Schizophrenia

No single defining characteristic - SZ is a collection of unrelated symptoms 

2 classification systems:

• 1. DSM 5 - one positive system must be present for diagnosis
• 2. ICD 10 - two or more negative symptoms are sufficient for diagnosis 

ICD 10 recognises subtypes of SZ:

• 1. paranoid SZ: powerful positive symptoms
• 2. hebephrenic SZ: primarily negative symptoms
• 3. catatonic SZ: disturbance of movement; sufferer immobile or overactive

Positive symptoms = additional experiences beyond those of ordinary existence

• 1. Hallucinations: sensory experiences - some relative to the environment whereas others hold no relationship eg. criticising voices heard by the sufferer - can distort any sense
• 2. Delusions: irrational beliefs - believing they are someone else or their body is under external control - behave in a way that makes sense to them, but is bizarre to others
• (3. Speech disorganiation) 

Negative symptoms = loss of usual abilities and experiences

• 1. Avolition: severe loss of motivation to carry out everyday tasks - results in lowered activity levels and unwillingness to carry out goal-directed behaviours
• 2. Speech poverty: a redution in the amount and quality of speech - may include a delay in verbal responses during conversation 
  • ICD 10 recognises this as a negative symptom bcos emphasis on reduction in the amount of speech
  • DSM recognises as positive symptom bcos places emphasis on speech disorganisation 

1. Reliability: the extent to which the diagnosis of SZ is consistent

2. Validity: the extent to which the diagnosis and classification techniques measure what they are designed to measure, in this case to measure SZ

3. Co-morbidity: occurence of two illnesses together which confuses diagnosis and treatment

4. Symptom overlap: when two or more conditions share symptoms , questioning the validity of the classification

low reliability - Cheniaux had 2 psychiatrists idependently diagnose 100 patients using both DSM and ICD criteria and found inter-rater relibility was poor:

• 1st psychiatrist diagnosed 26 using DSM, and 44 using ICD
• 2nd psychiatrist diagnosed 13 using DSM and 24 using ICD

this inconsistency between mental health professionals and the different classification systems is a limitations of the diagnosis

poor validity - in Cheniaux's study, SZ is much more likely to be diagnosed using ICD than DSM - suggests SZ is either over-diagnosed in ICD or under-diagnosed in DSM = poor validity

co-morbidity - 2 or more conditions occur together - Buckley et al concluded that half patients with SZ also have depression - possibly that they could be the same condition

gender bias - Longenecker reviewed studies of SZ and concluded that men have been diagnosed with SZ more than women - Cotton et al found female patients typically function better than men which may explain why women escape diagnosis, possibly causing under-diagnosis - problem bcos men n women with similar symptoms may have differing diagnosis

SZ runs in families: 

• strong relationship between genetic similarity of family members and likelihood of both developing SZ

Gottesman (1991) family study:

• MZ twins (shared genes = 100%) have a 48% shared risk of SZ
• DZ twins (shared genes = 50%) have a shared risk of 17%
• Grandchildren (shared genes = 25%) have a shared risk of 5%
• First cousins (shared genes = 12.5%) have a shared risk of 2%

Existence of candidate genes suggests the following:

• 1. each individual gene confers a small increased risk of SZ = SZ is polygenic
• 2. different combinations can lead to SZ = SZ is aetiologically heterogenous

Ripke et al (2014) studied 37,000 patients and found 108 separate genetic variations associated with increased risk; many coded for the dopamine neurotransmitter

Role of dopamine - DA is widely believed to be associated with SZ because it is featured in the functioning of brain systems related to the symptoms of SZ

Hyperdopaminergia: linked to subcortex - high dopamine activity in subcortex (central areas of the brain) associated with hallucinations and speech poverty (eg. excess of dopamine receptors in the Broca's area)

Hypodopaminergia: linked to prefrontal cortex - more recent versions of the hypothesis have focused on low levels of dopamine in the prefrontal cortex (responsible for thinking and decision making)

• limitation - mixed support for the dopamine hypothesis:
• Dopamine antagonists (eg. amphetamines) that increase dopamine can induce schizophrenic-like symptoms in people without SZ - antipsychotic drugs can be effective in reducing symptoms
• However, some of the candidate genes identified code for the production of other neurotransmitters such as glutamate
• This suggests that dopamine cannot provide a complete explanation for SZ and that it is just one important factor

brain activity linked with symptoms - neural correlates are measurements of the structure or function of the brain that correlate with the positive or negative symptoms of SZ

• avolition + ventral striatum - ventral striatum is involved in anticipation of reward (related to motivation) - loss of motivation (avolition) in SZ may be explained by low activity levels here
• Juckel et al (2006) found a negative correlation between ventral striatum activity and overall negative symptoms

Hallucinations + superior temporal gyrus - Allen et al (2007) found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus

• 1. Schizophrenic mothers = rejecting and controlling
• Fromm-Reichmann's (1948) psychodynamic explanation based on patients early experiences of 'schizophrenic mothers' (mothers who cause SZ)
• These mothers are cold, rejecting and controlling, and create a family climate of tension and secrecy - leads to distrust and paranoid delusions and SZ

• 2. Double-bind theory = conflicting family communication
• Bateson et al (1972) described how a child may be regularly trapped in situations where they fear doing the wrong thing, and recieve conflicting messages about what is wrong
• they cannot express their feelings about the unfairness of the situation
• when they 'get it wrong' the child is often punished by withdrawal of love - they learn the world is confusing and dangerous leading to disorganised thinking and delusions

