Optic neuritis means inflammation of the optic nerve, the “cable” that carries pictures from your eye to your brain. When this nerve gets inflamed, vision drops—often over hours to a few days—and colors look faded. Many people also feel a dull ache behind the eye, which gets worse when the eye moves. The optic nerve is part of the brain, so this is a neurologic problem, not a problem with glasses or the front of the eye.

Optic neuritis is inflammation of the optic nerve, the cable that carries visual signals from your eye to your brain. Inflammation makes this cable “swollen and irritable,” so vision from the affected eye becomes blurry or dim, colors (especially red) look washed-out, and moving the eye can hurt. Symptoms usually worsen over hours to a few days, and then—after the attack calms down—vision often gradually improves over weeks to months. Most people recover good visual acuity, though subtle problems (contrast or color) can linger. These features are the same in pregnancy, but some tests and medicines must be chosen more carefully to keep the baby safe. NCBI

Pregnancy changes the immune system. During pregnancy, the body usually becomes more tolerant to protect the baby; right after delivery, the immune system rebounds to its usual strength. Because of this swing, some immune-based problems that affect the optic nerve are quieter during pregnancy and more active in the first months after birth. This pattern is well known in multiple sclerosis (MS), where attacks drop during pregnancy and increase in the first 3 months postpartum before returning to baseline. PubMed

Not all optic neuritis is the same. In many people it’s related to demyelination (loss of the nerve’s insulating covering), as seen in typical “MS-type” optic neuritis. In others, antibodies against AQP4 (in NMOSD) or against MOG (in MOG-associated disease) drive the attack; these forms can behave differently in pregnancy. For example, NMOSD does not get the same protective effect during pregnancy and can relapse during pregnancy or after delivery unless the immune system is kept controlled. PubMedPMC
Safe diagnostic choices in pregnancy include MRI without contrast and noninvasive eye scans like OCT; gadolinium dye is generally avoided in pregnancy, and breastfeeding does not need to be stopped if gadolinium is given after birth. ACOG


Types of optic neuritis in pregnancy

These are practical buckets doctors use so they can plan tests and next steps. A single person’s case can fit more than one bucket.

  1. Typical demyelinating optic neuritis (MS-pattern).
    Short history (hours–days), eye pain with movement, color wash-out, a central blurry spot, and often a normal-looking optic disc at first (“retrobulbar” neuritis). Pregnancy tends to reduce MS activity; relapse risk increases in the early postpartum period. PubMed

  2. AQP4-positive optic neuritis (NMOSD).
    Can be severe, sometimes bilateral, and may involve long segments of the optic nerve. Pregnancy does not reliably protect against relapses; careful prevention around pregnancy and postpartum is important. PubMedPMC

  3. MOG-antibody–associated optic neuritis (MOGAD).
    Often shows disc swelling, can be bilateral, and may occur during or shortly after pregnancy. Vision often improves with steroids but relapses can occur. EyeWikiPMC

  4. Infectious optic neuritis/neuroretinitis.
    Due to germs such as syphilis, Lyme disease, tuberculosis, herpes viruses, varicella-zoster or Bartonella (cat-scratch). Needs targeted antibiotic or antiviral treatment once diagnosed.

  5. Autoimmune/systemic-inflammatory optic neuritis.
    Part of conditions like sarcoidosis, lupus (SLE), Behçet disease, granulomatosis with polyangiitis.

  6. Post-infectious (para-infectious) optic neuritis.
    Inflammation after a recent viral illness (immune system reacts after the infection rather than the germ directly causing damage).

  7. Chronic relapsing inflammatory optic neuropathy (CRION).
    Recurrent optic neuritis that responds to steroids but tends to relapse when steroids are tapered.

  8. Anatomic pattern: “retrobulbar” vs. “papillitis.”
    Retrobulbar = nerve looks normal at first; papillitis = optic disc is swollen on exam.

