Schizophrenia 16 marker essay plans
Diagnosis and classification of SZ
AO1: Background – 1% prevalence, more common in men/city-dwellers/those of low socio-
economic bg, late adolescence/early adulthood as cases before adolescence are rare, most
live with psychotic disorder for life as treatment only helps symptoms, only 1/5 fully recover.
Diagnosis – diagnostic system looking for cluster of symptoms, ICD used by WHO looks for 2
neg symptoms, DSM used by APA look for 1 positive symptom. Positive symptoms – atypical
symptoms in addition to normal experience e.g. delusions/paranoia, hallucinations,
disorganised speech. Negative symptoms – atypical symptoms representing loss of normal
experience e.g. speech poverty, avolition (poor hygiene, lack of persistence in work/school,
lack of energy)
AO3: Rosenhan’s study – pseudo patients faking SZ went to 12 diff hospitals (new, old,
private etc.) claiming to hear voices. Participants of study were doctors and patients of
psychiatric hospitals. Pseudo patients were all admitted and were asked to leave when their
symptoms disappeared. Reactions of doctors and patients were monitored. All but one
pseudo patient was diagnosed with SZ and were released from 7 to 52 days (avg = 19). DSM
2 was in use and patients were released based on their symptoms being in remission.
35/118 patients of psychiatric patients accused pseudo patients of faking SZ. Strengths of
diagnosis and classification – test re-test and reliability, Osorio et al – 180 SZ patients, pair
interviewed and found +.97 inter-rater reliability and +.92 test re-test reliability therefore
showing diagnosis consistency. Weaknesses – problem of validity as shown by Rosenhan’s
study, Chaniaux – 2 psychologists assessed 100 SZ patients using DSM and ICD, psychologist
using ICD diagnosed 68 and the one using DSM diagnosed 39 showing there is either an
under diagnosis or over diagnosis thus no criterion validity, symptom overlap with other
disorders – hard to distinguish with bipolar as both have avolition and delusions as
symptoms – could just be different variations of the same condition thus making diagnosis
flawed, co-morbidity – having 2 disorders at the same time so could just be one condition,
SZ and depression 50% and SZ and substance abuse 47%, gender bias as male to female
1.4:1 as some diagnostic criteria are biased towards pathologizing one gender – women
have more support so may deal with SZ better so could be underdiagnosed and not receive
the treatment that may benefit them, culture bias as minorities’ symptoms are
unrepresented, British Afro-Caribbeans 9 times more likely to be diagnosed than British
Whites, positive symptoms like hallucinations seen as appropriate in Haiti due to the belief
in communication with ancestors – this would be seen as irrational in Western culture.
Biological explanations of SZ (2017 specimen 1) Compare with family dysfunction
explanation for SZ (2020) (2018) (2023)
AO1: Genetic explanation – Gottesman stated that the closer a person is to someone with
SZ genetically the more likely to develop SZ (48% MZ 17% DZ). Neural correlates – best
known is dopamine, hyperdopaminergia = high levels of dopamine, hypodopaminergia =
low levels of dopamine. Dopamine hypothesis – high levels of dopamine in subcortical areas
of the brain e.g. excess dopamine receptors from subcortex pathways to Broca’s area
leading to speech poverty. Davis et al – updated dopamine hypothesis = low levels of
, dopamine in cortex linked to negative symptoms of SZ e.g. prefrontal cortex responsible for
thinking.
AO3: Heston’s adoption study – problem of genetic concordance studies is the shared enviro
people so to isolate enviro and genetic effects is to use adoption studies to study levels of SZ
and compare children to bio and adopted parents. Heston studied 47 children with SZ bio
mothers who had been adopted/fostered in the first month of their life and a control group
of 50 children who grew up in the same foster home. Found 0% SZ rates in control group
but 17% in those kids with SZ mothers = role for genetics. Ripke et al – meta-analysis of SZ
research and found many genetic variations meaning there is no one faulty gene
responsible for SZ = polygenetic, could be genes that code for NT like dopamine.
Weaknesses of genetic explanations – concordance rates not 100% so a role for something
other than genetics, genetics could just be a predisposition, biologically reductionist as
ignores factors like family dynamics. Strengths of dopamine hypothesis – implications for
treatments such as Clozapine which is more effective than typical
anti-psychotics/neuroleptics at relieving SZ behaviour. Suggests psychiatrists can see the
role of NT when treating SZ and improving their QOL. Weakness of dopamine hypothesis –
too simplistic as research shows that many NT linked to development of SZ, new drugs like
Clozapine more effective than traditional drugs as it effects dopamine but also other NT like
serotonin. Glutamate, a NT, is also implicated.
