PAPER 3 PSYCHOLOGY
SCHIZOPHRENIA
CLASSIFICATION AND DIAGNOSIS
Schizophrenia is a serious mental illness that affects 1% of people. It distorts
contact with reality and impairs a persons reality. It is more common in males,
city dwellers and lower socio-economic groups and is often diagnosed between
15-35 years.
ICD-10 suggests two or more negative symptoms are needed for a diagnosis
whilst DSM-5 says one positive symptom is sufficient for diagnosis.
Symptoms;
Positive - Hallucinations, delusions and disorganised speech.
Negative - Speech poverty, avoilition.
Reliability - Finding consistent results. This means having a consistent diagno-
sis of schizophrenia across patients or the same patient through test re-test.
Validity - Is what we are measuring what we are intending to measure? Do dif-
ferent assessment systems arrive at the same diagnosis?
EVALUATION
- The concept of co-morbidity. Buckley (2009) concluded that around half of
his patients with SZ also have diagnosis of depression and substance abuse.
Other common examples include PTSD. Therefore SZ may not exist as a sin-
gle condition, which is a problem for diagnosis as it suggests that some peo-
ple with SZ could have unusual cases of depression. This suggests that there
are low levels of validity of the diagnosis and classification of SZ.
- Symptom overlap. There is a considerable overlap between symptoms of
schizophrenia and other conditions such as bipolar with delusions and avoli-
tion. This suggests that SZ and bipolar may not be two conditions but varia-
tions of a single condition. This means SZ may not exist as a distinct condi-
tion and is hard to diagnose.
- Culture bias. Escobar found that Afro-Caribbean people living in the UK are
10x more likely to receive a diagnosis of SZ than white British people. Symp-
toms such as hearing voices have different meanings; for example Afro-Car-
ibbean societies may link hearing voices to communication with ancestors.
This may lead to an over interpretation of symptoms in black British people.
This means that particular people may be discriminated against.
- Gender bias. Cotton suggests men are more commonly diagnosed due to
women having closer social and family relationships, suggesting women
function better. This suggests that better interpersonal functioning may bias
practitioners into underdiagnosing. This suggests the validity of diagnosis is
poor.
,BIOLOGICAL EXPLANATION
Concerned with genetic vulnerability and the possible role of neural correlates. These are inter-
related - if schizophrenia is genetic than those genes lead to biological differences such as ab-
normal levels of dopamine.
Genetic Explanation consists of DNA strands inherited from parents. Evidence in favour of a
genetic link comes from family studies; which indicate that the closer the genetic relationship
to someone with schizophrenia, the greater the chance of developing the disorder.
Family studies argue genetic similarity increases in line with the probability of sharing
schizophrenia. Such studies have confirmed the risk of schizophrenia increases in line with ge-
netic similarity to a relative with the condition. Gottesman (1991) conducted a large scale fam-
ily study and found that children with two schizophrenic parents had a concordance rate of
46%, those with one parent was 13% and siblings was 9%. Identical twins was 48%.
Adoptive studies were researched by Heston who compared 47 children of schizophrenic moth-
ers who had been fostered or adopted during the first month of life with a control group of 50
children without schizophrenic mothers in the same home. Those 47 children were more likely
to be diagnosed with psychological abnormalities.
Schizophrenia appears to be polygenic.
EVALUATION
+ Supporting research. Research by Tienari found of 164 adoptees with schizophrenic
mothers, 11 received a diagnosis compared to just 2% of the 197 control group adoptees. Ad-
ditionally, Gottesman shows how genetic similarity is closely related to the development of
schizophrenia. These findings suggest genetic factors make some people more vulnerable to
developing schizophrenia than others.
- Family studies are studied retrospectively.
- Concordance rate is not 100%, therefore cannot wholly explain sz.
- Biologically reductionist.
Role of Mutation emphasises that 2/3rds of those with schizophrenia have no relative link and
therefore cannot inherit it. Sz can also have a genetic origin in the absence of family history.
