Schizophrenia

what is schizophrenia
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Terms in this set (88)
what is schizophrenia
lack of contact w/ reality
psychotic
diff symps for each indiv
characteristics
Scheinder pos + neg symptoms
pos = addition to regular behav
neg = inhibit reg behav
pos symptoms
hallucinations (Lewandowski 20% tactile)
delusions
disordered thinking
thought insertion
thought broadcasting
neg symptoms
agolia (no speech)
avoliation (unconcerned w/ surroundings)
anhendonia (inappro reaction to experiences)
flatness of effect
catatonia
stigma
declining. misunderstanding due to media portrayal
depression
symptoms seen in schizoprenia. diagnosis may cause depression
lack of insight
believe delus + perceptions are real. no lang skills to express beliefs. resistant to accept treatment
diagnostic criteria
ICD-10 v DSM IV, changes over time, limits generalisability (validity issue)
DH: initial
too much dopamine causes schizophrenia. JJ Griffiths induced psychosis w/ drug increases dopamine = cold responses and paranoid delusions. doesn't offer full explanation bc drugs that reduce dopamine have no effect on neg symps so only explains pos
DH: dopamine receptors
D1-D5 in cerebral cortex & limbic system. Seeman & Lee 1975 found antipsychotics impact D2 (D2 in subcortical region therefore limbic focus)
still no explanation for neg symp
DH: revised; limbic systemcontrols emotion + memory mesolimibic = carries dopamine ventral tegmental -> nucleus accumbens too much dop. oversimulation D2 receptors = pos sympt mesocortical = carries dopamine ventral tegmental -> frontal lobe. too little dop causes understimulation of D1 receptors = neg symtDH: imbalance may be caused by genes1`genetic predisposition - twin + fam studies. Gottesman - increased genetic sim = increased prob schiz. difficult to seperate environ + genetic factors. mz twins never have 100% concordance. 108 genetic loci - complexDH: measuring metabolitesmost research supporting dop hypo based on metabolic research. dopamine -> HVA measured in cerebral spinal fluid. diet + drugs also affect metabolite level. lumbar puncture = ethical issuesDH: serotoninpot influence on schiz. conven antipsychotics block D2. atypical block D2 + serotonin, could explain neg symDH: C or Eschiz ~~ dopa imblance. Cook 2000 - no dopa difference in schiz + non-schiz participants. less invasive techniques now more readily available; could establish c or emodifying schiz: drug treatmentsphenothiazine = antipsychotic; sedates and reduces symptoms by binding to dopa receptors. before, no treatment. Cole = 75% improved placebo - 25% improved, 28% worseSA: structural abnormalitiesKraeplin: organic brain disease. overshadowed by Freud view. modern brain scanning supports KraeplinSA: enlarged ventriclescativites in brain produce and transport cerebrospinal fluid. 4 ventricles. schizs seem to have enlarged ventricles. Weinberger 1979 used CAT + reported enlarged ventricles in chron schiz. Andreasen 1988 used MRI scans to show the size of ventricles in the brains of schizs were 20% to 50% larger than controlsSA: cortical atrophyloss of neurons from cerebral cortex giving shrunken appearance resulting in widening of sulci. characterizes 20-35% of chronic schizs. Vita 1988 used CAT scans to assess cortical atrophy in individuals w/ schiz. 33% morderate-severe atrophySA: reversed cerebral asymmetrynormally left hemis>right hemis (schizs opposite) may explain alogia & catatonia. Luchins 1979 compared 80 right handed people w/ schiz to 57 w/o using CAT; increased reversals in schizsSA: season of birth{ENVIRONMENTAL INFLUENCE ON PSYSIOLOGICAL STRUCTURE} Disanto 2012 schiz, bipolar, depression more likely diagnosed in winter. poss due to increased exposure to flu virus/lack of vitamin D during pregnancySA: replicable findingsMcCarley 1999 enlarged ventricles most reliable finding. Green links btwn atrophy + schiz confirmed w/ brain scans too. SA not always present in schiz. McCarley many factors can influence brain struc. diff in assessment, researchers, levels of schizSA: C or ESA may be caused by environmental influences (e.g. treatment drugs) Lyon 1981 antipsychotic medication -> decreased brain tissue density (therefore atrophy would occur after diagnosis)SA: not only linked to schizSA present in other conditions. Roy 1998 bipolar & schizoaffective disorder have enlarged ventricles. may indicate different disorders from common cause & classification