EDEXCEL A-LEVEL PSYCHOLOGY PAPER 2 (9PS 02) - 22nd May [Exam Chat]
Poll
How well did your EDEXCEL A-LEVEL PSYCHOLOGY PAPER 2 (9PS 02) exam go today?
EDEXCEL A-LEVEL PSYCHOLOGY PAPER 2 (9PS 02) - 22nd May [Exam Chat]
Welcome to the exam discussion thread for this exam.
Introduce yourself! Let others know what you're aiming for in your exams, what you are struggling with in your revision or anything else.
Wishing you all the best of luck.
General Information
Date/Time: 22nd May AM
Length: 2 hours
Good luck!
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Hey fellow Psychology Students!
Recently, I've been looking at ways to expand on the success of the weekly Study Together sessions we’re running every Tuesday evenings (https://www.thestudentroom.co.uk/showthread.php?t=7443741) and one idea we’ve had is to run similar sessions for students studying Psychology
.
The idea would be to have weekly sessions lasting an hour where you can come online and revise Psychology with other students. It feels like it could be a great way to build confidence with the content, as well as being a fun and sociable way to get some studying done.
Please let me know if this is something you would be interested in! If so, please comment on this post!
Recently, I've been looking at ways to expand on the success of the weekly Study Together sessions we’re running every Tuesday evenings (https://www.thestudentroom.co.uk/showthread.php?t=7443741) and one idea we’ve had is to run similar sessions for students studying Psychology
.The idea would be to have weekly sessions lasting an hour where you can come online and revise Psychology with other students. It feels like it could be a great way to build confidence with the content, as well as being a fun and sociable way to get some studying done.
Please let me know if this is something you would be interested in! If so, please comment on this post!
Original post by emm4nuella
Hey fellow Psychology Students!
Recently, I've been looking at ways to expand on the success of the weekly Study Together sessions we’re running every Tuesday evenings (https://www.thestudentroom.co.uk/showthread.php?t=7443741) and one idea we’ve had is to run similar sessions for students studying Psychology.
The idea would be to have weekly sessions lasting an hour where you can come online and revise Psychology with other students. It feels like it could be a great way to build confidence with the content, as well as being a fun and sociable way to get some studying done.
Please let me know if this is something you would be interested in! If so, please comment on this post!
Recently, I've been looking at ways to expand on the success of the weekly Study Together sessions we’re running every Tuesday evenings (https://www.thestudentroom.co.uk/showthread.php?t=7443741) and one idea we’ve had is to run similar sessions for students studying Psychology
.The idea would be to have weekly sessions lasting an hour where you can come online and revise Psychology with other students. It feels like it could be a great way to build confidence with the content, as well as being a fun and sociable way to get some studying done.
Please let me know if this is something you would be interested in! If so, please comment on this post!
this would be amazing. do you have any predictions for paper 1 in terms of topics, 8 markers etc?
Original post by pt12
Predictions ?
I think a practical investigation will come up and maybe biological explanation for schizophrenia
Original post by bob123445555
I think a practical investigation will come up and maybe biological explanation for schizophrenia
i also think ocd or carlsson, especially carlsson
carlsson and kroenke spin my brain
I hate carlsson, anyone got good notes on it?
Original post by RevisionisKey1
I hate carlsson, anyone got good notes on it?
AO1: The aim was to review studies into the relationship between levels of neurotransmitters and schizophrenia, particularly dopamine and glutamate.
There were two existing explanations of what might be responsible for schizophrenia:
-hyperdopaminergic (high levels of dopamine)
-hypoglutamatergic (low levels of glutamate).
This research was important because the priority was to support the production of drugs that reduce levels of relapse and also side effects, and this could only be achieved if we better understood the causes of SZ.
Procedure:
This is a literature review, as such the procedure was summarizing and analyzing the findings of other research. Looking at the results of brain scan studies (PET Scans), which look at the dopamine and glutamate activity in the brains of schizophrenic patients. PET scans involve injecting the patient with a radioactive tracer that is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. The scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red. Also looked at studies where people have consumed recreational drugs that lead to schizophrenia like psychotic symptoms. Overall, looking at all these studies together to investigate the effect of neurotransmitters on schizophrenia. Potentially discuss what kind of drug can be produced without side effects and improving compliance rates.
Findings: While dopamine has been shown through multiple brain scans and other studies to be a factor related to schizophrenia. It is not the only dysfunctional neurotransmitter related to SZ (noradrenaline, serotonin, acetylcholine, GABA, and glutamate also play roles). The relationship between dopamine and glutamate could be seen as a brake and an accelerator. Glutamate normally “breaks” or inhibits dopamine activity. But if glutamate is antagonized, it no long inhibits dopamine activity. Glutamate seems to be related in both positive and negative symptoms of schizophrenia. Hypoglutamatergia (Lack of glutamate) in the cerebral cortex is linked to negative symptoms of SZ. Hyperglutamatergia (too much glutamate) in the basal ganglia is linked to positive symptoms of SZ.
Conclusion: Overall, Carlsson et al suggested that SZ may have different subtypes that could be caused by different neurotransmitters such as glutamate, not just dopamine. This would have major implications for drug treatments because ny drug would need to be carefully targeted at particular neurotransmitters. Carlsson et al also concluded that further research is still needed to develop drugs that treat SZ and avoid major side effects. There are currently a number of drugs in development that can reduce dopamine but without serious side effects (e.g., muscle tremors), which would benefit patients.
-hyperdopaminergic (high levels of dopamine)
-hypoglutamatergic (low levels of glutamate).
This research was important because the priority was to support the production of drugs that reduce levels of relapse and also side effects, and this could only be achieved if we better understood the causes of SZ.
Procedure:
This is a literature review, as such the procedure was summarizing and analyzing the findings of other research. Looking at the results of brain scan studies (PET Scans), which look at the dopamine and glutamate activity in the brains of schizophrenic patients. PET scans involve injecting the patient with a radioactive tracer that is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. The scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red. Also looked at studies where people have consumed recreational drugs that lead to schizophrenia like psychotic symptoms. Overall, looking at all these studies together to investigate the effect of neurotransmitters on schizophrenia. Potentially discuss what kind of drug can be produced without side effects and improving compliance rates.
