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Schizophrenia - Psychology
Diagnosis of Schizophrenia
• WHO - ICD10
Two or more negative symptoms for diagnosis
1 month duration of symptoms
types:
paranoid schizophrenia - powerful delusions and hallucinations
hebephrenic schizophrenia - primary negative symptoms
catatonic - disturbance to movementleaving sufferer immobile or
overactive
• DSM5
One positive symptom needed
6 months for diagnosis
Symptoms
• Positive symptoms
Hallucinations - unreal manipulation of the senses e.g. hearing voices or
seeing facial expressions.
Delusions - irrational beliefs e.g. fear of being persecuted by aliens, this
can cause aggression.
• Negative symptoms
Avolition - apathy - inability to begin our keep up with goal directed activity.
Andreason ~ poor hygiene, lack of patience in education or work and a lack
of energy.
Speech poverty - reduction in the amount and quality of speech or delayed
responses.
Speech disorganisation - speech becomes incoherent or speaker changes
topic mid-sentence.
Evaluation
• poor inter-rater reliability, Chenxiaux - two psychiatrists independently diagnose
schizophrenia in 100 patients. A) 26 DSM, 44 ICD B) 13 DSM, 24 ICD.
• poor validity - unequal diagnosis via both diagnostic manuals means under or over
diagnosing schizophrenia.
• Co-morbidity - Buckley - 50% also diagnosed with depression, 23% OCD, 47%
substance abuse. This makes diagnosis confusing and tricky as it might be one
condition or a wrong diagnosis.
• Symptom overlap - Schizophrenia and bipolar disorder have similar symptoms which
can easily be incorrectly diagnosed.
• Longenecker - since the 80s more men are diagnosed than women.
• Cotton - gender bias, women seem to cope better with symptoms and men have higher
expectations of normality and thus defying these warrant diagnosis.
• Africans and west Indians are more likely to be diagnosed due to cultural bias, some
cultures may see hallucinations as positive, psychiatrists may not see as a good thing.
Biological Explanation
• Twin studies - Gottesman
48% risk for identical twins
17% fraternal twins
6% siblings + parents
• Candidate genes - Ripke
Polygenetic - requires a number of factors to work in combination.
Atelogical heterogeneous - different combinations of factors can lead to the condition.
108 gene variations were associated with risk of SZ.
Genes associated included ones that code for seretonin + dopamine.
• Dopamine hypothesis -
Neurotransmitters work differently in the brains of people with SZ.
HYPERdopaminergia - excess of dopamine in Brocas area may maybe associated with speech poverty and
auditory hallucinations.
HYPOdopaminergia - Goldman-Rakic - low levels of dopamine in the prefrontal cortex can explain negative
symptoms like avolition.
• Neural correlates - measurements of structure and function of the brain
Low levels of activity in the ventral striatum linked to negative symptoms.
Allen - low levels of activity in the superior temporal gyrus and anterior cingulate gyrus responsible for positive
symptoms e.g. hallucinations.
Evaluation
• Overwhelming evidence to support a generic link to SZ.
• Dopamine agonists help increase dopamine which makes symptoms of SZ
and produces SZ like symptoms.
• Lindstrom - dopamine is taken up faster in the brains of SZ suggesting they
produce more of it.
• Dopamine hypothesis may only be a partial explanation as genes identified
by Ripke identify certain genes are the cause of abnormal dopamine coding.
• Does low activity in certain areas of the brain cause symptoms or does SZ
cause abnormal functioning?
• Brown - parental age can cause gene abnormality in children which may lead
to SZ.
• The concordance rate for biological influences isn't 100% implying the role of
the environment is important.
Psychological Explanation
• Fromm-Reichman - SZ mother
SZ causing mother
Characteristics: cold, rejecting, controlling - family climate of tension and secrecy.
This distrust in the mother creates paranoia which leads to SZ.
• Bateson - Double-bind theory
Expressive communication style within the family.
