Schizophrenia Flashcards
AO1 Classification of Schizophrenia
1% of the population have the disorder, onset of first symptoms is around 15-45 years.
Men are more likely to develop the disorder, with males also having an earlier onset
The diagnostic and statistical manual / DSM is most often used for classification.
However the ICD / International classification of Disease can also be used. Two of the following symptoms need to be present for at least a month, one being positive
Positive Symptoms: Experiences that are in addition to normal experiences.
* Hallucinations - Additional sensory experiences such as seeing distortions in objects that look like faces, or hearing critical voices.
* Delusions - Irrational beliefs about themselves or the world. For example feelings of persecution “ i.e. the government” or feelings of grandeur “president”
Negative Symptoms: Loss of normal experiences and abilities.
. Avolition - A lack of purposeful, willed behaviour. No energy, sociability affection or attempt at personal hygiene. Generally apathetic.
. Speech poverty - Brief verbal communication style. Loss of quality and quantity of verbal responses. Can be classified as a positive symptom if speech is excessively disorganised, with sufferers wondering off the point.
Biological Explanations of Schizophrenia (Genetic) - A01
The genetic explanation for schizophrenia suggests that schizophrenia is inherited and results from a biological process driven by the activity of certain genes, such as brain structure development and neurotransmitter levels.
There is no one “schizophrenia gene”, however a collection of gene locations have been located that are associated with a higher risk of developing schizophrenia. This means schizophrenia is thought to be a polygenetic disorder. If Schizophrenia is genetic then we expect to see the more closely related two people are, if one person has the disorder the more likely the other person is to have the disorder (concordance rate)
Twin studies are particularly interesting for psychologists studying the genetic basis of schizophrenia as monozygotic twins are genetically identical and share environments
Gottesman (1991) reviewed cases of schizophrenia in famailes and found a concordance rate of 48% for identical twins (Monozygotic/MZ) and 17% for non identical twins (Dizygotic/DZ). This compares to the general population rate of 1%. This suggests schizophrenia has a genetic aspect as there is such a large difference between the two sets of twins. Both DZ and MZ twins should share similar environments. However concordance not 100% in MZ so not fully genetic.
Clinical Characteristics of Schizophrenia (A01)
- Perceptual symptoms
Auditory hallucinations - hearing things that aren’t there. People often hear voices saying abusive things. Auditory hallucinations are the most common type of hallucination in schizophrenia, but there are other types of hallucination too. Sometimes people see, feel, smell or taste things that aren’t there. - Social symptoms
Social withdrawal - not taking part in or enjoying social situations.
People might be aloof or avoid eye contact. - Cognitive symptoms
. Delusions - believing things that aren’t true. People can have delusions of grandeur (where they believe they’re more important than they are, e.g. that they’re the king) or of paranoia and persecution (where they believe people are out to get them). Some people with schizophrenia also experience delusions of control - they believe that their behaviour is being controlled by somebody else. For example, thought insertion is when someone feels that thoughts are being put into their head. Thought withdrawal is when they believe that someone is removing their thoughts. They might also believe that people can read their thoughts - this is thought broadcasting.
. Language impairments - irrelevant and incoherent speech. People often show signs of cognitive distractibility, where they can’t maintain a train of thought. They might also repeat sounds others say (echolalia), speak nonsense or gibberish (word salad), speak in nonsensical rhymes (clang associations), experience speech poverty (give very brief replies in conversation and show no extra, spontaneous speech) and invent words (neologisms). - Affective / emotional symptoms
. Avolition - a lack of drive, motivation or interest in achieving goals.
. Lack of interest in hygiene and personal care.
Lack of emotion - not reacting to typically emotional situations. This is also called emotional blunting.
Inappropriate emotions - reacting in an inappropriate way, e.g. laughing at bad news. - Behavioural symptoms
. Stereotyped behaviours - continuously repeating actions, which are often strange and don’t have a purpose.
. Psychomotor disturbance - not having control of your muscles. People may experience catatonia, where they sit in an awkward position for a long time. In this state people will sometimes stay in whatever position they re put in (so if you lift their arm over their head ill stay like that until you move it back). Catatonic stupo involves lying rigidly and not moving for long periods of time. People are conscious during these episodes and can remember what was going on around them, although they don’t seem aware of it at the time.
Clinical Characteristics of Schizophrenia (A03)
— There is a significant co-morbidity (high frequency of diagnosis of two disorders together) between schizophrenia and other mental health disorders, such as OCD and post-traumatic stress disorder, as suggested by Buckley et al (2009). These researchers found that 29% of their SZ patients suffered from post-traumatic stress disorder, whilst 50% suffered depression. Particularly in the case of depression, this suggests that if schizophrenia is so frequently diagnosed with other psychiatric disorders, then these two disorders may actually be the same, and so a more accurate and valid method of diagnosis would be to combine these two. Therefore, there are issues of validity in the
diagnosis of SZ and attempting to differentiate its symptoms from that of other disorders.
