n
A
- the conditioned withdrawal model , Wikler (1948)
- conditioned apetative-motivational model, Stewart et al., (1984)
models differ int he way they explain how cue responses are learned in the first place.
The conditioned withdrawal model argues that during drining, the drink is associated with induces withdrawal state, a drop in blood alcohol level (bad state). Next time n see cue e.g., bottle the cue will induce the withdrawal state (bad).
The conditioned apetative model argues that durign drinking the drink is associated with the pleasurable effects (good). next time n see cue e.g., bottle the cue will induce the same pleasurable state (good).
22
Q
how do we know whoch model - the withdrawal or apetative - actually reflects what happens when n see drug cue?
A
behavioural/physiological level
- We can jut look at what happens when they’re seeing it
- and compare this to the state of withdrawal and also to drug consumption
23
Q
FOOD CUES
neural level of cue reactivity - what areas do we see active?
the reward circuit
A
van der Laan et al., 2011
used method called the activation likelihood estimation method based on 28 studies. method computes the spatial overlap between different activation maps in different studies. then compares that overlap. tothe overlap generated by random maps.
looked at 3 contrasts
Contrast 1: compared activation to food vs control pictures
- extra striate visual cortex (e.g., fusiform gyrus), increased attention, percetual enhancment
- insula - motivational wanting or craving
- lateral OFC - representation of hedonic value, expected pleasentness
Contrast 2: compared activation to food pictures when n were hungry vs satiated
- amygdala - motivational salience detector
Contrast 3: compared responses to pictures of unhealthy vs healthy food
- ventral strriatum - nucleus accumbens (hedonic hotspot) , pleasure generator
24
Q
what areas might we expect active when seeing cue n like
A
- motivational processes - unconscious/conscious wanting or craving
- hedonic processes - liking, pleasure, expected pleasentness
- inhibition control
- self-regulation
- visual processing
- memory
25
what areas are active in both drug and food cue?
meta analysis by Tang et al., 2011 on drug cues active
those that we also saw earlier with food cues
* amygdala
* insula
* OFC
* striatum
additional areas active with drug cues only (Chase et al., 2011)
* ACC
* dorsolateral prefrontal cortex
26
wow fMRI has shown that picture of drug induces activation. ininsula. does this meant he drug caused that?
no, fMRI data is only ever correlational. we would need human and animal studies to determine whether it was causal
* microinjections of opioid agonists in hedonic hotspots (nucleus accumbens) produce reward responses e.g., licking
* patient studies in humans e.g., n undergoing lobotomy with part of forebrain removed; conditions in which n born without a forebrain e.g., hydrancephalic children; acquired brain injury - if any of these n they showed deficits in reward function then you can infer the damaged/missing area had something to do with reard
* deep brain stimulation - use electrodes. used to treat parkinsons. n agree to take part in research. placing pleasure electrodes in animals. before it was beleived the stimulation caused pleasure but later found out that it was just wanting/motivation system they were stimulating
27
how can we use reward cue reactivity research in a more practical context
1. use neural cue responses to rewards as biomarkers. Index people vulnerable to addiction, gage the severity of peoples dependence
2. use to predict future behaivour. scan n, produce drug cues to them, see the activations present in those who relapse later compared to those who dont
3. use to measure treatmetn sucess, explose to cues fmri, n do treatment, expose again to cues fmri - has the treatment helped?
28
do different people show different responses to cues?
Mahler and de wit (2010)
* yes
* study show n diff rewards then measure if they differ in their cue responses to different reward categories
* asked 15 smokers to stop smoking for a while
* then asked them to not eat for a while
* then show them pictures of foods and pictures of cigarrettes
* asked - rate how much this picture is making you crave X?