  9. Laterality: unilateral vs. bilateral.
    One eye vs both eyes—AQP4 and MOG disease are more likely to be bilateral.

  10. Timing: during pregnancy vs postpartum.
    Many immune-mediated cases cluster postpartum due to immune rebound. PubMed


Causes

These are possible causes or associated conditions doctors think about; tests are needed to sort them. Some are common; some are rare. The list mixes “diseases” and “triggers” because both matter in real life.

  1. Typical demyelinating optic neuritis (idiopathic MS-pattern).
    The immune system attacks myelin on the optic nerve; pregnancy often calms it, postpartum can flare it. PubMed

  2. Multiple sclerosis (MS).
    Optic neuritis can be the first sign of MS or a relapse in someone with MS. PubMed

  3. Neuromyelitis optica spectrum disorder (AQP4-IgG–positive).
    An antibody-driven disease that often relapses during pregnancy or postpartum without prevention. PubMed

  4. MOG-antibody–associated disease (MOGAD).
    Often disc-swelling optic neuritis, sometimes starting in or after pregnancy. EyeWiki

  5. Post-viral immune reaction.
    After a cold or flu-like illness, the immune system temporarily misfires and attacks the optic nerve.

  6. Varicella-zoster virus.
    The shingles virus can inflame the optic nerve or nearby tissues.

  7. Herpes simplex virus.
    Can cause optic neuritis, usually with other eye or neurologic signs.

  8. Syphilis.
    A bloodstream infection that can silently reach the eye and optic nerve; always test because it changes treatment completely.

  9. Lyme disease.
    Bacterial infection from ticks; can affect the optic nerve or mimic other patterns.

  10. Tuberculosis.
    Infection can involve the coverings of the brain and optic pathways or trigger immune inflammation.

  11. Sarcoidosis.
    Granulomas (tiny immune clusters) can affect the optic nerve or the brain covering around it.

  12. Systemic lupus erythematosus (SLE).
    Immune inflammation of small vessels can affect the optic nerve.

  13. Behçet disease.
    Blood-vessel inflammation can involve the optic nerve as part of broader eye inflammation.

  14. Granulomatosis with polyangiitis (ANCA-associated vasculitis).
    Vessel inflammation can reduce blood supply and trigger immune damage around the optic nerve.

  15. CRION (chronic relapsing inflammatory optic neuropathy).
    Recurrent, steroid-responsive optic neuritis that relapses when steroids are reduced.

  16. Bartonella henselae (cat-scratch) neuroretinitis.
    Inflamed optic nerve with a star-shaped pattern in the macula; needs antibiotics.

  17. Toxoplasma or other parasites (rare).
    Usually retinal disease, but nearby inflammation can involve the nerve.

  18. Medication-related immune optic neuritis (rare).
    Very uncommon reactions to immune-modulating drugs or checkpoint inhibitors can inflame the optic nerve.

  19. Toxic/nutritional optic neuropathy that mimics neuritis.
    Low B12 or toxins (e.g., methanol) usually cause a different type of nerve damage, but they are checked because they can look similar at first.

  20. Pressure or structural problems that mimic neuritis.
    A mass near the optic nerve or severe swelling of brain pressure (papilledema) can look like neuritis early on; tests separate them.


Common symptoms and signs

  1. Blurred or dim vision in one eye (sometimes both).

  2. Pain behind the eye, worse with eye movement.

  3. Washed-out colors, especially red looks pale (color desaturation).

  4. Central blurry or dark spot (central or cecocentral scotoma).

  5. Reduced contrast—gray looks the same as black or white.

  6. Edges look fuzzy or letters fade when reading.

  7. Flashes or flicker with eye movement (less common).

  8. Worse vision when hot or after exercise (Uhthoff phenomenon).

  9. Depth perception problems—harder to pour water or park a car.

  10. Headache or brow ache on the affected side.

  11. Tenderness when pressing gently around the eye.

  12. Colors look different between eyes when you compare them.

  13. Light seems dimmer in the affected eye (brightness mismatch).

  14. Pupil reacts differently to light (a doctor sees a relative afferent pupillary defect).

  15. Swollen optic disc on exam if the front of the nerve is inflamed (papillitis); the nerve can also look normal early in retrobulbar neuritis.