— There may be gender bias in the diagnosis of schizophrenia, as suggested by Longenecker et al (2010), who could not find an explanation for the sudden increase in the number of male SZ diagnoses made after 1980s. Cotton et al (2009) suggests that because there are no differences in genetic susceptibility for men and women in terms of SZ, then gender bias must be to blame. Dispositional traits of most women, such as high interpersonal functioning and being able to work even when suffering, means that such traits may mask the symptoms of schizophrenia or distort their severity so that they are not serious enough to call for a diagnosis. This means that the current system
of the diagnosis of SZ does not account for these biases or differences in functioning between men and women, increasing the likelihood of inaccurate diagnoses.
— A second type of bias which may reduce the validity of the diagnosis of SZ is the problem of gender bias, as suggested by Escobar et al (2012). For example, African Americans are far more likely to be diagnosed with SZ compared to patients belonging to Western cultures, due to their increased openness about admitting to certain SZ symptoms which may appear normal in their respective cultures. For example, the phenomenon of hearing voices may be considered a desirable sign of increased spirituality and connectedness with ancestors, and so may even be encouraged. However, both classification systems would view this as a hallmark characteristic of SZ and, combined with the potential distrust in African Americans that white psychiatrists may have, could increase the likelihood of false diagnoses.
Biological Explanations (Genetic) Schizophrenia - A03
+ There is evidence supporting the biological and genetic basis of schizophrenia. For example, Brown et al (2002) found that the risk of having offspring with SZ increased by over 1.3% if the father was over 50 years old, compared to if the father was under the age of 25. Therefore, this suggests that mutations in the sections of DNA containing the candidate genes, such as those coding for serotonin and dopamine production specifically, means that SZ is likely to have a strong heritability coefficient and biological basis. This supports the use of family studies and neural correlates as ways of studying and explaining incidence rates of SZ.
— The evidence for the dopamine hypothesis can be best described as ‘mixed’. On the one hand, support comes from Tauscher et al (2014) who found that antipsychotics, which act as dopamine antagonists and so reduce dopamine activity by binding to complementary receptors on the post-synaptic membrane, alleviated the symptoms of SZ, suggesting that dopamine has a key role in its development, in line with the predictions of the dopamine hypothesis. On the other hand, some researchers such as Moghaddam and Javitt (2012) have criticised the dopamine hypothesis and biological explanations of SZ as emphasising the role of dopamine too far. For example, the neurotransmitters glutamate and serotonin may also play a key role, as evidenced by the antipsychotic Clozapine acting upon both of these substances and being more effective than other atypical antipsychotics in reducing SZ symptoms, as suggested by Meltzer (2012).
— The main issue associated with the use of neural correlates as a means of explaining schizophrenia is that such evidence is correlational and so does not take into account the ‘third variable problem’, whereby a third unstudied factor could be affecting both outcomes. Taking the example of the link between lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus, and the experience of auditory hallucinations, one explanation would be the lowered activation levels causing the hallucinations, or the hallucinations themselves causing the lowered activation levels. A third possible explanation would be the third variable problem. Therefore, this demonstrates that correlational research cannot be used to reliably demonstrate a ‘cause and effect’ relationship between two variables.
Psychological Explanations For Schizophrenia (AO1)
- Psychological explanations suggest that the development of schizophrenia is due to abnormal family communication styles created by the schizophrenogenic mother, mixed messages according to double-bind theory, and the stress caused by high levels of expressed emotion. Despite none of these three factors explicitly causing schizophrenia, they are involved in its development and maintenance as contributory factors.
- Fromm-Reichmann suggested that there is a classic, schizophrenogenic mother who is characterised as being cold and rejecting. This means that the family climate is tense and lacking honesty, which leads to the development of paranoia and anxiety. These feelings manifest themselves in the (positive) schizophrenic symptom of paranoid delusions.
- Double-bind theory (Bateson) suggests that within a family, the child receives mixed messages from both parents about what is right or wrong. The tense atmosphere or controlling parenting style means that the child is unable to clarify these messages or voice their opinions about the unfairness of conflicting messages. When the child makes a mistake, as they often do, they are punished through a withdrawal of love. This means that the child sees the world as unfair and confusing due to this confliction, as reflected in the schizophrenic symptoms of disorganised thinking and paranoid delusions.
