Y2 Chapter 8 – Schizophrenia
Diagnosis and classification = Two major systems for the classification of mental disorders
are the ICD-10 and the DSM-5. In DSM-5, a positive symptom must be present, in ICD two
or more negative symptoms can be sufficient.
Evaluations:
o Inter-rater reliability (consistency)= Different psychiatrists reach the same diagnosis
for the same individual.
o Low validity = Whether we assess what we are trying to do. A test is done where 2
psychiatrists assessed the same 100 clients using DSM and ICD. 68 were diagnosed
with ICD and 39 with DSM. Shows schizophrenia is over or under-diagnosed
according to the diagnostic system
o Co-morbidity with other conditions = Schizophrenia is commonly diagnosed with
other conditions such as depression, so therefore may not exist as a distinct
condition. The issue with diagnosis as some people diagnosed with Schizophrenia
may have unusual cases of other conditions
Positive symptoms = Additional experiences beyond ordinary existence – hallucinations and
delusions
Hallucination = sensory experiences, such as voices or seeing things that aren’t there
Delusions (paranoia) = Irrational beliefs such as believing they are under external
control.
Negative symptoms = loss of usual abilities and experiences
Speech poverty = Reduction in amount and quality of speech. Also classified as
disorganization – in DSM this is a positive symptom but poverty is negative
Avolition (apathy) = Difficulty in the beginning or keeping up with goal-directed
activity. Includes: Poor hygiene, lack of persistence in work or education, and lack of
energy
Evaluations:
o Culture bias in diagnosis = Haiti some people believe voices are communication from
ancestors. British people from African Caribbean backgrounds are 9 times more likely
to be diagnosed than if they lived in their original background. Ruling out genetic
vulnerability. Shows may be discrimination
o Symptom overlap with other conditions = Schizophrenia and bipolar both include
delusions and negative symptoms. Hard to distinguish condition as with co-
morbidity, may not exist as a distinct condition
, Biological explanations for SZ
Genetic basis of SZ:
Family studies = large-scale family studies confirmed the risk of SZ increases in line
with genetic similarity to a relative with the disorder. For example, someone with an
aunt with SZ has a 2% chance of developing it
Candidate genes = early research looked for a single genetic variation to explain SZ.
However, SZ is polygenetic. In the study, a large number of genetic variations of
diagnosed versus control group was compared, and found 108 variations which
increase risk. Therefore SZ is also aetiologically heterogeneous (different
combinations of factors including genetic variation can lead to development)
Role of mutation = SZ can also have genetic origin in the absence of family history.
An explanation is a mutation in parental DNA caused by radiation, poison, or viral
infection.
Evaluation:
o Research support = family studies showed the risk of similarity of genes, adoption
studies showed biological children at higher risk even if brought up in an adopted
family, twin study showed concordance rate with higher in identical twins (MZ).
Showing genetic makeup’s effect on vulnerability. However, it is only an average
number so can’t be used to predict if a child may develop SZ.
o Environmental factors = biological such as birth complications and smoking THC in
teenage years. Psychological factors such as childhood trauma were shown in a
study where a high percentage of people with SZ reported at least one childhood
trauma.
Neural correlates of SZ
This is brain structure or function. The most common neural correlate of SZ is the NT
dopamine as it affects systems related to symptoms of SZ
The original dopamine hypothesis = is based on the discovery that drugs used to
treat SZ (reducing dopamine) caused symptoms similar to Parkinson’s (low DA level).
Therefore SZ may be the result of high DA. For example, an excess of DA receptors in
pathways from the subcortex to Broca’s area so may explain some symptoms of SZ
(B area responsible for speech production)
Updated version = abnormally low DA in cortex can explain symptoms. Such as low
DA in the prefrontal cortex (thinking) could explain cognitive issues (neg symptoms).
