SCHIZOPHRENIA
Diagnosis and classification
More common in men, city-dwellers and lower socio-economic groups
Diagnosis and Medical approach identifies symptoms that go together to be classified as a disorder.
classification Classification either from the DSM-5 or ICD-10 which differ slightly, (e.g. DSM-5 says one
positive symptom is needed for a diagnosis)
Positive symptoms Experience symptoms beyond normal experience:
- Hallucinations, unusual sensory experiences, distorted reality
- Delusions, beliefs not based in reality with bizarre behaviour
Negative symptom Loss of usual abilities:
- Speech poverty, poor or disorganised speech
- Avolition, loss of motivation and low activity
EVALUATION
One strength of the diagnosis process is its inter-rater reliability as it means clinicians are able to reach the same
diagnosis for an individual. Osorio et al found an inter-rater reliability of +.97 and test-retest reliability of +.92. This
means we can be reasonably sure the diagnosis is consistent, on the SSM scale.
A limitation is its validity. Cheniaux et al had two psychiatrists independently assess the same 100 clients and found 68
diagnosed under ICD and 39 to DSM. These results suggest that the condition is over under or over diagnosed according
to the system however either way validity is low.
Another limitation is its comorbidity with other conditions. If conditions occur together this can call into question the
classification as they may be a single condition. It can be diagnosed with depression or substance abuse. This is a
problem because it may mean schizophrenia is not a distinct condition which means some may actually have unusual cases
of depression.
A further limitation is the existence of gender bias. Fischer found the ratio of diagnosed men to women is 1.4:1. Some
consider this to be in relation to their closer relationships that give them access to greater support which may result in
the underdiagnosis of women. This means women may not receive treatment and services that may benefit them.
Another limitation is the existence of culture bias. Symptoms like hearing voices differ between cultures as in some
Afro-Caribbean cultures this may be attributed to communication from ancestors. Furthermore Afro-Carribeans in the
UK are ten times more likely to receive a diagnosis than a white British person which suggests an overinterpretation of
symptoms in black Brits. This means they may be discriminated against in a biassed diagnostic system.
A final limitation is the overlap of symptoms with other conditions. For example it shares positive symptoms with bipolar
disorder like delusions and negative symptoms like avolition. In terms of classification this means they may not be separate
, disorders, instead variations of the same condition. This means it is not a distinct condition that is hard to diagnose,
making both classification and diagnosis flawed.
Biological explanations
Genetic basis
Gottesman- family Risk increases with genetic similarity to someone with the condition, e.g. 9% for a sibling and
studies 48% of an identical twin
Candidate genes Polygenic and aetiologically heterogeneous (can result from different combinations of risk
factors). 108 genetic variations which each slightly increase the risk
Role of mutation Genetic vulnerability in people with no family history, found 2% risk with fathers 50+
EVALUATION
One strength is the strong evidence base. Family studies, like Gottesman, show risk increases with genetic similarity.
Adoption studies like Tienari et al show biological parents give children a higher risk than if they have grown up in an
adoptive family. This shows some people have a vulnerability to schizophrenia as a result of their genetic makeup.
One limitation is there is clear evidence environmental factors increase the risk of developing schizophrenia. These factors
are both biological and psychological influences, birth complications and long term smoking. In Morkved et al 67%
schizophrenic patients reported a childhood trauma compared to the matched group with 38%. Shows only genetic
factors alone cannot explain the condition.
Another limitation is the risk estimate of genetic counselling is just an average figure. This means it will not necessarily
reflect the probability of an individual developing the condition because the environmental risk factors must be assessed.
Neural correlates
Dopamine Levels in different brain regions correlate with symptoms
The original dopamine Antipsychotic drugs produce symptoms similar to Parkinson’s (low dopamine)
hypothesis
Schizophrenia caused by high dopamine in the subcortex (hyperdopaminergia) explains some
symptoms in connection to speech poverty - high dopamine receptors in Brocas
Updated hypothesis High dopamine in the subcortex and low in cortex (hypodopaminergia) explains negative
symptoms. For example low dopamine in the prefrontal cortex could explain cognitive problems.
Also suggested cortical hypordopaminergia may lead to subcortical hyperdopaminergia.
Dopamine levels are affected by both genetic vulnerability and childhood and adolescent stress
can make people more sensitive for hypodopaminergia and hence subcortical
hyperdopaminergia.