- Expressed emotion describes the level and type of emotion shown towards the patient by their carer, and is often a significant source of stress for the patient. This means that they are less likely to take their medication or comply to cognitive therapies provided by their hospital or institution, hence being a leading cause for relapse. Examples of high levels of negative expressed emotions include verbal criticism of the patient, needless ‘sacrifices’ for the patient and violence with hostility.
- Frith et al (1992) suggested that dysfunctional thought processes (abnormally-functioning thought processes which lead to unpleasant/ undesirable outcomes), including metarepresentation and central control, contribute to the development of schizophrenia.
- Metarepresentation is the cognitive ability to differentiate between our own actions and the actions of others, allowing us insight into the intentions and emotions as others, as well as maintaining a realistic/functional view of our own goals and intentions. Dysfunctions in metarepresentation have been associated with auditory hallucinations, and specifically thought insertion, due to the inability to Schizophrenia differentiate between our own thoughts and that of others. This may lead to paranoid delusions due to the contents of inserting others’ thoughts into the mind of the patient.
- Central control is the cognitive ability to carry out a deliberate action whilst suppressing an automatic response, and is often measured using the Stroop Test. This test involves identifying the colour of each word, where there is often a discrepancy e.g. the word ‘brown’ written in a yellow font. Therefore, the automatic response of reading the word must be suppressed, to allow for identification of the font colour. People with SZ often have dysfunctional central control abilities, and so often suffer from derailment because they cannot suppress the automatic associations that each new word in a sentence brings, and so begin to talk off-topic.
Psychological Explanations For Schizophrenia (AO3)
+ There is evidence supporting the idea that dysfunctional thought processes are implicated in the development of schizophrenia, and that faulty central control skills may be responsible for some SZ symptoms, as demonstrated by Stirling et al (2006). The researchers found that SZ sufferers made significantly more mistakes and twice as long to complete the task, compared to a healthy neurotypical control group. However, it should be emphasised that dysfunctional thought processing can only offer explanations for the indirect, proximal causes of SZ, and not the distal causes, meaning that such theories can explain the symptoms but not the origin of SZ. This limits the utility of psychological explanations for schizophrenia.
— A comparison can be made between biological and psychological explanations for SZ. A significant weakness of psychological explanations for SZ is that they do not accommodate for biological factors. Since such biological factors can explain the distal origins of schizophrenia (i.e. in terms of dopamine levels in the brain, candidate genes and patterns of activity coinciding with symptoms/ neural correlates), this suggests that psychological explanations would best be reserved for the proximal causes of SZ, as these causes are more likely to be most affected by psychological factors.
— A second major weakness would be the lack of support for family-based explanations. The idea of the schizophrenogenic mother was based upon historical observations of families with SZ members, where observers would be searching for ‘crazy-making characteristics’ (Harrington, 2012) which is hardly an objective and reliable indicator of the likelihood of developing SZ. Psychological explanations also place an increasing amount of blame on the families and caregivers of patients with SZ, as opposed to accommodating for the possibility of a genetic/biological predisposition. For example, caregivers/ parents are further hurt when they are forced to accept responsibility for their patient’s schizophrenia, which is likely to have already upset family life and relationships through the development of severe and intrusive negative and positive symptoms. This may explain the sudden popularity of community care in the 1980s, which could have marked parents refusing to take responsibility for their child’s condition, seeing as they are so dedicated to their care.
Problems with reliability for diagnosing schizophrenia
1) Schizophrenia diagnosis may be affected by cultural bias. For example, Harrison et al (1984) showed that there was an over-diagnosis of schizophrenia in West Indian psychiatric patients in Bristol. No research has found any cause for this, so it suggests that the symptoms of ethnic minority patients have been misinterpreted. This questions the reliability of the diagnosis of schizophrenia - it suggests that patients can display the same symptoms but receive different diagnoses because of their ethnic background.
2) Cultural bias has also been shown to stem from the medical staff themselves. Copeland et al (1971) found that 69% of American psychiatrists in the study diagnosed a particular patient (shown in a video) as having schizophrenia compared with only 2% of British psychiatrists asked to diagnose the same patient.
3) Reliably diagnosing schizophrenia can also be difficult due to gender bias. Loring and Powell (1988) conducted a study where 290 psychiatrists were asked to diagnose the same two patients. When they were told the patient was male, 56% diagnosed the patient as having schizophrenia. If they were told the patient was female, this dropped to around 20%, despite symptoms being identical. This gender bias wasn’t as clear if the psychiatrists were female. So, gender bias comes not only from the gender of the patient, but also from the gender of the practitioner.
