Schizophrenia Overview (Edexcel A-Level Psychology): Revision Notes

Schizophrenia Overview

Definition and diagnosis

Schizophrenia refers to a spectrum of psychological disorders characterised by abnormalities involving distortions of thought, perception and emotion, alongside social withdrawal. The disorder presents with both positive symptoms (adding to the patient's experience) and negative symptoms (subtracting from normal behaviour).

Diagnostic criteria: For a clinician to diagnose schizophrenia, a patient must have described two or more of the key symptoms for a substantial portion of the last month. At least one of these symptoms must be delusions, hallucinations, disorganised thinking/speech, disorganised behaviour or catatonia, or negative symptoms.

Clinicians must consider other factors when making a diagnosis. If a patient displays signs of disturbed mood (such as mania or depression), the symptoms of schizophrenia must have existed before the disturbed mood for the diagnosis to be valid. Additionally, the clinician must rule out whether brain damage or substance misuse could account for the altered behaviour.

Challenges in diagnosis

Clinician variables also affect diagnosis reliability. According to research by Aboraya et al. (2006), factors such as training and perception of presenting symptoms can influence diagnosis. Clinicians may focus more on acute symptoms whilst overlooking other symptoms. Patient variables during diagnosis—such as mood, memory and levels of shame—can lead to inaccurate information being provided to the clinician.

Symptoms

Positive symptoms (Type 1)

Positive symptoms add to the patient's experience. These include:

• Delusions: fixed false beliefs that cannot be changed by others, even when clear evidence contradicts them
• Hallucinations: perceptual experiences occurring without external stimulation
• Disorganised thinking/speech: inability to make connections between thoughts, resulting in incomprehensible language
• Abnormal motor behaviours: unexpected or rapidly changing behaviour that is out of context

Negative symptoms (Type 2)

Negative symptoms subtract from normal behaviour. The behaviours persist longer and result in a greater burden for the person compared to positive symptoms. These include:

• Lack of energy and enthusiasm
• Poverty of speech: reduced verbal communication
• Poor motivation: difficulty initiating or sustaining activities
• Social withdrawal: reduced social interaction
• Avolition: general lack of motivation to complete usual, self-motivated activities such as work

Detailed symptom descriptions

Delusions

Delusions are beliefs held by the individual that, despite not being true, cannot be changed by others even where clear evidence contradicts the belief. Common types of delusions in psychotic disorders include:

• Grandiose delusions: the individual believes they have remarkable qualities such as being famous or having special powers
• Persecutory delusions: the individual believes that others are 'out to get them' and trying to harm them in some way
• Referential delusions: the individual holds a belief that certain behaviours or language from others is being directed at them personally

Hallucinations

Hallucinations are experienced in the same way as the perception of an external stimulus would be, such as hearing or seeing something around you, but without any actual stimulus being present. For example, a person with a psychotic illness may hear voices talking to them that are not really there, or see people in front of them when there is no one there.

Hallucinations can occur in any sensory modality. However, the most common type of hallucination associated with schizophrenia is auditory hallucinations (hearing things that are not there). The hallucination must be experienced when the patient is fully awake and conscious to be classified as an actual symptom of disorder.

Disorganised thinking/speech

Disorganised thinking is best diagnosed from speech where ideas are loosely connected, or in severe cases, completely unconnected. In very severe cases the person's language may be completely incomprehensible because they are unable to make any connections between their thoughts—this may be referred to as 'word salad', which is a metaphor for the way individual words are tossed together during speech.

Disorganised thinking/speech means that the person randomly skips from topic to topic during conversation, and will answer questions with bizarre statements that do not seem to fit.

Abnormal motor behaviour/grossly disorganised behaviour (including catatonia)

The behaviour of individuals will be categorised as abnormal for many different reasons, but any motor movement that severely affects their ability to cope with daily life is categorised as grossly disorganised. This ranges from fidgeting to childish 'messing about' or even dressing bizarrely.

Within this category of symptoms is included catatonia, which is described as a significant decrease in the individual's responsiveness to the environment. They may sit completely still in odd postures, or refuse to speak to others, or even show continued, repetitive movements such as foot-tapping or hair-twirling that has no real meaning.

Features of schizophrenia

Prevalence and onset

The likelihood of a person developing schizophrenia is somewhere between 0.3 and 0.7 per cent, depending on factors such as their racial/ethnic background, where in the world they live, and their country of birth. There are also some gender differences in prevalence. For example, males are more likely to develop a higher proportion of negative symptoms and have a longer duration of the disorder, which are both associated with poor prognosis.

