schizophrenia case studies

cheniaux (2009)

2 psychiatrists, 100 clients independently assessed using icd and dsm-4

68 diagnosis with icd, 39 with dsm-4

osorio (2019)

high inter rater and test retest reliability with 180 individuals using the dsm-5

over 0.9 for both

gottesman (1991) + tienari (2004)

mz twins - 48% chance both get schizophrenia

dz twins - 17%

general pop - 1% chance

biological children of schizophrenics are still at above 1% risk of developing it, even when adopted into non schizophrenic families

but only 5% of children adopted into healthy families developed sz compared to 36% of those adopted into unhealthy families

ripke (2014)

schizophrenia is aetiologically heterogeneous

found 108 different candidate genes

dopamine hypothesis

original - due to high dopamine in subcortical areas of the brain

eg. high da in broca's area can lead to speech poverty

updated - low dopamine in the cortex can lead to negative symptoms

eg. low da in prefrontal cortex can lead to cognitive issues

biological eval

mz twin dna is not 100% shared so not entirely genetically influenced

study - 67% of a group with psychotic disorders reported a childhood trauma, compared to 38% of those with non psych disorders

antipsychotics that reduce da help with pos symptoms

there is also evidence for other neurotransmitters having roles like glutamate

determinism of this approach can make people feel like they will inevitably develop schizophrenia

read (2005)

people with schizophrenia and history of physical / sexual abuse (69% of women, 59% of men)

stirling (2006)

compared cognitive task performance in 30 people with schizophrenia and 30 without like stroop task (names of colours but the letters are in diff colours)

people with schizophrenia took longer due to central control impairment

drugs eval

meltzer (2012) - atypical effective in 30-50% cases where typical was ineffective

however the studies are short term effects only and the successful ones get published multiple times which inflates effectiveness

dopamine super sensitivity can lead to tardive dyskinesia

we dont really know why drugs work because theyre based off the original da hypothesis. in theory they shouldnt work for neg symptoms as in the updated hypothesis we know theyre from da already being too low

tarrier - drugs 81% effective, drugs + cbt 86% effective

burbach (2018)

phases of family therapy for schizophrenia

early phases involve mutual understanding, final phase involves maintenance for the future

small but significant effects on both pos and neg symptoms

mcfarlane (2016)

family therapy reduces relapse rates by 50-60% whereas standard outpatient care relapse is 70%+

glowacki (2016)

found seven studies that showed a reduction in neg symptoms with token economies

however seven studies is small = file drawer problem

meehls model

believed there was a single schizogene that would cause schizophrenia through diathesis-stress

tienari (2004)

combo of genetic vulnerability and environment

19000 adopted finnish children with biological schizophrenic mothers compared to adopted children without schizophrenic mothers

hostility in the adoptive parenting increased development of schizophrenia but only in the children with schizophrenic bio mothers

tarrier (2004)

divided participants into med + cbt, med + counselling and just meds

participants in both combo groups had lower symptoms than just the meds group

loring and powell

• gave 290 psychiatrists two identical case studies

• said the cases were from either a black male or female or a white male or female

• females were diagnosed with schizophrenia less and black people diagnosed more

leueht

• meta analysis of schizophrenia treated with drugs found that drugs were more effective than placebos

johnstone (1976) + eval

• people with schizophrenia found to have enlarged ventricles in brain

• but this evidence is correlational rather than causational

frith (1979)

• attention deficit theory = a faulty attention system that cannot filter out preconcious thoughts so they become hallucinations / delusions

• poor central control = cant supress automatic actions, like how schizophrenic people struggle with stroop tests because they cant supress saying the word rather than the colour

• metarepresentation issues = struggle to tell when their thoughts are their own or other peoples thoughts

typical antipsychotics (dopamine agonists)

• oldest ~ 1950s

• treat positive symptom by blocking dopamine receptors at the synapse

• good for anxiety due to having a sedative effect

• severe potential side effects like tardive dyskinesia (involuntary muscle movements)

• example - chlorpromazine

atypical antipsychotics

• block not just dopamine receptors but glutamate, serotonin etc

• treats both positive and negative symptoms

• risperidone binds to dopamine stronger than clozapine so its fast acting in small amounts

• clozapine binds to serotonin and glutamate which helps with depression

• side effects like weight gain and cardiovascular issues but far less chance of tardive dyskinesia

• example - clozapine