* left image - found people differ in terms of how much food cues make them crave a food and how much a smoking cue makes them crave a cigarrette
* also - found they are highly correlated with one another. the people showing strong craving to food cue show strong craving to cig cue x
* right image. -asked them to report their tonic - baseline craving. craving induced not by cue but natural hunger. smokers cravings for cigs varied but everyone had the same level of cravign for food naturally
29
study using cue reactivity as a biomarker
McClernont et al., 2008
* gave smokers different questionnairs to gave level of dependence
* scores on this correlated with responses to smoking-rekated vs neutral pictures in the key reward areas (ACC and OFC)
* study showed that neural cue reactivity is a good measure of dependence severity
30
study investigating brain activation in alcohol dependent n vs in n who just drink a lot
Ihssen et al., 2011
* students - heavy drinkers
* then exposed them to pictures of alcohol vsneutral pics
* indeed areas previously shown active with alcohol dependent n were active when shown alcohol
* right insula , left insula, ventral striatum
schlar argued this was probably indexing those with addictive dispositions (esp n with stronger activations)
part 2: exposed them to other rewards
* higher order socially accepted rewards - marriage, money, graduation
* found heavy drinkers showed reduced responses to these cues
* specifically in areas invovled in action planning and action goals
scholar suggestsit likely that the drug was valued more then the socially accepted reward. Placed further up in the motivational hierarchy. Alcohol has taken over as the main motivation.
31
study using reward cue reactivity research to predict future beahvoiur
Demos, Heatherton and kelly (2012)
* 58 female 1st year students
* 6 different categories: food, sexual scenes, n drinking alcohol, neutral people, animals, environmental scenes
* can nucleus accumbens activity predict: weight gain and sexual behaviour in 6 months?
* YES!! bold signal in nACC correlated with scores on sexual desire questionnaire and weight gain in 6 months
* really cool. -they could even differentiate the number of sexual partners diff ppl. inthe study had using this brai activiry
* importantly the effects were specific - so responses to food pictures did not predict sexual behaviour
scholars concluded nACC activity could serve as a proxy for future apetative behaviour and/or failed inhibition (self regulation) by higher order frontal region
32
study using reward cue reactivity research to predict future beahvoiur
addiction realm
neural cue responses detected with fMRI can predict relapse in range of different addictions
* cocaine addiction ( Prisciandaro et al., 2013)
* nicotine dependence (Janes et al., 2015)
* alcohol dependence (Heinz et al., 2009)
33
study using reward cue reactivity to measure treatment sucess
Vollstadt-Klein et al., 2011
* tested cue exposure therapy - a technique based on the principles of extinction
* CET group vs control who recieved standard treatment
* present organism te conditioned stimulus alone without the unconditioned response. the conditioned response then goes down. it is extinguished
* helps n with alcohol dependence deal with their cue responses
* abstinent alcohol dependent n - 9 sessions of CET
* n hold their favorite alcoholic drink and not allowed to consume it
* after the session found the CET group showed a larger decrease of cue responses in key reward areas (INSULA AND ACC )
34
what is neurofeedback aim?
to use responses to cues to actually treat people with addictions
35
what are the different levels of reward behaviour?
at every level we attach a certain value to the reward - how valuable is this?
* at the most basic level - we have wanted and liking responses
* then we have the drug value - thinking about how rewarding. it would be
* then we have the highest level of response - behavioural - the actual drug consumption
36
so we have 3 levels of reward behaviour. different treatments target different levels - which one does neurofeeback come in?
The highest level (the behavioural level) - behaviour modification, psychotherapy, social learning
mid-level (attaching a value to the drug) - reappraisal training
most basic level (liking/wanting responses to the drug) - this where neurofeeback comes in
37
definition of neurofeedback
it is a brain-computer interface that transforms the brain's natural outputs into available sensory outputs (feedback) which can be used to modify behaviour or mental states
## Footnote
basically it is training to self regulate activation in specific brain areas based on feedback
38
what does brain computer interface mean?
Anything that uses the brains output - brain signals to control an external device like a computer.
Neurofeedback is a special case of brain-computer interface
39
Can anyone just do neurofeedback from day 1 and reap the benefits?
No, it can only be achieved through training. they learn to self regulate brain activation in certain areas based on the feedback.
Based on the transformation of the natural output to the sensory output
40
what's umbrella term would neurofeedback fall under?
biofeedback, a broader term though that refers to any technique that provides information about a physiological system e.g., heart (ECR) or muscles (EMG) in order to increase awarness of it or modify it.
biofeedback uses a broad type of measurment techniques e.g., EEG or electrocardiographs.
