Review Article

Peripheral Neuropathies
Address correspondence to
Dr E. Wayne Massey, Division
of Neurology, Department of
Medicine, Duke University
Medical Center, DUMC 3909,
Durham, NC 27710,
masse010@mc.duke.edu.
in Pregnancy
Relationship Disclosure: E. Wayne Massey, MD, FAAN; Amanda C. Guidon, MD
Drs Massey and Guidon
report no disclosure.
Unlabeled Use of
Products/Investigational ABSTRACT
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Use Disclosure:
Drs Massey and Guidon
report no disclosure.
* 2014, American Academy
of Neurology.
Purpose of Review: This article provides an overview of the most common
peripheral neuropathic disorders in pregnancy with a focus on clinical recognition,
diagnosis, and treatment.
Recent Findings: The literature on this topic consists primarily of case reports, case
series, and retrospective reviews. Recent work, particularly in carpal tunnel syn-
drome, brachial neuritis, and inherited neuropathies in pregnancy, has added to our
knowledge of this field. Awareness of diabetic polyneuropathy with associated
autonomic dysfunction in pregnancy has grown as the incidence of diabetes
mellitus increases in women of childbearing age.
Summary: Women may develop mononeuropathy, plexopathy, radiculopathy, or
polyneuropathy during pregnancy or postpartum. Pregnancy often influences con-
sideration of etiology, treatment, and prognosis. In women of childbearing age with
known acquired or genetic neuromuscular disorders, pregnancy should be anticipated and
appropriate counseling provided. An interdisciplinary approach with other medical
specialties is often necessary.

Continuum (Minneap Minn) 2014;20(1):100–114.

INTRODUCTION of EMG and nerve conduction studies

Disorders affecting peripheral nerves,
plexus, or nerve roots are generally
rare in pregnancy and the postpartum
period. However, they may be com-
monly encountered in both inpatient
and outpatient neurology practice.
Acquired and inherited peripheral
nerve dysfunction affects the mother
and fetus in various ways. This article
reviews the most commonly encoun-
tered peripheral nerve disorders in
pregnancy (Table 5-1) with the goal
of facilitating rapid recognition, treat-
ment, symptom management, appro-
priate counseling, and interdisciplinary
collaboration.
After initial history and focused
symptom-specific neurologic examina-
tion, the clinician should strive to
localize the problem to one nerve,
multiple nerves, plexus, or nerve root.
Electrodiagnostic studies, consisting
100 www.ContinuumJournal.com
(NCS), both safe in pregnancy, further
refine the clinical localization and
provide additional information about
severity, chronicity, and prognosis. In
some cases, further laboratory or
imaging evaluation is warranted.
When choosing therapy, clinicians
should consider potential effects on
the fetus during pregnancy and
whether the patient is breast-feeding
postpartum.
UPPER EXTREMITY
Median Neuropathy at the
Wrist (Carpal Tunnel Syndrome)
Carpal tunnel syndrome (CTS) is the
most common mononeuropathy during
pregnancy. Estimates of the incidence
of pregnancy-related CTS vary from 1%
to 60% depending on study methodol-
ogy. Incidence is approximately 17%
in prospective studies describing
February 2014

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 KEY POINT

TABLE 5-1 Most Common Peripheral Neuropathic Disorders h Carpal tunnel syndrome
in Pregnancy is common in
pregnancy. Treatment
b Upper Extremity is typically conservative,
particularly when
Mononeuropathies (median, ulnar, radial)
symptoms start during
Brachial neuritis/neuralgic amyotrophy the third trimester.
b Lower Extremity
Mononeuropathies (femoral, obturator, lateral femoral cutaneous, fibular)
Lumbosacral plexopathy
Lumbosacral radiculopathy
b Facial Neuropathy (Bell Palsy)
b Intercostal Neuralgia
b Polyneuropathy
Immune-mediated neuropathies (eg, acute inflammatory demyelinating
polyradiculoneuropathy, chronic inflammatory demyelinating
polyradiculoneuropathy, multifocal motor neuropathy)
Diabetic polyneuropathy
Polyneuropathy due to nutritional deficiency
Genetic causes of polyneuropathy (eg, Charcot-Marie-Tooth, hereditary
neuropathy with liability to pressure palsies)