Findings: While dopamine has been shown through multiple brain scans and other studies to be a factor related to schizophrenia. It is not the only dysfunctional neurotransmitter related to SZ (noradrenaline, serotonin, acetylcholine, GABA, and glutamate also play roles). The relationship between dopamine and glutamate could be seen as a brake and an accelerator. Glutamate normally “breaks” or inhibits dopamine activity. But if glutamate is antagonized, it no long inhibits dopamine activity. Glutamate seems to be related in both positive and negative symptoms of schizophrenia. Hypoglutamatergia (Lack of glutamate) in the cerebral cortex is linked to negative symptoms of SZ. Hyperglutamatergia (too much glutamate) in the basal ganglia is linked to positive symptoms of SZ.
Conclusion: Overall, Carlsson et al suggested that SZ may have different subtypes that could be caused by different neurotransmitters such as glutamate, not just dopamine. This would have major implications for drug treatments because ny drug would need to be carefully targeted at particular neurotransmitters. Carlsson et al also concluded that further research is still needed to develop drugs that treat SZ and avoid major side effects. There are currently a number of drugs in development that can reduce dopamine but without serious side effects (e.g., muscle tremors), which would benefit patients.
AO3: A strength with the study draws from a large pool of 33 studies as secondary data to come up with results and conclusions. By using secondary data, Carlsson has a large sample size and dataset of patients of a relatively rare mental health disorder. Where otherwise it would have been time intensive to collect this many ppts. Therefore, the findings of the causes and suggestions for treatments for schizophrenia is applicable to schizophrenic patients and their therapists.
AO3: A weakness is that the study ignores the role of culture on schizophrenia. Luhrmann (2015) demonstrates that in California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in our West African sample, they were more likely to describe them as morally good and causally powerful. Therefore, this suggests that the intensity and the distress patients feel about SZ may be dependent on their culture.
AO3: A strength with the study is that it could lead to the development of new drug treatments. For example, Carlsson’s emphasis on serotonin and glutamate has pointed the pharmaceutical business to consider serotonin antagonists and glutamate agonists to reduce the symptoms of schizophrenia. The more precisely we understand the chemical underpinnings of the disorder, the more fine-tuned the drugs could be. This study could lead to new drugs, with little side effects and high compliance rates to be developed to help treat schizophrenia. As current dopamine-based drugs do not help a large percentage of patients.
Hopes that helps!
Original post by aleahlee2
AO1: The aim was to review studies into the relationship between levels of neurotransmitters and schizophrenia, particularly dopamine and glutamate.
AO3: A strength with the study draws from a large pool of 33 studies as secondary data to come up with results and conclusions. By using secondary data, Carlsson has a large sample size and dataset of patients of a relatively rare mental health disorder. Where otherwise it would have been time intensive to collect this many ppts. Therefore, the findings of the causes and suggestions for treatments for schizophrenia is applicable to schizophrenic patients and their therapists.
AO3: A weakness is that the study ignores the role of culture on schizophrenia. Luhrmann (2015) demonstrates that in California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in our West African sample, they were more likely to describe them as morally good and causally powerful. Therefore, this suggests that the intensity and the distress patients feel about SZ may be dependent on their culture.
AO3: A strength with the study is that it could lead to the development of new drug treatments. For example, Carlsson’s emphasis on serotonin and glutamate has pointed the pharmaceutical business to consider serotonin antagonists and glutamate agonists to reduce the symptoms of schizophrenia. The more precisely we understand the chemical underpinnings of the disorder, the more fine-tuned the drugs could be. This study could lead to new drugs, with little side effects and high compliance rates to be developed to help treat schizophrenia. As current dopamine-based drugs do not help a large percentage of patients.
Hopes that helps!
There were two existing explanations of what might be responsible for schizophrenia:
-hyperdopaminergic (high levels of dopamine)
-hypoglutamatergic (low levels of glutamate).
This research was important because the priority was to support the production of drugs that reduce levels of relapse and also side effects, and this could only be achieved if we better understood the causes of SZ.
Procedure:
This is a literature review, as such the procedure was summarizing and analyzing the findings of other research. Looking at the results of brain scan studies (PET Scans), which look at the dopamine and glutamate activity in the brains of schizophrenic patients. PET scans involve injecting the patient with a radioactive tracer that is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. The scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red. Also looked at studies where people have consumed recreational drugs that lead to schizophrenia like psychotic symptoms. Overall, looking at all these studies together to investigate the effect of neurotransmitters on schizophrenia. Potentially discuss what kind of drug can be produced without side effects and improving compliance rates.
Findings: While dopamine has been shown through multiple brain scans and other studies to be a factor related to schizophrenia. It is not the only dysfunctional neurotransmitter related to SZ (noradrenaline, serotonin, acetylcholine, GABA, and glutamate also play roles). The relationship between dopamine and glutamate could be seen as a brake and an accelerator. Glutamate normally “breaks” or inhibits dopamine activity. But if glutamate is antagonized, it no long inhibits dopamine activity. Glutamate seems to be related in both positive and negative symptoms of schizophrenia. Hypoglutamatergia (Lack of glutamate) in the cerebral cortex is linked to negative symptoms of SZ. Hyperglutamatergia (too much glutamate) in the basal ganglia is linked to positive symptoms of SZ.
Conclusion: Overall, Carlsson et al suggested that SZ may have different subtypes that could be caused by different neurotransmitters such as glutamate, not just dopamine. This would have major implications for drug treatments because ny drug would need to be carefully targeted at particular neurotransmitters. Carlsson et al also concluded that further research is still needed to develop drugs that treat SZ and avoid major side effects. There are currently a number of drugs in development that can reduce dopamine but without serious side effects (e.g., muscle tremors), which would benefit patients.
-hyperdopaminergic (high levels of dopamine)
-hypoglutamatergic (low levels of glutamate).
