my flashcards for schiz

Classification of schizophrenia

Schizophrenia is a psychological condition characterised by a loss of contact with reality. It affects around 0.7% of the population. There is no single defining symptom of schizophrenia but a cluster of (often seemingly unrelated) symptoms. These symptoms may be positive (experiences in addition to ordinary experience, such as hallucinations) or negative (a lack of abilities associated with normal experience, such as reductions in speech). Positive symptoms of schizophrenia Positive symptoms are additional experiences beyond those associated with normal psychological functioning. Positive symptoms associated with schizophrenia include hallucinations and delusions. Hallucinations Hallucinations are perceptions that are not based in reality, or distorted perceptions of reality. For example, a schizophrenic person may hallucinate hearing voices that aren’t really there, or seeing someone who isn’t really there. Delusions Delusions are beliefs that are not based in reality. For example, a schizophrenic person may have a delusion that they are the victim of a grand conspiracy, or that they are an important person with a unique mission (e.g. Jesus Christ reborn). Negative symptoms of schizophrenia Negative symptoms are a lack of abilities associated with normal psychological functioning. Negative symptoms associated with schizophrenia include speech poverty and avolition. Speech poverty Speech poverty is a reduction in the quality and amount of speech. For example, a schizophrenic person may give one-word answers to questions without elaborating any further detail. Avolition Avolition is a lack of desire and motivation for anything. For example, a schizophrenic person may sit around without engaging in everyday tasks such as work, socialising, or maintaining personal hygiene. Diagnosis of schizophrenia There are two main classification systems for diagnosing schizophrenia: The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the World Health Organisation’s International Statistical Classification of Diseases and Related Health Problems (ICD-10). These manuals enable doctors to label a patient’s symptoms as those of schizophrenia (rather than some other disorder). The criteria for DSM-5 and ICD-10 differ slightly: DSM-5 requires at least one positive symptom to be present, whereas diagnosis of schizophrenia using ICD-10 can be based on negative symptoms alone. Reliability of schizophrenia diagnosis Reliability refers to how consistently schizophrenia is diagnosed. For example, if multiple different doctors diagnose the same person as schizophrenic based on the same symptoms, then their diagnosis is reliable. Various studies have attempted to quantify the reliability of schizophrenia diagnosis. For example: Beck et al (1962) found a concordance rate of 54% among psychiatrists in their diagnosis of schizophrenia. Söderberg et al (2005) found a concordance rate of 81% among psychiatrists using the DSM classification to diagnose schizophrenia. Jakobsen et al (2005) found a concordance rate of 98% among psychiatrists using the ICD-10 classification to diagnose schizophrenia. In Cheniaux et al (2009), two psychiatrists evaluated 100 patients using both the DSM-4 and ICD-10 criteria. Psychiatrist 1 found 26 patients had schizophrenia according to DSM-4 and 44 according to ICD-10. Psychiatrist 2 found 13 patients had schizophrenia according to DSM-5 and 24 according to ICD-10. This suggests both low inter-observer reliability and low reliability between the two classification systems. AO3 evaluation points: Reliability of schizophrenia diagnosis

Validity of schizophrenia diagnosis Validity refers to how accurately schizophrenia is diagnosed. For example, if doctors frequently diagnose patients with autism as suffering from schizophrenia, then their diagnosis is not valid. Rosenhan (1973) questions the validity of schizophrenia diagnosis. In this study, eight healthy volunteers (i.e. subjects who did not have schizophrenia) presented themselves to various psychiatric hospitals claiming to hear voices. All eight volunteers were successfully admitted to the hospitals and diagnosed with schizophrenia. Depending on the ‘patient’, doctors took between 7-52 days to release them. In a later experiment, doctors were falsely told that healthy patients would attempt to admit themselves, which led doctors to turn genuine schizophrenic patients away because they thought they were actors. The results of these experiments suggest the doctors did not have valid methods for diagnosing schizophrenia. AO3 evaluation points: Validity of schizophrenia diagnosis

