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Multiple sclerosis, neuromyelitis optica spectrum disorder (NMOSD), MOG antibody-associated disease (MOGAD), autoimmune inflammatory myelitis, myasthenia gravis and chronic inflammatory demyelinating polyneuropathy (CIDP) often occur during the reproductive years. In most cases, having one of these disorders does not preclude pregnancy or the birth of a healthy child.
Management depends on the specific diagnosis, disease activity and current immunotherapy. Modern practice does not assume that treatment should automatically be stopped before conception. Some medications can be used during pregnancy, and many therapies are compatible with breastfeeding. In diseases with a high relapse risk, discontinuing effective treatment may pose a greater danger than drug exposure itself.
The main goal of pregnancy planning in a neuroimmune disease is to maintain disease control in the mother while minimizing fetal drug exposure.
Planning therefore includes not only the timing of conception, but also the treatment strategy during pregnancy, management of a possible relapse, care in the early postpartum period and compatibility of subsequent therapy with breastfeeding.
Pregnancy planning should ideally begin before contraception is stopped. For most autoimmune neurological diseases, clinical stability is preferable before conception, although the criteria for stability differ between conditions.
In multiple sclerosis, relapse frequency, MRI disease activity and the effectiveness of disease-modifying therapy are considered. In AQP4-IgG-positive NMOSD, the severity and frequency of previous attacks are especially important. In myasthenia gravis, generalized, bulbar and respiratory weakness must be assessed. In CIDP, the focus is on muscle strength, walking, neurological deficit and dependence on maintenance treatment.
Before pregnancy, it is useful to define:
One particularly undesirable situation is stopping effective treatment long before conception and then waiting several months for pregnancy to occur. This can make the period without disease control substantially longer than the pregnancy itself.
In diseases where a single attack can cause major irreversible neurological disability — especially AQP4-IgG-positive NMOSD — relapse prevention should be regarded as one of the central components of safe pregnancy management.
Pregnancy is not a contraindication to magnetic resonance imaging. MRI does not use ionizing radiation and can be performed in any trimester when the result is necessary for diagnosis or may change treatment.
If new myelitis, optic neuritis, active NMOSD or another inflammatory neurological disorder is suspected, an indicated investigation should not be postponed until after delivery simply because the patient is pregnant.
Gadolinium-based contrast agents are not routinely used during pregnancy. Gadolinium crosses the placenta, so contrast is considered only when it is expected to add substantial diagnostic information and the anticipated clinical benefit outweighs the potential fetal risk.
For most neuroimmune disorders, the information needed during pregnancy can be obtained with non-contrast MRI.
After maternal administration of gadolinium contrast, only a very small fraction of the dose enters breast milk, and oral absorption of the gadolinium complex by the infant is extremely low.
Current guidance from the American College of Radiology and ACOG does not require interruption of breastfeeding after standard gadolinium-enhanced MRI. When modern stable macrocyclic agents are used, a special waiting interval before breastfeeding is generally unnecessary.
| Disease | During pregnancy | Postpartum period | Main clinical task |
|---|---|---|---|
| Multiple sclerosis | On average, inflammatory relapse frequency falls, particularly in the second half of pregnancy. Actual risk depends greatly on the treatment used before pregnancy and on the consequences of stopping it. | Relapse frequency may rise during the first months after delivery, especially after a prolonged treatment interruption or withdrawal of therapies associated with rebound disease activity. | Define the disease-modifying treatment strategy before conception, during pregnancy and after delivery. |
| AQP4-IgG-positive NMOSD | Pregnancy does not reliably suppress disease activity. Severe attacks can occur. | Relapse risk is particularly important during the first months after delivery. | Maintain effective attack prevention and avoid unjustified treatment gaps. |
| MOGAD | Available observational series suggest a relatively low relapse rate during pregnancy. | The evidence is less consistent. Postpartum activity is strongly influenced by the previous disease course. | Distinguish monophasic from relapsing disease and individualize indications for maintenance treatment. |
| Myasthenia gravis | The course is variable. Worsening has been reported most often during the first trimester. | Postpartum worsening is relatively common. | Maintain stable neuromuscular function, prevent respiratory and bulbar complications and plan delivery. |
| CIDP | Most data come from small series. Both stable disease and onset or relapse during pregnancy have been described. | Disease reactivation may occur; muscle strength and walking require clinical monitoring. | Maintain effective therapy with the best-established safety profile. |
Pregnancy management in multiple sclerosis is now a distinct clinical task because the strategy depends not only on disease activity, but also on the mechanism of action of a particular disease-modifying therapy, the risk of reactivation after withdrawal and whether treatment can be continued during pregnancy and breastfeeding.
