Purpose <p>This study assessed the diagnostic potential of chromatic pupil campimetry (CPC) using relative maximal constriction amplitude (relMCA), pupillary light response (PLR) latency, and pupillary escape to differentiate optic neuropathies (ON) from healthy individuals and identify specific ON subtypes.</p> Methods <p>CPC testing used red and blue stimuli at central (0°) and peripheral (20°) locations to measure relMCA, latency, and pupillary escape. Patients with various ON etiologies, including glaucoma (n = 20), optic nerve compression by meningioma (n = 18), chiasm compression (n = 4), Leber hereditary optic neuropathy (LHON; n = 4), and autosomal dominant optic atrophy (ADOA; n = 3), were tested. Linear mixed-effects models and post hoc Tukey tests were used to analyze differences across subgroups of ON etiologies and a healthy control group (n = 40), regarding signal eccentricities and locations.</p> Results <p>Pupillary escape was significantly higher in ON patients during central red stimulation (<i>p</i> = 0.0007). Glaucoma and meningioma groups showed reduced relMCA and prolonged latency for both stimuli compared to controls (<i>p</i> &lt; 0.0001 to <i>p</i> = 0.0058). RelMCA during blue stimulation was lower in glaucoma patients than in ADOA (<i>p</i> = 0.0183). LHON patients exhibited significantly prolonged PLR latency during blue stimulation compared to healthy (<i>p</i> = 0.0284).</p> Conclusion <p>CPC effectively distinguished glaucoma and meningioma from healthy controls but was less reliable for differentiating ON subtypes. Our results indicate, that central pupillary escape is associated with inner retinal dysfunction.</p>

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Chromatic pupil campimetry as objective diagnostic tool for progressive optic neuropathies

  • Márton Viktor Edelmayer,
  • Torsten Strasser,
  • Ronja Jung,
  • Anton Sonntag,
  • Ricarda Jendritza,
  • Felix Tonagel,
  • Tobias Peters,
  • Helmut Wilhelm,
  • Barbara Wilhelm,
  • Carina Kelbsch

摘要

Purpose

This study assessed the diagnostic potential of chromatic pupil campimetry (CPC) using relative maximal constriction amplitude (relMCA), pupillary light response (PLR) latency, and pupillary escape to differentiate optic neuropathies (ON) from healthy individuals and identify specific ON subtypes.

Methods

CPC testing used red and blue stimuli at central (0°) and peripheral (20°) locations to measure relMCA, latency, and pupillary escape. Patients with various ON etiologies, including glaucoma (n = 20), optic nerve compression by meningioma (n = 18), chiasm compression (n = 4), Leber hereditary optic neuropathy (LHON; n = 4), and autosomal dominant optic atrophy (ADOA; n = 3), were tested. Linear mixed-effects models and post hoc Tukey tests were used to analyze differences across subgroups of ON etiologies and a healthy control group (n = 40), regarding signal eccentricities and locations.

Results

Pupillary escape was significantly higher in ON patients during central red stimulation (p = 0.0007). Glaucoma and meningioma groups showed reduced relMCA and prolonged latency for both stimuli compared to controls (p < 0.0001 to p = 0.0058). RelMCA during blue stimulation was lower in glaucoma patients than in ADOA (p = 0.0183). LHON patients exhibited significantly prolonged PLR latency during blue stimulation compared to healthy (p = 0.0284).

Conclusion

CPC effectively distinguished glaucoma and meningioma from healthy controls but was less reliable for differentiating ON subtypes. Our results indicate, that central pupillary escape is associated with inner retinal dysfunction.