Optic Neuropathy after COVID-19

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Article initiated by:
Alicia Chen, Bohan Kim
All contributors:
Alicia Chen, Andrew Go Lee, MD, Bohan Kim, Nagham Al-Zubidi, MD, Noor Laylani, MD, Osama Al Deyabat, MBBS, Nagham Al-Zubidi, MD, Pamela Davila-Siliezar, MD, Osama Al Deyabat, MBBS, Sanjana Jaiswal
Assigned editor:
Osama Al Deyabat, MBBS
Review:
Assigned status Up to Date
 by Osama Al Deyabat, MBBS on October 09, 2024.


Optic neuropathy has been reported in COVID19 and although the precise mechanisms remain ill-defined, several hypotheses have been proposed including inflammatory cytokines and a transient hypercoagulable state. There are two main types of optic neuropathy observed with COVID-19: ischemic optic neuropathy (ION) and optic neuritis (ON). In cases of ischemic optic neuropathy, both anterior ION and posterior ION have been reported with COVID19. In cases of optic neuritis as well, both papillary and retrobulbar forms have been reported. Clinicians should be aware of the possibility of ION or optic neuritis in COVID19.

Background

ION

Ischemic optic neuropathy (ION) is a sudden, painless loss of vision due to an interruption of blood supply to the optic nerve[1]. ION can be classified as anterior with disc edema (AION) or posterior without disc edema (PION). AION is typically divided into arteritic (A-AION) and non-arteritic (NA-AION) etiologies[1].

Recently, cases of optic neuropathy have been reported following infection with the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the virus that causes the Corona Virus Disease-19 (COVID19)[2] [3][4][5][6][7][8][9]. Proposed mechanisms of how SARS-CoV-2 might cause ION (AION or PION) include inducing a severe inflammatory response, endothelial damage, hypercoagulable state, and hypoxemia, which leads to hypoperfusion and subsequent ischemia of the optic nerve[3] [10][11][12][13].

Typical non-COVID19 related NA-AION is associated with risk factors: (1) structural factors which make the optic nerve head susceptible to ischemic events (e.g., small cup to disc ratio or “disc at risk”) and (2) vascular factors which predispose to acute hypoperfusion of the optic nerve head (e.g., diabetes mellitus, systemic hypertension, nocturnal arterial hypotension, ischemic heart disease, anemia)[1]. Non-arteritic posterior ischemic optic neuropathy (NA-PION) is thought to have similar vascular risk factors as NA-AION, but no structural risk has been found[14]. Typical AION is the common presentation, while PION is rare[14].

Optic Neuritis

Optic neuritis (ON) is an inflammatory demyelinating optic neuropathy causing acute uniocular or binocular loss of vision.[15] ON is mainly a clinical diagnosis based on history and examination findings (e.g., decreased VA, RAPD, dyschromatopsia, optic nerve head edema/atrophy), as well as investigations such as magnetic resonance imaging (MRI) (e.g., demonstrating post-contrast enhancement in the optic nerve/sheath), optical coherence tomography (OCT) (e.g., swelling of the RNFL), and lumbar puncture. The association of ON ranges from several infectious etiology (viral, bacterial, parasitic and fungal) to primary demyelination (MS, NMO spectrum disorders, MOGAD) as well as secondary demyelinating etiologies (sarcoidosis, SLE, Sjogren, PAN, Behcet, vasculitis). In reported cases of COVID-19 associated optic neuritis, both papillary (accompanying with optic disc edema) and retrobulbar forms (enhancement in the posterior portion of optic neuritis) were seen. Interestingly, inflammatory orbital apex syndrome (e.g., pain/restriction with EOM) accompanied some reported cases of COVID-19 associated optic neuritis.[16]

Once the diagnosis is established , the treatment typically follows the recommendations of the Optic Neuritis Treatment Trial (ONTT) protocol. [17] It is not clear if the ONTT guidelines however would apply to COVID19 related ON. Neurotropism of the virus was postulated as one of the mechanisms for neuro-ophthalmic manifestations. [18] Another mechanism involves molecular mimicry where the viral antigens trigger host immune response directed toward the central nervous system (CNS) myelin proteins.[19]

Pathophysiology of COVID-19-related ION

ION

The coronavirus has been reported to cause activation of inflammatory cells (e.g. neutrophils and monocytes) and endothelial cells leading to high levels of circulating inflammatory cytokines (e.g., CRP, ferritin, IL-2, TNF-α) and excess production of pro-coagulants (e.g., tissue factor and von Willebrand factor)[3] [11]. Extensive complement involvement and membrane attack complex-mediated microvascular endothelial cell injury have also been reported to lead to COVID19-associated coagulopathy, which can include venous, arterial, and microvascular thrombosis[12][13]. COVID19 has also been reported to cause clinically significant hypoxemia[14].

In ION, it has been hypothesized that these factors in COVID19 (inflammatory response, hypercoagulable state, and hypoxemia) may lead to thrombosis of the blood vessels (e.g., ciliary vessels) supplying the optic nerve and subsequent ischemia of the optic nerve[2][3][4][5][7][8][9]. However, there have been no studies to confirm this pathogenesis.

Savastano et al. reported the impact of SARS-CoV-2 infection on the microvascular network of optic nerve head in patients who recovered from COVID19. The study reported that in the patients who recovered from COVID19, there was an impairment in the blood supply to the peripapillary retinal nerve fiber layer, characterized by a reduction of radial peripapillary capillary plexus (RPCP) density. RPCP density has been previously correlated to visual acuity and visual field loss in NAION patients[20].

Optic Neuritis

COVID-19-related ON is thought to result from an autoimmune reaction triggered by SARS-CoV-2, leading to demyelination. The neurotropism of the SARS-CoV-2 virus, although poorly understood, is believed to involve pathways such as crossing the blood-brain barrier or transport via infected leukocytes. [21] Parainfectious and postinfectious demyelination has been described in other neurological conditions related to COVID-19, such as Guillain-Barré syndrome and acute transverse myelitis.[22][23] Negative RT-PCR results in cerebrospinal fluid (CSF) do not necessarily exclude CNS infection, as testing for SARS-CoV-2 in CSF remains unreliable in clinical settings.

The immune response in ON may also involve molecular mimicry, in which viral antigens trigger an autoimmune reaction against self-proteins, particularly myelin, potentially explaining the demyelination observed in COVID-19-associated ON. [19] Another mechanism includes the production of MOG-IgG antibodies, as seen in MOGAD, where antibodies target oligodendrocytes, potentially following SARS-CoV-2 infection.[24] This immune response is believed to involve T-cells and complement fixation, causing demyelination once these antibodies cross the blood-brain barrier.

COVID-19-associated ON can be either parainfectious, as seen in cases where the patient was asymptomatic or mildly symptomatic, or postinfectious, occurring days to weeks after recovery. In cases involving recent infection or vaccination, the pathophysiology may vary, as seen in one patient who developed ON soon after receiving a COVID-19 booster.[25] The rapid onset of symptoms in this case, compared to previously reported cases, suggests that the combination of recent infection and vaccination may have led to a heightened immune response. The association between COVID-19 and ON is further complicated by reports of other COVID-related ocular events, such as retinitis and uveitis, seen in conjunction with ON. [26]

Case Reports of Presumed ION after COVID-19 Infection

Case Sex Age Past Medical History Ophthalmic Symptoms Physical Exam Labs Diagnosis
1[2] F 50 HTN, HLD Acute, painless vision loss OD; 1 week after testing positive for COVID 20/70 OD. Temporal and inferior nasal field loss OD.

No RAPD. Normal fundoscopic exam with no optic disc edema.

Normal CBC, BMP, ESR. CRP 7 and d dimer 206 ng/ml. PION
2[3] M 52 None Acute, painless vision loss and floater OD; 2 weeks after COVID hospitalization Hand motion perception OD. RAPD OD. Central and nasal field loss OD.

Pale optic disc without swelling OD, small optic disc OS.