only electrodiagnostically confirmed cause edema in the tissues of the carpal

pregnancy-related CTS.1 EMG and
NCS can distinguish pregnancy-related
CTS from other forms of pregnancy-
related hand pain.
Key presenting features include
nocturnal or activity-related hand par-
esthesias, which can be painful. Sen-
sory disturbance classically occurs in a
median distribution in the hand; how-
ever, more widespread hand and arm
symptoms are commonplace. Patients
often describe hand stiffness and
clumsiness, and in severe cases, weak-
ness of the abductor pollicis brevis
may occur.2
Although it is a common disorder in
pregnancy, the etiology of pregnancy-
related CTS is poorly understood. In
general, CTS is caused by compression
of the median nerve at the wrist due to
reduced space in the carpal tunnel.
Pregnancy-induced fluid retention may
tunnel. Most women with pregnancy-
related CTS develop symptoms in the
third trimester when they have more
generalized edema, which supports this
hypothesis. Other hypotheses include
the effect of relaxin and other hor-
mones on ligamentous laxity, changes
in sleep position, and increased adipose
tissue in pregnancy. Although diabetes
mellitus is a known risk factor for CTS in
the general population, an association
between gestational diabetes mellitus
and pregnancy-related CTS is not
known. Pregnancy-related CTS may
occur postpartum and is most typically
associated with breast-feeding, possibly
due to altered hand positioning.3
Given the high likelihood that
pregnancy-related CTS will resolve in
the postpartum period, management
is typically conservative, as illustrated
by Case 5-1. Pregnancy-related CTS

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 Peripheral Neuropathies in Pregnancy

KEY POINTS
h While carpal tunnel
syndrome in pregnancy
Case 5-1
A 35-year-old right-handed woman developed severe bilateral hand
is often less severe than
pain and paresthesia during her third trimester. Her symptoms intermittently
nonYpregnancy-related
extended to her forearms and were particularly severe at night. She
carpal tunnel syndrome,
described hand clumsiness and swelling. Carpal tunnel syndrome (CTS)
a significant percentage
was suspected. A trial of wrist splints recommended by her obstetrician
of women may have
provided no relief. Neurologic examination was notable for normal
ongoing symptoms
strength, decreased sensation in a median distribution in the right hand,
postpartum.
and a Tinel sign over the median nerve at both wrists. Electrodiagnostic
Electrodiagnostic
studies showed mild, bilateral, right greater than left median neuropathies
studies are
at the wrist. No evidence of more widespread polyneuropathy was present.
recommended to
Given the symptom severity and failed trial of wrist splints, the option of
support the diagnosis
injections for CTS was discussed. The patient declined but stated that she
in cases of severe,
was relieved to know the cause of her symptoms, which resolved
atypical, or persistent
3 months postpartum.
symptoms.
Comment. This patient was diagnosed with pregnancy-related CTS.
h Carpal tunnel syndrome By electrodiagnostic criteria, pregnancy-related CTS is typically mild,
may present or worsen although patients may describe severe symptoms with significant
postpartum. functional impairment. As this case illustrates, symptoms often resolve
postpartum, particularly when they first appear in the third trimester.
Recent longitudinal data, however, suggest that a larger percentage of
women than previously suspected may have persistent symptoms after
delivery, particularly when symptom onset occurs early in pregnancy.
Conservative measures and anticipatory guidance are typically
recommended for pregnancy-related CTS.

is typically less severe than nonY
pregnancy-related CTS, thus justifying
more conservative management. Ini-
tial recommendations include using
wrist splints to maintain a neutral
position and avoiding repetitive ma-
neuvers that may worsen symptoms.
Few data compare the effects of
various nonoperative therapies (eg,
analgesics, low-salt diet, rest, splinting,
local steroid or lidocaine injections).
The belief that symptoms resolve
in 75% of patients in the first month
postpartum was recently challenged. A
3-year longitudinal study that included
a control group of age-matched,
nonpregnant women showed that per-
sistent symptoms were more common
than previously estimated. Approxi-
mately 50% of all patients with
pregnancy-related CTS had improve-
ment of symptoms in 1 year, and
between 60% and 70% improved in 3
years. However, among women not
treated surgically, at 3 years 50% of
those with pregnancy-related CTS still
had symptoms, in comparison with 83%
of women in the control group.4 Pa-
tients with symptom onset earlier in
pregnancy and with greater pregnancy-
associated weight gain were more
likely to have persistent symptoms.
Surgical therapy should be consid-
ered if conservative measures fail,
symptoms are severe, or progression
occurs after delivery. Surgery can
nearly always be postponed until after
delivery. It is important to remember
that surgery may restrict hand and arm
use in the postpartum period, when
newborns require handling and care.
Ulnar and Radial
Neuropathies
Ulnar and radial neuropathies occur
infrequently in pregnancy. If severe or

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atypical or if localization is uncertain
clinically, electrophysiologic evalua-
tion may be considered. Therapy for
ulnar neuropathy first involves care
not to traumatize the olecranon
groove or other site of compression,
such as the wrist.3 Radial neuropathy
near the spiral grove associated with
prolonged use and inappropriate po-
sitioning of a birthing bar during labor
has been reported.5 A birthing bar
attaches to the labor bed and creates a
shelf on which a woman may rest her
upper arms. It is sometimes used to
facilitate a squatting position during
the second stage of labor.
Neuralgic Amyotrophy
Neuralgic amyotrophy, also known as
Parsonage-Turner syndrome or brachial
neuritis, has both an idiopathic and
autosomal dominant hereditary form.
Both forms are characterized by attacks
of severe neuropathic pain, typically in
the shoulder, followed by multifocal
upper limb weakness and atrophy. The
upper trunk of the brachial plexus is
usually affected, scapular winging is
frequently present, and sensory symp-
toms can be patchy. However, the
clinical presentation is often heteroge-
neous; it may be bilateral or involve
nerves outside the brachial plexus, such
as the phrenic or spinal accessory nerves.
Progression is rapid initially, and recov-
ery may take months to years.
Altered immunity and resulting in-
flammation are thought to underlie
both the idiopathic and hereditary
forms of neuralgic amyotrophy. He-
reditary neuralgic amyotrophy is ge-
netically heterogenous, but mutations
in the SEPT9 gene on chromosome
17q25 have been reported in the
majority of affected families. Features
suggesting hereditary rather than idio-
pathic neuralgic amyotrophy include
repeated episodes (especially post-
partum), family history, involvement of
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KEY POINTS
nerves outside the brachial plexus, and h Neuralgic amyotrophy
the presence of mild dysmorphic fea- has both idiopathic and
tures. Dysmorphic features in hereditary autosomal dominant
neuralgic amyotrophy include short hereditary forms. Both
stature, hypotelorism, epicanthic folds, forms may occur
redundant cervical skin folds, and dys- postpartum. The
morphic ears.6 In one series of 246 inherited variety can
patients, four of the 10 cases of neural- recur with subsequent
gic amyotrophy associated with preg- pregnancies, and no
nancy were hereditary, whereas the known method exists
to prevent attacks.
remaining six were idiopathic.7 The
method of delivery (eg, vaginal or h Attention to positioning
cesarean delivery) does not appear to in labor helps prevent
influence the incidence of postpartum lower extremity
mononeuropathies.
attacks in hereditary neuralgic amyo-
Femoral, fibular, and
trophy, and no proven way to prevent
(less commonly)
episodes exists. Anecdotally, early treat- obturator neuropathies
ment with corticosteroids in hereditary may occur.
neuralgic amyotrophy and idiopathic
neuralgic amyotrophy may stop progres-
sion, limit pain, or improve outcome.6
LOWER EXTREMITY
During pregnancy or after delivery,
women may develop lower extremity
weakness or sensory loss. Postpartum
peripheral nerve injuries are now un-
common as a result of prevention strat-
egies during labor.8 In general, frequent
leg position changes, shortened active
labor time, and avoidance of prolonged
hip flexion, extreme thigh abduction, or
hip external rotation are protective.
Particular attention is warranted in
women receiving epidural anesthesia,
which is associated with a longer second
stage of labor. Sensory blockade makes
women less likely to sense pressure
and change their own position.9
Femoral and Obturator
Neuropathies
The femoral nerve is formed by the
L2 to L4 nerve roots and arises from
the lumbar plexus. The nerve passes
between the psoas and iliacus muscles
and under the inguinal ligament. Dur-
ing delivery, the femoral nerve may be
compressed at the inguinal ligament
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 Peripheral Neuropathies in Pregnancy
KEY POINT
h The etiology of
compression or stretch
should be evaluated
when women develop
lower extremity
mononeuropathies
or plexopathy
postpartum.
Electrodiagnostic studies
confirm localization and
assist with assessment of
severity and prognosis,
which is typically
favorable.
104 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
or stretched through hip abduction
and external rotation.10 In femoral
neuropathy, patients report difficulty
standing and may describe a buckling
sensation in the leg. This results from
weakness of the quadriceps femoris
and, in lesions proximal to the ingui-
nal ligament, the iliopsoas. Sensory
loss and paresthesia may be seen in
the distribution of the femoral nerve
over the distal anteromedial thigh
and, if involved, the saphenous nerve
over the anteromedial aspect of the
lower leg. The patellar reflex can be
diminished or absent. Weakness of
both hip flexion and adduction sug-
gests a plexus or root lesion instead of
an isolated femoral neuropathy.11
Although obturator neuropathy is rare
postpartum, it should be considered in a
patient with isolated hip adduction weak-
ness and numbness over the proximal
medial thigh. The obturator nerve may
be affected by the lithotomy position. A
cadaver study suggested that hip abduc-
tion, as is used in the lithotomy position,
increases strain on the obturator nerve
to a degree that has been associated
consistently with subsequent nerve dys-
function. This strain was lessened by
using concomitant hip flexion.12 The
nerve may also be compressed against
the pelvic brim during forceps delivery or
due to hematoma from pudendal nerve
block.9 In both femoral and obturator
neuropathy in the postpartum, pelvic
imaging is often indicated if symptoms
are persistent or compression from hem-
orrhage is suspected.13 If no cause is
found, treatment is supportive. Symptoms
often improve within 2 to 6 months.9
Fibular (Peroneal) Neuropathy
Following reviewed terminology pub-
lished in 1998 by the Federative
Committee on Anatomical Termi-
nology (FCAT), the peroneal nerve is
known as the fibular nerve, to distin-
guish it from other nerves with similar
names; both terms are still used
interchangeably by many texts. During
pregnancy or following labor, women
who have a fibular (peroneal) neurop-
athy may report paresthesia along the
lateral aspect of the leg and may notice
foot drop; examination reveals weakness
of ankle dorsiflexion and eversion, and
toe extension. Sensory loss may involve
the lateral aspect of the leg and dorsum
of the foot. The deep or superficial
branches of the fibular nerve may be
affected together or in isolation. Me-
chanical injury, neuroma, fat, or cysts
can compress the common fibular nerve
at the fibular head. Cysts may enlarge
during pregnancy. Electrodiagnostic
evaluation can confirm fibular neuropa-
thy and exclude lumbosacral plexopathy
and L5 radiculopathy. Peripheral nerve
ultrasound may further aid in localiza-
tion or in identification of structural
causes of focal compression. Prognosis
for recovery from pregnancy-related
lower extremity nerve injury is typically
good; however, the number of patients
with peroneal neuropathy in one study
of postpartum nerve injuries was small.9
The potential etiology of injury and
severity of deficits should be considered
in each case to help guide assessment
of prognosis. Patients should be
counseled to avoid pressure at the
fibular head from activities such as
prolonged squatting or crossing the
legs. Ankle-foot orthoses may be re-
quired to assist with ambulation if
severe ankle dorsiflexion weakness is
present.3
Lateral Femoral Cutaneous
Neuropathy (Meralgia
Paresthetica)
Meralgia paresthetica is a sensory
mononeuropathy that occurs from in-
jury to the lateral cutaneous nerve of
the thigh (also called the lateral femo-
ral cutaneous nerve). The course of the
nerve is highly variable, and locations
February 2014

