Schizophrenia Quiz- Psychology (A2)

Match the definition to the key term

Schizophrenia Facts: 1. Schizophrenia is more commonly diagnosed in [blank_start]men[blank_end] 2. About [blank_start]1%[blank_end] of the population suffer from schizophrenia 3. People are more likely to be diagnosed if they live in the [blank_start]city[blank_end] 4. [blank_start]Working[blank_end] class people are more likely to suffer from schizophrenia

DSM [blank_start]5[blank_end]: Must have [blank_start]one[blank_end] [blank_start]positive[blank_end] symptoms to be diagnosed ICD [blank_start]10[blank_end]: Must have [blank_start]two+[blank_end] [blank_start]negative[blank_end] symptoms to be diagnosed

There are 3 main types of delusions in schizophrenia: 1. [blank_start]Delusions of grandeur:[blank_end] the false belief that the sufferer is someone of extreme importance 2. [blank_start]Delusions of persecution:[blank_end] the false belief that the sufferer is being targeted- makes them very suspicious. These are the most common form of delusions for sufferers. 3. [blank_start]Somatic delusions:[blank_end] a preoccupation with one's body- the false belief that something is wrong/odd with their body e.g. tumours, blood made of silver

Reliability references the [blank_start]consistency[blank_end] of a study. One important measure of reliability is [blank_start]inter-rater[blank_end] reliability. This is the consistency of [blank_start]multiple[blank_end] researchers' diagnoses- do they all come to [blank_start]the same[blank_end] conclusion?

[blank_start]Cheniaux[blank_end] et al. (2009) asked two psychiatrists to [blank_start]independently[blank_end] diagnose 100 patients using the DSM and ICD criteria. Inter-rater reliability was [blank_start]poor[blank_end]: One psychiatrist diagnosed 26 patients using the [blank_start]DSM[blank_end] and 44 patients using the [blank_start]ICD[blank_end] The other psychiatrist diagnosed 13 patients with the [blank_start]DSM[blank_end] and 24 using the [blank_start]ICD[blank_end]. This shows that the results are not consistent; if they were, both psychiatrist would have diagnosed the same number of patients e.g. both diagnosed 26 using the DSM.

One way of assessing validity of diagnosis is [blank_start]criterion validity[blank_end]. This is whether two diagnostic systems come to [blank_start]the same[blank_end] conclusion in terms of diagnosis of a patient. Good criterion validity would mean two diagnostic systems (e.g. DSM and ICD) give the same diagnosis to the same patient.

Cheniaux et al. (2009) did a study in which two psychiatrists independently diagnosed 100 patients using the DSM and the ICD. It was found that DSM diagnosed [blank_start]almost half as many[blank_end] patients with schizophrenia in comparison to the ICD e.g. one psychiatrist diagnosed 13 people using the DSM and 24 using the ICD. This clearly indicates that the two diagnostic systems [blank_start]are not[blank_end] reaching the same conclusions in terms of diagnosis, and therefore the [blank_start]criterion validity[blank_end] is poor.

[blank_start]Morbidity:[blank_end] how common a medical disorder is [blank_start]Co-morbidity:[blank_end] when two or more disorders occur at the same time If conditions occur together a lot of the time, this questions the reliability and validity of the diagnosis and classification, because they may in fact be [blank_start]a single condition[blank_end].

[blank_start]Buckley[blank_end] et al. investigated the extent to which schizophrenics also suffered from other conditions. Findings: 50% also suffer from [blank_start]depression[blank_end] 47% also suffer from [blank_start]substance abuse[blank_end] 29% also suffer from [blank_start]PTSD[blank_end] 23% also suffer from [blank_start]OCD[blank_end]

Buckley's study into comorbidity suggested that substance abuse and schizophrenia were the most commonly comorbid, with PTSD being the least.

Both schizophrenia and bipolar disorder involve positive symptoms such as [blank_start]delusions[blank_end], and negative symptoms such as [blank_start]avolition[blank_end]. Based on the [blank_start]DSM[blank_end], in which you must have one positive symptom, you may be diagnosed with schizophrenia when you actually have bipolar disorder, or vice versa.

Symptom overlap has one main issue: [blank_start]misdiagnosis[blank_end]. This can lead to either incorrect [blank_start]treatment[blank_end] (could actually worsen the illness) and [blank_start]labelling[blank_end] (affects mortgages, employment, and insurance).

