Optic Neuritis in Pregnancy

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Article initiated by:

Andrew Go Lee, MD, Jennifer Dunnigan, Michael Y Zhao, Tala Al Shawa, Vikas Dodda, Kameron Spanburg, Saif Aldeen Alryalat, MD, Osama Al Deyabat, MBBS, Sanjana Jaiswal

All contributors:

Nagham Al-Zubidi, MD, Sanjana Jaiswal

Assigned editor:

Noor Laylani, MD

Review:

Assigned status Up to Date

 by Noor Laylani, MD on July 28, 2025.

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Contributing Editors:	add

Optic neuritis (ON) is a vision-threatening condition that often affects women of childbearing age. This article will review the diagnosis, evaluation, and management of optic neuritis in pregnancy, with special attention to the physiological, hormonal, and immunological changes unique to this state. It will explore typical and atypical ON etiologies—including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD)—and their impact on pregnancy outcomes. Special focus will be placed on pregnancy-safe imaging and treatment modalities, including the use of corticosteroids, therapeutic plasma exchange, and postpartum disease-modifying therapy (DMT) considerations.

Optic Neuritis in Pregnancy

Disease

Optic neuritis (ON) is an inflammatory or demyelinating condition of the optic nerve associated with vision impairment and vision loss that often recovers but depending upon etiology may be only partially reversible or irreversible. In typical ON, there is inflammatory/demyelinating damage to the axons that can lead to death and apoptosis of the retinal ganglion cells. Although most ON is demyelinating, autoimmune, infectious, inflammatory, granulomatous, and other etiologies may produce an acute optic neuropathy.

Typical ON predominantly affects young adults with peak incidence between the ages of 30-50 years old, with a higher prevalence in females. Pregnancy is known to impose physiological stress on the body and has been associated with an increased incidence of ON in females, particularly in the postpartum period. Interestingly, women with a history of ON have increased risks of pregnancy complications including preeclampsia and preterm delivery, suggesting that the inflammatory condition can impact pregnancy outcomes. This article examines the evaluation, management, and prognosis of ON during pregnancy.

Epidemiology

Optic neuritis is the most common cause of decreased vision due to optic nerve dysfunction in adults aged 20 to 40 years. The annual incidence of new-onset ON has been reported between 0.56 and 14 cases per 100,000. Overall, the exact prevalence of ON during pregnancy remains unclear; however, recent studies are showing that women with a history of ON have a higher likelihood of experiencing ON during their pregnancy.

Pregnancy is generally considered to be an immunotolerant state through an increase in T regulatory cells which play a crucial role in maintaining immune tolerance against fetal antigens. Studies have shown that episodes of ON are more likely to occur during the postpartum period. After delivery, there is a rapid decline in hormones that stimulate immunoprotection to the fetus, allowing for remission of autoimmune disease and recurrence of ON. A review of 54 cases of pregnancy-related ON found 11 episodes (16.4%) during pregnancy and 56 (83.6%) within one year postpartum or after fetal loss including 33 (49.3%) in the first three months after birth.

Etiology

The various etiologies of ON can be broadly categorized into typical (commonly multiple sclerosis [MS]) or atypical (including antibody-associated ON) forms. As mentioned, pregnancy is one of the few medical states that may be protective against immune related ON, specifically related to MS.  Other forms of ON include neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), systemic lupus erythematosus (SLE), and Sjögren syndrome. In addition, some infectious etiologies have been linked to ON in pregnancy. Other uncommon forms of ON include chronic relapsing inflammatory optic neuropathy (CRION), glial fibrillary acidic protein (GFAP), collapsing response mediator protein 5 (CRMP5), as well as systemic causes including sarcoidosis, Behcet’s syndrome, and granulomatosis with polyangiitis.

Ocular Manifestations

The core symptoms and signs of ON in pregnancy are similar to those seen in non-pregnant patients. Clinical presentations can include any combination of acute or subacute vision loss (can be unilateral or bilateral), color vision impairment visual field loss, and a relative afferent pupillary defect. The fundus exam in retrobulbar ON is typically normal but mild optic disc edema may also occur.

Pathophysiology

During pregnancy, high levels of estrogen and progesterone hormones generally promote a Th2-dominant state to prevent fetal rejection. However, fluctuations in these hormones, particularly the rapid decline after delivery, can disrupt this balance and lead to periods of increased autoimmune activity. Specifically, the postpartum drop in estrogen and progesterone levels can reactivate suppressed Th1 and Th17 responses, triggering heightened autoimmune activity. This shift may exacerbate conditions like optic neuritis (ON), which is often associated with demyelinating diseases such as multiple sclerosis (MS). Some studies suggest that viral illnesses can also precipitate auto-immune reactions and may induce bilateral ON attacks in pregnancy.

