Schizophrenia

Serious mental disorder affecting 1% of population.

More common in men, city-dwellers and lower socio-economic groups.

Diagnosis and classification are interlinked. To diagnose a specific disorder we need to be able to distinguish one disorder from another.

Diagnosis - identify symptoms and use classification system to identify the disorder (e.g. depression, OCD, schizophrenia, etc.)

identify symptoms that go together = a disorder

One of the main classification systems.

One positive symptom must be present (delusions, hallucinations or speech disorganisation) to be diagnosed with schizophrenia.

One of the main classification systems.

(V11 published but not used for diagnosis until 2022) - two or more negative symptoms are sufficient for diagnosis (e.g. avolition and speech poverty).

Additional experiences beyond those of ordinary existence.

Unusual sensory experiences that have no basis in reality or distorted perceptions of real things. Experienced in relation to any sense.

For example, hearing voices or seeing people who aren’t there.

Beliefs that have no basis in reality - make a person with schizophrenia behave in ways that make sense to them but are bizarre to others.

For example, beliefs about being a very important person or the victim of a conspiracy.

Loss of usual abilities and experiences.

A reduction in the amount and quality of speech. May include a delay in verbal responses during conversation.

DSM emphasises speech disorganisation and incoherence as a positive symptom.

Severe loss of motivation to carry out everyday tasks (e.g. work, hobbies, personal care).

Results in lowered activity levels and unwillingness to carry out goal-directed behaviours.

Strength of the diagnosis of schizophrenia - A reliable diagnosis is consistent between clinicians (inter-rater) and between occasions (test-retest).

Osório et al. (2019) report excellent reliability for schizophrenia diagnosis (DSM-5) - inter-rater agreement of +.97 and test-retest reliability of +.92.

This means that the diagnosis of schizophrenia is consistently applied.

Limitation of the diagnosis of schizophrenia - Criterion validity involves seeing whether different procedures used to assess the same individuals arrive at the same diagnosis.

Cheniaux et al. (2009) had two psychiatrists independently assess the same 100 clients. 68 were diagnosed with schizophrenia with ICD and 39 with DSM.

This means that schizophrenia is either over - or under - diagnoses, suggesting that criterion validity is low.

In the Osório study there was excellent agreement between clinicians using different procedures both dervived from the DSM system.

This means that criterion validity for schizophrenia is good provided it takes place within a single diagnostic system.

Limitation of the diagnosis of schizophrenia - If conditions often co-occur then they might be a single condition. Schizophrenia is commonly diagnosed with other conditions.

For example, Buckley et al. (2009) concluded that schizophrenia is co-morbid with depression (50% of cases), substance abuse (47%) or OCD (23%).

This suggests that schizophrenia may not exist as a distinct condition.

Limitation of the diagnosis of schizophrenia - Men are diagnosed with schizophrenia more often than women, in a ratio of 1.4:1 (Fischer and Buchanan 2017).

This could be because men are more genetically vulnerable, or women have better social support, masking symptoms.

This means that some women with schizophrenia are not diagnosed so miss out on helpful treatment.

Limitation of the diagnosis of schizophrenia - Some symptoms, e.g. hearing voices, are accepted in some cultures, e.g. Afro-Caribbean societies ‘hear voices’ from ancestors.

Afro-Caribbean British men are up to ten times more likely to receive a diagnosis as white British men, probably due to overinterpretation of symptoms by UK psychiatrists.

This means that Afro-Caribbean men living in the UK appear to be discriminated against by culturally-biased diagnostic system.

Limitation of the diagnosis of schizophrenia - There is overlap between the symptoms of schizophrenia and other conditions, e.g. both schizophrenia and bipolar disorder involve delusions and avolition.

Schizophrenia and bipolar disorder may be the same condition (a classification issue). Schizophrenia is hard to distinguish from bipolar disorder (a diagnosis issue).

This means that schizophrenia may not exist as a condition and, if it does, it is hard to diagnose.

Strong relationship between the degree of genetic similarity and shared risk of schizophrenia.

Gottesman’s (1991) large-scale study found (for example) someone with an aunt with schizophrenia has a 2% chance of developing it, 9% for a sibling and 48% for an identical twin.

Family members also share environment but still indicates support for genetic view.

Early research looked unsuccessfully for a single genetic variation to explain schizophrenia.

Schizophrenia is polygenic - requires several genes.

It is also aetiologically heterogenous, i.e. risk is affected by different combinations.

Ripke et al. (2014) combined all previous data from genome-wide studies. Found 108 separate genes associated with slightly increased risk of schizophrenia.