Evaluation:
o Evidence for DA = amphetamines increase DA and symptoms. Antipsychotic drugs
reduce DA and symptoms. Some candidate genes act on the production of DA. Study
– rats’ symptoms on amphetamines
Diagnosis and classification = Two major systems for the classification of mental disorders
are the ICD-10 and the DSM-5. In DSM-5, a positive symptom must be present, in ICD two
or more negative symptoms can be sufficient.
Evaluations:
o Inter-rater reliability (consistency)= Different psychiatrists reach the same diagnosis
for the same individual.
o Low validity = Whether we assess what we are trying to do. A test is done where 2
psychiatrists assessed the same 100 clients using DSM and ICD. 68 were diagnosed
with ICD and 39 with DSM. Shows schizophrenia is over or under-diagnosed
according to the diagnostic system
o Co-morbidity with other conditions = Schizophrenia is commonly diagnosed with
other conditions such as depression, so therefore may not exist as a distinct
condition. The issue with diagnosis as some people diagnosed with Schizophrenia
may have unusual cases of other conditions
Positive symptoms = Additional experiences beyond ordinary existence – hallucinations and
delusions
Hallucination = sensory experiences, such as voices or seeing things that aren’t there
Delusions (paranoia) = Irrational beliefs such as believing they are under external
control.
Negative symptoms = loss of usual abilities and experiences
Speech poverty = Reduction in amount and quality of speech. Also classified as
disorganization – in DSM this is a positive symptom but poverty is negative
Avolition (apathy) = Difficulty in the beginning or keeping up with goal-directed
activity. Includes: Poor hygiene, lack of persistence in work or education, and lack of
energy
Evaluations:
o Culture bias in diagnosis = Haiti some people believe voices are communication from
ancestors. British people from African Caribbean backgrounds are 9 times more likely
to be diagnosed than if they lived in their original background. Ruling out genetic
vulnerability. Shows may be discrimination
o Symptom overlap with other conditions = Schizophrenia and bipolar both include
delusions and negative symptoms. Hard to distinguish condition as with co-
morbidity, may not exist as a distinct condition
, Biological explanations for SZ
Genetic basis of SZ:
Family studies = large-scale family studies confirmed the risk of SZ increases in line
with genetic similarity to a relative with the disorder. For example, someone with an
aunt with SZ has a 2% chance of developing it
Candidate genes = early research looked for a single genetic variation to explain SZ.
However, SZ is polygenetic. In the study, a large number of genetic variations of
diagnosed versus control group was compared, and found 108 variations which
increase risk. Therefore SZ is also aetiologically heterogeneous (different
combinations of factors including genetic variation can lead to development)
Role of mutation = SZ can also have genetic origin in the absence of family history.
An explanation is a mutation in parental DNA caused by radiation, poison, or viral
infection.
Evaluation:
o Research support = family studies showed the risk of similarity of genes, adoption
studies showed biological children at higher risk even if brought up in an adopted
family, twin study showed concordance rate with higher in identical twins (MZ).
Showing genetic makeup’s effect on vulnerability. However, it is only an average
number so can’t be used to predict if a child may develop SZ.
o Environmental factors = biological such as birth complications and smoking THC in
teenage years. Psychological factors such as childhood trauma were shown in a
study where a high percentage of people with SZ reported at least one childhood
trauma.
Neural correlates of SZ
This is brain structure or function. The most common neural correlate of SZ is the NT
dopamine as it affects systems related to symptoms of SZ
The original dopamine hypothesis = is based on the discovery that drugs used to
treat SZ (reducing dopamine) caused symptoms similar to Parkinson’s (low DA level).
Therefore SZ may be the result of high DA. For example, an excess of DA receptors in
pathways from the subcortex to Broca’s area so may explain some symptoms of SZ
(B area responsible for speech production)
Updated version = abnormally low DA in cortex can explain symptoms. Such as low
DA in the prefrontal cortex (thinking) could explain cognitive issues (neg symptoms).
Evaluation:
o Evidence for DA = amphetamines increase DA and symptoms. Antipsychotic drugs
reduce DA and symptoms. Some candidate genes act on the production of DA. Study
– rats’ symptoms on amphetamines
