ok guys, i'm attempting to learning all of this 2nite. gna focus the most on ocd and the least on depression bcs of the recent exam questions. what would rly speed up the process is if ne1 would post model answers or just what needs to be in an answer for ocd, dpression and schiz! go on u know u want to... it'll help your revision as well...
I don't know how much this helps, but here is an essay I did on schitzophrenia that I got almost full marks on (-I am just gonna memorise it and hope that I can somehow inject it into whatever is asked..lol, thats what I usualy do, just memorise essays.)
“Psychological explanations of schizophrenia are an essential aspect of a fully understanding of this condition”. Discuss psychological explanations of schizophrenia with reference to this quote.
Schizophrenia is a mental disorder which affects about 1% of the population. The symptoms exhibited vary somewhat, but typically include problems with attention, thinking, social relationships, motivation, and emotion.
There are multiple psychological explanations of schizophrenia, one of which is the psychodynamic approach. While Freud was mostly concerned with neurotic disorders, he did develop a theory on schizophrenia. He saw it as a form of regression, happening because a person has a very weak ego which cannot deal with unacceptable id impulses. This produces a struggle which causes great anxiety which makes the person regress as a defence mechanism to a state characteristic of the oral stage (a time when the id is dominant and the ego hasn’t properly formed). When the child reaches adolescence, the id’s impulses for gratification become very strong and the anxiety this creates causes schizophrenia to commonly appear at this time.
A more modern psychodynamic explanation by Harry Stack Sullivan in 1962 places less emphasis on sexual impulses and looks more at personal relationships, particularly a damaged mother-child relationship. Stack believes that experiencing anxious and hostile relationships with the parents in early childhood causes the child to become withdrawn and lacking in trust and the ability to establish strong bonds with others. As time goes on this behaviour increases until the child retreats into a fantasy world and their problems get worse. This theory brought about the idea of the “schizophrenogenic mother”, which is a mother who is cold, rejecting, domineering and overprotective.
This theory has been shown to be very useful in the understanding of schizophrenia through the treatment it has brought about. The treatment brought up through this theory is verbal therapy which asks the person to think about their situation and understand the cause of it. Particular emphasis was put on family therapy and focusing on expressed emotion (EE) by Stack. There is considerable evidence to show that kids from a family with high EE are much more likely to have a relapse of their schizophrenia. (That is high expression of negative emotions such as rejection). The rate of relapse is 3to 4 times higher when a schizophrenic child goes home to a high EE family than a low one. 103 schizophrenic patients living within high EE families were randomly assigned to 4 groups and looked at for over a year. Group 1 where given medicine and family therapy, Group 2 medicine and social skills training, Group 3 a combination of what both Group 1 and Group 2 got and Group 4 received medicine only. The relapse rate showed 20% for Group 1, 20% Group 2, 0% for Group 3 and 41% for Group 4. This very strongly supports the idea that working on the high EE rate helps a patient not to relapse. This is useful information and would support the quote because it does give us a better understanding of the disorder. However the fact that drugs were used as well as therapy and EE work means that it was not entirely psychodynamic, so some may say that the biological approach is just important. It is perhaps not as important though because the group who received just medicine had the highest relapse rate. This would indicate that while this psychological approach is crucial in furthering our understanding of this disorder it needs to be looked at in conjunction with other approaches.
Another psychological approach to consider would be the behavioural approach. This is based on operant and classical conditioning, with a particular emphasis on operant conditioning. This approach suggests that a child has learned through the way the parent treats them that much of what he does is punished or ignored. This causes the child to become withdrawn and not learning to respond properly to social signals. (The wont understand these signals). This early experience makes the child withdrawn and idiosyncratic. When the child is punished they will withdraw or get attention which will reinforce the behaviour. It is possible that once people show this kind of behaviour the doctor labels them as schizophrenic and then they seem to be schizophrenic to other people, simply by having this label. There is no evidence to support the idea that schizophrenia develops in this way, however there is evidence that schizophrenic behaviour can be eliminated by the learning theory. Some studies have indicated that schizophrenics show weird behaviour more when psychiatric staff are near by. This may however be unconscious. Also, training programmes using operant conditioning in which desirable behaviour is rewarded and undesirable behaviour ignored have been shown to the very effective. It appears that you can change schizophrenia with this; however it does not work on some symptoms such as hearing voices, so it appears that perhaps this is more a method of dealing with the problem rather than actually eliminating it. This has been useful though and has led to treatments that have improved schizophrenia and it has introduced social skills learning which is very widely used, especially for those on medication. This too would support the quote in that it has been very useful in our fuller understanding of schizophrenia and has produced useful help for schizophrenics.
