schizophrenia Flashcards
(AO1) Diagnosis and classification *****
*positive symptoms = hallucinations (unusual sensory experiences) and delusions (irrational beliefs)
*negative symptoms = speech poverty (reduction in amount and quality of speech) and avolition (difficult to keep up with goal-directed activity)
*DSM-5 = 1 positive symptom and for 6 months
*ICD-10 = 2 negative symptoms for 1 month
(AO3) Diagnosis and classification *****
*Limitation. Cheniaux et al (2009) same psychologist. 68/100 diagnosed with sz with ICD-10 but 39/100 with DSM-5. Low criterion validity.
*Strength. Osorio et al (2019) reported good reliability. 180 patients diagnosed with sz. Inter rater reliability of +.97 and test retest = +.92
*Limitation. Gender bias. Fischer and Buchanan 2017 found ratio of men:women = 1.4:1 therefore women are diagnosed less. Cotton et al (2009) says women better at dealing with sz as they have better social relationships.
(AO1) bio explanation: genetics
*family studies - Gottesman (1991) found the chance of developing sz if your sibling has it is 9% compared to 48% for MZ twins.
*candidate genes - sz is polygenic. most likely gene would be those coding for neurotransmitters like dopamine. Ripke et al (2014) researched genetic make up of 37,000 people with sz and found 108 separate genetic variations. control of 113,000. sz is aetiologically heterogeneous.
*role of mutation - evidence for mutation comes from positive correlation between paternal age and risk of sz. Brown et al (2002) found sz was evident 0.7% for under 25 and over 2% in fathers over 50.
(AO3) bio explanation: genetics
*Strength for Gottesman. Tiernari et al (2004) adoption study in Finland. 197 adopted with sz mother and 6.7% developed sz. compared to a control group of 164 adoptees and only 2% developed sz. Also, Hilker et al (2018) showed a concordance rate of 33% for identical twins and 7% for non identical twins.
*Limitation. Many twin studies are difficult to separate nature and nurture. if the environment is the same then it is a confounding variable. high concordance rates could be due to environment and not genetics.
(AO1) bio explanations: dopamine hypothesis
the dopamine hypothesis is a neural correlate of sz.
*original idea was that sz was caused by excessive dopamine in sub cortex .
*Hyperdopaminergia - high dopamine levels in areas such as the basal ganglia (like the original idea)
*Hypordopaminergia - Davis et al added on to the hypothesis (1991) low dopamine levels in the brains cortex. E.g. low levels of dopamine in prefrontal cortex could explain cognitive problems
*Goldman Rakic (2004) identified low levels of dopamine in the prefrontal cortex in symptoms like avolition.
(AO3) bio explanations: dopamine hypothesis
*Limitation. Moncrieff (2009) claims dopamine activity can be affected by stress/smoking. demonstrates that evidence is far from conclusive. also, ripke suggests other significant neurotransmitters are involves with sz
*Limitation. McCutcheon et al (2020) found in post mortem and in scanning studies that people with sz had higher levels of glutamate in several brain regions. therefore equally strong role of glutamate as well as dopamine.
(AO1) bio explanations: neural correlates
*dopmaine hypothesis is an example of a neural correlate
*also, sz is caused by enlarged ventricles which causes damage to the central brain areas and prefrontal cortex.
*Juckel et al (2006) - negative correlation in ventral striatum activity and overall negative symptoms resulting in a loss of motivation, (hard to understand)
*ALLEN ET AL (2007) FOUND THAT PATIENTS WITH AUDITORY HALLUCINATIONS HAD LOW ACTIVATION IN SUPERIOR TEMPORAL GYRUS AND ANTERIOR CINGULATE GYRUS. therefore reduced activity in these areas correlate to auditory hallucinations.
(AO3) bio explanations: neural correlates
*correlation and not causation
(AO1) treatment: drug therapy *****
*typical antipsychotics - chlorpromazine works with dopamine theory. dopamine is blocked to reduce the level of hallucinations. also has sedative effect which calms the patient.
