In a nutshell: A subset of people with age-related eye diseases develop hallucinations because their brains overreact to images in their peripheral vision.

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Our brains can adapt in response to nerve damage, but sometimes those adaptations have unexpected effects. For example, changes in how the brain interprets nerve signals can lead to unpleasant sensations, such as tinnitus in the ears or pain in missing limbs.

Another example is found in people with non-inherited eye diseases – like age-related degeneration of the retina – who have lost their central vision but still have some peripheral vision.

About 40% of these people develop long-term hallucinations involving flashes of light, shapes, geometric patterns or more detailed visions. Rather than indicating brain disease or mental illness, these hallucinations seem to be a natural consequence of the brain adapting to changing sensory input.

Although this condition, known as Charles Bonnet syndrome (CBS), was discovered more than 250 years ago, researchers didn’t know what causes these hallucinations or why only some people suffer from them. One hypothesis is that when the retina is damaged, objects in our peripheral vision cause cells in the early visual cortex – where visual information is first processed in the brain – to become more active than normal. Under certain environmental conditions, which vary for each person with CBS, this hyperexcitability can cause the brain to create images that aren’t really there.

David Painter, a postdoctoral researcher working with Brain Function CoE chief investigator Jason Mattingley, wanted to test this hypothesis. He and his colleagues at the University of Queensland studied the brain activity of people with and without CBS.

The participants performed a task requiring their full visual attention, while coloured checkerboard patterns flickered on a computer screen in their peripheral vision. The researchers used electroencephalography (EEG) to record how brain cells in the participants’ visual cortex reacted to the checkerboard patterns, each of which flickered at a unique rate.

The researchers found that the brain cells in participants with CBS were much more active in response to certain images than the cells of people without any retinal damage or hallucinations. This hyperexcitability happened only when the participants’ peripheral visual field was stimulated, not during rest.

Their discovery directly supports the hypothesis that hyperexcitability in the early visual cortex is responsible for the hallucinations in CBS. By pinpointing how future treatments might alleviate these hallucinations – for example, by decreasing hyperexcitability in certain brain cells using methods such as transcranial magnetic stimulation – the researchers’ work also offers hope to the people with CBS who find their hallucinations distressing.

Next steps:
The researchers will use the same visual stimulation method to study how the brain processes information in people who have suffered a brain injury, such as a stroke. David Painter is also leading a project to extend these methods to create brain–computer interfaces that could help people to control their own brain activity.


Painter, D. R., Dwyer, M. F., Kamke, M. R., & Mattingley, J. B. (2018). Stimulus-driven cortical hyperexcitability in individuals with Charles Bonnet hallucinations. Current Biology, 28(21), 3475-3480.E3. doi: 10.1016/j.cub.2018.08.058

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Image by David Lloyd, University of Queensland