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Paper 2 - Coggle Diagram

- - - - brain injury
        frontal lobe- decision making
        limbic system- reoffending
        hippocampus- memory
        hypothalamus- control of rage and pleasure, explains torture
        / = CS charles whitman- found tumour in limbic area of brain
        / = blair- antisocial personality disorder usuaully have frontal dmg = more likely to be an offender
        x = polman- playing violent video games had bigger influence on agg levels of males = observation and imitation
        x = eysenck et al- criminal scored higher on p, e, n scales than non crims = personality
      - amygdala
        ^ determines emotional response, so if dmged could cause agg outbursts
        dmg to right- deficit in decision making in men, also more involed w impulsivity
        smaller amygdala = more likely to trigger fight/flight
        ^ predict- small amyg = violence
        / = pardini et al- smaller amygdala 3x more likely to exhibit agg
        / = CS of charles whitman- tumour on amygdala
        x = polman- playing violent video games had bigger influence on agg levels of males = observation and imitation
        x = eysenck et al- criminal scored higher on p, e, n scales than non crims = personality
      - XYY
        1:1000 male births, random mutation
        extra chromosome due to error when cells divide at fertilisation
        males with extra Y chromo (XYY) more likely to get into trouble w police than XY
        often have delayed speech, prone to adhd, impairment to social interaction, poor concentration
        more impulsive + phys active
        / = jacob- xyy males overrepresented in prisons 15/1000 instead of 1/1000
        / = stocholm- risk of conviction higher for xyy males, but if social factors eg edu controlled for then crime rates r similar to ctrls
        x = polman- playing violent video games had bigger influence on agg levels of males = observation and imitation
        x = eysenck et al- criminal scored higher on p, e, n scales than non crims = personality
      - eysenck- personality
        ppl who score highly in p, e, n most likely to commit crime
        extraversion
        high need for excitement- impulsive, agg = extra stimulation
        neuroticism
        controlled by ans, releases hormones eg adrenaline- usually nervous, moody = more likely to lash out in fear
        psychoticism- linked with high T levels- egocentric, impulsive - more males commit crime due to high T
        / = eysenck- criminal scored higher on pen scales than noncrims
        x = polman- playing violent video games had bigger influence on agg levels of males = observation and imitation
        x = raine et al- lower glucose metab in pre frontal cortex of NGRI = malfunction of brain
    - - self-fulfilling prophecy
        ^ happens before 1st crime
        expectation made by society of someones current bhvr based on past events
        person offends due to living up to whats expected of them by others in society
        once crime committed, treated diff by ppl in society
        causes them to adopt crim characteristics as part of normal bhvr = deviant
        ^ affects self image as criminal identity internalised- produces bhvr that will fulfil prophecy made abt them
        / = jahoda- ashanti ppl make prophecy abt crime based on day born- higher number arrests for boys born on a wednesday as believed to be agg = fulfil prophecy
        x = polman- playing violent video games had bigger influence on agg levels of males = observation and imitation
        x = raine et al- lower glucose metab in pre frontal cortex of NGRI = malfunction of brain
      - social learning theory
        attention- observe crim bhvr from sibling
        retention- important aspects of crim bhvr, how to pick locks
        reproduction- imitating by picking lock
        motivation- intrinsic- taking pride extrinsic- praise from peers
        vic rein- crim role model gaining lots of money
        / = polman- playing violent video games had bigger influence on agg levels of males = observation and imitation
        / = anderson- college students who heard violent songs felt more hostile- paying attention
        x = raine et al- lower glucose metab in pre frontal cortex of NGRI = malfunction of brain
        x = eysenck- criminal scored higher on pen scales than noncrims
      - labelling theory- reoffending
        self identity determined by society after committing crime
        bhvr only deviant if society sees it as- allows authority to maintain power
        ^ stigmatised- judged based on specific set of characteristics
        internalise label, little opp to change = commit crime in line w label
        causes of being labelled: related to crim, minority, high crime area
        retrospective label- persons past judged by current crim bhvr "what did u expect"
        / = lieberman- juveniles arrested previously go on to commit other crimes compared to those not previously arrested = label changes bhvr
        x = raine et al- lower glucose metab in pre frontal cortex of NGRI = malfunction of brain
        x = eysenck- criminal scored higher on pen scales than noncrims
    - - factors at time of event
        arousal
        witnessing crime can be very stressful = high arousal, making difficult to accurately take in info at time -> encoded wrong so later recall is diff
        giving evidence in court is stressful as have to recall unpleasant events + alien enviro = high arousal
        / = deffenbacher- accuracy poor when emotional arousal too high/low = optimum level of arousal needed for accurate recall
        x = loftus and palmer- more students reported broken glass when asked abt verb smashed than no verb- leading qs change memory
        weapon focus effect
        persons attention becomes diverted to immediate threat of weapon + being harmed = less attention to other details of scene
        ^ later recall less reliable as witness memory of event not accurate rep of what was initially seen during crime
        may be due to looking longer at unusual objects- may be unusualness of an event rather than danger posed by weapon that attracts attention = decreased accuracy
        / = loftus- ppts in gun condition less likely to identify customer than those who saw cheque book
        x = loftus and palmer- more students reported broken glass when asked abt verb smashed than no verb- leading qs change memory
      - post event
        reconstructive memory
        recall of event subject to personal interpretation of what happened, dependent on learnt/cultural norms and values, way we make sense of world
        info received after crime can affect stored memory, potentially changing it
        witnesses collate info heard into one version of event- not true rep = unrel
        leading questions
        leads witness to desired answer
        witnesses may not understand qs asked = memory changes
        witnesses often interrupted, cant give full answers
        / = loftus and palmer- more students reported broken glass when asked abt verb smashed than no verb- leading qs change memory
        x = deffenbacher- accuracy poor when emotional arousal too high/low = optimum level of arousal needed for accurate recall- arousal not rm
- - - - Validity
        +: Pihlajamma- produced diag of sz that matched diag of other classification systems
        +: Predictive val- Mason- 99 sz patients using icd-10, good predictor for future bhvr 13 years later
        +: Concurrent val- Andrews et al- 1500 ppl w dsm+icd, found overall agreement of 68%
        -: Overlapping symptoms
        -: Interpretation bias
        Reliability
        +: use set list of symptoms used to diag disorders
        +: High rel = similar patients given similar treatments, constantly predict how symptoms will be affected
        -: Interpretation bias- less consistent diag
        -: Cheniaux et al- sz diag more w icd10 than dsm5
        
