Schizophrenia 1 Diagnosis and Classification of Schizophrenia Outline

Schizophrenia

[1] Diagnosis and Classification of Schizophrenia Outline: Classification – schizophrenia is a collection of seemingly unrelated symptoms. There are 2 classifications: • DSM-5: one positive symptom • ICD-10: two or more negative symptoms Positive symptoms of schizophrenia are additional experiences beyond those of ordinary existence, such as: • Hallucinations: sensory experiences that have no basis in • reality or are distorted perceptions of real things e. g. hearing voices or seeing people that aren’t there Delusions: Beliefs that have no basis in reality that make sufferers behave in bizarre ways e. g. being an important person or a victim of conspiracy Outline: Negative symptoms of schizophrenia are the loss of usual abilities and experiences, such as: • Avolition: severe loss of motivation to carry out everyday • There are 4 key issues with classifying schizophrenia: 1. Reliability: extent to which diagnosis is consistent 2. Validity: extent to which classification techniques measure 3. 4. Eval 2: Diagnosis of schizophrenia has low validity – on way of testing validity is criterion validity which tests whether different assessments arrive at the same diagnosis for the same patient. Cheniaux et al’s study shows that schizophrenia is more likely to be diagnosed using ICD than DSM. This shows that it is either over diagnosed using ICD or underdiagnosed using DSM. Either way, it has low validity. tasks. Unwillingness to carry out goal-related behaviours Speech Poverty: reduced amount and quality of speech. May include delay in verbal responses during convo. DSM emphasises speech disorganisation and incoherence. Eval 1: Diagnosis of Schizophrenia has low reliability – Cheniaux et al: had two psychiatrists diagnose 100 patients using both DSM and ICD. Inter -rater reliability was poor. One psychiatrist diagnosed 26 patients using DSM and 44 using ICD. The second diagnosed 13 with DSM and 24 with ICD. This is a limitation as it shows that the classification of schizophrenia is inconsistent. what they are designed to measure Co-morbidity: occurrence of two illnesses together which confuse diagnosis and treatment Symptom overlap: when two or more conditions share symptoms, questioning the validity of the classification Eval 3: Diagnosis of schizophrenia suffers from co-morbidity – co-morbidity is when two or more conditions occur together a lot of times. This raises the question whether they are actually a single condition. Buckley et al: found that half of the patients that were diagnosed with schizophrenia also had a diagnosis of depression (50%) or substance abuse (47%). If severe depression looks like schizophrenia or vice versa, it may cause confusion. Eval 4: Gender bias in the diagnosis of schizophrenia – Longenecker: reviewed studies on schizophrenia and found that since 1980 s men have been diagnosed more than women. Cotton et al: found that female patients typically function better than men. This is because women are better able to avoid diagnosis because that have better interpersonal functioning so can hide their symptoms. Therefore, men and women suffering the same symptoms may experience different diagnoses. Extra Evaluation Point: Cultural bias in the diagnosis of schizophrenia – African-Americans and English people of African origin are more likely to be diagnosed in the UK. However rates in the West Indies and Africa are not so high, so it is not due to genetics. Instead it is because hearing voices of ancestors is normal in African cultures, but is seen as a positive symptom (hallucination) of schizophrenia in the UK. This shows that people from certain cultures are more likely to be diagnosed than others.

