WJEC A2 Psychology PY4 - Aetiologies of Schizophrenia

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

(?) 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

• 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

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

(+) 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

(+) 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

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

• 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

(+) 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