Schizophrenia - Biological explanations & treatments

Question 1

Genetics

Answer 1

Genes passed on through family

Question 2

Family studies

Answer 2

Compare concordance rates between different degree relatives -> higher concordance rates = genetic basis

Question 3

Twin studies

Answer 3

Compare concordance rates of monozygotic and dizygotic twins to find similar correlations

Question 4

Adoption studies

Answer 4

Is environment or genetics the cause -> compare adopted children to their biological & adoptive parents

Question 5

Candidates genes

Answer 5

Particular genes focused on to study development of features

Question 6

Polygenic

Answer 6

Multiple genes involved

Question 7

Aetiologically heterogenous

Answer 7

Different combinations of factors/genes lead to disorder

Question 8

Lifetime risk of schz

Answer 8

1%

Question 9

Genetic study: Riley & Kendler

Answer 9

First degree relative w/disorder -> 10x greater risk

Question 10

Genetic study: Gottesman (family study)

Answer 10

2% blood aunt, 9% sibling, 48% identical twin

Question 11

Genetic study: Tienari et al (adoption study)

Answer 11

7.5% when biological parents have schz, even if they grow up in adoptive family

Question 12

Genetic study: Hilker et al (twin study)

Answer 12

33% identical, 7% non-identical

Question 13

Genetic study: Ripke et al (candidate genes)

Answer 13

108 separate genetic variations associated with risk

Question 14

Genetic counselling

Answer 14

Discussions about physiological & mental health and how it will impact individual’s family/children, understand their own genetics & family’s genes/risks

Question 15

Other factors: Di Forti et al

Answer 15

Increased risk associated with high level THC smoking in teenagers

Question 16

Other factors: Morgan et al

Answer 16

Complication during birth increase the risk

Question 17

Other factors: Mokved et al

Answer 17

67% of their participants had at least 1 childhood trauma (compared to 38% in control group)

Question 18

Dopamine hypothesis (original)

Answer 18

Hyperdopaminergia on subcortical level (higher levels of dopamine) -> increased positive symptoms

Question 19

Dopamine hypothesis (updated)

Answer 19

Hypodopaminergia on cortical level (lower levels of dopamine) -> increased negative symptoms (+increased stress in early experiences -> more sensitive)

Question 20

Studies on dopamine: Falkai

Answer 20

Schizophrenic patients post-mortem -> increased dopamine in left amygdala

Question 21

Studies on dopamine: Tenn et al

Answer 21

Amphetamines induced schizophrenic-like symptoms in rats and reduced with other drugs

Question 22

Drug use & psychosis

Answer 22

Abuse of opioids
- experience psychotic-like symptoms (hallucinations)
- increases release of dopamine
- deficiency of endorphins increases dopamine release & result in psychosis (withdrawal)

Question 23

Other: Garson

Answer 23

Refutes ideas of drug-related psychosis imitating schizophrenia

Question 24

Other: McCutcheon et al

Answer 24

Glutamate (responsible for learning, attention & memory) differs for each schizophrenic patient (candidate genes impact)

Question 25

Brain abnormalities

Answer 25

• Enlarged ventricles & reduced grey matter
• 2.6% smaller brains (Haijma et al)
• 6% lighter (Brown et al)

Question 26

BA: Allen

Answer 26

Patients with auditory hallucinations -> lower activation levels in superior temporal gyrus & anterior cingulate gyrus

Question 27

BA: Juckel et al

Answer 27

Negative correlation between avolition & activity in ventral striatum

Question 28

Treatment: typical antipsychotics

Answer 28

Dopamine antagonists developed in 1950s -> block D2 receptors

Question 29

Typical: Chlorpromazine

Answer 29

• Reduce action of dopamine
• Makes dopamine build up initially
• Production then decreases
• Decreases positive symptoms
• Indiscriminately blocks all dopamine activity
• Side effects: tardive dyskinesia, sedative effect (histamine receptor impacted), agitation

Question 30

Treatment: Atypical antipsychotics

Answer 30

Dopamine antagonists & other neurotransmitters developed in 1970s to act on both symptoms

Question 31

Atypical: Clozapine

Answer 31

• Weak binding to inhibit D2 & D5 receptors
• Inhibits S2, norepinephrine and histamine receptors
• Mood-enhancing effects
• Initially led to agranulocytosis (deaths)
• Only given when others fail
• Must have regular blood tests

Question 32

Atypical: Risperidone

Answer 32

• Developed in 90s
• Stronger binding to dopamine & serotonin receptors
• Fewer side effects

Question 33

Positive of biological treatments

Answer 33

+ Cost-effective (only £15 for 28 x 10mg chlorpromazine compared to £60 therapy)
+ Economic impact (fewer hospitalisations & people able to function/work)
+ Ethical (independent living without need for institutionalisation and sedatives mean they are calm enough to engage in additional treatments)

Question 34

Effectiveness of biological treatments (+)

Answer 34

+ Bagnall & atypicals (more effective - fewer movement disorders, fewer leave treatment early, Clozapine effective in 30-50% resistant cases [Meltzer])
+ Leucht et al (more effective than placebos)
+ Thornly et al (chlorpromazine reduced severity of symptoms & improved functioning)

Question 35

Negatives of biological treatments

Answer 35

• Ethics (severe side effects cause harm, reduce adherence)
• Outdated research i.e. dopamine hypothesis (drug treatments may not be appropriate, typical only help pos. symptoms, treatment fallacy)

Question 36

Effectiveness of biological treatments (-)

Answer 36

• Tarrier et al (improved severity of symptoms better paired with CBT than alone)
• Healy (only focus on short-term effects rather than long-term and could just be because of the powerful calming effect)
• Moncrieff (easier for staff to manage than help patient [chemical cosh] which misleads patients)