        Validity
        External val- generalised to pts with same symptoms
        concurrent val- research gains similar results to other research carried out at same time
        predictive val- predict future outcomes
        internal val- whether diag given due to symptoms in classification system and not culture/gender
        Reliability
        External rel- how much diag varies every time tested w class system
        test retest rel- proportion of ppl who receive same diag when reassessed at later date
        interrater rel- how consistent class system is over time
  - - - Neurotransmitter explanation
        
        Sz caused by flunctuation in dopa lvls in brain pathways
        mesolimbic
        pos symptoms, rewards + pleasure
        excess dopa in ML = pos symptoms
        lower glutamate levels = gaba receptors stop inhibiting dopa activity
        inc in dopa and low gluta causes thalamus to stop filtering sensory info = hallucinations due to sensory overload
        d2 receptors in ML have higher density in sz pts
        hyperactivity in these receptors = more sensitive to dopa, binds more easily, causes signal transmission to inc = pos symptoms
        excess of serotonin = inc in 5HT2 receptors, reduction in gluta in ML, causing inc in dopa + pos symptoms
        mesocortical
        too little dopa = neg symptoms
        MC important in higher cog functioning, emotion
        Lower levels of gluta in sz pts act as a brake, causing lower levels of dopa = neg symptoms
        blocking d2 receptors in MC leads to lack of sensitivity to dopa + inc in neg symptoms
        / = Carlson- ppl given amphetamines have higher dopa release in basal ganglia than ctrls, more likely to exhibit sz symptoms- excess dopa credible
        / = seeman- d4 receptors 6x more dense in sz pts, leads to psychotic symptoms
        x = gottesman- 75% MZ twins diag w sz, 24% DZ- genetic not dopa
      - Bio explanation (genetics)
        
