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ACD Addiction and compulsive disorders interim exam 1 summary
ACD Addiction and compulsive disorders interim exam 1 summary
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Voorbeeld 4 van de 41 pagina's
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Addiction and Compulsive DisordersSummary Interim Exam
Week 1
Module 1 - Background Info
The relapse rate per drug differs tremendously. Another factor is comorbidity. Addiction used to
be seen as a sign of moral weakness (moral model). Later it was thought that the highly addictive
characteristic of the substance was what caused the addiction (pharmacological model). Later it
was thought that drug abuse was a symptom of an underlying problem (symptomatic model).
Then the disease model came, in which fundamental (premorbid) biological and psychological
differences exist between addicts and non-addicts, as a result of which the former are unable to
use alcohol and other drugs in moderation. Then the learning theory model came, that addiction
can be unlearned again with the help of behavioral therapeutic interventions. After a while, the
bio-psycho-social development model came to attention, here, both the onset and termination of
the addiction are seen as the result of a continuous interaction between innate vulnerability
(biological), personal development (psychological) and circumstances (social). The brain disease
model is explained in the lecture. Pharmacological and behavioural therapeutic interventions are
seen as the most promising within this model. Drugs can be sedative, stimulants or psychedelics.
They have different effects on the brain. What they have in common is that they directly or
indirectly result in a release of dopamine in the nucleus accumbens, which plays an important
role in their addictive effect. Besides tolerance, withdrawal symptoms often occur.
Lecture - Module 1
Substance abuse is highly prevalent.
There are some risk and protective
factors about developing substance
,abuse. Many of these factors relate to SOS. not everyone gets treated due to stigma, attitudes,
readiness, finances and structural issues. The relapse rate is high. Society pays the costs of
substance abuse.
A theory of addiction is the Moral model of addiction: substance abuse results from a lack of
willpower. Often drugs are initially used voluntarily, afterwards, they are needed and craved,
turning into an addiction. Brain disease model:
addiction should be seen as an acquired disease of
the brain (Nora Volkow).
Addiction is a chronic relapsing brain disease
(dopamine system) resulting from compulsive
drug use despite negative consequences. This
comes from a hyperactive reward system (craving,
habits and cognitive dysfunction). It is a complex
disease. There are some criticisms towards the
brain disease model (taking responsibility away
from the person).
Strong craving is common across SUD. dopamine
activity is seen in response to rewards (food, sex)
in the nucleus accumbens. The same dopamine response is seen with drugs. It is seen that drugs
hijack the reward system (Mesolimbic dopamine pathway: dopamine neurons in the VTA project
to the NuAcc). PET studies show a lower density of dopamine D2 receptors in clinical people,
relative to controls. This structural change is a result of drug overuse, and the decrease of 2
receptors is somewhat a compensation/balance the brain does. Pet research in monkeys shows
that chronic drug use over time leads to decreased D2 receptor density. D2 receptor density can
recover after a period of abstinence. Low Dopamine D2 receptor density is also seen in relatives
of drug addicts as well, suggesting a predisposed lower reward sensitivity (and vulnerability for
addiction). The dominant theory is the former. Classical conditioning plays a part in addiction as
well, due to addiction associated stimuli, such as CS(beer brand) US(beer). In a study, neutral
and substance-related stimuli are presented in an MRI, and BOLD is measured. In substance
cues, NuAcc is activated more (in contrast to neutral stimuli). In pavlovian learning, single-cell
recordings are done to pavlovian cues with animals. Monkeys learned to predict the US from the
,CS. At the beginning of training, dopamine neurons spike to unexpected reward, and at the end,
response transfers to reward predictors, and the peak/response to the actual reward disappears.
This is due to the surprise aspect of the stimuli, something that is unexpected fires dopamine, not
something expected (prediction error). During training, response slowly shifts from the US to
CS. cocaine
particularly elicits a
much stronger
response than food
(over repeated drug
use, the repetition
of DA signals
continue to reinforce drug-related cues and actions to pathological levels). Some of these may be
linked to genetic vulnerability. D2 receptor downregulation is building tolerance basically.
Berridge believes that mesolimbic suppressions are more the consequence rather than the cause
of drug addiction. Incentive sensitization theory (Berridge and Robinson): A pathological
motivation for drugs is the core problem in addiction. Repeated substance abuse leads to a
decrease in liking and an increase in wanting (not necessarily conscious). The DA system
becomes sensitized (hyperreactive) to the incentive effects of drugs and associated cues. Neural
sensitization explains this paradoxical difference: the drugs have an increased ability to elevate
dopamine transmission in brain regions (NuAcc). Liking can be measured by taste reactivity.
According to IS theory, the incentive salience of drug-associated stimuli increases in substance
abuse. Drug-associated stimuli elicit attention and approach, become reinforcers, and can induce
relapse. Research has shown that
● Drug associated cues become motivational targets (stimuli, context)
● Drug associated cues become conditioned reinforcers in their own right
● Drugs reinstate drug-seeking (can be prevented by blocking the mesolimbic pathway)
● Motivation to work for the drug increases (rats pressing levers to obtain drugs)
There is little human research in incentive-sensitization, but some use progressive ratio schedule
to measure, but many studies are self-report. Some research shows that cue-induced recovery of
responding continues to increase for weeks-months (incubation of craving). Stimulus control and
cue exposure are used as treatment, but relapse is high.
, Literature Module 1 - DSM-5 criteria for Substance Use Disorder
Literature Module 1 - Drug Addiction as Incentive Sensitization
(Berridge and Robinson)
Addiction and Incentive Sensitization
IS is a persistent “sensitization” or hypersensitivity to the incentive motivational effects of drugs
and drug-associated stimuli. IS causes biased attention to drug-associated stimuli and a
pathological wanting/craving of drugs. an addictive drug is a stimulus that both potently activates
the mesolimbic brain system and initiates neurobiological events that enduringly sensitize that
system. Liking decreases as wanting increases. Specific contexts, stimuli, or mood states can
facilitate the expression of a sensitized “wanting” response. This could be related to
drug-induced prefrontal cortex dysfunction.
What Is Drug Sensitization?
It is basically the increase in a drug effect that occurs after repeated exposures to the drug.
Incentive sensitization refers to particular neurobiological changes in brain mesolimbic
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