A final psychological explanation to consider would be the cognitive approach. This states the idea that problems paying attention in a family leads to over aroused, unpredictable behaviour which may be particularly bad in families with negative attitudes (shouting) and early experience of this kind can develop into psychosis. This links with brain functioning which is a biological approach. Type 1 symptoms can be seen as a result of over attention, for example, being unable to focus on one thing which shows itself in disorganised speech. Auditory hallucination is a sign of over attention because they cannot filter out noise. There is strong evidence from lab experiments that schizophrenics with type 1 symptoms are worse than normal at filtering out stimuli and paying attention to one thing. Type 2 patients cannot pay enough attention which may lead to withdrawal. There is some evidence that 40-50% of schizophrenics fail to show normal physiological arousal to stimuli. This has not lead to any type of treatment which would suggest that it is not particularly important in our overall understanding of schizophrenia, however even through not producing any treatment, it has shown us which areas need to be concentrated on and which need less attention and can help our general knowledge and therefore our attitude towards schizophrenia.
A general point to bear in mind is that people do not always agree on whether someone is schizophrenic. In the 60’s agreement between psychiatrists was between 50-70% on if someone was schizophrenic, however thanks to the DSM IV it is now clearer on what a patient needs to be showing in order to be diagnosed as schizophrenic, so the agreement is now about 90%. Most people now accept the diathesis stress approach which states that a patient will only develop full blown schizophrenia is they have predisposing factors of either genetics, or mother having a viral infection during the second trimester of pregnancy, and then a stressor such as drugs, or a major negative life event, which triggers the disease.
In conclusion, it would seem that the quote is correct in saying that psychological explanations of schizophrenia are an essential aspect of a fully understanding of this condition. These approaches have either produced very useful treatments or they have simply added to our overall knowledge, all of which help us to have a much broader understanding of schizophrenia. It is however obvious that psychological explanations can only explain so much and need to be considered in conjunction with other approaches to fully aid in the treatment and understanding of schizophrenia.
probably not very helpful,but let me know if it is and I can see if I have any others. probs have one on depression, but not OCD cause we don't do that..
xx
Heres some notes on biological explanations of schizophrenia, AO1= black, AO2 = blue:
Clinical characteristics
Delusions – these are beliefs that seem real to the patient but are not real. It may be a belief that the behaviour or comment on someone on TV was specifically meant for them alone.
Experience of control – the person may believe they are under the control of an alien force that has invaded their mind and body.
Hallucinations – bizarre unreal perceptions of the environment, they are usually auditory (hearing voices) but can also be visual (seeing faces).
Disordered thinking – the feeling that someone has put in or taken thought out of the mind. The person may believe their thoughts are being broadcast so everyone can hear them.
Biological explanations
1) Genetic factors
According to this explanation schizophrenia runs in the family and genes are responsible for the disorder. Gottesman summarised 40 studies; concordance rates are 48% if you have a MZ twin with schizophrenia and 17% if you have a DZ twin with schizophrenia. Schizophrenia is more common in biological relatives, the closer the relatedness the greater the risk. For example there is a greater risk of schizophrenia if a first degree relative (e.g. sibling) has it than if a second degree relative (e.g. nephew) has it.
Rosenthal studies 4 identical girls (quadruplets), they all developed schizophrenia, although at different ages and slightly different symptoms were shown. However, they did have a dreadful childhood so the conclusion is not clear.
- These studies show a strong genetic link with schizophrenia, however, the concordance rates are not 100%, which suggests that environmental influence is also involved.
- The high concordance in MZ twins may be because they are treated more similarly than DZ twins, so this greater environmental similarity rather than genetic similarity may be responsible.