        Inherited from parents, one sz parent = 1/5 chance of sz two sz parents = 1/3
        DRD2- d2 receptors, involved in reward system so linked to devel of pos symptoms as d2 receptor activity affects cog dysfunction, oversensitive to dopa = pos symptoms
        COMT- provides instructions to make enzymes that break down nts, problems w production can inc/dec dopa levels = sz symptoms
        located on chromosome 22, defect = 30x more likely sz
        diathesis-stress model- ppl born vulnerable to developing sz due to genetic make-up, need to be raised in specific enviro for disorder to develop, more stress in early life = sz more likely
        / = gottesman- 75% MZ twins diag w sz, 24% DZ- genetics involved
        / = nkam- DRD2 involved w attention problems in sz patients- affects sz devel
        x = carlsson- ppl given amphetamines have higher dopa release in basal ganglia- dopa not genes
        x = seeman- d4 receptors 6x more dense in sz patients, causing sz symptoms- d4 not genes
      - Non-bio explanation (social causation)
        
        Sz is a reaction to social enviro someone lives in, more common in wc
        Unemployment + poverty
        lack of volition- dont have money to do things they enjoy
        disorganised thinking- high stress
        adversity to adult life
        childlike state to avoid adult responsibilities, causes emotional bluntness
        social isolation
        lack of volition- alone for long periods of time
        paranoia- dont go out a lot
        poor housing/overcrowding
        hallucinations and stress/paranoia- noise in small, overcrowded houses
        areas w high crime
        delusions- fear of someone trying to hurt
        emotional disturbance- desensitisation to crime
        separation from parents as child
        lack of volition- withdraw socially, fear of relationships for fear of hurt
        emotional blunting- shut off emotions to avoid being hurt
        / = copper et al- single unskilled males 4x more likely to develop sz = skills taught in childhood can help reduce chance of sz
        / = veiling et al- immigrants in neighbourhoods away from own culture higher chance of sz
        x = carlsson- amphetamines = higher dopa in basal ganglia causing symptoms- dopa not sc
        x = gottesman- 75% MZ 24% DZ = genetic not sc
    - - Bio treatment (drugs)
        
        Change biochem of brain to reduce symptoms
        mostly tablets, but can be injected
        not a cure- just a way to manage symptoms
        antipsychotic drugs used as work to block receptors, reducing amount of nts in brain
        typical/atypical as drugs- trial and error between which is best
        typical as drugs
        reduce dopa levels, only treat pos symptoms as “antagonist”, block function of dopa in brain
        work by blocking d2 receptors on post synaptic neuron, stopping dopa from binding w receptor + slowing ability to pass msgs between neurons
        atypical as drugs
        reduce dopa and serotonin levels- antagonist and agonist = treat pos and neg symptoms by inc/dec dopa activity in brain
        improve cog function and memory
        ML- bind to d2 receptors and reduce activity of dopa, slow msg passing to normal level = pos
        MC- bind to 5HT2a receptors (reduce action of sero) block so dopa levels raised = reduce neg
        stimulate 5HT1a receptors on gaba neurons- reduces gaba activity = activates gluta neurons, changing dopa in MC = higher cog functioning
        / = hartling et al- meta analysis, found typical as more effective at reducing pos symptoms, but atypical better at reducing neg symptoms
        x = side effects like tongue protrusion, weak immune system make ppl not want to take
        x = rector- cbt and routine care more effective than any other treatment
      - Psych treatment (CBT)
        
        CBT
        Works on developing sz patients self esteem by educating abt their sz
        try to normalise their psychotic experiences
        adapted to meet needs of individual
        takes 12-20 sessions
        stage 1:
        identifying symptoms and setting goals
        identify stressors associated w symptoms
        realistic, measurable goals for therapy are agreed
        coping mechs agreed- eg antipsychotic drugs to cope w hallucinations
        stage 2:
        develop/practise coping strats
        A- identify activating events (hearing voices) that cause consequences
        C- categorise consequences (social withdrawal) as emotional/bhvrl
        emphasise connection between A&C
        B- patients false beliefs discussed as actual causes of these events/emotions
        therapist teaches strats for managing stressful situations
        combat hallucinations/delusions by verbally challenging perceived reality, encourage patient to collect evidence that they can challenge
        stage 3:
        maintaining therapy goals
        anxiety of treatment ending, ways to maintain
        review therapy outcomes + identify stressors + ways to deal w irl
        gradually reduce sessions over time
        
        = rector- CBT + routine care together more effective than any other sz treatment
        
        = barrowclough et al- improvements to neg symptoms when group therapy used compared to drugs
        
