3.3 schizophrenia

Question 1

schizophrenia

Answer 1

schizophrenia is a serious mental disorder characterised by a profound disruption to cognition, language, emotion and sense of self.

it is psychotic rather than neurotic, meaning it causes abnormal thought/perception and can cause sufferers to lose touch with reality.

more severe consequences of SZ could be homelessness, hospitalisation, or even attempted suicide.

Question 2

statistics

Answer 2

it is suffered by approximately 1% of the population. the onset of the disorder is between 15-35 years of age. in the past, it was more commonly diagnosed in:
- men than women
- cities than countryside
- working class than middle class people

Question 3

classification systems

Answer 3

diagnosing schizophrenia is based on positive and negative symptoms but varies based on the classification manual used.

the ICD-11 is used in europe and other parts of the world to diagnose schizophrenia. this was devised by the world health organisation (WHO).

its criteria is 2+ negative symptoms (like anhedonia or speech poverty/alogia) or 1 positive and 1 negative symptom for at least one month.

the DSM-5 is used in america to diagnose schizophrenia. this was devised by the american psychological association (APA).

the criteria is 2+ positive symptoms (like hallucinations or delusions) or 1 positive, 1 negative for at least one month. alongside this, extreme social withdrawal for at least six months.

Question 4

types of schizophrenia

Answer 4

crow (1980) suggested that type 1 SZ is characterised more by positive symptoms (an addition to an individual’s behaviour) eg. visual or auditory hallucinations or delusions. there is generally a better prospect for recovery.

type 2 is characterised more by negative symptoms (a loss to an individual’s behaviour) eg. loss of appropriate emotion or poverty of speech. there is generally a poorer prospect for recovery.

Question 5

positive symptoms

Answer 5

positive symptoms are those that appear to reflect an excess or distortion of normal functions.

hallucinations, delusions, disorganised speech, grossly disorganised or catatonic behaviour

Question 6

hallucinations

Answer 6

when sensory experiences of stimuli are distorted perceptions of things that are there.

there are different types of hallucinations. auditory (hearing voices, comments, or criticisms in their heads), visual (seeing things that are not real like distorted faces), olfactory (smelling things that are not real like disinfectant), and tactile hallucinations (touching/feeling things that are not there like bugs crawling on your skin)

Question 7

delusions

Answer 7

delusions (paranoia) are irrational, bizarre beliefs that seem real to the person with SZ. sufferers may believe that their bodies are under external control. some delusions can lead to aggression.

common delusions involve being an important historical, religious, or political figure like jesus. some believe they are being persecuted by the government, aliens, or even have superpowers.

Question 8

disorganised speech

Answer 8

abnormal thought processes lead to the individual being unable to organise their thoughts, which then translates to their speech.

they may slip from one topic to another (derailment) mid-sentence, or speak incoherently (gibberish).

this symptom is diagnosed in the DSM but not ICD.

Question 9

grossly disorganised or catatonic behaviour

Answer 9

the inability or motivation to initiate/complete a task.

disorganisation can lead to problems with personal hygiene or overactivity (engaging in many activities simultaneously rather than completing one).

catatonia refers to adopting rigid postures or aimless repetition of the same behaviour.

this symptom is diagnosed in the DSM but not ICD.

Question 10

negative symptoms

Answer 10

negative symptoms of SZ are those that appear to reflect a reduction or loss of normal functions. these persist even when positive symptoms are low.

speech poverty (alogia), avolition, affective flattening, anhedonia.

Question 11

speech poverty (alogia)

Answer 11

patients with SZ often have a reduced quality and amount of speech, and delay in verbal responses in conversation.

alogia may also be reflected in less complex syntax, meaning fewer clauses, shorter utterances, etc. this is associated with prolonged and earlier onset of the illness.

Question 12

avolition

Answer 12

(apathy) is the difficulty of managing goal-directed activity, which are actions performed to achieve a result. sufferers often have sharply reduced motivation to do so.

poor hygiene AND grooming, lack of persistence in work AND education, AND lack of energy are signs of avolition (ANDreason 1982)

Question 13

affective flattening

Answer 13

reduction in the range and intensity of emotional expression.

this includes fewer body and facial movements and deficits in prosody (tone of voice, intonation, tempo, loudness and pausing) that give cues for the emotional content of the conversation.

Question 14

anhedonia

Answer 14

the loss of interest in activities or reactivity to normally pleasurable stimuli.

there is physical anhedonia (related to physical pleasures like food, bodily contact, etc.) and social anhedonia (interaction in interpersonal situations)

Question 15

four issues associated with classification/diagnosis

Answer 15

co-morbidity, symptom overlap, gender bias, and culture bias negatively affect the reliability and validity in the classification and diagnosis of SZ.

Question 16

reliability and validity

Answer 16

reliability in diagnosis is the consistency of a measuring instrument (ICD or DSM).

inter-rater reliability is when two or more diagnosticians agree with the same diagnosis for the same individual – diagnosis should be done separately.

validity is the extent to which we measure what we intend to, or if the diagnosis of SZ is correct based on the symptoms in the manuals.

criterion validity is when different assessment systems arrive at the same diagnosis for the same patient (both ICD and DSM class the patient as SZ).

Question 17

three weaknesses of reliability and validity

Answer 17

- whaley (2001) found the inter-rater reliability between diagnosticians as low as +0.11 (using the DSM). poor reliability is a weakness of the diagnosis of SZ.

- cheniaux (2009) found low inter-rater reliability among diagnosticians. they asked two psychiatrists to independently diagnose 100 schizophrenic patients using both ICD and DSM criteria. IRR was poor, with one psychiatrist diagnosing 26 (DSM) and 44 (ICD) and the other psychiatrist diagnosing 13 (DSM) and 24 (ICD). SZ is more likely to be diagnosed using ICD (overdiagnosed) than DSM (underdiagnosed). this is a sign of poor validity.

- rosenhan (1973) found low validity in the diagnosis of SZ. 8 pseudo-patients were able to get themselves admitted to psychiatric hospitals by using the symptoms of hearing voices such as ‘hollow’, and ‘thud’. the pseudo-patients didn’t show any signs of mental illness during their stay, but all 8 patients stayed in for 7–52 days. all but one were discharged with SZ in remission. however, the study was done in the 70’s when the DSM was not as reliable/scientifically vigorous.

Question 18

two strengths of reliability and validity

Answer 18

+ osario (2019) reported that inter-rater reliability between pairs of psychiatrists was +0.97 and test-retest reliability was +0.92. this is more recent empirical evidence testing reliability in diagnosing schizophrenia (DSM 5), and shows high IRR.

+ as the reliability is so high using the DSM, the validity would also be high using this single diagnostic system. the ICD perhaps need more revision.

Question 19

co-morbidity

Answer 19

two or more mental disorders occur together at the same time in the same person.

this means the validity of SZ diagnosis can be questioned as SZ is commonly mistaken with other conditions.

Question 20

buckley (2009)

Answer 20

around 50% of the patients with SZ also have a diagnosis of depression or substance abuse. some cases also experience PTSD, and OCD.

this means that distinguishing the difference between the two disorders may prove difficult. an individual with severe depression may look like SZ, so they may be classified as the same condition.

co-morbidity is therefore a weakness of diagnosis and classification of SZ.

Question 21

symptom overlap

Answer 21

there is considerable overlap between the symptoms of SZ and other conditions such as depression and bipolar disorders.

ellason and ross (1995) found that people with DID have more symptoms of schizophrenia than people diagnosed with SZ. this means that most diagnosed SZ patients have sufficient symptoms to be diagnosed with at least one other disorder.

a patient may be diagnosed with SZ under one classification system (ICD or DSM) but another disorder under another, meaning symptom overlap can affect the diagnosis/classification of SZ.

Question 22

gender bias

Answer 22

(longnecker, 2010) men are more likely to be diagnosed with SZ than women, therefore there is gender bias in diagnosing SZ.

cotton (2009) suggests that this is because women seem to function better than men, by having good family relationships and interpersonal function.

Question 23

culture bias

Answer 23

some cultures get diagnosed with SZ more than others. for example, pinto and jones (2008) suggest that people of african american origin are nine times more likely to be diagnosed with SZ.

this may be because of culture differences between countries - in africa, communication with ancestors is seen as part of the culture, but in the USA (or according to the DSM) this may appear as positive symptoms (hallucinations) in SZ.