41
History of neurofedeback: what was a methodological pre-requisit of neurofeedback?
real time fMRI (rtfMRI)
real-time fMRI analyses and preprocesses images in real time during data acquisition
EEG neurofeedback was around way longer - 50 years - before fMRI neurofeedback
42
why was real time FMRI origionally developed?
to monitor the quality of the data during acquisition
but the authors of that first algorithm realised this might be something really cool - thought this could be used for interactive experiments
further work has refined the speed and speed of the technique
43
who were the guys that created the algorithm that allowed for rtfMRI
Cox, Jesmanowiczand Hyde (1995)
44
describe the neurofeedback paradigm to a child
closed loop
* someone is in the scanner and their brains area analysed
* and processed on a computer in real-time
* the output of this analysis is shown to them in the form of a thermometer which reflects how strong or weak the “alcohol area” it
* they then remember the cool tricks they learned in training to decrease the activity and apply it
* again this is processed, and reflected to them via the thermometer
* its a closed loop
45
https://www.brainvoyager.com/tbv/v20\_Demo/TBV\_20\_FFA\_PPA\_FLV.html
watch here, shows how through analysis the data comes in and using a specific software builds up the GLM
and how this is transformed into the feedback
illustrates how real time fMRI analysis works
46
so what can we do with this neurofeedback set up?
whys it so important dawg?
can address 2very important questions
1. are people able to regulate their own brain activity - what about. in areas previously thought to be inaccessible to voluntary control (reward circuits)? this q's about the feasibility of neurofeedback.
2. does this self regulation this brain activation lead to any real change in behaviour cognitive of affective processes?
47
what's the big difference with standard fMRI vs neurofeedback fMRI experiments?
the role of the brain activation
* in standard fMRI brain activation s the dependent variable
* in neurofeedback the brain activation is the independent variable - we manipulate it and see whether this changes emotions, behaviour and so on
48
what things do you need to think about before conducting neurofeedback study
# 1. define target brain area
2. how you present the feedback - thermometer
3. think about whether you want to test transfer - test if n maintain control of the target area outside the scanner
4. what it is you actually want to measure - subjective measure of emotions, behaviour (alcohol consumption)
5. controls to test for placebo effects
49
what target area should you pick?
it depends on the targetted goal. -e.g., if the goal is to improve movement for patients with Parkinson's then you might wanna target a motor area
for this reason knowledge about the neural mechanisms underlying certain behavioural effects therefore are important - e.g.,if trying to improve anxiety then target an emotional areas (Amygdala)
50
what 2 ways can you define target araeas?
* defined anatomically - based on existing theory of boundaries of an area
* defined by functional localiser - defined target area based on task or scan - presnt something you know will call this specific brain area
often we combine both - present task, get some peak activation in a subset of voxels, but these have anatomical constraints.
51
what are the different ways to classify different types of feedback?
* temporal contiguity
* modality
* signal content
* instructions
* direction of regulation
52
Different ways to classify feedback: temporal contiguity
what tf is this?
you can present feedback either continuously, as soon as the brain image has been acquired then feed the information back to the participant
* updated every TR (remember each TR = is one scan through the brain producing a single brain volume)
* or present feedback in intermittent way - wait a minute then present the thermometer
Bottom one has the advantage of n not being distracted while doing the task
53
Different ways to classify feedback: modalities
this is…?
* verbally: communicated it through intercom
* visually: thermometer, animation, virtual reality
* auditory: pitch of tone indicates activation level
Most typical is thermometer - communicates the activation level of an area
54
Different ways to classify feedback: signal content
* activation level
* functional connectivity
* multi voxel pattern analysis (MVPA)
55
Different ways to classify feedback: the instructions you tell n
wym?
so we tell n you need to self regulate your motor cortex - to do that…
* give very clear instruction e.g., imagine you are squeezing the fingers on your left hand
* implicitly - “try whatever works” - through trying diff stuff they learn which works - skill learning
Use Niklas study as an example of this - presented n food cues. then told them to imagine how bad it was for them but didnt give them a specific strategy to use (implicit approach)
56
Different ways to classify feedback: direction of activity
wym?
do we want n to up or downregulate activity of an area
* upregulation (most studies)
* downregulation (more difficult) - easier toincrease activity in an area than decrease it
57
There's different things you can feed in the stimulus e.g., thermometer that n see
58
Typical paradigm of neurofeedback set up
* 1 cycle = thermometer of self-regulation, fixation period, thermometer of self reg to see if it changed
* 1 block = 10 cylces per run
* 4-10 runs per session
* 1-4 sessions
Quite a lot tbh (long traiing)
59
Typical paradigm of neurofeedback set up : how do. wecompute the signal reflected in the thermometor
use the % signal change
to get feedback activation levels take current signal value (or a moving average of 3 brain images) and MINUS the average of the entire preceding fixation baseline
60
Typical paradigm of neurofeedback set up: scaling the thermometer
in what incremental steps do we scale that bitch?