Child often comes across times where they fear doing the wrong thing. Yet they receive mixed
messages and aren't told what exactly they did wrong.
The child is punished by a withdrawal of love.
This leaves the child feeling that the world is confusing and dangerous which causes paranoia.
• Expressed emotion and SZ
Negative emotion expressed by carers including:
verbal criticism --> followed by violence
Hostility, anger and rejection
Emotional over-involvement, needless self-sacrifice
This causes stress; it explains relapse in patients and how stress can trigger somebody genetically
vulnerable.
Cognitive Explanation
• Firth - dysfunctional thought processing
Metarepresentation - cognitive ability to reflect on thoughts
and behaviour. Dysfunctional Metarepresentation would
disrupt our ability to recognise our own actions and
thoughts as being carried out by ourselves rather than
somebody else. This would explain hallucinations and voice
insertion.
Central control - cognitive ability to suppress automatic
responses while we perform deliberate actions instead.
Evaluation
• Read - abuse in childhood
69% women
59% men
• Berry - insecure attachment also likely to develop sz.
• Data collected about childhood relies on the patient's recall, this may be
inaccurate or flawed which impacts the validity of the research.
• Parent blaming, more specifically, mother blaming.
• Stirling - patients with sz did worse on cognitive tasks like the stroop test
where they took twice as long to name ink colors on colored words.
• Cognitive explanation doesn't tell us about the origins of the disorder only the
causes of symptoms.
• Biological influences aren't really considered.
Drug Treatment
• Typical
Chlorpromazine; taken as a tablet, syrup or injection. In doses up to 1000mg per day.
Significant decline in use over last 50 years.
Antagonists in the dopamine system which reduce the action of dopamine. Antagonists
work by blocking the dopamine receptors in the synapses of the brain. This reduces
the action of doom dopamine.
Also a sedative, related to the histamine receptors. It is given to anxious patients in a
syrup form as it is quicker to be metabolised.
• Atypical
Clozapine; 300-400mg per day.
Acts the same way as chlorpromazine but is an antagonist for serotonin and glutamate.
Reduces symptoms of depression and anxiety and improves cognitive function.
Respiradone; taken in tablet, syrup and injection, 12mg per day. Effects lasts about two
weeks with an injection.
More efficient at binding to dopamine so it can be taken in smaller doses.
Evaluation
• Thornly - Chlorpromazine - more effective than a placebo. -1121
participants most of which showed beget overall functioning and reduced
symptom severity.
• Meltzer - Clozapine more effective in cases with anti-psychotic
resistance by 30-50%.
• Serious side effects including agranulocytosis which causes blood
clotting, long term uses of typical drugs can cause tardive dyskinesia
which manifests into involuntary facial movements.
• Hyperdopaminergia dictates that some areas of the brain have high
rather than low levels of dopamine activity.
• Is it ethical to sedate people using anti-psychotics, how does this relate
to quality of life.
Psychological Therapies
• CBT
Offering psychological explanations to the existence of their symptoms can help reduce anxiety, knowing where
these symptoms originated can dispel delusions and paranoia.
Challenge delusions so the patient learns that their beliefs are irrational.
• Family therapy
Improve the quality of communications and interactions between family members. This can reduce stress within
families which might contribute towards chance of relapse. Therapy aims to:
-Reduce stress for caring for a sufferer of sz
-Improving the ability to solve problems
-Reducing anger and guilt
-Developing a balance between caring for a patient and maintaining their own lives
-Improving beliefs and behaviour towards sz
• Token economy
Reward system to manage behaviour of sz, especially trying to reverse the effects of institutionalisation. Modifying
behaviour does not cure sz but helps to improve quality of life.
Tokens are given when the patient performs behaviours targeted for change, the tokens reinforce behaviour.
Although the tokens have no value, they can be exchanged for tangible rewards. Token economies rely on operant
conditioning.
Evaluation
• Jauhar - CBT has significant but fairly small effect on both
positive and negative symptoms.