However, Shields found that schizophrenia concordance rates for MZ twins brought up apart were similar to MZ twins brought up together. Kamin criticised these findings by suggesting that some of the separated twins used in Shields study hadn’t spent all their childhood apart, some were raised by relatives and some even went to the same school.
2) Biochemical factors
This explanation suggests that schizophrenia may be caused by high dopamine levels, or the dopamine receptors/neurones in schizophrenic patients may be too sensitive, this is known as the dopamine hypothesis.
Evidence for the dopamine hypothesis comes from antipsychotic drugs which block nerve impulses to dopamine receptors and seem to reduce the symptoms of schizophrenia. However, they have more effect on positive rather than negative symptoms.
Other evidence for the dopamine evidence comes from the study of Parkinson’s disease. Low levels of dopamine are often found in patients of Parkinson’s disease, when some patients were given L-dopa to increase their dopamine levels they produced many schizophrenic type symptoms. When L-dopa was given to schizophrenic patients, their symptoms became worse.
- However, antipsychotic drugs are only effective for positive symptoms, therefore excess dopamine levels can only explain some types of schizophrenia.
- Another criticism is that newer drugs which also affect serotonin levels are more effective in reducing schizophrenic symptoms. This suggests that dopamine levels alone cannot explain schizophrenia.
- Finally, the relationship between schizophrenia and dopamine levels is correlations. We cannot determine whether high dopamine levels are a cause or effect of schizophrenia.
3) Viral infections
Some researchers suggest schizophrenia maybe caused by exposure to viruses before birth. These may not have effect until puberty when they are activated by hormonal changes and cause schizophrenic symptoms.
Torrey found that a significant number of people with schizophrenia are born during the winter; this is when exposure to viruses is at its peak.
Van Os studied fingerprints of MZ twins and found that schizophrenics have fingerprint abnormalities e.g. more ridges than their non-schizophrenic twin. Fingerprints develop in the second trimester of pregnancy when the baby is most at risk from viruses. Therefore the abnormalities indicate viral infections during this period, which predispose a person to schizophrenia.
+ This explains why schizophrenia appears in people with no family history of schizophrenia.
- There is no evidence that all schizophrenics have been exposed to viruses.
1) Behavioural explanations
This explanation suggests schizophrenia is a consequence of faulty learning. If a child receives little or no social reinforcement early in life, the child will pay more attention to irrelevant environmental cues (e.g. the sound of a word rather than its meaning).
Their behaviour will eventually appear bizarre and others will label them as ‘weird’ and avoid them. According to Scheff’s labelling theory, individuals who have been labelled this way may continue to act in ways that match the label. The bizarre behaviours may be rewarded by attention and sympathy so are reinforced and will eventually become so bizarre that they are labelled as schizophrenic.
+ Behavioural explanations are supported by many behavioural therapies used on schizophrenic patients. Social skills training techniques have been used to help schizophrenics acquire useful social skills e.g. schizophrenics have learnt to make their own bed and comb their hair when rewarded. These programmes have been successful in reintegrating schizophrenics back into the community.
- However, behavioural explanations ignore the genetic evidence found by many studies (e.g. Gottesman).
+ Support for the labelling theory came from a member of the audience when Paul Meehl was giving a lecture. The man said he ‘kept his finger up his arse to prevent his thought from running out, and tried to tear his hair out with the other hand because it belonged to his father’. The man did all this because someone had called him a schizophrenic.
2) Family relationships
Bateson proposed the double bind theory which suggests that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia. For example, if a mother tells her child that she loves him, yet turns her head away in disgust or says it in a harsh tone, the child will receive conflicting messages.
The double bind theory explains the confused thinking of schizophrenics, however there is very little research supporting it.
+ Research evidence comes from Berger who found that schizophrenics reported higher recall of contradictory statements by their mother than non-schizophrenics. However, the evidence is unreliable as the schizophrenics recall may have been affected by their schizophrenia.
+ Mischler and Waxler also support the double bind theory. They found that mothers talked to their schizophrenic daughters in an unresponsive tone, whereas the same mothers talked to their normal daughters in a more normal and responsive way. However, the poor communication may be an effect of the schizophrenia patient rather than the cause.
