WJEC A2 Psychology PY4 - Aetiologies of Schizophrenia
3 Aetiologies of Schizophrenia
4.5 / 5 based on 7 ratings
- Created by: Zoey Jowett
- Created on: 19-10-12 21:34
Dopamine Hypothesis
1. Dopamine Hypothesis
- positive symptoms of Sz caused by excess amounts or increased sensitivity to the neurotransmitter dopamine; dopamine is substance that is known to be active in the limbic system, area of the brain responsible for governing emotion
- dopamine could be responsible for causing symptoms of Sz, could be due to excess amounts or sensitivities of the neurotransmitter that are genetically determined
EVALUATION
(+) Paul Charpentier (1940s)
- found that by giving his presurgical patients a new compound called chlorpromazine he could reduce their anxiety w/o causing mental confusion
- suggests that dopamine hypothesis may be correct; other drug companies investigated this effect and found drug had profound calming effects particularly in Sz patients, blocked dopamine receptor sites - possible link between dopamine and Sz
1 of 9
Dopamine Hypothesis
(?) Iversen (1979)
- post mortem study found more dopamine and dopamine receptor sites in the brains of dead Sz than dead non Sz, consistent with hypothesis
- however is a natural experiment = no direct manipulation of IV so the cause-effect relationship is more difficult to link
- also, even if there was higher levels of dopamine in the dead Sz, could be due to other environmental triggers
(+) Anti psychotic drugs
- block dopamine and reduce symptoms of Sz in many people; suggests dopamine does play a role in development of psychotic symptoms
(-) Lag Time Effects and Treatment Aetiology Fallacy
- lag time of several weeks before psychotic symptoms reduce even if neurotransmitter change is immediate, challenges aetiology as shows may not be a direct link between symptoms and dopamine
2 of 9
Dopamine Hypothesis
- MacLeod (1998) mistaken idea that the success of a treatment reveals cause of the disorder; dopamine blocking drugs may reduce psychotic symptoms but doesn't necessarily mean psychosis caused by dopamine
(+) Parkinson's Patients
- Parkinson's patients who have low dopamine levels, when given a drug that mimics dopamine (L-Dopa) patients can show Sz symptoms; supports dopamine theory; psychotic symptoms can be induced by increasing dopamine levels
(+) Davis (1974)
- found that amphetamines and cocaine drugs that increase dopamine levels can cause people to experience Sz symptoms
- consistent with hypothesis because Stevens (1982) stated rather than high levels of dopamine being the issue, sensitivity to dopamine may actually be the cause of Sz symptoms
- could be structural abnormalities in brain, maybe more receptor sites than usual for dopamine or normal amount of receptors but more sensitive in Sz patient
3 of 9
Genetic Theory
2. Genetic Theory
- suggests link between genetic makeup and Sz; possibility of the presence of genetic vulnerability to Sz could result in changes to dopamine levels, causing Sz symptoms
- more closely related you are to someone with Sz, more likely to develop it
EVALUATION
(+) Varma (1997)
- looked at first degree relatives (FDR) of about 1000 Sz and 1000 controls
- Sz/psychotic symptoms found in 16% of FDRs of Sz compared with 7% of controls
- supports assumption closer relatedyou are to a Sz family member, more likely to develop a psychiatric illnesslike Sz
(-) HOWEVER...
- only 160 out of 1000 Sz, small %, doesn't account for 84% which contradicts
4 of 9
Genetic Theory
(+) Joseph (2004)
- calculated pooled data for all Sz twin studies (if one twin had Sz) carried out prior to 2001; concordance rate for MZ twins was 40.4% and 7.4% for DZ twins
- supports the theory as it shows more closely related family members, like twins, are more likely to have Sz and therefore genetic factors must play a role
(-) HOWEVER...
- wasn't 100% concordance rate in MZ group, casts doubt on Sz being solely caused by genetics; MZ twins = 100% genesso if one has Sz, based on genetic theory, other twin should to, only 40.4%, must be other factors (environmental?)
- MZ twins more likely to have shared family environment (SRE) as 100% identical which could explain 40.4% as behaviours similar = weakens theory as makes CR less valid to support the genetic theory
5 of 9
Genetic Theory
(+) Heston (1966)
- adoption study 2 groups: group 1 = 47 adopted children with Sz bio mother
- group 2 which had 47 adopted children but bio mother didn't have Sz
- 16% of group 1 developed Sz however 0% of group 2 developed illness
- higher incidence in Sz bio relatives reared apart suggests genetics have level of significance in causing Sz, no affecting environmental factors or SRE
(-) Deterministic and emphasises role of nature
- deterministic = Sz inevitable if you have relative who suffers from Sz
- focuses solely on genetics, ignores the influence of environment and nurture
(?) Diathesis stress model
- realistic explanation of previous studies on impact of genes: suggests we must consider genes and environment collectively causing Sz
- even if we have genetic v such as FDR, may not be triggered unless certain environmental stressors present
6 of 9
Expressed Emotion Theory
3. Expressed Emotion Theory
- Brown's EE Theory (1966) suggests EE is a realistic maintenance/relapse factor in Sz
- EE = high levels of open criticism, hostility, emotional over involvement/over engagement and suffocating concern, normally by a family member
EVALUATION
(+) Brown (1966)
- found that 58% of Sz with high EE families relapsed whereas low EE families caused 10% relapse of Sz studied
- if Sz has a family with high levels of EE, increases chance of relapse, supporting Brown's theory that EE can be significant factor in maintaining control of Sz
(-) HOWEVER...
- highly natural experiment, variables weren't controlled and IV wasn't manipulated directly so cause-effect relationship difficult to establish
7 of 9
Expressed Emotion Theory
- could be that those with more serious psychotic symptoms, who are more likely to relapse, cause those around them to have higher EE
(+) Vaughn and Leff (1976)
- followed up 128 patients who had been hospitalised for Sz episodes, subsequently discharged and returned to families
- communication patterns between family members rated for EE
- found that patients with high EE families were more likely to relapse and be hospitalised (50%) than patients with low EE families (12%)
- prospective study, supports EE theory but also Brown theory as similar findings
(-) Liem (1974)
- failed to find a difference in patterns of communication in a prospective study
- he also suggests that classifying high EE and low EE is too subjective which weakens the validity
8 of 9
Expressed Emotion Theory
(+) Family Theory of Schizophrenia
- EE theory is one of the only family theories of Sz which is now taken into consideration by community mental health teams, responsible for re-settling patients into homes after being discharged from psychiatric wards
(+) Maintenance Theory
- EE may not explain cause of Sz but may help to explain some environmental triggers which can lead to relapse, or trigger symptoms of someone who is already vulnerable (possibly genetically?)
- EE theory useful as 'maintenance theory' of Sz, complementary to the diathesis stress (genetic) theory = how Sz can leave a genetic vulnerability if other relatives have it which can be triggered by specific environmental factors, such as EE
9 of 9
Similar Psychology resources:
0.0 / 5
5.0 / 5 based on 1 rating
0.0 / 5
5.0 / 5 based on 4 ratings
0.0 / 5
0.0 / 5
3.0 / 5 based on 2 ratings
0.0 / 5
Comments
Report
Report
Report
Report
Report
Report
Report
Report
Report
Report
Report