H Lew1, S Y Lee, J W Jang, H Y Kim, S J Kang, S J Kim. 1. Institute of Vision Research and Department of Ophthalmology, Yonsei University College of Medicine, Seoul, Korea. Hllew0332@yumc.yonsei.ac.kr
Abstract
PURPOSE: The objective of this study was to ascertain the effect of high-dose steroid therapy in traumatic optic neuropathy using the Heidelberg retina flowmeter (HRF) to detect changes in optic nerve head blood flow. METHODS: We experimentally damaged the optic nerves of 10 white rabbits with a Hartman mosquito clamp. The first group (n = 5) was treated with intravenous dexamethasone (0.25 mg/kg) every 6 h for a 48-hour period. The second group (n = 5) served as controls. Both groups were tested prior to operation, 1 week, 1 month and 2 months after surgery. RESULTS: Experimental optic nerve damage caused a significant decrease in optic nerve head blood flow of 50.51% (p = 0.001), with a volume decrease of 46.02% (p = 0.001) and a velocity reduction of 43.12% (p = 0.002) compared to the baseline. After 2 months, in the group treated with high-dose corticosteroid therapy, optic nerve head blood flow was increased by 76.90% (p = 0.012), volume by 77.53% (p = 0.012) and velocity by 47. 21% (p = 0.012) compared to the control group. CONCLUSION: The high-dose corticosteroid therapy improved the optic nerve head blood flow as demonstrated in experimental traumatic optic neuropathy. The HRF may be used to assess the therapeutic responses in traumatic optic neuropathy under variable conditions.
PURPOSE: The objective of this study was to ascertain the effect of high-dose steroid therapy in traumatic optic neuropathy using the Heidelberg retina flowmeter (HRF) to detect changes in optic nerve head blood flow. METHODS: We experimentally damaged the optic nerves of 10 white rabbits with a Hartman mosquito clamp. The first group (n = 5) was treated with intravenous dexamethasone (0.25 mg/kg) every 6 h for a 48-hour period. The second group (n = 5) served as controls. Both groups were tested prior to operation, 1 week, 1 month and 2 months after surgery. RESULTS: Experimental optic nerve damage caused a significant decrease in optic nerve head blood flow of 50.51% (p = 0.001), with a volume decrease of 46.02% (p = 0.001) and a velocity reduction of 43.12% (p = 0.002) compared to the baseline. After 2 months, in the group treated with high-dose corticosteroid therapy, optic nerve head blood flow was increased by 76.90% (p = 0.012), volume by 77.53% (p = 0.012) and velocity by 47. 21% (p = 0.012) compared to the control group. CONCLUSION: The high-dose corticosteroid therapy improved the optic nerve head blood flow as demonstrated in experimental traumatic optic neuropathy. The HRF may be used to assess the therapeutic responses in traumatic optic neuropathy under variable conditions.
Authors: K Kircher; G Weigert; H Resch; G Garhöfer; G T Dorner; G Fuchsjäger Mayrl; A Reitner; L Schmetterer Journal: Graefes Arch Clin Exp Ophthalmol Date: 2008-06-25 Impact factor: 3.117