Diagnostic tests

Doctors pick tests based on your story and exam. In pregnancy, they choose tests that are safe for you and the baby. MRI without contrast is preferred; if contrast is ever truly needed, experts limit gadolinium in pregnancy, and breastfeeding does not need to be stopped after gadolinium is given postpartum. ACOG

A) Physical-exam–based eye and neurologic tests

  1. Visual acuity (distance and near)
    Reading letters on a chart (and a near card) shows how sharp your vision is and tracks recovery over time.

  2. Color vision (Ishihara plates or D-15 test)
    These spot red-green weakness that is very common in optic neuritis; it’s an easy way to measure improvement.

  3. Pupil exam and the “swinging flashlight” test
    The doctor looks for a relative afferent pupillary defect (RAPD), which points to optic nerve trouble on one side.

  4. Confrontation visual fields
    You look straight ahead while the examiner brings small targets in from the sides; it roughly maps blind spots and field cuts.

  5. Fundus (dilated) exam
    A bright light and lenses let the doctor look at the optic nerve for swelling (papillitis) or pallor; in “retrobulbar” neuritis the nerve can look normal early on.

  6. Eye movement exam
    Looking in all directions checks for pain with movement and rules out double vision from muscle or brainstem problems.

B) “Manual” bedside checks you can often do in clinic without machines

  1. Red-cap desaturation test
    You look at a red object with each eye; if the affected eye sees “pink” instead of red, that supports optic nerve dysfunction.

  2. Brightness comparison test
    A simple lamp is alternated between eyes; the inflamed eye often sees dimmer light.

  3. Amsler grid
    A small square grid helps find central distortions or spots that align with your scotoma.

  4. Contrast-sensitivity chart (e.g., Pelli-Robson)
    Measures how well you see faint gray letters; this is often reduced in optic neuritis even when vision lines improve.

  5. Photostress recovery test
    A bright light briefly bleaches photoreceptors; slow recovery suggests macular disease, while normal recovery supports an optic-nerve problem—helpful to separate look-alikes.

C) Laboratory and pathological tests

  1. AQP4-IgG (aquaporin-4) blood test
    Finds NMOSD, which needs a different long-term plan and behaves differently in pregnancy. PubMed

  2. MOG-IgG blood test
    Detects MOG-associated disease, which often causes disc swelling and can debut in or near pregnancy. EyeWiki

  3. Infection screens guided by history
    Syphilis serology, Lyme testing, and TB screening (IGRA) are key when the story or exam points that way, because treatment is very specific.

  4. Autoimmune panels when needed
    ANA, ANCA, ACE (for sarcoid), and related tests help when systemic inflammation is suspected.

  5. Lumbar puncture (CSF studies) when atypical
    If the case does not fit the usual pattern, CSF can be checked for cell count, protein, oligoclonal bands, and infections; it’s reserved for special situations.

D) Electrodiagnostic tests

  1. Visual evoked potentials (VEP)
    Small scalp stickers record the brain’s response to a checkerboard pattern. Delayed signals support optic nerve demyelination. VEPs are noninvasive and considered safe in pregnancy. Hopkins Medicine

  2. Pattern electroretinogram (pERG)
    Checks macular/retinal function. A normal pERG with abnormal VEP favors an optic-nerve source rather than retina.

  3. Full-field electroretinogram (ERG)
    If the story suggests retinal disease (e.g., neuroretinitis), ERG helps separate retina problems from optic-nerve problems.

E) Imaging tests

  1. MRI of brain and orbits without gadolinium contrast
    This is the top imaging test because it shows optic nerve inflammation and looks for MS-type brain spots. MRI is the imaging of choice in pregnancy; gadolinium is usually avoided, and breastfeeding does not need to be interrupted if gadolinium is used postpartum. ACOG

  2. Orbital MRI with fat suppression (STIR or T2 fat-sat)
    Highlights the optic nerve and shows enhancement/swelling typical of neuritis.