Biological approach to schizophrenia

Biological explanations of schizophrenia Biological explanations of schizophrenia look at biological factors linked to schizophrenia. These include genetics, neural (brain) abnormalities, and abnormalities in dopamine. Genetics The genetic explanation of schizophrenia looks at hereditary factors – i.e. genes – that contribute to the development of schizophrenia. As always, twin studies are a useful way to determine whether or not a condition is inherited through genetics. If it is more common for both identical twins to suffer from schizophrenia than it is for both non-identical twins, this would suggest a genetic component to schizophrenia. The reason for this is that identical twins have 100% identical genetics whereas non-identical twins only share 50% of their genes and so any genetic condition would be equally common to both identical twins. Several studies have attempted to determine the genetic heritability of schizophrenia. Perhaps the most widely-cited source is Gottesman (1991), who looked at how different familial relationships to someone with schizophrenia are linked with risk of developing schizophrenia: Gottesman found that the closer the genetic relationship to the person with schizophrenia, the greater the risk of developing schizophrenia. For example, the concordance rate for schizophrenia among identical twins is 48%, whereas for non-identical twins it is 17%. This supports the idea that genetics play a role in developing schizophrenia. Other familial and twin studies into schizophrenia include: Cardno et al (1999) found identical twins had a concordance rate for schizophrenia of 40.8%, whereas non-identical twins had a concordance rate of 5.3%. Tienari et al (1985) conducted a longitudinal study comparing adopted children whose biological mothers had schizophrenia with a control group of adoptees whose biological mothers did not have schizophrenia. The researchers found that the children of schizophrenic mothers were more likely to develop schizophrenia compared to controls, supporting the role of genetics in the development of schizophrenia. Kety and Ingraham (1992) is another adoption study. Adoption studies like this are useful because they separate (and thus control for) environmental factors: If schizophrenia was passed on from parents to children through environmental factors only, you would expect adoptees whose biological parents had schizophrenia to have the same rates of schizophrenia as the control group. However, the researchers found that adoptees whose biological parents had schizophrenia were 10 times more likely to develop schizophrenia than a control group of adoptees whose biological parents did not have schizophrenia, supporting a genetic basis of the disorder. AO3 evaluation points: Genetic explanations of schizophrenia

Neural correlates The neural explanation of schizophrenia looks at correlations among the brain structures of people with schizophrenia. There are several ways to examine the brain, such as post-mortem and fMRI scanning. By using these methods, researchers can compare the brains of schizophrenic people with non-schizophrenic people to identify differences in brain structures that may cause schizophrenia.

For example, the images above from Kim et al (2010) show fMRI scans of a schizophrenic patient and a non-schizophrenic control during a working memory task. Other studies looking at the neural basis of schizophrenia include: Enlarged ventricles: Several studies have found correlations between enlarged ventricles in the brain and schizophrenia. For example, Johnstone et al (1976) and Suddath et al (1990). Enlarged ventricles are particularly linked with the negative symptoms of schizophrenia, as shown in studies such as Andreasen et al (1982). Reduced grey matter and cortical thinning: Boos et al (2012) compared MRI scans of 155 schizophrenic patients, 186 non-schizophrenic family members, and 122 non-schizophrenic controls. The researchers found that the schizophrenic patients had reduced grey matter and cortical thinning compared to their non-schizophrenic family members and the non-schizophrenic controls. This further supports the existence of a neural basis for schizophrenia. Facial emotion processing: A common symptom of schizophrenia is difficulty perceiving emotions. A meta-analysis by Li et al (2010) looked at fMRI scans of schizophrenic patients and non-schizophrenic controls during facial expression processing tasks. The researchers found that people with schizophrenia have reduced activity in the bilateral amygdala and right fusiform gyri compared to controls, suggesting a neural basis for this symptom. AO3 evaluation points: Neural explanations of schizophrenia

