Schizophrenia

Positive symptoms:

• Hallucinations: can be presented via any of the senses; often auditory
• Delusions: unreal beliefs; includes grandiose delusions (feelings of grandeur)
  
• Disordered thinking: jumping between topics without logical flow
• Echopraxia: copying movements of those around them; a form of catatonic behaviour

Negative symptoms:

• Alogia: poverty of speech
• Avolition: unwilling to take part in events around them; disinterested in things they used to enjoy
• Anhedonia: no longer react to things appropriately that they used to enjoy
• Flatness of effect: appear to have no emotions; speech is monotone, no facial expressions
• Catatonic behaviour: behaviour varies from no movement at all to rapid, repetitive movements that serve no purpose; may have waxy flexibility which means others could move their limbs for them but they remain rigid

• Poor reliability. Cheniaux had two psychiatrists separately diagnosed 100 patients using both DSM and ICD criteria. One got 26 using DSM and 44 using ICD, the other got 13 using DSM and 24 using ICD. Poor inter-rater reliability.
• Poor validity. From Cheniaux's study, scz is more likely to be diagnosed using ICD than DSM. This means it is either overdiagnosed with ICD or underdiagnosed with DSM. Criterion validity (i.e. if systems arrive at the same diagnosis) is low.
• Co-morbidity. Buckley et al. studied scz patients and found that 50% have depression and 23% have OCD, along with other problems as well. Causes problems in scz diagnosis because some conditions may look similar, so maybe they are the same condition.
• Symptom overlap. Both scz and bipolar disorder include positive symptoms such as delusions and negative symptoms such as avolition. May be diagnosed with scz under ICD and bipolar disorder under DSM. Suggests they may be the same condition.
• Gender bias. Longennecker et al. found that since the '80's men are more likely to be diagnosed with scz than women. May be because women can function better.
• Culture bias. African-Americans and English Afro-Caribbean people more likely to be diagnosed, but in some African cultures it is normal to hear voices. As psychiatrists are mostly white this creates culture bias.

• As genetic similarity increases, so does the chance of developing schizophrenia
• 20% chance if one parent is schizophrenic, 50% for both parents
• Twin studies often used to support genetic theory
• Gottesman -  where one twin has scz, there was a 17% risk of developing scz for dizygotic twins and 48% risk for monozygotic twins (1% for general pop.)
• No one gene blamed for scz, it is likely polygenic (requires a number of factors together)

Limitations:

• Twin studies never have a 100% concordance rate for MZ twins so it cannot be solely genetic
• Tienari - studied adopted children who had biological schizophrenic mothers. Found that a child-rearing style with high levels of criticism and low empathy were imlicated in the development of scz for those with a genetic risk only. Suggests there is a genetic component, but an environmental trigger is also needed (diathesis-stress model).
• Biological reductionism. Other factors such as environment are also involved, not just genetics. Also deterministic as people have no control over their genes; suggests they will inevitably develop scz which is not necessarily true.

• Dopamine hypothesis argues that neurotransmitters, especially dopamine, work differently for people with scz
• Hyperdopaminergia in the subcortex - excess dopamine receptors in the Broca's area may be associated with poverty of speech and/or auditory hallucinations
• Hypodopaminergia in the cortex - low levels of dopamine in the prefrontal cortex associated with the negative symptoms of schizophrenia, e.g. avolition (Goldman-Rakic et al.)

Strengths:

• Research has shown that drugs which increase levels of dopamine (e.g. amphetamines) produce psychotic (scz) symptoms. Link between excess dopamine and scz symptoms, can develop treatment from this.
• Led to successful treatment. Antipsychotic drugs reduce scz symptoms by blocking dopamine. Suggests correlation between dopamine and scz. However - only a short-term solution, so dopamine may not be the root cause of scz.

Limitations:

• High levels of dopamine may be a symptom of scz, so not a cause at all
• As low levels of dopamine have been linked to negative symptoms, the dopamine hypothesis can become confusing. Both high and low DA levels cause problems in different areas of the brain, which suggests they may not even be symptoms of the same illness.