[2] Biological Explanations for Schizophrenia Outline: The biological explanation state that schizophrenia has a genetic basis so runs in the family. Gottesman: found that MZ twins have a 48% shared risk of schizophrenia, DZ twins have a 17% risk and siblings have a 9% risk. Schizophrenia is polygenic which means that each individual gene only increases the risk of it a little bit. Schizophrenia is also aetiologically heterogenous which means that different combination lead to it in different people. Ripke: studied 37 k patients and found 108 separate genetic variations that increase the risk. Dopamine hypothesis: Dopamine is widely believed to be involved in schizophrenia, because it appears in functions linked to symptoms. High dopamine activity (hyperdopaminergia) in subcortex is associated with hallucinations and poverty of speech. Eval 2: There is mixed support for the dopamine hypothesis – Drugs that increase dopamine levels can cause schizophrenia symptoms in people that don’t have it. Antipsychotic drugs that lower dopamine levels can reduce those symptoms. However, some of the candidate genes identified code for the production of other neurotransmitters such as glutamate. This shows that dopamine can’t provide a complete explanation for schizophrenia and is only one factor. Outline: More recent versions of the dopamine hypothesis Eval 1: Strong evidence for genetic focus on low levels of dopamine (hypodopaminergia) in the vulnerability to schizophrenia – Gottesman’s prefrontal cortex which is responsible for decision-making. Neural Correlates: are measurements of the structure or function of the brain that correlate with the positive or negative symptom of schizophrenia. The ventral striatum is involved in the anticipation of reward. Avolition may be explained by low activity levels here. Juckel: found a negative correlation between ventral striatum activity and negative symptoms. Allen et al: found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus. Eval 3: Correlation-causation problems – whether unusual activity in the brain causes the symptoms or whethere are other possible explanations are yet to be answered. A negative correlation between the ventral striatum and avolition doesn’t mean that low activity in the ventral striatum causes avolition. It could be that avolition causes low activity in the ventral striatum. Neural correlates exist but tell us little about the causes of schizophrenia. family study shows that genetic similarity and the risk of schizophrenia is closely related. Tienari et al: Adoption studies also show that children of people with schizophrenia have an increased risk of developing it even if they are adopted by a healthy family. Overwhelming evidence shows that genetic factors make some people more vulnerable to developing schizophrenia. Eval 4: The role of mutation supports genetic explanation – schizophrenia can take place in the absence of family history of the disorder e. g. through mutation in paternal DNA through radiation. Brown et al: found a link between paternal age (older has higher risk of mutation) and risk of schizophrenia (0. 7% in fathers under 25 to 2% in fathers over 50). This shows that genetic factors are important. Extra Evaluation Point: It is clear that environment is also involved – the probability of developing schizophrenia, even if your twin is identical, is less than 50%. This means that environmental factors (e. g. family functioning during childhood) can also play a role in the development of schizophrenia. This suggests that schizophrenia may be the result of a combination of both biological and psychological processes.

[3] Psychological Explanations for Schizophrenia Outline: Family Dysfunction – Schizophrenogenic Mothers: Fromm-Reichmann’s psychodynamic explanation based on early experiences with schizophrenogenic mothers. These mothers were cold, rejecting, controlling and created a family climate of tension and secrecy. This leads to paranoid delusions. Double-blind theory: Bateson et al described how children fear doing the wrong thing and receive mixed signals as to whether something is wrong. If they do ‘get it wrong’, they are punished by withdrawal of love and view the world as a confusing place which leads to disorganised thinking and delusions. Expressed Emotion (EE): is the level of emotion expressed towards the patient: • Verbal Criticism • Hostility towards patient • Emotional over-involvement in their life High levels of EE cause stress in patient and leads to relapse. Eval 2: Evidence for family-based explanation is weak – although poor childhood experiences may be associated with schizophrenia, there is little evidence supporting the importance of schizophrenogenic mothers, expressed emotion or double-blind. These theories are based on clinical observations which are open to interpretation and often lead to blaming parent for their child’s symptoms. This undermines the credibility of the family-based explanation. Outline: Cognitive Explanations – Dysfunctional Thought Processing: low levels of info processing in some areas of the brain suggest an impairment in cognition e. g. low activity in ventral striatum is linked to negative symptoms. Metarepresentation: is the cognitive ability to reflect on thoughts and behaviour. A dysfunction disrupts our ability to recognise our thoughts as our own, which could lead to us hearing voices (hallucinations). Dysfunction of Central Control: Frith et al – central control is the cognitive ability to suppress automatic responses while performing deliberate actions. Patients experience derailment of speech as they can’t supress associations triggered by speech. Eval 3: Support for different information processing – Stirling et al: compared 30 patients with 18 non-patients (control) on cognitive tasks (Stroop Test). Patients took twice as long as the control group to supress the impulse, read the word and name the ink colour. This supports Frith’s dysfunction of central control theory. However, it is still unclear whether faulty cognitions are the cause of symptoms or the origins of the disorder. Eval 1: Evidence from family relationships is often retrospective – Read et al: reviewed 46 studies and concluded that 69% of all adult female patients with schizophrenia (59% of men) had a history of physical and/or sexual abuse. However, info gathered was based on childhood experiences recalled after the diagnosis. Symptoms may have distorted recall of childhood experience. This creates a problem with the validity of the evidence. Eval 4: Biological factors are sometimes overlooked – the biological explanation and the psychological explanations are hard to reconcile together. The question is how do they both fit in together? Perhaps they can separately produce same symptoms, however this raises the question of whether both outcomes are actually schizophrenia. We can view this in terms of the diathesis-stress model which states that the diathesis can be psychological or biological. Extra Evaluation Point: Direction of causality – it still remains unclear whether cognitive factors are a cause or result of neural correlates or abnormal neurotransmitter levels in schizophrenia. For example, we don’t know whether dysfunctional metarepresentation reduces dopamine in the superior temporal gyrus or the other way around. This questions the validity of the cognitive approach in explaining the origins of the condition.