The dopamine hypothesis The dopamine hypothesis explains schizophrenia (at least partly) as a result of abnormal activity of the neurotransmitter dopamine. The dopamine hypothesis became popular in the 1970s when studies (e.g. Seeman et al (1976), Creese et al (1976), and Snyder (1976)) reported that several drugs that reduce schizophrenia symptoms are dopamine receptor antagonists: They reduce dopamine activity. The implication is that schizophrenia is caused by increased dopamine activity and that these drugs work by reducing dopamine activity. Further evidence supporting the dopamine hypothesis includes: Dopamine agonists: Several studies have demonstrated that drugs that increase dopamine activity – dopamine agonists, such as amphetamines – can induce schizophrenic symptoms in non-schizophrenic people. For example, a systematic review by Curran et al (2004) found that amphetamine use makes schizophrenia symptoms worse in schizophrenic patients. Further, McKetin et al (2013) found that non-schizophrenic methamphetamine addicts demonstrated a 5-fold increase in schizophrenia-like symptoms during periods when they were using methamphetamine. This link is further supported by animal studies, such as Randrup and Munkvad (1966), who were able to induce schizophrenic behaviour in rats with amphetamines and then reverse these symptoms with dopamine-reducing drugs (antagonists). Post-mortem evidence: Bird et al (1979) used post-mortems to compare dopamine levels in the brains of 50 schizophrenic patients with 50 non-schizophrenic controls. The schizophrenic patients had increased dopamine concentrations in some areas of the brain compared to controls. Brain scans: Some studies using brain-scanning techniques have found increased dopamine activity in schizophrenic patients. For example, Lindström et al (1999) compared PET scans of 12 schizophrenic patients with 10 controls and found the schizophrenic patients had increased dopamine activity in the striatum and parts of medial prefrontal cortex. Further, a review of MRI scans by Alves et al (2008) found support for the (revised) dopamine hypothesis. Over the years, the dopamine hypothesis of schizophrenia has been refined. It’s not as simple as high dopamine = schizophrenia. Instead, research suggests that schizophrenia is linked with high dopamine activity in some areas of the brain (e.g. the subcortex) but low dopamine activity in other areas (e.g. prefrontal cortex). The dopamine hypothesis of schizophrenia remains somewhat controversial. The AO3 evaluation points below provide examples of evidence against the dopamine hypothesis. AO3 evaluation points: The dopamine hypothesis of schizophrenia

Biological treatment of schizophrenia: Drug therapy Antipsychotic drugs are the primary biological treatment for schizophrenia. These drugs are divided into two categories: Typical antipsychotics and atypical antipsychotics.

Typical antipsychotics

Atypical antipsychotics

Other names First-generation Second-generation Used since 1950’s 1970’s Aim Reduce symptoms of schizophrenia Reduce schizophrenia symptoms more effectively with less side effects Neurotransmitters targeted Dopamine Dopamine and others (e.g. serotonin and glutamate) Examples Chlorpromazine Haloperidol Clozapine Risperidone Typical antipsychotics Typical antipsychotic drugs for schizophrenia work by reducing dopamine activity – they are dopamine antagonists – and are thus strongly associated with the dopamine hypothesis of schizophrenia. They have been used since the 1950’s and are sometimes referred to as first-generation antipsychotics. Chlorpromazine was the first antipsychotic drug developed. It is a dopamine antagonist, which means it works by blocking dopamine receptors in the brain. Chlorpromazine also has sedative effects.