Longenecker found that [blank_start]men[blank_end] are more likely than [blank_start]women[blank_end] to be diagnosed with schizophrenia. However, this difference [blank_start]does not[blank_end] mean they are necessarily more likely to suffer from schizophrenia; it may actually be a case of [blank_start]gender[blank_end] bias. One argument is that they do suffer more than [blank_start]women[blank_end] do because they are [blank_start]genetically[blank_end] more vulnerable to developing schizophrenia. However, others argue that men are [blank_start]more[blank_end] likely to be diagnosed because women do not outwardly display symptoms so they may be [blank_start]underdiagnosed[blank_end] with schizophrenia. They may also be more high functioning than men, so can continue to work despite symptoms. This questions the [blank_start]validity[blank_end] of the diagnostic and classification systems.

African Americans are several times [blank_start]more[blank_end] likely than white people to be diagnosed with schizophrenia. However, rates of schizophrenia in Africa are relatively [blank_start]low[blank_end], so it can be concluded that these differences [blank_start]are not[blank_end] due to genetic vulnerability for schizophrenia, but rather the result of bias in diagnosis. For example, hearing voices in Africa is often seen as a form of communication with ancestors, and is therefore more acceptable. As well as this, white psychiatrist may over-interpret symptoms and distrust the honesty of black people. This is an example of [blank_start]cultural[blank_end] bias.

Label the image with the correct concordance rates and shared genes, as investigated by Gottesman (1991)

What can be concluded from Gottesman's study of concordance rates in schizophrenics?

Name one issue with Gottesman's study of concordance rates in schizophrenics

It is believed that schizophrenia is polygenic and has multiple candidate genes. What does the term 'polygenic' mean?

Which researcher investigated candidate genes and when?

Ripke et al (2014) carried out a [blank_start]wide scale[blank_end] study that combined the data of all previous human genome studies. The genetic make-up of 37,000 schizophrenics was compared to that of 113,000 healthy people. There were [blank_start]108[blank_end] separate variations that were linked to the onset of schizophrenia, with some of them coding for neurotransmitters such as [blank_start]dopamine[blank_end].

What is an issue with schizophrenia having multiple candidate genes?

Evidence for the genetic basis of schizophrenia suggests genes are the sole cause of schizophrenia.

Hyperdopaminergia: occurs in the [blank_start]sub cortex[blank_end] and involves [blank_start]high[blank_end] levels of dopamine. Symptoms include [blank_start]hallucinations[blank_end] and [blank_start]delusions[blank_end] Hypodopaminergia: occurs in the [blank_start]cortex[blank_end] and involves [blank_start]low[blank_end] levels of dopamine. Symptoms include [blank_start]avolition[blank_end] and [blank_start]speech poverty[blank_end]

[blank_start]High[blank_end] numbers of dopamine receptors in [blank_start]Broca[blank_end]'s area (associated with speech production) lead to [blank_start]high[blank_end] levels of dopamine activity in the area. One symptom this can cause is disorganised speech, a [blank_start]positive[blank_end] symptom. [blank_start]Low[blank_end] levels of dopamine in the pre-frontal cortex (associated with planning and decision making) lead to [blank_start]negative[blank_end] symptoms such as avolition and social withdrawal.

Why might it be possible for hyperdopaminergia and hypodopaminergia to both play a role in the onset/maintenance of schizophrenia?

[blank_start]Curran[blank_end] et al (2004) found that dopamine [blank_start]agonists[blank_end] (such as amphetamines, which [blank_start]increase[blank_end] the levels of dopamine in the brain) can produce schizophrenic symptoms such as hallucinations. This supports the idea that [blank_start]hyperdopaminergia[blank_end] plays a role in the development of schizophrenia. [blank_start]Tauscher[blank_end] et al (2014) found that dopamine [blank_start]antagonists[blank_end] (such as antipsychotics., which [blank_start]decrease[blank_end] the levels of dopamine in the brain) can reduce schizophrenic symptoms, supporting the role of [blank_start]hyperdopaminergia[blank_end]. However, [blank_start]Ripke[blank_end] et al found that some of the genes linked to schizophrenia don't code for dopamine, but rather for [blank_start]glutamate[blank_end], suggesting dopamine [blank_start]is not[blank_end] the sole cause of schizophrenia.

What are neural correlates?