Biological treatments for SZ
AO1: Typical anti-psychotics used for drug therapy – chlorpromazine during 1950s,
dopamine antagonist which blocks dopamine receptors at the synapse and regulates
dopamine levels in other areas of the brain which reduces hallucinations – can also be used
as a sedative. Atypical anti-psychotics used for drug therapy – clozapine and risperidone
used when other SZ treatments do not work as it targets a range of NT like dopamine,
serotonin, glutamate. Clozapine used as it reduces levels of anxiety and depression and
usually when someone is suicidal. Risperidone is safer and can be used in lower dosages as
it binds strongly to dopamine receptors. Side effects of drug therapy – agitation, sleepiness,
itchy skin, weight gain. Dystonia – muscle spasms, Parkinsonism – rigidity. Long term effect
= tardive dyskinesia – irregular jerky movements of body due to dopamine supersensitivity
(15% of patients) and involuntary muscle movements. Worst case scenario is neuroleptic
malignant syndrome due to blocking of dopamine action in hypothalamus – high bp, high
temp, coma, fatal.
AO3: Davis et al – meta-analysis on studies using anti-psychotics and placebo drugs. Found
that about 70% of patients had their symptoms improved after 6 weeks of anti-psychotics
but less than 25% in the placebo group = clinically beneficial. Lieberman et al – studied
ability to withstand neg side effects of anti-psychotics. Found that 70% stopped treatment
after 18 months and this was the same with typical and atypical drugs. Should anti-
psychotics be prescribed? – they are useful in mental institutions as it can calm down
patients and make them more susceptible to other forms of treatment such as CBT and
talking to social workers to figure out accom as only 3% of SZ patients in UK permanently
reside in mental institutions for life. Weakness in understanding drug therapy – based on
the dopamine hypothesis which states there are high levels of dopamine in cortex, but
newer research has shown low levels of dopamine in SZ brains = not a complete
Diagnosis and classification of SZ
AO1: Background – 1% prevalence, more common in men/city-dwellers/those of low socio-
economic bg, late adolescence/early adulthood as cases before adolescence are rare, most
live with psychotic disorder for life as treatment only helps symptoms, only 1/5 fully recover.
Diagnosis – diagnostic system looking for cluster of symptoms, ICD used by WHO looks for 2
neg symptoms, DSM used by APA look for 1 positive symptom. Positive symptoms – atypical
symptoms in addition to normal experience e.g. delusions/paranoia, hallucinations,
disorganised speech. Negative symptoms – atypical symptoms representing loss of normal
experience e.g. speech poverty, avolition (poor hygiene, lack of persistence in work/school,
lack of energy)
AO3: Rosenhan’s study – pseudo patients faking SZ went to 12 diff hospitals (new, old,
private etc.) claiming to hear voices. Participants of study were doctors and patients of
psychiatric hospitals. Pseudo patients were all admitted and were asked to leave when their
symptoms disappeared. Reactions of doctors and patients were monitored. All but one
pseudo patient was diagnosed with SZ and were released from 7 to 52 days (avg = 19). DSM
2 was in use and patients were released based on their symptoms being in remission.
35/118 patients of psychiatric patients accused pseudo patients of faking SZ. Strengths of
diagnosis and classification – test re-test and reliability, Osorio et al – 180 SZ patients, pair
interviewed and found +.97 inter-rater reliability and +.92 test re-test reliability therefore
showing diagnosis consistency. Weaknesses – problem of validity as shown by Rosenhan’s
study, Chaniaux – 2 psychologists assessed 100 SZ patients using DSM and ICD, psychologist
using ICD diagnosed 68 and the one using DSM diagnosed 39 showing there is either an
under diagnosis or over diagnosis thus no criterion validity, symptom overlap with other
disorders – hard to distinguish with bipolar as both have avolition and delusions as
symptoms – could just be different variations of the same condition thus making diagnosis
flawed, co-morbidity – having 2 disorders at the same time so could just be one condition,
SZ and depression 50% and SZ and substance abuse 47%, gender bias as male to female
1.4:1 as some diagnostic criteria are biased towards pathologizing one gender – women
have more support so may deal with SZ better so could be underdiagnosed and not receive
the treatment that may benefit them, culture bias as minorities’ symptoms are
unrepresented, British Afro-Caribbeans 9 times more likely to be diagnosed than British
Whites, positive symptoms like hallucinations seen as appropriate in Haiti due to the belief
in communication with ancestors – this would be seen as irrational in Western culture.
