ArticleJournal of neurology2025
Visual cortical activity in Charles Bonnet syndrome: testing the deafferentation hypothesis.
Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- 'Everywhere I turn, I'm blocked': a qualitative exploration of experiences of Charles Bonnet syndrome and its impact on physical activity and falls.Age and ageing · 2026Article
- Beyond Charles Bonnet Syndrome: A Scoping Review of Psychotic Symptoms in Vision Loss.Alpha psychiatry · 2026Review
- Psychological Profile and Visual Function in Charles Bonnet Syndrome: A Preliminary Cross-Sectional Study.Healthcare (Basel, Switzerland) · 2026Article
- Review
- Charles Bonnet Syndrome: associations between psychosocial measures and visual hallucination characteristics in the visually impaired.BMJ open ophthalmology · 2026Article
- Management of Charles Bonnet syndrome in routine eye care services.Eye (London, England) · 2026Article
- Persistent auditory hallucinations despite hearing aid use in bilateral sensorineural hearing loss without evidence of psychosis.SAGE open medical case reports · 2026Article
- Conscious vision: investigating visual hallucination awareness in Lewy body disease.Brain communications · 2026Article
- Article
- Article
- EEG changes associated with hallucinations caused by Charles Bonnet Syndrome.Frontiers in neurology · 2025Article
- Filling in the Blind Spot: Integrating Charles Bonnet Syndrome Screening in Ophthalmology.Clinical ophthalmology (Auckland, N.Z.) · 2025Review
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Authors and funding
6 authors.
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Abstract
Visual hallucinations in individuals following sight loss (Charles Bonnet syndrome; CBS) have been posited to arise because of spontaneous, compensatory, neural activity in the visual cortex following sensory input loss from the eyes-known as deafferentation. However, neurophysiological investigations of CBS remain limited. We performed a multi-modal investigation comparing visual cortical activity in 19 people with eye disease who experience visual hallucinations (CBS) with 18 people with eye disease without hallucinations (ED-Controls; matched for age and visual acuity) utilising functional MRI, EEG, and transcranial magnetic stimulation (TMS). A pattern of altered visual cortical activity in people with CBS was noted across investigations. Reduced BOLD activation in ventral extrastriate and primary visual cortex, and reduced EEG alpha-reactivity in response to visual stimulation was observed in CBS compared to ED-Controls. The CBS group also demonstrated a shift towards lower frequency band oscillations in the EEG, indicative of cortical slowing, with significantly greater occipital theta power compared to ED-controls. Furthermore, a significant association between reduced activation in response to visual stimulation and increased excitability (in the form of reduced TMS phosphene thresholds) was observed in CBS, indicating persistent visual cortical activation consistent with hyperexcitability, which was found to be significantly associated with increased hallucination severity. These results provide converging lines of evidence to support the role of increased visual cortical excitability in the formation of visual hallucinations in some people following sight loss, consistent with the deafferentation hypothesis.
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