One explanation for this is mutation in parental DNA which can be caused by viral infection. Ev-
idence comes from positive correlations between paternal age and a risk of SZ increasing from
0.7% with fathers under 25 to over 2% for fathers over 50 (Brown 2002).
Neural Correlates argue schizophrenia develops due to structural and functional brain abnor-
malities. Evidence originally limited to post-mortems, has developed with FMRIs which allow
comparisons from sufferers to non-sufferers, best achieved with a task.
This explanation proposes that sz is caused by enlarged ventricles. These are the fluid-filled
gaps between brain areas. Such damage to the central brain is often associated with negative
symptoms. Johnstone found that schizophrenics had enlarged ventricles whilst non-sufferers
did not.
EVALUATION
- Research suggests that enlarged ventricles may only explain certain schizophrenia symp-
toms. Weyant reported that enlarged ventricles are associated with negative symptoms only.
This implies that the explanation cannot explain all symptoms and all cases.
- Causation. Evidence suggests that schizophrenics that do not respond to medication are
those with enlarged ventricles. This could mean that it is an effect of suffering from sz over a
long period of time. Therefore the enlarged ventricles may be a consequence of the illness
rather than the cause.
Original Dopamine Hypothesis stated that sz was caused by excessive activity of
dopamine. This causes the messages from neurons that transmit dopamine to fire too early or
too often. Snyder stated that if too much dopamine is released into the synapse it can lead to
the onset of SZ.
,EVALUATION
+ Supporting research. The original hypothesis was based on the discovery that drugs
used to treat schizophrenia caused symptoms similar to those suffering Parkinson’s disease, a
condition associated with low dopamine levels. Therefore, schizophrenia may be a result of
high levels of dopamine in the subcortical areas of the brain.
+ Supporting evidence. Amphetamines increase dopamine and worsen symptoms in peo-
ple with sz and induce symptoms in people without (Curran).
BIOLOGICAL TREATMENTS
Antipsychotic drugs are used to reduce the intensity of the symptoms, in par-
ticular positive symptoms. Split into typical and atypical.
Typical are first generation which work as dopamine antagonists (Chlorpro-
mazine)
Atypicals were developed after typical and target a range of neurotransmitters
such as dopamine or serotonin (Clozapine and Risperidone)
These manage symptoms, they do not cure.
Atypical antipsychotics occupy the receptors and reduce the amount of
dopamine received. Also act upon the serotonin receptors to increase the lev-
els of serotonin the synapse.
Typical antipsychotics block receptor side to prevent abundance of dopamine.
Chlorpromazine (Typical) - Has a dosage of up to 1000mg daily, side effects in-
clude dizziness, agitation and insomnia.
Clozapine (Atypical) - Has a dosage of 300-450mg daily and side effects of
agranulocytosis. Prescribed to those with a high risk of suicide.
Risperidone (Atypical) - Has a dosage of 4-8mg, side effects include nausea and
low appetite.
EVALUATION
+ Real world application. Antipsychotics have been used in hospitals to
calm people with sz to enable staff to work with them rather than the benefits
of the drug itself. Calmed patients will therefore feel more inclined to engage
with therapy.
+ Supporting research. Thornby reviewed twin studies comparing the ef-
fects of chlorpromazine to control conditions. Data from 13 trials with a total
of 1121 participants. Results showed that chlorpromazine effectively tackled
symptoms better than the placebos. Meltzer reviewed typical antipsychotics
concluding that clozapine is more effective than typical and other atypical an-
tipsychotics. Its effective in 30-50% of treatment resistant cases where typi-
cal antipsychotics have failed.
- Series of side effects. Long term use can result in tardive dyskinesia - caused
by dopamine super sensitivity causing involuntary movement. The most seri-
ous side effect is (NMS) believed to be caused when the drug blocks
dopamine in the hypothalamus (the area associated with regulation of a
number of body systems). NMS can be fatal.
