Classification:

- Type of psychosis characterised by disruption of emotion and cognition. External relaity

and insight are impaired. Affects sense of self.
Positive symptoms: Atypical symptoms (in addition). Hallucinations, distortions.
Negative symptoms: loss of usual experience
Hallucinations: distorted perceptions with no nase in reality.

Delusions:
Persecution: belief that others want to harm or manipulate (government, aliens)
Grandeur: belief they are an important even god like individual with powers.
Control: Belief their body is under external control
Reference: belief that events in environment are directly related to them, (TV communicating to
them)

Negative Symptoms:
Avolition: Lack of purposeful, willed behaviour, inability to start and continue with goal-directed
behaviour. Results in lowered activity levels.
Speech poverty: Limited speech output with limited often repetitive content. Reduces quality of
speech too.

✅ Good reliability of diagnosis.

- Osorio (2019) reported good reliability for diagnosis with DSM-5
- Inter rater reliability of +.97
- Test retest of +.92

❌
- Diagnosis is consistently applied and ∴ reliable
Poor validity of diagnosis.
- Cheniaux (2009)
- Asked 2 psychologists to asses + diagnose 100 patients using DSM 5 and ICD 10
- ICD= 68 diagnosed, DSM= 39 diagnosed
- There is low criterion validity

❌Symptom overlap
-Despite claim that classifying positive and negative symptoms makes more valid
diagnoses, there is symptom overlap with schizophrenia and other conditions
- Lack of distinction calls into question the validity of schizophrenia having it’s own

❌
characteristics and signs
Comorbidity with other conditions.
- Common among patients with schizophrenia, like substance abuse, anxiety and
depression.
- 2 conditions frequently being diagnosed together means that validity of classification and
diagnosis both illnesses is reduced
- Psychiatrists may not be able to tell the difference
❌Cultural bias
-Positive symptoms of hearing voices is more acceptable in African cultures because of
cultural beliefs in communication with ancestors.
- Calls reliability of diagnosis into question
- May not be agreement on diagnosis by psychiatrists across cultures

❌
- Methods may not be suitable for use across all cultures.
Gender bias
- Longnecker (2010) reviewed studies of the prevalence of schizophrenia
- Found that since the 1980s men have been diagnosed more than women
- Prior, there had been no difference
- Women's better functioning may bias practitioners to under-diagnose schizophrenia
- Clinicians fail to consider these issues ∴ affect validity of diagnosis

Biological Explanations:

Genetic:
- Ripke, candidate genes
- Meta-analysis of genome wide studies of schizophrenia
- Genetic make compared- 37000 patients: 113000 contols
- Found 108 separate genetic variations associated with increased risk of SZ
➔ Gottesman (1991) - MZ twins have 48% risk rate and DZ twins have 17% risk rate
➔ Evidence that higher degree of genetic relativeness means higher risk of schizophrenia
● Benzel et al. 2007 found 3 genes, COMT , DRD4 , AKT1
● Have all been associated with excess dopamine in specific D2 receptors which lead to
positive symptoms such as delusions and hallucinations

Neural Correlates
- Measurements of structure or function of brain that correlate with symptoms of
schizophrenia, so may be implicated in origins of SZ
- Thought to be neural correlates of positive and negative symptoms
- Torres 2002 - found SZ people have larger ventricles in the brain.
Positive Symptoms
● Allen 2007 found lower activation levels in superior temporal gyrus and anterior cingulate
gyrus have been found in those experiencing auditory hallucinations
● Reduced activity in these areas is a neural correlate of auditory hallucinations
Negative symptoms
● Ventral striatum: may be involved in anticipation of reward (factor in motivations)
● Damage or reduced function in this part may explain avolition
- Juckel found lower activities in Ventral striatum in SZ patients compared to controls
- Found negative correlations between VS activity levels and severity of negative
symptoms
- ∴ VS activity is a neural correlate of negative symptoms
Dopamine hypothesis
- Neurotransmitter with excitatory effect
- Associated with sensation of pleasure
- Unusually high levels are associated with SZ, mainly positive symptoms
- SZ patients thought to have abnormally high levels of D2 receptors on postsynaptic
neurons = more dopamine binding and neurons firing
- Davis and Khan: revised hypothesis
- + symptoms caused by hyperdopaminergia in subcortex
- - symptoms = hypodopaminergia (Goldman et al 2004)

✅ Strong evidence for genetic vulnerability to schizophrenia from a variety of sources.

- Gottesman: showed that genetic similarity and SZ risk are closely correlated

❌
- May not be entirely genetic but genetic susceptibility is very important in SZ development
However this evidence does not explain how individuals with no family history of
schizophrenia develop the condition.

✅The role of genetic mutation supports the genetic explanation.

