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- 17%

biological children of schizophrenics are still at increased risk of developing it, even when adopted into non schizophrenic 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

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

atypical (clozapine, risperidone)

started in 80s and 90s

bind to dopamine and serotonin receptors, risperidone binds to dopamine stronger than clozapine so fast acting in small amounts

clozapine binds to serotonin and glutamate too which helps with depression

typical (dopamine agonists)

block dopamine receptors in the brain to reduce hallucinations

has a sedative effect so good for anxiety

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

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%

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