- Mechanism unclear. Our understanding is tied up with the original dopamine
hypothesis. We now know that the original dopamine hypothesis is incom-
, plete and in fact dopamine levels in other parts of the brain are too low.
Therefore this questions the effectiveness of antipsychotics.
PSYCHOLOGICAL EXPLANATION
Psychologists have attempted to link schizophrenia to childhood and adulthood
experiences of living in a dysfunctional family.
Family dysfunction (Reichmann) argues that abnormal processes within a fam-
ily such as cold parenting or anger can cause an onset of schizophrenia. For in-
stance, the mother causes schizophrenia (schizophrenogenic mother). Within
the family dysfunction explanation is the double bind theory and expressed
emotion.
The double bind theory argues family climate is important in the development
of schizophrenia as the child fears doing the wrong thing and will receive mixed
signals which leads to mistrust and reflects symptoms of sz (Bateson 1972).
Expressed emotion focuses on negative emotion expressed towards a patient
by their carer who are often family members. These high levels of (EE) are a
serious source of stress and could cause sz in someone who is genetically vul-
nerable (Diathesis stress model)
Cognitive explanation focuses on mental processes such as thinking, language
and attention. Frith identified two types of dysfunctional thought processing
that could lead to symptoms; meta representation (ability to reflect on
thoughts and behaviour) and central control (ability to suppress automatic
thoughts).
EVALUATION
- Socially sensitive. Parents who have already suffered at seeing their child’s
descent into sz likely bear lifelong responsibility for their care have under-
gone further trauma by receiving blame for the condition.
+ Strong evidence for dysfunctional thought processing. Stirling compared
30 patients with a diagnosis of sz with 10 non patients on a range of cognitive
tasks including the Stroop test. In line with Frith’s theories of central control,
patients took twice as long to name the ink colours than the control group.
A counter point however is that it does not tell us the origins of these cogni-
tions of sz. Cognitive theories can explain the proximal cause of sz but not
the distal cause.
SCHIZOPHRENIA
CLASSIFICATION AND DIAGNOSIS
Schizophrenia is a serious mental illness that affects 1% of people. It distorts
contact with reality and impairs a persons reality. It is more common in males,
city dwellers and lower socio-economic groups and is often diagnosed between
15-35 years.
ICD-10 suggests two or more negative symptoms are needed for a diagnosis
whilst DSM-5 says one positive symptom is sufficient for diagnosis.
Symptoms;
Positive - Hallucinations, delusions and disorganised speech.
Negative - Speech poverty, avoilition.
Reliability - Finding consistent results. This means having a consistent diagno-
sis of schizophrenia across patients or the same patient through test re-test.
Validity - Is what we are measuring what we are intending to measure? Do dif-
ferent assessment systems arrive at the same diagnosis?
EVALUATION
- The concept of co-morbidity. Buckley (2009) concluded that around half of
his patients with SZ also have diagnosis of depression and substance abuse.
Other common examples include PTSD. Therefore SZ may not exist as a sin-
gle condition, which is a problem for diagnosis as it suggests that some peo-
ple with SZ could have unusual cases of depression. This suggests that there
are low levels of validity of the diagnosis and classification of SZ.
- Symptom overlap. There is a considerable overlap between symptoms of
schizophrenia and other conditions such as bipolar with delusions and avoli-
tion. This suggests that SZ and bipolar may not be two conditions but varia-
tions of a single condition. This means SZ may not exist as a distinct condi-
tion and is hard to diagnose.
- Culture bias. Escobar found that Afro-Caribbean people living in the UK are
10x more likely to receive a diagnosis of SZ than white British people. Symp-
toms such as hearing voices have different meanings; for example Afro-Car-
ibbean societies may link hearing voices to communication with ancestors.
This may lead to an over interpretation of symptoms in black British people.
This means that particular people may be discriminated against.