This research was important because the priority was to support the production of drugs that reduce levels of relapse and also side effects, and this could only be achieved if we better understood the causes of SZ.
Procedure:
This is a literature review, as such the procedure was summarizing and analyzing the findings of other research. Looking at the results of brain scan studies (PET Scans), which look at the dopamine and glutamate activity in the brains of schizophrenic patients. PET scans involve injecting the patient with a radioactive tracer that is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. The scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red. Also looked at studies where people have consumed recreational drugs that lead to schizophrenia like psychotic symptoms. Overall, looking at all these studies together to investigate the effect of neurotransmitters on schizophrenia. Potentially discuss what kind of drug can be produced without side effects and improving compliance rates.
Findings: While dopamine has been shown through multiple brain scans and other studies to be a factor related to schizophrenia. It is not the only dysfunctional neurotransmitter related to SZ (noradrenaline, serotonin, acetylcholine, GABA, and glutamate also play roles). The relationship between dopamine and glutamate could be seen as a brake and an accelerator. Glutamate normally “breaks” or inhibits dopamine activity. But if glutamate is antagonized, it no long inhibits dopamine activity. Glutamate seems to be related in both positive and negative symptoms of schizophrenia. Hypoglutamatergia (Lack of glutamate) in the cerebral cortex is linked to negative symptoms of SZ. Hyperglutamatergia (too much glutamate) in the basal ganglia is linked to positive symptoms of SZ.
Conclusion: Overall, Carlsson et al suggested that SZ may have different subtypes that could be caused by different neurotransmitters such as glutamate, not just dopamine. This would have major implications for drug treatments because ny drug would need to be carefully targeted at particular neurotransmitters. Carlsson et al also concluded that further research is still needed to develop drugs that treat SZ and avoid major side effects. There are currently a number of drugs in development that can reduce dopamine but without serious side effects (e.g., muscle tremors), which would benefit patients.
AO3: A strength with the study draws from a large pool of 33 studies as secondary data to come up with results and conclusions. By using secondary data, Carlsson has a large sample size and dataset of patients of a relatively rare mental health disorder. Where otherwise it would have been time intensive to collect this many ppts. Therefore, the findings of the causes and suggestions for treatments for schizophrenia is applicable to schizophrenic patients and their therapists.
AO3: A weakness is that the study ignores the role of culture on schizophrenia. Luhrmann (2015) demonstrates that in California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in our West African sample, they were more likely to describe them as morally good and causally powerful. Therefore, this suggests that the intensity and the distress patients feel about SZ may be dependent on their culture.
AO3: A strength with the study is that it could lead to the development of new drug treatments. For example, Carlsson’s emphasis on serotonin and glutamate has pointed the pharmaceutical business to consider serotonin antagonists and glutamate agonists to reduce the symptoms of schizophrenia. The more precisely we understand the chemical underpinnings of the disorder, the more fine-tuned the drugs could be. This study could lead to new drugs, with little side effects and high compliance rates to be developed to help treat schizophrenia. As current dopamine-based drugs do not help a large percentage of patients.
Hopes that helps!
Your acc an Angel 🫶 whatever u need I got you, thank you so much
Original post by RevisionisKey1
Your acc an Angel 🫶 whatever u need I got you, thank you so much
No worries if you need anything else just PM
Original post by aleahlee2
AO1: The aim was to review studies into the relationship between levels of neurotransmitters and schizophrenia, particularly dopamine and glutamate.
AO3: A strength with the study draws from a large pool of 33 studies as secondary data to come up with results and conclusions. By using secondary data, Carlsson has a large sample size and dataset of patients of a relatively rare mental health disorder. Where otherwise it would have been time intensive to collect this many ppts. Therefore, the findings of the causes and suggestions for treatments for schizophrenia is applicable to schizophrenic patients and their therapists.
AO3: A weakness is that the study ignores the role of culture on schizophrenia. Luhrmann (2015) demonstrates that in California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in our West African sample, they were more likely to describe them as morally good and causally powerful. Therefore, this suggests that the intensity and the distress patients feel about SZ may be dependent on their culture.
AO3: A strength with the study is that it could lead to the development of new drug treatments. For example, Carlsson’s emphasis on serotonin and glutamate has pointed the pharmaceutical business to consider serotonin antagonists and glutamate agonists to reduce the symptoms of schizophrenia. The more precisely we understand the chemical underpinnings of the disorder, the more fine-tuned the drugs could be. This study could lead to new drugs, with little side effects and high compliance rates to be developed to help treat schizophrenia. As current dopamine-based drugs do not help a large percentage of patients.
Hopes that helps!
There were two existing explanations of what might be responsible for schizophrenia:
-hyperdopaminergic (high levels of dopamine)
-hypoglutamatergic (low levels of glutamate).
This research was important because the priority was to support the production of drugs that reduce levels of relapse and also side effects, and this could only be achieved if we better understood the causes of SZ.
Procedure:
This is a literature review, as such the procedure was summarizing and analyzing the findings of other research. Looking at the results of brain scan studies (PET Scans), which look at the dopamine and glutamate activity in the brains of schizophrenic patients. PET scans involve injecting the patient with a radioactive tracer that is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. The scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red. Also looked at studies where people have consumed recreational drugs that lead to schizophrenia like psychotic symptoms. Overall, looking at all these studies together to investigate the effect of neurotransmitters on schizophrenia. Potentially discuss what kind of drug can be produced without side effects and improving compliance rates.
Findings: While dopamine has been shown through multiple brain scans and other studies to be a factor related to schizophrenia. It is not the only dysfunctional neurotransmitter related to SZ (noradrenaline, serotonin, acetylcholine, GABA, and glutamate also play roles). The relationship between dopamine and glutamate could be seen as a brake and an accelerator. Glutamate normally “breaks” or inhibits dopamine activity. But if glutamate is antagonized, it no long inhibits dopamine activity. Glutamate seems to be related in both positive and negative symptoms of schizophrenia. Hypoglutamatergia (Lack of glutamate) in the cerebral cortex is linked to negative symptoms of SZ. Hyperglutamatergia (too much glutamate) in the basal ganglia is linked to positive symptoms of SZ.
