Clinical Psychology - Schizophrenia
Define SZ by Bleuler (1911)
Split of mind, in terms of splitting cognition from emotion
WHO (22) - Rate of number of SZ patients
24 million people have SZ or 1 in 300 worldwide
Rate of SZ diagnosis in mental hospitals
50% but only 31% receive specialist help
Rate of Pastor (2018)
Between 1990-2015, lifetime rate for SZ was 7.9 per 1000
Validity strength - rates of SZ
Shows precise number of patients treated so more valid and accurate representation of how many people suffer SZ in the real world
Validity weakness - rates of SZ
Subjective - records what is reported, many cases not reported, not true representation of disorders worldwide
Reliability strength - rates of SZ
Numbers of SZ patients in hospitals can be check in terms of admission rates so more reliable as able to see if data on SZ is consistent
Reliability weakness - rates of SZ
Not consistent diagnosis acorss cultures due to different manuals being used
Rena et al (2017) - Onset SZ for men
21-25 years old
Rena et al (2017) - Onset SZ for females
25-30 years old or after 45 years old
Sher (2019)- rate considering gender differences
Suicide rate 3.67 times higher in males compared to females
Rena (2017) - female symptoms
Late onset of SZ in females have less negative symptoms (so more positive symptoms) like hallucinations.
Validity strength - gender differences
Hospital admissions for SZ are objective numerical data, accurate record of who is being admitted
Validity weakness - gender differences
Diagnosis can be affected by gender bias as negative symptoms in women may be diagnosed as depression making gender rates less valid as not accurate
Reliability strength - gender differences
Hospital admissions used to check gender differences easier to replicate and look for consistency in data
Reliability weakness - gender differences
Gender rates for suicide due to SZ may not be consistent as suicide could be due to other factors such as loss of family so not consistent measure of impact of gender on disorder
Sher (2019) - life expectancy
Suicide rate in SZ is 10% and is the largest contributor to decreased life expectancy in SZ patients
Suicide rate comparison SZ patients and general population
20 times higher
WHO (20) - life expectancy comparison SZ and general population
SZ 2 to 3 times likely to die earlier
Validity strength - life expectancy
Use of death certificates is objective measure that can compare being SZ/not SZ to look at average life span/ accurate reflection of impact of disorder
Validity weakness - life expectancy
Death rates may be inaccurate as death of a patient may be put down to disorder but other factors such as drug overdose so making data less valid as not true representation of impact of SZ
Reliability strength - life expectancy
Death certificates are fixed document to check for patterns and trends consistent way to record impact of SZ on mortality rates.
Reliability weakness - life expectancy
Difficult to check consistency of death records linked to SZ due to symptoms not always being reported so not a consistent way to show how SZ affects mortality rates
positive symptom definition
unusual behaviours added to original behaviour
negative symptom definition
behaviours that go missing as the disorder develops
hallucinations
positive symptom, sensory experiences that seem real to patient but not to a neurotypical person like hearing voices
delusions
determined beliefs that a patient believes is true when it isn't. This includes paranoia and delusions of grandeur (feel like they are the most powerful)
disordered thinking
unable to organise incoming sensory information, easily distracted, poor working memory.
emotional disturbance
"blunting", turned off emotions
psychomotor disturbances
either mute and unmoving or wild and overexcited behaviours. may have an unusual posture they hold for hours like fetal position.
lack of volition
social withdrawal such as avoiding contact with family and friends becoming secluded and isolated. develops apathy as lack energy, loss of motivation or interest in daily activities, lack of pleasure in everyday events
Paranoid SZ
characterised by hallucinations, delusions of grandeur/ persecution
Disorganised SZ
innapropraitee emotonal responses to situation and disordered speech patterns, no hallucinations
Catatonic SZ
Little movement, unusual body positions, withdrawn from the world
Residual SZ
Low levels of positive symptoms, high levels of negative symptoms
Undifferentiated SZ
"Catch all" category, doesn't meet criteria for one of other types of SZ
Schizoaffective disorders
Episodes of SZ symptoms but prominent features of mood disorder not enough to classify as one disorder or the other
Neurotransmitter Theory - Mesolimbic pathway AO1
Reward pathway, excess dopamine transmission leads to positive SZ symptoms. Low glutamate levels, GABA receptors stops inhibiting dopamine activity, dopamine increase, thalamus stops filtering sensory information, sensory overload therefore hallucinations
Neurotransmitter Theory - Mesolimbic receptors AO1
- D2: greater density in patients. Hyperactivity causes patients to be more sensitive to dopamine (binds easily), transmission signal, positive symptoms.
- 5HT2: Increase activity as result of excess serotonin, reduce glutamate, increase dopamine, positive symptoms
Neurotransmitter Theory - Mesocortical pathway AO1
Little dopamine in pathway leads to negative symptoms, runs in cortex, motivation, emotion, high cognitive functioning. Low levels of glutamate acts as a brake, low dopamine.