typically we scale the thermometer in steps of 0.05% with a maximum of 0.5% signal change
## Footnote
remember that % signal change is very low in fMRI, the overall BOLD effect is tiny compared to these larger drifts in fMRI data (wut)
61
Typical paradigm of neurofeedback set up: what is something important to check
that the feedback is representing activation of the target area and not physiological or movment artefacts e.g., eye blinks
sometimes certain movments can affect the BOLDsignal - make sure it isnt in your study
62
whats the hemodynamic delay and is this a problem for neurofeedback?
the bold response only develops after 6 seconds
* not a problem because we have intermittent feedbackfrom some studies → wait 1 minute before telling participantshow strong their alcohol area is activates
* people can still learn to control it
neurofeedback studies using intermittent feedback show that delay did not prevent effective regulation as long as it was consistent. Posse et al.,
63
Transfer
Important to test in 1 additional fMRI run where you just leave out the thermometer (feedback)
does it still work
also in clinical studies its important to follow up subjects and inspect any behavioural change (e.g., after 3 months)
64
control conditions - what do you need to consider with these? what are the different types of control conditions we can use with NF?
* firstly if you will include them or not
different types
* **clinical studies**: one group of n to do NF training, other group receive treatment as usual e.g., counselling/medication
* **same mental training (imagery) but no feedback** - e.g., also think about how bad food is for them when shown food they just don't get any feedback
* **sham feedback** - most conservative, most stringent. still present the thermometer but it reflects either:
* computer-generated artificial feedback that is _non contingent_ on ANY brain changes
* from a different n (best, most conservative control condition)- also _not contingent_ of changes in the real n
* from a different region in the same n - _it is contingent. C_an still reflect effort, only this one allows you to make inferences about the effects in a the alcohol area
65
advantages of NF as a clinical treatment tool?
why use it to treat: mental disorders or behaviorus
* contrast to the pharmaceutical approach - non-invasive. no side effects
* tailor to individual. medications interact with someone's physiology and affect its efficiency.
* → remmeber we can present a localiser to each n and find the specific dysfunctional OR compensatory brain area that might differ across n
* → if we compare this to eeg feedback which has been around quite a while you can certainly be more specific areas in the areas you target (fMRI spatial resolution \> EEG spatial resolution)
* dysfunctional areas are often in deeper regions - basal ganglia, midbrain region, amygdala - inaccesible using TMS or EEG -NF
* self regulation sucess
* → also a psychological benefit - once learning this skill to change brain activation - improves the perception of self-efficacy (Bandura 1977). the expectation to achieve a desired outcome (key to motivation) is often lacking in patients
* → provides incentive for patients that lack motivation for psychotherpay to work
66
advantages of NF as a clinical treatment tool?
why use it to treat: mental disorders or behaviorus
* contrast to the pharmaceutical approach - non-invasive. no side effects
* tailor to individual. medications interact with someone's physiology and affect its efficiency.
* → remmeber we can present a localiser to each n and find the specific dysfunctional OR compensatory brain area that might differ across n
* → if we compare this to eeg feedback which has been around quite a while you can certainly be more specific areas in the areas you target (fMRI spatial resolution \> EEG spatial resolution)
* dysfunctional areas are often in deeper regions - basal ganglia, midbrain region, amygdala - inaccesible using TMS or EEG -NF
* self regulation sucess
* → also a psychological benefit - once learning this skill to change brain activation - improves the perception of self-efficacy (Bandura 1977). the expectation to achieve a desired outcome (key to motivation) is often lacking in patients
* → provides incentive for patients that lack motivation for psychotherpay to work
67
example study:
NF and pain (deChams 2005)
the classic study however some authors have questioned the results
Looked at the rACC (pain) and whether learning to regulate the ACC have any effects on pain experience.
