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Addiction & Compulsive 1 > L1: Drug Craving & Neural Basis > Flashcards

L1: Drug Craving & Neural Basis Flashcards

1
Q

Name the DSM criteria for substance use disorder

A

problematic pattern leading to clinically significant impairment or distress, as shown by min 2 occuring within 1y
1. substance is taken in larger amounts or for longer than intended
2. persistent desire / unsuccessful efforts to cut down / control use
3. spending a lot of time getting/using/recovering from use
4. craving & urges to use the substance
5. recurrent use resulting in failure to fulfill major role obligation (work, school, home etc)
6. continuing to use, even when it causes problems in relationships
7. giving up/reducing important social, occupation, or recreational activities because of use
8. using substances again and again, even when it puts you in danger
9. continuing to use, even when you know you have a physical/psych problem that could have been cause/exacerbated by the substance
10. needing more of the substance to get the effect you want (tolerance)
11. dev of withdrawal symptoms, which can be relieved by taking more of the substance

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2
Q

How does the national institute on drug abuse define addiction?

A

a chronic, relapsing disorder, characterised by compulsive drug seeking, continued use despite harmful consequences, and long-lasting changes in the brain

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3
Q

What are the 4 main reasons why people use?

A
  • to feel good (relaxation, confidence etc)
  • to feel better (self medication)
  • to do better (to perform better)
  • to explore (new experiences, feelings etc)
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4
Q

What is the difference between use and abuse?

A

when user loses voluntary ability to control its use
in DSM, to qualify as ABUSE: a problematic pattern is required, leading to clinically significant impairment or distress

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5
Q

What is the prevalence of substance abuse according to NEMESIS?

A

17% of nl ppl lifetime prevalence of substance abuse (13% alcohol 6% drugs)

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6
Q

according to NEMESiS, what were some sociodemographic factors relating to substance abuse? somet hat didnt relate?

A
  • younger age
  • men
  • living alone
  • being unemployed
  • very high degree of urbanization
    unrelated to income & country o origin
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7
Q

What are some protective factors for substance use?

A
  • parental monitoring & support
  • positive relationships
  • self efficacy (belief in self control)
  • academic performance
  • school anti drug policies
  • neighbourhood resources
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8
Q

What are some risk factors for substance use?

A
  • early aggressive behaviour in childhood
  • early drug use (-> importance of prevention!)
  • lack of parental supervision
  • substance abuse by caregivers
  • low refusal skills
  • poor social skills
  • drug availability
  • community poverty
  • genetic predispositions
  • personality traits: sensation seeking, impulsivity, diff w self regulation
  • other mental health issues (comorbidity w depression, trauma, anxiety, adhd etc)
  • addicitvity differs between drugs & way of administration
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9
Q

How does vicious cycle define substance abuse?

A

negative consequences of abuse can maintain or worsen the abuse: chrnoic drug use increases DA levels, leading to D2 receptor down regulation, leading to anhedonia & tolerance, thus contributing to escalation of drug use

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10
Q

What are some barriers to seeking treatment for substance use?

A
  • attitudinal (“didnt think anyone could help”)
  • readiness for change (“thought problem wasnt serious enough”)
  • stigma (“was embarassed to discuss it”)
  • finanical/cost (“insurance x cover treatment”)
  • structural (“didnt know where to go”)
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11
Q

What is the relapse rate in substance abuse?

A

40-60% despite treatment

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12
Q

What are common triggers for relapse?

A
  • returning to place/seeing someone associated w drug use
  • stressful circumstances
  • pre existing emotional or mental health struggles
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13
Q

What is the history of the models of addiction?

A

19th century: moral model
from mid 19th century: pharmacological model
1930-1950s: symptomatic model
1940-1960: disease model
1960-1970: learning theory model
1970-1990: bio-psycho-social dev model
since 1990: brain disease model

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14
Q

How does the moral model see addiction & its treatment?

A

drug abuse & drug seeking behaviour labelled as immoral, sign of moral weakness
-> ppl w an addiction were imprisoned or put in (questionable) re-education institution
- not supported by scienitific evidence, but still appears sometimes in society (care farms)

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15
Q

How does the pharmacological model see addiction & its treatment?

A
  • blame for addiction taken away from addicts and to the addictive substance
    -> prevent ppl from becoming involved w these substances (war on drugs)
  • now, seen as one-sided (its not just the availability & use of potentially addictive substances that leads to addiction)
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16
Q

How does the symptomatic model see addiction & its treatment?

A

addiction no longer viewed as condition in itself, but rather as a symptom of an underlying character-neurosis or personality disorder
-> long term, insight-oriented psychotherapeutic tratment of character neurosis (still used someplaces today)

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17
Q

How does disease model see addiction & its treatment?

A

there are fundamental (premorbid) biological & psychological differences between addicts & non-addicts, which leads to the former being unable to use substances in moderation
- main features of the addiction disease are the uncontrolled use & physical dependence (tolerance & withdrawal symptoms)
-> moderate use by non-addicts is possible, wile for addicts complete absitence is the only option (AA)

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18
Q

how does learning theory model see addiction & its treatment?

A

form of maladaptive learned behaviour that could be unlearned again w help of behavioural therapeutic interventions
-> aversion therapy & cue exposure are main interventions

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19
Q

how does the bio-psycho-social development model see addiction

A

there are only relative differences between addicts & non-addicts & smooth transitions between use, abuse, addiction etc
does not solely assume substance (pharmacological model) or individual (moral, symptomatic, disease models) as cause of addiction.
see addiction as interaction between innate vulnerability (bio), personal dev (psych), and circumstances (social)
-> intervention in which attention paid to bio, psych, & social influences

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20
Q

What are the 3 main substances of abuse? What do they all have in common?

A
  • sedatives: tend to make u feel calm & relaxed (alcohoo, opiatezs, benzodiazepines, barbiturates)
  • stimulants: tend to be invigorating (caffeine, nicotine, cocaine, amphetamine (speed))
  • psychedelics: altern state of consciousness & perception of world around you (cannabis, ecstasy, LSD)
    -> directly/indirectly result in release of dopamine in nucleus accumbens, which plays an important role in their addictive effect
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21
Q

How does brain disease model see addiction & its treatment

A
  • as acquired chronic relapsing brain disease.
  • innate vulnerability is basis for repeated use of substances, while repeated use in turn -> changes in brain.
    characterized by
  • compulsive drug seeking & use, despite harmful consequences
  • hyperactive reward system, sensitized to drug reward: craving & habits
  • cognitive dysfunction
  • complex disease w genetic & environmental contributions
  • puts the guilt aside so treatment can be prioritized
    -> treatment needs to involve pharmacolocal & behavioural therapeutic interventions
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22
Q

What role does dopamine play in the reward system? what role does it play in substance abuse?

A

anticipation of rewards -> release of dopamine in the mesolimbic reward system

drugs lead to much stronger dopamine release than natural rewards (like food or sex) -> hijack reward system so addicts are less sensitive to natural rewards (related to deficiency of dopamine D2 receptors in the nucleus accumbens) could be both vulnerability factor (already are less sensitive so then seek out drugs to compensate, or the result of drug use)
so exposure to drugs & drug associated cues -> dopamine release in NA -> craving

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23
Q

what does the “reward deficiency syndrome (RDS) account say?

A

that ppl w chronic deficiency of dopamine D2 recepotrs in the nucleu accumbens are less sensitive to simple natural rewards so look for stronger stimuli to compensate this (like through drugs)
addicts have this: cause or consequence of drug addiction?
-> little of both! homeostatic account & PET scan research shows that drug use decreased D2 receptors, while family research shows that low D2 density can precede it

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24
Q

How does the homeostatic account explain the structural differences in dopamine system in addicts?

