Pilot study reveals altered fixational eye movements in poorly controlled type 2 diabetes, suggesting fixational tracking can serve as an early functional marker of neurological dysfunction.
Type 2 diabetes mellitus (T2DM) is a prevalent metabolic condition associated with neuronal and vascular complications across multiple organ systems, including the eye, leading to vision impairment. Evidence suggests that structural and functional deficits may arise before funduscopically detectable changes in T2DM. Fixational eye movements (FEMs) reflect the integrity of the oculomotor control systems and may serve as early functional markers of neurological dysfunction. FEM parameters in T2DM with good vision and without retinopathy have not been comprehensively characterized. Using a tracking scanning laser ophthalmoscope (TSLO) during a perimetry task, this pilot study characterizes FEM parameters in 43 age-matched participants stratified by hemoglobin A1c (HbA1c): controls (HbA1c < 5.7%; n = 18), prediabetes (HbA1c ≥ 5.7 and < 6.5%; n = 11), well-controlled T2DM (HbA1c ≥ 6.5 and < 7%; n = 8), and poorly controlled T2DM (HbA1c ≥ 7%; n = 6). Poorly controlled T2DM exhibited significantly greater fixation instability, saccade vector amplitude, maximum excursion, and drift velocity compared with well-controlled T2DM, along with selective elevation of vertical saccade components. These findings indicate that oculomotor dysfunction in T2DM may be associated with glycemic control. Furthermore, FEM assessment may offer a non-invasive functional marker of subclinical neuro-visual impairment in T2DM.
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Kafle et al. (2026) studied this question.
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