Schizophreina Flashcards
What are positive symptoms?
Positive symptoms are an excess or distortion of normal functions, for example hallucinations, delusions and thought disturbances such as thought insertion.
What are the 3 positive symptoms and what are they?
Hallucinations are usually auditory or visual perceptions of things that are not present. Imagined stimuli could involve any of the senses. Voices are usually heard coming from outside the person’s head giving instructions on how to behave.
- Delusions are false beliefs. Usually the person has convinced him/herself that he/she is someone powerful or important, such as Jesus Christ, the Queen (e.g. Delusions of Grandeur). There are also delusions of being paranoid, worrying that people are out to get them.
- Psycho motor Disturbances: Stereotypical - Rocking backwards and forwards, twitches, & repetitive behaviours. Catatonia- staying in position for hours/days on end, cut off from the world.
What are the two types of negative symptoms and what are they?
Thought disorder in which there are breaks in the train of thought and the person appears to make illogical jumps from one topic to another (loose association). Words may become confused and sentences incoherent (so called ‘word salad). Broadcasting is a thought disorder whereby a person believes their thoughts are being broadcast to others, for example over the radio or through TV. Alogia - aka speech poverty – is a thought disorder were correct words are used but with little meaning.
• Avolition: Lack of volition (i.e. desire): in which a person becomes totally apathetic and sits around waiting for things to happen. They engage in no self motivated behavior. Their get up and go has got up and gone!
What are negative symptoms?
Negative symptoms are a diminution or loss of normal functions such as psycho motor disturbances, lack of volition, disturbances of mood and thought disorders.
How are hallucinations a limitation of the classification of schizophrenia?
Slater & Roth (1969) say that hallucinations are the least important of all the symptoms, as they are not exclusive to schizophrenic people.
How does the positive and negative symptom classification have good real life applicability?
Classification and diagnosis does have advantages as it allows doctors to communicate more effectively about a patient and use similar terminology when discussing them. In addition, they can then predict the outcome of the disorder and suggest related treatment to help the patient.
How can the positive and negative symptom diagnosis be harmful to sufferers or patients?
Scheff (1966) points out that diagnosis classification labels the individual, and this can have many adverse effects, such as a self-fulfilling prophecy (patients may begin to act how they are expected to act), and lower self-esteem.
How are the ethics of classification both advantages and weaknesses?
Ethics – do the benefits of classification (care, treatment, safety) outweigh the costs (possible misdiagnosis, mistreatment, loss of rights and responsibility, prejudice due to labelling).
What is reliability in classification?
For the classification system to be reliable, differfent clinicians using the same system (e.g. DSM) should arrive at the same diagnosis for the same individual.
How is self report a weakness of diagnosis?
Diagnosis of schizophrenia is difficult as the practitioner has no physical signs but only symptoms (what the patient reports) to make a decision on.
Who’s study demonstrated the high reliability of classifications of diagnosis in schizophrenia?
Jakobsen et al. (2005) tested the reliability of the ICD-10 classification system in diagnosing schizophrenia. A hundred Danish patients with a history of psychosis were assessed using operational criteria, and a concordance rate of 98% was obtained. This demonstrates the high reliability of the clinical diagnosis of schizophrenia using up-to-date classification.
How does co-morbidity make diagnosis and classification unreliable?
Co-morbidity describes people who suffer from two or more mental disorders. For example, schizophrenia and depression are often found together. This makes it more difficult to confidently diagnose schizophrenia. Co-morbidity occurs because the symptoms of different disorders overlap. For example, major depression and schizophrenia both involve very low levels of motivation. This creates problems of reliability. Does the low motivation reflect depression or schizophrenia, or both?
How is there a gender bias in classification and diagnosis?
Gender bias: Loring and Powell (1988) found that some behaviour which was regarded as psychotic in males was not regarded as psychotic in females.
What is validity in relation to classification and diagnosis?
For the classification system to be valid it should be meaningful and classify a real pattern of symptoms, which result from a real underlying cause.
How is the diagnosis and classification invalid due to the fact it is one disorder?
