The Cognitive Neuroscience of Addiction Flashcards
1
Q
SUBSTANCE USE REASONING
A
- psychoactive drugs used for various reasons:
1 . ALCOHOL = relaxing/enhancing social experiences/anxiety & depression reduction
2. COFFEE = to wake up
3. NICOTINE = experience/stimulant/social reasons
4. MDMA = improve social experience
5. COCAINE = confidence/enhance social experience/work focus
6. HEROINE = relax/belonging/safety
2
Q
ADDICTION
A
- 6% alcohol users meet alcohol disorder criteria
- addicts experience intense cravings for desired substances/severe withdrawal symptoms w/o it
- addicts oft go to extreme lengths to obtain drug; profound effect on physical/mental health -> potentially devastating effect on families/work/education/social life
- degrees of withdrawal dif between people/drugs
3
Q
ADDICTION DRUGS
A
DRUGS ASSOCIATED W/ADDICTION - nicotine - alcohol - amphetamine - caffeine - heroine - cocaine/crack - prescription drugs (ie. painkillers/Benzo's) LESS ASSOCIATED - MDMA - psychedelics ASSOCIATED BEH - gambling - gaming
4
Q
COCAINE
A
- addiction associated w/brain damage risk number appearing m-h post consumption incl. YA stroke (early 30s)/seizures
- lesions = movement disorders
- subtle pathology = reduced volume of inferior portion of frontal lobe
5
Q
HEROIN
A
- associated w/broad pathology range incl. grey matter reduction; brain hypoxia (reduced oxygen availability); cerebral edema (water saturation); stroke (blood supply loss); spongiform leukoencephalopathy (gen white matter axon loss); myelopathy (paralysis via spinal lesions)
- frontal/temporal regions = reduced grey matter density in heroin-dependents; correlation between grey matter density reduction associated w/longer heroin use
6
Q
ALCOHOL
A
- alcoholism linked strongly w/Wernicke-Korsakoff syndrome
- Wernicke encephalopathy = gen brain shrinkage
- Korsakoff syndrome = chronic Wernicke “end-stage”; psychiatric diagnosis characterised by anterograde amnesia (inability to remember new things); sometimes treated w/thiamine supplements; associated w/enlarged ventricles/cortical sulci; indicates brain tissue loss
7
Q
CANNABIS
A
YUCEL et al (2008)
- carefully selected long-term (>10y) heavy (>5 joints daily) cannabis using men w/19.7y on average w/o other neurologic/mental health complications
- pps contrasted w/16 controls
- user brain volume reduced in hippocampus/amygdala
8
Q
CANNABIS X PSYCHOSIS
A
MOORE et al (2007)
- way of testing if drug use -> mental illness = large scale longitudinal research assessing psychiatric youth status prior to drug use then again in adulthood post cannabis use
- odd ratios = increased psychosis diagnosis risk in heavy cannabis users VS others; doubling psychotic symptoms risk (ie. schizophrenia) in heavy cannabis
9
Q
ADDICATION CAUSES
A
- vast research done around it
- large inter-individual variability in addiction susceptibility
- 10-20% regular drug abusers = addicted; specific stats vary on drug
- similar estimates drawn from animal addiction models research; similar percentage in animals systematically administered potent drugs preferring drugs > sucrose
- genetic addiction attribution estimate = 50%
10
Q
LEARNING PERSPECTIVE OF RELAPSE
A
- associative learning addiction theories construe drug taking = conditioning
- instrumental conditioning paradigm = drug as reinforcer; strengthens drug-related cues/drug use associations
- ie. friends who smoke -> smoking -> nicotine euphoria
11
Q
LEARNING EXPLANATION OF RELAPSE
A
- stopping ie. smoking starts process of extinction-reducing association strength between various smoking cues/smoking ie. potent cues removed from equation BUT not extinguished
- context-driven relapse = cue re-exposure elicits conditioned response aka. smoking
- extinction procedures involving multiple cue exposure w/o reward = effective as potency reduction via relapse trigger BUT difficult pull off
- research suggests extinction treatments limited to rehab centres = less effective/long-term < treatments in equivalent contexts similar to addiction development (ie. addicts home)
12
Q
“WE ARE W/O DEFENCE AGAINST THE FIRST DRINK”
A
- first dose potential to produce enhanced craving = extensively documented; common to all drug abuse
- reasoning could incl. sensory experiences associated w/drug use (ie. tobacco smell) = strong cues alone
- if someone stops smoking extinction hasn’t affected cues; first re-exposure may elicit strong conditioned response (ie. smoking)
- cue relativity clearly detected in addict brain activity
13
Q
CCR (CONDITIONED COMPENSATORY RESPONSE)
A
SUBKOV & ZILOV (1937)
- Pavlov’s colleagues
- injected dogs w/adrenaline (epinephrine) severally
- raising blood adrenaline effect -> ^HR
- ^HR following each injection got constantly smaller
- dogs developed adrenaline tolerance
- aka. organism compensates for adrenaline effect via HR reduction around injection time
14
Q
CCR +
A
- to explore whether compensatory reaction actually required drug, researchers placed dogs in same stand; injected w/placebo (neutral substance ineffective on blood adrenaline)
- researchers observed substantial HR decrease following placebo injection
- dogs conditioned to reduce HR as injection-related context response
- following acquisition, compensatory response didn’t require drug -> it was conditioned compensatory response
- SO drug effect = US; cues associated w/administration = stimuli
15
Q
CCR: HEROIN
A
SIEGEL et al (1982)
- injected 3 rat groups w/large heroin dose
- group 1 = previously tested on small dose; same settings (same-tested c)
- group 2 = previously tested on small dose; dif cage (dif-tested c)
- group 3 = heroin-naive (first time tested c)
- fatality overdose = 1 -> 2 -> 3
