Schizophrenia Biological explanations
- Created by: Jess Hoskin
- Created on: 31-03-15 08:34
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- Biological Explanations
- Dopamine Hypothesis
- Theory
- Excess dopamine activity at synaptic sites
- Due to high number of D2 receptors on receiving neurones
- More dopamine binding so more neurones firing.
- Due to high number of D2 receptors on receiving neurones
- Dopamine is a neurotransmitter
- controls: movement, social functioning, memory and cognition, mood
- Causes positive symptoms of schizophrenia
- Excess dopamine activity at synaptic sites
- Research
- Support
- Seeman
- Post Mortem - Densities of D2 receptors average 20pmol/g on schizophrenics, this is 50% more than controls.
- Cannot infer cause and effect
- Post Mortem - Densities of D2 receptors average 20pmol/g on schizophrenics, this is 50% more than controls.
- Grilly
- L-dopa (Parkinson's medicine) raises dopamine levels and causes schizophrenic symptoms
- Amphetamine
- Dopamine agonist - causes hallucinations and delusions
- Biological treatments
- Chlorpromazine blocks dopamine receptors and removes symptoms.
- Seeman
- Limitations
- Amphetamine
- only mimics positive symptoms, so only explains 1/2 schizophrenia
- Dopamine cannot be the only cause, possibly another neurotransmitter e.g. serotonin
- only mimics positive symptoms, so only explains 1/2 schizophrenia
- Atypical anti-psychotic drugs only cure positive symptoms
- Dopamine cannot be the only cause, possibly another neurotransmitter e.g. serotonin
- Amphetamine
- Support
- Theory
- Enlarged ventricles
- Theory
- Ventricles are naturally occurring spaces in the brain containing cerebral fluid
- Torrey
- Schizophrenics have 15% bigger ventricles
- Research
- Support
- Andreasen
- CT scans - significant enlargement in schizophrenics.
- Andreasen
- Limitations
- Coplov and Crook
- 90 CT scans, overlap between normal and schizophrenics.
- Cause or effect? Caused by medicine?
- Lyon
- Increased medication = increased ventricles
- Lyon
- Coplov and Crook
- Support
- Theory
- Genetics
- Theory
- Gene for SZ passed on in DNA from parent to child.
- If correct a pattern should be seen.
- Same genes = normally same environment
- If correct a pattern should be seen.
- Gene for SZ passed on in DNA from parent to child.
- Research
- Support
- Family Studies
- Moldin
- Reviewed twin studies between 1920-1987.
- MZ = 46%, even when reared apart. DZ = 14%
- Reviewed twin studies between 1920-1987.
- Gottesman
- 40 twin studies, MZ concordance = 48%, DZ = 14%
- All more than 1% of general population.
- MZ not 100%, must be another factor. Diathesis stress model?
- MZ treated more similarly
- DZ = 14%, siblings = 9%. Same genes shared. DZ treated more similarly than siblings.
- 40 twin studies, MZ concordance = 48%, DZ = 14%
- When diagnosing twins researchers may be bias if they know if they are MZ or DZ
- Moldin
- Adoption Studies
- Tienari
- 164 adopted children, SZ mothers. 8.1% children with SZ mothers got schizophrenia 2.3% controls.
- Genes only activated in poor communication families
- 164 adopted children, SZ mothers. 8.1% children with SZ mothers got schizophrenia 2.3% controls.
- Heston
- 47 children SZ mothers, adopted at 2 months
- 17% test group got SZ, 0% control
- May have had a traumatic experience before adoption
- 17% test group got SZ, 0% control
- 47 children SZ mothers, adopted at 2 months
- Adoptive parents informed on background. Who would adopt these children?
- Tienari
- Family Studies
- Limitation
- No specific gene found. 12 genes implicated.
- Support
- Theory
- Dopamine Hypothesis
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