Biological explanations; Dopamine hypothesis Flashcards
History; previous DH
- The DH was developed out of successful treatment for schizophrenia.
- Evidence is correlational; lacks causality
- Inconsistent findings; drug treatment does not help all patients
Studies identifying causality
Two lines of evidence suggest a genuine causal role for dopamine in schizophrenia:
- Experimental: L-dopa, a drug which increases dopamine levels, leads to schizophrenic like symptoms in previously unaffected (Parkinson’s) patients.
- Prospective: Recreational use of amphetamines, which also increase dopamine activity, also induce schizophrenic like symptoms.
Inconsistency of findings
DH does not apply to all people with schizophrenia
- Drug treatment doesn’t help everyone
- Not all uses of L-dope or amphetamines develop s. symptoms
- Dopamine is not involved in Type 2/ Negative symptoms of S.
Recent developments: New DH
- About 6,000 papers have been published since 1990 alone.
- Howes & Kapur claim that dopamine is the common mechanism that produces psychotic symptoms of S.
- All those with S who have psychotic symptoms have pre-synaptic dopamine dysfunction.
Initial causes
- Multiple factors both genetic and environmental result in dopamine dysregulation; genes, stressful life events, obstetric complications, family factors, drug use.
- This addresses the second problem of causality; dopamine dysfunction results from multiple factors.
- These can then combine to give unique symptoms which results in unique pathways from the initial cause to the presynaptic dopamine dysfunction.
Locus of dysfunction
- The locus of dopamine dysregulation is presynaptic, involving increased synthesis and tendency to release the transmitter
- So excess dopamine is produced and released, but the dysfunction is presynaptic rather than at the dopamine receptor.
- Current drugs act ‘downstream’ rather than ‘upstream’ so they are not treating the primary cause of abnormality.
Effect of psychotic symptoms
-Dopamine dysregulation is linked specifically to the dimensions of positive psychotic symptoms and ‘psychosis proneness’ regardless of diagnosis.
Psychological effects
- Dopamine dysregulation alters the appraisal of stimuli through the process of aberrant salience (mistaken relevance)
- People with schizophrenia have difficulty telling the difference between relevant and irrelevant info. They do not filter out the irrelevant info and become confused in their thoughts.
Nature-nuture
Howes & Kapur see dopamine dysregulation as the common mechanism in schizophrenia. The precise causes are a mix of genetic and environmental factors, including EE and stressful life events.
Howes & Kapur: Review of evidence - Initial causes
- Genes: The genes that raise most risk are those associated with the dopaminergic pathways
- Environment: Factors are associated with unemployment, lack of close friends and subordination (hierarchies) Animal studies have shown these factors lead to dopamine dysfunction.
- Interaction: these factors interact e.g. early experiences lead to extreme reactions later due to dopamine dysfunction.
Howes & Kapur: Review of evidence - Locus of dysfunction
-A meta-analysis of brain scanning studies by Howes et al. found that high rates of presynaptic dopaminergic function in s patients, while other dopamine dysfunction seems to be less pronounced.
Howes & Kapur: Review of evidence - Effect on psychotic symptoms
- Schizophrenic patients with psychotic symptoms display dopamine dysfunction, while those without do not.
- Non-schizophrenics who experience psychotic symptoms also have dopamine dysfunction
- Drugs that reduce positive symptoms all work on the dopamine system.
Howes & Kapur: Review of evidence - Psychological effects
-Some studies have linked dopamine systems to motivational salience
Key study: Howes et al. (2012)
Aim: Investigating the nature of dopaminergic dysfunction in schizophrenia using meta-analysis of in vivo studies.
Method: 44 studies, with 618 patients with sz, and 608 controls. They used a variety of scans, computed tomography and pet scans to measure dopamine function. Studies were grouped into those of presynaptic function and those of dopamine transporter and receptor availability.
Results: Showed significant elevation (d=0.79) of dopaminergic function in sz patients. And so the conclusion is that the largest dopaminergic abnormality in sz is presynaptic.