neurofeedback Flashcards
food can be rewarding, why is this dangerous?
food is very enjoyable but we cant constantly indulge in it
what % of adults in the US are either overweight or obese?
68% (Alonso-Alonso et al., 2015)
Are people getting bigger over time? why?
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
ohw can we use neuroscience to help with weight gain/obesity increases
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)
how can reward cue research help us with drug addiction epidemic?
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.
does treatment for addiction work?
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
what is a reward
Anything that can that is positive reinforcer - so element of subjectivity - do n find this rewarding
do you have to enjoy the reward to keep chasing it if you have a problem e.g., heroin addiction
- 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.
are humans the only animals capable of experiencing reward?
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)
definition of a reward
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
some rewards are in-born while others we learn trough a form of classical conditioning: unconditioned vs conditioned reward
describe this
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
different ways to classify rewards
- 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)
classifying rewards in terms of the way they satiate the hunger
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
why does it make sense to look at food and drug rewards together
anatomical reasons
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
why does it make sense to look at food and drug rewards together
psychological reasons
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
how can we dissociate liking from wanting behaviour in humans/animals
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
dissociating liking from wanting is difficult in humans. can brain imaging help?
fmri studies on rewards - which type of response do they normally look at - wanting or liking?
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
what is the difference between an exterosceptive and interosceptive cue
- 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
what are 3 type of ways we can respond to a drug/food cue
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
what 2 models have been used to look at cue reactivity in alcohol addicted n
- 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).
how do we know whoch model - the withdrawal or apetative - actually reflects what happens when n see drug cue?
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
FOOD CUES
neural level of cue reactivity - what areas do we see active?
the reward circuit
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
what areas might we expect active when seeing cue n like
- motivational processes - unconscious/conscious wanting or craving
- hedonic processes - liking, pleasure, expected pleasentness
- inhibition control
- self-regulation
- visual processing
- memory
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
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
how can we use reward cue reactivity research in a more practical context
- use neural cue responses to rewards as biomarkers. Index people vulnerable to addiction, gage the severity of peoples dependence
- 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
- use to measure treatmetn sucess, explose to cues fmri, n do treatment, expose again to cues fmri - has the treatment helped?
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
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
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.
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
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)
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.,
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
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
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
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
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:
