Pregnancy: neuromuscular complications …

General Neurology

Updated 06.23.2025
Released 06.11.2004
Expires For CME 06.23.2028

Pregnancy: neuromuscular complications

Authors: Aparna M Prabhu MD MRCP, Rebecca Frawley DO

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Editor: Nicholas E Johnson MD MSCI FAAN

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Pregnancy: neuromuscular complications

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Introduction

Overview

A broad range of neuromuscular conditions affects women during pregnancy, including newly acquired conditions as well as progression or changes in chronic neuromuscular conditions. In this article, the authors examine a broad range of neuromuscular disorders. First, the authors focus on disorders that commonly present during pregnancy, including Bell palsy, carpal tunnel syndrome, radiculopathies, and other mononeuropathies; these disorders are felt to be self-limiting, but data suggest that there may be a high rate of neuropathy persisting into the postpartum period. Second, they explore the ramifications of pregnancy and delivery on pre-existing neuromuscular conditions, such as myasthenia gravis or muscular dystrophies.

Key points

	• Treatment of Bell palsy during pregnancy is controversial, but the majority of pregnant patients have an excellent recovery with or without treatment.
	• Mononeuropathies and radiculopathies occurring during pregnancy should be treated conservatively because most resolve weeks to months after delivery.
	• Pregnant women with hereditary neuropathies and muscular dystrophies can have a decline in muscle strength during pregnancy. They are also at risk for maternal and fetal complications during delivery that require close monitoring.
	• Pregnant women with myasthenia gravis should be monitored for clinical worsening during delivery and the postpartum period.
	• Newborn infants of mothers with myasthenia gravis need close observation in the first few days after birth for transient neonatal myasthenia gravis.

Neuromuscular disorders that present during pregnancy

Bell palsy. Bell palsy is an acute, unilateral lower motor neuron facial paralysis, often accompanied by periauricular pain, taste disturbance, and hyperacusis. It is a common condition that occurs in both the general and pregnant population at similar rates: approximately 11.5 to 53.3 per 100,000 for the general population and 50 per 100,000 pregnancies (08). Although prognosis is generally favorable, with recovery usually occurring within weeks to months, some studies have shown longer recovery and worse outcomes in pregnant populations as compared to the general population. A diagnostic workup is generally not indicated unless there are atypical features, such as an insidious onset, progressive course, or association with other neurologic deficits, which would be atypical for idiopathic Bell palsy.

The prevalence of Bell palsy in the pregnant population is controversial and not consistently described across the literature. According to some authors, Bell palsy during pregnancy occurs in approximately 45 cases per 100,000 compared with 20 cases per 100,000 in the general population (52). However, Vrabec and colleagues published data showing that the number of Bell palsy cases is not considerably different in pregnant women compared to all women of childbearing age (142). A large Korean study also did not find an increased rate of Bell palsy among pregnant women versus controls (18). All of these studies agree that when Bell palsy occurs in pregnancy, it most commonly occurs during the third trimester or early postpartum period.

The treatment of Bell palsy has not been fully established in pregnancy, and treatment is usually determined on an individual basis. Prednisone, which is commonly used to aid in recovery from Bell palsy, is a category C medication. There are data to support the use of steroids for Bell palsy in the general population, and several articles support its use in late stages of pregnancy or postpartum (142; 55). For example, a report demonstrated that complete recovery improved by 17% in all patients treated with steroids (104). Early treatment started within the first 3 days of symptoms with steroids can result in a greater than 94% chance of recovered facial nerve function (134). The recommended dose of steroids is 1 mg/kg for 5 days, followed by a taper. Hato and associates documented that treatment with both steroids and antivirals, compared to steroids alone, leads to a better outcome in the general population (51). However, another study found no benefit with the use of acyclovir given alone or in addition to steroids (134). The safety of both medications has been established. Both acyclovir and valacyclovir are category B medications and can be used in pregnancy and while breastfeeding, according to the American Academy of Pediatrics. However, it should be noted that because pregnant women are often excluded as participants in randomized trials, the American Academy of Otolaryngology-Head and Neck Surgery recommends individualized management for pregnant women, acknowledging that corticosteroids are associated with known risks, such as gastrointestinal disturbances, loss of glycemic control, elevated blood pressure, peripheral edema, and mood changes (08).

The prognosis for recovery of Bell palsy in pregnancy is also not clearly defined in the literature. Bell palsy that occurs during late pregnancy or postpartum often has worse or more prolonged recovery (98). One retrospective review of 31 cases of complete facial paralysis in pregnancy found that only 52% had satisfactory recovery by 6 weeks compared to 77% to 88% recovery in the control nonpregnant group. However, all 17 of the patients with incomplete facial nerve palsy eventually had satisfactory resolution (43). Another review article boosted higher rates of recovery. Roughly 90% of their pregnant patients with Bell palsy had complete recovery within 80 days, with a mean duration of about 7 weeks (21). Predictors of bad prognosis include bilateral facial nerve palsy and recurrence in subsequent pregnancies (21).

There also seems to be an association between Bell palsy and preeclampsia that is not well characterized in the literature thus far. Preeclampsia is up to five times more common in patients with Bell palsy (127; 71). Gestational hypertension or preeclampsia is present in 22.2% of pregnant women with Bell palsy, which is well above the national average of 5% (125). Chronic hypertension and obesity are also associated with the development of Bell palsy during pregnancy (62). Bell palsy can occur before preeclampsia is recognized, concurrently with preeclampsia, or in the postpartum period as preeclampsia is resolving (01).

Carpal tunnel syndrome. Carpal tunnel syndrome, also known as median mononeuropathy at the wrist, is common during pregnancy and can occur in any trimester. The patient-reported incidence of numbness and tingling affecting both hands during pregnancy is 34% (81). Diagnosis is often clinical, with EMG studies being reserved for atypical or severe cases (94; 83). However, the incidence of EMG-confirmed carpal tunnel syndrome is lower, with a reported incidence of 17% to 19% (96; 65). Pregnant women who develop carpal tunnel are more likely to be older (138).

Several reasons have been suggested to explain the increased prevalence of carpal tunnel syndrome in pregnancy. One idea is that during pregnancy, fluid retention or relaxin-induced hypertrophy of the transverse carpal ligament causes compression of the median nerve (121; 81). In fact, there does seem to be a correlation between large amounts of weight gain during pregnancy and the incidence of carpal tunnel syndrome. Turgut and colleagues found that women with carpal tunnel syndrome gained an average of 11.6 kg, whereas women who did not develop carpal tunnel syndrome gained an average of 8.5 kg (138). Onset appears to be more frequent in the third trimester and has been associated with higher levels of fluid retention, gestational diabetes, and possibly increased maternal age (91).

Treatment of carpal tunnel syndrome during pregnancy is primarily conservative, with splinting, activity modification, and reassurance (83; 45). In cases where conservative management does not control symptoms, local corticosteroid injections may be considered and have shown benefit. Moghtaderi and colleagues studied 20 patients with EMG-confirmed carpal tunnel syndrome who were treated with local injection of 4 mg dexamethasone and had significant improvement in pain levels (84). Surgical intervention is often deferred until the postpartum period but has been considered to be safe in refractory or severe cases (94). A retrospective study suggested that symptoms continue in 50% of patients at 1 year after delivery and in about 30% of patients at 3 years, showing that the patients who develop carpal tunnel syndrome would benefit from continued follow-up to ensure symptom improvement (96).

Lumbosacral radiculopathy. Low back pain is an extremely common complaint, both in the general population and among pregnant women. The incidence of low back pain was found to be 56% in a cohort of 200 pregnant women (31); in the same cohort, 60.7% experienced the onset of back pain between the 5th and 7th month of pregnancy. The incidence of symptomatic lumbar disc herniation in pregnancy is approximately 1 in 10,000, with most cases occurring during the third trimester, likely due to increased lumbar lordosis from weight gain and hormonal changes leading to ligamentous laxity and altered biomechanics of the body (25; 56).

Several factors may influence the incidence of low back pain and radiculopathy during pregnancy, including lumbar lordosis, direct pressure from the gravid uterus, postural stress, and ligamentous laxity due to the hormone relaxin (121). Spinal anesthesia during delivery may also be a factor in the development of back pain in the peri-delivery period. Complications of epidural anesthesia are rare (0.1% or less) but may include epidural hematoma, abscess, chemical radiculitis or arachnoiditis, direct needle injury to a nerve root, or anterior spinal artery infarction (59). Rarely, a sacral fracture secondary to pregnancy-induced osteoporosis may occur and mimic radiculopathy (97; 130).

In most patients, sacral and lumbar low back pain improves without intervention within 6 months (95). Initial management is conservative, including rest, physical therapy, and acetaminophen for pain (110; 56). Nonsteroidal anti-inflammatory drugs are generally avoided, especially in the third trimester, due to concerns of adverse effects on the fetus (25). In patients with examination findings indicating nerve root compression or myelopathy, MRI is the preferred imaging modality given its safety profile in pregnancy and ability to detect nerve compression syndromes clearly. However, according to the 2004 American College of Obstetricians and Gynecologists guidelines, contrast agents should be avoided unless medically necessary. Electromyography is another diagnostic test that could be considered. According to the American Association of Neuromuscular and Electrodiagnostic Medicine, EMG is safe in pregnancy as long as muscles near the developing fetus, such as the diaphragm, are avoided.

In cases of progressive neurologic deficit despite conservative treatment, refractory pain, or clinical evidence of spinal cord compression, such as cauda equina syndrome (saddle anesthesia, bowel or bladder dysfunction, etc.), surgical intervention is warranted and can safely be performed during pregnancy. Microdiscectomy or laminectomy are the most common surgical interventions, and multidisciplinary planning is recommended with special attention to maternal positioning and anesthesia to minimize fetal risk (30; 60).

Common mononeuropathies

Meralgia paresthetica. Meralgia paresthetica is a mononeuropathy that often occurs due to mechanical compression of the lateral femoral cutaneous nerve as it passes under the inguinal ligament. This condition often presents with pain and sensory disturbances overlying the lateral thigh without motor involvement (123). The mechanism is thought to be secondary to increased abdominal girth, weight gain, and fluid retention, which increases intra-abdominal pressure. Diagnosis is clinical, and treatment measures are often conservative, involving avoidance of tight clothing, weight management, and postural modifications (67; 123). For most patients, symptoms will resolve postpartum.

Femoral mononeuropathy. There are multiple proposed mechanisms for the development of femoral neuropathies, including injury during retraction in a cesarean delivery, compression due to prolonged lithotomy positioning during vaginal delivery, and other causes of mechanical compression both within the pelvis and as it passes under the inguinal ligament (145; 19). Femoral neuropathy often presents as weakness in hip flexion and knee extension, altered patellar reflexes, and sensory disturbances over the anterior thigh and medial aspect of the leg (19). Management is conservative, with emphasis on early physical rehabilitation and supportive measures. Most cases experience significant recovery in the months following diagnosis and treatment, but a portion may experience delayed or incomplete recovery (19).

Obturator mononeuropathy. Obturator mononeuropathy is a rare condition that occurs during pregnancy and is thought to occur secondary to compression, stretching of the nerve, or trauma during labor and delivery (145). The chance of this condition occurring increases with prolonged lithotomy positioning, difficult vaginal delivery, or pelvic surgeries (53). Patients often present with weakness in thigh adduction, medial thigh sensory disturbances, and ambulatory dysfunction secondary to instability. Diagnosis is clinical, and management is often conservative with physical therapy, but imaging can be obtained in severe cases where a compressive lesion is suspected. Prognosis is generally favorable, with most cases resolving spontaneously or with conservative management (03).

Sciatic mononeuropathy. Sciatic mononeuropathy is a rare condition that can occur during pregnancy secondary to mechanical compression of the sciatic nerve by an enlarged uterus or fetal head as the nerve passes through the pelvis, by compression secondary to prolonged lithotomy position, or, rarely, due to space-occupying lesions, such as tumors or endometriosis (111). This condition often presents as pain radiating from the buttock down the posterior thigh, with motor and sensory disturbances dependent on the site and severity of nerve involvement (67). Most cases are transient and will resolve without further intervention, but conservative management with physical therapy is often recommended. Patients experience a good prognosis, with most progressing to complete recovery.

Peroneal mononeuropathy. Peroneal mononeuropathy often presents as unilateral acute foot drop, secondary to weakness of ankle dorsiflexion and eversion, with sensory disturbances over the dorsum of the foot and lateral shin (78). More proximally, the peroneal component of the sciatic nerve is often preferentially affected by compression of the fetal head or forceps, due to its proximity to the bony pelvis (145). Distal to the pelvis, the mechanism is thought to be due to compression at the distal posterior thigh from patient hand placement or at the lateral knee due to inappropriate leg positioning in stirrups during vaginal delivery (145; 121; 103). Diagnosis is often clinical, but NCS/EMG can provide confirmation. The management is primarily conservative, with removal of causative compression, physical therapy, bracing to support ambulation, and patient education (117). Most cases are self-limited, with gradual recovery over the weeks and months following diagnosis, but early recognition and prevention are important to prevent nerve compression and symptom development.

Overall, the prognosis for recovery from a compression mononeuropathy is good. Most patients fully recover within 6 months. In a review article, the recovery was estimated to be between 3 and 6 months for demyelinating injuries or longer for axonal injury (121). Conservative measures, such as physical therapy, bracing, and walking aids, are often found to be helpful.

Demyelinating neuropathies.

Acute inflammatory demyelinating polyradiculoneuropathy. Acute inflammatory demyelinating polyradiculoneuropathy, also known as Guillain-Barré syndrome, is an immune-mediated demyelination of peripheral nerves that often presents with rapidly progressive, symmetric weakness, areflexia, and sensory disturbances. The literature suggests that the incidence of AIDP is not significantly different between the general population and pregnant women--approximately 0.75 to 2 in 100,000 (109; 16; 87). Case reviews suggest that AIDP most commonly occurs during the third trimester or in the initial 30 days postpartum (16). As in the general population, there is an association between vaccinations, infections (both bacterial and viral have been noted), and the development of AIDP. Notable connections have been observed following H1N1 vaccination, ZIKA infection, and both COVID-19 infection and vaccination (11; 17; 39; 136).

However, literature suggests that when AIDP does occur during pregnancy, women have increased rates of ICU admission, respiratory support (both invasive and non-invasive), and variations in response to treatment as compared to non-pregnant women (69). In general, most patients recover completely after AIDP, but about 10% have some residual disability. The mortality rate is 3% to 5%, with most deaths related to respiratory failure, aspiration, or complications of immobility (139). Fetal risks are primarily related to maternal complications and have not been connected to direct disease processes from AIDP. Case reports have shown that there is an increased risk of preterm delivery, fetal distress, and possible increased fetal mortality, particularly when the maternal disease is severe or complicated by infections or obstetric emergencies (12; 147; 69).

Early diagnosis and treatment are critical for maternal and fetal outcomes in AIDP. The gold standard treatment for AIDP remains either intravenous immunoglobulin or plasmapheresis, both of which are considered safe and effective in pregnancy (22; 69). IVIG is considered a first-line treatment due to its lower side-effect profile and ease of administration, as the primary concern is increased risk of thromboembolism (121). Plasmapheresis remains an appropriate treatment, particularly in severe or refractory cases, but risks include volume status fluctuations such as hypovolemia or hypervolemia, central-line related infections, and transfusion reactions such as urticaria and anaphylaxis (143; 12).

Regarding delivery, AIDP does not appear to impair uterine contraction. Thus, it is not felt that AIDP is an indication for cesarean section (14). Epidural anesthesia is generally considered safe, but there have been some reports of worsening in neurologic symptoms in patients with AIDP who undergo regional anesthesia (14). However, if general anesthesia is used during pregnancy, caution should be taken with the use of succinylcholine, which has been shown to cause hyperkalemia in patients with AIDP. This is thought to occur because of the postsynaptic receptor proliferation that is seen with AIDP (34).

Chronic inflammatory demyelinating polyradiculoneuropathy. Chronic inflammatory demyelinating polyradiculoneuropathy is an acquired, immune-mediated neuropathy characterized by progressive or relapsing symmetric weakness and sensory dysfunction due to demyelination of peripheral nerves. The literature suggests that pregnancy can both trigger new-onset and worsen relapses in CIPD (80; 68). Most reported cases occur during the first pregnancy, with women who carried pre-pregnancy diagnoses of CIPD experiencing relapse in all pregnancies (68). Long-term outcomes for both mother and fetus are generally reported as good following prompt recognition and treatment (68; 10).

The first-line treatment for CIPD during pregnancy is similar to that in AIDP, utilizing both IVIG and plasmapheresis without significant risk to mother or fetus (22; 69). IVIG is often preferred due to the favorable safety profile and support from randomized control trials (68). Plasmapheresis is effective for acute exacerbations but is less commonly used for maintenance therapy due to the risks, need for central venous access, and convenience. Unlike AIDP, intravenous or oral corticosteroids have been shown to be beneficial for short-term treatment of CIDP, as prolonged use carries risks such as gestational diabetes and hypertension (54; 76).

The effect of pregnancy and delivery on preexisting neuromuscular disorders

There are important considerations to be aware of in pregnant women with neuromuscular disorders such as hereditary neuropathies, myasthenia gravis, myopathy, and motor neuron disease. Women with hereditary neuromuscular conductions may experience worsening of their symptoms during pregnancy. Also, management may need to be modified during pregnancy.

Hereditary sensory and motor neuropathy. There is limited research on the effects of pregnancy on hereditary sensory and motor neuropathies, such as Charcot-Marie-Tooth disease and spinal muscular atrophy, but several international cohort studies and review papers have compared these populations with healthy cohorts.

Charcot-Marie-Tooth disease. Charcot-Marie-Tooth disease is the most common hereditary neuropathy characterized by progressive, length-dependent nerve degeneration leading to distal muscle atrophy and weakness, sensory disturbances, and characteristic foot deformities (09). The literature suggests that women with Charcot-Marie-Tooth disease have higher rates of preterm delivery, abnormal fetal presentation, and placenta previa than the general population (100). There is no significant risk noted to the fetus, with most newborns having normal birth weights (100; 113). Approximately 10% to 30% of patients across all subtypes of Charcot-Marie-Tooth disease were noted to have worsening of their symptoms during pregnancy, including progressive weakness, sensory deficits, cramping, and pain (04; 100; 113). The general care for patients with Charcot-Marie-Tooth disease is supportive. Prosthetic assist devices, walking assistance devices, and physical therapy are beneficial. At the time of delivery, if general anesthesia is needed, succinylcholine should be avoided because of the risk of hyperkalemia (124).

Spinal muscular atrophy. Spinal muscular atrophy is an autosomal recessive disorder characterized by progressive degeneration and loss of lower motor neurons in the anterior horn of the spinal cord and brainstem nuclei, leading to symmetric muscle atrophy and weakness (82). Studies have shown that women with spinal muscular atrophy have a higher incidence of preterm delivery and cesarean section than the general population, as well as progressive weakness both during and following pregnancy (04; 29; 126). Patients with spinal muscular atrophy are prone to respiratory distress, so baseline and serial pulmonary function testing is recommended during and after pregnancy due to the high risk of respiratory failure and maternal hypercapnia during pregnancy and delivery (29; 126). Given the risk for decompensation, regional anesthesia is preferred over general anesthesia in this population (126). For patients on disease-modifying therapy (nusinersen and gene therapies), discontinuation before conception is recommended due to unknown fetal risks, though recent studies have shown that nusinersen is safe when initiated in the third trimester (132).

In conclusion, there are no formal society guidelines for pregnancy management in hereditary neuropathies, but close monitoring and multidisciplinary care is recommended for these patients, given the potential for maternal and fetal complications.

Inflammatory myopathies. Inflammatory myopathies, such as dermatomyositis and polymyositis, are estimated to occur in 50 to 100 cases per million in the general population (105; 64), and only two cases per 100,000 pregnancies (137). The literature suggests that complications are associated with disease activity and that patients who are pregnant during periods of remission have more favorable outcomes than those who are pregnant during active disease (137). Active disease is consistently linked to increased rates of preterm birth, spontaneous abortion, stillbirth, low birth weight, intrauterine growth restriction, and the spectrum of hypertensive disorders of pregnancy, including preeclampsia (128; 15). One case series of four pregnant patients with inflammatory myopathy found no increase in disease activity during pregnancy. This was confirmed in a cohort of 14 women, 11 of whom had uncomplicated pregnancies and deliveries (99). Studies have shown a slight increased risk of disease activity or development of inflammatory conditions within the immediately postpartum period (133).

The first-line treatment for dermatomyositis and polymyositis disease activity is corticosteroids, which can be used with caution during pregnancy (class C). IVIG is also effective for steroid-resistant myositis (23). The combination of IVIG and corticosteroids has been successfully used to treat dermatomyositis in pregnancy (75). Uterine contractility is generally not affected by dermatomyositis or polymyositis, but these patients may need to be assisted with forceps or vacuum extraction if significant muscle weakness is present (121).

Muscular dystrophies. A variety of presentations and outcomes have been described in the literature regarding disease progression in women with myotonic dystrophy who become pregnant, as well as pregnancy complications, fetal presentations, and outcomes in these women. Muscle weakness may remain unchanged or gradually worsen, with an increased risk of disease progression in myotonic, limb-girdle, and facioscapulohumeral muscular dystrophies (58; 85; 66). This weakness often does not resolve postpartum, and nonambulant women are at a higher risk of both functional decline and obstetric complications, such as abnormal fetal presentations (eg, breech, transverse) during pregnancy as compared to their ambulatory counterparts (04). This weakness often persists after delivery, and postpartum care requires multidisciplinary management with early mobilization, tailored physiotherapy, mobility support, and assistance with breastfeeding due to muscle weakness (116; Awater and Rudnik-Schoneborn 2012; 85).

Several obstetric complications have been noted in this patient population. Overall, there is a higher incidence of operative deliveries due to involvement of uterine smooth muscle (85). Women with myotonic dystrophy type 1 have a higher risk of pregnancy complications, such as ectopic pregnancies, urinary tract infections, placenta previa, spontaneous abortions, premature deliveries, polyhydramnios, and neonatal death for causes not already described (58; 116; 121). Some studies have suggested there may be increased rates of postpartum maternal hemorrhage that can lead to emergent hysterectomy, but the available evidence suggests a similar rate when compared to the general obstetric population (121; 74; 85).

Fetal outcomes other than the previously described delivery-associated complications are also well-described in the literature. These are most notable in myotonic dystrophy type 1, where congenital myotonic dystrophy that is passed to an infant can result in hypotonia, respiratory insufficiency, and feeding difficulties (116; 74). Polyhydramnios and reduced fetal movement are also more frequent in myotonic dystrophy type 1 pregnancies. However, neonatal outcomes in other muscular dystrophies (eg, limb-girdle muscular dystrophy, facioscapulohumeral muscular dystrophy) are generally favorable unless the fetus is affected by the same disorder difficulties (116; 74).

The mode of delivery should be based on muscle strength, pelvic anatomy, and fetal presentation, with a low threshold to plan for operative-assisted delivery (79). Regional anesthesia is preferred with careful respiratory monitoring, and the patients should be informed of the potential need for respiratory support. Medications used during delivery can be associated with complications in patients with myotonic dystrophy. Whenever possible, general anesthesia should be avoided. Succinylcholine is often contraindicated due to the risk of severe hyperkalemia, rhabdomyolysis, and malignant hyperthermia-like reactions in this patient population (61; 122; 102). Nondepolarizing neuromuscular blocking agents (rocuronium, vecuronium, etc.) are preferred, but may result in prolonged neuromuscular blockage, and dosing should be carefully titrated to minimize effects. If overdosing occurs, sugammadex is the preferred reversal agent. Care should be taken to limit or avoid the use of magnesium sulfate for both tocolysis and preeclampsia management, as it may result in severe weakness and respiratory compromise in myotonic dystrophy type 1 (13).

Less is known about nondystrophic myotonias, such as myotonia congenita, during pregnancy. Two studies of pregnant patients with nondystrophic myotonia reported increased weakness and myotonia in just over half of the patients during pregnancy, with the majority returning to their previous baseline within 3 months postpartum when appropriate follow-up was obtained (135; 115). These patients should be monitored for functional decline to prevent injury, but the role of medication use in pregnancy is unclear, as the primary treatment, mexiletine, has not had a clearly studied safety profile in pregnancy (131). Overall, pregnancy outcomes are favorable, but multidisciplinary care and individualized management are recommended.

Metabolic and congenital disorders. Both metabolic and congenital myopathies are not well-studied in the pregnant population, and most of the data come from case reports.

Familial hypokalemic periodic paralysis is a rare neuromuscular disorder characterized by episodes of muscle weakness triggered by intense exercise, fasting, or consumption of carbohydrate-rich meals. In patients with familial hypokalemic periodic paralysis, the relationship between pregnancy and paretic attacks is variable. Several case series and reports describe an increased frequency or severity of attacks during pregnancy, but several studies have also shown little to no change in attack frequency (73; 115). Close monitoring of serum potassium is essential throughout the peripartum period, particularly during attacks (141). Epidural anesthesia is considered safe and may be beneficial in minimizing exertion during labor (106).

Mitochondrial myopathy refers to a group of disorders caused by defects in mitochondrial DNA or genes affecting mitochondrial function, which lead to impaired oxidative phosphorylation, particularly in tissues with high energy demands, such as muscle and the nervous system. Several studies have shown that patients with mitochondrial myopathy have a significantly increased risk of obstetric complications, including gestational diabetes, preeclampsia, hypertension, preterm delivery, intrauterine growth restriction, and higher rates of miscarriage (32; 118). Pregnancy can also exacerbate underlying myopathic symptoms, such as weakness and fatigue, and patients may have development or worsening of cardiorespiratory dysfunction and anemia during the peripartum period (129; 112). Preconception counseling, multidisciplinary management, and close monitoring are recommended for women with mitochondrial myopathies.

Congenital myopathies, such as nemaline myopathy, central core disease, multi-minicore disease, centronuclear myopathy, and myosin storage myopathy, are not well-studied due to the sparse case reports. The available literature, which includes cohort studies and reviews, suggests that women with congenital myopathies who are ambulatory at conception can expect pregnancy and delivery outcomes similar to the general population, with only a higher rate of elective cesarean and instrumental deliveries (04; 114). One study suggested that there is a higher risk for malignant hyperthermia with anesthesia (108). Deterioration of maternal muscle function during or after pregnancy is uncommon, but increased rates of falls and subjective weakness have been reported in nonambulatory patients (85). Cardiac involvement is rare, but there have been isolated cases of peripartum cardiac dysfunction, suggesting that individualized cardiac screening and subsequent monitoring may be beneficial for patients in selected subtypes (33). For example, there is a case report of a pregnant patient with Bethlem myopathy who had progressive cardiomyopathy during pregnancy (36).

There is little information available regarding pregnant women with metabolic myopathies, such as Pompe disease. However, there is a published cohort of pregnant women with Pompe disease who were able to successfully carry to term while on enzyme replacement (44). Given the scarcity of information available on every congenital and metabolic disorder, a multidisciplinary pre-conception discussion with the patient and family is recommended to ensure a thorough understanding of potential adverse outcomes.

Myasthenia gravis. Myasthenia gravis is an autoimmune disorder characterized by fluctuating and fatigable weakness of muscles due to impaired neuromuscular transmission mediated by autoantibodies affecting the post-synaptic membrane and altering cholinergic signal. Myasthenia gravis may develop for the first time during pregnancy or in the postpartum period. It occurs in one in 10,000 to one in 50,000 women of reproductive age, or 37 per 100,000 women of reproductive age (26; 107; 146).

The clinical outcome of pregnant women with myasthenia gravis is variable, and the relationship is thought to be bidirectional as pregnancy can influence the course of myasthenia gravis, and myasthenia gravis has clear implications for maternal and neonatal outcomes (02). The highest risk of exacerbation in a pregnant patient with myasthenia gravis appears to occur if pregnancy occurs within the first year of diagnosis, if an infection develops, or if the patient has an abnormal repetitive nerve stimulation test (26; 27). The primary maternal risks are secondary to disease state, with more frequent flares, acute respiratory failure, and risk of preterm birth being the most documented maternal complications (88). Worsening of symptoms was most likely to occur in the first or second trimester or first month postpartum but can occur throughout pregnancy (07; 27). Planned pregnancies were noted to be associated with fewer exacerbations and hospitalizations than unplanned pregnancies, and counseling is recommended for all women of reproductive age who express a desire or plan to become pregnant (90; 02).

The treatment of myasthenia gravis during pregnancy is multifactorial, based on patient stability, and often includes both symptomatic management as well as immunosuppression. Pyridostigmine has not been explicitly studied for safety during pregnancy, but the literature suggests that it does not cross the placenta in significant amounts, and it has not been associated with teratogenicity or an increased risk of congenital malformations (41). For this reason, pyridostigmine is the medication of choice for symptomatic treatment of patients not in myasthenic crisis or flare.

Neostigmine can be administered intramuscularly during labor or if oral medications cannot be given, but care must be taken to convert the pyridostigmine dose to neostigmine (70).

Prednisone or azathioprine are considered the preferred immunosuppressive therapies for women with myasthenia gravis during pregnancy, but risks should be discussed with patients as it is considered a class D medication in pregnancy (119; 46). Lab work is required to monitor leukopenia and liver toxicity while taking azathioprine. Both prednisone and methylprednisolone are category C medications and are considered safe in moderate doses. They are often used to treat myasthenia gravis during pregnancy and should be used at the lowest possible effective dose. However, fetal adrenal suppression after delivery has been reported in mothers treated with long-term prednisone (70).

Methotrexate is a folate inhibitor associated with congenital malformations and is absolutely contraindicated in pregnancy and breastfeeding. If used pre-pregnancy, a washout period of at least 3 months is recommended before conception.

Other immunosuppressants, such as cyclosporine, mycophenolate, methotrexate, cyclophosphamide, tacrolimus, rituximab, and eculizumab, are used to treat myasthenia in the general nonpregnant population but may need to be avoided during pregnancy. Cyclosporine does not appear to have any major risk for birth deformities and may also be considered for use during pregnancy. Mycophenolate is associated with miscarriage, premature birth, and birth defects and should be avoided during pregnancy.

Plasmapheresis and IVIG can safely be used and are effective for more severe symptoms of myasthenia gravis as well as exacerbations of symptoms during pregnancy. The main risk of plasmapheresis is hypotension due to massive fluid shifts and coagulopathy. Although IVIG can cause hyperviscosity, volume overload, aseptic meningitis, and hypercoagulability, it is generally the preferred treatment because of its established safety profile during pregnancy in other neurologic diseases, such as relapsing-remitting multiple sclerosis (28; 37). IVIG may even be used as monthly intravenous maintenance therapy (38).

Rituxan could be considered, although questions remain about the safety of rituximab during pregnancy and lactation (72).

Only prednisone, pyridostigmine, IVIG, and azathioprine have safety data to support their use during breastfeeding (24; 06).

Eculizumab may also be considered for use during pregnancy in refractory patients (120).

Table 1. Medications Commonly Used in Myasthenia Gravis: Safety During Pregnancy

Drug	Safe during pregnancy?	Does it enter breastmilk?	Safe during breastfeeding?	Comments	Possible adverse reactions
Pyridostigmine	Yes	Minimal < 1%	Yes		Gastrointestinal symptoms
Prednisone	Yes	No	Yes	Use least effective dose	Gestational diabetes
Rituximab	Unknown	Yes	Not recommended		Immune suppression in both mother and infant
Eculizumab	Unknown	Yes	Unknown
Azathioprine	Yes		Yes		Leukopenia
Mycophenolate mofetil	No		Unknown	Teratogenic	Major congenital malformations
Tacrolimus	Yes		Yes		Gestational diabetes and hypertension
Cyclosporine	Yes		Yes
Methotrexate	No		No	Teratogenic
IVIG	Yes		Yes		Fluid overload, coagulopathy
Plasma exchange	Yes		Yes		Fluid shifts
(90)

If a patient has been asymptomatic for more than a year before pregnancy, consideration should be given to reducing and stopping immunosuppressants at the beginning of the pregnancy or before conception (preferably). Although there are no published guidelines regarding the discontinuation of medications, as a rule, a taper can be attempted if a patient has achieved remission of myasthenic symptoms for 1 to 2 years. According to the Myasthenia Gravis Foundation of America class 1 definition, remission occurs when there is resolution of all muscle weakness and cranial nerve symptoms, except for mild eye closure weakness. The most successful tapers occur after the disease is under control or when it has been in remission for 4 to 5 years. About 30% to 50% of patients may experience a relapse after discontinuation of immunosuppressants, so close monitoring is necessary, especially if completion of taper immediately precedes pregnancy (47; 92).

Potential delivery-related complications also include acute respiratory failure due to crises triggered by stress, increased rates of labor induction and elective cesarean section, and the need for assisted vaginal delivery due to maternal muscle weakness. Myasthenia gravis does not affect uterine smooth muscle, but it may affect the striated muscles that are needed during voluntary pushing in the second stage of labor. However, the number of forceps deliveries or vacuum extractions needed during the second stage of labor is no greater than in the general population (144). Epidural anesthesia is preferred over general anesthesia for surgical delivery as surgery has been noted to be a potential trigger of myasthenic crisis (35). Nondepolarizing muscle relaxants may cause prolonged or exaggerated reactions in myasthenic patients. Spontaneous abortion in the first trimester may improve myasthenic exacerbations, but elective cesarean section can cause worsening of myasthenic gravis (20). Magnesium sulfate, used to treat preeclampsia, can also worsen myasthenia by inhibiting acetylcholine release and should be avoided (41). Also, caution should be used when treating hypertension in myasthenic patients with a beta blocker, as this can increase the risk of an exacerbation. Patients with myasthenia should be encouraged to proceed with vaginal delivery at term whenever possible because general anesthesia can lead to worsening disease (90; 27). Epidural anesthesia, combined spinal epidural anesthesia for caesarian section, and nitrous oxide are all considered safe methods of anesthesia in patients with myasthenia gravis, but the decision of delivery route and anesthesia provided should be a multidisciplinary discussion between the patient, family, and providers.

Neonatal complications include transient neonatal myasthenia gravis most commonly, but, rarely, arthrogryposis multiplex congenita or persistent myopathy can occur and is associated with an increased risk of spontaneous abortion (42; 40). Transient neonatal myasthenia gravis can occur in the newborn of myasthenia mothers in the first few hours to days after birth as hypotonia, weak cry, poor feeding, and, in severe cases, respiratory distress (40). Transient neonatal myasthenia gravis occurs in about 12% to 20% of infants of mothers with myasthenia gravis (86; 27). However, it is difficult to predict which infants will be affected by transient neonatal myasthenia gravis because there does not seem to be a clear correlation with the severity of active disease in the mother and the development of symptoms in the infant. High levels of acetylcholine receptor antibodies in the mother or infant do not necessarily correlate with more severe disease. Transient neonatal myasthenia can even occur in infants of myasthenic mothers who are in clinical remission. However, there does seem to be some correlation between the severity of transient neonatal disease and a high ratio of anti-fetal to anti-adult acetylcholine receptor antibodies (07). High levels of the anti-fetal acetylcholine receptor generated by the mother can rarely result in alteration in fetal muscle development, leading to persistent facial and bulbar weakness or fetal arthrogryposis (140; 93). Anti-muscle-specific kinase (MuSK) can also cross the placenta and result in transient neonatal myasthenia (89). However, one retrospective publication of 14 MuSK myasthenic pregnancies all resulted in healthy infants (50).

Motor neuron disease. Motor neuron diseases are a broad group of progressive neurodegenerative disorders characterized by selective loss of motor neurons in the central nervous system, with effect on the upper motor neurons in the motor cortex and the lower motor neurons in the brainstem and spinal cord. This group of conditions includes, but is not limited to, amyotrophic lateral sclerosis, primary lateral sclerosis, progressive muscular atrophy, spinal muscular atrophy, progressive bulbar palsy, hereditary spastic paraplegia, Kennedy disease, and multifocal motor neuropathy. There are few reported cases of motor neuron disease during pregnancy, and primary comments come from case reports due to the small sample size.

The most common motor neuron disease to occur is amyotrophic lateral sclerosis, though this still rarely occurs during pregnancy, as it typically affects older adults. There are multiple reports of women developing symptoms of amyotrophic lateral sclerosis during pregnancy, with concerns that the disease will progress rapidly during the peripartum period (48). However, the clinical course of amyotrophic lateral sclerosis during pregnancy appears variable, as there are case reports of a patient who remained stable during pregnancy and reports of stable patients who go on to develop worsening bulbar symptoms in the 6 weeks postpartum (101; 49). An analysis of five patients who developed amyotrophic lateral sclerosis during pregnancy found an increased rate of pathologic mutations in the superoxide dismutase 1 gene and an association with a particular vascular endothelial growth factor haplotype (77). This publication, along with previous case reports, suggests that patients who develop amyotrophic lateral sclerosis during pregnancy are more likely to have a family history of amyotrophic lateral sclerosis and have a genetic predisposition to develop the disease (57; 77). Riluzole has not been shown to cause complications when taken during pregnancy (63). There is little information on the use of edaravone in pregnancy.