needs to be reviewed.SA: neurodegenerative v neurodevelopmentalndevelopmental (harmful events) v ndegenerative (disease) Mathalon 2003 suggest both. ndevelopmental leave individual more vulnerable to ndegenerative diseases.PA: psychodynamic approachSchreber - judge w/ schiz wrote book on experiences. Freud based explanations on this bookPA: fixationfixated at oral stage (Freud)PA: regressionif an orally fixated individual experiences excessive stress they may regress back to oral stagePA: psychosisregression causes no ego/superego to control their impulses. id operates w/o restriction causing hall + delus. Freud - primary narcissism (selfish survival behaviour of infant)PA: schizophrenic motherFromm-Reichmann 1948 suggested mothers of schiz were overprotective + rejecting at same time causing impairments to emotional development so child vulnerable when faced w stress.PA: outdatedunscientific, unfalsifiable. no testable hypotheses. Popper - pseudo science. lack of empirical evidence. Solms 2000 PET during sleep. rational parts of brain inactive during sleep.PA: failure for effective treatmentlack of insight so not suited for psychoanalysis. Strupp 1977 psychoanalysis -> deterioration of schizophrenic symptoms bc focus on memories that schiz emotionally incapable of dealing w/. Rosen 1947 resolved symps in 36 individ w/ schiz using psychoanalysisPA: inconsistant support for schiz motherspsychodynamic = misoginistic. femininity = failed masculinity (Freud) Kasanin 1934 found maternal overprotection 33/45 cases of schiz. 1/3 cases didnt have overprotective mother. biased bc he knew hypoth so lacks objectivityPA: ignored geneticsnurture>nature. Gottesman 1991. Heston 1966 10% adopted children w/schiz mother developed schiz compared to 0% w/o (DIATHESIS STRESS)CA: cognitive approachschiz = breakdown of cog systems e.g. perception, attention + memoryCA: hallucinationsClaiborn 2.5%-4% of gen pop have had hallucin (most w/o psych prob) Morrison 1998 triggers cause audit hallucin which schiz associate inappro -> social withdrawal. emotions reinforce critical voices.CA: neg symptomsBecks Cog Triad 2008. schiz have dysfunctional beliefs of self, world, future. mental filters only allow neg messages + no info processing reinforces views -> neg sympsCA: lack of preconcious filtersFrith 1979 pos symps from inability to filter preconscious content. info from our senses is filtered (attentional systems) + the info that needs to be attended to is transferred to conscious awareness. schiz unable to do this so conscious flooded w/ irrelevant + ambiguous content causing hallucin + catatoniaCA: comprimised ToMFrith 1979 schizs have compromised theories of their own. e.g. delusions of persecution, auditory hallucinations. inner dialogue misinterprets as external. disorders in 3 cog symps; willed action (neg symps) self-monitoring (vocal halluncin) & monitoring others (delusions of persecu)modifying schiz: CBTorganises disorderded thinking. challenges thoughts w/ evidence. Nice CBT should be offered for recently diagnosed. success of treatment supports cog explanationsCA: supporting researchcog models Beck & Frith lot of research. Barch 1999 stroop test. schizs cannot filter information as fast/correctlyCA: reductionistFrith causal explanation. cog mechanism are faulty due to disconnection in frontal cortex + posterior areas. reductionist bc reduces complexity into cog mechanism functioningCA: not comprehensiveonly offers proximal not distal causes. lacks underlying mechanism to explan cog aspects, bio approach needed. Frith integrated bio, causal aspect to theory; faulty cog caused by disconnec. lead to futher criticisms of reductionismCA: integrated model of schizschiz needs to be considered more holisitically. Howes & Murray genes & early life factors w/ life events result in increased dopa -> probs w/ processing. stress->more dopa. cog explan alone insufficient but good in wider theoryDF: dysfunctional familiesresult of relationships w/ familyDF: double bind theoryBateson schiz symps due to comm difficulties. conflicting messages - child exposed to these in social interactions (unable to ignore/respond/comment on contradictions; reliant on parent) Bateson long term exposure to contradictions means child unable to discriminate btwn messages. hallucin & delus escapes contradictionsDF: expressed emotionmedication released patient from hosp but many relapse. Brown relapse linked to type or home released to w/ parents/wives = relapse more likely than those w/ lodgings/siblings. interviews w/ wives/parents found link btwn EE+relapseDF: EE componentslazy - high EE caregivers. low EE caregivers acknowledged illness. hostility - high EE. emotional overinvolvement in parent caregivers (guilt->excessive warmth) warmth - low EE. pos regard lacking in EEDF: C or ELiem comm during task of parents of sons w/ schiz no more disordered than comm in w/o schiz. Liem diff may have to adapt comm style to schiz child. suggested double bind theory based on effect not causeDF: origin of double bind commKoopmans 1997 incidental variations in family interactions at times of family distruption can cause DB. may be a symptom of pathology in parent (greater problem). explanation requires futher elaboration of origins of dysfunctional commDF: research support for EEVaughn + Leff 1976 53% schizophrenia w/ high EE relative relapsed within 9 mths - 12% low EE relatives relapse. McCreadie + Phillips 1998 did not find higher 6 & 12 mnth relapse rates in indiv w/ schiz in high EE rates. EE not only factorDF: shared environment or shared genesschiz may be due to comm issues in fam environ, but also due to family shared genes. Schiz Working Group of the PGC 2014 108 genetic loci. contradicts idea of fam relationships as cause. Diathesis stress - family relationships trigger genetically vulnerable to develop schizmodifying schiz: family interventionunderstanding fam comm -> interventions to reduce relapse. Pharoah 2000; form alliance w/ carers, lower emotional family climate by reducing stress + burden on relatives, increase capacity of relatives of anticipate & solve probs, reduce expressions of anger & guilt by fam members, maintain reasonable expectations for performance of ill family members, encourage relatives to set appropriate limits while maintaining degree of separatedness, promote desirable changes in relatives behaviour & belief systems. Pharoah 2010 53 controlled trials family intervention reduced relapse & hosp admissionSF: sociocultural factorsBoydell 2004 to understand caused of schiz the role of social environment cannot be ignoredSF: urbanicityhigher prevalence of schiz in urban areas. Faris + Dunham 1939 greater incidence of disorder comparing chicago city to outskirts. Os 2010 higher incidence of schiz in ppl born & raised in urban areas 0.5%. likely due to environ factors. Krabbendam + Os 2005 found factors e.g. socioeconomic issues, overcrowding, drugs & exposure to infectious agents. greater stress due to dense population. UN estimates 66% pop live in urban area by 2050.SF: self isolationschiz, solitary backgrounds. Faris 1934 schiz find social interactions stressful -> withdraw. urbanicity & overcrowding -> social isolation, restricts individual from feedback on appropriate behav causing strange behav. Jones 1994 study ppl born in specific week in march 1946. btwn 16-43 years 30 cases of schiz diagnosed. those diagnosed more likely to show solitary play preference btwn 4-6. at 13 more likely to rate themselves as less socially confident. suggests isolation starts earlySF: ethnicity & discriminationhigher schiz in afro-caribbean, Mahy 1999 cannot be genetic bc increased risk not seen in studies in caribbean. stress from migration to diff culture suggests reasonable explan. Harrison 1988 hw increased risk also seen in children of afro-caribbean migrants in the UK. therefore, suggestion that discrimination in society likely explanation for higher incidence of diagnosis in afro caribbean in UKSF: many risk factorshard to assess impact of each factor on develop of schiz. epidemiologists claim series of factors increase the risk of developing schiz, unclear if sociocultural risks work cocurrently or if some are more of a riskSF: urbanicity evalcannot be sure urban environ increases social stress of an individual compared to living in rural environ. general health better in urban areas, easier access to healthcare, high employment, better education. urban areas have higher social capital. McKenzie 2002 high levels of social capital protects us from stress. therefore unclear how mechanism underlying urbanicity works. may be combin environ risk factorsSF: C or Eurbanicity ~~ schiz. social drift hypothesis once diagnosed indiv show decline in socioeconomic status so move to less high class areas (inner city) gives flase impression of urbanicity being cause. Pederson + Mortensen 2001 those w/ high risk of