J Mov Disord.
2024 Jan;17(1):55-63. 10.14802/jmd.23102.
Retinal Thinning as a Marker of Disease Severity in Progressive Supranuclear Palsy
- Chen Y
1,2 - Wang H1
- Wang B1
- Li W3,4
- Ye P3,4
- Xu W3,4
- Liu P1,5
- Chen X1
- Cen Z1
- Ouyang Z1
- Wu S1
- Dou X5
- Liao Y6
- Zhang H6,7,8
- Tian M6,9
- Luo W1
- Affiliations
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- 1Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China
- 2Department of Ultrasound, Zhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, Zhejiang, China
- 3Department of Eye Center, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China
- 4Zhejiang Provincial Key Lab of Ophthalmology, Hangzhou, Zhejiang, China
- 5Department of Neurology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China
- 6Department of Nuclear Medicine and PET-CT Center, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China
- 7Key Laboratory for Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou, Zhejiang, China
- 8The College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, Zhejiang, China
- 9Huashan Hospital and Human Phenome Institute, Fudan University, Shanghai, China
- KMID: 2551211
- DOI: http://doi.org/10.14802/jmd.23102
Abstract
Objective
Progressive supranuclear palsy (PSP) involves a variety of visual symptoms that are thought to be partially caused by structural abnormalities of the retina. However, the relationship between retinal structural changes, disease severity, and intracranial alterations remains unknown. We investigated distinct retinal thinning patterns and their relationship with clinical severity and intracranial alterations in a PSP cohort.
Methods
We enrolled 19 patients with PSP (38 eyes) and 20 age-matched healthy controls (40 eyes). All of the participants underwent peripapillary and macular optical coherence tomography. Brain 11C-2β-carbomethoxy-3β-(4-fluorophenyl) tropane (11C-CFT) and 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography imaging were also performed in patients with PSP. We investigated the association between retinal thickness changes and clinical features, striatal dopamine transporter availability, and cerebral glucose metabolism.
Results
The peripapillary retinal nerve fiber layer (pRNFL) and macula were significantly thinner in patients with PSP than in controls. The thickness of the superior sector of the pRNFL demonstrated a significant negative relationship with the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale part III and Hoehn and Yahr staging scale scores. A significant negative correlation was found between outer inferior macular thickness and disease duration. Outer temporal macular thickness was positively correlated with Montreal Cognitive Assessment scores. In PSP, lower outer temporal macular thickness was also positively correlated with decreased dopamine transporter binding in the caudate.
Conclusion
The pRNFL and macular thinning may be candidate markers for monitoring disease severity. Additionally, macular thinning may be an in vivo indicator of nigrostriatal dopaminergic cell degeneration in PSP patients.
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