A

homeostatic account: the lower density of dopamine receptors in addicts is consequence of homeostatic compensatory brain changes after chronic drug use to lower dopamine transmission; increased dopamine activity due to drugs -> decrease of dopamine receptors
this down regulation may also underlie decreased (natural) reward sensitivity in addiction & tolerance in addiction
SO AS A CONSEQUENCE

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25
Q

Can D2 receptor densitiy increase following period of abstinence?

A

yes!

26
Q

What is the mesolimbic pathway?

A

striatum: small group of subcortical structures in basal ganglia, including: caudate, putamen, nucleus accumbens (aka ventral striatum aka center of craving)

27
Q

What happens in the mesolimbic dopamine pathway?

A

dopamine neurons in ventral tegmental area (VTA) project to the nucleus accumbens (or ventral striatum)

28
Q

What is the incentive sensitization theory?

A

pathological motivation for drugs + impaired cognitive control is core of addiction
- Berridge & Robinson
- suggest that the most crucial psychological change in addiction is a persistent “sensitization” or hypersensitivity to the motivational effects of drugs and drug related cues
-> drug associated stimuli gradually acquire incentive salience (means that these stimuli attract the attention of the addict & become attractive in themselves). in other words craving & wanting increases!
-> intensified “wanting’ of the drug (dopamine)-> elicits targeted behaviour to acquire the drug
- repeated substance abuse -> decrease in liking (hedonic experience during consumption) but increase in wanting
- wanting: extreme craving that can be subconscious, triggered especially by drug associated cues
- explains relapse, as exposure to drug associated cures incite craving for the drug long after withdrawal symptoms have dissapeared

29
Q

What is the incentive sensitization theory at the neurbiological level?

A

repeated drug use -> changes in mesolimbic dopamine system that plays role in motivational & pavlovian processes
specifically: system becomes sensitized (hyperreactive) to incentive effects of drugs & drug associated cues
this increased sensitization is associated w increased dopamine neurotransmission in brain regions like the nucleus accumbens

30
Q

What factors influence susceptibility to sensitization?

A
  • genetics
  • hormones
  • experiental factors
  • type of drug
  • higher doses & intermittent use -> greater sensitization
31
Q

How does the incentive sensitization theory work on a behavioural level?

A
  1. Drug-associated stimuli elicit attention and approach towards them (they become ‘wanted’), acting as ‘motivational magnets’.
  2. Drug-associated stimuli become (conditioned) reinforcers in their own right.
  3. Drug-associated stimuli (and drugs) exposure can lead to relapse (conditioned/drug/stressreinstatement)
  4. increasing willningness to work for the drug
32
Q

How does the traditional withdrawal-based explanation explain addiction?

A

suggests that ppl take drugs initially for pleasure, and then to avoid withdrawal symptoms
(also called positive-negative reinforcement, or hedonic homeostasis view)

33
Q

What is the shortcoming of the traditional withdrawal-based explanation of addiction?

A
  • drug withdrawal actually may be less powerful at motivating drug taking behaviour than ppl think (especially compared to positive incentive processes caused directly by drugs themselves & their cues as shown by animal studies)
  • only really works if person has already learned that drug taking will alleviate the withdrawal symptoms
  • addiction persists long after withdrawal symptoms dissapear so sensitization related changes in brain provide mechanism for continued addiction
34
Q

Could aberrant (dysfunctional) learning be an explanation for addiction?

A

yes addiction may result from drugs promoting aberrant learning processes (ex: instead of associating a reward w a certain behaviour, behaviours driven by drug cravings rather than natural rewards) of especially strong automatic stimluls response habits that lead to compulsivity

35
Q

What are the shortcoming of the (aberrant) learning explanations of addiction?

A

although learning is prob a component, its not the sole cause of addiction
- automatic habits do not necessarily become compuslive (u dont start brushing ur teeth compulsivley just cause its a habit) compulsive behaviour requires motivational components like incentive salience, which go beyond mere repetition. so learning view doesnt account for compulsivity in addiction
- learninga ccount also doesnt account for targeted flexibility in addiction (they will do anything to get drugs, which cannot be explained simply by automatic habits)

36
Q

How do learning processes interact w incentive sensitization in addiction?