Chlorpromazine (red diamond) blocks the receptor and prevents dopamine (purple circle) from exerting its effects. Typical antipsychotic drugs, such as chlorpromazine and haloperidol, can cause several side effects. Among the most serious of these side effects are extrapyramidal symptoms, which are problems with movement similar to Parkinson’s disease. Atypical antipsychotics Atypical antipsychotic drugs have been around since the 1970’s and are sometimes referred to as second-generation antipsychotics. The aim of these drugs is to improve upon the efficacy of typical antipsychotics while reducing side effects. Atypical antipsychotics target several neurotransmitters, not just dopamine. For example, clozapine is an atypical antipsychotic that acts on the neurotransmitters dopamine, serotonin, and glutamate. Risperidone, another atypical antipsychotic, targets dopamine and serotonin. Some evidence suggests atypical antipsychotics are superior to typical antipsychotics (see AO3 evaluation points below). However, atypical antipsychotics also carry a risk of side effects including weight gain, increased risk of heart attack, increased risk of diabetes, and extrapyramidal symptoms. AO3 evaluation points: Drug therapy for schizophrenia

Psychological approach to schizophrenia

Psychological explanations of schizophrenia Psychological explanations of schizophrenia include family dysfunction and cognitive explanations (e.g. dysfunctional thought processing). Family dysfunction Several psychologists have proposed that family dysfunction (e.g. high levels of conflict or difficulties communicating) can influence the development of schizophrenia. One example of this is Bateson et al (1956), who proposed the double bind explanation of schizophrenia. According to this explanation, children who often get conflicting messages from their parents are more likely to develop schizophrenia. For example, a mother who loves her child but has trouble expressing it may exhibit contradictory behaviours (e.g. hugging the child but being critical with her words). Another example is a parent who tells their child to be more spontaneous: Whatever the child does, they can’t fulfil this request because if they do act more spontaneous because their parent tells them then they aren’t acting spontaneously! Constant exposure to these mixed messages and impossible demands mean the child is unable to form a coherent picture of reality. This leads to disorganised thinking which in extreme cases can manifest as symptoms of schizophrenia such as delusions and hallucinations. Another familial explanation of schizophrenia is expressed emotion. An environment with a high degree of expressed emotion – particularly negative, such as criticism and hostility – causes stress, which increases the risk of schizophrenia. Expressed emotion is primarily associated with relapse in schizophrenic patients. AO3 evaluation points: Family dysfunction explanation of schizophrenia

Cognitive explanations Cognitive explanations of schizophrenia look at how schizophrenic patients think and process information. Schizophrenic cognition may differ from non-schizophrenic cognition in several ways: Dysfunctional thought processing: Metacognition is the ability to think about and reflect on one’s own thoughts, emotions, and behaviours. Schizophrenic patients are seen as suffering from metacognitive dysfunction, which may explain some symptoms of schizophrenia such as hallucinations. For example, an inability of schizophrenic patients to recognise their thoughts as their own may explain hearing voices: The patient attributes their own thoughts to some external source outside their mind. Cognitive biases: Positive symptoms of schizophrenia, such as delusions, can be explained as a result of cognitive biases. For example, bias may mean a schizophrenic person interprets the ordinary actions of other people as sinister, supporting their delusion that they are a victim of a conspiracy or that people are trying to harm them. Cognitive deficits: Bowie and Harvey (2006) describe various cognitive deficits associated with schizophrenia, such as: Attention deficits: Schizophrenic patients often have difficulty concentrating and paying attention. Speech deficits: Schizophrenic patients often have low verbal fluency and difficulty finding words. This may explain the symptom of speech poverty. Memory deficits: Schizophrenic patients often have impaired working memory, particularly verbal working memory. AO3 evaluation points: Cognitive explanations of schizophrenia

Psychological treatment of schizophrenia In addition to antipsychotic drugs, various psychological treatments for schizophrenia exist such as cognitive behavioural therapy (CBT), family therapy, and the use of token economies. Cognitive behavioural therapy (CBT) Cognitive behavioural therapy (CBT) is the main psychological treatment for schizophrenia. There are many different forms of CBT, but the main aim is to help patients identify and challenge the irrational and maladaptive thoughts underlying schizophrenia. For example, a schizophrenic patient may have delusional thoughts that there is a conspiracy to kill them. These thoughts cause negative emotions (e.g. fear, anxiety) and irrational behaviours (e.g. hiding from or attacking people). CBT involves talking through irrational thoughts like this. The patient is encouraged to describe their thoughts to the therapist. The therapist then helps the patient identify and challenge the reality of these thoughts. For example, the therapist may ask the patient to consider how likely these thoughts are to be true and consider alternative explanations. The therapist may also help the patient tackle their symptoms from the behavioural angle (e.g. by teaching behavioural coping skills) and the emotional angle (e.g. by teaching relaxation techniques). CBT is primarily used to treat positive symptoms of schizophrenia and is commonly used in combination with antipsychotic drug therapy. A typical course of CBT for schizophrenia might consist of 12 sessions spaced 10 days apart.

