eMedicine Specialties > Ophthalmology > Optic Nerve

Toxic/Nutritional Optic Neuropathy: Differential Diagnoses & Workup

Author: Aftab Zafar, MD, Consulting Staff, Department of Ophthalmology, St Mary's General Hospital
Contributor Information and Disclosures

Updated: Aug 27, 2008

Differential Diagnoses

Graves Disease
Ocular Manifestations of Syphilis
Optic Neuritis, Adult
Optic Neuropathy, Compressive
Thyroid Ophthalmopathy

Other Problems to Be Considered

Certain maculopathies/macular dystrophies
Dominantly inherited (Kjer) optic neuropathy
Mitochondrially inherited (Leber) optic neuropathy
Compressive or infiltrative lesion of optic chiasm
Bilateral inflammatory or demyelinative optic neuropathy
Syphilitic optic neuritis
Radiation optic neuropathy
Diabetic papillopathy
Nonphysiologic visual loss – Hysteria/malingering

Workup

Laboratory Studies

  • In any patient with bilateral central scotomas, serum B-12 (pernicious anemia) and red cell folate levels (marker of general nutritional status) need to be obtained. Other tests that could support the diagnosis of nutritional optic neuropathy are direct or indirect vitamin assays, serum protein concentrations, and antioxidant levels. Serologic testing for syphilis also should be completed.
  • Patients suspected of having a toxic optic neuropathy should have a CBC count, blood chemistries, urinalysis, and a serum lead level, particularly in those who have a coexisting peripheral neuropathy. The blood and urine also may be screened for other toxins if exposure to a particular one is not identified on history. On the other hand, if a specific intoxicant is suspected, one would try to identify it or its metabolites in the patient's tissues or fluids.

Imaging Studies

  • Although imaging studies yield normal results in toxic/nutritional optic neuropathy, they almost always are indicated, unless one is absolutely certain of the diagnosis. The most appropriate imaging study is an MRI of the optic nerves and chiasm with and without gadolinium enhancement.

Other Tests

  • Formal visual field evaluation, whether it is a static (Humphrey) or kinetic (Goldmann) field, is absolutely essential in the evaluation of any patient suspected of having toxic/nutritional optic neuropathy.
    • Central or cecocentral scotomata with preservation of the peripheral field are characteristic visual field defects of these optic neuropathies and are actually most prevalent in patients with these disorders. Rarely, patients may present with other defects, as mentioned below. Although the field defects do tend to be relatively symmetric, early on in a patient's presentation, the defect is usually more developed in one field than in the other field. Soft margins are another characteristic of these defects, which are easier to define/plot for colored targets, such as red, than for white stimuli. The anatomic basis of the cecocentral scotoma has yet to be established.
    • In ethambutol toxicity, central scotomas are the common visual field defect, but bitemporal defects1 and peripheral field constriction have been reported. The field defect in amiodarone toxicity may be simply a generalized constriction of fields or cecocentral scotomas.
  • Optical coherence tomography (OCT), which is now commonly used to measure nerve fiber layer thickness in patients with glaucoma, can also be used to quantify such changes in patients with other optic neuropathies, like the one caused by ethambutol.7,8 As discussed earlier, early changes are not clinically apparent in patients on ethambutol. With OCT, one can clearly quantify the loss of retinal nerve fibers from the optic nerves of these patients as a sign of early toxicity from the drug, which would not be apparent on funduscopy. Therefore, in conjunction with visual field testing, it is an additional objective test available to monitor patients on ethambutol.

More on Toxic/Nutritional Optic Neuropathy

Overview: Toxic/Nutritional Optic Neuropathy
Differential Diagnoses & Workup: Toxic/Nutritional Optic Neuropathy
Treatment & Medication: Toxic/Nutritional Optic Neuropathy
Follow-up: Toxic/Nutritional Optic Neuropathy
References
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References

  1. Lim SA. Ethambutol-associated optic neuropathy. Ann Acad Med Singapore. Apr 2006;35(4):274-8. [Medline].

  2. Orssaud C, Roche O, Dufier JL. Nutritional optic neuropathies. J Neurol Sci. Nov 15 2007;262(1-2):158-64. [Medline].

  3. Murphy MA, Murphy JF. Amiodarone and optic neuropathy: the heart of the matter. J Neuroophthalmol. Sep 2005;25(3):232-6. [Medline].

  4. Macaluso DC, Shults WT, Fraunfelder FT. Features of amiodarone-induced optic neuropathy. Am J Ophthalmol. May 1999;127(5):610-2. [Medline].

  5. Nagra PK, Foroozan R, Savino PJ, et al. Amiodarone induced optic neuropathy. Br J Ophthalmol. Apr 2003;87(4):420-2. [Medline].

