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  1. Amardeep Singh,
  2. Torben Lykke Sørensen
  1. Department of Ophthalmology, Copenhagen University Hospital, Roskilde, Denmark
  1. Correspondence to Dr Amardeep Singh, Department of Ophthalmology, Copenhagen University Hospital, Roskilde, Køgevej 7-13, DK-4000 Roskilde, Denmark; asingh{at}dadlnet.dk

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We thank Dr Meyer and colleagues for their valuable and relevant input on the incidence and regression of Charles Bonnet syndrome (CBS) in neovascular age-related macular degeneration (AMD).

We introduced intravitreal ranibizumab treatment for neovascular AMD in our clinic in 2007; our database for these patients therefore dates back to this year. Based on these data, the median duration of therapy in our CBS patients was 450 days (range 129–877). We do not have specific data regarding the presence of macular degeneration in these patients prior to therapy commencement and are therefore unable to provide a more precise duration.

We appreciate that CBS may occur in AMD of long duration, which is also suggested by our data on areas of geographic atrophy in patients with CBS.1 However, some reports have shown that brief visual deprivation in persons without ocular pathology has resulted in the development of visual hallucinations after a day.2 3 In our study, four out of five patients who reported an improvement in CBS following treatment had significantly impaired vision in the non-treated eye. Since only one of these patients reported symptoms of CBS prior to treatment, our data could indicate that when vision is acutely impaired in one eye, CBS may develop provided that vision in the other eye is also significantly impaired, and may also explain why treatment with ranibizumab may have an effect on CBS. This hypothesis is supported by the findings of Shiraishi and colleagues which suggest that CBS is more likely to be attributed to acute or dynamic vision deterioration than to low visual acuity per se.4 Meyer and colleagues linked the onset of structured visual hallucinations with intravitreal bevacizumab treatment in two subjects with vision impairment.5 They propose that reduced retinal oedema and realignment of the photoreceptors may promote the release phenomenon and trigger hallucinations, thereby supporting the hypothesis that dynamic and acute changes in visual acuity may contribute to the development of CBS.

The initial values for central retinal thickness as performed by spectral domain optical coherence tomography at the first consultation where therapy was commenced are in the range 200–550 μm (median 327 μm). In two eyes, the value for initial thickness was not available. The final central retinal thickness was found to be in the range 122–552 μm (median 264 μm). In one eye, the value for final thickness was not available.

We also find it important to highlight that reports on symptoms of CBS are highly subjective, and therefore we cannot be sure that all patients with CBS in our study did report the presence and characteristics of their symptoms. Hence, we feel caution should be exercised when drawing general conclusions on the subject.

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Footnotes

  • Competing interests None.

  • Provenance and peer review Commissioned; not externally peer reviewed.

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