Episodes of psychosis associated with schizophrenia tend to appear between late adolescence and mid-thirties, with the peak of onset being around early to mid-twenties in males, and late twenties for females. Often the episodes develop gradually over a period of time and may not be obvious at first. Patients who show psychotic episodes earlier than in late adolescence appear to be more likely to have worse prognosis over the long term.

Prognosis

Other features

Alongside the core symptoms associated with schizophrenia listed above, there are other common features associated with diagnosis of the disorder. For example, many patients will show general cognitive functioning deficits in areas such as working memory, language functioning and speed of information processing.

Mood abnormalities are also common. Many patients describe periods of low mood similar to those experienced in depressive episodes, as well as inappropriate displays of mood such as laughing for no reason.

Biological explanation of schizophrenia: the function of neurotransmitters

The dopamine hypothesis

It is a long-established idea that schizophrenia may, at least in part, be explained by an increase of certain neurotransmitters in areas of the brain. The key neurotransmitter thought to be associated with psychosis is dopamine.

The development of this theory emerged from research in the 1960s. It was noted that patients who had abused large amounts of the drug amphetamine often showed positive symptoms of psychosis, such as hallucinations and delusions. Randrup and Munkvad (1966) raised dopamine levels in the brains of rats by injecting them with amphetamine. The rats' behaviour changed, becoming more agitated, aggressive and isolated, showing that when the dopamine levels increased it resulted in psychotic-type behaviour consistent with that shown in patients with schizophrenia.

By investigating the action of the drug, researchers found that amphetamine acts on the brain in a way that increases the level of the neurotransmitter dopamine. This sparked the beginning of the development of the dopamine hypothesis of schizophrenia. In 1967, a paper published by J.M. Van Rossum made a link between overstimulation of dopamine receptors and schizophrenia.

Research by Lieberman et al. (1987) states that about 75 per cent of patients with schizophrenia show new symptoms or an increase in psychosis after using drugs such as amphetamine and methylphenidate, which mimic the action of dopamine in the brain. However, only a small proportion of people who regularly use these drugs suffer from psychotic symptoms, which suggests that there is something different about how some people's brains react to dopamine that may explain the development of schizophrenia.

This is supported by the fact that post-mortem examinations on the brains of people who had schizophrenia show a higher density of dopamine receptors in certain parts of the brain (cerebral cortex) than do patients not suffering from schizophrenia (Owen et al. 1978), suggesting that they are more sensitive to the action of dopamine than people who have not had schizophrenia.

Recent research developments

Recent research has found that the amount of receptors may only account for about a 6 per cent increase from what is normally found in the brain. People diagnosed with schizophrenia have a higher number of D2High receptors (Seeman, 2013). These receptors have a higher affinity to dopamine, which means they are more likely to bind to the neurotransmitter when it is present in the synapse, accounting for the higher degree of sensitivity shown by the brains of people with schizophrenia to dopamine-type drugs.

Evaluation of the neurotransmitter theory

Supporting evidence: Evidence to support the dopamine hypothesis as an explanation for schizophrenia comes from the fact that many traditional antipsychotic medications used to treat schizophrenia act by reducing the effect of dopamine by blocking dopamine receptors. However, there are many problems with this research as a support for the theory.

Evidence contradicting the dopamine hypothesis: Even more problematic for this explanation is evidence that has found that clozapine can actually increase dopamine levels in some parts of the brain, which would contradict the dopamine hypothesis completely.

Cause and effect issues: Another issue to consider is whether the increase in levels of and sensitivity to dopamine is the cause of schizophrenia, or whether developing the illness changes brain chemistry in a way that results in this. Evidence can only be gathered from the brains of patients with schizophrenia after they have been diagnosed so it is unclear whether the brain was like this prior to diagnosis or not.

It is also problematic that many patients are already diagnosed as schizophrenic and have been given antipsychotic medication to treat their symptoms. Dopamine antagonists can cause up-regulation where the number of dopamine receptors increases, which can also increase levels of dopamine detected in the body. As schizophrenia is a relatively rare disorder it would be extremely difficult to test the brains of a sample of people who had never been diagnosed, and then monitor them to see if there were changes later if they were diagnosed with the illness. We have no way to predict who will develop schizophrenia.

Post-mortem studies have shown that patients with schizophrenia who have taken antipsychotics for some time have elevated levels of dopamine, which are not found in the brains of those who have not received medication, suggesting that there may be up-regulation (Haracz, 1982).

Alternative dopamine pathways

The biochemical explanation can also successfully explain negative symptoms of the illness, which other explanations can sometimes struggle to account for. A reduction of dopamine in the mesocortical pathways, which links to the mesolimbic system (including the reward pathway in the brain associated with motivation to repeat behaviours), can lead to flattened affect, lack of motivation and the depressed mood state of individuals with schizophrenia.

