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Br J Ophthalmol. 2007 June; 91(6): 839–840.
PMCID: PMC1955581

Optical coherence tomography can monitor reversible nerve‐fibre layer changes in a patient with ethambutol‐induced optic neuropathy

Ethambutol (EMB) has been used as an antimycobacterial agent against tuberculosis since 1961, and its principal side effect is toxic optic neuropathy, which can be seen in up to 6% of patients.1,2

Through the use of optical coherence tomography (OCT), we can document evidence of reversible changes in nerve‐fibre layer (NFL) secondary to EMB‐induced optic neuropathy.

Case report

A 70‐year‐old man weighing 70 kg, who was being treated for Mycobacterium aviumintracellulare complex pneumonia, initially presented with a 3‐month history of gradual, painless loss of vision in both eyes. He had received EMB treatment for 7 months at 2 g/day (29 mg/kg/day). His visual complaints began 7 months after initiation of EMB treatment, and continued to worsen up to his presentation to our clinic. Before EMB treatment, his best‐corrected vision was 20/30 OU (with mild nuclear sclerotic cataracts), but with normal subjective colour and contrast sensitivity.

Our patient underwent a full neuro‐ophthalmological examination, which included an assessment of colour vision using the eight‐plate Ishihara Color Vision Test, Humphrey Field Analyzer (HFA) 30‐2 (SITA Fast test, Humphrey‐Zeiss Medical Systems, Dublin, California, USA), and contrast sensitivity using the Vision Contrast Test System (Vistech, Dayton, Ohio, USA). In addition, OCT (OCT 3000, Humphrey‐Zeiss) was performed on both eyes of the patient. All quantitative measurements were obtained by OCT using the retinal NFL (RNFL) analysis protocol (Stratus OCT 3). The basic principles and technical characteristics of the OCT have been described previously.3,4

The results are presented categorised by the clinical tests performed. The patient visits are abbreviated as A for the initial visit (3 months after discontinuing a 7‐month regimen of EMB), B for the second visit (5 months after discontinuing EMB) and C for the third visit (8 months after discontinuing EMB).

Humphrey visual field analysis

The patient presented with a new superior visual field (VF) defect in his right eye during visit B. By the third visit, the patient showed an improvement in his superior field VF defects when compared with his second visit. Figure 11 and table 11 give more detailed descriptions of the results.

figure bj107326.f1
Figure 1 (A) There is a new onset superior–temporal visual field (VF) defect on Humphrey VF analysis (HFA) mean deviation (MD) and pattern standard deviation (PSD) plots observed on second visit, arrow #1. This corresponds well ...
Table thumbnail
Table 1 Results for the subject's visual acuity, contrast sensitivity, colour vision, fundus examination, Humphrey visual field analysis and optical coherence tomography

Optical coherence tomography

OCT showed a significant increase in NFL thickness in the inferior quadrant of the right eye during visit B in comparison to visit A. This corresponded well with the HFA superior VF deficits. The average RNFL thickness of the inferior quadrant was 142 µm, ranging from a minimum 84 µm to a maximum 201 µm, or 156% thicker than the OCT data from the initial visit. We were unable to perform OCT of the left eye at this visit owing to patient non‐compliance. Hence, we excluded the left eye from any further OCT or HFA analysis. By the third visit (C), OCT revealed a significant decrease in the inferior quadrant RNFL, down to an average 123 µm, or a 13.4% loss of NFL thickness when compared with the second visit, but still 135% thicker than that seen on the patient's initial presentation (fig 11).

Comment

OCT is a useful tool for examining the NFL thickness of certain optic neuropathies.5,6 In this study, we used OCT to monitor reversible axonal swelling in a patient with EMB‐induced optic neuropathy. The marked thickening of the inferior quadrant nerve fibre on OCT corresponded well with the VF defects in the superior quadrant observed on HFA. Furthermore, as the thickness of the inferior quadrant NFL decreased, we saw a concurrent improvement in the patient's VF defects within the superior quadrant. We attribute these reversible NFL changes to retinal ganglion cell axonal swelling that resolved over time after cessation of EMB.

We believe that the heavier distribution of magnocellular axons (M cells) within the peripheral RNFL may play an important role in the reversible changes in NFL that we observed. Unlike parvocellluar axons (P cells), M cells are larger, serve low spatial frequency of contrast sensitivity and motion stereopsis.6,7,8 The large‐calibre M cell axons fire (neuronal activity/second) less often owing to their transient response characteristics and hold an anatomical advantage of having more mitochondria because of their larger volume in comparison to P cells.6,7,8,9 It is reasonable to suggest that the reversible axonal changes we observed within the peripheral RNFL were due to a significant recovery of the retinal ganglion cells, most notably M cells, after the cessation of EMB.

Footnotes

Funding: This study was supported by the Research to Prevent Blindness (RPB) Foundation, senior investigator award.

Competing interests: None declared.

References

1. Barron G J, Tepper L, Iovine G. Ocular toxicity from ethambutol. Am J Ophthalmol 1974. 77256–260.260 [PubMed]
2. Leibold J E. The ocular toxicity of ethambutol and its relation to dose.Ann NY Acad Sci 1966. 135904–909.909 [PubMed]
3. Huang D, Swanson E A, Lin C P. et al Optical coherence tomography. Science 1991. 2541178–1181.1181 [PubMed]
4. Schuman J S, Hee M R, Puliafito C A. et al Quantification of NFL thickness in normal and glaucomatous eyes using optical coherence tomography. Arch Ophthalmol 1995. 113586–596.596 [PubMed]
5. Zoumalan C I, Agarwal M, Sadun A A. Optical coherence tomography can measure axonal loss in patients with ethambutol‐induced optic neuropathy. Graefes Arch Clin Exp Ophthalmol 2005. 243410–416.416 [PubMed]
6. Barboni P, Savini G, Valentino M L. et al Retinal NFL evaluation by optical coherence tomography in Leber's hereditary optic neuropathy. Ophthalmology 2005. 112120–126.126 [PubMed]
7. Sadun A A, Win P H, Ross‐Cisneros F N. et al Leber's hereditary optic neuropathy differentially affects smaller axons in the optic nerve. Trans Am Ophthalmol Soc 2000. 98223–235.235 [PMC free article] [PubMed]
8. Carelli V, Ross‐Cisneros F N, Sadun A A. Mitochondrial dysfunction as a cause of optic neuropathies. Prog Retin Eye Res 2004. 2353–89.89 [PubMed]
9. Carelli V, Ross‐Cisneros F N, Sadun A A. Optic nerve degeneration and mitochondrial dysfunction: genetic and acquired optic neuropathies. Neurochem Int 2002. 40573–584.584 [PubMed]

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