Current evidence no longer supports a universal approach in which all therapy is stopped before conception. Interferon beta and glatiramer acetate can be used during pregnancy and lactation; anti-CD20 therapy can be used as a strategy to maintain prolonged disease control while pregnancy is being planned; and in highly active MS, natalizumab may be continued during pregnancy. S1P receptor modulators — particularly fingolimod — require special attention because discontinuation is associated with a risk of marked disease reactivation.
Other important issues include management of unplanned pregnancy while taking a disease-modifying therapy, MRI, relapse treatment, postpartum risk and the timing of treatment resumption.
Pregnancy planning, use of individual MS therapies, MRI, relapse management and breastfeeding are discussed in detail on a separate page:
Neuromyelitis optica spectrum disorder, especially AQP4-IgG-positive NMOSD, requires a strategy different from that used in multiple sclerosis. A single NMOSD attack may cause profound and sometimes irreversible visual loss, paraparesis or tetraparesis, bladder dysfunction or brainstem involvement. Preventing new attacks is therefore the central task of pregnancy management.
Unlike multiple sclerosis, pregnancy does not produce a consistent reduction in AQP4-IgG-positive NMOSD activity. The most reproducible observation is a higher relapse risk during the early postpartum period.
Attack risk is greater in patients with active disease before pregnancy and when effective immunotherapy is discontinued. Current recommendations therefore do not support automatic withdrawal of preventive treatment when pregnancy is planned.
The 2026 MENACTRIMS recommendations suggest, where possible, planning conception after at least 12 months of clinical stability, while also emphasizing that immunotherapy should not be stopped or postponed without good reason during pregnancy planning.
Azathioprine has extensive experience in autoimmune disease during pregnancy. It may be continued in patients with NMOSD if it maintains clinical disease control and there is no reason to change treatment.
Azathioprine metabolites are found in breast milk at very low concentrations, and accumulated experience supports compatibility with breastfeeding under appropriate clinical monitoring.
Rituximab is widely used off label in AQP4-IgG-positive NMOSD and can be incorporated into pregnancy planning. Its prolonged biological effect allows an infusion to be given before conception while maintaining relapse prevention as circulating drug concentrations gradually fall.
MENACTRIMS 2026 allows an attempt at conception one month after rituximab or inebilizumab. Official product labels may specify more conservative contraception intervals, which should also be considered during individual planning.
If B-cell-depleting therapy is given during the second half of pregnancy, transient B-cell depletion may occur in the newborn. In this situation, lymphocyte and B-cell counts should be checked after birth, and live vaccines postponed until the B-cell pool has recovered.
Eculizumab and ravulizumab inhibit complement component C5 and are highly effective preventive therapies for AQP4-IgG-positive NMOSD.
The largest pregnancy experience is available for eculizumab, mainly in paroxysmal nocturnal hemoglobinuria and atypical hemolytic uremic syndrome. These are not direct NMOSD studies, but they substantially expand the information available about C5 inhibition during pregnancy.
Pregnancy experience with ravulizumab is much more limited. MENACTRIMS 2026 states that eculizumab and ravulizumab may be continued during pregnancy when the need to control NMOSD outweighs the potential risk of drug exposure.
International recommendations are not fully concordant. Some more conservative expert documents do not recommend routine use of newer targeted therapies during pregnancy because prospective data remain limited. The decision to continue C5 inhibition should therefore reflect disease activity, severity of previous attacks and the consequences of treatment withdrawal.
Satralizumab is a monoclonal antibody against the interleukin-6 receptor and is approved for AQP4-IgG-positive NMOSD.
There are no controlled pregnancy trials. However, several case reports describe continuation or initiation of satralizumab during pregnancy without NMOSD relapse and without identified serious adverse neonatal outcomes.
In individual cases, satralizumab concentrations in breast milk and infant blood were below the assay detection threshold. These data are clinically interesting but remain too limited to support a universal recommendation.
Use of satralizumab during pregnancy or lactation should therefore be considered in the context of the individual relapse risk of NMOSD and the uncertainty associated with limited reproductive data.
Inebilizumab depletes CD19-positive B cells and has a prolonged biological effect. MENACTRIMS considers it a possible pre-pregnancy strategy, with an attempt at conception one month after infusion.
There are insufficient data on administration during pregnancy itself. As with other B-cell-depleting treatments, meaningful exposure in the second half of pregnancy requires assessment of the newborn's B cells before live vaccines are administered.
Mycophenolate mofetil is associated with an increased risk of pregnancy loss and a characteristic pattern of congenital anomalies. It should be replaced before planned conception.
Methotrexate is teratogenic and embryotoxic and is contraindicated in pregnancy.
Cyclophosphamide has embryofetal and gonadotoxic effects and is not used as routine maintenance therapy during pregnancy. It may be considered only in exceptional severe situations when no acceptable alternative exists.
A clinically significant attack requires early treatment. High-dose intravenous methylprednisolone usually remains first-line therapy.
For a severe attack or insufficient recovery after corticosteroids, therapeutic plasma exchange is used. Pregnancy is not a contraindication to plasma exchange; with appropriate obstetric and hemodynamic monitoring, its effectiveness and complication profile are comparable to use outside pregnancy.
In a severe NMOSD attack with major visual loss or motor deficit, delaying plasma exchange solely because of pregnancy may reduce the likelihood of functional recovery.
MOG antibody-associated disease (MOGAD) is a distinct inflammatory disease of the central nervous system and may present with optic neuritis, myelitis, ADEM, brainstem involvement and other syndromes.
Reproductive data in MOGAD are much more limited than in multiple sclerosis or AQP4-IgG-positive NMOSD, so risk estimates must take the small size of published cohorts into account.
In a French series of pregnancies after MOGAD onset, relapses during pregnancy were uncommon and some attacks occurred during the early postpartum period.
A two-center study published in 2025 analyzed 22 pregnancies in 15 women with MOGAD. No confirmed attacks occurred during pregnancy. In the postpartum period, two attacks occurred in one patient with a pre-existing steroid-dependent relapsing course.
An international Asian cohort published in 2026 likewise found lower MOGAD activity during pregnancy but a return of activity after delivery; some patients who had previously appeared monophasic subsequently developed relapsing disease.
Pregnancy itself is not an indication to start long-term immunotherapy in a patient with a single MOGAD episode, prolonged clinical stability and no evidence of relapsing disease.
In relapsing MOGAD, treatment strategy depends on the frequency and severity of previous attacks, residual neurological disability and response to previously used treatments.
Intravenous immunoglobulin is the maintenance treatment with the best-established pregnancy experience. Azathioprine or B-cell-directed therapy may be considered in selected clinical situations, although the evidence base is substantially smaller than in NMOSD.
Acute optic neuritis, myelitis or another clinically significant MOGAD episode during pregnancy is treated with high-dose corticosteroids. Plasma exchange is used for severe attacks or inadequate steroid response. Intravenous immunoglobulin is used in selected situations.
The term “myelitis” describes inflammatory involvement of the spinal cord but does not by itself determine prognosis or the risk of another episode. For pregnancy planning, it is essential to establish which disease caused the previous myelitis.
Inflammatory spinal cord lesions may occur in:
A woman with a single seronegative myelitis many years earlier and no subsequent clinical or MRI activity therefore has a very different prognosis from a patient with AQP4-IgG-positive NMOSD or relapsing MOGAD.
If the diagnosis was made before modern cell-based AQP4-IgG and MOG-IgG assays became widely available, or if the cause of the myelitis remained unclear, it may be useful to review the clinical history, brain and spinal MRI and previous serological testing before pregnancy.
Repeat antibody testing is not required for every patient. The decision depends on how long ago the disease occurred, the original laboratory method, the clinical syndrome and the subsequent course.
Progressive weakness in the legs or arms, a new sensory level, marked deterioration in walking or new bladder dysfunction require urgent neurological assessment.