        = jauhar et al- cbt has small effect on sz symptoms after systematic review
        
        = hartling et al- typical more effective at reducing pos symptoms, atypical neg symptoms = drugs
  - - - Bio explanation
        hypothalamus- regulates eating, so dmg can explain avoidance of food and binge eating due to hypothalamus controlling appetite
        feeling and reasoning part of brain- happy when lose weight
        hypothalamus sends signals to other areas of brain that tell us we are hungry, stimulates us to eat
        hormone ghrelin is produced in stomach when hungry- ghrelin levels rise before a meal and decrease afterwards- signals hypo that we r full
        ana pts- elevated ghrel as person is starving. when do eat, ghrel lvls drop signif, could explain why ana pts find it hard to put on weight- hunger signals not working correctly
        ^ if ghrelin cant bind to receptors, brain interprets as person not being hungry
        leptin- produced in fatty tissue and travels thru blood to brain
        signals to hypo that we r full
        ana pts have high leptin levels- starving, when eat something small, high leptin lvls produced, sending faulty signal to hypo = dont need to eat more
        / = anand- dmg to lateral hypo led to pts not eating as body never feels hunger, no signal to eat received = exp avoidance bhvr
        x = cause and effect- dont know whether ana dmgs hypo/hypo dmg causes ana
        x = becker- 0% vomited -> 11.3%
      - non bio explanation
        social learning theory
        attention
        retention- rehearse diets
        reproduction- excessive dieting
        motivation- intrinsic- excessive exercising makes them feel proud extrinsic- praised by friends for weight loss
        vicarious reinforcement- rms rich and famous, motivates pts
        / = becker - 0% 1995 11.3% 1998
        / = sui-wah - ana rare in black populations as being slim not viewed as attractive- diff types of rms observed and imitated
        x = scott van zeeland - variant of EPHX2 gene causes ana development
        x = anand- dmg to lateral hypo caused pts not to eat as didnt get hunger signals- not slt
    - - bio treatment- drugs
        cant treat ana, but help w comorbid conditions eg anxiety, depression
        anti-depressants:
        SSRIs (selective serotonin reuptake inhibitors) most commonly used as they work by blocking sero reuptake back into presynaptic neuron, leaving more sero available to pass msgs to post synaptic neuron = reduce depression symptoms
        ^ inc appetite due to inc in sero
        anti-psychotics:
        reduce anxiety + delusion of distorted body image by blocking dopa receptors in ML pathway = reduced dopa so ctrls unrealistic ideas abt weight
        flood reward pathways during eating- ana pts get pleasure from eating food
        / = kaye et al- ana pts given ssri had lower relapse rates
        / = jensen et al- giving 3 patients olanzapine daily increased perception of their body image
        x = grave- more than 88% of ana pts who started cbt have improved bmi after completing therapy, CBT effective treatment
        x = bower- after cbt ana pts had sig changes to eating bhvrs + depressive symptoms = not drugs
      - psychological treatment- CBT
        works to develop ana pts self esteem + destigmatise their eating bhvrs
        can be adapted to meet needs of individual, takes 12-20 sessions
        stage 1:
        identifying symptoms and setting goals
        identify stressors associated w symptoms
        realistic, measurable goals for therapy are agreed
        coping mechs agreed- eg antipsychotic drugs to cope w faulty thoughts
        stage 2:
        develop/practise coping strats
        A- identify activating events (calories on packaging) that cause consequences
        C- categorise consequences (not meeting friends for lunch) as emotional/bhvrl
        emphasise connection between A&C
        B- patients false beliefs discussed as actual causes of these events/emotions
        therapist teaches strats for managing stressful situations
        combat obsession with checking calories by verbally challenging perceived reality, encourage patient to collect evidence that they can challenge
        stage 3:
        maintaining therapy goals
        anxiety of treatment ending, ways to maintain
        review therapy outcomes + identify stressors + ways to deal w irl
        gradually reduce sessions over time
        / = grave- more than 88% of ana pts who started cbt have improved bmi after completing therapy, CBT effective treatment
        / = bower- after cbt ana pts had sig changes to eating bhvrs + depressive symptoms
        x = kaye et al- ana pts given ssri had lower relapse rates
        x = jensen et al- giving 3 patients olanzapine daily increased perception of their body image