Conclusion: Overall, Carlsson et al suggested that SZ may have different subtypes that could be caused by different neurotransmitters such as glutamate, not just dopamine. This would have major implications for drug treatments because ny drug would need to be carefully targeted at particular neurotransmitters. Carlsson et al also concluded that further research is still needed to develop drugs that treat SZ and avoid major side effects. There are currently a number of drugs in development that can reduce dopamine but without serious side effects (e.g., muscle tremors), which would benefit patients.
-hyperdopaminergic (high levels of dopamine)
-hypoglutamatergic (low levels of glutamate).
This research was important because the priority was to support the production of drugs that reduce levels of relapse and also side effects, and this could only be achieved if we better understood the causes of SZ.
Procedure:
This is a literature review, as such the procedure was summarizing and analyzing the findings of other research. Looking at the results of brain scan studies (PET Scans), which look at the dopamine and glutamate activity in the brains of schizophrenic patients. PET scans involve injecting the patient with a radioactive tracer that is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. The scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red. Also looked at studies where people have consumed recreational drugs that lead to schizophrenia like psychotic symptoms. Overall, looking at all these studies together to investigate the effect of neurotransmitters on schizophrenia. Potentially discuss what kind of drug can be produced without side effects and improving compliance rates.
Findings: While dopamine has been shown through multiple brain scans and other studies to be a factor related to schizophrenia. It is not the only dysfunctional neurotransmitter related to SZ (noradrenaline, serotonin, acetylcholine, GABA, and glutamate also play roles). The relationship between dopamine and glutamate could be seen as a brake and an accelerator. Glutamate normally “breaks” or inhibits dopamine activity. But if glutamate is antagonized, it no long inhibits dopamine activity. Glutamate seems to be related in both positive and negative symptoms of schizophrenia. Hypoglutamatergia (Lack of glutamate) in the cerebral cortex is linked to negative symptoms of SZ. Hyperglutamatergia (too much glutamate) in the basal ganglia is linked to positive symptoms of SZ.
Conclusion: Overall, Carlsson et al suggested that SZ may have different subtypes that could be caused by different neurotransmitters such as glutamate, not just dopamine. This would have major implications for drug treatments because ny drug would need to be carefully targeted at particular neurotransmitters. Carlsson et al also concluded that further research is still needed to develop drugs that treat SZ and avoid major side effects. There are currently a number of drugs in development that can reduce dopamine but without serious side effects (e.g., muscle tremors), which would benefit patients.
AO3: A strength with the study draws from a large pool of 33 studies as secondary data to come up with results and conclusions. By using secondary data, Carlsson has a large sample size and dataset of patients of a relatively rare mental health disorder. Where otherwise it would have been time intensive to collect this many ppts. Therefore, the findings of the causes and suggestions for treatments for schizophrenia is applicable to schizophrenic patients and their therapists.
AO3: A weakness is that the study ignores the role of culture on schizophrenia. Luhrmann (2015) demonstrates that in California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in our West African sample, they were more likely to describe them as morally good and causally powerful. Therefore, this suggests that the intensity and the distress patients feel about SZ may be dependent on their culture.
AO3: A strength with the study is that it could lead to the development of new drug treatments. For example, Carlsson’s emphasis on serotonin and glutamate has pointed the pharmaceutical business to consider serotonin antagonists and glutamate agonists to reduce the symptoms of schizophrenia. The more precisely we understand the chemical underpinnings of the disorder, the more fine-tuned the drugs could be. This study could lead to new drugs, with little side effects and high compliance rates to be developed to help treat schizophrenia. As current dopamine-based drugs do not help a large percentage of patients.
Hopes that helps!
do you have anything for the POTS study? this is so helpful
Original post by hi2007
do you have anything for the POTS study? this is so helpful
whats the POTS study?
Original post by aleahlee2
whats the POTS study?
the contemporary study for OCD unless u do anorexia or depression
Original post by hi2007
the contemporary study for OCD unless u do anorexia or depression
Ohhh sorry i only do anorexia
Classic study Rosenhan
Aim
At the time of Rosenhan’s study, there were growing concerns about the validity and reliability of diagnoses for mental illness. Inspired by the ‘anti-psychiatry’ movement of the time, the aim of Rosenhan’s study was to find out whether mental health professionals could distinguish between those who were genuinely mentally ill and those who were not.
Procedure
· Rosenhan’s study was a combination of a field experiment and a participant observation. · It took place in 12 psychiatric hospitals that varied in size and location. The sample was 8 ‘pseudopatients’ (5 men, 3 women) from various occupations including a painter, housewife and some psychologists including Rosenhan himself. None had ever been diagnosed with a mental illness and were obtained using opportunity sampling. · The procedure began with the pseudopatients calling up various hospitals for an appointment and complaining of ‘hearing voices’ (auditory hallucinations) and said they could hear the words ‘empty’ ‘thud’ and ‘hollow’. As a result, 7 pseudopatients were admitted to the hospitals with a diagnosis of schizophrenia and 1 was admitted with a diagnosis of manic depression with psychosis. · They described their mental state accurately, acted normally with both staff and genuine patients, accepted but did not take medication given to them, and did not report any more symptoms. · The pseudopatients observed the behaviour of the staff (doctors and nurses) and tried to interview them and recorded their responses as well as comments by genuine patients. They gathered both quantitative and qualitative data. Hospital authorities were informed of the study, but managers were not. · A follow-up study took place in another hospital after the staff asked Rosenhan to send more pseudopatients over there over a period of three months, claiming they would definitely notice whether or not they were real or fake patients. Rosenhan did not actually send any patients.