Spinal MRI without gadolinium can be performed during pregnancy. If an inflammatory attack is confirmed, treatment is determined by the likely cause and severity of neurological deficit.
Pregnancy is possible in most women with autoimmune myasthenia gravis, but the disease course remains variable. Symptoms may remain stable, improve or worsen.
The largest systematic review and meta-analysis available to date, published in 2026, included 34 studies and 3,720 pregnancies in women with myasthenia gravis.
Across the included studies, worsening of myasthenic symptoms occurred in approximately 30% of pregnancies, most often during the first trimester.
Exacerbation or worsening after delivery was reported in approximately 27% of cases.
Among 1,530 newborns, transient neonatal myasthenia was reported in approximately 9%.
These estimates come from heterogeneous studies of varying quality and represent population averages rather than an individual patient's probability of complications.
Pregnancy is preferably planned during stable disease control. Bulbar symptoms, respiratory weakness, previous myasthenic crises and the need for high-dose immunotherapy are particularly important.
If thymectomy is indicated, elective surgery is preferably performed before pregnancy. Pregnancy itself is not an indication for thymectomy.
Pyridostigmine remains standard symptomatic treatment and may be used during pregnancy. Because pharmacokinetics may change during pregnancy, dosing sometimes needs to be adjusted according to clinical response.
The drug is compatible with breastfeeding: concentrations in breast milk are low and clinically significant infant exposure is not expected.
Prednisolone and other systemic corticosteroids may be used when necessary to maintain myasthenia control. During prolonged treatment, the lowest effective dose is preferred, with monitoring of blood pressure, glucose metabolism and other steroid-related complications.
Azathioprine has substantial clinical experience during pregnancy in a range of autoimmune diseases. Current recommendations allow it to be continued in patients with myasthenia gravis when needed to maintain clinical stability.
Azathioprine may also be used during breastfeeding.
Intravenous immunoglobulin and therapeutic plasma exchange are used for clinically important exacerbations, rapid worsening or myasthenic crisis.
Both can be used during pregnancy. The choice depends on disease severity, speed of symptom progression, comorbidities, availability and previous clinical response.
Plasma exchange itself does not create drug exposure through breast milk and does not require interruption of breastfeeding; feeding may need to be modified only because of accompanying medication or the mother's clinical condition.
Complement inhibitors and FcRn inhibitors have substantially expanded treatment options for generalized myasthenia gravis. However, pregnancy experience with these agents remains much smaller than the accumulated evidence for pyridostigmine, corticosteroids, azathioprine, intravenous immunoglobulin and plasma exchange.
For eculizumab, substantial pregnancy experience exists in paroxysmal nocturnal hemoglobinuria. Published data overall do not suggest a major teratogenic signal, although direct experience in myasthenia gravis is limited. Continuation may be considered in severe disease when stopping treatment carries a substantial risk of deterioration.
Reproductive data for ravulizumab are much more limited. Despite the similar C5-inhibition mechanism, experience with eculizumab cannot automatically be regarded as equivalent evidence for ravulizumab.
For efgartigimod, rozanolixizumab and nipocalimab, the clinical evidence base during pregnancy remains insufficient. This is particularly relevant to the mechanism of FcRn inhibition: FcRn participates in transplacental transport of maternal IgG, so blocking this receptor could potentially reduce transfer of protective maternal antibodies to the fetus.
FcRn inhibitors are therefore not standard pregnancy strategies and require individualized assessment of myasthenia severity, effectiveness of alternative treatments and the potential consequences of inadequate disease control.
Mycophenolate mofetil is proven teratogenic and should be replaced before planned conception. Methotrexate is also contraindicated.
Cyclophosphamide is not used as routine maintenance treatment during pregnancy because of embryofetal and gonadotoxic effects.
Myasthenia gravis itself is not an indication for cesarean delivery. The first stage of labor depends predominantly on uterine smooth muscle and is generally not impaired by a neuromuscular junction disorder.
During the second stage, striated muscle activity becomes more important, so obstetric assistance may be required if significant weakness or fatigability is present.
Regional anesthesia is generally feasible in stable myasthenia. The anesthetic strategy depends on the severity of generalized, bulbar and respiratory weakness.
Magnesium sulfate requires particular caution in myasthenia gravis.
