Type I has positive symptoms and better prospects of recovery so type II has negative symptoms and
worse prospects of recovery. This is diagnosed using the two axes called ICD-10 and DSM-V.
Both of these describe positive symptoms (additional to reality) like auditory, olfactory, visual and
tactile hallucinations, delusions of grandeur/persecution , disorganised speech or made up words
(neologisms) and catatonic behaviour. Negative symptoms (reduction of reality) include speech
poverty and avolition which means having no motivation, and not being able to follow goals or make
choices.
However the ICD-10 emphasises cognitive functioning with a focus on thought insertion (someone
putting thoughts into your head), thought withdrawal (someone taking them away) and thought
broadcasting (believing everyone can hear them). The DSM–V focuses on social/occupational
functioning like whether they have a job, relationship or comorbidities.
Males normally get diagnosed in their late teens, females in their early twenties. 0.5-1% of people
have it nationally and symptoms must occur for a month in a period of six months.
Validity = accuracy of diagnosis
1) Symptoms overlap, eg delusions of grandeur in bipolar too, so which is it? Hewitt et al 14
autistic and 14 sz and 7 autistics had symptom overlap e.g. flat emotions.
2) Comorbidity, when you have two at once so which symptoms are sz?
3) Gender bias, loring and powell gave psychs patient descriptions and if they mentioned male
sz = 56% but female = 20%
reliability = consistency of diagnosis across psychologists
1) Cultural bias, copeland gave british/us psychs and 2% sz from brits but 69% sz from
americans so psychs need to understand their cultural background
Labelling = implications of invalid diagnosis
1) Rosenhan got 8 volunteers admitted to asylums by saying I heard voices and then acted
normally. It took 7-52 days to be released as they were interpreted as symptoms so labels
stick and effect on social life/work/ self esteem (historical bias 70s standards)
Schizophrenia is hereditary and polygenic (e.g. NRG3 or PCM1) as shown by Gottesman's study
which found that MZ twins have 48% concordance rate but DZ twins have 17%.
Excess dopamine in the subcortical areas of the brain cause positive symptoms (eg auditory
hallucinations from the broca's area) due to hyperdopaminergia and low levels within the cerebral
cortex causes negative symptoms (eg in the prefrontal cortex which makes decision causing avolition)
due to hypodopaminergia
Neural correlates are the enlarged ventricles causing negative symptoms (andreason compared sz
and normal and found sz had 20% bigger) lower levels of activity in the ventral striatum causing
avolition and lower levels of activity in the superior temporal gyrus (allen found patients with auditory
hallucinations have lower levels compared to a control) causing positive symptoms as its used for
processing sounds
- But MZ twins have a more similar environment and are raised/treated to be exactly the same
(assuming they are identical and all differences are DNA) so concordance rates could be
showing environmental differences that create two types of twins
- Noll, antipsychotics don't help hallucinations/delusions in ⅓ of patients and some people
experience these but have normal dopamine levels
- No causal relationship, does sz cause enlarged ventricles or the other way round so no
concrete conclusions reduces validity and usefulness
- Treatment implications as in the US they use neuroimaging to do treatment as prevention and
predict who will develop it, e.g. those with enlarged ventricles are at risk patients. This
benefits society, treating them before they become psychotic.
Chlorpromazine - typical (first generation) antipsychotic, developed in the 50’s. A dopamine
antagonist so it binds to D2 receptors to reduce the level that reaches the postsynaptic neurons and
prevent hyperdopaminergia so less positive symptoms
worse prospects of recovery. This is diagnosed using the two axes called ICD-10 and DSM-V.
Both of these describe positive symptoms (additional to reality) like auditory, olfactory, visual and
tactile hallucinations, delusions of grandeur/persecution , disorganised speech or made up words
(neologisms) and catatonic behaviour. Negative symptoms (reduction of reality) include speech
poverty and avolition which means having no motivation, and not being able to follow goals or make
choices.
However the ICD-10 emphasises cognitive functioning with a focus on thought insertion (someone
putting thoughts into your head), thought withdrawal (someone taking them away) and thought
broadcasting (believing everyone can hear them). The DSM–V focuses on social/occupational
functioning like whether they have a job, relationship or comorbidities.
Males normally get diagnosed in their late teens, females in their early twenties. 0.5-1% of people
have it nationally and symptoms must occur for a month in a period of six months.
Validity = accuracy of diagnosis
1) Symptoms overlap, eg delusions of grandeur in bipolar too, so which is it? Hewitt et al 14
autistic and 14 sz and 7 autistics had symptom overlap e.g. flat emotions.
2) Comorbidity, when you have two at once so which symptoms are sz?
3) Gender bias, loring and powell gave psychs patient descriptions and if they mentioned male
sz = 56% but female = 20%
reliability = consistency of diagnosis across psychologists
1) Cultural bias, copeland gave british/us psychs and 2% sz from brits but 69% sz from
americans so psychs need to understand their cultural background
Labelling = implications of invalid diagnosis
1) Rosenhan got 8 volunteers admitted to asylums by saying I heard voices and then acted
normally. It took 7-52 days to be released as they were interpreted as symptoms so labels
stick and effect on social life/work/ self esteem (historical bias 70s standards)
Schizophrenia is hereditary and polygenic (e.g. NRG3 or PCM1) as shown by Gottesman's study
which found that MZ twins have 48% concordance rate but DZ twins have 17%.
Excess dopamine in the subcortical areas of the brain cause positive symptoms (eg auditory
hallucinations from the broca's area) due to hyperdopaminergia and low levels within the cerebral
cortex causes negative symptoms (eg in the prefrontal cortex which makes decision causing avolition)
due to hypodopaminergia
Neural correlates are the enlarged ventricles causing negative symptoms (andreason compared sz
and normal and found sz had 20% bigger) lower levels of activity in the ventral striatum causing
avolition and lower levels of activity in the superior temporal gyrus (allen found patients with auditory
hallucinations have lower levels compared to a control) causing positive symptoms as its used for
processing sounds
- But MZ twins have a more similar environment and are raised/treated to be exactly the same
(assuming they are identical and all differences are DNA) so concordance rates could be
showing environmental differences that create two types of twins
- Noll, antipsychotics don't help hallucinations/delusions in ⅓ of patients and some people
experience these but have normal dopamine levels
- No causal relationship, does sz cause enlarged ventricles or the other way round so no
concrete conclusions reduces validity and usefulness
- Treatment implications as in the US they use neuroimaging to do treatment as prevention and
predict who will develop it, e.g. those with enlarged ventricles are at risk patients. This
benefits society, treating them before they become psychotic.
Chlorpromazine - typical (first generation) antipsychotic, developed in the 50’s. A dopamine
antagonist so it binds to D2 receptors to reduce the level that reaches the postsynaptic neurons and
prevent hyperdopaminergia so less positive symptoms