  3. Optical coherence tomography (OCT)
    A painless light-scan that measures the retinal nerve fiber layer and ganglion-cell layer—it tracks nerve fiber loss after an attack and is safe in pregnancy. PubMed

  4. OCT angiography (OCTA)
    A dye-free scan of the retinal micro-vessels—useful when fluorescein angiography is best avoided in pregnancy. PMC

  5. Automated perimetry (formal visual-field testing)
    A computerized test that maps exact blind spots and compares them over time; it’s essential to document recovery or relapse.

Non-pharmacological treatments

Each item explains what it is, purpose, and how it helps (“mechanism,” in simple terms). These are adjuncts—not substitutes for urgent medical care if vision is dropping.

  1. Prompt specialist assessment. Purpose: rule out dangerous mimics (infection, swelling from another cause) and confirm ON. Mechanism: early diagnosis guides safe pregnancy-appropriate care. NCBI

  2. Education about red flags & recovery. Purpose: reduce anxiety and prevent delays. Mechanism: knowing that pain with eye movement and color wash-out are typical, and that improvement often takes weeks, sets expectations. NCBI

  3. Temperature management (avoid overheating). Purpose: keep vision from temporarily worsening (Uhthoff). Mechanism: heat can slow nerve conduction in demyelinated fibers; cooler showers, fans, and breathable clothing help. NCBI

  4. Vision rest and pacing. Purpose: reduce eye strain during the acute painful phase. Mechanism: frequent breaks lower discomfort.

  5. Lighting and contrast optimization. Purpose: help reading and screen tasks. Mechanism: high-contrast fonts, good ambient lighting, and dark-mode/large fonts improve signal-to-noise through a weakened nerve.

  6. Low-vision strategies (temporary). Purpose: keep you functional at work/home while vision recovers. Mechanism: larger print, audiobooks, screen readers, and magnifiers bypass contrast/color deficits.

  7. Safe driving practices. Purpose: avoid accidents during acute vision loss. Mechanism: delay driving until cleared; consider daytime driving only if legally permitted.

  8. *Eye patching for disabling light sensitivity or diplopia. ** Purpose: symptom relief in selected cases (note: classic ON is monocular, but binocular issues can co-exist). Mechanism: reduces visual conflict.

  9. Sleep optimization. Purpose: immune balance and healing. Mechanism: adequate sleep supports inflammatory recovery and pain tolerance.

  10. Stress-reduction (mindfulness/CBT). Purpose: reduce pain perception and anxiety. Mechanism: stress heightens central pain and fatigue; simple breathing or guided mindfulness helps.

  11. Gentle exercise approved by obstetrics. Purpose: mood, sleep, and metabolic health. Mechanism: improves overall resilience; avoid overheating; prefer cool indoor walks/stretching.

  12. Hydration and regular meals. Purpose: prevent fatigue and headaches that worsen visual strain. Mechanism: stable glucose and fluids support nerve function.

  13. Smoking cessation. Purpose: better nerve and vascular health; lower MS risk and relapse severity. Mechanism: toxins and oxidative stress harm myelin and blood vessels (general neuro-ophthalmic guidance).

  14. Infection prevention. Purpose: infections can trigger relapses or pseudo-relapses. Mechanism: hand hygiene, vaccinations recommended by obstetrics (inactivated vaccines), and prompt care if fever develops. (Vaccine choices are obstetric-guided.)

  15. Workplace accommodations. Purpose: maintain employment safely. Mechanism: larger monitors, high-contrast themes, extra breaks, and flexible deadlines.

  16. Sunlight & vitamin D within obstetric advice. Purpose: general immune balance (especially relevant for MS biology). Mechanism: adequate vitamin D status supports immune regulation (supplement dosing under “Dietary supplements”). (General evidence base from neurology and obstetrics; confirm levels individually.)

  17. Ergonomics for screen use. Purpose: minimize eye/neck strain. Mechanism: proper monitor height, glare control, and 20-20-20 rule.