- Gender bias. Cotton suggests men are more commonly diagnosed due to
women having closer social and family relationships, suggesting women
function better. This suggests that better interpersonal functioning may bias
practitioners into underdiagnosing. This suggests the validity of diagnosis is
poor.
,BIOLOGICAL EXPLANATION
Concerned with genetic vulnerability and the possible role of neural correlates. These are inter-
related - if schizophrenia is genetic than those genes lead to biological differences such as ab-
normal levels of dopamine.
Genetic Explanation consists of DNA strands inherited from parents. Evidence in favour of a
genetic link comes from family studies; which indicate that the closer the genetic relationship
to someone with schizophrenia, the greater the chance of developing the disorder.
Family studies argue genetic similarity increases in line with the probability of sharing
schizophrenia. Such studies have confirmed the risk of schizophrenia increases in line with ge-
netic similarity to a relative with the condition. Gottesman (1991) conducted a large scale fam-
ily study and found that children with two schizophrenic parents had a concordance rate of
46%, those with one parent was 13% and siblings was 9%. Identical twins was 48%.
Adoptive studies were researched by Heston who compared 47 children of schizophrenic moth-
ers who had been fostered or adopted during the first month of life with a control group of 50
children without schizophrenic mothers in the same home. Those 47 children were more likely
to be diagnosed with psychological abnormalities.
Schizophrenia appears to be polygenic.
EVALUATION
+ Supporting research. Research by Tienari found of 164 adoptees with schizophrenic
mothers, 11 received a diagnosis compared to just 2% of the 197 control group adoptees. Ad-
ditionally, Gottesman shows how genetic similarity is closely related to the development of
schizophrenia. These findings suggest genetic factors make some people more vulnerable to
developing schizophrenia than others.
- Family studies are studied retrospectively.
- Concordance rate is not 100%, therefore cannot wholly explain sz.
- Biologically reductionist.
Role of Mutation emphasises that 2/3rds of those with schizophrenia have no relative link and
therefore cannot inherit it. Sz can also have a genetic origin in the absence of family history.
One explanation for this is mutation in parental DNA which can be caused by viral infection. Ev-
idence comes from positive correlations between paternal age and a risk of SZ increasing from
0.7% with fathers under 25 to over 2% for fathers over 50 (Brown 2002).
Neural Correlates argue schizophrenia develops due to structural and functional brain abnor-
malities. Evidence originally limited to post-mortems, has developed with FMRIs which allow
comparisons from sufferers to non-sufferers, best achieved with a task.
This explanation proposes that sz is caused by enlarged ventricles. These are the fluid-filled
gaps between brain areas. Such damage to the central brain is often associated with negative
symptoms. Johnstone found that schizophrenics had enlarged ventricles whilst non-sufferers
did not.
EVALUATION
- Research suggests that enlarged ventricles may only explain certain schizophrenia symp-
toms. Weyant reported that enlarged ventricles are associated with negative symptoms only.
This implies that the explanation cannot explain all symptoms and all cases.
- Causation. Evidence suggests that schizophrenics that do not respond to medication are
those with enlarged ventricles. This could mean that it is an effect of suffering from sz over a
long period of time. Therefore the enlarged ventricles may be a consequence of the illness
rather than the cause.
Original Dopamine Hypothesis stated that sz was caused by excessive activity of
dopamine. This causes the messages from neurons that transmit dopamine to fire too early or
too often. Snyder stated that if too much dopamine is released into the synapse it can lead to
the onset of SZ.
,EVALUATION
+ Supporting research. The original hypothesis was based on the discovery that drugs
used to treat schizophrenia caused symptoms similar to those suffering Parkinson’s disease, a
condition associated with low dopamine levels. Therefore, schizophrenia may be a result of
high levels of dopamine in the subcortical areas of the brain.
+ Supporting evidence. Amphetamines increase dopamine and worsen symptoms in peo-
ple with sz and induce symptoms in people without (Curran).