Question 24

two advantages of classification and diagnosis

Answer 24

+ communication shorthand: a patient with a mental disorder often has numerous symptoms. it is simpler to incorporate these symptoms into a single diagnosis and this makes communication between mental health professionals easier.

+ treatment: treatments are often specific to certain disorders e.g. symptoms of schizophrenia respond well to certain anti-psychotic drugs but not anti-anxiety. a reliable diagnosis can point to a therapy that will alleviate symptoms.

Question 25

biological explanations of SZ

Answer 25

the genetic basis and neural correlates (including the dopamine hypothesis).

Question 26

the genetic basis

Answer 26

genetic factors are normally tested through family, twin and adoption studies.

family studies use SZ patients’ biological relatives to determine if they are similarly affected, compared to non-biological relatives. the closer the genetic relatedness, the greater the risk.

twin studies use monozygotic (identical) twins, who share 100% of their genes, and dizygotic (non-identical) twins, who share 50%. if SZ is genetic, then concordance rates for having SZ should be higher in MZ than DZ twins (as the same DNA means the same vulnerability to the disorder).

genetic and environmental influences in twin and family studies are difficult to separate, so adoption studies are carried out to understand the influence of nature vs nurture.

adoption studies compare adopted children from biological families with SZ (nature/genetics) compared to adopted children from families without SZ (nurture/environment).

Question 27

candidate genes

Answer 27

also, there are specific candidate genes that are implicated in SZ that may increase a person’s risk of developing the disease. as there are a combination of these genes, SZ is referred to as polygenic.

gurling et al (2006) used family studies to discover that SZ was associated with chromosome 8p21-22. the PCM1 gene was also implicated. this provides evidence for genetics.

Question 28

three strengths of the genetic basis

Answer 28

there is research evidence to support biological explanations.

+ gottesman (1991) conducted family studies. he found that if both parents were schizophrenic, then the likelihood of the offspring also having SZ was 46%. if one parent was schizophrenic, then the likelihood dropped to 13% and if a sibling had SZ, the likelihood was 9%. this suggests there is a genetic basis for SZ, as the closer the DNA match is, the higher the likelihood of developing SZ is.

+ joseph (2004) did a review of twin studies that were carried out up to 2001, and found an overall concordance rate for MZ twins as 40% but 7.4% for DZ twins. as the concordance rate is higher for more genetically similar individuals (identical twins), genetics must play a part in the onset of SZ.

+ tienari et al (2001) conducted an adoption study, with 164 finnish adoptees whos biological mothers had been diagnosed with SZ. they found that 11/164 (around 7%) were also diagnosed later on. the control group showed only 4/197 diagnoses (2%). this shows a genetic link in explaining schizophrenia.

Question 29

two weaknesses of the genetic basis

Answer 29

- the genetic explanation of SZ is also biologically reductionist as it reduces behaviour to purely genes (such as the PCM1). the explanation ignores other factors such as environment/upbringing. an example of this is the schizophrenogenic mother, a parenting style in childhood that could trigger symptoms of SZ in adulthood.

- the diathesis stress model states that there is a genetic vulnerability in schizophrenia but this is only triggered by an external stressor in the individual’s life. genetic factors alone may not trigger SZ. taking a more holistic perspective in understanding the causes of SZ may lead to more effective treatments rather than just focusing on genes alone.

Question 30

neural correlates

Answer 30

the specific brain regions/structures/functions that are implicated in the symptoms and behaviours associated with the disorder. different neurotransmitters such as dopamine and serotonin (either excessive levels or low levels) can also play a part in SZ.

Question 31

different brain regions

Answer 31

there are neural correlates for both the positive and the negative symptoms of schizophrenia.

research shows that deficits in the nerve connections between the hippocampus and prefrontal cortex (planning, reasoning, judgement) have found to correlate with the degree of memory impairments in schizophrenics.

Question 32

one strength of neural correlates

Answer 32

+ brain scan evidence supports neural correlate research. it is objective - it relies on observed structural brain changes that occurs in SZ patients. the method has face validity and can help tailor treatments that reduce the symptoms for SZ.

Question 33

three weaknesses of neural correlates

Answer 33

- when looking at different brain regions, there are individual differences SZ sufferers. not all patients have deficits in the functioning of different brain regions.