Schizophrenia can also have a genetic origin in the absence of a family history because of mutation in parental DNA.

Evidencce comes from the correlation between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia (Brown et al. 2002).

Dopamine (DA) is widely believed to be involved in schizophrenia because it is features in the functioning of brain systems related to the symptoms of schizophrenia.

High dopamine activity in subcortex (central areas of the brain) associated with hallucinations and poverty of speech (e.g. excess of DA receptors in pathways linking from subcortex to Broca’s area).

May explain specific symptoms e.g. poverty of speech and auditory hallucinations.

Updated hypothesis has added low levels of DA in the prefrontal cortex (responsible for thinking), could explain negative symptoms.

Explains origins of abnormal DA - genetic variations and early experiences of stress make some people more sensitive to cortical hypodopaminergia and hence subcortial hyperdopaminergia (Howes et al).

Strength of the biological explanations for schizophrenia - Family studies (e.g. Gottesman) show risk increases with genetic similarity. Twin study found 33% concordance for MZ and 7% for DZ twins (Hiker et al. 2018).

Adoption studies (e.g. Tienari et al. 2004) show that biological children of parents with schizophrenia are at greater risk even if they grow up in an adoptive family.

This shows that some people may be more vulnerable to schizophrenia because of their genes.

Limitation of the biological explanations for schizophrenia - Biological risk factors include birth complications (Morgan et al. 2017) and smoking THC-rich cannabis in teenage years (Di Forti et al. 2015).

Psychological risk factors include childhood trauma e.g. 67% with schizophrenia (38% matched controls) reported at least one childhood trauma (Mørkved et al. 2017).

This means genes alone cannot provide a complete explanation for schizophrenia.

If potential parents have a relative with schizophrenia, they can be advised of risk of having a child with the condition.

However the risk estimate is just as average figure based on genetic similarity to relatives, doesn’t take account of the future child’s environment.

This means that genetic counselling only provides a crude idea of vulnerability and is of limited use.

Strength of dopamine in symptoms of schizophrenia - Amphetamines (increase DA) mimic symptoms (Curran et al. 2004). Antipsychotic drugs (reduce DA) reduce intensity of symptoms (Tauscher et al. 2014).

Candidate genes act on the production of DA or DA receptors.

This strongly suggests that dopamine is involved in the symptoms of schizophrenia.

Limitation of dopamine in symptoms of schizophrenia - Theres evidence for a central role for glutamate.

Post-mortem and scanning studies found raised glutamate in people with schizophrenia (McCutcheon et al. 2020).

Also, several candidate genes for schizophrenia are believed to be involved in glutamate production or processing.

This means that a strong case can be made for a role for other neurotransmitters in schizophrenia.

Fromm-Reichmann’s (1948) psychodynamic explanation of patients’ early experiences of ‘schizophrenogenic mothers’ (mothers who cause schizophrenia).

These mothers are cold, rejecting, controlling, and create a family climate of tension and secrecy. This leads to distrust and paranoid delusions and schizophrenia.

Bateson et al. (1972) described how a child may be regularly trapped in situations where they fear doing the wrong thing, but receive conflicting messages about what counts as wrong. They cannot express their feelings about the unfairness of the situation.

When they ‘get it wrong’ (often) the child is punished by withdrawal of love - they learn the world is confusing and dangerous, leading to disorganised thinking and delusions.

Expressed emotion (EE) is the level of emotion (mainly negative) expressed including:

• verbal criticism of the person with schizophrenia

• hostility towards them

• emotional over-involvement in their life

High levels of EE cause stress in the person, may trigger onset of schizophrenia or relapse.

Lower level of information processing in some areas of the brain suggest cognition is impaired.

For example, reduced processing in the ventral striatum is associated wit negative symptoms.

Metarepresentation is the cognitive ability to reflect on thoughts and behaviour (Frith et al. 1992)

This dysfunction disrupts our ability to recognise our thoughts as our own - could lead to the sensation of hearing voices (hallucination) and experience of having thoughts placed in the mind by others (thoughts insertion, a delusion).

Frith et al. (1992) also identified dysfunction of central control as a way to explain speech poverty - central control being the cognitive ability to suppress automatic responses while performing deliberate actions.

People with schizophrenia experience derailment of thoughts because each word triggers automatic associations that they cannot suppress.

Strength of family dysfunction explaining schizophrenia - A review by Read et al. (2005) reported that adults with schizophrenia are disproportionately likely to have insecure attachment (Type C or D).

Also, 69% of women and 59% of men with schizophrenia have a history of physical and/or sexual abuse.

This strongly suggests that family dysfunction does make people more vulnerable to schizophrenia.

