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Classification of Schizophrenia

Schizophrenia is a serious mental disorder siffered by about 1% of the world population. The symptoms of schizophrenia can interfere with everyday tasks so many sufferers end up homeless or hospitalised.

The two major systems for the classification of mental disorder are the International Classification of Disease edition 10 (ICD-10) and the Diagnostic and Statistical Manual edition 5 (DSM-5).

The DSM-5 system only requires one of the positive symptoms - delusions, hallucinations or speech disorganisation - must be present for diagnosis whereas two or more negative symptoms are sufficient under ICD.

ICD-10 recognises a range of subtypes of schizophrenia and the DSM also used to do this but this has been dropped in the DSM-5.

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Positive Symptoms

Positive symptoms of schizophrenia are additional experiences beyond those of ordinary existence. They include hallucinations and delusions.

Hallucinations: unusual sensory experiences. Some are related to events in the environment but others have no relationship to the environment. Voices that are heard either talking to or commenting on the sufferer, often criticising them. The sufferer may see distorted facial expressions or occasionally people or animals that are not there.

Delusions: irrational beliefs. Common delusions involve being an important historical, political or religious figure, such as Jesus. They also commonly involve being persecuted, perhaps by government or aliens. Another class of delusions concerns the body. They believe that a part of them is under external control - it makes sense to them but is bizarre to others. Some delusions can lead to aggression.

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Negative Symptoms

Negative symptoms of schizophrenia involve the loss of usual abilites and experiences. Examples include avolition and speech poverty.

Avolition: finding it difficult to begin or keep up with goal-directed activity i.e. actions performed in order to achieve a result. Sufferers of schizophrenia often have sharply reduced motivation to carry out a range of activities. Andreason (1982) indentified three indentifying signs of avolition; poor hygiene and grooming, lack of persistence in work or education and lack of energy.

Speech Poverty (Alogia): changes in patterns of speech. The ICD-10 recognises speech poverty as a negative symptom. The emphasis is on reduction in the amount and quality of speech in schizophrenia. This is accompanied by a delay in sufferer's verbal responses during conversation. The DSM places its emphasis on speech disorganisation in which speech becomes incoherent or the speaker changes topic mid-sentence. This is classified in DSM-5 as a positive symptom.

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  • Reliability: an important measure of reliability is inter-rater reliability - the extent to which different assessors agree on their assessments. Elie Cheniaux et al (2009) has two psychiatrists independently diagnose 100 patients using both DSM and ICD criteria. One psychiatrist diagnosed 26 with schizophrenia according to DSM and 44 according to ICD and the other diagnosing 13 according to the DSM and 24 according to ICD. This shows poor reliability.
  • Validity: there are a number of validity issues to consider. We can see that schizophrenia is much more likely to be diagnosed using ICD than DSM. This suggests that schizophrenia is either over-diagnosed in ICD or under-diagnosed in DSM. This is poor validity.
  • Co-Morbidity: morbidity refers to a medical condition or how common it is. Co-morbidity is the phenomenon that two or more conditions. If conditions occur together a lot then it calls into question the validity of their diagnosis and classification because they might actually be a single condition. In terms of classification, if very severe depression looks a lot like schizophrenia and vice versa. This is a weakness of diagnosis and classification.
  • Symptom Overlap: there is a considerable overlap between the symptoms of schizophrenia and other conditions. This again calls into question the validity of both the classifcation and diagnosis of schizophrenia. Under ICD a patient may be diagnosed with schziophrenia but DSM may be diagnosed with bipolar disorder.
  • Gender bias in diagnosis: Julia Longenecker et al (2010) reviewed studies of the prevalence of schizophrenia and concluded that since the 1980's men have been diagnosed with schizophrenia rather more often than women.
  • Cultural bias in diagnosis: African Americans and English people of Afro-Caribbean origin are several times more likely than white people to be diagnosed with schizophrenia.
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Genetic Basis of Schizophrenia

Schizophrenia runs in families: it has been noted that schizophrenia runs in families. This is quite weak evidence in itself for a genetic link as families share the majority of their genes and environment. The more closely related you are to the person with schizophrenia the more likely you are to have schizophrenia. Gottesman (1991) found that identical twins have 48% chance of both of them developing schziophrenia if they have the genes and fraternal twins have a 17% chance.

