READINGS Flashcards
Multi-sourced model of addition
SOCIAL, HISTORICAL + CULTURAL ENVIRONMENT
- diff addictions shave more in common than not
- addictive behaviours have unstable, ever-changing tendencies (characterisation, meaning and definitions change across cultures, social settings and time)
- specific stimulating arrangements influence dev of addiction
- consumption-stimulating contexts
- social pressures, pop culture and the media
- availability, exposure, social norms
PAST ACTIONS/CURRENT CHOICES
- temporal discounting + time-discounting (delayed courses of action are less ‘counted on’ than immediate effects)
- patterns of previous consumption (accumulated momentum)
- future-orientated > value present consumption more, discount possible future costs of consumption
- impulsivity > choose drugs NOW, no consideration of future consequences
PRE-DISPOSITIONS
- genetics (but GxE interactions)
- shared genetic inheritance with other dx?
- personality dispositions (sensation-seeking, impulsivity, future-time orientation, harm avoidance, reward dependence)
NEUROBIOLOGY
- DA > increased neurotransmission + DA cell density in nucleus accumbens
- “pleasure centre” > many interconnected brain areas
- must interpret in terms of psych, cog, social and behavioural processes
UNDERLYING PROCESSES
- associative strengths: elicited by context cues > part of unconscious, automated, habitual processes
- goal pursuit outside conscious awareness
- addictive responses elicited + strengthened based on associative links (environmental cues/stimuli + responses) > operant and classical conditioning
What does the multi-sourced model of addiction emphasise?
- addiction as synergy > no. of factors work together
- each case a unique combo of potentially unfortunate circumstances
- individually-tailored treatments
- explains why some people quick abruptly, some after a while, some with major difficulties and some never
- focus on why people who are well aware of harmful consequences continue to perform addictive behaviours
- mechanisms work together to form behaviours which are extremely resistant to change
- majority of contemporary accounts of addiction are not mutually exclusive
- all the processes and mechanisms can be functional and supportive of each other
How does psychology interact with gambling?
- gamble to deal with underlying psych problems
- psych factors: conditioned response, schedules of reinforcement, erroneous cognitions
What is the problem with gambling research?
- very limited
- conflicts of interest: agenda largely set by government and they have veto power
- no high-impact journals
- few large-scale clinical outcome studies
What sets Aus apart from the rest of the world in gambling?
- impact of electronic gaming machine gambling
- 80% of gambling problems
- 60% gambling revenue
- highly available > SA has over 600 venues with EGMs
- highlights the contradiction and conflicts of interest in gambling in Aus
4 theories of conversion disorder?
- PSYCHOANALYTICAL: internalised prohibition against expressing unconscious desires (sexuality, aggression, dependency). Treatment = help client move to more mature defense mechanisms
- LEARNING THEORY: maladaptive operant behaviours that act on the environment to produce reinforcing consequences. Treatment = reduce external reinforcement + alter client’s beliefs through counter-suggestion
- SOCIOCULTURAL: more acceptable form of communication in cultures where direct expression of intense emotions is prohibited
- NEUROPSYCH: voluntary commands blocked from activating the pathways that control the arm > inhibition of willed movement
Cognitive Model of IAD
- misinterpret benign bodily sensations as signs of disease
- overestimate likelihood of serious illness
- cognitive bias > attend to info that confirm illness concerns + ‘avoidance’ behaviours
- selective attn. to illness-related threat info
- personality and temperament: high N, low E/C
- effortful control/C moderates rship b/w health anxiety and clinical IAD > helps explain why some neurotic people go on to develop IAD and others do not
SOCIAL DEVELOPMENTAL FACTORS:
- childhood separation anxiety
- insecure attachment
- childhood experience with sig illness (personal, family, close friend)
- overly concerned parents
What are the 5 key cluster symptoms in psychotic disorders?
- psychosis (delusion, hallucinations, +ve sx)
- alterations in drive and volition (all the -ve sx)
- altered neurocognition (memory, attn., exec fn)
- depression
- mania
What are the risk factors for schizophrenia?
PERINATAL + EARLY CHILDHOOD: hypoxia, maternal infection/stress/malnutrition
- non-specific emo/behav disturbances, language alterations, subtle motor delays
- childhood trauma
ENVIRONMENT: urban, migrant, cannabis
- social isolation + disadvantage play a role
GxE INTERPLAY: 80% heritable
PATHOPHYSIOLOGY: large ventricles, decreased grey matter, DA (meds block receptors), abnormalities in brain response to cog tasks, decrea sed brain response to new stimulus/higher to repeated
COGNITION: attn., WM, exec function, social cognition, LTM, processing speed (typically 1SD below norm) > limit return to work etc.