  18. Coordination of care (neuro-ophthalmology + obstetrics ± neurology). Purpose: align imaging, labs, and treatments with pregnancy safety. Mechanism: team ensures MRI without contrast when sufficient; uses contrast only if absolutely necessary. ACOG

  19. Vision rehabilitation if recovery is incomplete. Purpose: maximize independence. Mechanism: guided training helps compensate for contrast/field deficits. NCBI

  20. Postpartum plan. Purpose: reduce higher postpartum relapse risk (especially MS/NMOSD). Mechanism: schedule early postpartum follow-up; discuss breastfeeding-compatible medications in advance. PubMed


Drug treatments used in optic neuritis

Always individualize with your neuro-ophthalmologist and obstetric team. Doses below are typical adult regimens used outside pregnancy; in pregnancy the team weighs risks/benefits, trimester, and breastfeeding plans. Do not self-treat.

  1. Intravenous methylprednisolone (IVMP)Corticosteroid, first-line for acute ON to speed recovery.
    Typical regimen: 1,000 mg IV daily for 3 days (some use 3–5 days). Timing: within the first 14 days of vision loss is ideal. Purpose: shortens time to visual recovery. Mechanism: calms immune inflammation around the optic nerve. Side effects: insomnia, mood change, high blood sugar/pressure, reflux, infection risk. Pregnancy note: high-dose steroids can be used in pregnancy when benefits outweigh risks; teams often prefer IV methylprednisolone in the 2nd/3rd trimester. (In early 1st trimester, risks and alternatives are weighed carefully.) Evidence from the Optic Neuritis Treatment Trial (ONTT) supports high-dose steroids to speed recovery. PMCNCBI

  2. Oral prednisone/prednisolone taper after IVCorticosteroid continuation.
    Typical regimen: e.g., prednisone ~1 mg/kg/day for ~11 days, then taper (protocols vary). Purpose & mechanism: continue anti-inflammatory control while the nerve settles. Important safety point: standard-dose oral prednisone alone (without the IV pulse) is not recommended because ONTT showed higher recurrence with oral-only therapy; if an oral-only route is needed, studies suggest very high-dose oral regimens (e.g., 1,250 mg/day) can be bioequivalent to IV, but pregnancy suitability must be assessed by specialists. Side effects: similar to IV steroids. PMC+1EyeWiki

  3. Gastro-protection (e.g., pantoprazole)Proton-pump inhibitor (supportive).
    Dose: common adult dose 20–40 mg daily while on high-dose steroids. Purpose: reduce steroid-related reflux/ulcer risk. Mechanism: lowers stomach acid. Side effects: headache, diarrhea; long-term use has other risks—short courses are typical. (Use only if your clinician advises.)

  4. Analgesia (paracetamol/acetaminophen)Pain control for eye-movement pain.
    Dose: as advised (avoid exceeding daily max). Mechanism: central pain relief. Pregnancy: generally considered first-line analgesic when needed at standard doses; always confirm with your obstetric clinician.

  5. Intravenous immunoglobulin (IVIG)Immunomodulator for steroid-refractory ON (selected cases).
    Typical dose: 0.4 g/kg/day for 5 days (varies). Purpose: alternative immune modulation when steroids fail or are contraindicated. Mechanism: modulates antibodies and immune signaling. Side effects: headache, thrombosis risk (rare), infusion reactions. (Evidence for ON is mixed; more often used in NMOSD/MOGAD contexts or when PLEX is unsuitable.) Wiki Journal Club

  6. Therapeutic plasma exchange (PLEX/TPE)Procedure, not a drug, but often the next step for severe, steroid-refractory ON—especially in NMOSD.
    Protocol: 5–7 exchanges over ~10–14 days. Purpose: rapidly remove harmful antibodies (e.g., AQP4-IgG). Mechanism: filters plasma to reduce pathogenic immune factors. Side effects: catheter risks, low blood pressure, infection. Pregnancy: has been used during pregnancy when necessary, with specialist teams. PubMedAjoWiley Online Library

