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56 Cards in this Set
- Front
- Back
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Who is Harry Kakavas? |
- Man who sued Crown for $30 million for exploiting his pathological gambling addition - Gambled over $1.5 billion in 15 months, attempted to sue Crown for $30 million - Crown used their private jets to fly him to Casino - Lost the case, Judge ruling that he was responsible for his own actions |
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What is the largest contributor to disease burden in Australia? |
Dependent drug use |
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What are the two highest causes of preventable death in Australia? (App. 15,000 per year) |
Alcohol abuse and Cigarette Smoking |
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What percentage of Australians will use an illicit drug in their lifetime? |
38% |
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What percentage of regular drug users will develop a dependency? |
10-15% |
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How has addiction been traditionally viewed? |
As a social problem |
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What social stigmas exist around addiction? |
Rather than being treated as patients, people are blamed for their illness, discriminated against and criminalised |
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How is specialised treatment for addiction viewed? |
Unnecessary and/or ineffective |
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How do Government policies view addiction as an illness? |
Still a strong emphasis on personal responsibility, as opposed to a disease which is out of their control |
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What was the aim of addiction neurobiology? |
To provide scientific evidence to support the medicalisation, or 'disease principle' of addiction |
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Describe Robbins et al. (1973; 1993) study on opiate addiction in vietnam war veterans. |
- Vietnam war soldiers had a high rate of heroin usage. (45% used, 20% dependent) - Investigated ongoing rates once vets returned home (only 5% of those who said they were dependent, relapsed upon returning home; only 12% had any use at all after 3 years) |
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How do drugs produce euphoria? |
By overactivating the 'pleasure/limbic' centers in the brain, via the release of dopamine in the nucleus accumbens |
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What are the mechanisms behind drug use becoming association with euphoria over time? |
- Limbic system is closely tied to learning centers such as the hippocampus - repeated pair of drug induced europhia with drug related stimuli creates an association |
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How do cue induced brain activations compare to drug induced brain activations? |
- For both active and abstinent users, drug-related stimuli activates the limbic regions usually activated with the effects of the drugs. - This cued activation does not result in the euphoria of drug use, but can generate cravings |
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How does the strength of the cued activation in the limbic system relate to the strength of cravings? |
The magnitude of activation of limbic and medial prefrontal regions predicts relapse in alcohol dependent individuals. |
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How does damage to the Insula cortex impact addiction? |
- Insula cortex is critical to the awareness of cravings - Damage to the insula removes the awareness of cravings - Smokers with damaged insula 100 times more likely to quit, than smokers with damage to other areas |
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How does the availability of Dopamine D2 receptors influence vulnerability to addiction? |
- Low availability of Dopamine D2 receptors linked to increased vulnerability to addiction - High availability of Dopamine D2 receptors shown to be a protective factor in siblings of drug dependent individuals |
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Describe the inverted U-shape curve that models Dopamine stimulation. |
- There exists an optimum level of dopamine stimulation that results in pleasure. Too much or too little dopamine results in unpleasantness - People with low d2 start below the optimal pleasure line, thus drugs can push them in pleasure - People with high d2 sit at pleasant, thus drugs can push them into unpleasant feelings |
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How is the gene Taq1A allele linked to dopamine D2 levels? |
- Possession of two copies of the allele is associated with reduced density of D2 in the midbrain - Reduced expression is associated with low dopaminergic tone, which benefits from external stimulation to increase dopamine levels |
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How is the reinforcement of both positive and negative factors associated with dopamine stimulation linked to the source of the stimulation? |
Greater dopamine stimulation results in the source of the stimulation being given greater salience and increased desire to seek it. |
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How can indirect stimuli result in dopaminergic stimulation? |
Indirect stimuli such as risky activities have an ability to stimulate the dopaminergic system via outcomes that are better than expected. |
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How does possession of the Taq1A gene predict the risk of developing drug dependence? |
- Longitudinally, people who possess Taq1A are 2 to 5 times more likely to develop a drug dependence in their lifetime - People who possess Taq1A are more likely to have a poor response to treatment, and higher rates of relapse |
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How is impulsivity linked to levels of D2 and D3 receptors available in the midbrain areas? |
People who self report high levels of impulsiveness have low levels of D2 and D3 receptor availability in midbrain areas. |
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How do people with low levels of D2 and D3 receptors react to dopaminergic stimulation? |
- People with low levels of dopamine, and self report poor self control have an enhanced response to dopaminegeric stimulation - Elevated response is associated with stronger subjective desire or wanting of the drug |
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What role might dopamine play in response inhibition? |
- Modulate tension between seeking stimulation and avoiding overstimulation - Transform top down inputs into a focused, context dependent signal that is able to suppress or facilitate behaviour |
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What other conditions have low tonic levels of depression and poor inhibitory control? |
- Parkinson's - Schizophrenia - OCD - Frontotemporal dementia - Tourette's - Huntington's |
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How does dopamine and cognitive control influence Parkison's disease |
Parkison's disease is associated with decreased inhibitory control and low dopamine levels |
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How does dopamine replacement therapy affect patients with Parkison's disease? |
- No clear evidence of significant improvements in cognitive control - Subset of patients (15-20%) actually develop impulse-compulsive behaviours |
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How is TaqA1+ linked to learning mechanisms? |