The validity of schizophrenia as a single disorder is questioned by many. This is a useful point to emphasise in any essay on the disorder. There is no such thing as a ‘normal’ schizophrenic exhibiting the usual symptoms.
How is the problem of the validity of classification lead to another limitation?
Since their are problems with the validity of diagnosis classification, unsuitable treatment may be administered, sometimes on an involuntary basis. This raises practical and ethical issues when selecting different types of treatment.
How are there problems in validity of diagnosis and classification due to a misrepresentation in what we are actually testing?
Problems of validity: Are we really testing what we think we are testing? In the USA only 20% of psychiatric patients were classed as having schizophrenia in the 1930s but this rose to 80% in the 1950’s . In London the rate remained at 20%, suggesting neither group had a valid definition of schizophrenia.
How is the idea of schizophrenia as an umbrella term a limitation?
Neuropsychologist Michael Foster Green suggests that neurocognitive deficits in basic functions such as memory, attention, central executive and problem solving skills may combine to have an outcome which we are labelling “Schizophrenia” as if it was the cause when in fact it is simply an umbrella term for a set of effects.
How is diagnosis invalid due to the assigning of treatments?
Predictive validity. If diagnosis leads to successful treatment, the diagnosis can be seen as valid. But in fact some Schizophrenics are successfully treated whereas others are not. Heather (1976) there is only a 50% chance of predicting what treatment a patient will receive based on diagnosis, suggesting that diagnosis is not valid.
How is validity of diagnosis ruined through cause?
Aetiological validity – for a diagnosis to be valid, all patients diagnosed as schizophrenic should have the same cause for their disorder. This is not the case with schizophrenia: The causes may be one of biological or psychological or both.
Who conducted research into diagnosis of schizophrenia and what did they show as an limitation?
David Rosenhan (1972) famous experiment involving Pseudo patients led to 8 normal people being kept in hospital despite behaving normally. This suggests the doctors had no valid method for detecting schizophrenia. They assumed the bogus patients were schizophrenic with no real evidence. In a follow up study they rejected genuine patients whom they assumed were part of the deception.
How does schizophrenia have a culture bias and therefore lacks validity?
Culture - One of the biggest controversies in relation to classification and diagnosis is to do with cultural relativism and variations in diagnosis. For example in some Asian countries people are not expected to show emotional expression, whereas in certain Arabic cultures public emotion is encouraged and understood. Without this knowledge a person displaying overt emotional behaviour in a Western culture might be regarded as abnormal.
What is the genetic basis of schizophrenia?
Benzel et al. (2007) three genes: COMT , DRD4 , AKT1 - have all been associated with excess dopamine in specific D2 receptors, leading to acute episodes, positive symptoms which include delusions, hallucinations, strange attitudes.
Who’s (2 studies) research into DNA has provided a basis for the genetic basis of schizophrenia?
Research by Miyakawa et al. (2003) studied DNA from human families affected by schizophrenia and found that those with the disease were more likely to have a defective version of a gene, called PPP3CC which is associated with the production of calcineurin which regulates the immune system. Also, research by
Sherrington et al. (1988) has found a gene located on chromosome 5 which has been linked in a small number of extended families where they have the disorder.
Who’s study ( 2 studies) showed how closeness of biological relationship can affect schizophrenia?
Evidence suggests that the closer the biological relationship, the greater the risk of developing schizophrenia. Kendler (1985) has shown that first-degree relatives of those with schizophrenia are 18 times more at risk than the general population. Gottesman (1991) has found that schizophrenia is more common in the biological relatives of a schizophrenic, and that the closer the degree of genetic relatedness, the greater the risk.
How do mono zygotic twins act as limitation of biological diagnosis of schizophrenia?
Very important to note genetics are only partly responsible, otherwise identical twins would have 100% concordance rates.
How are there methodological problems with the biological diagnosis of schizophrenia?
One weakness of the genetic explanation of schizophrenia is that there are methodological problems. Family, twin and adoption studies must be considered cautiously because they are retrospective, and diagnosis may be biased by knowledge that other family members who may have been diagnosed. This suggests that there may be problems of demand characteristics.
How is the issue of nature nurture a limitation of the biological diagnosis of schizophrenia?