Candidate genes: individual genes are believed to be associated with risk of inheritance. Because a number of genes each appear to confer a small increased risk of schizophrenia it appears that schizophrenia is polygenic - it requires a number of factors to work in combination. Schizophrenia is aetiologically heterogeneous - different combinations of factors can lead to the condition. Stephen Ripke et al (2014) carried out a study where the genetic make-up of 37,000 patients was compared to that of 113,000 controls; 108 seperate genetic variations with increased risk of schizophrenia.

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The Dopamine Hypothesis

Neurotransmitters: the brains chemical messengers work differently in the brain of a patient with schizophrenia. Dopamine is widely believed to be involved. Dopamine is important in the functioning of several brain systems that may be implicated in the symptoms of schizophrenia.

Hyperdopaminergia in the subcortex: the original version of the dopamine hypothesis focused on the possible role of high levels or activity of dopamine in the subcortex (the central areas in the brain). An excess of dopamine receptors in Broca's area (which is responsible for speech production) may be associated with poverty of speech and/or the experience of auditory hallucinations.

Hypodopaminergia in the cortex: more recent versions of the dopamine hypothesis have focused on abnormal dopamine systems in the brain's cortex. Goldman-Rakic et al (2004) have identified a role for low levels of dopamine in the prefrontal cortex (responsible for thinking and decision making) in the negative symptoms of schizophrenia.

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Neural Correlates of Schizophrenia

Neural correlates are measurements of the structure or function of the brain that correlate with an experience. Both positive and negative symptoms have neural correlates.

Neural correlates of negative symptoms: motivation involves the anticipation of a rewards and certain regions of the brain. The ventral striatum are believed to be particularly involved in anticipation and abnormalities may be involved in the development of avolition. Juckel et al (2006) measured activity levels in the vental striatum in schizophrenia and found lower levels of activity than those observed in controls. They observed a negative correlation between activity levels in the ventral striatu, and the severtiy of overall negative symptoms.

Neural correlates of positive symptoms: Allen et al (2007) scanned the brains of patients experiencing auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as theirs or others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group. Reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.

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  • Multiple sources of evidence for genetic susceptibility: there is very strong evidence for genetic vulnerability to schizophrenia from a variety of sources. The Gottesman (1991) study clearly shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies (Pekka Tienari et al, 2004) show that children of schizophrenia sufferers are still at a heightened risk of schizophrenia if adopted into families with no history of schizophrenia.
  • Mixed evidence for the dopamine hypothesis: dopamine agonists that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers (Curran et al, 2004). Antipsychotic drugs reduce the dopamine activity and both kinds of drug study suggest an important role for dopamine in schizophrenia. Some genes identified show that not only dopamine is important in the development of schizophrenia. (can be used as strength or weakness)
  • Correlation-Causation problem: most of the studies leave a lot of questions unanswered such as does the unusual activity in a region of the brain cause the symptom? The existence of neural correlates in schizophrenia therefore tells us relatively little in itself.
  • The role of mutation: schizophrenia can develop due to a mutation in the parental DNA which can be caused by radiation, poison or viral infection. Evidence shows a positve correlation in paternal age and development of schizophrenia (Brown et al, 2002)
  • The role of the psychological environment is important but unclear: the evidence supporting the role of biological factors in schizophrenia - but there is evidence to suggest an important role for environmental factors.
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Family Dysfunction

There are a range of psychological explanations for schizophrenia and some of these have focused particularly on the family and it's role in making individuals particularly vulnerable to schizophrenia.

The Schizophrenogenic Mother: Freida Fromm-Reichmann (1948) proposed a psychodynamic explanation for schizophrenia based on the accounts she heard from patients about their childhoods. Fromm-Reichmann noted that many of her patients spoke of a particular type of parent, the schizophrenogenic (schizophrenia-causing) mother. The schizophrenogenic mother is cold, rejecting and controlling and creates a family climate characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions and eventually schizophrenia.

Double-Bind Theory: Gregory Bateson et al (1972) agreed that family climate is important in the development of schizophrenia but emphasised the role of communication style within the family. The developing child finds themselves trapped where they fear they are doing the wrong thing, but receive mixed messages and feel unable to comment on the unfairness of the situation. When they get it wrong, they are punished and this leaves them with an understanding of the world as confusing and dangerous. Bateson was clear that this was neither the main type of communication in the family, nor the only factor in developing schizophrenia.