BIOLOGICAL TREATMENTS
Antipsychotic drugs are used to reduce the intensity of the symptoms, in par-
ticular positive symptoms. Split into typical and atypical.
Typical are first generation which work as dopamine antagonists (Chlorpro-
mazine)
Atypicals were developed after typical and target a range of neurotransmitters
such as dopamine or serotonin (Clozapine and Risperidone)
These manage symptoms, they do not cure.
Atypical antipsychotics occupy the receptors and reduce the amount of
dopamine received. Also act upon the serotonin receptors to increase the lev-
els of serotonin the synapse.
Typical antipsychotics block receptor side to prevent abundance of dopamine.
Chlorpromazine (Typical) - Has a dosage of up to 1000mg daily, side effects in-
clude dizziness, agitation and insomnia.
Clozapine (Atypical) - Has a dosage of 300-450mg daily and side effects of
agranulocytosis. Prescribed to those with a high risk of suicide.
Risperidone (Atypical) - Has a dosage of 4-8mg, side effects include nausea and
low appetite.
EVALUATION
+ Real world application. Antipsychotics have been used in hospitals to
calm people with sz to enable staff to work with them rather than the benefits
of the drug itself. Calmed patients will therefore feel more inclined to engage
with therapy.
+ Supporting research. Thornby reviewed twin studies comparing the ef-
fects of chlorpromazine to control conditions. Data from 13 trials with a total
of 1121 participants. Results showed that chlorpromazine effectively tackled
symptoms better than the placebos. Meltzer reviewed typical antipsychotics
concluding that clozapine is more effective than typical and other atypical an-
tipsychotics. Its effective in 30-50% of treatment resistant cases where typi-
cal antipsychotics have failed.
- Series of side effects. Long term use can result in tardive dyskinesia - caused
by dopamine super sensitivity causing involuntary movement. The most seri-
ous side effect is (NMS) believed to be caused when the drug blocks
dopamine in the hypothalamus (the area associated with regulation of a
number of body systems). NMS can be fatal.
- Mechanism unclear. Our understanding is tied up with the original dopamine
hypothesis. We now know that the original dopamine hypothesis is incom-
, plete and in fact dopamine levels in other parts of the brain are too low.
Therefore this questions the effectiveness of antipsychotics.
PSYCHOLOGICAL EXPLANATION
Psychologists have attempted to link schizophrenia to childhood and adulthood
experiences of living in a dysfunctional family.
Family dysfunction (Reichmann) argues that abnormal processes within a fam-
ily such as cold parenting or anger can cause an onset of schizophrenia. For in-
stance, the mother causes schizophrenia (schizophrenogenic mother). Within
the family dysfunction explanation is the double bind theory and expressed
emotion.
The double bind theory argues family climate is important in the development
of schizophrenia as the child fears doing the wrong thing and will receive mixed
signals which leads to mistrust and reflects symptoms of sz (Bateson 1972).
Expressed emotion focuses on negative emotion expressed towards a patient
by their carer who are often family members. These high levels of (EE) are a
serious source of stress and could cause sz in someone who is genetically vul-
nerable (Diathesis stress model)
Cognitive explanation focuses on mental processes such as thinking, language
and attention. Frith identified two types of dysfunctional thought processing
that could lead to symptoms; meta representation (ability to reflect on
thoughts and behaviour) and central control (ability to suppress automatic
thoughts).
EVALUATION
- Socially sensitive. Parents who have already suffered at seeing their child’s
descent into sz likely bear lifelong responsibility for their care have under-
gone further trauma by receiving blame for the condition.
+ Strong evidence for dysfunctional thought processing. Stirling compared
30 patients with a diagnosis of sz with 10 non patients on a range of cognitive
tasks including the Stroop test. In line with Frith’s theories of central control,
patients took twice as long to name the ink colours than the control group.
A counter point however is that it does not tell us the origins of these cogni-
tions of sz. Cognitive theories can explain the proximal cause of sz but not
the distal cause.
