Do all cases of acute optic neuritis require high-dose corticosteroids?

admin
9 Min Read

Michela Cimberle , 2025-05-15 20:20:00

Key takeaways:

  • One physician said intravenous corticosteroids are useful for treating optic neuritis.
  • Another argued corticosteroids may increase the risk for infection in some cases.

SEVILLE, Spain — Treatment of optic neuritis with corticosteroids, findings from the Optic Neuritis Treatment Trial and the validity of previous treatment paradigms were debated at the Congress on Controversies in Ophthalmology.

For

Do all patients with acute optic neuritis (ON) require high-dose corticosteroids? The answer is yes, according to Andrew G. Lee, MD.

Eye and brain
Treatment of optic neuritis with corticosteroids, findings from the Optic Neuritis Treatment Trial and the validity of previous treatment paradigms were debated at the COPHy meeting. Image: Adobe Stock

The Optic Neuritis Treatment Trial (ONTT) dates back to 1992 and was based on the knowledge of the disease that was available at that time. The discovery of specific antibodies associated with inflammatory disorders of the central nervous systems has altered the overall picture of ON and its mechanisms, prognosis and treatment.

Andy Lee, MD

Andrew G. Lee

“You need to know that optic neuritis has changed. … Now there are two bad guys you need to worry about. One guy’s name is MOG, myelin oligodendrocyte glycoprotein, and the other guy’s name is NMOSD, neuromyelitis optica spectrum disorder,” Lee said.

In light of these new findings, some of the recommendations (“the little white lies,” as Lee called them) of the ONTT have become obsolete.

“No. 1 is that optic neuritis always gets better. That’s not true anymore. Optic neuritis usually gets better, and the demyelinating and idiopathic forms do get better, but the bad guys, MOG and NMO, need steroids,” Lee said.

According to the ONTT, IV steroids only help to speed up the recovery process that would occur naturally, regardless of treatment. This conclusion, Lee said, was wrong.

“In the ONTT, we only did MRI of the brain with no contrast, no orbit, no gadolinium, no fat suppression. You cannot do that anymore. You need MRI of the head and orbit, gadolinium and fat suppression to see the extent of the enhancement and whether the enhancement is in the sheath or in the back,” he said.

In the trial, a normal MRI scan was good news because it excluded the diagnosis of multiple sclerosis (MS). However, it is now known that a normal MRI scan, or a scan that shows lesions that are not typical for MS, could indicate that “the ugly antibody, NMOSD, and MOG, the bad, might be lurking in there.”

Lee added that, according to the trial, no laboratory testing was needed, such as syphilis serology and antimitochondrial antibody, and neither was a lumbar puncture. This is no longer true because these tests may be relevant in the context of MOG-associated disease and NMOSD.

The geography of MS can give important diagnostic insights. Lee showed that in the equatorial regions of both the Northern and Southern Hemisphere, MS is significantly less prevalent.

“When it’s a Black, Afro Caribbean or African American person or somebody from these areas, you should be thinking about a non-MS-related optic neuritis,” he said.

The rates of NMOSD, as he showed in another map, are significantly higher in these populations.

Optic neuritis needs prompt treatment, particularly when related to NMOSD and MOG, Lee said. A delay of even 4 days reduces the chance of regaining 20/20 vision by a factor of eight. Treatment, he said, should be intravenous, while oral steroids would have the effect of “poking the bear.”

“The bear’s name is antibody-mediated NMOSD and MOG. … Do not give oral steroids — that is poking the bear,” he said.

NMOSD is misdiagnosed as MS in 50% of cases, and this is a concern because urgent diagnosis and treatment make a difference in NMOSD, Lee said. If not treated promptly, within 10 months a relapse will occur in half of cases, and within 25 months, 80% of patients will progress to transverse myelitis, which can lead to paralysis, blindness and death.

Against

Dan Milea, MD, PhD, agreed with Lee’s point that high doses of IV steroids are beneficial in most cases of optic neuritis. Most, but not all, “because as Andy said, there’s the bad and the ugly, but there is somebody else in the game: the bad, the ugly and the horrible,” Milea said. “The horrible is infection, and steroids on an infection are not good.”

Dan Milea, MD, PhD,

Dan Milea

He described the case of a 27-year-old patient with bilateral, painless, rapidly progressing vision loss and questionable optic disc swelling. The patient was treated with steroids, and vision decreased further. OCT showed he had central serous retinopathy induced by steroids.

“It’s an exceptional case after 3 days to have central serous due to steroids, but it has been described. And guess what? Did this help him? Not really because the diagnosis was not even optic neuritis, and the patient did not improve but got worse. The final diagnosis was Leber’s hereditary optic neuropathy, and we know that 30% of patients with Leber’s neuropathy get steroids for nothing or just for an encounter with the horrible,” Milea said.

Toxoplasmosis is another entity that is not usually investigated up-front because it is not a common cause of optic neuritis, “but the Jensen’s visual field defect could put you on the track,” he said. Steroids are not ideal when dealing with toxoplasmosis.

For all the good reasons explained by Lee, there is a current shift toward steroids for optic neuritis, but it should never be “always,” Milea said.

“Remember, steroids can be harmful and can increase the risk of infection, central serous retinopathy and more,” he said.

References:

  • Beck RW, et al. N Engl J Med. 1992;doi:10.1056/NEJM199202273260901.
  • Beekman J, et al. Neurol Neuroimmunol Neuroinflamm. 2019;doi:10.1212/NXI.0000000000000580.
  • Huda S, et al. Clin Med (Lond). 2019;doi:10.7861/clinmedicine.19-2-169.
  • Jarius S, et al. J Neurol. 2023;doi:10.1007/s00415-023-11634-0.
  • Matiello M, et al. Neurology. 2008;doi:10.1212/01.wnl.0000303817.82134.da.
  • Smith AD, et al. Mult Scler Relat Disord. 2023;doi:10.1016/j.msard.2023.104498.
  • Stiebel-Kalish H, et al. Neurol Neuroimmunol Neuroinflamm. 2019;doi:10.1212/NXI.0000000000000572.
  • Weinshenker BG, et al. Ann Neurol. 2006;doi:10.1002/ana.20770.
  • Zoric L, et al. Medicina (Kaunas). 2024;doi:10.3390/medicina61010007.


Source link

Share This Article
error: Content is protected !!