Reductionism

Brown and Birley (1968) found that 50 per cent of schizophrenic patients reported a major life event in the three weeks prior to relapse, suggesting that social conditions may trigger schizophrenia relapse. Although this does not directly propose that social triggers cause schizophrenia, it does indicate that we should be looking beyond the synaptic level when explaining schizophrenia.

Biological explanation of schizophrenia: genetics

Another biological explanation for schizophrenia is that there is evidence of a strong heritable factor in the development of the disorder. The risk of developing schizophrenia at some point in your lifetime for the general population is less than 1 per cent. However, if you have a second degree relative (for example, aunt/uncle, niece/nephew) with the illness, that risk increases to between 2 and 6 per cent.

If you have a first degree relative (for example, parent, sibling, dizygotic twin) with schizophrenia, the risk increases even more significantly to between 6 and 17 per cent. However, the biggest risk seen was in people who had an identical or monozygotic twin with schizophrenia, where there was a 48 per cent chance that they would be diagnosed with the illness too (Gottesman, 1991). The greater the degree of genetic relatedness, the higher the risk of developing the disorder, suggesting a strong genetic element to schizophrenia.

Evaluation of the genetic explanation

Family studies evidence: Family studies like this have established that there does appear to be some inherited component in the development of schizophrenia, as lifetime risk increases when the level of genetic similarity with a sufferer increases. However, research has failed to isolate a single recessive or dominant gene that seems to cause the illness (Tamminga and Schulz, 1991).

Criticisms of family studies: Family studies can also be criticised for failing to acknowledge that the incidence of schizophrenia in families may be a result of environmental influences. Research into dysfunctional family communication patterns and schizophrenic relapse rates indicate that schizophrenia may be a result of stress caused by negative emotions within families.

Twin studies analysis: It is important to note here that research such as that by Gottesman (1991) has found that in DZ twins the concordance rate is only around 17 per cent, while in MZ twins it is 48 per cent. Both sets of twins will have shared prenatal and post-birth environments, but MZ twins share 100 per cent of the same genes while DZ twins only share 50 per cent. The fact that MZ twins show such an increased concordance suggests that genes must play a role in the development of schizophrenia.

In comparison to other siblings, where the concordance found was 9 per cent in Gottesman's (1991) research, concordance rates in twins are increased. This could be accountable to a higher risk of birth complications in twins than in other pregnancies or the possibility that MZ twins are raised more similarly than DZ twins or siblings and are more likely to experience identity confusion (Joseph, 2004), products of environment and upbringing rather than genetics.

Adoption studies: Family and twin research has indicated that the greater degree of family relatedness, the higher concordance for schizophrenia, but it fails to control for environmental influences. Adoption studies remove this problem because they examine concordance of children that have been separated from their biological parents, thereby removing the influence of the environment.

An alternative biological theory: neuroanatomical theory

In 1919, Kraepelin first suggested that schizophrenia was a 'brain-based' illness, but there was a limited opportunity to test out this theory because it was impossible to study the brains of those diagnosed with schizophrenia until after death. Since the 1980s when there were advances in the use of brain-imaging techniques in research, psychologists have been interested in whether schizophrenia had any anatomical components.

There is a lot of research that has found that patients with schizophrenia have enlarged ventricles in the brain—these are cavities in the brain that store cerebrospinal fluid. Johnstone et al. (1976) used CAT scans to compare the brain structures of a group of schizophrenic patients, and a group of matched controls, and found that those with schizophrenia had significant enlargement in ventricular areas.

There was a significant increase in the size of ventricles throughout adolescence as the disorder progressed, and there was a relationship between the severity of negative symptoms measured in the patients and the increase in ventricle size. However, criticism of this explanation is that it is difficult to identify cause and effect as brain abnormalities may be the result of developing schizophrenia rather than the cause of the illness.

Developmental psychology

Schizophrenia is a disorder that can be explained through the process of development. The two biological explanations of schizophrenia dealt with here (neurochemicals and genetics) could be used to discuss issues in developmental psychology. The neurochemical balance in the brain is something that could be affected by many things including the genes you have from conception, prenatal factors such as maternal illness, and chemical exposure such as drugs used throughout life.

Non-biological explanation: cognitive theory

Frith's cognitive theory

The cognitive explanation of schizophrenia begins by attributing Type 1 (positive) symptoms of schizophrenia to biological causes. The experience of hallucinations and delusions is thought to be associated with biological factors, such as increased dopamine levels, but when the patient tries to make sense of this experience they begin to experience other symptoms of the illness. This is where the cognitive explanation can help us understand the disorder.