Results
The quantitative findings were that the pseudopatients were hospitalised between 7 and 52 days (averaging 19 days) prior to being considered sane enough to be discharged. · No doctors or nurses questioned their genuineness. In some hospitals, genuine patients questioned the pseudopatients as they thought they may have been journalists. · In 4 of the 12 hospitals, no staff answered the pseudopatients when they asked them questions. It was found that 71% of doctors and 88% of nurses and other staff ignored the pseudopatient when questioned. · The qualitative findings were that three ‘normal’ behaviours were misinterpreted as ‘abnormal’, including note writing being interpreted by a nurse as ‘engaging in writing behaviour’ as though it was something only a person with a mental illness would do. Another interpreted pacing up and down as a sign of nervousness, when the pseudopatient was just bored. · The follow-up study showed that out of 193 cases, 41 of the patients were identified as being fake by at least one staff member, and 23 were suspected as being fake by a psychiatrist, when in fact Rosenhan did not send any pseudopatients.
Conclusion
From these results it can be concluded that mental health professionals cannot distinguish between real and false patients, and they were willing to make a diagnosis based on one fake symptom. ‘Normal’ behaviour was misinterpreted as ‘abnormal’ to support their idea that the pseudopatients had a mental illness. This suggests the validity of psychiatric diagnoses was low. Ironically, due to the consistency of diagnoses they are reliable but incorrect.
AO3- STRENGTH
· A strength of Rosenhan’s study was that it had high internal validity.
· The doctors and nurses in the 12 hospitals were unaware they were being observed by the pseudopatients and therefore it is likely that they treated the them in exactly the same way as they would have treated any of their real patients.
· This lack of demand characteristics means that the study is very useful in highlighting issues surrounding the difficulty of diagnosing mental disorders.
AO3- WEAKNESS
· A weakness of Rosenhan’s study was that it was ethnocentric.
· The study was conducted across 12 hospitals in five states of America and focused on the use of the DSM-II manual for diagnosing mental disorders.
· This is a weakness because other cultures may not use the DSM-II manual and also may not share the westernised view of some symptoms, particularly hallucinations, so we cannot assume that the process of diagnosing mental disorders will show similar problems in other cultures and countries.
Aim
At the time of Rosenhan’s study, there were growing concerns about the validity and reliability of diagnoses for mental illness. Inspired by the ‘anti-psychiatry’ movement of the time, the aim of Rosenhan’s study was to find out whether mental health professionals could distinguish between those who were genuinely mentally ill and those who were not.
Procedure
· Rosenhan’s study was a combination of a field experiment and a participant observation. · It took place in 12 psychiatric hospitals that varied in size and location. The sample was 8 ‘pseudopatients’ (5 men, 3 women) from various occupations including a painter, housewife and some psychologists including Rosenhan himself. None had ever been diagnosed with a mental illness and were obtained using opportunity sampling. · The procedure began with the pseudopatients calling up various hospitals for an appointment and complaining of ‘hearing voices’ (auditory hallucinations) and said they could hear the words ‘empty’ ‘thud’ and ‘hollow’. As a result, 7 pseudopatients were admitted to the hospitals with a diagnosis of schizophrenia and 1 was admitted with a diagnosis of manic depression with psychosis. · They described their mental state accurately, acted normally with both staff and genuine patients, accepted but did not take medication given to them, and did not report any more symptoms. · The pseudopatients observed the behaviour of the staff (doctors and nurses) and tried to interview them and recorded their responses as well as comments by genuine patients. They gathered both quantitative and qualitative data. Hospital authorities were informed of the study, but managers were not. · A follow-up study took place in another hospital after the staff asked Rosenhan to send more pseudopatients over there over a period of three months, claiming they would definitely notice whether or not they were real or fake patients. Rosenhan did not actually send any patients.
Results
The quantitative findings were that the pseudopatients were hospitalised between 7 and 52 days (averaging 19 days) prior to being considered sane enough to be discharged. · No doctors or nurses questioned their genuineness. In some hospitals, genuine patients questioned the pseudopatients as they thought they may have been journalists. · In 4 of the 12 hospitals, no staff answered the pseudopatients when they asked them questions. It was found that 71% of doctors and 88% of nurses and other staff ignored the pseudopatient when questioned. · The qualitative findings were that three ‘normal’ behaviours were misinterpreted as ‘abnormal’, including note writing being interpreted by a nurse as ‘engaging in writing behaviour’ as though it was something only a person with a mental illness would do. Another interpreted pacing up and down as a sign of nervousness, when the pseudopatient was just bored. · The follow-up study showed that out of 193 cases, 41 of the patients were identified as being fake by at least one staff member, and 23 were suspected as being fake by a psychiatrist, when in fact Rosenhan did not send any pseudopatients.
Conclusion
From these results it can be concluded that mental health professionals cannot distinguish between real and false patients, and they were willing to make a diagnosis based on one fake symptom. ‘Normal’ behaviour was misinterpreted as ‘abnormal’ to support their idea that the pseudopatients had a mental illness. This suggests the validity of psychiatric diagnoses was low. Ironically, due to the consistency of diagnoses they are reliable but incorrect.
AO3- STRENGTH
· A strength of Rosenhan’s study was that it had high internal validity.
· The doctors and nurses in the 12 hospitals were unaware they were being observed by the pseudopatients and therefore it is likely that they treated the them in exactly the same way as they would have treated any of their real patients.
· This lack of demand characteristics means that the study is very useful in highlighting issues surrounding the difficulty of diagnosing mental disorders.
AO3- WEAKNESS
· A weakness of Rosenhan’s study was that it was ethnocentric.
· The study was conducted across 12 hospitals in five states of America and focused on the use of the DSM-II manual for diagnosing mental disorders.
· This is a weakness because other cultures may not use the DSM-II manual and also may not share the westernised view of some symptoms, particularly hallucinations, so we cannot assume that the process of diagnosing mental disorders will show similar problems in other cultures and countries.
CONTEMPORARY STUDY- GUARDIA
Aim
The aim of the study was to continue previous research by the same team that had found that patients with anorexia nervosa found it difficult to gauge their own body size and misjudged their ability to fit through a 'door frame' that was clearly big enough for them. This study wanted to test this phenomenon further by considering whether this perceptual problem extended beyond the individual to other people - would they also misjudge the body size of other people in the same task?
