Biological: Neural Correlates (AQA A-Level Psychology): Revision Notes
Biological: Neural Correlates
What are neural correlates?
Neural correlates refer to the idea that schizophrenia development is linked to structural and functional brain abnormalities, including biochemical changes. Originally, research was limited to post-mortem examinations of deceased patients' brains. However, modern non-invasive scanning techniques like functional magnetic resonance imaging (fMRI) now allow researchers to observe brain activity in living patients through magnetic fields and radio waves.
These techniques enable scientists to compare brain functioning between people with and without schizophrenia by giving participants tasks associated with abnormal functioning in schizophrenia, such as social cognition, thought processing, and working memory tasks.
A key question in this research is whether brain abnormalities in schizophrenia patients are caused by genetic factors or result from the disorder itself. This can be investigated by comparing patients' brains with non-schizophrenic family members - if similar abnormalities appear in both groups, this suggests a genetic link.
Structural brain differences
Research has consistently identified enlarged ventricles (fluid-filled gaps between brain areas) in people with schizophrenia. These enlarged ventricles are particularly associated with damage to central brain areas and the prefrontal cortex. More recent scanning studies have also linked this damage to negative symptoms of schizophrenia.
The consistent finding of enlarged ventricles across multiple studies provides strong evidence for structural brain differences in schizophrenia, though the relationship between these changes and symptom development remains complex.
Key research studies
Johnstone et al. (1976)
- Participants: People with schizophrenia compared to controls
- Findings: Patients showed enlarged ventricles while controls did not
- Conclusion: Suggests schizophrenia relates to loss of brain tissue
Weyandt (2006)
- Findings: Enlarged ventricles were associated only with negative symptoms
- Implication: This means enlarged ventricles cannot explain all symptoms and aspects of schizophrenia
Research Example: Brain Activity and Thought Disorder
Study: Tilo et al. (2001)
- Participants: Six patients with schizophrenia and six controls
- Procedure: fMRI scans while participants looked at and discussed Rorschach ink-blots
- Findings: In schizophrenic patients, severity of thought disorder was negatively correlated with activity levels in the Wernicke brain area (associated with coherent speech production)
- Conclusion: Supports the idea that abnormal functioning in specific brain areas relates to schizophrenia
Li et al. (2010)
- Procedure: Meta-analysis of fMRI studies investigating facial emotion processing difficulties in schizophrenia patients
- Findings: Both groups activated bilateral amygdala and right fusiform gyri when processing facial emotions, but activation was severely limited in schizophrenia patients
- Conclusion: Abnormal brain functioning may explain difficulties processing facial emotions in schizophrenia
Boos et al. (2012)
- Participants: 155 schizophrenia patients, 186 non-schizophrenic siblings, and 122 unrelated controls
- Findings: Schizophrenic participants showed decreased grey matter density and cortical thinning compared to other participants
- Conclusion: Brain tissue differences in schizophrenia patients are an effect of having the disorder rather than genetic factors
Research Example: Brain Circuit Dysfunction
Study: Yoon et al. (2013)
- Participants: 18 schizophrenia patients and 19 controls performing memory tasks
- Findings: Patients showed heightened activity in substantia nigra, decreased activity in prefrontal cortex, and diminished connectivity between brain regions. Higher connectivity between substantia nigra and striatum correlated with stronger symptoms
- Conclusion: Abnormal functioning of the prefrontal cortex-basal ganglia brain circuit may relate to cognitive deficits in schizophrenia
The dopamine hypothesis
The dopamine hypothesis proposes that schizophrenia development relates to abnormal levels of the neurotransmitter dopamine. Dopamine increases neuron firing rates during synapses, enhancing communication between neurons. Snyder (1976) argued that excessive dopamine release during synapses can lead to schizophrenia onset.
This theory developed after discovering that phenothiazine antipsychotic drugs lessen schizophrenia symptoms by decreasing dopamine activity. Additionally, the dopamine-releasing drug L-dopa creates schizophrenic symptoms in people without the condition. Other drugs affecting the dopaminergic system, such as LSD and hallucinogens, also create schizophrenic-like behaviour in healthy individuals and heighten symptoms in those with schizophrenia.
Updated dopamine theory
Davis et al. (1991) refined the theory after discovering that not all schizophrenia patients have high dopamine levels, and that the modern antipsychotic drug clozapine works effectively despite having little dopamine-blocking activity. They suggested that:
Updated Dopamine Theory Key Points:
- High dopamine levels in the mesolimbic dopamine system are associated with positive symptoms
- High dopamine levels in the mesocortical dopamine system are associated with negative symptoms
The neurotransmitter glutamate may also be involved, as there is reduced function of NMDA glutamate receptors in people with schizophrenia, with dopamine involved in restricting glutamate release.