- as there are different brain regions involved in SZ, it may be difficult to pinpoint which brain region is causing the symptoms.

- it may be difficult to establish cause and effect in terms of neuroanatomy. evidence is correlational, and does not establish whether the sufferer had abnormalities in a particular brain region and then developed schizophrenia or vice versa.

Question 34

the dopamine hypothesis

Answer 34

dopamine is a neurotransmitter associated with reward, motivation, reinforcement (and strongly implicated in the mechanisms of addiction).

the dopamine hypothesis claims that excess dopamine in certain brain regions is associated with positive SZ symptoms.

schizophrenics have high levels of D2 receptors on recieving dopamine neurones. this leads to more dopamine binding and neurones firing too easily and often. this causes hallucinations and delusions.

Question 35

consequences of the dopamine hypothesis

Answer 35

hyperdopaminergia - high dopamine levels in the subcortex. eg. an excess of dopamine receptors in broca’s area (which is responsible for speech production) may be associated with problems in speech and/or the experience of auditory hallucinations

hypodopaminergia - lower dopamine levels in the cortex. this area is responsible for decision making and thinking, and is associated with the negative symptoms of SZ.

Question 36

two strengths of the dopamine hypothesis

Answer 36

+ drug research supports the dopamine hypothesis. dopamine agonists like amphetamines increase dopamine levels and make schizophrenic symptoms worse in sufferers. they can also produce schizophrenic-like symptoms in non-sufferers. this supports hyperdopaminergia.

+ antipsychotic drugs act like antagonists. these reduce the levels of dopamine in SZ patients (helping to control symptoms of SZ). this supports the idea that dopamine levels are high in SZ and must be reduced through drugs.

Question 37

three weaknesses of the dopamine hypothesis

Answer 37

- the dopamine hypothesis is biologically determinist, meaning individuals have no control over the onset of SZ. it alone cannot be seen as the sole cause of SZ since there are other biological and psychological factors that contribute such as family dysfunction, the schizophrenogenic mother and impaired cognitions like hallucinations and delusions.

- glutamate is another neurotransmitter that has been implicated in SZ (moghadamm and javitt, 2012) suggesting that dopamine might not be the only neurotransmitter responsible for SZ and others may be involved.

- the dopamine hypothesis does not explain whether abnormal levels of dopamine cause schizophrenia, or vice versa. also, high and low levels of dopamine are implicated in the disorder - this means it is hard to identify the exact cause for vulnerability.

Question 38

psychological explanations for schizophrenia

Answer 38

family dysfunction and cognitive explanations.

Question 39

family dysfunction

Answer 39

vulnerability to developing schizophrenia can be explained by familial dysfunction (eg. abuse, divorce, criminal activities, high poverty etc), in child and adulthood.

the schizophrenogenic mother, double-bind theory and expressed emotion can explain this.

Question 40

schizophrenogenic mother

Answer 40

fromm-reichmann (1948) noted that her SZ patients spoke about a certain type of parent which she called the schizophrenogenic mother. characteristics included being cold, rejecting, controlling, and as well as creating a tense/secretive family climate.

this leads to the child lacking trust in relationships, which can develop into paranoid delusions (and ultimately developing SZ). the father is often passive and doesn’t get involved in child upbringing.

Question 41

double bind theory

Answer 41

bateson et al. (1972) focused on family communication style as an explanation for SZ.

children who frequently receive contradictory messages from their parents may fear doing the wrong thing but not understand what this is. for example a mother telling a child that she loves him, but showing disgust.

the child is unable to comment about the unfairness of the situation or seek clarification. when the child gets it wrong, they are punished by withdrawal of love leaving them confused. this may be reflected in SZ symptoms such as paranoid delusions.

family communication style may be a risk factor in the development of SZ but not the only cause.

Question 42

expressed emotion

Answer 42

EE is the level of negative emotion expressed towards a patient by their carers. this can include verbal criticism, violence, hostility, anger and rejection.

also, emotional over-involvement in the patient’s life, including needless self-sacrifice.

high EE increases patient’s stress levels. this may cause relapse, or trigger the onset of SZ if the person has a genetic vulnerability to the disorder (diathesis-stress model)

Question 43

four strengths of family dysfunction

Answer 43

+ tienari et al (2001) adoption study. the adopted children who had schizophrenic biological parents were more likely to have SZ themselves than those without.

however, this difference only emerged in situations where the adopted family was rated as disturbed or ‘dysfunctional’. as the illness only manifested itself under appropriate environmental conditions, genetic vulnerability and family dysfunction both contributed to the onset of SZ.

+ read (2005) reviewed 46 studies of child abuse and SZ. they concluded that 69% of adult women with SZ had a history of physical/sexual abuse or both in childhood. for men the figure was 59%. this study shows that family dysfunction contributes to an individual developing SZ.

+ adults with insecure attachments to their primary carer are also more likely to develop SZ thus strengthening the family dysfunction explanation.

+ berger (1965) found that SZ patients reported more double-blind statements by their mothers than non-SZ patients. though, the evidence may not be reliable. patient recall may be affected by their SZ (eg. hallucinations and delusions).

Question 44

three weaknesses of family dysfunction

Answer 44

- the evidence for family dysfunction as an explanation is not strong. liem (1974) measured parental communication patterns in families with and without SZ children, and found no difference. the double bind theory may not be specifically related to SZ.

- parents of patients have already suffered seeing their child develop SZ and have taken on the reponsibility of caring for them for life. they may suffer further trauma by being blamed for their child’s condition, which is unethical and may cause more harm than good for all involved. the family dysfunction explanation promotes parent blaming.

- environmentally reductionist, as it simplifies the cause of SZ to family upbringing. it ignores other factors such as the biological explanations (eg. PCM1 gene implicated in the vulnerability to developing SZ). it is therefore important to look at a more holistic explanation of SZ.

Question 45

cognitive explanations

Answer 45

these focus on the role of dysfunctional mental processes. frith et al (1992) identified two kinds:

1. metarepresentation – this is the cognitive ability to reflect on thoughts and behaviour. a dysfunction would disrupt the ability to recognise our own actions/thoughts as our own. this could explain auditory hallucinations and delusions.

2. central control – this is the cognitive ability to suppress automatic responses while we perform other actions instead (eg. thinking ‘don’t do this’, then choosing to do it or not). the inability to ignore automatic thoughts could lead to speech poverty and thought disorder. SZ patients also experience derailment, a consequence of losing control of thoughts.

Question 46

two strengths of cognitive explanations

Answer 46

stirling et al (2006) compared 30 patients with a diagnosis of SZ to 18 non-patient controls on a range of cognitive tasks, such as the stroop effect. this is when a colour is written in a different colour and one is asked to identify the colour of the word. he found that patients took twice as long to say the colour compared to controls.

this shows dysfunctional thought processing in SZ, as they struggled to separate the colour from the written word.

+ CBT is a sucessful treatment used alongside drugs to treat schizophrenia, therefore cognitive elements must be implicated in explaining SZ. SZ is a thought disorder, so CBT questions and challenges symptoms like hallucinations and delusions. behavioural techniques (such as positive reinforcement) are also used.

Question 47

two weaknesses of cognitive explanations

Answer 47

- it is difficult to establish cause and effect with cognitive explanations. essentially, whether dysfunctional thought processing caused SZ or vice versa.

- it fails to take into account biological factors and does not acknowledge the fact that dysfunctional thought processing could also be due to abnormal dopamine levels in the brain. this explanation is therefore reductionist because it is simplifying SZ to very basic elements e.g. dysfunctional thoughts rather than considering other factors such as genes, neurotransmitters and stress which have all been shown to contribute to schizophrenia.

Question 48

biological therapies for SZ

Answer 48

the most common treatment for SZ is antipsychotic drugs (tablets, syrup or even injections for those who may not take meds properly). these are given for different lengths of time depending on the patient.

this may be accompanied with psychological therapies like family therapy or CBT.

there are typical (traditional or first generation) and atypical (second generation) antipsychotics

Question 49

typical antipsychotics

Answer 49

typical antipsychotics are dopamine antagonists, meaning they reduce the effects of dopamine to reduce the positive symptoms of SZ.

they bind to, but do not stimulate, dopamine receptors (like D2) and block their action. this fits with the dopamine hypothesis, as it suggests high levels of dopamine are present in those with SZ.