Biological explanations of SZ (2017 specimen 1) Compare with family dysfunction
explanation for SZ (2020) (2018) (2023)
AO1: Genetic explanation – Gottesman stated that the closer a person is to someone with
SZ genetically the more likely to develop SZ (48% MZ 17% DZ). Neural correlates – best
known is dopamine, hyperdopaminergia = high levels of dopamine, hypodopaminergia =
low levels of dopamine. Dopamine hypothesis – high levels of dopamine in subcortical areas
of the brain e.g. excess dopamine receptors from subcortex pathways to Broca’s area
leading to speech poverty. Davis et al – updated dopamine hypothesis = low levels of
, dopamine in cortex linked to negative symptoms of SZ e.g. prefrontal cortex responsible for
thinking.
AO3: Heston’s adoption study – problem of genetic concordance studies is the shared enviro
people so to isolate enviro and genetic effects is to use adoption studies to study levels of SZ
and compare children to bio and adopted parents. Heston studied 47 children with SZ bio
mothers who had been adopted/fostered in the first month of their life and a control group
of 50 children who grew up in the same foster home. Found 0% SZ rates in control group
but 17% in those kids with SZ mothers = role for genetics. Ripke et al – meta-analysis of SZ
research and found many genetic variations meaning there is no one faulty gene
responsible for SZ = polygenetic, could be genes that code for NT like dopamine.
Weaknesses of genetic explanations – concordance rates not 100% so a role for something
other than genetics, genetics could just be a predisposition, biologically reductionist as
ignores factors like family dynamics. Strengths of dopamine hypothesis – implications for
treatments such as Clozapine which is more effective than typical
anti-psychotics/neuroleptics at relieving SZ behaviour. Suggests psychiatrists can see the
role of NT when treating SZ and improving their QOL. Weakness of dopamine hypothesis –
too simplistic as research shows that many NT linked to development of SZ, new drugs like
Clozapine more effective than traditional drugs as it effects dopamine but also other NT like
serotonin. Glutamate, a NT, is also implicated.
Biological treatments for SZ
AO1: Typical anti-psychotics used for drug therapy – chlorpromazine during 1950s,
dopamine antagonist which blocks dopamine receptors at the synapse and regulates
dopamine levels in other areas of the brain which reduces hallucinations – can also be used
as a sedative. Atypical anti-psychotics used for drug therapy – clozapine and risperidone
used when other SZ treatments do not work as it targets a range of NT like dopamine,
serotonin, glutamate. Clozapine used as it reduces levels of anxiety and depression and
usually when someone is suicidal. Risperidone is safer and can be used in lower dosages as
it binds strongly to dopamine receptors. Side effects of drug therapy – agitation, sleepiness,
itchy skin, weight gain. Dystonia – muscle spasms, Parkinsonism – rigidity. Long term effect
= tardive dyskinesia – irregular jerky movements of body due to dopamine supersensitivity
(15% of patients) and involuntary muscle movements. Worst case scenario is neuroleptic
malignant syndrome due to blocking of dopamine action in hypothalamus – high bp, high
temp, coma, fatal.
AO3: Davis et al – meta-analysis on studies using anti-psychotics and placebo drugs. Found
that about 70% of patients had their symptoms improved after 6 weeks of anti-psychotics
but less than 25% in the placebo group = clinically beneficial. Lieberman et al – studied
ability to withstand neg side effects of anti-psychotics. Found that 70% stopped treatment
after 18 months and this was the same with typical and atypical drugs. Should anti-
psychotics be prescribed? – they are useful in mental institutions as it can calm down
patients and make them more susceptible to other forms of treatment such as CBT and
talking to social workers to figure out accom as only 3% of SZ patients in UK permanently
reside in mental institutions for life. Weakness in understanding drug therapy – based on
the dopamine hypothesis which states there are high levels of dopamine in cortex, but
newer research has shown low levels of dopamine in SZ brains = not a complete
