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Spontaneous spatial navigation circuitry in schizophrenia spectrum disorders.
Leanne K Wilkins1, Todd A Girard1, Bruce K Christensen2
1Department of Psychology, Ryerson University, 350 Victoria St, Toronto, ON M5B 2K3, Canada.
Psychiatry Research
|June 8, 2019
Summary
Individuals with schizophrenia show impaired spatial navigation and memory when using cognitive mapping strategies. However, response-based strategies reveal intact memory, suggesting strategy use is key to understanding navigation in schizophrenia.
Area of Science:
- Neuroscience
- Cognitive Psychology
- Psychiatry
Background:
- Spatial memory is crucial for navigation and daily life.
- Schizophrenia patients exhibit deficits in spatial navigation, particularly when employing cognitive mapping strategies.
- Response-based navigation strategies appear less affected in schizophrenia.
Purpose of the Study:
- To investigate brain communication patterns during spatial navigation in schizophrenia.
- To compare neural activity between individuals with schizophrenia using different navigation strategies.
- To understand the role of strategy selection in memory performance in schizophrenia.
Main Methods:
- A virtual-reality navigation task was employed.
- Functional brain imaging was used to observe brain communication.
- Participants with schizophrenia were categorized based on their navigation strategy (spatial vs. response-based).
Main Results:
- Schizophrenia participants using spatial strategies showed abnormal communication between temporal and frontal brain regions.
- Schizophrenia participants using response strategies recruited similar brain systems to healthy controls, but with increased activation.
- Strategy use significantly impacts observed memory performance and neural recruitment in schizophrenia.
Conclusions:
- Navigation strategy is a critical factor in understanding memory and brain function in schizophrenia.
- Abnormal brain connectivity is associated with impaired spatial navigation in schizophrenia.
- Response-based strategies may offer a compensatory mechanism for memory deficits in schizophrenia.
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