Scientific Background
Neurology, cognition, and genetics of aphantasia – the current state of research
Scientific research on aphantasia began only in 2015 with Adam Zeman's groundbreaking study. Since then, research has yielded important insights into neurological foundations, cognitive differences, and possible genetic factors.
Researchers describe mental imagery as 'Vision in Reverse' – the brain activates the visual cortex top-down instead of bottom-up like actual seeing. In aphantasia, this top-down signal chain appears to be interrupted.
- Reduced activity in primary visual cortex (V1) during imagery tasks
- Normal activity during actual seeing – the 'hardware' works
- Differences in connectivity between prefrontal cortex and visual system
People with aphantasia show characteristic cognitive profiles. Autobiographical memory is often less episodic-detailed, instead relying more on semantic (factual) knowledge. This is not a deficit – just a different strategy.
- Autobiographical memory: fewer sensory details, more facts
- Semantic memory (factual knowledge): fully intact
- Problem-solving: conceptual instead of visual – equally effective
Initial studies suggest a genetic component. Aphantasia runs in families – first-degree relatives of aphantasics have a 10-fold increased probability of having aphantasia themselves.
- Familial clustering observed in multiple studies
- ~10x increased risk in first-degree relatives
- Specific genes not yet identified
Three main methods are used to measure aphantasia: two subjective questionnaires and one objective test.
The gold standard since 1973. 16 questions about visual imagery vividness. Scores from 16 (aphantasia) to 80 (hyperphantasia).
Start testMeasures imagery across all 7 senses. Ideal for detecting multisensory aphantasia.
Start testThe only objective test. Uses the priming effect: Imagined images 'win' in rivalry. Aphantasics don't show this effect.
Start test