* training comprised 60 second blocks, alternated in which way n were told to direct the activation (either upregulate or downregulate) the rACC
* while did this they had to submerget heir hands in an ice cold bath (painful stimulus)
* after each regulation run (upregulation vs downregulation) - n rate pain intensity
* compared ratings to see if the regulation affected subjective pain processing
feedback
* presented burning fire increasing and decreasing in size
results
* showed both healthy and chronic pain n could do this
* learned to control ACC - reflected in ratings of pain intensity
* effects were maintained in post-test tranfer when they didn't see the burning fire anymore
* controls didn't show this pattern, never controlled ACC, no changes in the pain ratings compared to the up and down-regulation
* thus the effects were NOT attributable to the mental strategy itself or ability to regulate any brain region
68
why use NF method to treat cue-reactivity in addiction
alcohol dependence
* bc treatment options just don't work
* 5-10 % of the population are alcohol dependent (high prevelance)
* pharmacutical treatment (e.g., acamprosate) has only small effects
* relapse rates are really high in addiction (50-70%) within one year of detoxification
we know one key factor for relapse is the dysfunctional response (e.g., craving) to alcohol cues in our environment
69
design a neurofeedback study to tackle cue reactivity and craving:
1. passive viewing localiser scan - alcohol and neutral images - the difference between these can identify the alcohol areas
2. ask n to downregulate the activation of the alcohol area e.g., “do whatever strategy works for you!”
Alternatively
1. localise for the area responding to the healthy goal images.
2. ask n to upregulate activation (attemept to shift motivational hierarchy)
what's the problem with this task design?
Dual-task issue. N needs to monitor both picture and feedback stimulus (thermometor)
70
how can we contend with the dual-task issue
The motivational neurofeedback approahc
* brain activation is reflected via the size of the cues that elicit the brain activation
* n instructed to make the picture smaller - the smaller reflecting lower activation in the alcohol area
* when they failed to do this the picture grew larger
* big advantage with this approach provides real motivational consequences, you can actually push the nice drink picture away from you
* control needed as activation may just decrease due to the picture becoming smaller so they added a condition where they presented the same sized images but just in a passive viewing context
* can investigate how much of the reduced activation is down to mental efforts and how much is due to the size of the image
71
big pic small pic neurofeedback version
Ihssen et al., (2017)
* women fasted 4h before session
* down-regulate target area - identified by localiser
* during exposure to energy-dense food pictures
* measured food craving, subjective hunger levels after training (ratings), implicit measure where a free bowl of crisps placed next to them then measured how much they ate
see pic for areas identified with the localiser - amygdala was chosen in the end
See graph for activation in the target areas during down-regulation in different training runs VS. passive viewing condition where they saw the same pic size changes but without neurofeedback regulation
omg sick - can see consistently activation was lower in the experimental group
72
what does the small pic bic pic NF method (Ilhessen et al., 2017) tell us?
This method of using the picture sizes (motivation method) may enable a more effective downregulation than other approaches (thermometor based approach)
basically, that n can actually learn to do this.
remember as well the results were from only 1 session, if we had more than 1 session then we would probably have been better at doing this
73
what are the whole brain effects from the picture-size guided down regulation? (Issen et al., 2017)
* downregulation led to a more widespread deactivation of areas
* specifically areas functionally relative to reward
* downregulation led to deactivation of various reward-related areas but interestingly
* excluded early visual areas - this tells us n didn't just close their eyes
74
what were the behavioural effects of the picture-size guided down regulation? (Issen et al., 2017)
* decrease in food cravings from before-to-after training however this wasnt significant
* correlation between how successful they were in downregulating the ting and their hunger rating.
* the better they were at regulating their amygdala the lower they rated their hunger
this is still preliminary data and only on 10 people. more research certainly needed.
nothing found in the implicit measures (crisps eaten)
75
NF study on alcohol addiction (Kirsch et al., 2016)
* 38 heavy student drinkers
* arget area: ventral striatum
* localiser: monetry reward task
* instruction: downregulate the temperature using any strategy that works for you
* different control conditions - yoke-feedback; no-feedback
results:
76
key summary - NF and addiction
* studies support the feasibility of neurofeedback in terms of upregulation and down-regulation
* but what we need to show is there is sustained behavioural change
* need to improve future studies - have multiple training sessions, facilitate transfer (E.g., homework to practice self-regulation techniques outside of the scanner)
current issues
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