In neural correlates, negative symptoms are associated with the [blank_start]ventral striatum[blank_end], which is linked to [blank_start]anticipation[blank_end]. It therefore causes symptoms such as avolition and low mood. Jukel et al. found [blank_start]low[blank_end] levels of activity in the ventral striatum of schizophrenic patients. Lower activity was linked to [blank_start]more[blank_end] severe symptoms ([blank_start]negative[blank_end] correlation). Positive symptoms are associated with the [blank_start]superior temporal gyrus[blank_end] in the [blank_start]temporal[blank_end] lobe, which is linked to [blank_start]auditory processing[blank_end]. It therefore cause symptoms such as auditory hallucinations. [blank_start]Low[blank_end] levels of activity were found in patients who suffered [blank_start]hallucinations[blank_end]. These patients make more errors when identifying pre-recorded speech as their own, when compared to a control group.

'One issue with neural correlates is that it is unclear as to whether the abnormality is the cause or effect of schizophrenia. For example, low activity in the ventral striatum may actually be due to the schizophrenia, rather than causing it. ' Is this statement true or false?

[blank_start]Fromm-Reichmann[blank_end] (1948) suggested the psychological explanation for schizophrenia that a schizophrenogenic mother can influence the development of schizophrenia. A schizophrenogenic mother is [blank_start]cold and dominant[blank_end], causing conflict and tension in the family. This causes [blank_start]secrecy[blank_end], leading to distrust and, eventually, [blank_start]paranoia[blank_end]. This therefore causes schizophrenic symptoms such as [blank_start]persecutory delusions[blank_end].

Bateson (1972) proposed the [blank_start]double[blank_end] bind theory: [blank_start]faulty[blank_end] communication in families causes schizophrenia. This involves [blank_start]contradictory[blank_end] messages, e.g. mother telling child to do something, but when they do it they are punished. This leads to confusion and fear of doing the wrong thing. The individual will then develop strategies and behaviours to [blank_start]avoid[blank_end] the double bind situation, which results in symptoms such as avolition, social withdrawal and the flat effect.

The three forms of negative expressed emotions: 1. [blank_start]Verbal criticism[blank_end]- scrutinising the individual, sometimes involves violence 2. [blank_start]Hostility[blank_end]- anger and rejection of individual 3. [blank_start]Emotional over-involvement[blank_end]- being overly involved in the individual's personal life

What are high levels of negative expressed emotions often correlated with?

What does negative expressed emotion cause in an individual?

Cognitive explanations for schizophrenia revolve around [blank_start]dysfunctional[blank_end] thought processing. Lowered processing in the ventral striatum and superior temporal gyrus [blank_start]support[blank_end] the cognitive explanation, as they emphasise how changes in thought processing can cause schizophrenic symptoms. There are two main explanations: 1. Dysfunctional [blank_start]meta-representation[blank_end]- disruption in the ability to recognise [blank_start]our own[blank_end] actions and thoughts as being carried out by ourselves, causing [blank_start]hallucinations[blank_end]. 2. Lack of central control- the [blank_start]inability[blank_end] to supress [blank_start]automatic[blank_end] thoughts, causing disorganised speech. The Stroop test found that schizophrenics take [blank_start]twice[blank_end] as long to supress their automatic thoughts compared to a control group.

Why is it a problem that Fromm-Reichmann observed patients who already had schizophrenia when investigating the schizophrenogenic theory?

Berger (1965) found that schizophrenic patients reported [blank_start]higher[blank_end] recall of double bind statements compared to non-schizophrenics. This is therefore is [blank_start]supporting[blank_end] evidence for the double bind theory, however it lacks [blank_start]reliability[blank_end]; the patients already have schizophrenia, so they may be experiencing delusions which make them believe they experienced double bind situations, when they actually didn't. For example, if they were questioned before the onset of the symptoms, they may have had lower recall, meaning there [blank_start]would not[blank_end] be consistency over time.

Liem (1974) found that communication patterns in families with a schizophrenic child was the same as with families with a non-schizophrenic child. What does this evidence suggest about the double bind theory?

'Kavanagh (1992) reviewed 26 studies of negative expressed emotion, and found the relapse rates in schizophrenics who reported high levels of negative expressed emotions was 48%, compared to 21% in patients who returned to families with low levels of negative expressed emotion.' Is this statement true or false?

