Toxic/Nutritional Optic Neuropathy 

  • Author: Aftab Zafar, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Dec 5, 2011
 

Background

The anterior visual pathway is susceptible to damage from toxins or nutritional deficiency. These disorders tend to be classified under the heading toxic/nutritional optic neuropathy, a syndrome characterized by papillomacular bundle damage, central or cecocentral scotoma, and reduction of color vision. Both toxicity and malnutrition, acting either independently or together, have been implicated in the pathogenesis of these disorders. Although these problems have been classified as optic neuropathies, in most of these entities, the primary lesion has not actually been localized to the optic nerve and may possibly originate in the retina, chiasm, or even the optic tracts.

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Pathophysiology

The exact mechanism(s) by which nutritional deficits damage the optic nerve has not been elucidated. Although the etiology is likely multifactorial, most clinicians agree that in patients who abuse ethanol and tobacco, undernutrition is the principal cause of the amblyopia. Others believe that specific deficiencies in vitamin B-12, thiamine, folic acid, proteins with sulfur-containing amino acids, or any combination of these also play a role. Whether tobacco or ethanol has a direct effect on the optic nerve remains unclear. Why certain agents are toxic to the optic nerve, particularly the portion that comprises the papillomacular bundle, also remains largely unestablished. Whether the unusual configuration of the vascular supply of the optic nerve head predisposes it to the accumulation of toxic agents has been questioned.

It has been hypothesized that the chelating properties of ethambutol are what contribute to its neurotoxicity, but this has yet to be proven. The mechanism of the neurotoxicity that occurs from the antiarrhythmic amiodarone remains unclear. Researchers believe that it may relate to a lipidosis that is induced by the drug.

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Epidemiology

Frequency

United States

Toxic and nutritional optic neuropathies are not common in the United States. In the general population, nutritional amblyopia is more common among tobacco and alcohol abusers and those who are undernourished. Toxic optic neuropathies usually are associated with exposure of employees in a workplace, ingestion of materials/foods containing toxic substances, or systemic medications.

International

Nutritional optic neuropathy is definitely more prevalent in regions of famine, such as in Africa, where it may take on epidemic proportions.

Mortality/Morbidity

Morbidity of these disorders depends on risk factors, the underlying etiology, and the duration of symptoms before the institution of treatment. A patient with advanced optic atrophy is less likely to recover visual function than a patient who does not have such pathologic changes.

Race

These disorders have no racial predilection. All races are susceptible.

Sex

These disorders are found equally in both males and females.

Age

Any age may be affected by toxic optic neuropathies, but nutritional optic neuropathies are very rare in children since drinking and smoking are much less frequent in this age group. Toxic optic neuropathy used to be seen in youngsters with chronic pulmonary conditions, such as cystic fibrosis, when treated with chloramphenicol.

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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.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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.

Ralph Garzia, OD  Assistant Dean for Clinical and Academic Programs, Associate Professor, College 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.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Robert C Sergott, MD, to the development and writing of this article.

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. Grzybowski A, Holder GE. Tobacco optic neuropathy (TON) - the historical and present concept of the disease. Acta Ophthalmol. Aug 2011;89(5):495-9. [Medline].

  8. Becker M, Masterson K, Delavelle J, Viallon M, Vargas MI, Becker CD. Imaging of the optic nerve. Eur J Radiol. May 2010;74(2):299-313. [Medline].

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

  10. 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].

  11. 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].

  12. 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].

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

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

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

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

  17. 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.

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

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

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

  21. 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.

  22. 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.

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

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

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

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