[4] Biological Therapies for Schizophrenia: Drug Therapy Outline: Typical Antipsychotics – such as chlorpromazine have been around since the 1950 s. They are dopamine antagonists as they reduce the level of dopamine. They are based on the dopamine hypothesis. They work by blocking dopamine receptors in the synapses in the brain. When taking chlorpromazine, dopamine level initially rises but then reduces. This normalises neurotransmission in the brain which reduces symptoms such as hallucinations. Chlorpromazine also has an effect on histamine receptors which cause a sedative effect. It is used to calm patients when they are first admitted. Eval 2: Antipsychotics have side effects – Typical antipsychotics are associated with dizziness, agitation, sleeplessness, weight gain etc. long term use can lead to lip smacking and grimacing. The most serious side effect is neuroleptic malignant syndrome (NMS) which is when dopamine activity is blocked in the hypothalamus which disrupts several body systems. Atypical antipsychotics were developed to reduce side effects, but some still exist which may cause patient to avoid antipsychotics as a treatment. Outline: Atypical Antipsychotics – such as Clozapine have been used since the 1970 s. The aim of them was to improve effectiveness of supressing psychoses and reduce side affects. They target a range of neurotransmitters including dopamine and serotonin. Clozapine binds to dopamine, serotonin and glutamate receptors. They are more effective than typical antipsychotics as they reduce depression and anxiety as well as improving cognitive functions. It also improves mood which is important (50% of sufferers commit suicide). Risperidone was developed as Clozapine was involved in many deaths due to agranulocytosis. Risperidone binds to serotonin and dopamine receptors. It binds more strongly to dopamine receptors so is more effective at smaller doses and has fewer side effects. Eval 3: Theoretical objection to the use of antipsychotics – antipsychotics are based on the dopamine hypothesis and the idea that high dopamine activity in the subcortex causes symptoms. However, the modern version states that low levels of dopamine in the prefrontal cortex is linked to symptoms which means that antipsychotics shouldn’t work. This raises the question about whether antipsychotics are the cause of positive effects. Eval 1: Evidence shows antipsychotics are moderately effective – Thornley et al: reviewed data from 13 trials (1, 121 participants) and found that Chlorpromazine was associated with better functioning and reduced symptom severity than a placebo. Meltzer et al: concluded that clozapine is more effective than typical antipsychotics and is 30 -50% more effective in treatment-resistant cases. This evidence shows that psychotics are effective. Eval 4: Doubts about the true effectiveness of antipsychotics – Healy et al: suggests that data from successful trials have been published multiple times which exaggerates the positive effects. Moreover, most studies show short-term effects only. Antipsychotics have a sedative effect, so seem as though they have a positive effect, but that doesn’t mean that it is effective at reducing psychosis. This shows that the effectiveness of psychotics may be overestimated by research. Extra Evaluation Point: Antipsychotic drugs my simply be a ‘chemical cosh’ – antipsychotics may be used in hospitals to calm patients down to make them easier to deal with rather than to benefit them. Short-term use of antipsychotics to calm patients is recommended by the National Institute for Health and Care Excellence (NICE). However, this is seen by some as humans rights abuse and raises ethical issues in the use of antipsychotics.