*atypical antipsychotic - clozapine reduces negative symptoms of sz. binds to block dopamine receptors however it also acts on serotonin and glutamate receptors. also enhances mood which is positive for highly suicidal patients
*another atypical antipsychotic is risperidone. binds more strongly to dopamine receptors than clozapine. highly effective in low doses.
(AO3) treatment: drug therapy *****
*Strength. Thornley et al (2003) reviewed studies comparing chloropromazine and placebo effects. In 13 trials studying 1121 ppts, chlorpromazine was clearly more effective than placebos. Meltzer (2012) portrays a strength for atypical also. Clozapine is effective 30-50% of the time when typical treatments fail. shows that both work
*counterpoint - Healy (2012) said most are short term effects. does not treat patient from the psychosis but just calms them down.
*limitation. serious side effects. typical = tardive dyskinesia, dizziness, stiff jaw, itchy skin. Antipsychotic = neuroleptic malignant syndrome. this can result in high temperature that leads to comas and fatal effects
(AO1) psychological explanations - family dysfunction
*schizophrenic mother - Fromm-Reichmann (1948) noticed many of her ppts shared similar parenting. the sz mother is cold, rejecting and controlling and leads to family climate of tension and secrecy. this develops into paranoid delusions and eventually sz
*double bind theory - Bateson et al (1972)emphasised role of communication in a family. child fears doing wrong things but gets mixed signals about what is right and what is wrong. when they get it wrong they are punished with withdrawal of love. leads them to thinking the world is confusing and dangerous leading to disorganised thinking and paranoid delusions
*expressed emotion - level of emotion expressed towards person with sz by carers which are often family
1) verbal criticism of the person
2) hostility towards the person
3) emotional over involvement in the life of the person
- high levels of emotion causes stress to the sz person. this could also trigger sz for anyone with a genetic vulnerability
(AO3) psychological explanations - family dysfunction
*indicators of family dysfunction include insecure attachment and exposure to childhood trauma. Read et al (2005) found adults with sz are disproportionally likely to have insecure attachment. Also, Read found that 69% of women and 59% of men with sz have a history of physical/sexual abuse.
*Limitaiton. Lacks evidence base for any of the explanations. No support to show the importance of family based theories like sz mother and double bind. both theories are made of clinical observations and informal assessments but not systematic evidence.
(AO1) psychological explanations - cognitive explanations
*dysfunctional thinking - reduced thought processing in ventral striatum associated with negative symptoms. reduced processing of info in the temporal and cingulate gyri associated with hallucinations
*metarepresentation dysfunction - Frith et al (2012) identified metarepresentation which is the cognitive ability to reflect on thoughts and behaviour. allows insight into our own intentions and goals. dysfunction in metarepresentation would disrupt ability recognised own actions and thoughts as being carried out by ourselves. this would explain hallucinations of hearing voices and delusions
*central control dysfunction - Frith et al discovered speech poverty and thought disorder could result from inability to suppress automatic thoughts and speech triggered by other thoughts.
(AO3) psychological explanations - cognitive explanations
*Strength. evidence for dysfunctional thought processing. Stirling et al (2006) compared performance on range of cognitive tasks in 30 people with schizophrenia. control group of 30 without. Task was a stroop task and people with sz took over twice as long on average to name font colours. shows correlation of sz and slower cognitive processes
*limitation. only explains proximal origins of symptoms. only explains what is happening now with the diagnosis and not what happened initially through genetics and childhood therefore only partial explanation
(AO1) psychological therapies: CBT
*most likely 5-20 sessions. CBt deals with both thoughts and behaviour.
*CBT works by making the client make sense of how their irrational cognitions impact their behaviour. understanding how the symptoms form can help become less worried about things like auditory hallucinations. e.g. if therapist helps the client realise the auditory hallucinations are from the malfunctioning speech centre in their own brain, it will be less frightening as person knows they cannot be hurt. helps people cope with sz.