- Presence of TaqA1+ more likely to learn following rewards, rather than punishment. - Opposite is true for those without TaqA1+ |
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Describe the delay discounting task in Kirby and Markovic (1996) |
- Participants presented a fixed set of 27 choices between smaller, immediate rewards and larger, delayed rewards - Heroin addicts would only wait 40 days to make an extra $25, whilst controls would wait 77 days. - Greater control |
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How does DSM-IV (1994) view control as a component of substance dependence? |
- A key criteria of substance dependence - Persistent desire or unsuccessful efforts to cut down or control substance use - Substance is taken in larger amounts or over a longer period than was intended |
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What is top down cognitive control? |
- When conscious internal goals take precedence over automatic processes - Exhibited in inhibitor control and selective attention |
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What areas of the brain are associated with carrying out the Stroop test? |
- Anterior Cingulate Cortex (ACC) - detects the need for greater levels of control - Dorsolateral prefrontal cortex (DLPFC) - exerts the control |
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What occurs in the ACC and DLPFC during a stroop test? |
- ACC detects that the response conflict between the word and the colour - DLPFC resolves this conflict through biasing attention to colour processing, rather than word reading |
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What mediates the conflict resolution involved in a stroop task? |
- Unclear if it's the amplification of relevant information, or the inhibition of irrelevant information, or both |
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What tasks are used to evaluate inhibitory control? |
- Go / Nogo tasks - Stop-Signal Tasks |
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What areas of the brain has fMRI research consistently shown to be involved in successful response inhibition? |
Right inferior frontal, right parietal and dorsal ACC regions |
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What affect on response inhibition is typically caused by a lesion to the right inferior frontal gyrus? |
- Increased response times on Stop Signal response times |
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What impact does drug use have on the Right inferior frontal, right parietal and dorsal ACC regions? |
Compromised cognitive control and dysfunction in the Right inferior frontal, right parietal and dorsal ACC regions |
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What results do dependent drug users and gamblers show on control tasks such as GNG and SST |
- Significantly poorer performance on control tasks |
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How are the negative performance of drug users on control tasks associated with brain activation in the DLPFC and dorsal ACC regions of the brain? |
Poor performance on control tasks associated with significantly lower activity in DLPFC and ACC regions |
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How is prefrontal dysfunction associated with drug-naive children with a family history of drug dependence |
- Increased pre-frontal dysfunction - Poor cognitive control performance - Greater risk of developing subsequent drug addiction later in life |
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How do Dependent drug users perform on attention tasks including drug related stimuli |
- Demonstrate a greater attentional bias for drug related stimuli, than controls - Only for stimuli directly related to the individuals drug usage (i.e. joint v bong) - Greater bias predicts poorer treatment outcomes |
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How do dependent drug users perform on a drug related emotional stroop task? |
- Both active and abstinent drug users show significantly slower response times for drug related words or pictures compared to neutral items, items from a single category or simple coloured configurations. |
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What are the mechanisms involved in the performance of dependent drug users on an emotional stroop task? |
- The presence of the drug related stimuli induces cravings, that activate limbic regions (Increases cravings) - Prefrontal control regions simultaneously downregulate showing less activity than necessary to regulate control (Reduces control) - In practice, this makes drug related cues in the environment very difficult to ignore |
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How is cognitive performance associated with successful treatment? |
Cognitive impairment is generall associated with poor treatment retention |
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What results did Paulus et al. (2005) find in respects of cognitive control and relapse? |
- Poor cognitive control and associated hypoactivity in DSLPF, parietal temporal cortices and anterior insula accurately predicted relapse in 89% of relapsers, and 95% of non-relapsers |
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How does cognitive performance predict the response to treatment? (Carroll et al. 2011; Aharaonvich et al. 2008) |
-Less predicative power of response to treatment from interventions |
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How do dependent drug users recover? |
- Evidence suggests recovery of cognitive function with abstinence is slow and piecemeal, if at all - Participants who continue to take the drug have better cognitive performance up to 6 months later - Abstinence of 12 mons does not relate to better neuropsych performance |
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How does maintenance treatments affect cognitive performance? |
Maintenance treatments are associated with cognitive impairment |
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What outcomes can dependent drug users expect from abstinence? |
- Current evidence suggests enduring cognitive control problems and hyperactive responsiveness to drug related stimuli |
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Can you improve cognitive control? |
- Noradrenergic drugs improve SST performance, but not Serotonergic drugs - Serotonergic drugs improve reward learning performance, but not Noradrenergic drugs |
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How does Ritalin improve a child diagnosed with ADHD on attentional tasks? |
- Significant improvements to performance on attentional tasks, stop-signal tasks - associated with significant increases in right IFG activity during stop trials
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How do Neuroenhancers such as Modafinil and Methylphenidate improve recovery from drug dependence? |
- Generally no improvement, or at best mixed results - Modafinil - conflicting findings - Methylphenidate - no improvement |
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What did Cochrane's meta-analysis of congitive enhancers impact on drug dependence report? |
- Did not reduce cocaine use - Trend for improving abstinence - No influence on treatment retention |
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How did Methylphenidate influence cognitive control in dependent psychostimulant users? |
- Improved performance in stop-signal in adult cocaine users taking ritalin - Improvements associated with increases in ventromedial prefrontal activity |