psychotic disoders reduce likelihood of developing schiz if they moved to a more rural environ. suggests linkSF: self isolation C or EOs 2000 claimed single ppl living in neighbourhoods w/ few single ppl greater risk of developing schiz bc increased isolation & loneliness. suggests social isolation is valid explanation. hw we cannot be certain social isolation is cause of schiz or early indicator of psychosis. Jones'. more intervention strategies necessarySF: ethnicity or discrimination may be the casual factorethnicity gives higher risk of schiz, or symptoms are a result of prejudice & social discrimination. ethnic minorities may appear to be mistrustful of psychiatrists bc of pevious neg encounters w/ authority figures (paranoia) increased risk of diagnosis. Boydell 2001 incidence of schiz increased in ethnic minorities as the no. of ethnic minorities in the area fell. suggests social experience contributed to development of schiz. cannot assess impact of ethnicity & discrimination until we have prejudice free society.SF: sluggish schizpolitical groups within society impacts prevelance of schiz. 1974 Russia 6/1000 schiz in pop, 3/1000 UK. 1980s Moscow highest incidence of schiz in world, Russia most cases in any western country. increase in prevalence due to diagnosis of sluggish schiz - not diagnosed in west. Snezhnevsky claimed certain indiv were schiz even w/o symptoms at time of diagnosis. were then able to put thousands of political activists in mental institutions. fall of communism in Russia -> use of ICD-10; prevalence levels have fallen.MMB; ANTIP antipsychotics: conventional1950s. chlorpromazine blocks action of neurotransmitter dopamine by blocking D2 receptors. c/antipsych work by blocking dopamine receptors on the post synaptic neuron; reducing activity in neuron. causes increase of dopamine from presynaptic neuron. later the production of dopamine decreases bc it is depleted so the amount of dopamine in synapse decreases. blocking of receptor & lower level of dopamine in the synapse in combination leads to decrease in neural activity. decrease in activity in mesolimbic pathway is responsible for decrease in pos symptomsMMB: ANTIP antipsychotics: atypical1990s clozapine. works as dopamine antagonistMMB: ANTIP atypical differencedatypical = received at fewer dopamine D2 receptor sites & more D1 + D4. atypical bind to nearly all serotonin receptors as much as dopamine receptors. Seeman 2002 atypical bind more loosely to D2 receptors than conventional. means that blocking from atypical lasts enough to produce effect, not long enough to produce side effects (e.g. in conventional) half-life is less than conventional (less than 24 hrs)MMB: ANTIP effectiveness of coventional antipsychoticsCole 1964 mental disorders treated same way as physical - drugs. found that 75% given conventional antipsychotic improved > 25% placebo. none given antipsychotics worsened, 48% placebo worsened.MMB: ANTIP conventional v atypicalatypical = more effective. Ravanic 2009 effectiveness clozapine (atypical) chlorpromazine (conven) & haloperidoland (conven) over 5 yrs clozapine fewer adverse effects. suggests atypical more effective so preferable. some may respond better to conventional so cannot be made redundantMMB: ANTIP difficulty assessing effectiveness of antipsychoticsnon-compliance major issue bc indiv lack insight to their condition so don't take the medication. Rettenbacher 2004 found full compliance 54.2% schiz. partial 8.3%. non-compliance 37.5%. suggests antipsychotics not as effective as they seem when usedMMB: ANTIP side effectsboth types have side effects e.g. tardive dyskinesia. psychiatrists must consider whether benefits worth more than the side effects. individual may be administered antipsychotics w/o valid consent - defo do not want side effectsMMB: ANTIP chemical straightjacketsantipsychotics similar to chemical straightjackets - keep people quiet & under control. Szasz 1960 argued using physical treatments for mental disorders is bad; suggested concept of mental illness excludes non-conformistists from society.MMB: ANTIP asylums or care in communityLowrie antipsychotic drugs revolutionised care of schiz; treated in community>asylum. introduction beneficial for both patients & societyMMB: ANTIP risk of violenceschiz w/o drug therapy may pose threat. NCISH 2015 ppl w/ history of schiz account 6% total homicide rate in Eng. 29% don't adhere to drug treatment b4 homicide. lack of