of trauma include the psoas or tensor
fascia lata muscles, the iliacus compart-
ment in the pelvis, the inguinal liga-
ment, or the thigh. No cause is
identified in many cases. Symptoms
may be bilateral. Physical examination
reveals sensory loss in the anterolateral
thigh in the distribution of the lateral
cutaneous nerve of the thigh. Impor-
tantly, because the lateral cutaneous
nerve of the thigh is an exclusively
sensory nerve, strength and deep ten-
don reflexes are normal. Standing,
walking, and flexion or extension ma-
neuvers of the hip can exacerbate
symptoms.11
During pregnancy and delivery, the
lateral cutaneous nerve of the thigh
can be stretched or compressed. This
nerve is unlikely to be damaged
during regional anesthesia because it
originates more caudal and lateral
than the site typically used for epidu-
ral placement.2,14 Presence of meralgia
paresthetica should not preclude the
use of regional anesthesia. Man-
agement of meralgia paresthetica in
pregnancy focuses on symptom man-
agement. Most cases resolve sponta-
neously within several months of
delivery. Avoiding aggravating posi-
tions and tight-fitting clothing is
recommended.15 Tricyclic antidepres-
sants or anticonvulsants, which are
first-line medications in nonpregnant
patients, are all FDA pregnancy cate-
gory C or D.10 These are not recom-
mended for use in pregnancy because
the risk to the fetus outweighs po-
tential benefit to the patient with
meralgia paresthetica.
Lumbosacral Plexopathy
Injuries to the lumbosacral plexus can
occur during the third trimester or
delivery, due to compression from the
fetal head or forceps. The plexus is
relatively unprotected at the pelvic
brim. Therefore, fetal macrosomia
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KEY POINT
and malpresentation are risk factors.9 h Meralgia paresthetica
Symptoms include pelvic and proxi- involves sensory loss
mal leg weakness and pain with asso- and paresthesia of the
ciated weakness in ankle dorsiflexion, anterior and lateral
inversion, and eversion. Muscles in- thigh. While symptoms
nervated by L4 and L5 roots are most are bothersome to the
affected. Sensory impairment predom- patient, it is typically a
inates in an L5 distribution. The benign disorder, which
Achilles (S1) reflex is often spared. is diagnosed clinically.
Electrodiagnostic studies show a plex- Electrodiagnostic
studies can be
us lesion (ie, sparing the paraspinal
performed if the
muscles).3 Outcome data are limited,
localization is in
and after excluding an ongoing com- question. Normal
pressive lesion, management is typi- strength and deep
cally conservative. tendon reflexes help
distinguish this from
Low Back Pain and Lumbosacral other causes of sensory
Radiculopathy disturbance of the
Low back pain from musculoskeletal thigh.
causes is reported in approximately
50% of pregnancies. However, low
back pain due to herniated disc is rare
and occurs in an estimated 1 in 10,000
pregnancies. Pregnancy does not in-
crease the risk of disc herniation.16
Back pain without neurologic deficits
can be managed symptomatically.
Changes in sensation, strength, or
reflexes, however, should prompt in-
vestigation for radiculopathy with
noncontrasted MRI and electro-
diagnostic studies. Most common
causes of radiculopathy can be inves-
tigated without contrast. Gadolinium
agents are FDA pregnancy category C
and should only be used if the poten-
tial clinical benefit outweighs the risk
(for more on this topic, see ‘‘Neuro-
radiology in Women of Childbearing
Age’’ by Drs Riley Bove and Joshua
Klein in this issue of ).
Contrast is typically indicated only if
concern exists for infection, inflamma-
tion, or malignancy causing radi-
culopathy.17 Conservative measures
such as rest, physical therapy, postural
education, and lumbar support are
generally recommended.18 Surgery is
typically avoided in pregnancy except
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 Peripheral Neuropathies in Pregnancy
KEY POINTS
h Back pain with focal in cases of significant progressive
neurologic deficits neurologic deficits or cauda equina
should prompt further syndrome.18
investigation for The risk of neurologic complication
radiculopathy, which from epidural anesthesia is low, esti-
occurs only rarely in mated at 0.1%. Potential complications
pregnancy. include epidural hematoma, drug
h Epidural anesthesia toxicity, chemical radiculitis, arach-
very uncommonly noiditis, and direct needle injection
results in neurologic injury into the nerve root. Therefore,
complications, including urgent MRI is recommended in women
radiculitis, arachnoiditis, who develop radiculopathy or myelop-
or epidural hematoma. athy after epidural anesthesia.19 Al-
h Women have an though electrodiagnostic studies have
increased risk of Bell limited ability to detect abnormalities
palsy in the third in the acute setting, studies may be
trimester and postpartum. performed to establish a baseline for
Pregnancy-related Bell future comparison if symptoms persist.
palsy may be more severe
than nonYpregnancy- Idiopathic Facial Nerve Palsy
related Bell palsy. The
(Bell Palsy)
risks versus benefits of
treatment with steroids Bell palsy is the most common disor-
should be considered for der of the facial nerve. Pregnant
each patient. women, particularly in the third tri-
mester and in the first 2 weeks
postpartum, have 3 times the risk for
developing Bell palsy over their
nonpregnant counterparts. The path-
ophysiology of Bell palsy in pregnancy
is poorly understood. Relative immu-
nosuppression hypothetically may
lower the threshold for reactivation
of herpes viruses in the geniculate
ganglion. Increased extracellular vol-
ume, hypertension, hypercoagulable
states, and changes in hormonal levels
have also been suggested. Retrospec-
tive studies have shown a significant
association with chronic or gestational
hypertension, preeclampsia, and dia-
betes mellitus.10
Bell palsy presents identically in
pregnant and nonpregnant women,
but the course may be more severe
in pregnant women. Although most
patients regain normal or near-normal
function, retrospective data suggest
that pregnant women are more likely
to have complete facial paralysis,
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Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
which is a poor prognostic factor.20
Whether this difference is due to the
disease process or treatment-related
factors is unknown.
Pregnant and breast-feeding women
have traditionally been excluded from
corticosteroid and antiviral trials for
Bell palsy. The decision to treat preg-
nant women or not involves con-
sideration of the potential risks and
benefits. Recent evidence-based guide-
lines published by the American
Academy of Neurology (AAN) recom-
mended using corticosteroids for Bell
palsy in the general population when
started within 3 to 7 days of symptom
onset to maximize the chance for
facial nerve recovery.21 Steroids are
FDA pregnancy category C and prob-
ably safe during lactation. As in the
general population, comorbid condi-
tions need to be considered when
making the decision to start these
agents in pregnancy or postpartum. If
the patient has poorly controlled hy-
pertension or hyperglycemia, the risk
may outweigh the benefit. The same
AAN guidelines found that antiviral
agents have not conclusively shown
efficacy in Bell palsy, and their benefit
may only be modest. These agents are
FDA pregnancy category B and con-
sidered generally safe in breast-
feeding. No clear evidence-based
guidelines for treating pregnant or
breast-feeding patients who have Bell
palsy have been published. Typically,
in an otherwise uncomplicated preg-
nancy, the potential benefit of treat-
ment with corticosteroids after the
first trimester is likely to outweigh
the risk, in the authors’ opinion.
Because of the uncertain benefit and
possible risk, antiviral agents can
probably be forgone in pregnancy
when no additional manifestations of
viral infection are present. In all pa-
tients, the eye should be lubricated to
prevent corneal abrasion. Patients can be
February 2014

