Transcript Lecture Slides - University of Warwick

Module: Health Psychology
Lecture: Addiction
Date:
02 March 2009
Chris Bridle, PhD, CPsychol
Associate Professor (Reader)
Warwick Medical School
University of Warwick
Tel: +44(24) 761 50222
Email: [email protected]
www.warwick.ac.uk/go/hpsych
Aims and Objectives
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Aim: To provide an overview of the psychology of addiction
Objectives: By the end of the session you should be able to
describe …
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Basic brain functions and how drugs function in the brain
The nature of addiction and the distinction between
physical and psychological dependency
The key features and efficacy of a stepped care
treatment protocol for addiction
Risks factors for relapse, and appropriate tasks and
techniques for preventing relapse
Task-Specialisation and the Reward Pathway
Neuronal Transmission
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Electrical impulse travels
down axon towards terminal
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Soma
Release of neurotransmitter
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Dendrite
Dopamine; Serotonin; GABA;
Endorphines; Glutamate;
Acetylcholine
Axon
Neurotransmitter binds to its
receptor on next neuron
Binding generates a new
impulse in next neuron
… and so on …
Terminal
Synaptic Neurotransmission and Modulation
Drug Functions in the Brain
Cocaine Inhibits Uptake
Opiates Increase Release
Accumbens
1100
1000
900
800
700
600
500
400
300
200
100
0
AMPHETAMINE
% of Basal Release
400
DA
DOPAC
HVA
0
250
1
2
3
4
Time After Amphetamine
Accumbens
Caudate
150
100
0
0
1
2
3 hr
Time After Nicotine
COCAINE
DA
DOPAC
HVA
200
100
0
5 hr
NICOTINE
200
Accumbens
300
250
% of Basal Release
% of Basal Release
% of Basal Release
Drug Effects on Dopamine Levels
0
1
Accumbens
2
3
4
Time After Cocaine
5 hr
MORPHINE
Dose (mg/kg)
0.5
1.0
2.5
10
200
150
100
0
0
1
2
3
4
Time After Morphine
5hr
Drug use changes the brain
in fundamental and long lasting ways
These changes are both
functional and structural
Long-Term Effects of Short-Term Drug Use
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PET depicting brain activity
in monkeys during cognitive
tasks - learning and memory
Pre and Post design: monkey
acts as own control
Exposure = 10 days of
amphetamine
Significant decrease in brain
activity for at least 1 year
Relatively short-term drug
use can have long-term
effects on brain function
Pre-amphetamine
Post-amphetamine
Long-Term Metabolic Changes
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PET depicting brain activity
during cognitive tasks - decision
making, learning, and memory
Controls (no history of drug
use) and (same) cocaine users
after 10 & 100 days abstinence
Short and long-term brain in
cocaine users is significantly
less than in non-drug users
Control
Cocaine Abuser (10 days)
Unknown whether activity in
some brain areas will ever
return to normal
Cocaine Abuser (100 days)
Glucose Utilisation  +
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Changes in Brain Structure
Case
Heroin
Alcohol
Amphetamine
Cocaine
Non-Case
Dopamine neurons in the
nucleus accumbens have more
dendritic spines/connections in
amphetamine exposure
What is Addiction?
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A chronic, often relapsing brain disease that causes
compulsive drug seeking and use despite harmful
consequences to self and others
Addiction develops because the brain (neurons) adapts to
repeated drug exposure such that normal functioning
occurs only in presence of drug
Adaptation negatively influences:
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Affect: magnified emotional instability
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Behaviour: uninhibited and substance-led
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Cognition: impaired, distorted and egocentric
What is Dependency?