Diagnosis

History/Signs/Symptoms

The signs and symptoms of optic neuritis in pregnancy are similar to that of ON in non-pregnant patients and may include:

●      Visual acuity and/or visual field loss (typically central or ceco-central scotomas)

●      Mild ocular pain on movement

●      Reduced color vision

●      Relative afferent pupillary defect

●      Normal optic disc or mild disc swelling

Diagnostic Procedures

●      Best-corrected visual acuity (BCVA) assessment

●      Visual field testing (e.g., automated perimetry)

●       Color vision testing (e.g., Ishihara plates)

●       Pupillary examination for a RAPD

●       Fundoscopic examination

●      Optical coherence tomography (OCT) evaluation of the retinal nerve fiber layer (RNFL)

●      Magnetic resonance imaging (MRI) of the brain and orbits with and without contrast to look for demyelinating disease and enhancement of the optic nerve

●      Lumbar puncture with cerebrospinal fluid (CSF) analysis

●      Serum aquaporin 4 (AQP4) and myelin oligodendrocytic glycoprotein (MOG) antibodies

●      Additional autoimmune testing may be indicated based on clinical presentation and history

Imaging and Electrophysiology

●      Preconception MRI can establish a baseline for patients with known MS

●      Gadolinium-enhanced MRI is recommended for ON but may not be suitable during pregnancy due to its category C teratogenic risk

●      Visual evoked potentials (VEPs) may be helpful in select cases

●      Optical coherence tomography (OCT) can assess the optic nerve

Differential Diagnosis

Other optic neuropathies can occur during pregnancy and may mimic signs and symptoms of demyelinating or inflammatory ON. Visual field testing may assist in differentiating these by revealing localizing patterns of visual field loss (e.g., junctional scotoma or junctional scotoma of Traquair (monocular hemianopic loss), bitemporal, or homonymous hemianopia). Pituitary adenomas, meningiomas, schwannomas, and pituitary apoplexy can all occur during pregnancy causing acute optic neuropathy that can mimic ON. Finally, para-ophthalmic aneurysms may mimic ON and may become symptomatic due to blood pressure and fluid shifts common in pregnancy.

Management

A non-contrast cranial MRI can still be performed safely in pregnancy even though gadolinium is not generally recommended for pregnant patients. Typically, gadolinium MRI of the brain and orbit with fat suppression is recommended for ON but if no gadolinium is advised then T2 MRI of brain can still show demyelinating white matter lesions or evaluate for structural compressive lesions (e.g., pituitary tumor).  If a diagnosis of ON is reached, corticosteroids can still be considered as first-line treatment but caution should be exercised and consultation with obstetrics obtained before the tenth week of gestation to avoid any theoretical risks of complications during organogenesis. Methylprednisolone, prednisone, and prednisolone are preferred in pregnancy as they are inactivated by placental 11-β-hydroxysteroid dehydrogenase and therefore, do not enter the fetal circulation .

Usually, once prednisolone-related drugs are degraded, approximately 10% of the total amount will ultimately reach the fetus. However, when taken in high doses and for a long period, prednisolone and methylprednisolone can saturate the placental enzymes and cross the placental barrier, causing significant suppression of the fetal glands and fetal adrenal insufficiency at birth. Additionally, repeated administration of high-dose steroids during the second and third trimester may be associated with hypertension, preeclampsia, intrauterine growth restriction, and low birth weight. Specific correlations between dosage and length of exposure are unknown.

Thus, a risk-benefit decision must be made with an obstetrics and gynecology physician (OB-GYN); if approved, a course of intravenous (IV) methylprednisolone (500-1000 mg once daily) can be given during pregnancy for three days. Typical demyelinating ON usually resolves spontaneously but IV corticosteroids can facilitate the speed of recovery. If clinically indicated (e.g., NMOSD ON) then some studies have shown that therapeutic plasma exchange represents a viable alternative form of treatment and may even have better long-term visual outcomes.

After delivery, surveillance neuroimaging should be considered within the first few months postpartum to establish a new baseline and to evaluate for silent inflammatory activity in women not resuming effective disease-modifying therapies (DMTs) early. In this post-pregnancy period, gadolinium contrast may be used as it is considered compatible with breastfeeding. Exclusive breastfeeding appears to be protective against MS relapse in the early postpartum period, however, the resumption of DMTs must be carefully monitored due to the risk of transfer through breast milk. Table 1 summarizes the risks of MS therapies in pregnancy.