Procedure
Participants were a group of 25 female patients from a clinic for eating disorders in Lille, France, all of whom met the DSM IV criteria for anorexia nervosa, and another 25 healthy, female controls who were all students. · Each group was matched for age (mean approximately 24 years old) and level of education (around 13 years of education after primary school). · In the anorexic group, 12 were diagnosed restricting type, and 13 were diagnosed with binge/purge type. ANOREXIA NERVOSA GROUP CONTROL GROUP Average BMI: 15.6 Average BMI: 22.1 Average shoulder width: 37.7cm Average shoulder width: 41.5cm · A door-frame shape was projected onto a wall to give the illusion of an opening that the participants could possibly walk through. In total, 51 different width shapes were projected onto the walls varying from 30-80cm wide. · The projections were presented in a random order, and each one was presented four times to each participant. Every participant, tested alone, was asked to predict if they could walk through each 'door frame' at normal speed without turning to the side (first person perspective). · They were then asked whether another female researcher standing in the room could fit through the frame (third person perspective). The researcher had a similar BMI and shoulder width to the control group.
Results
Supporting previous findings, the group of patients with anorexia showed a significant overestimation of body size in themselves, judging that they would be unable to fit through door frames that were considerably bigger than their actual body size. · However, the same was not found in judgements of whether the researcher could pass through. Here they were much more accurate in predicting the body size of the ‘other person' in relation to their ability to pass through the ‘frame’. · The evidence from the control group found that they showed no significant difference in their ability to accurately predict the 'passability' of either themselves or the 'other person'. · It was also discovered that patients who had lost weight in the six months before the study was conducted showed a greater difference between their own and the 'other person' passability perceptions – and there was a positive correlation between amount of weight lost and amount of difference between the two measures of passability.
Conclusion
Evidence in this study suggests that the patients have not adapted their internal body image to take into account their 'new' body size after developing the disorder. They suggest that the brain still perceives the body to be a larger size despite visual information that would contradict this. The correlation between losing weight before the study and passability perceptions suggests that when anorexics lose weight their central nervous system cannot update the body image schema quickly enough to provide an accurate representation of current body size. This might explain why patients with anorexia continue to see themselves as bigger than they are and strive to continue to lose weight because their brain does not perceive their current size accurately.
AO3- STRENGTH
A strength of the study is that the researchers used a matched pairs design The researchers matched the anorexia group and the control group for age and education level. This was to ensure that the only difference between the two groups is that one group contained anorexia patients and the other did not. This reduces the likelihood of individual or participant differences affecting the DV, thus increasing the internal validity of the study as the researchers can be sure that differences between the group’s perceived possibility ratio was only due to the presence of anorexia in one group affecting how they perceive their bodies.
AO3- WEAKNESS
However, there are also problems with the design of the study. The researchers may suggested that there were significant differences between the control group and the anorexia group – their shoulder width and BMI. The weight and size of the experimenters body matched those in the control group much more than those in the AN group. This may have been a confounding variable which affected the findings. Perhaps the researchers could have used an experimenter with a similar body size of those in the AN group when they gave their judgements about the experimenter fitting through the doorway, to measure third person perspective. Although this would raise further ethical concerns.
AO3- STRENGTH
Although there are questions over the internal validity of the study, the reliability of the findings is likely to be good since other research has gained similar findings. Previous research by Guardia (2010) had found that anorexics did not think they could pass through an opening that was clearly wide enough and Schneider et al (2009) also found that people with AN misjudge their own body size, overestimating their body parts (particularly thighs and waists) by about 30% which is significantly higher compared to healthy controls. This evidence suggests that there is reliability in the idea that those with AN overestimate their body size.
Hope these help!
Aim
The aim of the study was to continue previous research by the same team that had found that patients with anorexia nervosa found it difficult to gauge their own body size and misjudged their ability to fit through a 'door frame' that was clearly big enough for them. This study wanted to test this phenomenon further by considering whether this perceptual problem extended beyond the individual to other people - would they also misjudge the body size of other people in the same task?
Procedure
Participants were a group of 25 female patients from a clinic for eating disorders in Lille, France, all of whom met the DSM IV criteria for anorexia nervosa, and another 25 healthy, female controls who were all students. · Each group was matched for age (mean approximately 24 years old) and level of education (around 13 years of education after primary school). · In the anorexic group, 12 were diagnosed restricting type, and 13 were diagnosed with binge/purge type. ANOREXIA NERVOSA GROUP CONTROL GROUP Average BMI: 15.6 Average BMI: 22.1 Average shoulder width: 37.7cm Average shoulder width: 41.5cm · A door-frame shape was projected onto a wall to give the illusion of an opening that the participants could possibly walk through. In total, 51 different width shapes were projected onto the walls varying from 30-80cm wide. · The projections were presented in a random order, and each one was presented four times to each participant. Every participant, tested alone, was asked to predict if they could walk through each 'door frame' at normal speed without turning to the side (first person perspective). · They were then asked whether another female researcher standing in the room could fit through the frame (third person perspective). The researcher had a similar BMI and shoulder width to the control group.
Results
Supporting previous findings, the group of patients with anorexia showed a significant overestimation of body size in themselves, judging that they would be unable to fit through door frames that were considerably bigger than their actual body size. · However, the same was not found in judgements of whether the researcher could pass through. Here they were much more accurate in predicting the body size of the ‘other person' in relation to their ability to pass through the ‘frame’. · The evidence from the control group found that they showed no significant difference in their ability to accurately predict the 'passability' of either themselves or the 'other person'. · It was also discovered that patients who had lost weight in the six months before the study was conducted showed a greater difference between their own and the 'other person' passability perceptions – and there was a positive correlation between amount of weight lost and amount of difference between the two measures of passability.
Conclusion
Evidence in this study suggests that the patients have not adapted their internal body image to take into account their 'new' body size after developing the disorder. They suggest that the brain still perceives the body to be a larger size despite visual information that would contradict this. The correlation between losing weight before the study and passability perceptions suggests that when anorexics lose weight their central nervous system cannot update the body image schema quickly enough to provide an accurate representation of current body size. This might explain why patients with anorexia continue to see themselves as bigger than they are and strive to continue to lose weight because their brain does not perceive their current size accurately.