A

learning doesnt cause inecentive sensitization but plays role in shaping and regulating how incentive sensitization (pathological desire)
- learning helps specify the objects of desire by assocating them past experiences
- influences when & where neural sensitization (when brain becomes increasingly sensitive to certain stimuli) is expressed
- contributes to contextual control over the expression of sensitization (explains why addicts may experience heightened desire for drugs in environments associated w drug use)

37
Q

What are spillover effects?

A

Incentive sensitization can extend beyond drug targets to other stimuli such as food, sex, or gambling

38
Q

Does incentive sensitization apply to any other form of addiction beyond drugs?

A
  • Overactivation of dopamine circuits linked to excessive “wanting” in behaviors like sex, binge eating, and gambling
  • but unknown if sensitization-like states occur w/o drug use, except for stress-exposure periods
  • could be the case in binge eating (that excessive wanting powers the episodes)
39
Q

How have the 4 behavioural components of incentive sensitization been studied?

A
  1. CSs become motivational magnets = conditioned place preference paradigm
  2. CSs become reinforcers in their own right = conditioned reinforcement paradigm
  3. CS (and drug) exposure leads to relapse (reinstatement) = reinstatement paradigm
  4. Increased willingness to work for the drug = progressive ratio experiments
40
Q

How do progressive ratio self administration experiments work?

A

instrumental response requirement to obtain a substance graduallly increases
the max nr of responses that the subject makes in order to receive substance = break point (outcome variable)
- results: rats will work harder to self administer a drug (reach breakpoint later) if pre exposed to this drug)
- effort put in is signaled by dopamine transmission in nucleus accumbens

41
Q

Define conditioned reinstatement vs drug resinstatement vs stress reinstatement

A

ability of drug-associated cues (CS) to powerfully reinstate a previously extinguished instrumental response.
– ex: after period of abstinence in rehab, return to original drug-associated context may trigger relapse to the same level of drug seeking as before.

drug reinstatement ex: just having one drink (or hit) leads to full blown relapse
stress reinstatement ex: stressful episode at work leads to relapse

42
Q

How has reinstatement (relapse) been studied?

reinstatement paradigm

A
  1. acquisition: lever press -> light CS + drug, so will start pressing lever more and more
  2. extinction: lever press -> nothing, so will stop pressing lever
  3. reinstatement test (in extinction): light CS(cue)/shock(stress)/drug: will start pressing lever again at same level as before (reinstatement)
    in humans
    R1 -> cigarettes; R2 -> chocolate
    smokers preferentially choose R1 in choice reinstatment test

results: reinstatement can be prevented by systemic/local manipulation of the VTA & nucleus accumbens, thus implicating the mesolimbic pathway in reinstatement

43
Q

What is the conditioned place preference paradigm?

A

dopamine necessary in drug induced conditioned place preference (animal/humans learns to prefer a place associated w the effects of a drugs)

44
Q

What is the conditioned reinforcement paradigm?

A

phase 1 (pavlovian/classical): light (CS) -> drug (US)
phase 2 (instrumental): response 1 -> light; response 2 -> nothing
results: rats will perform R1 more vigorously than R2
becomes even stronger if you stimulate dopamnie release in the nucleus accumbens

45
Q

what is tolerance?

A

reduction of a (desired or undesired) effect of a substance when administered chronically. so we become less sensitive & need larger doses -> higher risk of overdose

46
Q

What are some common withdrawal symptoms?

A

anxiety, irritability, malaise, dysphoria, hyperkatifeia (i.e., hypersensitivity to emotional distress), a feeling that “everything is gray,” and alexithymia (i.e., an inability to express one’s feelings).

47
Q

How is dopamine’s relation to substance use measured by research methods? What were the results?