ESR 42 (high), CRP 39 (high). Lymphopenia (WBC 6800/ul; lymphocyte: 11.5%) NAION
3[4] M 43 DM, HLD Acute, painless vision loss OD; 4 weeks after COVID symptoms and testing positive 20/30 OD. RAPD OD. Inferior hemifield defect OD. Temporal pallor of optic nerve OD. Normal CBC, ESR, BMP. NAION
4[5] M 45 DM, HTN Acute, blurry vision OD followed by blurry vision OS 2 weeks later; started 1 month after COVID-19 infection 6/6 OD, 6/24 OS. RAPD OS. Inferior field defect OS. Superior and inferior field defects OS. Hyperemic optic disc with blurred margins (OD), pale edematous disc (OS). Normal CBC, ESR, BMP. Bilateral sequential NAION
5[6] F 67 CAD s/p PCI 7 years ago, HTN Decreased vision OS preceded by 2-day headache; tested positive for Sars-CoV-2 2 days later 20/800 OS (with dense posterior subcapsular cataract). No RAPD. Superior visual field loss OS. Normal labs NAION
6[7] F 69 DM, HTN Vision loss OS with severe headaches near eyes and occiput, and scalp tenderness; 2.5 weeks after positive SARS-CoV-2 test Light perception from nasal and superior side OS. No direct response and slow indirect response to light OS. Blurring of optic margins with flame hemorrhages OS. Elevated ESR (63 mm/h; range, 3-15 mm/h). Ultrasound of temporal arteries revealed wall thickening and a “halo.” GCA/AAION
7[8] M 72 DM, HTN, smoking Acute, painless, blurred vision OD; 13 days after COVID-19 symptoms 0.3 OD. No RAPD. Inferior visual field loss OD. Optic disc swelling OD. Normal labs NAION
8[9] M 64 None Vision loss OD; 5 weeks after COVID-19 symptoms and hospitalization 20/20 OD. RAPD OD. Inferior visual field loss OD. Pale optic disc with sectorial papillary edema OD Normal labs NAION

Case Reports of Presumed Optic Neuritis after COVID19 Infection

Case Sex Age Past Medical History Ophthalmic Symptoms Physical Exam Labs & Imaging Diagnosis & Management & F/U
1[27] F 30 None Headache, low vision. Symptoms started four days after  positive PCR,  vaccinated year ago. 20/640 OS, RAPD OS, mild disc edema OS, Edema and leakage on OCT and FFA, HVF Completedly Closed OS on 24-2 MRI- linear enhancement 3 Days of IV steroid, then oral steroid. Two weeks F/U, marked reduction in disc edema and 20/32 VA
2[25] F 58 None Bilateral eye pain,  within two hours of receiving COVID booster vaccine. Pain with eye movement. Three weeks ago, mild case confirmed by rapid antigen. VA 20/20, no RAPD, L HT on R gaze, -3 deficit on supraduction on R eye, Mild nasal and inferior ON rim elevation without swelling, OCT, HVF normal R Optic Nerve enhancement, Full lab work up for ON negative 3-day course of intravenous methylprednisolone 250 mg every six hours for right mild optic neuritis.
3[16] M 16 None Decreased vision in L eye, pain with EOM. + PCR for COVID 2 weeks prior LP on OS, RAPD on L eye, Normal optic disc and no disc edma both eyes None Retrobulbar neuritis
4[16] M 35 None Sudden Vision Loss and Pain with EOM in L eye. + PCR 6 months ago 20/600 LE, RAPD in L eye, Disc edema w blurred margins and peripallipary, Edema on OCT None Papillary optic neuritis
5[16] M 38 None Sudden loss of vision and pain on EOM in the L eye for 5 days. + PCR 1.5 months prior HM OS, RAPD OS, Normal Discs None Retrobulbar neuritis
6[26] F 8 mo None Loss of parallelism in OU, High Viral Titer, Mother diagnosed 2 wks ago ET OS, bilateral disc edema T2 hyperintensity of the intraorbital part of both optic nerves Injectable pulse methylprednisolone therapy (15 mg/kg/day for 3 days) followed by a tapering dose of oral prednisolone initiated at 1 mg/kg
7[26] F 21 None Progressive dimness of vision in her right eye associated with periorbital pain on EOM 3/60 OD, RAPD, disc edema R eye Post-contrast enhancement of the intraorbital part of right optic nerve, NMO/MOG neg IV methylprednisolone for 3 days followed by a tapering dose of oral prednisolone (1 mg/kg/day), after which she had a partial recovery and was followed up after 3 weeks with a visual acuity of 6/60 in her right eye
8[26] M 16 None Sudden onset color desaturation followed by blurring of vision in his left eye which progressed to an extent of near blindness within a week. + rPCR COVID-19 LP OD, RAPD, disc edema Post-contrast enhancement of optic nerve was seen on imaging Oral steroids following pulse methylprednisolone therapy and achieved a vision of 6/60 in left eye after 4 weeks of follow-up.