The primary maternal risks during pregnancy with motor neuron disease are that the disease can progress and lead to respiratory compromise, nutritional deficiencies due to worsened bulbar symptoms, and increased risk of thromboembolic events due to immobility (48). The timing and method of delivery should be tailored to patient disability, but vaginal delivery is often possible because the uterine smooth muscle is not affected by disease progression (121; 85). Cesarean section should be favored if there is respiratory compromise or concern for progressing respiratory failure. Infants born to mothers with motor neuron disease generally have similar outcomes to children born to mothers without motor neuron disease, though the primary adverse events reported have been preterm birth or fetal growth restriction (48).

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Aparna M Prabhu MD MRCP

Dr. Prabhu of Thomas Jefferson University and Jefferson Einstein Medical Center has no relevant financial relationships to disclose.
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Rebecca Frawley DO

Ms. Frawley of Jefferson Einstein Philadelphia Hospital has no relevant financial relationships to disclose.
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Editor

Nicholas E Johnson MD MSCI FAAN

Dr. Johnson of Virginia Commonwealth University received consulting fees and/or research grants from AMO Pharma, Avidity, Dyne, Novartis, Pepgen, Sanofi Genzyme, Sarepta Therapeutics, Takeda, and Vertex, consulting fees and stock options from Juvena, and honorariums from Biogen Idec and Fulcrum Therapeutics as a drug safety monitoring board member.
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Former Authors

Timothy Miller MD PhD
Ann Poncelet MD
Zachary N London MD
Jackie Whitesell MD
Emma Ciafaloni MD FAAN

Patient Profile

Age range of presentation: 15 to 48 years
Sex preponderance: female only
Heredity: Myotonic muscular dystrophy: autosomal dominant

Fascioscapulohumeral muscular dystrophy: autosomal dominant

Limb girdle muscular dystrophy: autosomal recessive or dominant

Hypokalemic periodic paralysis: autosomal dominant

Spinal muscular atrophy: autosomal recessive
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Complication of the puerperium, unspecified: O90.9

Pregnancy-related condition, unspecified: O26.9

Carpal tunnel syndrome: G56.0

Cramp and spasm: R25.2

Bell palsy: G51.0

Lumbosacral root disorders, not elsewhere classified: G54.4

Muscular dystrophy: G71.0

Amyotrophic lateral sclerosis: G12.2

Myasthenia gravis: G70.0

Myotonic disorders: G71.1

Spinal muscular atrophy, unspecified: G12.9

Hereditary motor and sensory neuropathy: G60.0
ICD-11: Complications predominantly related to the puerperium, unspecified: JB4Z

Maternal care for other conditions predominantly related to pregnancy: JA65

Carpal tunnel syndrome: 8C10.0

Cramp or spasm: MB47.3

Bell palsy: 8B88.0

Other specified nerve root or plexus disorders: 8B9Y

Muscular dystrophy: 8C70

Amyotrophic lateral sclerosis: 8B60.0

Myasthenia gravis: 8C60

Myotonic disorders: 8C71

Spinal muscular atrophy: 8B61

Hereditary motor and sensory neuropathy: 8C20

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Pregnancy: neuromuscular complications

Associated Disorders

Acute inflammatory demyelinating polyradiculoneuropathy
Bell palsy
Carpal tunnel syndrome
Chronic inflammatory demyelinating polyradiculoneuropathy
Demyelinating neuropathies
- Femoral mononeuropathy
- Hereditary sensory and motor neuropathy I and II
- Inflammatory myopathies
- Lumbosacral radiculopathy
- Meralgia paresthetica
- Metabolic myopathies
- Motor neuron disease
- Muscular dystrophies
- Myasthenia gravis
- Obturator mononeuropathy
- Peroneal mononeuropathy
- Sciatic mononeuropathy

Also Relevant

Acute inflammatory demyelinating polyradiculoneuropathy
Bell palsy
Carpal tunnel syndrome
Chronic inflammatory demyelinating polyradiculoneuropathy
Headache associated with hormonal fluctuations
- Lumbosacral plexus injuries
- Motor and multifocal motor neuropathies
- Myasthenia gravis
- Myotonic dystrophy
- Neurogenetics and genetic and genomic testing
- Pregnancy and epilepsy
- Pregnancy and stroke
- Pregnancy: CNS complications

Pregnancy: neuromuscular complications …

Pregnancy: neuromuscular complications

Cite this article

Introduction

Overview

Key points

Neuromuscular disorders that present during pregnancy

Common mononeuropathies

The effect of pregnancy and delivery on preexisting neuromuscular disorders

Table 1. Medications Commonly Used in Myasthenia Gravis: Safety During Pregnancy

Clinical vignette

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Mental status examination

Turcot syndrome

Upadacitinib

Dextromethorphan hydrobromide and quinidine sulfate

DNA- and RNA-directed gene therapies

Amblyopia

Coma due to supratentorial and cerebellar lesions

Nystagmus

Pregnancy: neuromuscular complications

Cite this article

Introduction

Overview

Key points

Neuromuscular disorders that present during pregnancy

Common mononeuropathies

The effect of pregnancy and delivery on preexisting neuromuscular disorders

Table 1. Medications Commonly Used in Myasthenia Gravis: Safety During Pregnancy

Clinical vignette

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Mental status examination

Turcot syndrome

Upadacitinib

Dextromethorphan hydrobromide and quinidine sulfate

DNA- and RNA-directed gene therapies

Amblyopia

Coma due to supratentorial and cerebellar lesions

Nystagmus

This is an article preview.
Start a Free Account
to access the full version.