reassured that recurrence of Bell palsy
in future pregnancies is rare.3
Intercostal Neuralgia
Intercostal neuralgia occurs rarely in
pregnancy (when it is also called
thoraconeuralgia gravidarum). Patients
experience mild to severe pain and
sensory change in the distribution of
one to two thoracic roots, typically in
the lower thoracic region. Pain can
worsen with palpation of the paraspinal
muscles or radiate to the abdomen. The
etiology is unknown and may relate to
stretch injury. Because symptoms typi-
cally remit within hours of delivery, a
physiologic rather than structural cause
of nerve injury has been hypothesized.
EMG may reveal abnormal spontaneous
activity in the paraspinal muscles of the
corresponding symptomatic level. This
abnormality is not required for diagno-
sis.22 Intra-abdominal and spinal (spinal
cord or radicular) etiologies should be
considered in the differential diagnosis,
and imaging of the thoracic spine may
be considered. Herpes zoster should
be considered in the presence of a skin
rash. Treatment with topical lidocaine
patches, FDA pregnancy category B,
may be considered after a discussion of
the risk of treatment to the fetus versus
potential benefit to the patient. Ex-
tended epidural anesthetic until delivery
has been reported in a severe case.23
POLYNEUROPATHY
The general approach to the evalua-
tion of polyneuropathy is not sig-
nificantly changed by pregnancy.
Clinicians use the history, physical
examination, and electrodiagnostic
studies to characterize the polyneu-
ropathy systematically and narrow the
differential diagnosis of potential etiol-
ogies. A series of questions helps focus
the evaluation (Table 5-224). With this
framework in mind, the authors focus
this discussion on several forms of
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KEY POINTS
polyneuropathy with particular rele- h Intercostal neuralgia
vance to pregnancy and the postpar- results in pain and
tum period. sensory change in the
distribution of one or
AUTOIMMUNE NEUROPATHIES two thoracic roots. The
Acute Inflammatory etiology in pregnancy
Demyelinating is unknown, and
Polyradiculoneuropathy symptoms typically
Acute inflammatory demyelinating resolve within hours
polyradiculoneuropathy (AIDP), or of delivery.
Guillain-Barré syndrome, is an acute h The approach to
neuropathy that may affect women evaluation of
during pregnancy or the postpartum polyneuropathy is not
period. The incidence of AIDP is ap- significantly changed
by pregnancy.
proximately 0.75 to 2 in 100,000 per year
and increases with age. During preg-
nancy, the age-adjusted incidence is
identical to that of the general popula-
tion. Nearly all of these cases, however,
occur in the second or third trimesters
or the first month postpartum.25
The clinical presentation of AIDP
and approach to therapy in pregnancy
is the same as in the general popula-
tion. Patients develop progressive
weakness, sensory disturbance, and
loss of deep tendon reflexes that often
follow an ascending pattern. Extra-
ocular movement abnormalities, facial
weakness, ataxia, respiratory compro-
mise, and autonomic dysfunction may
occur. Diagnosis is made based on the
clinical history, the presence of
cytoalbuminologic dissociation in CSF,
electrodiagnostic studies that support
an acute neuropathy, and the exclusion
of mimic diagnoses. Importantly, CSF
and electrodiagnostic studies may be
normal very early in the disease course.
AIDP is most frequently demyelinating;
however, some autoimmune polyneu-
ropathy variants are axonal. Pregnant
women may be less likely than the
general population to have serologic
evidence of associated Campylobacter
jejuni infection. The 10% incidence of
cytomegalovirus infection in pregnant
women with AIDP mirrors the general
population. Testing for these agents is
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 Peripheral Neuropathies in Pregnancy

KEY POINT
h Acute inflammatory
TABLE 5-2 Characterization of Polyneuropathy
demyelinating
polyradiculoneuropathy
can be treated with
plasma exchange or IV
immunoglobulin in
pregnancy and does not
appear to have adverse
perinatal or neonatal
outcomes. Testing for
cytomegalovirus should
be performed because
cytomegalovirus can be
transmitted to the fetus.
a
b What is the time course?
Acute or chronic
Progressive or relapsing/remitting
b What is the distribution?
Length-dependent or independent
Multifocal
b What types of nerve fibers are affected?
Motor and/or sensory
Large and/or small
Somatic and/or autonomic
b What portion of the nerve is affected?
Axon, myelin, or both
b Is there a family history or other features that would suggest a hereditary
neuropathy?
Lack of positive sensory symptoms
Associated skeletal abnormalities (eg, scoliosis, high-arched feet)
Early age at onset or very slowly progressive course
a
Data from Alport AR, Sander HW, Continuum (Minneap Minn).24 journals.lww.com/continuum/
Fulltext/2012/02000/Clinical_Approach_to_Peripheral_Neuropathy_.6.aspx.

recommended because their presence is
often associated with more severe dis-
ease and residual disability. Cytomegalo-
virus is also important to identify because
it may be transmitted to the fetus.26
The treatment for AIDP is either a
course of plasma exchange or IV
immunoglobulin. One review of a
small series of treatment outcomes
and complications in pregnant pa-
tients with AIDP found no treatment-
related complications with either
therapy.25 Termination of pregnancy
because of AIDP is not recommended,
as it has no proven benefit in short-
ening disease course or improving
maternal outcome. Additionally, peri-
natal and neonatal outcomes appear
reasonable, without defined risk due
to AIDP. In this review,25 35% of patients
had preterm delivery; however, in most
of the patients, labor was induced for
maternal neurologic decline. Sixty-one
percent of patients delivered via ce-
sarean delivery. However, vaginal de-
liveries were achieved even in patients
with severe weakness and ventilator
dependence. Therefore, in general,
AIDP does not appear to affect uterine
contractility, and operative delivery
can be reserved for obstetric indica-
tions. General anesthesia has been used
without complication but may be com-
plicated by autonomic instability. One
report of succinylcholine precipitating
severe hyperkalemia and maternal
death in AIDP has been published27;
depolarizing neuromuscular blocking
agents should be avoided in patients
with AIDP. Epidural anesthesia has
generally been used in this group
without complications, although one