Magnesium depresses neuromuscular transmission and can markedly worsen weakness, potentially causing respiratory failure. Standard treatment of preeclampsia or eclampsia with magnesium sulfate in a patient with myasthenia therefore requires an alternative obstetric and anesthetic strategy.
Maternal acetylcholine-receptor antibodies may cross the placenta. As a result, some newborns develop transient neonatal myasthenia.
Possible symptoms include hypotonia, a weak cry, impaired sucking and swallowing and, less commonly, respiratory insufficiency. The symptoms result from circulating maternal antibodies and gradually resolve as those antibodies are cleared.
The absence of neonatal myasthenia in a previous pregnancy does not exclude it in a later pregnancy, and the reverse is also true. A newborn of a mother with myasthenia therefore requires clinical observation regardless of previous pregnancy outcomes.
A rare but more severe complication of transplacental antibody exposure is fetal AChR-antibody-associated disease with reduced fetal movement and arthrogryposis. This is particularly relevant in women who have had such complications in a previous pregnancy.
Chronic inflammatory demyelinating polyneuropathy is much less common than multiple sclerosis or myasthenia gravis, so reproductive evidence remains limited.
A systematic review identified only 24 well-documented patients with CIDP onset or relapse related to pregnancy. In 17 cases, the disease first appeared during pregnancy; some women with established CIDP relapsed during subsequent pregnancies.
These data do not define an exact individual risk. They confirm that CIDP can begin or reactivate during pregnancy but do not mean that pregnancy routinely causes disease worsening.
IVIG is one of the best-studied CIDP treatments during pregnancy. It has no known teratogenic effect, is widely used in pregnant patients with immune and neurological disorders and is compatible with breastfeeding.
If a patient is clinically dependent on regular IVIG before pregnancy, stopping treatment solely because of pregnancy is usually unjustified. Dose and infusion interval are determined by clinical response.
Corticosteroids remain an effective treatment for CIDP and can be used during pregnancy if they previously provided stable disease control.
Long-term treatment requires monitoring of blood pressure, glycemia, infection risk and other steroid-related complications.
Plasma exchange is a first-line treatment for CIDP and may be performed during pregnancy when clinically necessary. Standard monitoring of hemodynamics, electrolytes and coagulation is required, taking physiological changes of pregnancy into account.
Plasma exchange is not a reason to discontinue breastfeeding.
Azathioprine is sometimes used as additional treatment in CIDP, although evidence for efficacy is substantially weaker than for IVIG, corticosteroids and plasma exchange. If it is necessary to maintain previously achieved stability, pregnancy does not always require withdrawal.
Mycophenolate, methotrexate and cyclophosphamide are not suitable for planned maintenance therapy during pregnancy.
Efgartigimod alfa is now used for CIDP, but clinical pregnancy data are insufficient.
A dedicated pregnancy registry is included in the current prescribing information to collect pregnancy outcome data.
FcRn mediates transplacental transfer of maternal IgG. Because efgartigimod lowers IgG concentrations, fetal exposure could theoretically reduce passive immune protection in the newborn. This should also be considered when live vaccines are planned after birth.
Preclinical studies have not identified adverse effects on embryofetal development, but the absence of a signal in animal experiments does not substitute for human pregnancy data.
As of 2026, IVIG remains a substantially better studied maintenance treatment for CIDP during pregnancy.
Data on efgartigimod alfa concentrations in human breast milk and the clinical consequences for the infant remain insufficient. The prescribing information emphasizes balancing the benefits of breastfeeding against the mother's clinical need for treatment and possible infant exposure.
Unlike IVIG, corticosteroids or azathioprine, the evidence for efgartigimod is therefore not sufficient to formulate an equally definite recommendation during lactation.
The table mainly relates to NMOSD, MOGAD, myasthenia gravis and CIDP. MS medications are discussed in detail on the separate page on multiple sclerosis and pregnancy.
| Treatment | Main indications | Pregnancy | Breastfeeding | Clinical comment |
|---|---|---|---|---|
| Intravenous immunoglobulin | CIDP, myasthenia gravis, MOGAD; selected situations in other diseases | Compatible | Compatible | Extensive pregnancy experience. May be used as maintenance or short-term treatment depending on the diagnosis. |
| Prednisolone / methylprednisolone | NMOSD, MOGAD, myasthenia gravis, CIDP | May be used | Compatible | For long-term treatment, the lowest effective dose is preferred. High-dose methylprednisolone is used for clinically significant acute attacks. |
| Therapeutic plasma exchange | Severe NMOSD/MOGAD attacks, myasthenia gravis, CIDP | May be used | Does not require interruption | Used for severe attacks or insufficient corticosteroid response, and for marked deterioration in myasthenia gravis or CIDP. |
| Pyridostigmine | Myasthenia gravis | Compatible | Compatible | Standard symptomatic treatment for myasthenia gravis. |
| Azathioprine | NMOSD, myasthenia gravis; selected cases of MOGAD and CIDP | Acceptable when indicated | Compatible | Long-standing pregnancy experience. It is not an evidence-based first-line CIDP treatment. |
| Rituximab | NMOSD; selected cases of MOGAD and refractory myasthenia gravis | Individual strategy | May be used when indicated | Often used before conception. After in-utero exposure during the second half of pregnancy, newborn B-cell counts should be assessed before live vaccines. |
| Inebilizumab | AQP4-IgG+ NMOSD | Limited data | Individual assessment | MENACTRIMS allows a pre-pregnancy strategy with an attempt at conception one month after infusion. Data on administration during pregnancy itself are insufficient. |
| Eculizumab | NMOSD, generalized myasthenia gravis | May be considered if clinically necessary | May be considered when indicated | Substantial reproductive experience exists in other complement-mediated disorders; direct NMOSD and myasthenia data are less extensive. |
| Ravulizumab | NMOSD, generalized myasthenia gravis | May be considered if clinically necessary | Limited data | Mechanism is similar to eculizumab, but the reproductive evidence base is substantially smaller. |
| Satralizumab | AQP4-IgG+ NMOSD | Limited clinical experience | Limited clinical experience | Several favorable pregnancy and lactation cases have been published, including milk concentration measurements. Data remain insufficient for a universal recommendation. |
| FcRn inhibitors efgartigimod, rozanolixizumab, nipocalimab | Generalized myasthenia gravis; efgartigimod also CIDP | Insufficient evidence | Insufficient evidence | FcRn participates in transplacental IgG transfer. A pregnancy registry exists for efgartigimod; possible reduction in passive neonatal immunity should be considered. |
| Mycophenolate mofetil | NMOSD, myasthenia gravis | Contraindicated | Not used | Associated with increased pregnancy loss and a characteristic pattern of congenital anomalies. Requires replacement before conception. |
| Methotrexate | Rarely used in these disorders | Contraindicated | Not used | Teratogenic and embryotoxic. |
| Cyclophosphamide | Severe refractory autoimmune disease | Not used routinely | Contraindicated | Embryofetal and gonadotoxic effects. Use during pregnancy is limited to exceptional severe situations. |
Recommendations for individual drugs can differ between expert guidelines and official prescribing information in Israel, the European Union, the United States and other countries. Both sources should be considered when pregnancy is planned.
Compatibility of breastfeeding with treatment depends on the pharmacokinetics of the specific drug, its concentration in breast milk, oral bioavailability to the infant and possible pharmacological effects after systemic absorption.
For several treatments, accumulated evidence allows therapy to continue without stopping breastfeeding. These include intravenous immunoglobulin, pyridostigmine, corticosteroids and azathioprine.
The approach to monoclonal antibodies during lactation has also changed. Because IgG monoclonal antibodies have a large molecular size, concentrations of most such agents in mature breast milk are low, and oral bioavailability to the infant is extremely limited.
For this reason, current expert recommendations allow breastfeeding during treatment with several anti-CD20 agents and some other monoclonal antibodies when continuation of therapy is clinically necessary.
This issue is particularly important in NMOSD because of the high risk of a postpartum attack. MENACTRIMS recommends early resumption of immunotherapy after delivery and allows administration of monoclonal antibodies to breastfeeding mothers after the very early postpartum period.
For satralizumab, individual reports have found either undetectable drug levels in breast milk or concentrations below the analytical threshold. These observations are encouraging but do not yet replace larger prospective data.
Clinical information during lactation remains insufficient for FcRn inhibitors, including efgartigimod, so recommendations are much less certain.