[5] Psychological Therapies for Schizophrenia Outline: Cognitive Behaviour Therapy (CBT) – general aims are to identify irrational thoughts and challenge them e. g. by considering less threatening possibilities. CBT helps patients understand their symptoms e. g. how delusions/hallucinations can affect their feelings and behaviour. Explaining these may reduce anxiety as patients know they aren’t based on reality. Family Therapy – aims to reduce EE in family. It involves the family rather than the individual. It attempts to improve communication and interaction within the family. Therapists try to reduce stress that may cause a relapse. Eval 2: Therapies may help but not cure – CBT helps patients make sense of their symptoms. Family therapy reduces the stress of living with the condition. Token economies help make patients’ behaviour more socially acceptable. Although these are worth doing, they don’t cure schizophrenia. Biological therapies also don’t cure schizophrenia but they do reduce the severity of symptoms so are more desirable. Outline: Pharoah et al – identified strategies family therapists use: 1. 2. 3. 4. Reduce stress of caring for a relative Improving ability of family to anticipate and solve problems Reduce guilt and anger in members Improve beliefs about behaviour towards schizophrenia Token economies – are reward systems used on operant conditioning. They are used to manage behaviour of patients who spend long periods in hospital. Tokens are given to those that display desirable behaviour which can be traded in for privileges. Tokens act as secondary reinforcers as they only have vale because they are associated with rewards. Eval 3: Ethical Issues – In token economy systems, severely ill patients are unable to get privileges as they are less able to comply with desirable behaviours than moderately ill patients. Severely patients therefore suffer discrimination. Moreover, CBT challenges a person’s paranoia, but may interfere with their freedom of thought. Ethical issues make psychological therapies controversial. Eval 1: Research shows limited benefits – Juahar et al: found that CBT had a small effect on symptoms of schizophrenia. Mc. Monagle and Sultana: found that only one on three studies of token economies using random allocation showed improvement. Pharoah et al: reviewed effectiveness of family therapy and moderate evidence of a reduction in hospital readmission and quality of life, but evidence was inconsistent. Overall, there isn’t much support for the effectiveness of psychological therapies. Eval 4: Quality of evidence – small-scale studies that compare patients before and after therapies have found positive results. But these studies often lack a control group or random allocation, but are included in reviews. Therefore, the effectiveness of psychological therapies may be overestimated by evidence. Extra Evaluation Point: Alternative psychological therapies are under-researched – NICE recommends art therapy if a qualified art therapist is available that has experience working with schizophrenia patients. However, these therapies aren’t well researched so it is unclear how effective they are. This raises the question of whether under-researched therapies should be made available to patients.

[6] The Interactionist Approach to Schizophrenia Outline: Diathesis-stress model – states that a vulnerability (diathesis) and a stress trigger (stressor) are needed to develop schizophrenia. In the original diathesis-stress model, diathesis was entirely a result of a single ‘schizogene’. Meehl argued that someone without this gene can never develop schizophrenia no matter how much stress they were exposed to. People who do have the gene are vulnerable to the effects of chronic stress e. g. schizophrenogenic mother. Modern understanding of diathesis assume that many genes increase vulnerability – it doesn’t have to be genetic and can be psychological trauma e. g. child abuse Eval 2: The original diathesis-stress model is too simplistic – multiple genes increase the risk of schizophrenia by a small amount – there is no single schizogene. Stress comes in many forms such as dysfunctional parenting. Research shows that stress can also be biological factors e. g. Houston et al: found that childhood sexual trauma was a diathesis and cannabis was a trigger. This shows that the old view of diathesis as biological and stress as psychological is overly simple. Outline: Modern understanding of stress includes Eval 1: Support from the dual role of anything that can trigger schizophrenia e. g. cannabis vulnerability and stress – Tienari et al: studied can increase risk up to 7 times depending on dose as it interferes with the dopamine system. Treatment according to the interactionist approach – Turkington et al: suggest that it is possible to believe in biological causes of schizophrenia and still practice CBT to relieve psychological symptoms. This requires an interactionist model. In the UK, it is increasingly common to treat patients with a combination of drugs and CBT. In the US there is a conflict between the biological approach and the psychological approach, so adoption of the interactionist approach has been slower. adopted children whose biological mother had schizophrenia. The parenting style of the adoptive mothers were assessed and compared with a control group of kids who had no genetic risk. Childrearing styles with high levels of criticism and conflict were implicated in the development of schizophrenia only if the child had a genetic risk. This shows that a combination of genetic vulnerability and stress contribute to developing schizophrenia. Eval 3: Usefulness of interactionist approach in treatment – Tarrier et al: randomly allocated Eval 4: We don’t know exactly how diathesis and stress work – there is strong evidence that 315 patients to (1) medication + CBT group or (2) a medication and supportive counselling group or (3) a control group (medication only). Those in group 1 and 2 showed lower symptom levels than those in group 3, but there was no difference in hospital readmission. This shows that there is a practical advantage to adopting an interactionist approach in the form of superior treatments outcomes. vulnerability coupled with stress can lead to schizophrenia. But we don’t understand the mechanisms by which symptoms appear and how vulnerability and stress produce them. This means that we have an incomplete understanding of the actual mechanism. Extra Evaluation Point: Treatment-causation fallacy – Turkington et al: argue the fact that biological and psychological therapies work better together than on their own doesn’t mean that the interactionist approach is correct. Similarly, the fact that drugs help, doesn’t mean that schizophrenia is biological in origin. This is called treatment-causation fallacy. This means that superior outcomes of research shouldn’t be over interpreted in terms of evidence in support of the interactionist approach.