Psychology of Addiction: Brain Functions, Treatment, and Relapse Prevention

1. Module: Health PsychologyLecture: AddictionDate: 02 March 2009 Chris Bridle, PhD, CPsychol Associate Professor (Reader) Warwick Medical School University of Warwick Tel: +44(24) 761 50222 Email: C.Bridle@warwick.ac.ukwww.warwick.ac.uk/go/hpsych

2. Aims and Objectives • Aim: To provide an overview of the psychology of addiction • Objectives: By the end of the session you should be able to describe … • 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

3. Task-Specialisation and the Reward Pathway

4. Neuronal Transmission • Electrical impulse travels down axon towards terminal • Release of neurotransmitter • Dopamine; Serotonin; GABA; Endorphines; Glutamate; Acetylcholine • Neurotransmitter binds to its receptor on next neuron • Binding generates a new impulse in next neuron • … and so on … Soma Dendrite Axon Terminal

5. Synaptic Neurotransmission and Modulation

6. Drug Functions in the Brain Cocaine Inhibits Uptake Opiates Increase Release

7. COCAINE AMPHETAMINE Accumbens 1100 Accumbens 400 1000 900 DA 800 DA 300 DOPAC 700 DOPAC HVA % of Basal Release HVA 600 % of Basal Release 500 200 400 300 100 200 100 0 0 0 1 2 3 4 5 hr Time After Amphetamine Time After Cocaine NICOTINE MORPHINE 250 Accumbens 250 Dose (mg/kg) 200 Accumbens 0.5 200 Caudate 1.0 2.5 150 % of Basal Release 10 150 % of Basal Release 100 0 1 2 3 hr 100 0 1 2 3 4 5 hr 0 0 0 1 2 3 4 5hr Time After Nicotine Time After Morphine Drug Effects on Dopamine Levels

8. Drug use changes the brain in fundamental and long lasting ways These changes are both functional and structural

9. Long-Term Effects of Short-Term Drug Use • 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

10. Long-Term Metabolic Changes • 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 • Unknown whether activity in some brain areas will ever return to normal Control Glucose Utilisation  + Cocaine Abuser (10 days) Cocaine Abuser (100 days)

11. Changes in Brain Structure Non-Case Case Cocaine Amphetamine DA D2 Receptor Availability  + Alcohol Dopamine neurons in the nucleus accumbens have more dendritic spines/connections in amphetamine exposure Heroin

12. What is Addiction? • 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: • Affect: magnified emotional instability • Behaviour: uninhibited and substance-led • Cognition: impaired, distorted and egocentric

13. What is Dependency? • Dependence is used synonymously to avoid the pejorative connotations of addiction • Permits useful distinction between physical dependence and psychological dependency • 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

14. Substance Dependence Criteria (ICD 10) • Three or more of the following during the past year: • Evidence of tolerance • Strong desire / compulsion to take the substance • Difficulty controlling substance-taking behaviour • Increasing effort to obtain the substance • Progressive neglect of alternative pleasures or interests • Continued substance use despite negative consequences • Physiological withdrawal state when substance use is ceased or reduced

15. Stepped Care Treatment Model Abstinence Harm Minimization 1 2 Step 3 4 (DoH, 2001)

16. Relapse Curves After Treatment:Heroin, Nicotine & Alcohol What do these data demonstrate? • 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

17. Thinking About Relapse Name the colour, ignore the word table paper beer golf centre drink year pub object bottle tyre drive people chaser shot orange beach whiskey tum whistle rum Response times for alcohol-related and unrelated words by alcohol-dependent and non-dependent people

18. Alcohol Stroop Task • Result: Alcohol dependent people took longer to name ink colour for alcohol-related words • additional processing time • Explanation: Alcohol-related words must activate additional cognitive processes • drain available cognitive resources • Conclusion: Automatic attentional bias for alcohol-related stimuli • unable to stop ‘cues to action’

19. Effect of Substance-Related Stimuli Amygdalanot activated Amygdalaactivated Amygdala is critical for memory and responsible for evoking emotions 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

20. Relapse Risk Factors • Common predictors of relapse: • Onset age and duration • Negative affect – previous and current • High risk situations – social and/or stressful • Lack of social support – adaptive, not available • Lack of pre-arranged follow-up • Ineffective coping skills • Poor response to/interpretation of initial lapse

21. Relapse Prevention Key Techniques • 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 Key Tasks • Identify high risk situations • Develop effective coping strategies • Mobilise adaptive social support • Prevent lapse from slipping into relapse • Preparing response to (inevitable) lapse

22. Conclusions • 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

23. Summary • 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

24. Any questions? • What now? • 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