  7. AzathioprineImmunosuppressant (for relapse prevention in NMOSD or MOGAD; not for acute ON).
    Dose: often 2–2.5 mg/kg/day (with TPMT testing and blood monitoring). Purpose: reduce future attacks. Mechanism: dampens lymphocyte DNA synthesis. Pregnancy: can be used when needed under specialist care; widely referenced in pregnancy fact sheets. Side effects: bone-marrow suppression, liver issues, infections. PMC

  8. RituximabAnti-CD20 B-cell depleter (off-label for NMOSD/MOGAD in many regions; sometimes given pre-pregnancy or postpartum).
    Dose: 1 g IV on days 1 and 15, or 375 mg/m² weekly ×4; repeat q6–12 months. Purpose: relapse prevention in antibody-mediated disease. Mechanism: depletes B-cells that make pathogenic antibodies. Pregnancy: data are limited; some clinicians avoid during pregnancy but may use pre-conception or postpartum; breastfeeding compatibility is improving in new reports—decisions are individualized. Side effects: infusion reactions, infections. MotherToBaby

  9. EculizumabComplement C5 inhibitor for AQP4+ NMOSD (attack prevention; not for acute ON itself).
    Dose: typical adult: 900 mg weekly ×4, then 1,200 mg every 2 weeks. Mechanism: blocks complement-mediated astrocyte injury. Pregnancy: case series (often in PNH and NMOSD) suggest use when benefits outweigh risks; requires meningococcal vaccination planning. Side effects: infection risk. SpringerLink

  10. Satralizumab / InebilizumabIL-6 receptor blocker / anti-CD19 (for NMOSD prevention).
    Dose: satralizumab 120 mg SC at weeks 0, 2, 4 then q4 weeks; inebilizumab 300 mg IV on days 1 & 15 then q6 months. Purpose: reduce NMOSD relapses. Pregnancy: limited data—specialist decision-making is essential. Side effects: infections; lab monitoring. SpringerLink

Important: In classic, typical ON, high-dose steroids speed recovery but do not change long-term vision, and oral prednisone alone at standard doses should be avoided because it increases recurrence. PMCEyeWiki


Dietary (molecular) supplements in pregnancy

Supplements do not treat an ON attack but support general neuro-immune and obstetric health. Always coordinate with your obstetric clinician to avoid excess or interactions with your prenatal vitamin.

  1. IodineGoal: ~220–250 mcg/day in pregnancy (often via prenatal with 150 mcg). Function/mechanism: supports maternal and fetal thyroid hormones, vital for baby’s brain development. Avoid excess iodine. Office of Dietary Supplements+1

  2. CholineGoal: 450 mg/day (many prenatals are low; eggs are rich). Function: brain and placental development; methylation. Office of Dietary SupplementsInfantRisk Center

  3. DHA (omega-3)Goal: commonly 200–300 mg DHA/day from low-mercury fish or supplements. Function: neuronal membranes, fetal eye/brain development. Follow FDA/EPA fish advice (8–12 oz/week of low-mercury fish). U.S. Food and Drug Administration

  4. Vitamin DDose: individualized to labs; many prenatals have 400–800 IU; clinicians often target higher if deficient. Function: immune regulation and bone health (mom/baby).

  5. Folate (Folic acid)Goal: 600 mcg DFE/day in pregnancy (prenatals). Function: neural tube & DNA synthesis.

  6. Vitamin B12Goal: 2.6 mcg/day (prenatal). Function: myelin and red blood cell formation; deficiency can cause optic neuropathy mimic.

  7. IronDose: as directed (commonly 27 mg/day prenatal). Function: prevent anemia-related fatigue and support oxygen delivery.

  8. Iodine-fortified salt (used moderately) — supports iodine intake; avoid overuse to keep sodium appropriate. Office of Dietary Supplements

  9. Zinc — present in prenatals; supports immune function.

  10. Lutein/Zeaxanthin (optional) — dietary carotenoids found in leafy greens/eggs that concentrate in retina; generally regarded as safe in foods; supplement use in pregnancy should be discussed with your OB.