Treatment

ION

While there are no definite treatments for NAION, the underlying cause should be treated to prevent further complications. Risk factors for atherosclerosis should be controlled, including blood pressure and diabetes[28]. Most of the recommended treatments are intended to prevent thrombosis (e.g., aspirin) or reduce the edema of the optic disc [6]. While corticosteroids can lead to improvement in systemic symptoms and prevention of blindness in arteritic ION/giant cell arteritis (GCA), corticosteroids are not suggested for NAION[29]. In the context of COVID19, the benefits of steroids have not been explored[6].

Optic Neuritis

The treatment of ON typically involves high-dose corticosteroids, initiated as soon as possible after diagnosis to prevent further optic nerve damage. In reported COVID-19-related ON cases, pulse methylprednisolone followed by oral prednisone taper has been the standard approach, leading to gradual improvement of vision. [30][27][16]

Prognosis

About 40% of patients with non-COVID19 related NAION will spontaneously recover some vision[28]. The prognosis for COVID-19-related ON, like other forms of ON, is typically favorable with appropriate treatment. Visual recovery is usually good with the early use of high-dose corticosteroids, such as pulse methylprednisolone followed by tapering doses of oral steroids. However, the exact pathogenesis remains elusive, especially in distinguishing between parainfectious and postinfectious ON. Continued follow-up is crucial to monitor for other neurological complications or the onset of demyelinating diseases in the future. While COVID-19’s role in causing ON and other neurological conditions is still being explored, it is clear that the virus can trigger significant immune responses that may lead to demyelination.

Summary

Optic neuropathy has been increasingly reported in COVID-19 patients, although the exact mechanisms remain unclear. Two primary types of optic neuropathy are observed: ischemic optic neuropathy (ION), including both anterior (AION) and posterior (PION) forms, and optic neuritis (ON). Proposed mechanisms for these COVID-19-associated optic neuropathies include an inflammatory response, endothelial damage, hypercoagulable states, and hypoxemia. Despite this, the ischemic origin of ION in COVID-19 patients is not yet fully confirmed, and further studies are needed to clarify the pathogenesis and explore potential treatments.

In typical AION, differentiating between arteritic (e.g., giant cell arteritis, GCA) and non-arteritic AION (NAION) presents a diagnostic challenge, particularly in the context of COVID-19, where elevated inflammatory markers such as ESR, CRP, and platelet counts might be mistaken for signs of GCA. Thorough evaluation, including temporal artery biopsy, remains essential, particularly in elderly patients. It is possible that some reported cases of AION in COVID-19 may be coincidental rather than causal, potentially attributable to underlying GCA.

Clinicians should maintain awareness of the potential for both ION and ON in COVID-19 patients. While treatments such as corticosteroids have shown promise in managing optic neuritis, no definitive treatments for NAION in COVID-19 have been established. Ongoing research is crucial to better understand the relationship between COVID-19 and optic neuropathies and to guide future therapeutic strategies.

References

  1. ↑ 1.0 1.1 1.2 Hayreh S. S. (2011). Management of ischemic optic neuropathies. Indian journal of ophthalmology, 59(2), 123–136. https://doi.org/10.4103/0301-4738.77024
  2. ↑ 2.0 2.1 2.2 Selvaraj V, Sacchetti D, Finn A, Dapaah-Afriyie K. (2020). Acute Vision Loss in a Patient with COVID-19. Rhode Island Medical Journal, 103(6), 37-38.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Golabchi, K., Rezaee, A., Aghadoost, D., & Hashemipour, M. (2021). Anterior ischemic optic neuropathy as a rare manifestation of COVID-19: a case report. Future virology, 10.2217/fvl-2021-0068. https://doi.org/10.2217/fvl-2021-0068
  4. ↑ 4.0 4.1 4.2 Rho, J., Dryden, S. C., McGuffey, C. D., Fowler, B. T., & Fleming, J. (2020). A Case of Non-Arteritic Anterior Ischemic Optic Neuropathy with COVID-19. Cureus, 12(12), e11950. https://doi.org/10.7759/cureus.11950
  5. ↑ 5.0 5.1 5.2 Sanoria, A., Jain, P., Arora, R., & Bharti, N. (2022). Bilateral sequential non-arteritic optic neuropathy post-COVID-19. Indian journal of ophthalmology, 70(2), 676–679. https://doi.org/10.4103/ijo.IJO_2365_21
  6. ↑ 6.0 6.1 6.2 6.3 Babazadeh, A., Barary, M., Ebrahimpour, S., Sio, T. T., & Mohseni Afshar, Z. (2022). Non-arteritic anterior ischemic optic neuropathy as an atypical feature of COVID-19: A case report. Journal francais d'ophtalmologie, 45(4), e171–e173. https://doi.org/10.1016/j.jfo.2021.12.001
  7. ↑ 7.0 7.1 7.2 Szydełko-Paśko, U., Przeździecka-Dołyk, J., Kręcicka, J., Małecki, R., Misiuk-Hojło, M., & Turno-Kręcicka, A. (2022). Arteritic Anterior Ischemic Optic Neuropathy in the Course of Giant Cell Arteritis After COVID-19. The American journal of case reports, 23, e933471.
  8. ↑ 8.0 8.1 8.2 Yüksel, B., Bıçak, F., Gümüş, F., & Küsbeci, T. (2021). Non-Arteritic Anterior Ischaemic Optic Neuropathy with Progressive Macular Ganglion Cell Atrophy due to COVID-19. Neuro-ophthalmology (Aeolus Press), 46(2), 104–108.
  9. ↑ 9.0 9.1 9.2 Moschetta, L., Fasolino, G., & Kuijpers, R. W. (2021). Non-arteritic anterior ischaemic optic neuropathy sequential to SARS-CoV-2 virus pneumonia: preventable by endothelial protection?. BMJ case reports, 14(7), e240542. https://doi.org/10.1136/bcr-2020-240542
  10. ↑ Kaur, S., Bansal, R., Kollimuttathuillam, S., Gowda, A. M., Singh, B., Mehta, D., & Maroules, M. (2021). The looming storm: Blood and cytokines in COVID-19. Blood reviews, 46, 100743. https://doi.org/10.1016/j.blre.2020.100743
  11. ↑ 11.0 11.1 Magro, C., Mulvey, J. J., Berlin, D., Nuovo, G., Salvatore, S., Harp, J., Baxter-Stoltzfus, A., & Laurence, J. (2020). Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases. Translational research : the journal of laboratory and clinical medicine, 220, 1–13. https://doi.org/10.1016/j.trsl.2020.04.007
  12. ↑ 12.0 12.1 Goshua, G., Pine, A. B., Meizlish, M. L., Chang, C. H., Zhang, H., Bahel, P., Baluha, A., Bar, N., Bona, R. D., Burns, A. J., Dela Cruz, C. S., Dumont, A., Halene, S., Hwa, J., Koff, J., Menninger, H., Neparidze, N., Price, C., Siner, J. M., Tormey, C., … Lee, A. I. (2020). Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study. The Lancet. Haematology, 7(8), e575–e582. https://doi.org/10.1016/S2352-3026(20)30216-7
  13. ↑ 13.0 13.1 Tobin, M. J., Laghi, F., & Jubran, A. (2020). Why COVID-19 Silent Hypoxemia Is Baffling to Physicians. American journal of respiratory and critical care medicine, 202(3), 356–360. https://doi.org/10.1164/rccm.202006-2157CP