Neurotransmitter Theory - Mesocortical receptors AO1
D2: blocks, lack of sensitivity to dopamine, emotional disturbances, heightened negative symptoms
Neurotransmitter Theory - S AO3
Seeman (1993): Density of receptors like D4 6 times greater in SZ than no SZ, increase sensitivity to neurotransmitter leads to psychotic symptoms more than excess of dopamine
Neurotransmitter Theory - C AO3
Depatie and Lal (2001): giving people drugs increasing productin of dopamine doesnt create SZ symptoms as would be expected if excess dopamine caused so limited explanation
Neurotransmitter Theory - O AO3
Non biological explains SZ is a reaction to social environment rather than excess dopamine as poor living conditions can create sensory overload causing hallucinations therefore not full explanation of cause of SZ
Neurotransmitter Theory - D AO3
Reductionist: Reduces down to the factor that excess dopamine in either mesocortical and mesolimbic pathways can cause positive and negative symptoms in SZ therefore can establish cause and effect of SZ
Neurotransmitter Theory - A AO3
Treatment programmes including medication to help reduce symptoms if good understanding of theory. Not one treatment programme will treat all symptoms as doesnt consider ID
Carlsson et al (99) - Research method AO1
Meta-analysis used on 33 alternative studies based on neurotransmitter involvement in SZ. Collected secondary data from PET scans from Carlsson (14) and animal research of rats and mice.
Carlsson et al (99) - Glutamate levels in pathways results AO1
- Mesolimbic: Glutamate low, GABA low, dopamine release not inhibited. If levels become too high, positive symptoms
- Mesocortical: Glutamate low, accelerator function of glutamate to increased dopamine doesnt work, dopamine drops, negative symptoms
Carlsson et al (99) - Another way glutamate involved in SZ AO1
Acts as accelerator and brake in different parts of the brain to cause positive and negative SZ symptoms
Carlsson et al (99) - Conclusion AO1
Glutamate deficiency may lead to more responses to dopamine (excess). Requires further study to help understand SZ. Needs to investigate serotonin being involved in SZ
Carlsson et al (99) - Secondary data AO3
Available to be replicated by other researchers to check for consistency therefore reliable
Carlsson et al (99) - Animal ethics AO3
Morally wrong to hold prejudices towards one species for another species benefit so humans shouldn't discriminate animals
Carlsson et al (99) - Reductionist AO3
Shows clear explanation of relationship between dopamine and SZ
Carlsson et al (99) - Scans AO3
Images taken from scans so subject to interpretation bias. Less accurate measure to find relationship between SZ and dopamine
Carlsson et al (99) - Conclusion AO3
If relationship between dopamine and SZ, treatment programmes can be developed however, labelling can occur if media backs up the criticism of SZ with scientific evidence
AO1: Case studies - Unique
Unique circumstance, unique unusual symptoms of mental health not observed before in patient.
AO1: Case studies - Methods
Variety of methods used to gather data about patients including interviews of thought processes and tasks to assess cognitive ability
AO1: Case studies - Data
Primary and Secondary used to compare information about patient throughout length of study
AO1: Case studies - Triangulation
Use triangulation to compare methods used for information aboout the patient
AO3: Case studies - Generalisability
Only uses one person or small group, low G
AO3: Case studies - Bias
Researcher bias as could develop relationship with patient, low V
AO3: Case studies - Population validity
Measure symptoms of real patients, accurate measure, high V
AO3: Case studies - Holism
methods can help investigate symptoms, comprehensive overview of possible causes
AO1: Bradshaw (1998) - Case study
Case study of long term SZ female patient to discover effectiveness of CBT
AO1: Bradshaw (1998) - Time assessed
Assessed periodically over 3 years and followed up one year later based on severity of symptoms and hospitalisations
AO1: Bradshaw (1998) - 4 phases
- Building rapport (bond)
- Understanding CBT and SZ
- Treatment
- Maintainence strategies for coping in the future
AO1: Bradshaw (1998) - Findings
Number of days in hospital reduced to 60 before CBT to 1 day a year after. Goals attained like taking on college course and volunteering.
AO3: Bradshaw (1998) - Generalisability
Case study only focuses on 1 individual, low G
AO3: Bradshaw (1998) - Validity
Researcher gains relationship with patient through building rapport phase therefore results of effectiveness of CBT will be biased, low V
AO3: Bradshaw (1998) - Ecological Validity
Real patient, real symptoms, patient treated by CBT therefore accurate, high EV
AO3: Bradshaw (1998) - Reliability
Follows the 4 phases, will produce results that can be checked for consistency
AO3: Bradshaw (1998) - Useful
Provides a full understanding of effectiveness of CBT that can be used for many patients worldwide.
AO3: Bradshaw (1998) - Not useful
Not all patients want to take part in the treatment therefore the CBT treatment is less effective
Genes explanation - Risk AO1
Can run in families in that having one parent with SZ has chance of inheriting 1 in 5 and both parents 1 in 3
Genes explanation - DRD2 AO1
Codes for D2 receptors, involved in reinforcement and reward system so links to SZ symptom development. D2 receptor activity affects cognitive dysfunction so oversensitivity to dopamine in synapse causes hallucinations
Genes explanation - COMT AO1
Provides instructions to make enzymes that are used to breakdown neurotransmitters like dopamine. MB-COMT enzyme work in prefrontal cortex, production problems can increase and decrease dopamine levels causing SZ. Located on chromosome 22 and defect in gene leads to 30 times more likely of SZ.