Medical Therapy

Table 1: Multiple Sclerosis Therapies in Pregnancy

Drug Name	Category	Side Effects In Pregnancy	Fetal Toxicity	Compatible with Lactation	Detectable in Breast Milk? (Y/N)
Interferon Beta	Immunomodulator	Low birth weight, preterm birth weight	Unclear	Possibly	Yes
Glatiramer acetate	Immunomodulator	Injection site reactions	Low	Yes	No
Natalizumab	Anti-a4 Integrin	Anemia, thrombocytopenia	Potential risk	No	Yes
Fingolimod	Sphingosine 1-phosphate receptor modulator	Bradycardia	Yes	No	Yes
Teriflunomide	Pyrimidine synthesis inhibitor	Teratogenic, hepatotoxicity	Yes	No	Yes
Dimethyl fumarate	Nrf2 Pathway activator	Gastrointestinal issues, flushing	Unclear	Possibly	Yes
Ocrelizumab	Anti-CD20	Immunosuppression, infection risk	Unclear	Possibly	Yes
Methylprednisolone	Corticosteroid	Hypertension, gestational diabetes	Unclear	Yes	Yes
Prednisone	Corticosteroid	Gestational diabetes, hypertension	Low	Yes	Yes

Table 2: NMOSD Therapies in Pregnancy

Drug Name	Category	Side Effects in Pregnancy	Fetal Toxicity	Compatibility with Lactation	Detectable in Breast Milk?
Rituximab	Anti-CD20	Immunosuppression	Potential risk	No	Yes
Azathioprine	Immunosuppressant	Teratogenicity, leukopenia	Yes	No	Yes
Mycophenolate Mofetil	Immunosuppressant	Teratogenicity, miscarriage	Yes	No	Yes
Eculizumab	Anti-C5 Complement	Infection, anemia	Unclear	Possibly	Yes
Inebilizumab- Con	Anti-CD19	Infusion reaction, infection	Potential risk	Unknown	Unknown

Table 3: MOG-AD Therapies in Pregnancy

Drug Name	Category	Side Effects in Pregnancy	Fetal Toxicity	Compatibility with Lactation	Detectable in Breast Milk?
Rituximab	Anti-CD20	Immunosuppression	Potential risk	Not recommended	Yes
Azathioprine	Immunosuppressant	Teratogenicity, leukopenia	Yes	Yes	Yes
Intravenous Immunoglobulin	Immunomodulator	Infusion reactions	Low	Yes	Yes

Prognosis

Like ON in non-pregnant patients, signs and symptoms of typical ON in pregnancy typically improve over time. Pain with eye movement usually resolves within days to weeks. Visual acuity and color perception improve over two weeks to three months, and nearly 90% of patients achieve near-normal function by six months. Only 3% of patients have BCVA of 20/200 or worse after 5 years. Studies have demonstrated that patients with ON have a significantly lower likelihood of pregnancy and delivery compared to age-matched control demonstrating that the underlying autoimmune mechanisms, or the medications used to treat ON, have impaired impacts on fertility.

In roughly 20% of cases, ON symptoms mark the onset of MS during pregnancy. Treatment of this condition requires immunosuppressive and/or disease-modifying therapies to minimize autoimmune sequelae. Patients with ON during pregnancy should work closely with their obstetricians to discuss the careful initiation of immunosuppressive agents, as well as the cessation of treatments before stopping contraceptives if they wish to become pregnant.

Summary

ON in pregnancy can usually be managed as ON in non-pregnant patients with the exception of gadolinium for the MRI. Some cases of ON however may not be due to MS but may be seropositive for NMOSD or MOGAD. These cases pose unique challenges due to the immunological changes during pregnancy and the risks to the mother of untreated antibody mediated disease. The diagnosis of ON involves clinical evaluation, MRI if appropriate, and serum antibody testing for AQP4 (cell based assay) and MOG. Management may include observation for typical ON, or IV corticosteroids, though their use must be carefully balanced against potential risks to the fetus, and plasma exchange is an alternative for severe cases. Prognosis is generally favorable with most patients achieving significant visual recovery. However, some studies have shown that ON in pregnancy leads to an increased risk of pregnancy complications such as pre-eclampsia, preterm delivery, and delayed fetal growth. Postpartum monitoring and appropriate resumption of disease-modifying therapies are crucial to manage and prevent relapses. NMOSD and MOGAD however may require long term postpartum immunosuppression.