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Expressed Emotion

Expressed Emotion is the level of emotion, particularly negative emotions, expressed towards a patient by their carers. It contains several elements:

  • Verbal criticism of the patient, occasionally accompanied by violence.
  • Hostility towards the patient, including anger and rejection.
  • Emotional over-involvement in the life of the patient, including needless self-sacrifice.

These high levels of expressed emotion in carers directed towards the patient are a serious source of stress for the patient.

This is primarily an explanation for relapse in patients with schizophrenia. It has also been suggested that it may be a source of stress that can trigger the onset of schizophrenia in a person who is already vulnerable.

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Cognitive Explanations

Cognitive explanations focus on the role of mental processes. 

Schizophrenia is characterised by disruption to normal though processing. This lower than usual level of information processing suggests that cognition is likely to be impaired.

Christopher Frith et al (1992) identified two kinds of dysfunctional thought processing that could underlie some symptoms:

  • Metarepresentation: the cognitive ability to reflect on thoughts and behaviour. Dysfunction in metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else.
  • Cental Control: the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers associations, and they cannot suppress the automatic response to these.
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  • Support for family dysfunction: Read et al (2005) reviewed 46 studies of child abuse and schizophrenia and concluded that 69% of adult women in-patients with a diagnosis of schizophrenia had a history of physical abuse, sexual abuse or both in childhood. For men the figure was 59%. Adults with insecure attachments to their primary carer are also more likely to have schizophrenia (Berry et al, 2008).
  • Weak evidence for family-based explanations: there is almost no evidence to support the importance of the schizophrenogenic mother or double bind. Both of these studies are based on clinical observations of patients and early evidence involved assessing the personality of the mothers of patients for 'crazy-making characteristics'.
  • Strong evidence for dysfunctional information processing: Stirling et al (2006) compared 30 patients with a diagnosis of schizophrenia with 18 non-patient controls on a range of cognitive tasks including the Stroop Test, where participants have to name the ink colours of colour words, suppressing the impulse to read the words. Patients took over twice as long to name the ink colours as the control group.
  • Evidence for biological factors is not adequately considered: psychological explanations for schizophrenia can be hard to reconcile with the biological explanations. It could be that they both produce symptoms.
  • Direction of causailty: there is a lot of information concerning abnormal cognitions as well as a mass of information about abnormal biology in schizophrenia. It remains unclear what causes what.
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The most common treatment of schizophrenia involved the use of antipsychotic drugs.

These drugs can be taken as a tablet or in the form of syrup. For those particularly at risk of failing to take their medication, some antipsychotics are given as an injection every 2-4 weeks.

Antipsychotics may be required in the short or long term.

Some patients can take a short course of the drugs and stop their use without the return of symptoms and other patients may require antipsychotics for life of face the likelihood of a recurrence of schizophrenia.

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Typical Antipsychotics

These have been around since the 1950s and include chlorpromazine. Chlorpromazine can be taken as tablets, syrup or by injection. If taken orally it is taken daily.

There is a strong association between the use of typical antipsychotics and the dopamine hypothesis. They work by reducing the action of a neurotransmitter - it blocks the dopamine receptors which reduces the action of dopamine. This normalises neurotransmissions in key areas of the brain.

Chlorpromazine is also an effective sedative. This is believed to be related to its effect on histamine receptors. It is often used to calm patients not only with schizophrenia but also with other conditions. This has often been done when patients are first admitted to hospitals and are very anxious.

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Atypical Antipsychotics

Atypical antipsychotics have been used since the 1970s and their purpose was to maintain or improve the effectiveness of drugs in suppressing the symptoms of psychosis and also minimise the side effects. There are a range of atypical antipsychotics and they do not all work in the same way.

Clozapine: developed in the 1960s and first trialled in the early 1970s. It was withdrawn as some patients died due to a blood condition called agranulocytosis (lowered white blood cell count) when taking the drug. Clozapine was remarketed in the 1980s and was to be used when other treatments failed. Now, people have to take multiple blood tests throughout their use of clozapine. Clozapine acts on dopamine in the same way as chlorpromazine, but also acts on serotonin and glutamate receptors. This helps improve mood and reduce depression and anxiety in patients. 

Risperidone: developed in the 1990s as an attempt to produce a srug as effective as clozapine but without the side effects. Like clozapine, risperidone binds to the dopamine and serotonin receptors but binds more strongly to dopamine receptors, making it more effective in much smaller doses. There is evidence to suggest that this leads to fewer side effects.

