Biological explanations; Dopamine hypothesis Flashcards

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1
Q

History; previous DH

A
  • The DH was developed out of successful treatment for schizophrenia.
  • Evidence is correlational; lacks causality
  • Inconsistent findings; drug treatment does not help all patients
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2
Q

Studies identifying causality

A

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.
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3
Q

Inconsistency of findings

A

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.
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4
Q

Recent developments: New DH

A
  • 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.
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5
Q

Initial causes

A
  • 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.
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6
Q

Locus of dysfunction

A
  • 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.
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7
Q

Effect of psychotic symptoms

A

-Dopamine dysregulation is linked specifically to the dimensions of positive psychotic symptoms and ‘psychosis proneness’ regardless of diagnosis.

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8
Q

Psychological effects

A
  • 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.
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9
Q

Nature-nuture

A

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.

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10
Q

Howes & Kapur: Review of evidence - Initial causes

A
  • 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.
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11
Q

Howes & Kapur: Review of evidence - Locus of dysfunction

A

-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.

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12
Q

Howes & Kapur: Review of evidence - Effect on psychotic symptoms

A
  • 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.
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13
Q

Howes & Kapur: Review of evidence - Psychological effects

A

-Some studies have linked dopamine systems to motivational salience

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14
Q

Key study: Howes et al. (2012)

A

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.

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