One disadvantage of the negative expressed emotion theory is that 52% of schizophrenics who return to homes with high expressed emotions [blank_start]don't relapse[blank_end]. The reason for this may be [blank_start]individual[blank_end] differences such as the types of symptoms the experience (negative vs. positive), their personality and the severity of symptoms. This indicates that negative expressed emotion [blank_start]is not[blank_end] a full explanation for schizophrenia.

One main limitation of all family dysfunction explanations is that they all place [blank_start]blame[blank_end] and responsibility on the [blank_start]family[blank_end]. This is an ethical issue as it may cause [blank_start]distress[blank_end] to family members.

Which researcher investigated a lack of central control's link to schizophrenia and found that schizophrenics take twice as long to complete the Stroop test?

Which treatment for schizophrenia supports cognitive explanations for schizophrenia?

Typical drug therapy for schizophrenia was introduced in the 19[blank_start]50[blank_end]s, with a drug called [blank_start]chlorpromazine[blank_end] that could either be injected or consumed. This therapy involves dopamine [blank_start]antagonists[blank_end]: the drug blocks the receptor sites for dopamine in post-synaptic neurons, hence [blank_start]decreasing[blank_end] levels of the neurotransmitter, meaning symptoms such as [blank_start]hallucinations[blank_end] are reduced. Chlorpromazine is also used as a sedative, as it is linked to the neurotransmitter [blank_start]histamine[blank_end] as well.

Atypical drug therapy for schizophrenia was introduced in the 19[blank_start]70[blank_end]s, with a drug called [blank_start]clozapine[blank_end]. The aim of this type of drug therapy was to reduce the side effects of typical drug therapy. Like chlorpromazine, this drug also binds to dopamine receptors on the post-synaptic neuron, hence blocking them, but it also does the same for neurotransmitters [blank_start]serotonin[blank_end] and [blank_start]glutamate[blank_end]. It is often prescribed to [blank_start]suicidal[blank_end] patients for its mood-enhancing effects. However, this drug is also known to cause [blank_start]agranulocytosis[blank_end], a fatal blood disorder, so a new drug was made in the 19[blank_start]90[blank_end]s, risperidone. It has the same binding qualities as clozapine, but binds [blank_start]more[blank_end] strongly, so the doses are smaller and the side effects are reduced.

What percentage of schizophrenic patients attempt suicide? (linked to typical drug therapies)

Thornley (2003) did a meta-analysis of studies comparing the effects of Chlorpromazine to a placebo. What did the study find?

What did Meltzer (2012) suggest about the effectiveness of clozapine?

Label the table with the correct side effects associated with the different types of drug therapy. (definition is below the unlabeled term)

What do severe side effects to drug therapies cause?

What do both types of drug therapy treat in order to cure schizophrenia?

While drug therapy does support the [blank_start]dopamine[blank_end] hypothesis as an explanation for schizophrenia, it can also be said that it [blank_start]does not take[blank_end] into account other biological factors such as genes and neural correlates, or external factors such as family dysfunction. This is therefore [blank_start]a limitation[blank_end] of drug therapy.

Who is likely to over-emphasise the effectiveness of drug therapies?

What is the aim of CBT?

[blank_start]Reality[blank_end] testing in CBT involves the patient and psychologist discussing how likely their beliefs are to be [blank_start]true[blank_end]. It also involves considering less [blank_start]threatening[blank_end] possibilities linked to their beliefs. As well as this, CBT helps patients recognise the link between hallucinations/delusions and their feelings/behaviour.

CBT helps patients cope with their symptoms, but does not cure them.

Personal therapy is an approach to [blank_start]CBT[blank_end]. The aim of personal therapy is to [blank_start]evaluate[blank_end] the experiences of a patient, including triggers and consequences. Patients are then provided with strategies to cope with their issues. There are four techniques developed: 1. [blank_start]Distraction for[blank_end] intrusive thoughts 2. [blank_start]Challenging[blank_end] meaning of thoughts 3. [blank_start]Increase/decrease[blank_end] in social activity to distract from low mood 4. [blank_start]Relaxation[blank_end] techniques Personal therapy also helps patients recently discharged from hospital to deal with daily life e.g. recognising signs of relapse.

What did NICE discover about CBT when comparing it to drug therapy?

[blank_start]Jauhar[blank_end] (2014) did a [blank_start]meta-analysis[blank_end] of CBT as a treatment for schizophrenia, and found it had [blank_start]a small[blank_end] therapeutic effect. Additionally, if researchers didn't know which patients were treated with CBT, the effect [blank_start]disappeared[blank_end], suggesting the researcher may have been actively looking for improvements when they knew who had been through CBT, so the improvements may be over-emphasised. This therefore indicates that CBT [blank_start]isn't[blank_end] as effective as previously suggested.