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  • Evidence for effectiveness: there is a large body of evidence to support the idea that both typical and atypical antipsychotics are at least moderately effective in tackling the symptoms of schizophrenia. Ben Thornley et al (2003) reviewed studies comparing the effects of chlorpromazine to control conditions in which patients received a placebo. Data from 13 trials showed that chlorpromazine was associated with better overall functioning and reduced symptom severity. 
  • Serious side effects: there is a range of side effects that come with taking antipsychotic drugs which range from mild to serious and potentially fatal. Typical antipsychotics are associated with a range of side effects including dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. Long-term use can result in tardive dyskinesia, which is caused by dopamine supersensitivity and is involuntary facial movements such as grimacing, blinking and lip smacking. The most serious side effect is neuroleptic malignant syndrome (NMS) which can result in high temperature, deliruim and comas.
  • Use of antipsychotics depends on the dopamine hypothesis: there is evidence to show that the original dopamine hypothesis is not a complete explanation for schizophrenia. If this is true then it is not clear how antipsychotics can help with schizophrenia and the modern understanding suggests that the drugs shouldn't work.
  • Problems with evidence for effectiveness: David Healy (2012) has suggested that some successful trials have had their data published multiple times, exaggerating the evidence for positive effects. Most published studies also only assess short-term rather than long-term benefits.
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Cognitive Behaviour Therapy (CBT)

CBT is now commonly used to treat patients with schizophrenia. It takes place between five and twenty sessions and the aim is to help patients identify irrational thoughts and try to change them. It will not get rid of the symptoms of schizophrenia but can make patients understand them and cope with them.

How CBT helps: patients can be helped to make sense of their delusions and hallucinations and how it impacts their feelings and behaviours. Understanding where symptoms come from can be very helpful to some patients. By offering psychological explanations for the existence of hallucinations and delusions, it can help reduce anxiety. CBT also helps as delusions can be challenged so that a patient can come to learn that their beliefs are not based on reality.

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Family Therapy

Family therapy takes place with families rather than the patients alone and aims to improve the quality of communication and interaction between family members. Some therapists see the family as the root cause of schizophrenia - but most family therapists are more concerned with reducing stress within the family which may contribute to a patients risk of relapse.

How family therapy helps: Fiona Pharoah et al (2010) identify a range of strategies by which family therapists aim to improve the functioning of a family with a member suffering from schizophrenia:

  • Forming a therapeutic alliance with all family members.
  • Reducing the stress of caring for a relative with schizophrenia.
  • Improving the ability of the family to anticipate and solve problems.
  • Reduction of anger and guilt in family members.
  • Helping family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives.
  • Improving families' beliefs about and behaviour towards schizophrenia.

It is suggested that these strategies work by reducing levels of stress and expressed emotion, whilst increasing the changes of patients' complying with medication.

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Token Economies

Token economies are reward systems used to manage the behaviour of patients with schizophrenia, especially those who have patterns of maladaptive behaviour through spending long periods in psychiatric hospitals. Doing this does not cure schizophrenia but improves the patient's quality of life and makes it more likely that they can live outside a hospital.

Tokens: tokens are given immediately to patients when they have carried out a desirable behaviour that has been targeted for reinforcement. This may be getting dressed in the morning, making a bed or having a shower - it depends on the patient's individual behaviour issues. This immediacy of reward is important because it prevents 'delay discounting', the reduced effect of a delayed reward.

Rewards: the tokens have no value in themselves but they can be swapped later for more tangible rewards. Token economies are a kind of behavioural therapy based on operant conditioning. Tokens are secondary reinforcers because they only have value once the patient has learned that they can be used for rewards. The rewards may be in the form of material items or in the form of services and privileges.