Question 50

typical antipsychotics: example

Answer 50

chlorpromazine: the maximum dosage is 1000mg, but patients should start at about 400mg and build up to 800mg. it also acts as an effective sedative as it is absorbed faster in syrup form than tablet.

Question 51

atypical antipsychotics

Answer 51

atypical antipsychotics emerged later, and were used to improve effectiveness and minimise the side effects of typical antipsychotics. they work on the negative symptoms of SZ.

similarly to typical antipsychotics, they block D2 receptors, but temporarily. they then rapidly dissociate to allow normal dopamine transmission. this is why there are lower levels of side effects.

Question 52

atypical antipsychotics: examples

Answer 52

clozapine: a more effective, alternative treatment for SZ than typical drugs.

it is only available in syrup or tablet form as it has fatal side effects. the dosage is 300 – 450mg per day, much lower than chlorpromazine.

clozapine acts on serotonin and glutamate receptors, as well as dopamine, which reduces depression/anxiety and improves cognitive functioning. it is generally given to those at high risk of suicide as it improves mood (around 40% of SZ patients attempt).

risperidone: attempts to reduce the serious side effects of clozapine but still be as effective. it binds more effectively to D2 receptors, leading to less side effects. much smaller doses are required. it can be taken as syrup, tablets or injection, and the dosage is 4-8mg, maximum of 12mg.

Question 53

strengths of biological therapies

Answer 53

+ thornley et al (2003) compared the use of chlorpromazine (typical AP) with a placebo. 13 trials and 1121 pps showed that chlorpromazine reduced SZ symptoms and improved overall functioning. 3 trials and 512 pps showed that chlorpromazine reduced relapse rates as well. as typical antipsychotics were more effective in reducing the symptoms of SZ compared to a placebo, drug therapy is an effective treatment for SZ.

+ meltzer (2012) found that clozapine (atypical AP) is more effective than other atypical AP in treating SZ, as well as all typical drugs. they found clozapine to be effective in 30-50% of cases where typical AP had failed.

+ there is inconclusive evidence in finding out whether clozapine or risperidone is more effective. this means some patients responded better to one drug than the other, supporting the idea that SZ is a complex psychotic disorder.

+ leucht (2012) found that relapse rates are much lower when patients take antipsychotic drugs (both typical and atypical) as opposed to placebos. they found out of 6000 patients 64% of the placebo group had relapsed compared to 27% in the antipsychotic (medicated) group. this was after 12mo.

Question 54

three weaknesses of biological therapies

Answer 54

- there are serious side effects in using drugs to treat SZ. examples for typical AP are: dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin.

more extreme effects include ‘tardive dyskinesia’ which is caused by dopamine hypersensitivity (involuntary face movements like grimacing, blinking, lip smacking). also, AP drugs can also cause neuro malignant syndrome, NMS (rare, life threatening reaction that can cause high temperature, delirium and coma).

- there are side effects for atypical drugs too. regular blood tests still need to be taken to test for signs of agranulocytosis (a rare blood condition where the production of white blood cells is prevented – leads to problems with immunity).

- healy (2012) suggests that successful drug trials hav had their research ublished numerous times, and exaggerate the effectiveness of the drug in data. also, antipsychotics calm nerves so it may seem as if thed drugs are successful. in reality they do not show reduction in symptoms. studies also only show short term benefits of the drugs, especially in those that stopped taking the drugs after the trials.

- ethical issues. patients with SZ may not be able to give informed consent to take the drugs as SZ is a psychotic disorder. the drugs have severe side effects, meaning patients may be put under physical and mental harm, espcially in more severe irreversible cases like NMS or tardive dyskinesia.

Question 55

psychological therapies for SZ

Answer 55

cbt, family therapy and token economies.

Question 56

CBTp

Answer 56

CBTp (cognitive behavioural therapy for psychosis) is used in the treatment of SZ. it’s used to treat residual positive/negative symptoms that persist despite the use of AP drugs, to improve functioning.

CBTp can be delivered in groups or alone for at least 16 sessions (NICE) to treat SZ.