• 3. Expressed emotion = criticism and hostility lead to relapse
• EE is the level of (negative) emotion expressed towards the SZ patient and includes:
  • Verbal criticism of the patient
  • Hostility towards the patient
  • Emotional over-involvement in their life
• High levels of EE cause stress in the patient, a primary explanation for relapse

limitation - Read et al reviewed 42 studies and concluded that 69% of all female, adult patients with SZ and 59% of men had a history of physical and/or sexual abuse

most of this evidence is based on info about childhood experiences gathered after the diagnosis - symptoms may have distorted the patients recall of their childhood experiences - questions validity of evidence

limitation - poor childhood experiences may be associated with SZ, but there is little evidence to support the importance of SZ mothers, EE or double bind - these theories are mainly based on clinical observation of patients (open to interpretation) + also historically led to blaming patients already suffering over their child's symptoms - undermines credibility of family explanations

• 1. Dysfunctional thought processing
• low levels of information processing in some areas of the brain suggest cognition is impaired
• eg. reduced progressing in the ventral striatum is associated with negative symptoms

• 2. Metarepresentation leads to hallucinations
• metarepresentation is the cognitive ability to reflect on thoughts and behaviour (Frith et al)
• this dysfuntion disrupts our ability to recognise our thoughts as our own 
• leads to hallucinations (hearing voices) + delusions (thoughts placed in mind by others)

• 3. Dysfunction of central control leads to speech poverty
• dysfunction of central control (the cognitive ability to suppress automatic responses while performing deliberate actions) as a way to explain speech poverty (Frith et al)
• People with SZ experience derailment of thoughts and spoken sentences bcos each word triggers automatic associations that they cannot suppress

Strength - Stirling et al compared 30 patients with SZ with control group of 18 non-patients on cognitive tasks, eg. Stroop test (naming ink colour of colour words)

Patients took twice as long as the control group to suppress the impulse to read the word and to read the ink colour instead - supports Frith's theory of central control dysfunction - other evidence also shows that processing differs in SZ patients

However, it is not clear whether these faulty cognitions are merely the proximal cause (ie. cause of the symptoms) or the underlying distal cause (ie. the origins of the disorder)

Limitation - unclear whether cog factors are a cause or result of neural correlates + abnormal neurotransmitter levels in SZ, eg. does dysfunctional metarepresentation reduce or increase levels of dopamine in the temporal gyrus - questions validity of cog approach in explaining SZ

• typical antipsychotics (eg. chlorpromazine) work by acting as antagonists in the dopamine system - reduce the action of dopamine by blocking dopamine receptors in the synapses in the brain
• 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
• Chlorpromazine also has an effect on histamine receptors which appears to lead to a sedation effect - also used to calm anxious patients when they are first admitted to hospital

• eg. Clozapine, introduced later than typical antipsychotics
• The aim of these drugs was to improve effectiveness of drugs in suppressing psychoses such as SZ and also minimise these effects
• Clozapine binds to dopamine receptors the same as chlorpromazine does but also acts on serotonin and glutamate receptors
• This drug was more effective than typical antipsychotics - clozapine redces depression and anxiety in patients as well as improving cognitive functioning
• also improves mood - important as up to 50% of people suffering from SZ attempt suicide

• Risperidone was developed bcos clozapine was involved in deaths of some patients from a blood condition called agranulocytosis
• like clozapine, binds to dopamine and serotonin receptors - binds more strongly to dopamine receptors and is therefore more effective in smaller doses than most antipsychotics and has fewer side effects

aims: help patients identify irrational thoughts and try to change them

may involve discussion of how likely a patients beliefs are to be true, and consideration of less threatening possibilities 

CBT helps patients to understand their symptoms (delusions and hallucinations) and how these impact their feelings - offering explanations for these symptoms reduces anxiety and helps the patient realise their beliefs are not based on reality

• includes the family rather than individual patients
• aims: to improve communication and interaction in the family
• therapists try to reduce stress within the family that may contribute to patients risk of relapse (reduces levels of EE)

Pharaoh et al (2010) identified a range of strategies family therapists use to reduce the likelihood of relapse and readmission to hospital:

• 1. reduce stress of caring for a relative with SZ
• 2. improve ability of family to anticipate and solve problems
• 3. reduce guilt and anger in family members
• 4. improve beliefs about and behaviour toward SZ

Token economies are reward systems (operant conditioning) used to manage the behaviour of patients with SZ who spend long periods in psychiatric hospitals

Tokens: 

• (eg. coloured discs) are given to patients who carry out desirable behaviours (eg. getting dressed, making a bed, etc)
• reinforces desriable behaviour and bcos it is given immediately, prevents 'delay discounting'
• Hold no value in themselves, but can be exchanged later for a tangible reward, eg. sweets
• secondary reinforcers bcos they only have value due to the learned associations (classical conditioning) with innate primary reinforcers

vulnerability + trigger = SZ - both a vulnerability and a stress trigger are needed to develop SZ

Meehl's model (old understanding): gene + stress = SZ

• diathesis was entirely the result of a single 'schizogene' - Meehl argued that someone without the gene would never develop SZ, no matter how much stress they are exposed to
• But a person who does have the gene is vulnerable to the effects of chronic stress eg. schizophrenogenic mother ie. the schizogene is necessary but not sufficient for the development of SZ

Modern understanding:

• not down to a single 'schizogene', but that many genes increase vulnerability
• diathesis doesnt have to be genetic, could be early psychological trauma affecting brain development, eg. child abuse affects the HPA system, making child vulnerable to stress
• modern definition of stress = anything that risks triggering SZ, eg. cannabis can increase risk of SZ up to 7x depending on dose - probably bcos interferes with the dopamine system

Antipsychotic medicine and CBT:

• Turkington et al (2006) suggest it is possible to believe in biological causes of SZ and still practise CBT to relieve psychological symptoms
• This requires adopting an interactionist model - not possible to adopt a purely biological approach and then use CBT treatment