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  • Evidence for effectiveness: Sameer Jauhar et al (2014) reviewed the results of 34 studies of CBT for schizophrenia and concluded that CBT has a significant but fairly small effect on both positive and negative symptoms. Pharoah et al concluded there is moderate evidence to show that family therapy significantly reduces hospital readmission. A review of evidence for token economies by McMonagle and Sultana (2009) found that some patients showed improvement in symptoms.
  • Treatments improve quality of life but do not cure: all the things that psychological treatments aim to do is worth doing, but should not be confused with curing schizophrenia. Biological treatments do not cure schizophrenia either but reduce the severity of some symptoms.
  • Ethical issues: token economy systems have proved controversial and the major issue is that privileges, services etc bcome more available to patients with mild symptoms and less so for those with more severe symptoms of schizophrenia that prevent them from complying. CBT may involve challenging a person's paranoia but this can interfere with their freedom of thought.
  • Quality of the evidence for effectiveness: many small studies in which mental health professionals have compared patients before and after psychological treatments have found more positive results - but there is often a lack of a control group and these studies are generally more optimistic.
  • Alternative psychological treatments: there are other psychological therapies that can be helpful for some people with schizophrenia that are less well-known and less likely to be available to patients. 
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The Interactionist Approach

The interactionist approach is an approach that acknowledges that there are biological, psychological and societal factors in the development of schizophrenia.

The diathesis-stress model is a good example of the interactionist approach as it says that both a vulnerability to schizophrenia and a stress-trigger are necessary in order to develop the condition. One or more underlying factors make a person particularly vulnerable to developing schizophrenia.

Meehl's Model: the originial diathesis-stress model (Meehl 1962) said that schizophrenia was a result of a single schizogene. According to Meehl, if a person does not have the schizogene then no amount of stress would lead to schizophrenia. In carriers of the gene, chronic stress through childhood and adolescence could result in the development of the condition.

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The Diathesis-Stress Model

Modern understanding of diathesis (vulnerability): our understanding of diathesis has changed as it is now cleae that many genes increase genetic vulnerability slightly and there is no single schizogene (Ripke et al, 2014). Modern views also include a range of factors beyond the genetic including psychological trauma (Ingram and Luxton, 2005). Read et al (2001) proposed a neurodevelopmental model in which early trauma alters the developing brain. Early and severe enough trauma, such as child abuse, can seriously affect many aspects of brain development.

Modern understanding of stress (negative psychological experience): stress was seen as psychological in nature, especially related to parenting. Although psychological may still be considered important, a modern definition of stress includes anything that risks triggering schizophrenia (Houston et al, 2008). Most of the recent research into factors triggering schizophrenia has concerned cannabis use - it is a stressor as is increases the risk of schizophrenia by up to seven times according to dose. Most people do not develop schizophrenia after smoking cannabis so it seems there must also be one or more vulnerabilty factors.

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Interactionist Treatment

The interactionist approach to schizophrenia acknowledges both biological and psychological factors in schizophrenia and is therefore compatible with both biological and psychological treatments.

The model is associated with combining antipsychotic medication and psychological therapies, most commonly CBT.

Douglas Turkington et al (2006) say that is it possible to believe in biological causes of schizophrenia and still practise CBT to relieve psychologcal symptoms. This requires adopting an interactionist model; it is not possible to adopt a purely biological approach and tell patients that their condition is purely biological and that there is no psychological explanation.

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

It is unusual to treat schizophrenia using psychological therapies alone. CBT, family therapy and the use of token economies are usually carried out with patients who are also taking antipsychotics.

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  • Evidence for the role of vulnerability and triggers: Pekka Tienari et al (2004) investigated the combination of genetic vulnerability and parenting style. Children adopted from 19,000 Finnish mothers with schizophrenia between 1960 and 1979 were followed up and their adoptive parents were assesed for child-rearing style. The rates of schizophrenia were compared to those in a control group of adoptees. A child-rearing style characterised by high levels of criticim and conflict and low levels of empathy was involved in the development of schizophrenia - but only for children with a high genetic risk.
  • The original diathesis-stress model is over-simple: the classic model of a single schizogene and schizophrenia parenting syle as the major source of stress is now known to be very over-simple. Multiple genes increase vulnerability to schizophrenia; there is no single schizogene. 
  • Support for the effectiveness of combinations of treatments: Nicholas Tarrier et al (2004) did a study on 315 patients who were randomly allocated to a medication and CBT group, medication and supportive counselling or a control group. Patients in the two combination groups showed lower symptom levels than those in the control group, who only had medication, although there was no difference in rates of hospital readmission.
  • We don't know exactly how diathesis and stress work: we do not yet fully understand the mechanisms by which the symptoms of schizophrenia appear and how both vulnerability and stress produce them.
  • The treatment-causation fallacy: the fact that combined biological and psychological treatments are more effective than either on their own does not necessarily mean the interactionist approach to schizophrenia is correct.
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