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Dependence is used synonymously to avoid the pejorative
connotations of addiction
Permits useful distinction between physical dependence
and psychological dependency
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Physical dependency: defined by the appearance of
characteristic withdrawal symptoms when the substance is
discontinued
Psychological dependency: defined by the need to use a drug
out of desire for the effects it produces, rather than to relieve
symptoms of withdrawal
Dependency-specific consumption motivations may drive
compulsive use, and require different treatment strategies
Substance Dependence Criteria (ICD 10)
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Three or more of the following during the past year:
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Evidence of tolerance
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Strong desire / compulsion to take the substance
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Difficulty controlling substance-taking behaviour
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Increasing effort to obtain the substance
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Progressive neglect of alternative pleasures or interests
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Continued substance use despite negative consequences
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Physiological withdrawal state when substance use is ceased
or reduced
Stepped Care Treatment Model
Abstinence
Harm
Minimization
Advice and
information;
1
Planned
counselling;
Controlled
consumption
2
Structured
programme of
counselling,
substitute
medication and
detoxification
Step
3
Inpatient
programme
with medically
supervised
detoxification
4
(DoH, 2001)
Relapse Curves After Treatment:
Heroin, Nicotine & Alcohol
What do these data demonstrate?
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12-month relapse between 65-80%
Heroin and Smoking follow almost
identical relapse pattern
Alcohol has highest initial but
lowest long-term relapse rate
All patients vulnerable to relapse
within first 3 months - >50%
Relapse vulnerability reduced for
alcohol after 3 months
Reduced vulnerability not evident
in Heroin or Smoking until 6 mnths
Relapse is a huge problem
Name the colour, ignore the word
table
pub
shot
paper
object
orange
beer
bottle
beach
golf
tyre
whiskey
centre
drive
tum
drink
people
whistle
year
chaser
rum
Response times for alcohol-related and
unrelated words by alcohol-dependent
and non-dependent people
Thinking About Relapse
Alcohol Stroop Task
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4
3.5
Result: Alcohol dependent people
took longer to name ink colour for
alcohol-related words
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3
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2.5
Alcohol
Neutral
2
1.5
1
0.5
0
Explanation: Alcohol-related
words must activate additional
cognitive processes
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Non-Case
drain available cognitive resources
Conclusion: Automatic attentional
bias for alcohol-related stimuli
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Case
additional processing time
unable to stop ‘cues to action’
Effect of Substance-Related Stimuli
Amygdala is critical for
memory and responsible for
evoking emotions
Amygdala
not activated
Amygdala
activated
In addicts, the amygdala is
active during craving
Recovering addicts (>10 yrs)
watched videos in PET scan
Drug-related video activated
the amygdala and triggered
negative emotion and
substance craving
Neutral
Drug-related
Relapse Risk Factors
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Common predictors of relapse:
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Onset age and duration
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Negative affect – previous and current
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High risk situations – social and/or stressful
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Lack of social support – adaptive, not available
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Lack of pre-arranged follow-up
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Ineffective coping skills
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Poor response to/interpretation of initial lapse
Relapse Prevention
Key Tasks
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Identify high risk
situations
Key Techniques
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Develop effective coping
strategies
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Mobilise adaptive social
support
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Prevent lapse from
slipping into relapse
Preparing response to
(inevitable) lapse
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Behaviour analysis –
scheduling and monitoring
Coping skills training – cues,
affect, peers
Cognitive restructuring understanding relapse as
both a process and as an
event
Integration into social
supportive networks
Contingency planning
Conclusions
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Addiction is a chronic, often relapsing brain disease that
changes both the structure and function of the brain
Characterised by uncontrolled compulsive drug use despite
negative effects for the individual and those around them
Interventions are effective, but rates of relapse are high,
especially in the first 3 months
Risk of relapse has many influences, including background,
stable, social and situational factors
Relapse can be reduced by preparing patients in advance,
and by effective inter-professional management
Summary
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This session would have helped you to understand …




Basic brain functions and how drugs function in the brain
The nature of addiction and the distinction between
physical and psychological dependency
The key features and efficacy of a stepped care
treatment protocol for addiction
Risks factors for relapse, and appropriate tasks and
techniques for preventing relapse
Any questions?
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What now?
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Obtain / download one of the recommended
readings
In your small groups consider today’s lecture in
relation to your tutorial tasks:
a) integrated template
b) ESA question