• Pharaoh - family therapy reduced hospital readmissions over
the course of a year and improves quality of life. Although he
notes that the effects were inconsistent.
• The treatments improve quality of life but does not cure sz.
• Ethical consideration as token economies can be discriminative
against patients with severe symptoms.
• Small scale studies with small samples.
• Anti-psychotics maybe necessary to help some patients engage
in therapy, otherwise patients with severe symptoms may be too
distressed to actively participate.
Interactionist Approach
• Diathesis stress model
Vulnerability and stress is needed in order to develop sz.
The condition is triggered by a stressful event.
Meehl - schizogene which led to a schizotypic personality which is vulnerable to stress. The
development of this personality can be caused by stress in childhood like the schizophragenic
mother.
~Modern understanding - there is no schizogene, instead sz is polygenetic. Stress is important in
developing the disorder.
Read - trauma early on in childhood can cause neurological damage and prevents the
development of a normal psyche which makes a person vulnerable to stress.
e.g. hypothalamic-pituitary-adrenal system becomes overactive.
~Understanding of stress - Anything that increases the risk of developing sz.Examples include
canabis can increase chances of developing sz buy 7x.This is because canabis interferes with the
dopamine system.
Treatment:
Combination method of Anti-psychotics and CBT. Increasingly, in Britain, it is becoming the
standard practice. However, it is more costly and dominating ideas about biology being the cause
has meant that drug treatments is the most common method.
Evaluation
• Tienari - in an adoptee study, the children raised in an adopted family full of
conflict, criticism and low empathy, with biological parents who had sz were
more likely than a control to develop sz.
• The original stress model was over simplistic. There is no schizogene - recent
research implies that multiple genes are responsible for sz.
• Houston - childhood sexual trauma coupled with canabis use caused sz.
• Tarrier - patients in the experimental group who received drugs and
CBT/supportive counselling showed lower levels of symptoms than those only
given drugs.
• Unsure how the mechanisms of vulnerability and stress cause symptoms to
appear.
• Treatment-causation fallacy - the assumption that because a certain therapy
works, that it automatically means that's the cause e.g. drug treatments work
to reduce symptoms but that isn't to say that sz is biologically caused.

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Schizophrenia - Psychology AQA

  • 2. Diagnosis of Schizophrenia • WHO - ICD10 Two or more negative symptoms for diagnosis 1 month duration of symptoms types: paranoid schizophrenia - powerful delusions and hallucinations hebephrenic schizophrenia - primary negative symptoms catatonic - disturbance to movementleaving sufferer immobile or overactive • DSM5 One positive symptom needed 6 months for diagnosis
  • 3. Symptoms • Positive symptoms Hallucinations - unreal manipulation of the senses e.g. hearing voices or seeing facial expressions. Delusions - irrational beliefs e.g. fear of being persecuted by aliens, this can cause aggression. • Negative symptoms Avolition - apathy - inability to begin our keep up with goal directed activity. Andreason ~ poor hygiene, lack of patience in education or work and a lack of energy. Speech poverty - reduction in the amount and quality of speech or delayed responses. Speech disorganisation - speech becomes incoherent or speaker changes topic mid-sentence.
  • 4. Evaluation • poor inter-rater reliability, Chenxiaux - two psychiatrists independently diagnose schizophrenia in 100 patients. A) 26 DSM, 44 ICD B) 13 DSM, 24 ICD. • poor validity - unequal diagnosis via both diagnostic manuals means under or over diagnosing schizophrenia. • Co-morbidity - Buckley - 50% also diagnosed with depression, 23% OCD, 47% substance abuse. This makes diagnosis confusing and tricky as it might be one condition or a wrong diagnosis. • Symptom overlap - Schizophrenia and bipolar disorder have similar symptoms which can easily be incorrectly diagnosed. • Longenecker - since the 80s more men are diagnosed than women. • Cotton - gender bias, women seem to cope better with symptoms and men have higher expectations of normality and thus defying these warrant diagnosis. • Africans and west Indians are more likely to be diagnosed due to cultural bias, some cultures may see hallucinations as positive, psychiatrists may not see as a good thing.
