Purpose: To determine if orbital blood flow is altered in traumatic optic neuropathy. Methods: A patient with isolated traumatic optic neuropathy was identified and Color Doppler Imaging (CDI) was performed. Results: Initial clinical evaluation revealed isolated right optic neuropathy with visual acuity of 20/200. Intravenous corticosteroid therapy improved visual acuily to 20/40. Humphrey visual field demonstrated an absolute superior altitudinal defect. CDI four days after injury revealed significant decrease in peak systolic velocity (PSV) and end diastolic velocity (EDV) of the central retinal artery (CRA) of the affected eye (OD: PSV=5.62 mm/sec, EDV=0.92 mm/sec; OS: PSV=10.22 mm/sec, EDV=1.66 mm/sec). The PSV and EDV of the ophthalmic arteries showed no significant difference (OD: PSV-46.40 mm/sec, EDV=10.89 mm/sec; OS: PSV=51.13 mm/sec, EDV 12.31 mm/sec). Repeat CDI 14 weeks after injury demonstrated persistent decrease in PSV but not EDV in CRA of the affected eye (OD: PSV=5.75 mm/sec, EDV=1.57 mm/sec; OS: PSV-9.15 mm/sec, EDV 1.57 mm/sec). The ophthalmic artery demonstrated a significant decrease in PSV and EDV (OD: PSV=19.88 mm/sec, EDV=5.21 mm/sec, OS: PSV-38.00 mm/sec, EDV=11.51 mm/sec). Posterior ciliary artery (PCA) PSV demonstrated no significant differences between eyes (OD: nasal PSV=6.28 mm/sec, temporal PSV= 11.50 mm/sec; OS: nasal PSV=8.11 mm/sec, temporal PSV= 8.89 mm/sec). The resistive indices of all arteries demonstrated no significant differences. Conclusion: The etiology of traumatic optic neuropathy remains elusive. We found decreased CRA blood flow velocities using CDI in a patient with traumatic optic neuropathy. Further studies regarding orbital hemodynamics in traumatic optic neuropathy are indicated.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience