Severe Course and Contingent Risk Factors in Tuberculostatic Optic Neuropathy

¹Frisch I. B., ²Kunze A., ¹Castro A., ¹Pavlovska V., ²Meinck H.-M., ¹Krastel H.,
¹Ruprecht-Karls-Universität Heidelberg, Universitäts-Augenklinik (Heidelberg)
²Ruprecht-Karls-Universität Heidelberg, Neurologische Klinik (Heidelberg)

Purpose: To draw attention to risk and causal factors of tuberculostatic optic neuropathy. Due to the resistance pattern of mykobacteria, ethambutol has remained indispensable as tuberculostatic compound. Local risks comprise any present or previous opticopathy, systemic risks are increased serum levels of ethambutol or exposure of the optic nerve to additional toxicity. Cumulative strain bears particular danger.
Methods: Standard acuity, Octopus-perimetry, colour arrangement tests, the Kolling plate and VEP provided monitoring of visual functions.
Results: At the age of 20, cervical biopsy ascertained specific lymphadenopathy in our patient of east asian origin. A 4 drugs therapy (ethambutol, rifampicin, isoniacid, pyrazinamid) was required. His initial symptom of opticopathy was glare. Thereafter he developped bitemporal scotomata and undetectable VEP. Cranial MRI revealed no pathology and so, a diagnosis of paraxial toxic optic neuropathy was etablished. Despite discontinuation of ethambutol, visual fields, colour vision and acuity declined (the latter to 1/20). Isoniazid and, later on, any tuberculostatic compounds were withdrawn. During the subsequent 30 months with vitamines B₆ and B₁₂ supplementation, acuity slowly recovered to 1,0 O.U., colour vision improved stepwise from a red-green to a tritan defect, finally arriving at a near normal pattern with arrangement tests. Along with VEP improvement, scotomata tended to shrink. Eventually there remained no more overlap of defects in the right and in the left visual field, respectively.
Conclusions: Here, cumulative strain to the optic nerve may be due to several compounds of potential toxicity and the intravenous application of ethambutol with consequently high serum levels. An ethnically low activity of ethanol-dehydrogenase may have contributed as well. Paraxial affection of the optic fascicles rendered detection of toxic opticopathy more difficult. We recommend to define glare as an early symptom of toxic opticopathy, to regard low activity of ethanol-dehydrogenase as potential risk, to check regularly for acuity and colour vision and to perform regularly visual field screening and paraxial colour vision screening. For the latter two purposes, the Kolling plate may be useful.

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