(For 1–3, Iodine, Choline, DHA, we relied on NIH ODS and FDA/EPA resources.) Office of Dietary Supplements+1U.S. Food and Drug Administration


Regenerative” drugs & stem cells

There are no approved “regenerative” or stem-cell drugs for optic neuritis during pregnancy. However, in antibody-mediated diseases (NMOSD/MOGAD), clinicians sometimes use immune-modifying therapies before pregnancy or postpartum to prevent future attacks. During pregnancy, choices are highly individualized:

  1. Rituximab (anti-CD20). Typical adult: 1 g IV day 1 & 15 or 375 mg/m² ×4; used for relapse prevention (often pre-pregnancy or postpartum). Limited pregnancy data; breastfeeding compatibility improving in recent evidence. MotherToBaby

  2. Eculizumab (C5 inhibitor). Adult: 900 mg weekly ×4 then 1,200 mg q2wk; prevents NMOSD relapses; used in selected pregnancies when benefits outweigh risks; vaccination planning required. SpringerLink

  3. Inebilizumab (anti-CD19). Adult: 300 mg day 1 & 15 then q6mo; limited pregnancy data—specialist decision. SpringerLink

  4. Satralizumab (IL-6R blocker). Adult: 120 mg SC at weeks 0, 2, 4 then q4wk; limited pregnancy data—specialist decision. SpringerLink

  5. Azathioprine. Adult: ~2–2.5 mg/kg/day; may be used during pregnancy when needed (careful monitoring). PMC

  6. Intravenous immunoglobulin (IVIG). Adult: 0.4 g/kg/day ×5 (varies); pregnancy-compatible and sometimes chosen for prevention in special cases. (Evidence base varies by condition.) Wiki Journal Club

Not recommended: “stem-cell clinics” or unregulated “regenerative” injections—unsafe and not evidence-based for optic neuritis, especially in pregnancy.


Procedures/surgeries

True surgery is almost never needed for optic neuritis. When procedures are discussed, it’s usually because the case is atypical or severe:

  1. Therapeutic plasma exchange (PLEX/TPE). Why: severe steroid-refractory ON (especially NMOSD). What happens: blood is cycled through a machine to remove antibodies; usually 5–7 sessions over ~2 weeks. PubMedAjo

  2. Central venous catheter insertion (to do PLEX). Why: reliable access for exchange therapy.

  3. Lumbar puncture (spinal tap). Why: look for oligoclonal bands (MS) or other inflammatory/infectious clues when diagnosis is uncertain. (Procedure, not surgery.)

  4. Optic nerve/orbital biopsy (extremely rare). Why: if a tumor, sarcoid, or unusual infection mimics ON and all noninvasive tests are inconclusive.

  5. Optic nerve sheath fenestration/decompression is not a treatment for ON; it’s used for intracranial hypertension with papilledema. It’s listed here only to clarify it’s not indicated for typical optic neuritis.


Prevention strategies

  1. Early evaluation of any new visual symptoms in pregnancy.

  2. Cool-down strategies to limit heat-triggered blurring.

  3. Adequate sleep and stress management.

  4. Infection prevention and vaccinations per obstetrics (avoid live vaccines in pregnancy).

  5. Smoking cessation and avoiding secondhand smoke.

  6. Prenatal nutrition: prenatal vitamin with iodine and folate, consider DHA, and check vitamin D with your clinician. Office of Dietary SupplementsU.S. Food and Drug Administration

  7. Plan postpartum follow-up early, since relapse risk can increase in the first 3 months after delivery for MS/NMOSD. PubMed

  8. Coordinate medications (stop teratogenic drugs before conception; pick pregnancy-appropriate alternatives).

  9. Treat infections promptly (fever and illness can worsen symptoms).

  10. Safe activity: avoid driving until your vision is cleared as safe.


When to see a doctor urgently

  • Sudden vision loss in one or both eyes.

  • Eye pain worsened by movement.

  • Color suddenly looks dull/grey, or a central dark spot appears.

  • New neurological symptoms (weakness, numbness, severe headache, balance problems).

  • No improvement within 1–2 weeks, or worsening despite treatment.