AO3- STRENGTH
A strength of the study is that the researchers used a matched pairs design The researchers matched the anorexia group and the control group for age and education level. This was to ensure that the only difference between the two groups is that one group contained anorexia patients and the other did not. This reduces the likelihood of individual or participant differences affecting the DV, thus increasing the internal validity of the study as the researchers can be sure that differences between the group’s perceived possibility ratio was only due to the presence of anorexia in one group affecting how they perceive their bodies.
AO3- WEAKNESS
However, there are also problems with the design of the study. The researchers may suggested that there were significant differences between the control group and the anorexia group – their shoulder width and BMI. The weight and size of the experimenters body matched those in the control group much more than those in the AN group. This may have been a confounding variable which affected the findings. Perhaps the researchers could have used an experimenter with a similar body size of those in the AN group when they gave their judgements about the experimenter fitting through the doorway, to measure third person perspective. Although this would raise further ethical concerns.
AO3- STRENGTH
Although there are questions over the internal validity of the study, the reliability of the findings is likely to be good since other research has gained similar findings. Previous research by Guardia (2010) had found that anorexics did not think they could pass through an opening that was clearly wide enough and Schneider et al (2009) also found that people with AN misjudge their own body size, overestimating their body parts (particularly thighs and waists) by about 30% which is significantly higher compared to healthy controls. This evidence suggests that there is reliability in the idea that those with AN overestimate their body size.
Hope these help!
Original post by aleahlee2
Classic study Rosenhan
Aim
At the time of Rosenhan’s study, there were growing concerns about the validity and reliability of diagnoses for mental illness. Inspired by the ‘anti-psychiatry’ movement of the time, the aim of Rosenhan’s study was to find out whether mental health professionals could distinguish between those who were genuinely mentally ill and those who were not.
Procedure
· Rosenhan’s study was a combination of a field experiment and a participant observation. · It took place in 12 psychiatric hospitals that varied in size and location. The sample was 8 ‘pseudopatients’ (5 men, 3 women) from various occupations including a painter, housewife and some psychologists including Rosenhan himself. None had ever been diagnosed with a mental illness and were obtained using opportunity sampling. · The procedure began with the pseudopatients calling up various hospitals for an appointment and complaining of ‘hearing voices’ (auditory hallucinations) and said they could hear the words ‘empty’ ‘thud’ and ‘hollow’. As a result, 7 pseudopatients were admitted to the hospitals with a diagnosis of schizophrenia and 1 was admitted with a diagnosis of manic depression with psychosis. · They described their mental state accurately, acted normally with both staff and genuine patients, accepted but did not take medication given to them, and did not report any more symptoms. · The pseudopatients observed the behaviour of the staff (doctors and nurses) and tried to interview them and recorded their responses as well as comments by genuine patients. They gathered both quantitative and qualitative data. Hospital authorities were informed of the study, but managers were not. · A follow-up study took place in another hospital after the staff asked Rosenhan to send more pseudopatients over there over a period of three months, claiming they would definitely notice whether or not they were real or fake patients. Rosenhan did not actually send any patients.
Results
The quantitative findings were that the pseudopatients were hospitalised between 7 and 52 days (averaging 19 days) prior to being considered sane enough to be discharged. · No doctors or nurses questioned their genuineness. In some hospitals, genuine patients questioned the pseudopatients as they thought they may have been journalists. · In 4 of the 12 hospitals, no staff answered the pseudopatients when they asked them questions. It was found that 71% of doctors and 88% of nurses and other staff ignored the pseudopatient when questioned. · The qualitative findings were that three ‘normal’ behaviours were misinterpreted as ‘abnormal’, including note writing being interpreted by a nurse as ‘engaging in writing behaviour’ as though it was something only a person with a mental illness would do. Another interpreted pacing up and down as a sign of nervousness, when the pseudopatient was just bored. · The follow-up study showed that out of 193 cases, 41 of the patients were identified as being fake by at least one staff member, and 23 were suspected as being fake by a psychiatrist, when in fact Rosenhan did not send any pseudopatients.
Conclusion
From these results it can be concluded that mental health professionals cannot distinguish between real and false patients, and they were willing to make a diagnosis based on one fake symptom. ‘Normal’ behaviour was misinterpreted as ‘abnormal’ to support their idea that the pseudopatients had a mental illness. This suggests the validity of psychiatric diagnoses was low. Ironically, due to the consistency of diagnoses they are reliable but incorrect.
AO3- STRENGTH
· A strength of Rosenhan’s study was that it had high internal validity.
· The doctors and nurses in the 12 hospitals were unaware they were being observed by the pseudopatients and therefore it is likely that they treated the them in exactly the same way as they would have treated any of their real patients.
· This lack of demand characteristics means that the study is very useful in highlighting issues surrounding the difficulty of diagnosing mental disorders.
AO3- WEAKNESS
· A weakness of Rosenhan’s study was that it was ethnocentric.
· The study was conducted across 12 hospitals in five states of America and focused on the use of the DSM-II manual for diagnosing mental disorders.
· This is a weakness because other cultures may not use the DSM-II manual and also may not share the westernised view of some symptoms, particularly hallucinations, so we cannot assume that the process of diagnosing mental disorders will show similar problems in other cultures and countries.
Aim
At the time of Rosenhan’s study, there were growing concerns about the validity and reliability of diagnoses for mental illness. Inspired by the ‘anti-psychiatry’ movement of the time, the aim of Rosenhan’s study was to find out whether mental health professionals could distinguish between those who were genuinely mentally ill and those who were not.
