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Summary Exam 1 Addiction & Compulsive Disorders UvA Year 2
Summary of Addiction & Compulsive Disorders Exam 1
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Voorbeeld 3 van de 26 pagina's
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Voorbeeld van de inhoud
W1.2 (MODULE 1)ARTICLE BY LESHNER (1997) – ADDICTION IS A BRAIN DISEASE, AND IT
MATTERS
There is a wide gap between the scientific facts and public perceptions about drug abuse and
addiction → Factors unique to the drug abuse arena that compound the problem:
- Normal delay in transferring any scientific knowledge into practice and policy
- Tremendous stigma that is attached to being an addict
- Ingrained ideologies of people working in the field – Many drug abuse workers are
themselves former drug users who have had successful treatment experiences with a
particular treatment method, due to which they may defend a single approach
All drugs of abuse have common effects on the mesolimbic reward system, which extends
from the ventral tegmentum to the nucleus accumbens, with projections to areas such as the
limbic system and the orbitofrontal cortex → Addiction as a consequence of fundamental
changes in brain function, marked by a metaphorical switch in the brain triggered by
prolonged drug use, leading to compulsive drug seeking and use
↓
When addiction is viewed as a chronic, relapsing disorder, then treatment outcomes involve
reductions in drug use and long periods of abstinence, with occasional relapses considered as
normal – Goal of treatment is typically the management of the condition rather than a cure
ARTICLE BY BERRIDGE & ROBINSON (2011) – DRUG ADDICTION AS AN
INCENTIVE SENSITIZATION
Addiction: A pathological and compulsive pattern of drug-seeking and drug-taking behaviour,
which occupies an inordinate amount of an individual’s time and thoughts, and persists
despite adverse consequences
Hedonic hypothesis/Opponent-process theory: Suggests that addictive drugs are taken initially
simply to achieve pleasant drug highs, and after addiction, to escape withdrawal lows
↓ Issue with hedonic theories:
Drug withdrawal actually may be much less powerful at motivating drug-taking behaviour
than people generally think
- Experiment: A priming cocaine or heroin injection is more effective at reinstating
Reaction of drug-seeking behaviour in rats than naltrexone (which makes rats nauseous)
- Withdrawal symptoms are maximal within a few days after the cessation of drug use,
hedonic theorists
but the susceptibility to reinstatement continues to grow for weeks to months
Conditioned withdrawal symptoms: Reactions that occur in response to cues associated with
drug use, rather than the direct effects of the drug itself (E.g.: seeing drug paraphernalia can
trigger physiological changes similar to those experienced during actual withdrawal)
↓ However:
1. Many addicts report that cues often fail to elicit conditioned withdrawal
2. Drug cues often elicit different effects than withdrawal symptoms
,Learning theory of addiction: Suggests that addiction is primarily driven by learned
associations between drug-related cues and pleasurable effects of the drug – Argues that
addiction arises from the formation of strong automatic stimulus-response (S-R) habits, which
confer compulsivity to drug-seeking behaviour
↓ However:
1. Habitual behaviours do not make an action compulsive – Compulsive behaviour in
addiction involves motivational factors beyond mere habit formation
2. Targeted flexibility: The capacity of individuals to engage in a variety of complex
behaviours aimed at obtaining drugs or fulfilling drug-related needs
Incentive-sensitisation theory of addiction: Repeated exposure to drugs can sensitise the
brain’s reward system, making individuals more sensitive to drug-related cues and cravings
- Intense craving, triggered by familiar contexts or stress, combined with impaired
cognitive control due to substance abuse, contributes to addiction symptoms
- ‘Wanting’ and ‘liking’ do not always occur together, as in addiction, the craving of a
substance increases, while the hedonic experience during consumption decreases
- Suggests that dopamine in the mesolimbic system plays a crucial role in ‘wanting’
- After sensitisation occurs, the mesolimbic dopamine system becomes hyperreactive to
exposure to drugs and drug-related cues
- While learning is not the direct cause of hypersensitivity, it plays a significant role in
directing motivation towards specific drug-related cues → It is the non-associative
adaptations in brain circuits (such as an increase in D2 receptors) that mediate
incentive-motivational processes that ultimately drive motivation for drugs
How incentive sensitisation is manifested:
- Biologically → Increased dopamine activity in relevant brain regions
- Psychologically → Increased desire triggered by cues related to the rewards
Individual susceptibility to sensitisation varies:
- Previous drug experiences
- Previous experiences with major stresses in life
- Characteristics of the drug itself
- Dose of the drug
- Frequency and pattern of drug use – Drug use with periods of abstinence contributes
to sensitisation specifically
- Route of administration of the drugs
- Extended access to drugs
- Speed with which drugs reach the brain
The brain’s nucleus accumbens (NAcc) and dopamine-related circuitry play a role in reward
learning → Cues predicting rewards can activate NAcc-related circuitry strongly, sometimes
even more than the reward itself → The transition to addiction may stem from drugs
promoting aberrant learning, involving maladaptive associations between drug-related cues
and rewarding experiences
, The applicability of incentive sensitisation to addictions beyond drugs, such as sex, gambling,
and binge eating, remains uncertain – While there is some evidence suggesting that
overactivation of dopamine circuits may contribute to excessive wanting in these behaviours,
it is not yet established whether sensitisation-type states can emerge without drug exposure
Incentive salience, or ‘wanting’ is distinct from cognitive wanting, as incentive salience is
psychologically evident in cue-triggered wanting and motivational magnet effects, drawing
individuals strongly towards specific reward stimuli, even without conscious awareness of the
reward, whereas cognitive wanting involves conscious desires
Different types of utility (Kahneman):
1. Predicted utility: The expectation of how much a future reward will be liked
2. Decision utility: What we actually decide to do, manifest in choice and pursuit →
Incentive salience ‘wanting’ is a form of decision utility
- Incentive salience ‘wanting’ is closely linked to sensory precepts and cues
associated with rewards
- Manifests as a phasic peak triggered by encountering rewards or cues and does
not necessarily require conscious awareness
- May have evolved as a subcortical mechanism to guide behaviour towards
innate incentives, preceding conscious goal-directed behaviour – Cognitive
forms of desire are more dependent on higher cortex-based brain systems
3. Experienced utility: The hedonic impact experienced when the reward is gained
4. Remembered utility: The memory of how good a previous reward was in the past –
Chief determinant of predicted utility
Stephens & Graham: Compulsion typically involves external forces acting against internal
desires → Although a person may cognitively desire one thing (such as abstinence from
drugs), the sensitised incentive salience ‘wanting’ for drugs can emerge spontaneously in
response to drug-related cues → When ‘wanting’ becomes strong enough and overrides
cognitive desires, it can exhibit compulsive properties, even if it originates internally rather
than from external forces
BACKGROUND MODULE CANVAS
Spontaneous remission: Many people suffering from
addiction recover without formal treatment –
Suggests that the high relapse rates reported in the
scientific literature may in part be due to including
only clinical samples
Different models of addiction:
- Moral model: Viewed addiction as a sign of moral weakness – Drug abusers and
addicts were considered immoral, in conflict with societal norms, and lacking the
willpower to overcome their addiction – Prevalent in the 19th century – Led to the
‘War on Drugs’ in the US
- Pharmacological model: Shifted the blame away from the individual and attributed
addiction to the highly addictive nature of certain substances – Focus was on
preventing access to substances to curb addiction – Prevalent in mid-19th century
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