Research supporting the dopamine hypothesis
Randrup & Munkvad (1966)
- Procedure: Created schizophrenic-like behaviour in rats using amphetamines (which activate dopamine production), then reversed effects using neuroleptic drugs (which inhibit dopamine release)
- Conclusion: Supports the dopamine hypothesis
Iversen (1979)
- Procedure: Post-mortem examinations of people who had schizophrenia
- Findings: Found excess dopamine in the limbic system
- Conclusion: Suggests neurotransmitter involvement in the disorder
Research Example: Brain Imaging Evidence
Study: Kessler et al. (2003)
- Procedure: Used PET and MRI scans to compare people with and without schizophrenia
- Findings: People with schizophrenia had elevated dopamine receptor levels in basal forebrain and substantia nigra/ventral tegmental brain areas. Cortical dopamine level differences were also found
- Conclusion: Suggests dopamine importance in schizophrenia onset
Javitt et al. (2000)
- Findings: Glycine (a glutamate receptor agonist) reversed phencyclidine hydrochloride-induced psychosis in rats and improved symptoms in people with schizophrenia
- Conclusion: Supports the glutamate theory
Javitt (2007)
- Findings: Phencyclidine and ketamine induce schizophrenic symptoms in people without the condition by blocking neurotransmission at NMDA-type glutamate receptors, leading to abnormal dopamine system functioning in striatal and prefrontal brain areas
- Conclusion: Supports the connection between dopamine and glutamate in schizophrenia onset
Evaluation of neural correlates
Strengths:
- Modern brain scanning technology provides objective, scientific evidence of brain differences in schizophrenia patients
- Research consistently shows structural abnormalities like enlarged ventricles across multiple studies
- Can help distinguish between genetic factors and disorder effects by comparing patients with family members
Weaknesses:
- Some people without schizophrenia have enlarged ventricles, while not all patients with schizophrenia do, challenging the idea that brain abnormalities directly cause the condition
- Patients who don't respond to medication mainly show enlarged ventricles, possibly indicating that suffering from schizophrenia over time leads to physical brain damage rather than brain damage causing schizophrenia
- Brain abnormalities may result from environmental factors like substance abuse and stress, which also damage brain tissue
- Medication non-response might occur because structural brain damage prevents antipsychotic medications from effectively reducing symptoms
- Longitudinal studies show brain damage is evident at first onset but worsens over time, even with medication, suggesting progressive deterioration
- Only certain brain scanning methods can assess whether damage worsens as the disorder continues
Evaluation of dopamine hypothesis
Strengths:
- Supported by drug evidence - antipsychotic drugs that reduce dopamine also reduce symptoms
- Animal studies provide controlled evidence for dopamine's role
- Modern brain scanning shows differences in dopamine receptor levels between patients and controls
Weaknesses:
- Evidence is inconclusive, as there's no consistent difference in dopamine levels between drug-free schizophrenic patients and people without schizophrenia
- The theory may be over-simplistic, as many other neurotransmitters (serotonin, glutamate) may also be involved in schizophrenia development
- Healy (2000) suggests pharmaceutical companies promoted the dopamine theory because they could profit from manufacturing dopamine-inhibiting antipsychotic drugs
- Cannot explain why patients only recover slowly when given neuroleptic drugs, despite medication having immediate effects on dopamine levels
- Lloyd et al. (1984) argue that even if dopamine is a causative factor, it may work indirectly through environmental factors, as abnormal family circumstances can lead to high dopamine levels which trigger symptoms
- Biochemical differences could just as easily be an effect rather than a cause of the disorder
- Dopamine appears more associated with positive symptoms, so may only contribute to certain aspects of schizophrenia, suggesting multiple types exist with dopamine linked to specific types only
Key Points to Remember:
- Neural correlates focus on brain structure and function differences in people with schizophrenia, identified through modern scanning techniques like fMRI
- Key findings include enlarged ventricles and prefrontal cortex abnormalities, though these don't appear in all patients
- The dopamine hypothesis suggests excessive dopamine in mesolimbic systems causes positive symptoms, while issues in mesocortical systems cause negative symptoms
- Research evidence supports both approaches but also reveals limitations - not all patients show expected brain changes or dopamine differences
- Both explanations may be over-simplified, as schizophrenia likely involves multiple neurotransmitters and brain systems working together