Limitation of family dysfunction explaining schizophrenia - There is almost no evidence to support the importance of traditional family-based theories e.g. schizophrenogenic mother and double bind.

Both theories are based on clinical observation of patients and informal assessment of the personality of the mothers of patients.

This means that family explanations have not been able to explain the link between childhood trauma and schizophrenia.

Strength of cognitive explanations for schizophrenia - Stirling et al. (2006) compared performance on a range of cognitive tasks (e.g. Stroop task) in people with and without schizophrenia.

As predicted by central control theory, people with schizophrenia took over twice as long on average to name the font-colours.

This supports the view that the cognitive processes of people with schizophrenia are impaired.

Limitation of cognitive explanations for schizophrenia - Cognitive explanations for schizophrenia are proximal explanations - they explain what is happening now to produce symptoms.

Cognitive explanations are weaker as distal explanations (i.e. what causes cognitive problems), possible distal explanations are genetic and family dysfunction.

This means that cognitive theories alone only provide partial explanations.

Drugs use to reduce the intensity of symptoms, in particular the positive symptoms, of psychotic conditions like schizophrenia.

The first generation of antipsychotic drugs, having been used since the 1950s. They work as dopamine antagonists and include Chlorpromazine.

Typical antipsychotic drugs (e.g. chlorpromazine) have been around since the 1950s.

They work by acting as antagonists in the dopamine system and aim to reduce the action of dopamine - they are strongly associated with the dopamine hypothesis.

Dopamine antagonists work by blocking dopamine receptors in the synapses in the brain, reducing the action of dopamine.

Initially, dopamine levels build up after taking chlorpromazine, but then production is reduced.

This normalises neurotransmission in key areas of the brain, which in turn reduces symptoms like hallucinations.

Also has sedation effect.

Chlorpromazine also has an effect on histamine receptors which appear to lead a sedation effect.

It is also used generally to calm anxious patients when they are first admitted to hospital.

The aim of developing newer antipsychotics was to maintain or improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and also to minimise the side effects of the drugs used.

Binds to dopamine receptors as chlorpromazine does but also acts on serotonin and glutamate receptors.

This drug was more effective than typical antipsychotics - clozapine reduces depression and anxiety as well as improving cognitive functioning.

It also improves mood, which is important as up to 50% of people with schizophrenia attempt suicide.

Risperidone was developed in the 1990s because clozapine was involved in the deaths of some people from a blood condition called agranulocytosis.

Risperidone like clozapine binds to dopamine and serotonin receptors.

But risperidone binds more strongly to dopamine receptors and is therefore more effective in smaller doses than most antipsychotics and has fewer side effects.

Strength of antipsychotic drugs - Thornley et al. (2003) reviewed data from 13 trials (1121 participants) and found that chlorpromazine was associated with better functioning and reduced symptom severity compared with placebo.

There is also support for the benefits of atypical antipsychotics. Meltzer (2012) concluded that clozapine is more effective than typical antipsychotics, and that it is effective in 30-50% of treatment-resistant cases.

This means that, as far as we can tell, antipsychotics work.

Most studies are of short-term effects only and some data sets have been published several times, exaggerating the size of the evidence base (Healy 2012). Also benefits may be due to calming effects of drugs rather than real effects on symptoms.

This means the evidence of effectiveness if less impressive than it seems.

Limitation of antipsychotic drugs - Typical antipsychotics are associated with dizziness, agitation, sleepiness, weight gain, etc. Long-term use can lead to lip-smacking and grimacing due to dopamine super-sensitivity (= tardive dyskinesia)

The most serious side effect is neuroleptic malignant syndrome (NMS) caused by blocking dopamine action in the hypothalamus (can be fatal due to disrupted regulation of several body systems).

This means that antipsychotics can do harm as well as good and individuals may avoid them (reducing effectiveness).

Limitation of antipsychotic drugs - The use of most of these drugs is strongly tied up with the dopamine hypothesis and the idea that there are higher-than-usual levels of dopamine in the subcortex of people with schizophrenia.

But there is evidence that this may not be correct and that dopamine levels in other parts of the brain are too low rather than too high. If so, most antipsychotics shouldn’t work.

This means antipsychotics may not be the best treatment to opt for - perhaps some other factor is involved in their apparent success.

A method for treating mental disorders based on both cognitive and behavioural techniques. From the cognitive viewpoint the therapy aims to deal with thinking, such as challenging negative thoughts. The therapy also includes behavioural techniques.

The aims of CBT in geneal are to help clients identify irrational thoughts (e.g. delusions and hallucinations) and try to change them.

5-20 sessions, individually or in a group

Clients are helped to make sense of how their delusions and hallucinations impact on their feelings and behaviour.

For example, a client may hear voices and believe they are demons so they will be very afraid.

Normalisation involves explaining to the client that hearing voices is an ordinary experience.

Turkington et al. (2004) treated a paranoid client who believed the Mafia were plotting to kill him.

The therapist acknowledged the client’s anxiety, and explained that there were other, less frightening possibilities and gently challenged the client’s evidence of his belief in the Mafia explanation.

A psychological therapy carried out with all or some members of a family with the aim of improving their communication and reducing the stress of living as a family.

Family therapy aims to reduce the levels of expressed emotion (EE), especially negative emotions such as anger and guilt which create stress.

Reducing stress is important to reduce the likelihood of relapse.

The therapist encourages family members to form a therapeutic alliance whereby they all agree on the aims of therapy.

The therapist also tries to improve families’ beliefs about and behaviour towards schizophrenia.

A further aim is to ensure that family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives.

• Phases 1 and 2 - share information and identify resources family can offer.

• Phases 3 and 4 - learn mutual understanding, and look at unhelpful patterns of interaction.

• Phases 5, 6 and 7 - skills training (e.g. stress management techniques), relapse prevention and maintenance.

Strength of CBT - Jauhar et al. (2014) reviewed 34 studies of CBT for schizophrenia, and concluded that there is evidence for significant effects on symptoms.

Pontillo et al. (2016) found reductions in auditory hallucinations. Clinical advice from NICE (2019) recommends CBT for people with schizophrenia.

This means both research and clinical experience support CBT for schizophrenia.

Limitation of CBT - Thomas (2015) points out that different studies have focused on different CBT techniques and people with different symptoms.

Overall modest benefits of CBT for schizophrenia may conceal a range of effects of different techniques on different symptoms.

This means that is is hard to say how effective CBT will be for treating a particular person with schizophrenia.

CBT may improve quality of life but not ‘cure’ As schizophrenia is a biological condition CBT should only improve ability to live with schizophrenia.

But studies report significant reductions in positive and negative symptoms. This suggests CBT does more than enhance coping.

On balance then it may well be that CBT may be a partial cure for schizophrenia.

Strength of family therapy - McFarlane (2016) concluded family therapy is effective for schizophrenia. Relapse rates were reduced by 50-60%.

Particularly promising during time when mental health initially starts to decline. NICE recommends family therapy.

This means that family therapy is good for people with both early and ‘full-blown’ schizophrenia.

Strength of family therapy - Therapy is not just for benefit of identified patient but also for the families that provide bulk of care for people with schizophrenia (Lobban and Barrowclough).

Family therapy lessens the negative impact of schizophrenia on the family and strengthens ability of the family to give support.

This means family therapy has wider benefits beyond the obvious positive impact on the identified patient.

A from of behavioural therapy, where desirable behaviours are encouraged by the use of selective reinforcement. For example, people are given rewards (tokens) as secondary reinforcers when they engage in correct/socially desirable behaviours. The tokens can then be exchanged for primary reinforcers - favourite foods or privileges.

Ayllon and Azrin (1968) used a token economy in a schizophrenia ward. A gift token was given for every tidying act. Tokens were later swapped for privileges e.g. films.

Token economies were extensively used in the 1960s and 70s. Decline in the Uk due to a shift towards care in the community rather than hospitals and because of ethical concerns.

Token economies still remain a standard approach to managing schizophrenia in many parts of the world.

Institutionalisation occurs in long-term hospital treatment.

Matson et al (2016) identified three categories of institutional behaviour that can be tackled using token economies: personal care, condition-related behaviours (e.g apathy) and social behaviour.

Modifying these behaviours does not cure schizophrenia but has two major benefits:

• Quality of life

• ‘Normalises’ behaviour

Token economies improve the quality of life within the hospital setting, e.g. putting on make-up or becoming more sociable with other residents.

Encourages return to more ‘normal’ behaviour, making it easier to adapt back into the community e,.g. getting dressed or making your bed.

Tokens (e.g. coloured discs) given immediately after a desirable behaviour. Target behaviours are decided individually based on knowledge of the person (Cooper et al. 2007).

Tokens have no value themselves but are swapped for rewards, e.g. sweets or magazines, or activities like a film or a walk outside.

Tokens are given immediately following target behaviours because delayed rewards are less effective.

Token economies are an example of behaviour modification based on operant conditioning.

Tokens are secondary reinforcers - exchanged for rewards (primary reinforcers which are directly rewarding e.g. food).