A
  • microdialysis studies
  • showed that natural rewards -> increased release of dopamine levels in nucleus accumbens, which reflects CRAVING
48
Q

What is the role of withdrawal symptoms in substance abuse

A

Opponent-processes theory
drug is intially used to bring pleasure, but later in the addiction, tolerance occures & drugs are mainly taken to avoid the unpleasant withdrawal symptoms (negative reinforcement)
BUT relapse can occur long after withdrawal symptoms have dissapeared (so craving also plays role)

49
Q

What is the difference between pavlovian/classical & instrumental conditioning

A

pavlovian conditioning: where stimuli that predict a reward can evoke conditioned responses & craving. change in behaviour due to experience w CS-US relationship (where CS is bell, and US is food)

50
Q

How is pavlovian learning in substance abuse studied?

A
  • cue reactivity fMRI studies: participants shown substance images & neutral images. BOLD signal at substance images vs neutral images compared
  • single cell recording in monkeys midbrain near or inside DA neurons to detect action potentials (dopamine activity)
51
Q

What were the results of cue reactivity fMRI studies?

A

more nucleus accumbens activity at substance images vs neutral images in drug useres
this correlates w cue induced self reported craving

52
Q

How is “prediction error” encoded by the mesolimbic dopamine pathway? how is it affected by substances of abuse?

A

when the prediction of a reward (like juice) is not yet completely accurate (CS-US training hasnt been going on for that long), this leads to suprise & a reward prediction error occurs
- midbrain dopamine neurons encode this prediction error as a signal to the cortico-striatal brain circuits that the current reward value doesnt match the expected value (functions as a teaching signal)
- once CS-US has been learned, the predictive cue CS will evoke dopamine response so DA fires at (unexpected) presentation of CS (instaed of the fully predicted US)

53
Q

What were the results of single cell recordings in monkeys to pavlovian cues?

A
  • monkeys learned to predict the delivery of US (fruit juice) based on visual icons (CS)
    -burst of dopamine at unexpected rewards (US without CS, at beginning of training)
  • this burst of dopamine transfers to the reward predictor as training continues (CS)
54
Q

What is the role of incubation of craving in addiction

A

increases in drug seeking have been observed after a period of absitence/extinction, craving may increase during extinction: “incubation of craving”

55
Q

Which brain region plays an important role in craving?

A

nucleus accumbens

56
Q

What are the barriers that make it so difficult to practically implement our scientific knowledge on substance abuse as a health issue (not just a social one)?

A
  1. stigma around addicts: they are often seen as weak/amoral ppl, and as bad ppl who dont deserve the fulll treatment & compasion
  2. some of the ppl who work in the fields of addiction treatment & prevention hold specific ideologies that they like to stick to
57
Q

According to Leshner’s article, where is the focus on addiction currently, and where should it actually be?

A

currently: focus on addictiviness, which is often measured by the withdrawal symptoms. doesnt make sense cus severity of withdrawal symptoms x always correlate w the drugs danger, a lot of withdrawal symptoms can be managed w meds, and some highly addictive substances have minimal withdrawal symptoms
should focus on compuslivie drug seeking and use despite negative consequences, not the withdrawal symptoms

,

58
Q

How does Leshner argue that Addiction is a Brain Disease?

A
  • addiction affects the brains mesolimbic reward system
  • prolonged drug use causes lasting changes in brain function
  • these brain changes underlie addiction, shifting voluntary drug use -> compulsive behaviour
  • treatment goals should reverse/compensate for these brain changes through meds or beh interventions
59
Q

How does Leshner argue that there is also more to addiction than it being a Brain Disease?

A
  • influenced by social contexts: conditioned environmental cues can trigger cravings/relapses
  • treatment should address bio, behavioural, and social factors
60
Q

How does Leshner argue that Addiction is a chronic, relapsing disorder?

A

requires management rather than cure, since most ppl suffer from it for most of their lives to some extent
treatment success measured by significant decrease in drug use & periods of abstinence, w relapses being normal

Addiction & Compulsive 1 (5 decks)

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