Revised hypothesis: Excess dopamine in subcortical areas (mesolimbic pathway) causes positive symptoms. Deficit of dopamine in prefrontal cortex (mesocortical pathway) causes negative symptoms. Patel et al (2010) found lower levels of dopamine in dorsolateral prefrontal cortex of schizophrenic patients.
Genetic factors: Adoption studies
Tienari et al. (2000) in Finland: Adoptees with schizophrenic biological mothers: 6.7% developed schizophrenia. Adoptees with non-schizophrenic biological mothers: 2% developed schizophrenia. Concluded that genetics decisively confirms liability to schizophrenia.
Genetic factors: Family studies
Schizophrenia is more common among biological relatives. The closer the genetic relationship, the higher the risk. Gottesman's study: Children with 2 schizophrenic parents: 46% concordance. Children with 1 schizophrenic parent: 13% concordance. Siblings: 9% concordance.
Neural correlates: Evaluation 1
Evidence from Drug Treatment
* Back:
* Leucht et al. (2013) found antipsychotics more effective than placebos, supporting the dopamine hypothesis.
* Challenges typical/atypical antipsychotic classification, as effectiveness differences were small.
* This suggests dopamine plays a key role in schizophrenia.
Neural correlates: evaluation 2
Challenges to the Dopamine Hypothesis
* Back:
* Noll (2009) argues antipsychotics don't alleviate symptoms in 1/3 of people.
* Some have symptoms despite normal dopamine levels.
* This suggests other neurotransmitters may be involved in positive symptoms.
Neural correlates: Evaluation 3
Challenges to the Dopamine Hypothesis
* Back:
* Noll (2009) argues antipsychotics don't alleviate symptoms in 1/3 of people.
* Some have symptoms despite normal dopamine levels.
* This suggests other neurotransmitters may be involved in positive symptoms.