Optic Atrophy Treatment & Management

  • Author: Rashmin Gandhi, MBBS, FRCS(Edin), FRCS(Glasg); Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: May 10, 2010
 

Medical Care

No proven treatment exists for optic atrophy. However, treatment that is initiated before the development of optic atrophy can be helpful in saving useful vision. The role of intravenous steroids is proven in a case of optic neuritis or arteritic anterior ischemic optic neuropathy. Early diagnosis and prompt treatment can help patients with compressive and toxic neuropathies.

Idebenone, a quinone analog, has been used recently in a few cases of Leber hereditary optic neuropathy to ameliorate the net ATP synthesis by providing an alternate pathway, as well as by scavenging free radicals, with the advantage of concentrating readily in the mitochondria. The results were modest.

Stem cell treatment can hold a key in the future treatment of neuronal disorders. Neural progenitor cells delivered to the vitreous can integrate into the ganglion cell layer of the retina, turn on neurofilament genes, and migrate into the host optic nerve.

At present, the best defense is an early diagnosis because if the cause can be found and corrected, further damage can be prevented.

Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Rashmin Gandhi, MBBS, FRCS(Edin), FRCS(Glasg)  Faculty, Departments of Ocular Physiology and Neuro-ophthalmology, Elite School of Optometry; Faculty, CU Shah Ophthalmic Postgraduate Center, Consulting Staff, Department of Ophthalmology, Sankara Nethralaya Hospital

Rashmin Gandhi, MBBS, FRCS(Edin), FRCS(Glasg) is a member of the following medical societies: All India Ophthalmological Society and American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Coauthor(s)

Gangaprasad Muthaiah Amula, MBBS, DNB  Fellow, Sankara Nethralaya Hospital, India

Disclosure: Nothing to disclose.

Specialty Editor Board

Edsel Ing, MD, FRCSC  Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Toronto East General Hospital, Canada

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

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.

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

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.

References

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  3. Albert DM, Jakobeic FA. Optic atrophy. In: Principles and Practice of Ophthalmology. 2nd ed. Philadelphia: WB Saunders; 2000:4108- 4113.

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  5. Glaser JS. Neuro-Ophthalmology. 2nd ed. Philadelphia: JB Lippincott; 1990:115–117.

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  8. Kline LB, ed. Optic nerve disorders. In: Ophthalmology Monographs. Vol 10. San Francisco, Calif: American Academy of Ophthalmology; 1996.

  9. Kuppersmith MJ, Krohn D. Cupping of the optic disc with compressive lesions of the anterior visual pathway. Ann Ophthalmol. 1984;16:948–953.

  10. Miller NR, Newman NJ. Walsh & Hoyt's Clinical Neuro-ophthalmology. 6th ed. Philadelphia: JB Lippincott; 208- 218.

  11. Miller NR, Newman SA. Transsynaptic degeneration. Arch Ophthalmol. Sep 1981;99(9):1654. [Medline].

  12. Newman NJ. Optic disc pallor: a false localizing sign. Surv Ophthalmol. Jan-Feb 1993;37(4):273-82. [Medline].

  13. Patel DA, Hove MW. Focal Points. Vol XXIV. No 2. San Francisco, Calif: American Academy of Ophthalmology; March 2006.

  14. Schwartz B. Cupping and pallor of the optic disc. Arch Ophthalmol. Apr 1973;89(4):272-7. [Medline].

  15. Tasman W, Jaeger EA. Topical diagnosis of optic nerve lesions. In: Duane's Ophthalmology. Philadelphia: JB Lippincott; 2007.

  16. Thompson HS. Pupillary signs in the diagnosis of optic nerve disease. Trans Ophthalmol Soc U K. Sep 1976;96(3):377-81. [Medline].

  17. Trobe JD, Glaser JS, Cassady J, et al. Nonglaucomatous excavation of the optic disc. Arch Ophthalmol. Jun 1980;98(6):1046-50. [Medline].

  18. Trobe JD, Glaser JS, Cassady JC. Optic atrophy. Differential diagnosis by fundus observation alone. Arch Ophthalmol. Jun 1980;98(6):1040-5. [Medline].

 
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Normal optic nerve histopathology.
Glaucomatous optic atrophy histopathology.
Healthy optic disc.
Nonarteritic anterior ischemic optic neuropathy.
Arteritic anterior ischemic optic neuropathy, cilioretinal artery occlusion.
Primary optic atrophy.
Optic atrophy following papilledema (secondary).
Glaucomatous optic atrophy.
Juvenile open-angle glaucoma (JOAG) with optic pallor.
Consecutive optic atrophy following panretinal photocoagulation (PRP).
Table 1. Various Common Groups of Disorders Presenting with Optic Atrophy
PostneuritisIschemic



Arteritic



Ischemic



Nonarteritic



Compressive
Age15-50 yApproximately 70 ySixth decadeVaries based on cause
SexMultiple sclerosis F>MF>MF=MVaries based on cause
Visual acuityVaries from mild blurring (34%) and moderate loss of acuity (12%) to severe or total loss of light perception (complete blindness) in 54% of cases, to no light perception. The loss of vision is acute and progressive.--Vision usually recovers within 2 mo< 20/200 (6/60)>20/200 (6/60)Varies from mild blurring to no light perception
Color visionColor vision > vision lossColor vision loss = vision lossColor vision loss = vision lossColor vision = vision loss
RAPD*++++
MotilityPainful movement in cases of retrobulbar neuritisNormalNormalDepends on the site of compression
NystagmusIn multiple sclerosis, beating nystagmus (upbeating or downbeating) may be seenNoNoSee-saw nystagmus in optic chiasm compression
Optic discTemporal pallorPallid disc edemaSegmental disc edema Bow-tie pallor seen in optic chiasm compression; varies in other instances
Electrophysiologic studyVEP-increased latency <†>VEP-reduced amplitudeVEP-reduced amplitudeReduced VEP amplitude
Neuroimaging



(CT, MRI)



In multiple sclerosis, hyperechoic lesions are seen in the brain on MRI--Can delineate the exact location of compression
Other associationsHeadache, scalp tenderness, jaw claudicationHypertension and diabetesHeadache, vomiting, and focal neurologic deficits
*RAPD - Relative afferent pupil defect



<†>VEP - Visual-evoked potential



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