Schizophrenia - Biological explanations & treatments Flashcards
genetics, family studies, twin studies, adoption studies, other studies, neural - dopamine, brain structures, typical & atypical antipsychotics, evaluations
Genetics
Genes passed on through family
Family studies
Compare concordance rates between different degree relatives -> higher concordance rates = genetic basis
Twin studies
Compare concordance rates of monozygotic and dizygotic twins to find similar correlations
Adoption studies
Is environment or genetics the cause -> compare adopted children to their biological & adoptive parents
Candidates genes
Particular genes focused on to study development of features
Polygenic
Multiple genes involved
Aetiologically heterogenous
Different combinations of factors/genes lead to disorder
Lifetime risk of schz
1%
Genetic study: Riley & Kendler
First degree relative w/disorder -> 10x greater risk
Genetic study: Gottesman (family study)
2% blood aunt, 9% sibling, 48% identical twin
Genetic study: Tienari et al (adoption study)
7.5% when biological parents have schz, even if they grow up in adoptive family
Genetic study: Hilker et al (twin study)
33% identical, 7% non-identical
Genetic study: Ripke et al (candidate genes)
108 separate genetic variations associated with risk
Genetic counselling
Discussions about physiological & mental health and how it will impact individual’s family/children, understand their own genetics & family’s genes/risks
Other factors: Di Forti et al
Increased risk associated with high level THC smoking in teenagers
Other factors: Morgan et al
Complication during birth increase the risk
Other factors: Mokved et al
67% of their participants had at least 1 childhood trauma (compared to 38% in control group)
Dopamine hypothesis (original)
Hyperdopaminergia on subcortical level (higher levels of dopamine) -> increased positive symptoms
Dopamine hypothesis (updated)
Hypodopaminergia on cortical level (lower levels of dopamine) -> increased negative symptoms (+increased stress in early experiences -> more sensitive)
Studies on dopamine: Falkai
Schizophrenic patients post-mortem -> increased dopamine in left amygdala
Studies on dopamine: Tenn et al
Amphetamines induced schizophrenic-like symptoms in rats and reduced with other drugs
Drug use & psychosis
Abuse of opioids
- experience psychotic-like symptoms (hallucinations)
- increases release of dopamine
- deficiency of endorphins increases dopamine release & result in psychosis (withdrawal)
Other: Garson
Refutes ideas of drug-related psychosis imitating schizophrenia
Other: McCutcheon et al
Glutamate (responsible for learning, attention & memory) differs for each schizophrenic patient (candidate genes impact)
Brain abnormalities
- Enlarged ventricles & reduced grey matter
- 2.6% smaller brains (Haijma et al)
- 6% lighter (Brown et al)
BA: Allen
Patients with auditory hallucinations -> lower activation levels in superior temporal gyrus & anterior cingulate gyrus
BA: Juckel et al
Negative correlation between avolition & activity in ventral striatum
Treatment: typical antipsychotics
Dopamine antagonists developed in 1950s -> block D2 receptors
Typical: Chlorpromazine
- 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
Treatment: Atypical antipsychotics
Dopamine antagonists & other neurotransmitters developed in 1970s to act on both symptoms
Atypical: Clozapine
- 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
Atypical: Risperidone
- Developed in 90s
- Stronger binding to dopamine & serotonin receptors
- Fewer side effects
Positive of biological treatments
+ 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)
Effectiveness of biological treatments (+)
+ 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)
Negatives of biological treatments
- 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)
Effectiveness of biological treatments (-)
- 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)