AO3 evaluation points: CBT for schizophrenia

Family therapy Family therapy is a treatment for schizophrenia based on the family dysfunction explanation of schizophrenia. According to this explanation, schizophrenia is caused (at least in part) by familial dysfunction and so family therapy aims to address this dysfunction rather than focusing on the schizophrenic patient in isolation. This involves talking openly about the patient’s illness and how it affects them with an aim to: Improve communication patterns: Increase positive communication and decrease negative communication among the family (i.e. reduce levels of expressed emotion) Increase tolerance and understanding: Educate family members about schizophrenia and how to deal with it (e.g. how to support each other) Reduce feelings of guilt and anger: Family members may feel guilty (e.g. that they are responsible for causing schizophrenia) or angry towards the schizophrenic patient A typical course of family therapy may consist of weekly sessions for a year, after which the family members will have developed skills that they can use after therapy has ended. AO3 evaluation points: Family therapy for schizophrenia

Token economies Token economies is a behaviourist approach to schizophrenia based on operant conditioning: Schizophrenic patients are awarded tokens (that can be exchanged for rewards) in return for desirable behaviour. Token economies are mainly used to treat negative symptoms of schizophrenia, such as avolition. For example, avolition may mean the patient has little motivation to undertake tasks such as getting out of bed, washing, and socialising. Token economies provide an incentive for the patient to undertake these tasks, changing their behaviour. Token economies are primarily used for schizophrenic patients who are in institutions for long time periods. As well as schizophrenia, token economies are also used to deal with criminal behaviour (see the forensic psychology page for more details). AO3 evaluation points: Token economies for schizophrenia

Interactionist approach to schizophrenia

Rather than trying to reduce schizophrenia to either a psychological or biological phenomena, interactionist approaches to schizophrenia explain the disorder as a combination of various factors. One example of this is the diathesis-stress model. Diathesis-stress model The diathesis-stress model of schizophrenia explains the disorder as a combination of genetic and environmental factors. According to this model, biology determines a person’s vulnerability to schizophrenia (biological diathesis), but schizophrenia is only triggered in response to environmental stressors (stress). So, a person with a high genetic predisposition towards schizophrenia may never develop the disorder (e.g. if they live in a supportive low-stress environment) but a person with a lower genetic disposition may develop schizophrenia if exposed to enough environmental stress (e.g. dysfunctional family upbringing, drug abuse, etc.). In other words, genetic disposition is necessary to developing schizophrenia, but not sufficient by itself. The diathesis-stress model originated with Meehl (1962), who proposed the existence of a single ‘schizogene’ – the effects of which are activated in response to stress. However, more recent research (e.g. Ripke et al (2014)) suggests multiple genes contribute to genetic risk for schizophrenia. Also, ‘stress’ in the diathesis-stress model is not just the emotion – it includes anything that increases the risk of triggering schizophrenia (e.g. drug use, illness, physical trauma, sexual abuse). AO3 evaluation points: Diathesis-stress model of schizophrenia

Interactionist treatment of schizophrenia Interactionist treatment approaches to schizophrenia tackle the disorder from multiple angles. For example, a patient may be given antipsychotic drug therapy (a biological approach to treatment) in combination with cognitive behavioural therapy (a psychological approach to treatment). In general, research suggests such interactionist approaches are more effective than either treatment in isolation.