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Inner retinal thickening affects microperimetry thresholds in the presence of photoreceptor thinning in patients with RPGR retinitis pigmentosa
  1. Jasleen Kaur Jolly1,2,3,
  2. Moreno Menghini1,3,
  3. Piers A Johal2,
  4. Thomas M W Buckley1,3,
  5. Holly Bridge2,
  6. Robert E Maclaren1,3
  1. 1 Nuffield Laboratory of Ophthalmology, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK
  2. 2 Oxford Centre for Functional MRI of the Brain (FMRIB), Wellcome Centre for Integrative Neuroimaging, University of Oxford, Oxford OX3 9DU, UK
  3. 3 Oxford Eye Hospital, Oxford University Hospitals NHS Foundation Trust, Oxford OX3 9DU, UK
  1. Correspondence to Jasleen Kaur Jolly, NDCN, Oxford University, Level 6 WW JR Hospital, Oxford OX3 9DU, UK; Jasleen.jolly{at}eye.ox.ac.uk

Abstract

Background Loss of photoreceptors cause degeneration in areas of the retina beyond the photoreceptors. The pattern of changes has implications for disease monitoring and measurement of functional changes. The aim of the study was to study the changes in inner retinal structure associated with photoreceptor disease, and the impact of these on microperimetry threshold.

Methods This retrospective cohort study was conducted on optical coherence tomography (OCT) images and microperimetry tests collected between 2013 and 2019. 22 eyes with RPGR retinitis pigmentosa completed both OCT imaging and microperimetry assessment. 18 control eyes underwent OCT imaging. Photoreceptor layer and inner retinal thickness calculated for different eccentric areas were obtained. The relationship between the photoreceptor layer and inner retinal thickness, and microperimetry threshold was explored.

Results Central 1° photoreceptor layer and inner retinal thickness were 96±34 and 139±75 μm in RPGR patients, and 139±15 and 62±14 μm in controls. Photoreceptor layer thickness differed between patient and control groups across increasing visual field areas (p<0.01, Kruskal-Wallis 1-way ANOVA), whereas the inner retinal thickness significantly differed between groups for the central 1° and 3° only. Microperimetry thresholds were explained by a combination of photoreceptor thickness (coefficient 0.15, 95% CI 0.13 to 0.18) and inner retinal thickness (coefficient 0.05, 95% CI 0.03 to 0.06).

Conclusion OCT shows evidence of remodelling in the inner retinal layers secondary to photoreceptor disease. This appears to have an impact on microperimetry threshold measurements.

  • Imaging
  • Dystrophy
  • Retina
  • Degeneration
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Footnotes

  • JJ and MM contributed equally

  • Twitter Jasleen Jolly @jkjolly4.

  • Contributors Conception: JKJ and MM. Data acquisition: MM, JKJ, TMWB and REM. Data analysis: JKJ, PAJ and MM. Code writing: JKJ. Interpretation: JKJ, MM, TMWB, HB and REM. Writing of first draft of manuscript: JKJ. Manuscript amendements: MM, PAJ, TMWB, HB and REM.

  • Funding This study is funded by the National Institute for Health Research (NIHR) [Clinical Doctoral Research Fellowship CA-CDRF-2016-02-002 for Jasleen K Jolly], and the NIHR Oxford Biomedical Research Centre (REM). Moreno Menghini received funds by Retina Suisse, OPOS foundation, Schweizerischer Fond zur Verhütung und Bekämpfung von Blindheit (no funder number). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care. The sponsor and funding organization had no role in the design or conduct of this research.

  • Competing interests REM receives grant funding from Biogen Therapeutics. REM is a consultant to Nightstar Therapeutics and Spark Therapeutics. These companies did not have any input into the work presented. No other authors have a conflict of interest.

  • Ethics approval Data used for this retrospective review were anonymised data acquired from screening visits between 2013 and 2019 for ongoing clinical trials at the Oxford Eye Hospital (NCT03116113). Healthy control data were obtained from volunteers acquired in 2017 and held on an in-house database as part of ongoing clinical research.

  • Provenance and peer review Not commissioned; externally peer-reviewed.

  • Data availability statement Data are available on request.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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