3) Stress
Stressful life events (e.g. death of a close relative, break-up of an intimate relationship, job loss) may also trigger schizophrenia. This may be due to neurotransmitter changes but no definite cause has been made.
Day found that across many countries, schizophrenics tend to have experienced a high number of stressful life events in the weeks before they developed schizophrenia.
- However a cause-effect relationship cannot be made because schizophrenia may have been the cause of the life event rather than the effect. For example, someone may have lost their job due to their bizarre behaviour caused by schizophrenia, rather than develop schizophrenia due to losing their job.
Depression Clinical characteristics
There are two types of depression; unipolar (major) and bipolar depression. The following symptoms must be present continuously for at least two weeks.
Emotions – Sad and depressed mood with loss of interest in pleasure activities.
Cognitive – Feeling worthless, thoughts of suicide and death.
Physical – Sleeping difficulties, weight loss/gain, and tiredness.
Biological Explanations
1) Genetic factors
MZ twins have 100% same genes and DZ twins have 50% same genes. McGuffin studied 177 twins with depression and found that concordance rates are 46% if you have a MZ twin with depression and 20% if you have a DZ twin with depression. This suggests that depression is largely dependant on genes. Research also found that there was higher concordance for bipolar than unipolar depression.
Research has also found that there is a greater risk of depression if a first degree relative (e.g. sibling) has it than if a second degree relative (e.g. nephew) has it.
- These studies show a strong genetic link with depression, however, the concordance rates are not 100%, which suggests that environmental influence is also involved.
- Concordance rates are also lower for depression than for schizophrenia (Gottesman) suggesting that depression has a more psychological rather than genetic components.
- Similarities between close relative could be due to similar environments rather than similar genes. Families tend to have similarities in certain characteristics e.g. lifestyle and social class, so are more likely to be exposed to similar environments and life events.
The diathesis-stress model is a way of combining biological and environmental explanations. The model suggests that individuals are born with a predisposition to mental disorders e.g. depression. The gene for predisposition is inherited and when combined with environmental factors/stressors it may cause depression.
+ Kendler found that women with a depressed sibling were more likely to become depressed than those without one. Also, the highest levels of depression were found in those who were exposed to significant negative life events and were most genetically at risk.
2) Biochemical factors
This explanation suggests that low levels of serotonin are thought to be a cause of depression. Serotonin controls the levels of the neurotransmitter noradrenaline. A serotonin deficiency means that noradrenaline levels are not controlled and so fluctuate wildly. Noradrenaline acts on synapses, allowing nerve impulses to pass through. It is associated with increasing the activity of nerve impulses and causing physiological arousal. If noradrenaline levels drop too low, nerve impulses cannot cross synapses, reducing the activity of the body. This explains why depressed individuals generally feel tired and hopeless as they are not physiologically aroused.
+ Post mortems of depressed suicide victims revealed an increased density of noradrenaline receptors. When noradrenaline molecules are limited in synapses, postsynaptic cells expand their receptors to pick up whatever signals are available.
+ Antidepressants (e.g. Prozac) increase levels of serotonin and noradrenaline and have been successful in reducing the symptoms of depression. They work by blocking the reuptake of serotonin from the postsynaptic membrane so it stays binded to the receptor proteins for longer. This increases nerve activity and reduces depressive symptoms.
- However, there is no evidence that abnormal levels of serotonin and noradrenaline are the cause of depression; they may just be the effect of depression.
- Serotonin based drugs do not help everyone with depression, therefore there must be other causes. Also, not everyone with low neurotransmitter levels becomes depressed.
A study found that out of the women admitted into hospital for depression, 43% entered on the day before their menstrual period. Around this time the levels of oestrogen and progesterone are fluctuating and many women develop symptoms e.g. irritability, mood swings, depression due to the hormonal fluctuations. Therefore depression may be caused by hormones, not just neurotransmitter changes. Many women also reported depression after giving birth when massive hormonal changes occur.
I know exactly how you're feeling I don't feel as if I can regurgitate it all without my notes in front of me, arrghhh!
This time tomorrow it will be in the past
Psychology discussion, revision and homework help.
Useful Resources:
psychopathology
im so stressed!! panic panic panic!!!!! i feel like i dont know anything - i want another day 