Problems with validity with diagnosing Schizophrenia
1) Rosenhan (1973) conducted a study where people with no mental health problem got themselves admitted into a psychiatric unit by saying they heard voices - they became pseudo patients. Once they’d been admitted they behaved ‘normally’. However, their behaviour was still seen as a symptom of their disorder by the staff in the unit. For example, one pseudo patient who wrote in a diary was recorded as displaying writing behaviour’. This questions the validity of the diagnosis of mental disorders - once people are labelled as having a disorder, all of their behaviour can be interpreted as being caused by the disorder.
2) Symptom overlap can also cause problems with the validity of diagnosis. Lots of the most common symptoms in schizophrenia are also found in other disorders. For example, avolition is also a symptom of depression. This makes it hard to determine which disorder the patient may have.
Comorbidity
- Comorbidity can also be an issue in making a reliable and valid diagnosis of schizophrenia.
- Comorbidity means having two or more conditions at the same time. For example, patients with schizophrenia may also have depression. Having more than one condition makes it really difficult for healthcare professionals to diagnose schizophrenia as a distinct mental illness.
- It could be that some of their symptoms belong to one known disorder, but that the others belong to an untreated mental disorder which hasn’t been recognised yet.
Biochemical Factors
Post-mortems and PET scans have shown that people with schizophrenia have abnormally high levels of the neurotransmitter dopamine. These findings led to the development of the dopamine hypothesis, which states that synapses that use dopamine as a neurotransmitter are overactive in the brains of people with schizophrenia.
Evidence For:
1) Antipsychotic drugs reduce the symptoms of schizophrenia by blocking dopamine receptors. This suggests that it’s the overactive dopamine receptors causing the symptoms.
2) Drugs like amphetamines, which increase dopamine function, can sometimes cause schizophrenia-like symptoms in people without schizophrenia.
Evidence Against:
1) Antipsychotic drugs only work on the positive symptoms of schizophrenia, e.g. hallucinations. This means increased dopamine function doesn’t explain negative symptoms like social withdrawal.
2) The link with dopamine is correlational, so it doesn’t show cause and effect. It may be that increased dopamine function is a symptom of schizophrenia, rather than a cause of It.
Neurological Factors
Neural correlates, such as abnormal brain structure, could explain schizophrenia
1) Johnstone et al (1976) compared the size of the ventricles (hollow areas) The dopamine hypothesis is also an example of a neural correlate in the brains of people with schizophrenia with the brains of those without schizophrenia. They found that the people with schizophrenia had enlarged ventricles, which suggests that schizophrenia is linked to a reduction in the temporal and frontal lobe volume.
2) Buchshaum’s (1990) MRI scans on the brains of people with schizophrenia found abnormalities in the prefrontal cortex.
Evidence against.
1) People without schizophrenia can also have enlarged ventricles, showing the relationship isn’t that simple.
2) These findings are correlational, so they don’t show cause and effect. It may be that abnormal brain structure is a symptom of schizophrenia, rather than a cause of it.
Evolutionary Explanation
. Some evolutionary explanations of schizophrenia suggests that there must have been an advantage to having schizophrenia for it to remain in the population.
. One evolutionary idea is that people diagnosed with schizophrenia today share similar characteristics to shamans of the past.
. They were likely to lead people to split off from a group when it got too big, starting new cultures.
Evidence for…
There is such a strong genetic link to schizophrenia, that there must be some form of evolutionary explanation.
Evidence against…
There is little evidence and the theory is difficult to prove.
Psychological Factors Family Dysfunction (A01)
Family Dysfunction
* Psychologists have suggested that conditions in dysfunctional families could cause schizophrenia.
. One idea is that a cold and dominant ‘schizophrenogenic’ mother could create conflict, causing schizophrenia.
- Another idea is Bateson’ (1956) Double Bind Theory, which suggested that faulty communication in families could lead to contradictory messages for children and cause schizophrenia.
- Expressed emotion (EE) environments contain high levels of hostility and criticism towards the person with schizophrenia. EE has been found in dysfunctional families and correlates with relapse in people with schizophrenia. For example, Vaughn and Leff (1976) found that people with schizophrenia were more likely to relapse once discharged from hospital in environments of high EE.
Psychological Factors Family Dysfunction (A03)
Other research investigating the role of the family on schizophrenia supports the theory of family dysfunction. For example, Lidz et al (1958) investigated families and proposed that dysfunctions such as emotionally distant parents and unequal marriages could have an impact on the children in the family, ultimately leading to schizophrenia.
The theory ignores the biological evidence for schizophrenia and puts the blame on the family and parents. Most of the studies into the effects of family dysfunction were also retrospective - the families were only studied after the disorder had developed, and so it could have been the condition itself that had disrupted family life.