- Brown et al established a link between: fathers age at conception time- and risk of child
developing SZ later in like
- 0.7% chance for fathers under 25, 2% for those over 50

❌
- Supports importance of genetic factors
Environmental factors must play a role as concordance rates never exceed 50% in twin
studies. SZ cannot be sufficiently explained by only biology

✅Supporting Evidence: Effectiveness of drug therapies.

-Leucht et al found antipsychotics were significantly more effective than placebo in the
treatment of + and - symptoms
- Normalisation of dopamine activity treats SZ so there must be link between SZ and

❌
dopamine hypothesis
Undermining evidence: Ineffectiveness of drug therapies in some patients.
- Noll 2009 argues that antipsychotics don’t get rid of hallucinations in ⅓ of patients
- Other candidate genes code for other types of neurotransmitters that may be the cause
of + symptoms
Biological Therapies

All antipsychotics work by reducing dopaminergic transmission.

Typical (traditional) antipsychotics
- Act as dopamine antagonists
- They bind to (and block) dopamine receptors but don’t stimulate them, reducing the
action of dopamine.
- normalises neurotransmission, reducing positive symptoms such as hallucinations.
(Chlorpromazine),
Atypical (newer) antipsychotics
Helps positive and negative symptoms
Clozapine
- temporarily occupy the receptors and then rapidly dissociate to allow normal dopamine
transmission.
Act on other neurotransmitters, particularly serotonin, address negative symptoms too
- Reduces depression + anxiety and improves cognitive function.
(potential fatal blood condition)

Risperidone: (90s) binds more strongly to the dopamine

receptors than Clozapine allowing smaller doses
meaning fewer side effects.

✅ Research evidence shows the effectiveness of antipsychotics.

- Meltzer, concluded that Clozapine = more effective than typical antipsychotics and other
atypical antipsychotics, effective in around 40% of treatment resistant cases where
typical aps have failed

❌Cognitive factors are also important

- Leucht, research 36% patients didn’t relapse when on placebo
- Implies: cognitive factors are important in treatment of SZ
- Drugs may not be entirely necessary in all cases
❌Antipsychotics have side effects that range from mild to fatal.
- Typical antipsychotics= associated with range of side effects: dizziness, agitation, stiff
jaw, weight gain and itchy skin
- APS may not be appropriate for all patients
- Side effects so distressing it may discourage patients from taking meds

❌Potential ethical concerns with antipsychotics being used as a ‘chemical Cosh’.

- Used in hospitals for convenience of staff
- Makes patients calmer and easier to deal with
- Seen as human rights abuse by some

❌There is a possible theoretical objection to the use of antipsychotics.

- Use of drugs is closely related to dopamine hypothesis but there is evidence to show
that this explanation may not be correct
- Can undermine faith in some researchers that positive effects attributed to the drugs
may be a result of other factors and not the drugs

❌There are doubts about the true effectiveness

- Healy (2012)
- Argues some successful trials of effectiveness have had their data published multiple
times
- Exaggerates evidence for positive effects
- They have calming effects, easy to demonstrate that they have positive effects on
patients
- Suggests effectiveness of DT’s may be exaggerated
Family Dysfunction

Schizophrenogenic mothers

- Fromm-Reichmann’s psychodynamic explanation of patients early experiences of SZG

mothers

Double bind

- Bateson et al 1972 described how a child may be regularly trapped in situations -they
fear doing wrong thing, recieve conflicting messages about what counts as wrong.
- They cannot express their feelings
- punished by withdrawal of love

Expressed emotion

Level of emotion [mainly negative] expressed including:

- Verbal criticism of the person with schizophrenia

- Hostility, emotional over involvement in their life
- High levels of EE cause stress in the person , may trigger onset schizophrenia or relapse

✅ evidence linking family dysfunction to schizophrenia

- review by Read et al 2005: adults with SZ = disproportionately likely to have insecure
attachment type C or D
- 69% of women and 59% of men with SZ have history of physical and or sexual abuse
- suggests that family dysfunction makes people more vulnerable to schizophrenia

❌poor evidence base for any of the explanations

- Next to no evidence supporting importance of traditional family-based theories
- Evidence is based on clinical observation of patients + informal assessment of the
personality of the mothers of patients
- family explanations have not been able to explain the link between childhood trauma and
schizophrenia

✅ parent blaming research in this area may be useful, eg showing that insecure attachment
and childhood trauma affect vulnerability to schizophrenia

❌However parent blaming research is socially sensitive

- It creates additional stress for parents already seeing their child experienced
schizophrenia and taking responsibility for their care
 - This means that research into family dysfunction and schizophrenia will always be very
controversial but worth it for potential benefits

Cognitive explanations

- Low levels of info processing in some of the brain suggest cognition = impaired
- Reduced processing in the ventral striatum associated w/ negative symptoms

Metarepresentation

- The cognitive ability to reflect on thoughts and behaviour [Frith et al 1992]

- This dysfunction disrupts ability to recognise thoughts as our own - may lead to hearing
voices + the experience of having thoughts placed in mind by others

Central control

- Frith et al [1992] identified dysfunction of central control as way to explain speech

poverty - central control is cognitive ability to suppress automatic responses while
performing deliberate actions
- People with SZ experience derailment of thoughts as each word triggers automatic
associations they cannot suppress

✅ evidence for dysfunctional thought processing.