Diagnosis and classification
More common in men, city-dwellers and lower socio-economic groups
Diagnosis and Medical approach identifies symptoms that go together to be classified as a disorder.
classification Classification either from the DSM-5 or ICD-10 which differ slightly, (e.g. DSM-5 says one
positive symptom is needed for a diagnosis)
Positive symptoms Experience symptoms beyond normal experience:
- Hallucinations, unusual sensory experiences, distorted reality
- Delusions, beliefs not based in reality with bizarre behaviour
Negative symptom Loss of usual abilities:
- Speech poverty, poor or disorganised speech
- Avolition, loss of motivation and low activity
EVALUATION
One strength of the diagnosis process is its inter-rater reliability as it means clinicians are able to reach the same
diagnosis for an individual. Osorio et al found an inter-rater reliability of +.97 and test-retest reliability of +.92. This
means we can be reasonably sure the diagnosis is consistent, on the SSM scale.
A limitation is its validity. Cheniaux et al had two psychiatrists independently assess the same 100 clients and found 68
diagnosed under ICD and 39 to DSM. These results suggest that the condition is over under or over diagnosed according
to the system however either way validity is low.
Another limitation is its comorbidity with other conditions. If conditions occur together this can call into question the
classification as they may be a single condition. It can be diagnosed with depression or substance abuse. This is a
problem because it may mean schizophrenia is not a distinct condition which means some may actually have unusual cases
of depression.
A further limitation is the existence of gender bias. Fischer found the ratio of diagnosed men to women is 1.4:1. Some
consider this to be in relation to their closer relationships that give them access to greater support which may result in
the underdiagnosis of women. This means women may not receive treatment and services that may benefit them.
Another limitation is the existence of culture bias. Symptoms like hearing voices differ between cultures as in some
Afro-Caribbean cultures this may be attributed to communication from ancestors. Furthermore Afro-Carribeans in the
UK are ten times more likely to receive a diagnosis than a white British person which suggests an overinterpretation of
symptoms in black Brits. This means they may be discriminated against in a biassed diagnostic system.
A final limitation is the overlap of symptoms with other conditions. For example it shares positive symptoms with bipolar
disorder like delusions and negative symptoms like avolition. In terms of classification this means they may not be separate
, disorders, instead variations of the same condition. This means it is not a distinct condition that is hard to diagnose,
making both classification and diagnosis flawed.
Biological explanations
Genetic basis
Gottesman- family Risk increases with genetic similarity to someone with the condition, e.g. 9% for a sibling and
studies 48% of an identical twin
Candidate genes Polygenic and aetiologically heterogeneous (can result from different combinations of risk
factors). 108 genetic variations which each slightly increase the risk
Role of mutation Genetic vulnerability in people with no family history, found 2% risk with fathers 50+
EVALUATION
One strength is the strong evidence base. Family studies, like Gottesman, show risk increases with genetic similarity.
Adoption studies like Tienari et al show biological parents give children a higher risk than if they have grown up in an
adoptive family. This shows some people have a vulnerability to schizophrenia as a result of their genetic makeup.
One limitation is there is clear evidence environmental factors increase the risk of developing schizophrenia. These factors
are both biological and psychological influences, birth complications and long term smoking. In Morkved et al 67%
schizophrenic patients reported a childhood trauma compared to the matched group with 38%. Shows only genetic
factors alone cannot explain the condition.
Another limitation is the risk estimate of genetic counselling is just an average figure. This means it will not necessarily
reflect the probability of an individual developing the condition because the environmental risk factors must be assessed.
Neural correlates
Dopamine Levels in different brain regions correlate with symptoms
The original dopamine Antipsychotic drugs produce symptoms similar to Parkinson’s (low dopamine)
hypothesis
Schizophrenia caused by high dopamine in the subcortex (hyperdopaminergia) explains some
symptoms in connection to speech poverty - high dopamine receptors in Brocas
Updated hypothesis High dopamine in the subcortex and low in cortex (hypodopaminergia) explains negative
symptoms. For example low dopamine in the prefrontal cortex could explain cognitive problems.
Also suggested cortical hypordopaminergia may lead to subcortical hyperdopaminergia.
Dopamine levels are affected by both genetic vulnerability and childhood and adolescent stress
can make people more sensitive for hypodopaminergia and hence subcortical
hyperdopaminergia.