  • 5. Biological Explanation • Twin studies - Gottesman 48% risk for identical twins 17% fraternal twins 6% siblings + parents • Candidate genes - Ripke Polygenetic - requires a number of factors to work in combination. Atelogical heterogeneous - different combinations of factors can lead to the condition. 108 gene variations were associated with risk of SZ. Genes associated included ones that code for seretonin + dopamine. • Dopamine hypothesis - Neurotransmitters work differently in the brains of people with SZ. HYPERdopaminergia - excess of dopamine in Brocas area may maybe associated with speech poverty and auditory hallucinations. HYPOdopaminergia - Goldman-Rakic - low levels of dopamine in the prefrontal cortex can explain negative symptoms like avolition. • Neural correlates - measurements of structure and function of the brain Low levels of activity in the ventral striatum linked to negative symptoms. Allen - low levels of activity in the superior temporal gyrus and anterior cingulate gyrus responsible for positive symptoms e.g. hallucinations.
  • 6. Evaluation • Overwhelming evidence to support a generic link to SZ. • Dopamine agonists help increase dopamine which makes symptoms of SZ and produces SZ like symptoms. • Lindstrom - dopamine is taken up faster in the brains of SZ suggesting they produce more of it. • Dopamine hypothesis may only be a partial explanation as genes identified by Ripke identify certain genes are the cause of abnormal dopamine coding. • Does low activity in certain areas of the brain cause symptoms or does SZ cause abnormal functioning? • Brown - parental age can cause gene abnormality in children which may lead to SZ. • The concordance rate for biological influences isn't 100% implying the role of the environment is important.
  • 7. Psychological Explanation • Fromm-Reichman - SZ mother SZ causing mother Characteristics: cold, rejecting, controlling - family climate of tension and secrecy. This distrust in the mother creates paranoia which leads to SZ. • Bateson - Double-bind theory Expressive communication style within the family. Child often comes across times where they fear doing the wrong thing. Yet they receive mixed messages and aren't told what exactly they did wrong. The child is punished by a withdrawal of love. This leaves the child feeling that the world is confusing and dangerous which causes paranoia. • Expressed emotion and SZ Negative emotion expressed by carers including: verbal criticism --> followed by violence Hostility, anger and rejection Emotional over-involvement, needless self-sacrifice This causes stress; it explains relapse in patients and how stress can trigger somebody genetically vulnerable.
  • 8. Cognitive Explanation • Firth - dysfunctional thought processing Metarepresentation - cognitive ability to reflect on thoughts and behaviour. Dysfunctional Metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than somebody else. This would explain hallucinations and voice insertion. Central control - cognitive ability to suppress automatic responses while we perform deliberate actions instead.
  • 9. Evaluation • Read - abuse in childhood 69% women 59% men • Berry - insecure attachment also likely to develop sz. • Data collected about childhood relies on the patient's recall, this may be inaccurate or flawed which impacts the validity of the research. • Parent blaming, more specifically, mother blaming. • Stirling - patients with sz did worse on cognitive tasks like the stroop test where they took twice as long to name ink colors on colored words. • Cognitive explanation doesn't tell us about the origins of the disorder only the causes of symptoms. • Biological influences aren't really considered.
  • 10. Drug Treatment • Typical Chlorpromazine; taken as a tablet, syrup or injection. In doses up to 1000mg per day. Significant decline in use over last 50 years. Antagonists in the dopamine system which reduce the action of dopamine. Antagonists work by blocking the dopamine receptors in the synapses of the brain. This reduces the action of doom dopamine. Also a sedative, related to the histamine receptors. It is given to anxious patients in a syrup form as it is quicker to be metabolised. • Atypical Clozapine; 300-400mg per day. Acts the same way as chlorpromazine but is an antagonist for serotonin and glutamate. Reduces symptoms of depression and anxiety and improves cognitive function. Respiradone; taken in tablet, syrup and injection, 12mg per day. Effects lasts about two weeks with an injection. More efficient at binding to dopamine so it can be taken in smaller doses.