Question 57

process of CBTp

Answer 57

the patient establishes realistic goals for therapy with a therapist in the initial assessment. the patient is encouraged to engage with the therapist to find explanations for current thoughts/distress and allow for change.

ellis’s ABC model is used. the patient identifies their activating events (A) that cause their emotional and behavioural (B) consequences (C). beliefs can then be rationalised, disputed and changed.

patients may feel alone in their experiences (eg. delusions/hallucinations) so CBTp is used to normalise symptoms, and convey to patients that many with SZ experience the same thing. this can reduce stigmatisation and anxiety/isolation. recovery seems more likely.

the therapist helps the patient come to logical conclusions using gentle questioning eg. ‘if your voices are real, why can’t other people hear them?’. the therapist should remain empathetic, non-judgemental and trustworthy whilst helping patients to find alternative explanations.

Question 58

two strengths of CBTp

Answer 58

+ CBTp is more effective in treating SZ than standard care (AP drugs alone). NICE (2014) found CBTp reduced rehospitalisation rates up to 18 months following the end of treatment. CBTp also reduced the severity of symptoms and improved social functioning. however, patients were treated with both meds and CBTp, so assessing just CBTp as an effective treatment is difficult

+ addington and addington (2005) suggested that the effectiveness of CBTp depends on the stage of SZ. they found that CBTp is less effective in the initial acute phase, where self reflection is inappropriate.

rather, it should be made available after a patient is stabilised with medication. group therapy that normalises symptoms is also helpful here. so, individuals with more experience of living with SZ and a greater realisation of their problems are most likely to benefit from CBTp.

Question 59

two weaknesses of CBTp

Answer 59

- CBTp lacks availability. despite being recommended by NICE as a treatment for SZ. only 1/10 diagnosed individuals have access to the therapy. haddock (2013) found that in the north west of england, only 7% of patients were offered CBTp.

- CBTp’s success depends on the willingness of patient’s to cooperate and accept treatment. a significant amount of patients refused treatment or did not attend in haddock’s study, limiting its effectiveness further (freeman, 2013)

Question 60

family therapy

Answer 60

family therapy aims to provide support for carers of SZ patients, reduce stress in family life and the risk of rehospitalisation for patients (in conjunction with AP drugs). it gives carers guidance on the treatment and management of SZ.

family therapy is used when there is a high risk of relapse: this is often with families that have high levels of expressed emotion (high levels of criticism, hostility or emotional over-involvement).

family therapy is offered for 3-12 months and at least 10 sessions. techniques used include psychoeducation on the illness and reducing tensions/burdens of care for family members.

it also involves reducing emotions such as guilt and anger and replacing these with reasonable expectations for patient performance. family therapy also allows for learning about how to anticipate and solve issues.

Question 61

three strengths of family therapy

Answer 61

+ pharoah (2010) reviewed 53 studies published (2002-2010) from europe, asia and north america to investigate the effectiveness of family intervention. the studies compared family therapy to standard care (AP meds alone). overall, assessment of mental state/social functioning (eg. living independently, employment) was mixed. however, compliance with medication increased, and there was a reduction in the risk of relapse and hospital readmission during treatment and after 24mo.

+ garety (2008) found relapse rates in those that took part in family therapy was 25% compared to 50% for those who receive standard care alone. as relapse rates for SZ are half of what they are in those who do not take part in family therapy, it must be an effective treatment.

+ economic benefits. NICE reviewed family therapy studies and found that when offered to SZ sufferers alongside standard care, costs are saved. the extra cost of therapy is offset by a reduction in costs of hospitalisation because of the lower relapse rates, and rehospitalisation as the measure is preventative in the long term.

Question 62

one weakness of family therapy

Answer 62

- 10/53 studies in pharoah’s meta-analysis did not use blinding in their trials. raters knew the conditions allocated to the patients, so there is a risk of rater bias (scientists may have scored those who took part in family therapy as more highly improved than those who didn’t). therefore we don’t know if the therapy is actually effective.

Question 63

token economies

Answer 63

token economies are reward systems used to manage SZ patient behaviour in hospitals. it does not treat the patient, but makes it easier to undo maladaptive behaviour that institutionalisation may have caused eg. bad hygiene. this can improve quality of life and make it more likely that they are able to live out of a hospital setting.

token economies are based on the positive reinforcement idea in operant conditioning. if a patient carries out a good behaviour that should be repeated (eg. making their bed), they are given a token (secondary reinforcer) which can be exchanged for a reward (primary reinforcer), e.g. sweets, cigarettes or a walk outside the hospital. behaviour should then be repeated in hoped for more tokens and tangible rewards.

tokens should be given immediately to the patients so rewards and good behaviours are associated. ‘good’ behaviours differ person to person eg. bathing vs speaking to others politely.