compliance = risk factorMMB: CBTdeveloped by Beck to treat depressionMMB: CBT; irrational thinkingpurpose of CBT = help organise disordered thinking rationally. helps make client aware of connections btwn disordered thinking & illness. challenges their interpretations of events by asking for evidence for beliefs. these help deal w/ pos symptoms & help make client more self-reliant when dealing w/ illness.MMB: CBT: key components of CBTidentified Smith 2003; engagement studies, psychoeducation, behavioural skills training, relapse prevention strategies, cognitive strategiesMMB: CBT; engagement studiespreliminary sessions; worries & symptoms talked about. builds up rapport w/ client (espc important w/ client w/ prev neg experience, or exper paranoia) natural coping strategies of client also discussedMMB: CBT; psycho-educationnormalises experience of psychotic symptoms, offering alternative explanations. client increases understanding of context of symptoms. futher assessmentMMB: CBT; behavioural skills trainingbehavioural strategies e.g. relaxation & activity scheduling taught. strategies useful to cope w/ symptoms not managed by medication & 2ndary symptoms of anxiety & depressionMMB: CBT; relapse prevention strategiestherapist & client identify indicators of relapse. identify thoughts & behav experiences b4 becoming unwell. asked to assess how they get on w/ others & what others noticed b4 they become unwell. plans developed by therapist & client that can be employed when indicators seenMMB: CBT; cognitive strategiesEllis ABC model to explain irrational thinking; Activating event -> Belief (rational/irrational) -> Consequence (healthy/unhealthy emotions). model was extended to ABCDE (Disputing beliefs & Effects of beliefs becoming more rational) clients asked to keep thought diary recording how they feel, what they did, thoughts. asked to think differently about an event & record different views & provide evidence that their thinking is appropriate. diary entry discussed w/ therapist. behav experiments used to challenge beliefs. clients asked to identify actions that could be employed to lessen voices. (e.g. music, talking) patient rates severity of voices - allows them to realise they can control voices.MMB: CBT; effective form of treatmentKuipers 1997 participants w/ distressing symp medication resistant randomly allocted standard care cond or CBT + standard care cond. after 9 mths found change in sympt experienced. CBT + stand care cond 50% participants considered to have improved. stand care cond 31% considered improved. suggests even marginal benefits CBT significantly betterMMB: CBT; contradictory evidenceJauhar 2014 only small therapuetic effect of CBT. Morrison 2014 reported CBT reduced psychiatric symp in schiz. lack of consistancy = CBT ineffective. hw Morrison cohort had choice in their treatment plan Jauhar didn't. choice important confounding variable & critcal to success of CBTMMB: CBT; short-term effectivenessonly short term studies available. long term = not positive. Tarrier 2004 CBT + standard care same relapse rate as stand care. effects CBT short lived. participants in CBT cond less neg affected by sympt than those w/o CBT. suggests long term benefits of symptom reduction.MMB: CBT; neg experience clientsmay add to neg burden of schiz after suffering sympt & prescribed strong sedative medication. Kuipers 1997 clients satisfied w/CBT experience & appropriate way of dealing w/ symp. reviewing suitability from client POV important w/ ethicsMMB: CBT; some psychiatrists may limit access to CBTpsychiatric services may feel CBT not viable option (lack of insight, cannot engage in CBT, good w/ medication) Kingdon + Kirschen 2006 only 49% schiz referred to CBT. ethical issue psychiatric prejudice limiting access to CBT when could be beneficialMMB: CBT; is CBT being offered to everyone?NHS organised into trusts. providing services to people living in geographisl catchment. Royal College Psychiatrists 2014 found significant variations in no. ppl offered CBT 67%-14%, average of 50% ppl reporting their trust did not offer CBT. NHS should offer all treatment to everyoneMMB: CBT; cost effectiveKuipers 1998 economic impact. CBT + antipsychotic med. CBT initally more costly, long term schiz less likely to need emergency psychiatric services. budgets regarding healthcare trusts only allow trusts to deal w/ immediate care requirements>long term. trusts don't balance short & long term costs