• Neural correlates - patterns/structures in brain activity that occur in conjunction with schizophrenia
• Negative symptoms - Juckel et al. found lower levels of activity in the vental striatum in people with schizophrenia than in controls.
  • Avolition is the loss of motivation. Motivation involves anticipation of a reward. Certain regions of the brain, such as the ventral striatum, are believed to be involved in this anticipation.
• Positive symptoms - Allen et al. scanned the brains of patients with auditory hallucinations and compared them to controls whilst they identified recorded speech as their own or others'. Found lower activation levels in the superior temporal gyrus and the anterior cingulate gyrus were found in the hallucination group. Hallucination group also made more errors.
  • Reduced activity in these areas is a neural correlate of auditory hallucinations. Negative correlation - as activation reduced, positive symptoms increased.

Strengths:

• Biological explanations have led to effective treatments which also has an effect on the economy as fewer people are in institutions and more people with scz can return to work.
• Ethical, as the patients or their families are not blamed.

Limitations:

• Only a correlation, not causation. Abnormalities may be caused by scz, not the other way around. Neural correlates may not provide much information about what actually causes scz.
• Deterministic, suggests people have no control over their illness
• Reductionist. Diathesis-stress model considers the environmental as well as the biological factors involved in scz, which is a more complete explanation.

• Typical antipsychotics (e.g. chlorpromazine) are dopamine antagonists - they bind to and block dopamine receptors without stimulating them, reducing the action of dopamine
• Initially dop. levels build up but then production is reduced
• This normalises neurotransmission levels by reducing stimulation of the dop. system, reducing positive symptoms such as hallucinations

• Atypical antipsychotics (e.g. clozapine) are also dopamine antagonists
• Only temporarily occupy the receptors and then rapidly dissociate to allow normal transmission
• Thought to be responsible for fewer side-effects
• Act on other neurotransmitters as well, particularly serotonin
• Addresses negative symptoms such as avolition as well as positive symptoms

Strengths:

• Tihonen et al. - 37-fold increase in suicide when scz patients stopped taking medication. NCISH reported 346 homicides in England between 2003-2013 by people with scz history; 29% of those had stopped taking medication.
• Social and economic implications. Lawrie claimed that antipsychotics have led to a social revolution that allows people with scz to live normally and not end up hospitalised at great cost. Also led to a reduction in violence (to self and others).

Limitations:

• Side-effects. Typical anti-psychotics have serious side-effects such as tardive dyskenesia. Atypicals have fewer side-effects because of how they work but they still have some such as agranulocytosis.
• Drugs may be administered without consent. Szasz called them chemical straitjackets and a form of social control. Ethical dilemma, as people may be dangerous if not medicated. Question of whether drugs are given to reduce suffering or to increase complicance in the hospital.

• Fromm-Reichmann - based on accounts of her patients, she described a parent (mother) who caused their scz
• Mothers of people with scz were overprotecting and controlling, while at the same time being distant and rejecting
• Causes an emotional disturbance in the person, who develops a distrust that can become paranoid delusions which can lead to schizophrenia

Evaluation:

• Kasanin - hospital records showed that 33/45 patients had evidence of maternal overprotection
  • However - that means almost 1/3 didn't; lacking in objectivity as he wasn't blind to the hyp.
• Methodological weaknesses. Methods used to assess the mothers' personality for 'crazy-making' characteristics has been criticised by modern psychologists such as Harrington. Internal validity questionable.
• Parent blaming.  Parents given the responsibility of caring for the child as well as blaming them for causing the problem.The popularity of all family dysfunction theories decreased in popularity at the same time as the increase in community care.

• Bateson - symptoms of scz caused by communication issues between parent and child
• Conflicting messages are a risk factor - child starts to see the world in terms of contradictory messages and cannot distinguish between the contradictions because they have internalised the double bind situation
• Can cause delusions and hallucinations to try and escape the demands of the DB situation

Evaluation:

• Liem - during structured tasks, communication between families of boys with scz was no more disordered than that of control families. Suggests that families with scz members adapt their communication to help them deal with the child. Effect, not cause.
• Koopmans - occassional DB may have started as a result of family disruption, but there is little empirical evidence to support this. May be a symptom of pathology in the parent, which is a greater causal factor than poor communication.

• Brown - studied 156 men discharged from hospital and prescribed antipsychotics
• Found that those who went to live with wives or mothers were more likely to relapse than those living with siblings or in lodgings
• Interviewed the wives/mothers, found a link between the amount of expressed emotion and chances of relapse
• EE characteristics - expression of critical comments, hostility, emotional over-involvement, lack of warmth and positive regard

Evaluation:

• Vaugn and Leff - 53% of individuals with high EE relatives relapsed within 9 months compared to 12% of those with low EE relatives.
• McCreadie and Phillips - failed to find higher relapse rates between 6-12 months. Suggests EE relatives may be a factor, but not the only factor.