When the patient experiences a hallucination they may look to others to confirm what they think they have seen or heard, but when others cannot confirm this the patient may become wary of them and feel they are keeping information from them.

This can then, in turn, create further delusions of persecution or paranoia as the patient can feel that others are deliberately denying the experience they believe they are having. Therefore, many of the symptoms of schizophrenia are seen as a mistaken attempt by the patient to understand the experiences resulting from abnormal biological functioning in the brain.

But he argued that schizophrenic patients are unable to ignore these minor processes, and as such they experience an increased level of cognitive awareness that they cannot make sense of. Imagine, for example, having the experience of being told to check your watch to make sure you are not late for work. We may unconsciously keep checking our watch when we know we are due to arrive at work soon, but often this would not be something we would actually think about.

Someone with schizophrenia may experience this 'thought' as a voice telling them to check their watch because they might be late. For most of us, this thought would go unnoticed, but to a person with schizophrenia this might be experienced as an external voice telling them what to do. When they try to make sense of this and cannot, this can then lead to further delusions and worsening symptoms.

Social drift theory

Evidence has suggested that schizophrenia is more prevalent in lower social classes in society and this has been explained by the social drift hypothesis. This theory suggests that the symptoms of schizophrenia make it difficult for patients to hold down jobs, achieve well in education, and maintain relationships and so they often drop down into lower social and economic classes in society.

Consequently, there are greater concentrations of people with schizophrenia in the more deprived areas than there are in more affluent areas in society. People with schizophrenia also drift into the more urban areas because they can gain better access to support services than is possible in rural areas. For example, there is generally more cheap housing, food kitchens and social service provision available in cities than in small towns or villages, which can encourage people with schizophrenia to drift into these different societal areas.

Evaluation of the cognitive theory of schizophrenia

Supporting evidence: Research evidence has supported the idea that cognitive deficits are often associated with schizophrenia. For example, Gold and Harvey (1993) report that people with schizophrenia often score lower on tests of attention, memory and problem solving, than similar people without the disorder.

Evidence from theory of mind studies: Evidence from Corcoran et al. (1995) has found that patients with schizophrenia also show deficits in tasks requiring 'theory of mind', which is the cognitive skill associated with the ability to read and interpret the intentions of other people's behaviour. This means there is a strong evidence base behind the claim that schizophrenia has a cognitive cause.

This suggests that there is a pre-existing biological risk factor, which then affects the person's cognitive abilities. If there is a stressor in the individual's life, this will lead to continuing decline in cognitive processing, which could result in schizophrenia. Thus, although focusing on cognitive explanations for the disorder, separating out the biological factors is not easy and ultimately the explanation may be rooted in biology.

Genetic component in cognitive deficits: Sitskoom et al. (2004) found that the cognitive deficits found in patients with schizophrenia were also found in relatives of the patients who did not have the disorder. This suggests that there may be some genetic component underlying the cognitive deficit that is triggered in some people and not others.

Measurement difficulties: Another criticism would be that there is no easy way to measure whether the cognitive impairments seen in schizophrenic patients are the cause of the illness, or whether they are actually the effect of having schizophrenia. There may in fact be a combination of factors associated with developing schizophrenia and the cause of the illness could be a combination of all of these. This brings us back to the diathesis-stress model of mental illness mentioned earlier in the topic.

Nature-nurture debate

Biological explanations of schizophrenia suggest nature has the biggest influence on developing the illness, while social explanations would focus more on nurture as the cause. These two opposing views are part of a fundamental debate in determining work in clinical psychology in relation to whether disorders are something that develop due to internal factors mostly beyond our control, or whether mental health problems stem from external factors.

The cognitive explanation of schizophrenia suggests that the disorder is rooted in nature as the ability of the brain to process information will be best explained by biological factors. However, cognitive psychologists often talk about 'stressors' triggering the underlying problem, and these are usually external/environmental issues. This may suggest that there is a combination of factors that must be present in order for a person to develop schizophrenia.

Wider issues and debates

Use of psychological knowledge in society

The dopamine hypothesis emphasised to society that schizophrenia is an illness with a physical cause and therefore encouraged a change in opinions about treating those with mental health problems. The change in attitude towards medical treatment for disorders like schizophrenia has led to improvements in the understanding of how drugs can be used to alter brain chemistry.

Ethical issues

Drugs to treat schizophrenia have been well developed since the 1970s, but this is only possible through trials that have investigated the effects of different forms of medication. Many people have raised concerns about the ability of patients with psychotic illnesses such as schizophrenia to give informed consent regarding their participation in research. Someone who has lost touch with reality may not be able to consider all of the implications involved in their taking part in drug trials and this can cause problems with the ethics of such research.

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