Question 64

one strength of token economies

Answer 64

+ dickerson (2005) found that 11/13 studies that investigated treating SZ reported beneficial effects directly attributable to token economies. he concluded that token economies increased adaptive behaviours of patients, but many had methodological issues which could have effected the overall validity of token economies.

Question 65

three weaknesses of token economies

Answer 65

- there are ethical concerns in using token economy programmes in psychiatric settings. in order to make reinforcement effective, clinicians may exercise control over important reinforcers such as food, privacy or activities. however, all humans have basic rights that should not be violated regardless of positive consequences - things such as food should not be restricted, even as part of the token economy programme.

- it lacks ecological validity. token economy effectively reduces the negative symptoms of those with SZ, but only in a hospital setting. it is difficult to administer token economies with outpatients as they do not recieve 24 hour care (rewards are not immediately given after postive behaviour).

- token economies only manage he symptoms of SZ behviour and do not treat the actual disease. this means it is not an effective psychological treatment as SZ behaviour is still prevalent.

Question 66

the interactionist approach

Answer 66

this acknowledges that there are biological, psychological and societal factors in the development of SZ.

biological factors include genetic vulnerability, neurochemical (dopamine), and neurological (brain) abnormality.

psychological factors include stress resulting from life events and daily hassles, including poor quality interactions in the family.

Question 67

diathesis-stress model

Answer 67

the diathesis stress model suggests that there is a genetic vulnerability to developing SZ, but an external stressor (negative psychological experience) is needed to trigger the onset of the disorder.

meehl (1962) suggested that SZ was entirely genetic and that the ‘schizogene’ caused it.

modern understanding disputes this, and suggests many different genes increase genetic vulnerability alongside psychological trauma, where trauma becomes the diathesis rather than the stressor.

‘stress’ is anything that triggers schizophrenia, for example, cannabis users are 7x more likely to develop SZ symptoms because cannabis interferes with dopamine systems.

Question 68

treatment

Answer 68

the interactionist approach suggests biological and psychological factors are important in the onset of SZ, so is compatible with both treatments.

the model is used to treat SZ patients with both antipsychotic medication and psychological therapies such as CBT. drug therapy controls the symptoms of SZ (typical for positive, atypical for negative etc.) and CBT/family therapy precedes this to reduce any residual symptoms.

Question 69

three strengths of the interactionist approach

Answer 69

+ read (2001) proposed a neurodevelopmental model in which early trauma affects brain development. he found that early and severe enough trauma such as child abuse can seriously affect brain development, and make an individual more vulnerable to stress.

+ tienari (2004) found evidence for the dual role of genetic vulnerability and stress triggers in SZ. they studied the parenting styles of parents who children adopted away from their schizophrenic mothers compared to a control group of parents with no genetic risk. they found a high risk of developing SZ in those who’s parents were more critical and less empathetic, but only for children with a high genetic risk. this strongly supports the interactionist approach – genetic vulnerability and family-related stress combine in the development of SZ.

+ tarrier (2004) found that when 315 participants were randomly allocated to (1) medication + CBT group (2) medication + supportive counselling, or (3) control group, the combination groups showed lower symptom levels than those in the control group (meds only). however, there was no difference in hospital readmission. therefore, there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes.

Question 70

two weaknesses of the interactionist approach

Answer 70

- the original diathesis-stress model is too simplistic. schizophrenia is polygenic, meaning multiple genes increase vulnerability rather than one ‘schizogene’. this idea is biologically reductionist. houston (2008) found childhood sexual trauma was a diathesis and cannabis use a trigger. this shows diathesis as biological and stress as psychological is overly simple, and not accurate anymore.

- turkington (2006) argues that just because combining biological and psychological treatments is effective, it does not mean that the interactionist approach to explaining the onset of schizophrenia is.

this is called treatment-causation fallacy. for example, just because AP drugs work, does not been therE is a biological basis to SZ.