It is very difficult to separate out the influence of nature-v-nurture. The fact that the concordance rates are not 100% means that schizophrenia cannot wholly be explained by genes and it could be that the individual has a pre-disposition to schizophrenia and simply makes the individual more at risk of developing the disorder. This suggests that the biological account cannot give a full explanation of the disorder.
How is the reductionist approach of biological diagnosis a limitation?
A final weakness of the genetic explanation of schizophrenia is that it is biologically reductionist. The Genome Project has increased understanding of the complexity of the gene. Given that a much lower number of genes exist than anticipated, it is now recognised that genes have multiple functions and that many genes behaviour. Schizophrenia is a multi-factorial trait as it is the result of multiple genes and environmental factors. This suggests that the research into gene mapping is over simplistic as schizophrenia is not due to a single gene.
What is the dopamine hypothesis and what does high dopamine levels relate to?
Dopamine is a neurotransmitter. It is one of the chemicals in the brain which causes neurons to fire. The original dopamine hypothesis stated that schizophrenia suffered from an excessive amount of dopamine. This causes the neurons that use dopamine to fire too often and transmit too many messages.
• High dopamine activity leads to acute episodes, and positive symptoms which include: delusions, hallucinations, confused thinking.
Where does evidence for the dopamine hypothesis come from?
Evidence for this comes from that fact that amphetamines increase the amounts of dopamine. Large doses of amphetamine given to people with no history of psychological disorders produce behaviour which is very similar to paranoid schizophrenia. Small doses given to people already suffering from schizophrenia tend to worsen their symptoms.
What is the second dopamine hypothesis refering to the receptors?
A second explanation developed, which suggests that it is not excessive dopamine but that fact that there are more dopamine receptors. More receptors lead to more firing and an over production of messages. Autopsies have found that there are generally a large number of dopamine receptors (Owen et al., 1987) and there was an increase in the amount of dopamine in the left amygdala (falkai et al. 1988) and increased dopamine in the caudate nucleus and putamen (Owen et al, 1978).
How is the cause and effect argument a limitation of the dopamine hypothesis?
One criticism of the dopamine hypothesis is there is a problem with the cause and effect. Is the raised dopamine levels the cause of the schizophrenia, or is it the raised dopamine level the result of schizophrenia? It is not clear which comes first. This suggests that one needs to be careful when establishing cause and effect relationships in schizophrenic patients.
How is a study done on normal non schizophrenic individuals, a limitation of the biological diagnosis?
One of the biggest criticisms of the dopamine hypothesis came when Farde et al found no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals in 1990.
How is evidence for no association between anti psychotics and schizophrenia a limitation?
Noll (2009) also argues around one third of patients do not respond to drugs which block dopamine so other neurotransmitters may be involved.
How is the biological diagnosis of schizophrenia a weakness?
A final weakness of the dopamine hypothesis is that it is biologically deterministic. The reason for this is because if the individual does have excessive amounts of dopamine then does it really mean that thy ey will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
What are neural correlates?
• People with schizophrenia have abnormally large ventricles in the brain. Ventricles are fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste. This means that the brains of schizophrenics are lighter than normal. The ventricles of a person with schizophrenia are on average about 15% bigger than normal (Torrey, 2002).
What is a strength of neural research into neural correlates in diagnosis?
A strength is that the research into enlarged ventricles and neurotransmitter levels have high reliability. The reason for this is because the research is carried out in highly controlled environments, which specialist, high tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the basil ganglia, the hippo campus and the amygdale. This suggests that if this research was tested and re-tested the same results would be achieved.
Who’s study supports neural correlates as a diagnosis for schizophrenia?
Supporting evidence for the brain structure explanation comes from further empirical support from Suddath et al. (1990). He used MRI (magnetic resonance imaging) to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic. The schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the schizophrenic twins could be easily identified from the brain images in 12 out of 15 pairs. This suggests that there is wider academic credibility for enlarged ventricles determining the likelihood of schizophrenia developing.
How are neural correlates deterministic and how is this a weakness?
A second weakness of the neuroanatomical explanations is that it is biologically deterministic. The reason for this is because if the individual does have large ventricles then does it really mean that they will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.