  14. ↑ 14.0 14.1 14.2 Sadda SR, Nee M, Miller NR, Biousse V, Newman NJ, Kouzis A. (2001). Clinical spectrum of posterior ischemic optic neuropathy. American Journal of Ophthalmology, 132(5):743-750.
  15. ↑ Abel A, McClelland C, Lee MS. Critical review: Typical and atypical optic neuritis. Surv Ophthalmol 2019;64:770‑9.
  16. ↑ 16.0 16.1 16.2 16.3 16.4 Jossy A, Jacob N, Sarkar S, Gokhale T, Kaliaperumal S, Deb AK. COVID-19-associated optic neuritis - A case series and review of literature. Indian J Ophthalmol. 2022;70(1):310-316. doi:10.4103/ijo.IJO_2235_21
  17. ↑ Beck RW. The optic neuritis treatment trial. Arch Ophthalmol. 1988;106:1051‑3.
  18. ↑ Sen M, Honavar SG, Sharma N, Sachdev MS. COVID‑19 and eye: A review of ophthalmic manifestations of COVID‑19. Indian J Ophthalmol 2022;70:488‑509.
  19. ↑ 19.0 19.1 Alomari SO, Abou‑Mrad Z, Bydon A. COVID‑19 and the central nervous system. Clin Neurol Neurosurg 2020;198:106116. doi: 10.1016/j.clineuro.2020.106116
  20. ↑ Savastano, A., Crincoli, E., Savastano, M. C., Younis, S., Gambini, G., De Vico, U., Cozzupoli, G. M., Culiersi, C., Rizzo, S., & Gemelli Against Covid-Post-Acute Care Study Group (2020). Peripapillary Retinal Vascular Involvement in Early Post-COVID-19 Patients. Journal of clinical medicine, 9(9), 2895. https://doi.org/10.3390/jcm9092895
  21. ↑ Ellul MA, Benjamin L, Singh B, Lant S, Michael BD, Easton A, et al. Neurological associations of COVID-19. Lancet Neurol. 2020;19(9):767–83. https://doi.org/10.1016/S1474-4422(20)30221-0.
  22. ↑ Sedaghat Z, Karimi N. Guillain Barre syndrome associated with COVID-19 infection: a case report. J Clin Neurosci. 2020;76:233–5. https://doi.org/10.1016/j.jocn.2020.04.062.
  23. ↑ Chakraborty U, Chandra A, Ray AK, Biswas P. COVID-19-associated acute transverse myelitis: a rare entity. BMJ Case Rep. 2020;13(8): e238668. https://doi.org/10.1136/bcr-2020-238668.
  24. ↑ Chen JJ, Bhatti MT. Clinical phenotype, radiological features, and treatment of myelin oligodendrocyte glycoprotein-immunoglobulin G (MOG-IgG) optic neuritis. Curr Opin Neurol. 2020;33(1):47–54. https://doi.org/10.1097/WCO.0000000000000766.
  25. ↑ 25.0 25.1 Zhang J, Joiner D, Zhang C. Hyperacute optic neuritis in a patient with COVID-19 infection and vaccination: a case report. BMC Ophthalmol. 2023;23(1):80. Published 2023 Feb 28. doi:10.1186/s12886-023-02825-4
  26. ↑ 26.0 26.1 26.2 26.3 Chakraborty, U., Chaudhuri, J., Datta, A.K. et al. COVID-19 and optic neuritis: a series of three cases and a critical review. Egypt J Neurol Psychiatry Neurosurg 59, 172 (2023). https://doi.org/10.1186/s41983-023-00772-x
  27. ↑ 27.0 27.1 Duran M, Aykaç S. Optic neuritis after COVID-19 infection: A case report. J Fr Ophtalmol. 2023;46(1):e4-e7. doi:10.1016/j.jfo.2022.09.005
  28. ↑ 28.0 28.1 Garrity, J. (2021). Ischemic Optic Neuropathy. Merck Manual. https://www.merckmanuals.com/home/eye-disorders/optic-nerve-disorders/ischemic-optic-neuropathy
  29. ↑ Aiello, P. D., Trautmann, J. C., McPhee, T. J., Kunselman, A. R., & Hunder, G. G. (1993). Visual prognosis in giant cell arteritis. Ophthalmology, 100(4), 550–555. https://doi.org/10.1016/s0161-6420(93)31608-8
  30. ↑ Azab MA, Hasaneen SF, Hanifa H, Azzam AY. Optic neuritis post-COVID-19 infection. A case report with meta-analysis. Interdiscip Neurosurg. 2021;26:101320. doi:10.1016/j.inat.2021.101320
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