应用光学相干断层成像术(OCT)测量乙胺丁醇诱导性视神经病变患者视神经轴突缺失的研究

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Purpose: To map and identify the pattern, in vivo, of axonal degeneration in e thambutol-induced optic neuropathy using optical coherence tomography (OCT). Et hambutol is an antimycobacterial agent often used to treat tuberculosis. A serio us complication of ethambutol is an optic neuropathy that impairs visual acuity, contrast sensitivity, and color vision. However, early on, when the toxic optic neuropathy is mild and partly reversible, the funduscopic findings are often su btle and easy to miss. Methods: Three subjects with a history of ethambutol (EMB )-induced optic neuropathy of short-, intermediate-, and long-term visual de ficits were administered a full neuro-ophthalmologic examination including visu al acuity, color vision, contrast sensitivity, and fundus examination. In additi on, OCT (OCT 3000, Humphrey-Zeiss, Dublin, CA) was performed on both eyes of ea ch subject using the retinal nerve fiber layer (RNFL) analysis protocol. OCT int erpolates data from 100 points around the optic nerve to effectively map out the RNFL. Results: The results were compared to the calculated average RNFL of norm al eyes accumulated from four prior studies using OCT, n=661. In all subjects wi th history of EMB-induced optic neuropathy, there was a mean loss of 72%nerve fiber layer thickness in the temporal quadrant (patient A, with eventual recover y of visual acuity and fields, 58%loss; patient B, with intermediate visual def icits, 68%loss; patient C, with chronic visual deficits, 90%loss), with an average mean optic nerve thickness of 26±16 μm. There was a combined mean loss of 46%of fibers from the superior, inferior, an d nasal quadrants in the (six) eyes of all three subjects (mean average thicknes s of 55±29 μm). In both sets (four) of eyes of the subjects with persistent vi sual deficits (patientsBandC), therewas an average loss of 79%of nerve fiber th ickness in the temporal quadrant. Conclusions: The OCT results in these patients with EMB-induced optic neuropathy showconsiderable loss especially of the temp oral fibers. This is consistent with prior histopathological studies that show p redominant loss of parvo-cellular axons (or small-caliber axons) within the pa pillo-macular bundle in toxic or hereditary optic neuropathies. OCT can be a va luable tool in the quantitative analysis of optic neuropathies. Additionally, in terms of management of EMB-induced optic neuropathy, it is important to proper ly manage ethambutol dosing in patients with renal impairment and to achieve pro per transition to a maintenance dose once an appropriate loading dose has been r eached. Purpose: To map and identify the pattern, in vivo, of axonal degeneration in e thambutol-induced optic neuropathy using optical coherence tomography (OCT). Et hambutol is an antimycobacterial agent often used to treat tuberculosis. A serio us complication of ethambutol is an However, early, when the toxic optic neuropathy is mild and partly reversible, the funduscopic findings are often su btle and easy to miss. Methods: Three subjects with a history of ethambutol (EMB) -induced optic neuropathy of short-, intermediate-, and long-term visual de ficits were administered a full neuro-ophthalmologic examination including visu al acuity, color vision, contrast sensitivity, and fundus examination. In additi on, OCT (OCT 3000, Humphrey-Zeiss, Dublin, CA) was performed on both eyes of ech ch subject using the retinal nerve fiber layer (RNFL) analysis protocol. OCT int erpolates data from 100 points around t he optic nerve to effectively map out the RNFL. Results: The results were compared to the calculated average RNFL of norm al eyes accumulated from four prior studies using OCT, n = 661. In all subjects wi th history of EMB-induced optic neuropathy, there was a mean loss of 72% nerve fiber layer thickness in the temporal quadrant (patient A, with eventual recover y of visual acuity and fields, 58% loss; patient B, with intermediate visual def icits, 68% loss; patient C, with was visual deficits of 90%, with an average mean optic nerve thickness of 26 ± 16 μm. There was a combined mean loss of 46% of fibers from the superior, inferior, an d nasal quadrants in the (six) eyes of all three subjects (mean average thicknes of 55 ± 29 μm). In both sets (four) of eyes of the subjects with persistent vi sual deficits (patientsBandC), therewas an average loss of 79% of nerve fiber thickness in the temporal quadrant. Conclusions: The OCT results in these patients with EMB-induced optic neuropat hy sThis is consistent with prior histopathological studies that show p redominant loss of parvo-cellular axons (or small-caliber axons) within the pa pillo-macular bundle in toxic or hereditary optic neuropathies. OCT can be a va luable tool in the quantitative analysis of optic neuropathies. In, of terms of management of EMB-induced optic neuropathy, it is important to proper ly manage ethambutol dosing in patients with renal impairment and to achieve pro per transition to a maintenance dose once an appropriate loading dose has been r eached.
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