- Starling et al 2006: compared performance on a range of cognitive tasks EG stroop task
in people w/ and w/o SZ
- people w/ SZ took over twice as long on average to name the font colours in Stroop task
- This supports the view that the cognitive process is of people with schizophrenia are
impaired

❌only proximal margins of symptoms explained.

- Cognitive explanations for SZ are explanations - they explain what is happening now to
produce the symptoms
- Cognitive exp are weaker as distal explanations
- possible distal explanations are genetic and family dysfunction
- means cognitive theories alone only provide partial explanations

✅The cognitive approach provides excellent explanation for the symptoms of SZ

- suggesting it is a psychological condition
❌abnormal cognition is probably partly genetic in origin and the result of abnormal brain
development

- This means that although it has psychological symptoms schizophrenia is perhaps best
seen as a biological condition

Psychological Therapies

Beck’s CBT:

1. identify the thoughts/ delusions

2. challenges thoughts/ delusions
3. Therapist set homework + behavioural assignments to improve patients functioning
4. Homework is used to show the patient that they are able to cope

CBTp

- uses the ABCDE model.

- identifying activating events (A)
- resulting beliefs (B) from these events appear to cause their emotional consequences
- (C). beliefs can then be rationalised,
- disputed (D) changed through critical collaborative analysis,
- leading to the effect (E) of restructured beliefs.

→ Critical collaborative analysis - e.g. “if your voices are real, why can no-one else hear them?”

✅evidence for effectiveness.

- Jauhar et al. 2014 reviewed 34 studies of CBT for schizophrenia,
- concluded that there 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.

❌evidence quality.
- Thomas (2015): different CBT techniques and people with different symptoms.
- modest benefits of CBT for SZ may conceal range of effects of diff techniques on diff
symptoms.
- Means it’s hard to say how effective CBT is for treating diff patients with SZ.

❌CBT may improve quality of life but it is not classified as a 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.

Family Therapy: Aims to improve quality of communication w/ family members + reduce the
stress of living

Methods

- Form alliance with other family members

- Reduce stress of caring for someone with schizophrenia
- Improve the ability of family members to care for someone with schizophrenia
- Reduce guilt in family members
- Help family balance care with their own lives
- Improves family beliefs about schizophrenia

Burbach’s (2018) model for family therapy:

- Phases 1 and 2: share info, identify resources that the family can offer.
- Phases 3 and 4: learn mutual understanding, look for unhelpful patterns of interactions.
- Phases 5 and 6: skills training, families are taught skills such as stress management and
relapse prevention and maintenance.

✅evidence for effectiveness

- McFarlane (2016) concluded family therapy is effective for SZ.
- Relapse rates were reduced by 50-60%.
- Particularly promising during time when mental health initially starts to decline.
- NICE recommends family therapy.-
- means family therapy is good for people w/ both early and full blown SZ.

✅ benefits for the whole family.

- benefit for the families who provide the bulk of care for people with schizophrenia
(Lobban and Barrowclough)
- Family therapy lessens negative impact of SZ on the family + strengthens ability of
family to give support.
- means family therapy has wider benefits beyond the impact on patient.

✅reduces relapse rate

- makes families better able to provide the bulk of care so it has economic benefits.
 - also has therapeutic benefits for people with schizophrenia and their families.
- suggests everyone wins, therapy should be for the benefit of the person and then their
family.

Token Economies

Maladaptive behaviours prevent patients from adapting to new or difficult situations.

- Good behaviours earn tokens to be exchanged for a reward.

- TES are a means of changing the behaviour of a patient with schizophrenia. They are
based on operant conditioning
- Maladaptive behaviours tend to develop during prolonged hospital stays, which was a
common problem in the 1960s when TES was widely used
1. Primary reinforcer: reward is intended to show the patient what they can achieve by
engaging in desirable behaviours. sweets, magazines,etc
2. Secondary reinforcer: patients can tangibly earn what they can then be exchanged for a
reward.

Matson et al. (2016) identified 3 categories of problematic behaviours that develop in a

hospital, can be addressed through the use of token economies:

- Personal hygiene
- Illness-related behaviours (problems with positive and negative symptoms).
- Social behaviour (problems in dealing with other people).

❌limited to use within a hospital environment.

- hard to conduct outside of a hospital setting due to the patients not being monitored
closely enough to allow them to be given the secondary reinforcers after displaying the
desired behaviour.
- means that the patient may struggle to associate the reward with the desired behaviour
reducing the effectiveness of the therapy.
- token economies limited outside of a hospital setting; reduces the overall effectiveness
for managing schizophrenia.

✅TE’s have been shown to be effective in hospitals:

- some patients may not get to live outside until they’ve shown improvement self care +
social interactions
 - suggest that on balance the use of token economies are worth using despite external
limitations as they let patients avoid being institutionalised

✅ evidence to support the effectiveness

- Glowaki(2016) used 7 high quality studies between 1999 and 2013 on effectiveness of
TE’s in a hospital setting.
- All studies showed reduction in negative impact of symptoms + decline in the frequency
of undesirable behaviours.
- findings TE’s are effective method of managing schizophrenia; supports the value of its
use.

❌7 studies are a limited evidence base

- makes it harder to generalise findings; limited samples across such a long time frame.
- questionable validity of Glowaki’s study
- means we must also question the true effectiveness of token economies in the
management of schizophrenia.

❌ethical concerns about the use of token economies.

- require deliberate manipulation of a patient’s behaviour
- mental health professionals have the power to manipulate patient’s behaviour and
actions.
- TE’s require imposing the therapist’s ideas of norms and values onto patient, forces
them to change ‘normal’ behaviour to the therapist’s idea of ‘normal’.

❌Additionally, TE’s restrict pleasures (the rewards) from those who won’t cooperate w/ therapy
- means those patients who are very ill and may not be cognitively able to take part in the
token economy
- will be unable to gain access to rewards; may make them even more distressed than
they are already making
- Means benefits of token economies may be outweighed ethical concerns about impact
on personal freedoms + short term distress
Interactionist approach

diathesis stress model

- argues SZ to be result of genetic vulnerability (diathesis) and environmental trigger

(stresser).

Meehl’s Diathesis stress model

- Diathesis for SZ is entirely genetic.

- Genes are assumed to cause neurochemical abnormalities that in turn, result in an
increased risk for schizophrenia
- If person doesn’t have the genetic vulnerability, no amount of stress would give SZ .

Stressers

- negative psychological experience e.g. dysfunctional parents and stressful life events
- Chronic stress in someone who carries the genetic vulnerability could result in SZ.

Modern understanding:

- believed that diathesis is not caused by 1 single gene

- Stress includes anything that risks triggering schizophrenia

Modern Understanding:

Read et al (2001)

- theory that early trauma actually could alter the brain’s development,
- E.g the development of hypothalamic-pituitary-adrenal system can be made overactive
by childhood trauma rendering individual much more vulnerable to stress later in life

recently Houston et al (2008) changed definition of stress to include anything (both physical and
psychological) that can increase the risk of triggering schizophrenia.
 - cannabis works by interacting with the dopamine system; has been identified as a
potential stressor increasing risk of developing SZ up to 7 times.

The interactionist model acknowledges biological + psychological factors in SZ, associated with
combining antipsychotic medication and psychological therapies (most commonly CBT).

Turkinson suggests that adopting interactionist viewpoints, makes it possible to believe in

biological causes as well as utilise CBT to alleviate symptoms.

- It’s a common approach in the UK with most patients being provided a combination of
both medication and therapies (mostly CBT).

✅support for dual role of vulnerability and stress

- Tienari (2004) studied children adopted away from mothers who had SZ
- Adoptive parents style of parenting assessed and compared with control group of
adoptees w/ no diathesis
- Child-rearing style w/ high criticism and conflict w/ low empathy was implicated in SZ
development only with kids who had high predisposition

❌Diathesis-stress model is over simplistic

- Multiple genes increase vulnerability, no specific SZ gene
- Researchers also believe stress can be biological
- E.g Houston found; childhood sexual trauma was diathesis and cannabis use was a
trigger
- Multiple factors affecting diathesis (bio, psycho)

✅Real world application;

- Tarrier ‘04 random allocation of 315 ppts
- 1: medication+CBT 2: meds + counselling group 3: control group (meds only)
- Participants in 2 combo groups showed lower symptoms
- Clear practical advantage to adopting interactionist approach

❌Jarvis 2019
- Says this argument is same as treatment causation fallacy
- We can’t automatically assume that success of combo therapies means interactionist
exp are correct
✅Urbanisation:
- SZ is more commonly diagnosed in urban areas, supporting interactionist position

❌However SZ may be more noticed in cities or people with diathesis for SZ may move to cities
- Overall, the greater chances of diagnosis in cities is not a strong support for the
interactionist position