Retinal nerve fiber layer in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

Wong, Bryan M.; Hudson, Christopher; Snook, Emily; Tayyari, Faryan; Jung, Hyejung; Binns, Malcolm A.; Samet, Saba; Cheng, Regina; Balian, Carmen; Mandelcorn, Efrem D.; Margolin, Edward; Finger, Elizabeth; Black, Sandra E.; Tang‐Wai, David F.; Zinman, Lorne; Tan, Brian; Lou, Wendy; Masellis, Mario; Abrahão, Agessandro; Frank, Andrew; Beaton, Derek; Sunderland, Kelly M; Arnott, Stephen R.; Tartaglia, Maria Carmela; Hatch, Wendy

doi:10.3389/fnins.2022.964715

Cited by 1 publication

(1 citation statement)

References 33 publications

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“…Only one study has compared ocular changes between patients with a tauopathy (i.e., progressive supranuclear palsy) and patients with a transactive response DNA binding protein 43 (TDP-43) proteinopathy (i.e., ALS and frontotemporal dementia). 27 Those authors found that the peripapillary RNFL in the temporal sector was significantly thinner in the TDP-43 than the tauopathy patients prior to correcting for multiple comparisons.…”

Section: Discussionmentioning

confidence: 98%

Longitudinal Changes in the Retinal Nerve Fiber Layer Thickness in Amyotrophic Lateral Sclerosis and Parkinson’s Disease

Taufik,

Ramli,

Tan

et al. 2024

J Clin Neurol

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Background and Purpose There is increasing evidence that the anterior visual pathways are involved in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD). This study investigated longitudinal changes in retinal nerve fiber layer (RNFL) thickness in patients with ALS and PD with the aim of better understanding their roles as biomarkers of disease progression. Methods This study recruited 21 ALS patients, 19 age-matched PD patients, and 21 agematched healthy controls. Patient demographics and clinical scores relating to the respective diseases were documented. The RNFL thickness was measured using optical coherence tomography at baseline and after 6 months. Results At baseline, the RNFL in the superior quadrant was significantly thinner in the patients with ALS than in healthy controls (109.90±22.41 µm vs. 127.81±17.05 µm [mean±standard deviation], p =0.008). The RNFL thickness did not differ significantly between the ALS and PD patients or between the PD patients and healthy controls. At 6 months, there was further significant RNFL thinning in patients with ALS, for both the overall thickness (baseline: median=94.5 µm, range=83.0–106.0 µm; follow-up: median=93.5 µm, range=82.5–104.5 µm, p =0.043) and the thickness in the inferior quadrant (median=126 µm, range=109.5–142.5 µm; and median=117.5 µm, range=98.5–136.5 µm; respectively, p =0.032). However, these changes were not correlated with the ALS functional scores. In contrast, the patients with PD did not demonstrate a significant change in RNFL thickness between the two time points. Conclusions The RNFL thickness is a promising biomarker of disease progression in patients with ALS but not in those with PD, which has a slower disease progression.

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Section: Discussionmentioning

confidence: 98%