  6. Nazarian SM, Jay WM. Bilateral optic neuropathy associated with amiodarone therapy. J Clin Neuroophthalmol. Mar 1988;8(1):25-8. [Medline].

  7. Santaella RM, Fraunfelder FW. Ocular adverse effects associated with systemic medications : recognition and management. Drugs. 2007;67(1):75-93. [Medline].

  8. Zoumalan CI, Agarwal M, Sadun AA. Optical coherence tomography can measure axonal loss in patients with ethambutol-induced optic neuropathy. Graefes Arch Clin Exp Ophthalmol. May 2005;243(5):410-6. [Medline].

  9. Chai SJ, Foroozan R. Decreased retinal nerve fibre layer thickness detected by optical coherence tomography in patients with ethambutol-induced optic neuropathy. Br J Ophthalmol. Jul 2007;91(7):895-7. [Medline].

  10. Johnson LN, Krohel GB, Thomas ER. The clinical spectrum of amiodarone-associated optic neuropathy. J Natl Med Assoc. Nov 2004;96(11):1477-91. [Medline].

  11. Danesh-Meyer H, Kubis KC, Wolf MA. Chiasmopathy?. Surv Ophthalmol. Jan-Feb 2000;44(4):329-35. [Medline].

  12. Glaser JS. Nutritional and toxic optic neuropathies. In: Glaser JS, ed. Neuro-ophthalmology. 3rd ed. Philadelphia: Lippincott; 1999.

  13. Grant WM, Schuman JS. Toxicology of the Eye. 4th ed. Springfield, Ill: Charles C Thomas Publisher; 1993.

  14. Kerrison JB. Optic neuropathies caused by toxins and adverse drug reactions. Ophthalmol Clin North Am. Sep 2004;17(3):481-8; viii. [Medline].

  15. Lessell S. Nutritional deficiency and toxic optic neuropathies. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology. 2nd ed. Philadelphia: WB Saunders Co; 2000.

  16. Mantyjarvi M, Tuppurainen K, Ikaheimo K. Ocular side effects of amiodarone. Surv Ophthalmol. Jan-Feb 1998;42(4):360-6. [Medline].

  17. Melamud A, Kosmorsky GS, Lee MS. Ocular ethambutol toxicity. Mayo Clin Proc. Nov 2003;78(11):1409-11. [Medline].

  18. Miller NR. Anterior toxic optic neuropathies. In: Walsh and Hoyt's Clinical Neuro-Ophthalmology. 4th ed. Baltimore: Lippincott Williams & Wilkins; 1982:254-260.

  19. Miller NR. Retrobulbar toxic and deficiency optic neuropathies. In: Walsh and Hoyt's Clinical Neuro-ophthalmology. 4th ed. Baltimore: Lippincott Williams & Wilkins; 1982:289-307.

  20. Phillips PH. Toxic and deficiency optic neuropathies. In: Miller NR, Newman NJ, eds. Walsh and Hoyt's Clinical Neuro-ophthalmology. 6th ed. Baltimore: Lippincott Williams & Wilkins; 2005:447-463.

  21. Rizzo JF 3rd, Lessell S. Tobacco amblyopia. Am J Ophthalmol. Jul 15 1993;116(1):84-7. [Medline].

  22. Sadun AA. Metabolic optic neuropathies. Semin Ophthalmol. Mar 2002;17(1):29-32. [Medline].

  23. Woon C, Tang RA, Pardo G. Nutrition and optic nerve disease. Semin Ophthalmol. Sep 1995;10(3):195-202. [Medline].

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Further Reading

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Keywords

toxic/nutritional optic neuropathy, toxic-nutritional optic neuropathy, toxic and nutritional optic neuropathy, toxic optic neuropathy, nutritional optic neuropathy, optic neuropathy, optic neuropathies, metabolic optic neuropathy, nutritional deficits, undernutrition, nutritional amblyopia

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Contributor Information and Disclosures

Author

Aftab Zafar, MD, Consulting Staff, Department of Ophthalmology, St Mary's General Hospital
Aftab Zafar, MD is a member of the following medical societies: Canadian Medical Association, Canadian Ophthalmological Society, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Brian R Younge, MD, Professor of Ophthalmology, Mayo Clinic School of Medicine
Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society
Disclosure: Nothing to disclose.

CME Editor

Ralph Garzia, OD, Assistant Dean for Clinical Programs, Associate Professor, School of Optometry, University of Missouri at St Louis
Ralph Garzia, OD is a member of the following medical societies: American Academy of Optometry and American Optometric Association
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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