• Diathesis-stress model - this type of family relationship may trigger those who are genetically predisposed to develop scz.

• Scz characterised by disruption to normal throught processes
• Frith - identified two types of dysfunctional thought processes in his 'compromised theory of mind'
  • Metarepresentation - recognising one's thoughts as one's own. When dysfunctional, can lead to symptoms including hallucinations and delusions.
  • Dysfunctional Central Control - cannot suppress automatic responses and perform deliberate actions instead. Leads to disorganised speech and throughts as talking triggers too many associations which cannot be overcome.

Evaluation:

• Stirling - Patients with scz took twice as long to name the colour of the words in the Stroop test compared to controls
• Can't explain all symptoms as they are not all cognitive, e.g. catatonic behaviour
• Ethical, as CBT suggests they can change their faulty thoughts - some level of free will
• Explains a proximal, but not ultimate cause. May just be a symptom of scz and not a cause.

Key assumption of CBT is that people's distorted thoughts affect their behaviour in maladaptive ways. In scz treatment, patients learn to change these thoughts to decrease symptoms such as delusions. The stages followed are:

• Assessment - patient expresses their thoughts and experiences. Realistic goals are dicussed, using the patiet's current distress as motivation for change
• Engagement - therapist empathises with patient's feelings
• ABC model - patient explains the activating events (A) that appear to cause their emotional and behavioural (B) consequences (C). Patient's beliefs, which are the actual cause of C, can then be rationalised and changed.
• Normalisation - telling patient that they are not alone in experiencing these symptoms
• Critical collaborative analysis - therapist uses gentle questioning to help the patient understand illogical deductions and conclusions
• Developing alternative explanations - patient develops healthier explanations for their previous unhealthy assumptions, with the help of the therapist.

Strengths:

• Gould et al. - meta analysis, all 7 studies reported a statistically significant decrease in positive symptoms post-treatment. Suggests there is a need to address psychological abnormalities as well as neurotransmitters, but may be due to placebo effect.
• CBT and medication meant fewer hallucinations and delusions, 25-50% reduction in recovery time (Drury), lower dropout rates and greater patient satisfaction (Kuipers et al.) Difficult to separate effects of CBT and medication.

Limitations:

• Subject attrition. May lead to a biased sample, as patients with more severe scz may be more likely to drop out. Results may then show CBT to be more effective than it really is.
• Not suitable for all patients. Kingdon and Kirschen studied 142 patients, found that many were deemed unsuitable for CBT as they could not engage with it, older patients particularly. CBT should in theory be applicable to everyone because they all suffer with maladaptive thoughts.

• Form therapeutic alliance with all family members
• Reduce stress of caring for relative with scz
• Improve families' ability to predict and solve problems
• Reduce anger and guilt of family members
• Improve families' attitude towards scz

Evaluation:

• Economic implications. NICE review suggested family therapy associated with cost savings when offered to patients alongside standard care by decreasing relapse hospitalisation.
• Lobban et al. - 60% of studies reported positive impact on relatives, e.g. relationship quality.
• Pharoah et al. - meta-analysis, lower relapse rates and improvement in social functioning. Authors suggested family therapy actually just increased medication compliance.
• Methodological issues with research. Many of the studies in Pharoah et al's study were from China, which stated that random allocation had been used but it was not.
• Garety et al. - no difference between patients who had family therapy and patients who just had carers. Carers expressed low EE, so good standard care had the same effect on relapse.

• Tokens given immediately for desirable behaviour, e.g. dressing, making their bed
• Act as secondary reinforcer, exchanged for primary reinforcers, e.g. walk outside the hospital
• Patient learns to engage with socially desirable behaviour which will improve their quality of life when they return home

Evaluation:

• McGonagle and Sultana - only found 3 studies that used random allocation, only 1 of these showed improvement in symptoms and none provided useful data on changes to behaviour. Unreliable evidence for the effectiveness of token economy.
• May not be appropriate because it is based on the assumption that the undesirable behaviours are due to institutionalisation, not symptoms of scz. Will only be successful with people who have milder symptoms.
• Ethical concerns. Can be seen as a form of discrimination as their symptoms may prevent them from complying to the expected desirable behaviours. Complaints from family members means it is rarely used in hospitals, so it has limited application.