Procedure
· Rosenhan’s study was a combination of a field experiment and a participant observation. · It took place in 12 psychiatric hospitals that varied in size and location. The sample was 8 ‘pseudopatients’ (5 men, 3 women) from various occupations including a painter, housewife and some psychologists including Rosenhan himself. None had ever been diagnosed with a mental illness and were obtained using opportunity sampling. · The procedure began with the pseudopatients calling up various hospitals for an appointment and complaining of ‘hearing voices’ (auditory hallucinations) and said they could hear the words ‘empty’ ‘thud’ and ‘hollow’. As a result, 7 pseudopatients were admitted to the hospitals with a diagnosis of schizophrenia and 1 was admitted with a diagnosis of manic depression with psychosis. · They described their mental state accurately, acted normally with both staff and genuine patients, accepted but did not take medication given to them, and did not report any more symptoms. · The pseudopatients observed the behaviour of the staff (doctors and nurses) and tried to interview them and recorded their responses as well as comments by genuine patients. They gathered both quantitative and qualitative data. Hospital authorities were informed of the study, but managers were not. · A follow-up study took place in another hospital after the staff asked Rosenhan to send more pseudopatients over there over a period of three months, claiming they would definitely notice whether or not they were real or fake patients. Rosenhan did not actually send any patients.
Results
The quantitative findings were that the pseudopatients were hospitalised between 7 and 52 days (averaging 19 days) prior to being considered sane enough to be discharged. · No doctors or nurses questioned their genuineness. In some hospitals, genuine patients questioned the pseudopatients as they thought they may have been journalists. · In 4 of the 12 hospitals, no staff answered the pseudopatients when they asked them questions. It was found that 71% of doctors and 88% of nurses and other staff ignored the pseudopatient when questioned. · The qualitative findings were that three ‘normal’ behaviours were misinterpreted as ‘abnormal’, including note writing being interpreted by a nurse as ‘engaging in writing behaviour’ as though it was something only a person with a mental illness would do. Another interpreted pacing up and down as a sign of nervousness, when the pseudopatient was just bored. · The follow-up study showed that out of 193 cases, 41 of the patients were identified as being fake by at least one staff member, and 23 were suspected as being fake by a psychiatrist, when in fact Rosenhan did not send any pseudopatients.
Conclusion
From these results it can be concluded that mental health professionals cannot distinguish between real and false patients, and they were willing to make a diagnosis based on one fake symptom. ‘Normal’ behaviour was misinterpreted as ‘abnormal’ to support their idea that the pseudopatients had a mental illness. This suggests the validity of psychiatric diagnoses was low. Ironically, due to the consistency of diagnoses they are reliable but incorrect.
AO3- STRENGTH
· A strength of Rosenhan’s study was that it had high internal validity.
· The doctors and nurses in the 12 hospitals were unaware they were being observed by the pseudopatients and therefore it is likely that they treated the them in exactly the same way as they would have treated any of their real patients.
· This lack of demand characteristics means that the study is very useful in highlighting issues surrounding the difficulty of diagnosing mental disorders.
AO3- WEAKNESS
· A weakness of Rosenhan’s study was that it was ethnocentric.
· The study was conducted across 12 hospitals in five states of America and focused on the use of the DSM-II manual for diagnosing mental disorders.
· This is a weakness because other cultures may not use the DSM-II manual and also may not share the westernised view of some symptoms, particularly hallucinations, so we cannot assume that the process of diagnosing mental disorders will show similar problems in other cultures and countries.
thank you so much!!
Original post by hi2007
does anyone have good notes for the interview for clinical the vallentine one for research methods
Vallentine et al. (2010):
Aim:
The aim of this study was to determine the usefulness of psycho-educational material provided via groupwork for offender patients within a high secure forensic psychiatric hospital.
Background:
Variables under investigation included: relapse (inferred from changes in medication), level of care (e.g., high vs. low dependency wards), engagement in therapy and the number of violent incidents.
A semi-structured interview was developed to capture post-group evaluation – and the experience of group members’ of their relationships with the group leaders.
Hypotheses:
1. It was predicted that patients would report improvements in their general well-being and mental state following the group
2. It was also expected that participants would be able to describe some benefits with regards their level of understanding (of their condition, of their own behaviour)
3. It was predicted that patients would show more willingness to comply with other suggested treatments recommended within the high-security setting
Method:
Participants.
The sample consisted of 42 male patients detained in a high-security hospital under the Mental Health Act (1983). Each patient had been assessed as having the potential to gain from information about illness and/or lacking insight or information about their diagnosis, and therefore referred for an ‘Understanding Mental Illness’ (UMI) psycho-educational group
The ICD-10 was used to diagnose patients: 33 were diagnoses with schizophrenia of which 26 were paranoid Sz.
Group therapy:
1. Four 20-session UMI groups were run over a period of 3 years
2. The focus of the intervention is to provide information on three target areas of mental illness; schizophrenia, depression and anxiety. The emphasis is on future relapse prevention
3. Tasks are designed to encourage spontaneous discussion and reflection on issues concerning mental illness and its treatment in both hospital and community settings
Interview element:
A semi-structured interview was undertaken to evaluate participants’ experience of the group including feedback on how they felt the group could be improved and what they had gained.
Interview and analysis:
1. Following completion of the groups, participants were approached to request their feedback via a semi-structured interview with the lead researcher
2. Content analysis was used to extract themes from semi-structured interview data. Units of coding were generated inductively (i.e letting the data bring out the categories, rather than having pre-conceived categories) from the data by a member of the research team
3. To ensure consistency of coding an independent second rater with no involvement in the delivery of the groups coded the data. Inter-rater reliability was found to be on average 60% across themes, suggestive of a ‘substantial’ level of agreement
Results:
Note: several participants had been transferred from high security at the time of the study and 3 refused to be interviewed
All patients reported that:
1. They felt the group was ‘valuable’ and contained useful information that would be of benefit to people diagnosed with mental illness
2. They experienced a lack of understanding when first diagnosed due to not receiving an explanation of the diagnosis or not understanding the explanation
3. It was information they wanted and felt they should be entitled to
4. They found the visit from the pharmacist helpful in explaining medication and recommended keeping it in future groups
5. They would recommend the group to other
Conclusions and actions:
1. Participants valued knowing about their mental illness and the sense of hope and empowerment they felt it provided
2. The analysis identified the lack of information they felt they had received previously
3. The process provided important feedback for the service on what was helpful and difficult about the group overall
4. Where possible, these suggestions were implemented
5. Patients emphasised the positive impact of the intervention on their sense of control and empowerment
Hope this helps! Good luck
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