What is the UHR criteria? What are Basic Symptoms? How do they overlap?
UHR >1 of:
- attenuate psychotic sx
- brief limited intermittent psychotic ep
- trait vulnerability + decline in psychosocial functioning
- unspecified prodromal sx
BS:
- subjective disturbance in diff domains (perception, thought processing, language, attn.)
- insight, reality testing
^^^ all rely on help-seeking individuals
What is the key difference between BS and UHR?
- BS: earlier prodromal phase
- UHR: later phase
What are the associated features in and outcomes of HR individuals?
OUTCOMES: <40% dev psychotic dx
- continue to dev. dx up to 10yrs after initial presentation
- little known about those who not convert (limited studies)
CLINICAL + FUNCTIONAL:
- comorbid: anx, dep, substance, suicide
- academic/vocational fn. impaired
- interpersonal difficulties
- poorer QOL
NEUROCOG:
- small-med impairments across no. of domains (more severe in those who end up converting to dx - esp. verbal fluency and memory)
- fall b/w healthy and those with SCZ
- social cog deficits
NEURO: smaller hippo + ACC
- dysfunction in DA and glutamate systems
What are 5 key predictors of psychosis? What can we do to prevent transition?
- genetic risk with functional decline
- high unusual thought content scores
- high suspicion/paranoia scores
- low social functioning
- hx substance use
- HR with high suspiciousness/anhedonia/asociality scores > esp. high transition risk
PREVENT:
- CBT, omega-3
Explain the cog approach to hallucinations/delusions (Morrison)
MISINTERPRETATIONS
- interpreted as threatening to physical/psych integrity of individual > increase -ve mood + arousal > safety behaviours (hypervigilance, distraction, wacth Tv) > prevent confirmation + increase recurrence
- influenced by experiences (trauma) + beliefs
- maintained by safety behaviours, faulty self/social knowledge, mood, physiology
- determine cog, behavioural, affective + phys responses/consequences
- associated with level of distress
- social meanings play a role (culturally unacceptable)
- influenced by current environment (stressful life events, family environment > high EE)
METACOGNITION
- intrusive thoughts attributed to external source to reduce cog dissonance
- appraisal and response is key (NOT content) > attribute intrusions to external source to reduce cog dissonance
- +ve and -ve beliefs about intrusions (influence development and maintenance)
- +ve: provide company, soothing, exciting, make them special
- -ve: attempts to suppress, associated w unhelpful coping strats, uncontrollable, dangerous
KEY DIFF TO ANXIETY:
- culturally unacceptable interpretations
INTRUSIONS COMMON RESPONSE: sexual abuse, bereavement, sleep/sensory deprivation, solitary confinement
- in psychosis: less wanted + less controllable, more distressing/uncontrollable/unacceptable
APPRAISALS ARE KEY:
- +ve rship w malevolence + resistance of voices
- +ve rhsip w benevolence + engagement w voices
- selective attn. + attentional biases + excessive self-awareness
- over-confident in judgment/guessing
- more punishment and worry-based control strategies
Explain PDs across the lifespan
- traits in childhood stabilize throughout life (mod. stable in childhood > increased stability from adolescence to adulthood > changes more slowly after 30yrs > continue to stabilise until at least 60yrs)
^^^ rate of change slows over time, doesn’t cease - traits 50% heritable
- we should tak on a broad, life-course perspective on adaptive and maladaptive traits > consider PDs at all ages
- change in traits can predict change in PD but not vice versa
- PD becomes increasingly apparent during transition from childhood to adulthood
- lifespan approach could help reduce stigma > view it as more treatable
YOUNG PEOPLE
- caution against dx <18yrs (say they are protecting children against stigma?) > but this is preventing the adoption of a lifespan view
- will allow prevention, early detection and interventions to change the life-course trajectory of PD
LATER LIFE: scarcity of research (only cross-sectional)
- neurotic/-ve affective decrease w age + cluster A increase
- stability of personality in older adults tends to be over-estimated
- bias toward minimisation of personality problems in later life
- cog decline/ALZ related to changes in personality