Which two of the below statements are evaluative statements about CBT?

[blank_start]Family[blank_end] therapy aims to improve faulty communication in families, specifically treating [blank_start]negative[blank_end] expressed emotion (hostility, criticism, emotional over-involvement). It involves the presence of [blank_start]all[blank_end] family members, and all must be [blank_start]completely[blank_end] open. Strategies to improve communication include [blank_start]removing[blank_end] burden of care (sharing care of schizophrenic family member), removing feelings of guilt, and [blank_start]decreasing[blank_end] negative forms of communication.

Name 3 aims of the strategies used in family therapy

Pharoah (2010) found that [blank_start]family therapy[blank_end] [blank_start]increased[blank_end] compliance to medication and therefore [blank_start]decreased[blank_end] relapse rates.

Pick three evaluative statements for family therapy as a treatment for schizophrenia

Token economies are a form of management for schizophrenia, used to [blank_start]modify[blank_end] maladaptive symptoms caused by [blank_start]institutionalisation[blank_end]. It is based on [blank_start]operant[blank_end] conditioning and is useful for [blank_start]long[blank_end] term patients in psychiatric wards. Clinicians develop a list of behaviours that they believe will improve a patient's engagement in daily life, such as getting out of bed or brushing teeth. If a patient carries out this behaviour, they are [blank_start]immediately[blank_end] rewarded with a token ([blank_start]secondary[blank_end] reinforcer) which can be exchanged for a reward such as sweets or magazines.

Azran and Ayllan (1968) did a study into the effectiveness of [blank_start]token economies[blank_end]. They studied [blank_start]female[blank_end] patients in a psychiatric wards and found that those who did token economy systems [blank_start]exhibited[blank_end] the desired behaviours set by clinicians, suggesting token economy [blank_start]is[blank_end] effective.

Pick 3 evaluative statements for token economy

The interactionist approach to schizophrenia This approach suggests that the interaction of 3 main factors causes the onset of schizophrenia 1. [blank_start]Biological[blank_end]: genes, dopamine hypothesis, neural correlates 2. [blank_start]Psychological[blank_end]: stress, anxiety, poor cognitive functioning 3. [blank_start]Social[blank_end]: family dysfunction

The diathesis-stress model [blank_start]Diathesis[blank_end]: vulnerability [blank_start]Stressor[blank_end]: trigger Original diathesis-stress model for schizophrenia Diathesis: [blank_start]genetic[blank_end] vulnerability- the schizogene (one gene which leads to development of the schizotypic personality, characterised by sensitivity to stress) Stressor: [blank_start]environmental[blank_end] trigger- stress in childhood e.g. schizophrenogenic mother Modern diathesis-stress model Diathesis: [blank_start]not necessarily[blank_end] a genetic vulnerability, and multiple genes are involved. Psychological trauma can also cause vulnerability Stressor: the stressor is [blank_start]not necessarily[blank_end] just psychological, it is simply any factor which increases the risk of the onset of schizophrenia e.g. smoking cannabis

What is the most common combination of treatments in the interactonist approach?

Houston (2008) concluded that childhood sexual trauma created vulnerability for schizophrenia, while cannabis use acted as the trigger. However, this research has been criticised. What is a limitation of the findings?

Which researcher found that adopted children with schizophrenic biological mothers and with adoptive mothers that showed high levels of negative expressed emotion were more likely to develop schizophrenia themselves, hence supporting the interactionist approach?

What did Tienari's research suggest about the interactionist approach?

Name limitations of Tienari's study of the interactionist approach

Which researcher carried out a study into interactionist treatment for schizophrenia in which one group received medication and CBT, one group received medication and support counselling, and one group received just medication, and found the 2 combination groups showed greater reduction in symptoms compared to the medication. These findings also indicated that schizophrenia isn't solely biological.

'While research such as Tarrier's support the interactionist approach, it is possible that the cause of schizophrenia is not necessarily an interaction between biological and psychological. It is difficult to tell if, in the experiments where effectiveness of interactionist treatments is measured, it is actually just one treatment making the difference. We cannot be entirely sure, therefore, whether an interaction between the two factors is the cause of schizophrenia.' Is this statement true or false?