  • 11. Evaluation • Thornly - Chlorpromazine - more effective than a placebo. -1121 participants most of which showed beget overall functioning and reduced symptom severity. • Meltzer - Clozapine more effective in cases with anti-psychotic resistance by 30-50%. • Serious side effects including agranulocytosis which causes blood clotting, long term uses of typical drugs can cause tardive dyskinesia which manifests into involuntary facial movements. • Hyperdopaminergia dictates that some areas of the brain have high rather than low levels of dopamine activity. • Is it ethical to sedate people using anti-psychotics, how does this relate to quality of life.
  • 12. Psychological Therapies • CBT Offering psychological explanations to the existence of their symptoms can help reduce anxiety, knowing where these symptoms originated can dispel delusions and paranoia. Challenge delusions so the patient learns that their beliefs are irrational. • Family therapy Improve the quality of communications and interactions between family members. This can reduce stress within families which might contribute towards chance of relapse. Therapy aims to: -Reduce stress for caring for a sufferer of sz -Improving the ability to solve problems -Reducing anger and guilt -Developing a balance between caring for a patient and maintaining their own lives -Improving beliefs and behaviour towards sz • Token economy Reward system to manage behaviour of sz, especially trying to reverse the effects of institutionalisation. Modifying behaviour does not cure sz but helps to improve quality of life. Tokens are given when the patient performs behaviours targeted for change, the tokens reinforce behaviour. Although the tokens have no value, they can be exchanged for tangible rewards. Token economies rely on operant conditioning.
  • 13. Evaluation • Jauhar - CBT has significant but fairly small effect on both positive and negative symptoms. • Pharaoh - family therapy reduced hospital readmissions over the course of a year and improves quality of life. Although he notes that the effects were inconsistent. • The treatments improve quality of life but does not cure sz. • Ethical consideration as token economies can be discriminative against patients with severe symptoms. • Small scale studies with small samples. • Anti-psychotics maybe necessary to help some patients engage in therapy, otherwise patients with severe symptoms may be too distressed to actively participate.
  • 14. Interactionist Approach • Diathesis stress model Vulnerability and stress is needed in order to develop sz. The condition is triggered by a stressful event. Meehl - schizogene which led to a schizotypic personality which is vulnerable to stress. The development of this personality can be caused by stress in childhood like the schizophragenic mother. ~Modern understanding - there is no schizogene, instead sz is polygenetic. Stress is important in developing the disorder. Read - trauma early on in childhood can cause neurological damage and prevents the development of a normal psyche which makes a person vulnerable to stress. e.g. hypothalamic-pituitary-adrenal system becomes overactive. ~Understanding of stress - Anything that increases the risk of developing sz.Examples include canabis can increase chances of developing sz buy 7x.This is because canabis interferes with the dopamine system. Treatment: Combination method of Anti-psychotics and CBT. Increasingly, in Britain, it is becoming the standard practice. However, it is more costly and dominating ideas about biology being the cause has meant that drug treatments is the most common method.
  • 15. Evaluation • Tienari - in an adoptee study, the children raised in an adopted family full of conflict, criticism and low empathy, with biological parents who had sz were more likely than a control to develop sz. • The original stress model was over simplistic. There is no schizogene - recent research implies that multiple genes are responsible for sz. • Houston - childhood sexual trauma coupled with canabis use caused sz. • Tarrier - patients in the experimental group who received drugs and CBT/supportive counselling showed lower levels of symptoms than those only given drugs. • Unsure how the mechanisms of vulnerability and stress cause symptoms to appear. • Treatment-causation fallacy - the assumption that because a certain therapy works, that it automatically means that's the cause e.g. drug treatments work to reduce symptoms but that isn't to say that sz is biologically caused.