The breastfeeding plan should be decided at the same time as the postpartum treatment plan. In a patient at high risk of a severe NMOSD attack, myasthenia deterioration or another active neurological disease, delaying necessary treatment solely to continue breastfeeding may be clinically unjustified.
Paternal drug exposure is fundamentally different from drug exposure in a pregnant woman. For most biological therapies, clinically meaningful embryonic exposure through semen is not expected.
The main concern is with medications that may impair spermatogenesis or have genotoxic effects.
Cyclophosphamide and some other cytotoxic drugs can cause substantial and sometimes prolonged reductions in fertility. If such treatment is planned in a man of reproductive age, sperm cryopreservation should be discussed before therapy begins.
Contraception intervals after a particular treatment should follow the current prescribing information for that drug.
Pregnancy should not be a reason to delay evaluation of a serious new neurological syndrome.
Urgent assessment is required for:
If an NMOSD or MOGAD attack or inflammatory myelitis is suspected, non-contrast MRI may be performed during pregnancy, and necessary anti-inflammatory treatment should not be delayed solely because of pregnancy.
No. The strategy depends on the disease and the medication. IVIG, pyridostigmine, azathioprine and corticosteroids can be used during pregnancy when indicated. For some monoclonal antibodies, continuation or pre-conception use is also possible. In NMOSD, unjustified withdrawal of effective treatment can substantially increase the risk of a severe attack.
Yes. Pregnancy is preferably planned after stable disease control has been achieved and a preventive treatment strategy has been defined in advance. Preventing severe attacks and planning the first postpartum months are especially important because relapse risk increases after delivery.
Not necessarily. Risk depends on the cause of the myelitis. A single seronegative transverse myelitis followed by years of stability is fundamentally different from AQP4-IgG-positive NMOSD or relapsing MOGAD. If an old diagnosis remains unclear, re-evaluation before pregnancy may be useful.
In modern small series, relapse frequency during pregnancy itself has been low. Activity may return after delivery, especially in patients with previously relapsing disease. The evidence base remains much smaller than in MS or NMOSD.
Yes. MRI without gadolinium contrast can be performed in any trimester when it is needed for diagnosis or treatment decisions. Routine gadolinium use during pregnancy is not recommended.
In most cases, yes. Myasthenia gravis itself is not an indication for cesarean delivery. Obstetric assistance may be needed during the second stage if significant fatigability is present. Planning is individualized by the obstetric, neurological and anesthetic teams.
According to a 2026 meta-analysis, transient neonatal myasthenia was reported in approximately 9% of newborns of mothers with myasthenia gravis. It results from transplacental transfer of maternal antibodies and usually resolves as those antibodies are cleared.
Yes. Intravenous immunoglobulin has substantial pregnancy experience and is used, among other situations, in CIDP, myasthenia gravis and selected cases of MOGAD. It is also compatible with breastfeeding.
Yes. Therapeutic plasma exchange can be used during pregnancy for severe NMOSD or MOGAD attacks, marked deterioration in myasthenia gravis and selected cases of CIDP. Standard hemodynamic and obstetric monitoring is required.
For many treatments, yes. IVIG, pyridostigmine, corticosteroids and azathioprine are compatible with breastfeeding. Favorable pharmacokinetic and clinical data have also accumulated for several monoclonal antibodies. Information remains insufficient for some newer drugs, particularly FcRn inhibitors.
Pre-conception treatment planning is particularly important in AQP4-IgG-positive NMOSD, relapsing MOGAD, generalized myasthenia gravis, CIDP requiring maintenance treatment, and after previous inflammatory myelitis when the underlying cause remains unclear.
During consultation, disease activity can be assessed, the need to modify treatment before conception can be determined, the risk of drug exposure can be weighed against the risk of treatment withdrawal, and a plan can be created in advance for pregnancy, treatment of a possible relapse and postpartum therapy.
Consultation with Dr. Lidiia PrakhovaThis information is educational and does not replace an individual consultation with a neurologist, obstetrician-gynecologist and, when needed, a maternal-fetal medicine specialist. Decisions to continue, stop or replace a specific medication depend on the diagnosis, disease activity, previous treatment response and the current prescribing information.