  • Fever or signs of infection, especially if you are using steroids or have NMOSD.

These are reasons to call your obstetric clinician and go to an emergency or urgent eye/neurology service. NCBI


What to eat — and what to avoid

Helpful foods (examples):

  • Low-mercury fish (salmon, sardines, trout) 8–12 oz/week for DHA—great for baby’s brain and your neural membranes. U.S. Food and Drug Administration

  • Eggs (choline, lutein/zeaxanthin), leafy greens, beans/lentils, lean meats, dairy/yogurt (pasteurized), nuts/seeds, whole grains—a balanced prenatal pattern. ACOG

Avoid or limit:

  • High-mercury fish (shark, swordfish, king mackerel, bigeye tuna). U.S. Food and Drug Administration

  • Unpasteurized cheeses/milk and deli meats unless heated until steaming (to prevent Listeria). ACOG

  • Raw or undercooked meats/eggs/sushi; unpasteurized juices. Mayo Clinic

  • Caffeine > 200 mg/day (roughly one 12-oz coffee). ACOG

  • Alcohol—avoid entirely in pregnancy.


FAQs

1) Is optic neuritis dangerous for my baby?
ON itself affects your optic nerve, not the fetus. The main concern is choosing tests and treatments safely—which is why MRI is done without contrast unless absolutely essential. ACOG

2) Will my vision come back?
In typical ON, vision often improves over weeks to months, with many people near their previous acuity by ~6 months, though contrast/color may remain a bit off. High-dose steroids help you improve faster but don’t change long-term vision. NCBIPMC

3) Is MRI safe while I’m pregnant?
YesMRI without gadolinium is acceptable in pregnancy. Gadolinium is usually avoided unless the diagnostic need is compelling. ACOG

4) Can I breastfeed if I needed steroids?
Most corticosteroids are compatible with breastfeeding; for very high doses, some clinicians suggest timing feeds after infusions. Check specific drugs in LactMed. NCBI

5) Why not just take oral steroids at home?
Standard-dose oral prednisone alone increased recurrence in ONTT. If an oral-only route is necessary, very high-dose oral regimens (bioequivalent to IV) may be considered by specialists. PMC+1

6) What if steroids don’t work?
For severe, steroid-refractory attacks, plasma exchange (PLEX) can improve outcomes—especially in NMOSD. Ajo

7) Could this mean I have MS?
Sometimes. About 15–20% of people have ON as the first sign of MS, and MRI findings help estimate risk. Your team will explain your personal risk and follow-up plan. NCBI

8) What about NMOSD or MOGAD?
These antibody-mediated diseases can cause ON and need different long-term prevention. Testing for AQP4-IgG and MOG-IgG helps guide therapy. NCBI

9) Will delivery trigger a relapse?
For MS, relapse risk is higher in the first 3 months postpartum; planning follow-up and postpartum therapy is important. NMOSD can also flare postpartum—close monitoring is key. PubMed

10) Are OCT and VEP safe?
Yes. These are noninvasive eye/brain signal tests without radiation. Nature

11) Can vitamins or diet cure ON?
No. Supplements support general health but do not stop an attack. Use them to meet pregnancy needs (iodine, choline, DHA, folate), not as a replacement for medical care. Office of Dietary Supplements+1U.S. Food and Drug Administration

12) Do I need gadolinium contrast for MRI?
Usually no in pregnancy; use only if the diagnostic benefit is essential. ACOG

13) If I have NMOSD/MOGAD, can I stay on preventive therapy?
Possibly. Some medications (e.g., azathioprine) can be used when needed in pregnancy; others are timed pre-pregnancy or postpartum. This is specialist territory. PMC

14) How fast should I seek care?
Immediately when vision drops—early assessment and treatment speed recovery and ensure no dangerous mimic is missed. NCBI

15) Will I need surgery?
Almost never. ON is treated with medicines and procedures (like PLEX) rather than operations. Surgery is considered only to diagnose or treat an unusual mimic. NCBI

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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 18, 2025.

 

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