Tokens that can be exchanged for a range of different primary reinforcers are called generalised reinforcers. These have a more powerful effect.

Strength of token economies to manage schizophrenia - Glowacki et al. (2016) identified seven high quality studies published between 1999 and 2013 on the effectiveness of token economies in a hospital setting.

All the studies showed a reduction in negative symptoms and a decline in frequency of unwanted behaviours.

This supports the value of token economies.

Seven studies is quite a small evidence base. One issue with such a small number of studies is the file drawer problem - a bias towards publishing positive findings.

This means that there is a serious question over the effectiveness of token economies.

Limitation of token economies in managing schizophrenia - Professional have the power to control people’s behaviour and this means imposing one person’s norms on to others (e.g. a patient may like to look scruffy).

Also restricting the availability of pleasure to people who don’t behave as desired means that very ill people, already experiencing distressing symptoms, have an even worse time.

This means that benefits of token economies may be outweighed by the impact on freedom and short-term reduction in quality of life.

Limitation of token economies in managing schizophrenia - Other approaches do not raise ethical issues, e.g. art therapy is a high-gain low-risk approach to managing schizophrenia (Chiang et al. 2019)

Even if the benefits of art therapy are modest, this is true for all approaches to treatment and management of schizophrenia and art therapy is a pleasant experience.

This means that art therapy might be a good alternative to token economies - no side effects or ethical abuses.

A broad approach to explaining schizophrenia, which acknowledges that a range of factors, including biological and psychological factors, are involved in the development of schizophrenia.

Diathesis means vulnerability. Stress in this context refers to negative experiences that trigger the vulnerability.

The diathesis-stress model says both vulnerability and a trigger are needed to develop schizophrenia - its is the interaction that is key.

In the original diathesis-stress model, diathesis was entirely the result of a dingle ‘schizogene’.

Meehl (1962) argued that someone without this gene should never develop schizophrenia, no matter how much stress they were exposed to.

But a person who does have the gene is vulnerable to the effects of chronic stress (especially a schizophrenogenic mother).

The schizogene is necessary but not sufficient for th development of schizophrenia.

It is now believed that diathesis is not due to a single ‘schizogene’. Instead it is thought that many genes increase vulnerability.

Also, diathesis doesn’t have to be genetic. It could be early psychological trauma affecting brain development.

For example, child abuse affects the hypothalamic-pituitary adrenal (HPA) system, making a child vulnerable to stress.

A modern definition of stress (in relation to diathesis-stress) includes anything that risks triggering schizophrenia. Can be psychological (e.g. parenting) or biological (e.g. cannabis use).

Cannabis use can increase the risk of schizophrenia up to seven times depending on dose - probably because it interferes with the dopamine system.

Antipsychotic drugs taken in combination with CBT.

But this requires adopting an interactionist model - it is not possible to adopt a purely biological approach, tell patients that their condition is purely biological (no psychological significance to their symptoms) and then treat them with CBT (Turkington et al. 2006).

The UK adopts more interactionist approach compared to the US.

In Britain it is increasingly standard practice to treat patients with a combination of drugs and CBT.

In the US there is more of a conflict between psychological and biological models of schizophrenia and this may have led to slower adoption of the interactionist approach.

Strength of the diathesis-stress model in explaining schizophrenia - Tienari et al. (2004) studied children adopted away from mothers diagnosed with schizophrenia. The adoptive parents’ parenting styles were assessed and compared with a control group of adoptees with no genetic risk.

A child-rearing style with high levels of criticism and conflict and low level of empathy was implicated in the development of schizophrenia but only for children with a high genetic risk.

This shows that a combination of genetic vulnerability and family stress leads to increased risk of schizophrenia.

Limitation of the diathesis-stress model in explaining schizophrenia - Multiple genes increase vulnerability, each with a small effect on its own - there is no schizogene. Stress comes in many forms, including dysfunctional parenting.

Researchers now believe stress can also include biological factors. For example, Houston et al. (2008) found childhood sexual trauma was a diathesis and cannabis use a trigger.

This means that there are multiple factors, biological and psychological, affecting both diathesis and stress.

Tarrier et al. (2004) randomly allocated 315 participants to (1) medication + CBT group, or (2) medication + supportive counselling group, or (3) control group (medication only).

Participants in the two combination groups showed lower symptom levels than those in the control group - but no difference in hospital readmission.

This means that there is a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes.

Jarvis and Okami (2019) suggest this argument is the same as claiming that because alcohol reduces shyness, shyness is caused by lack of alcohol, the treatment-causation fallacy.

Therefore we cannot automatically assume that the success of combined therapies means interactionist explanations are correct.