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case of worsening weakness has been
reported.28,29 The authors recommend
communication with the obstetrician
and anesthesiologist regarding method
of delivery in AIDP. Additional important
treatment considerations include deep
vein thrombosis prophylaxis and preven-
tion of secondary infections, such as
pneumonia or urinary tract infection.
Chronic Inflammatory
Demyelinating
Polyradiculoneuropathy
Chronic inflammatory demyelinating
polyradiculoneuropathy (CIDP) is a
group of immune-mediated neuropa-
thies with a relapsing or progressive
course. Because they usually present in
older adults, with a peak incidence
between the ages of 40 and 60, informa-
tion about pregnancy is limited. In case
reports and a small series of nine women
with CIDP who became pregnant, an
increased risk of relapse during the third
trimester and postpartum period was
observed.30 A similar pattern of worsen-
ing has been reported in multifocal
motor neuropathy (MMN), another un-
common disease in pregnancy. Risk to
the fetus is not well established in
either disorder. Interestingly, one case
of neonatal transmission of MMN asso-
ciated with anti-ganglioside M1 (anti-
GM1) antibodies and monoclonal
gammopathy has been reported.31
METABOLIC AND NUTRITIONAL
NEUROPATHIES
Diabetic Polyneuropathy
Diabetic polyneuropathy is estimated to
affect 50% of patients with either type 1
or type 2 diabetes mellitus. Risk factors
include duration of disease and poor
glycemic control. Other vascular risk
factors, such as obesity and hyperlipid-
emia, may play a role. The most com-
mon form of diabetic polyneuropathy is
a length-dependent, small and large
fiber, sensory greater than motor
Continuum (Minneap Minn) 2014;20(1):100–114
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
KEY POINTS
polyneuropathy. This neuropathy is of- h Communication with
ten painful and may be accompanied by the obstetrician and
autonomic abnormality. Manifestations anesthesiologist
of autonomic neuropathy include regarding the method
gastroparesis, vomiting, constipation, di- of delivery in women
arrhea, urinary frequency or retention, with acute inflammatory
and postural hypotension. Many of these demyelinating
symptoms are common during preg- polyradiculoneuropathy
nancy in nondiabetics and thus may go is recommended.
unrecognized as related to diabetic h Autonomic dysfunction
neuropathy by women and their doc- in diabetic
tors. Diabetes mellitus also predisposes polyneuropathy may
patients to cranial, nerve root, and focal cause gastroparesis or
entrapment neuropathies. cardiac complications
during pregnancy and
Limited information, mostly from case
delivery. Diabetes also
reports, exists about whether symptoms
predisposes pregnant
of diabetic polyneuropathy or autonomic women to focal
neuropathy worsen with pregnancy. compressive
Moreover, the effect of diabetic poly- neuropathies.
neuropathy on pregnancy outcomes is
difficult to separate from other known
risk factors, such as poor metabolic
control, hyperemesis, inadequate nutri-
tion, or coexisting vascular disease. Preg-
nancy does not appear to increase the
risk for development or progression of
diabetic polyneuropathy or autonomic
neuropathy. Adjustments in pharmaco-
therapy for painful diabetic neuropathies
may be indicated during pregnancy. Partic-
ular attention to positioning and padding
during delivery may help avoid superficial
nerve injuries at sites of compression.32
Gastroparesis and cardiac compli-
cations from autonomic neuropathy
pose significant challenges during
pregnancy. Gastroparesis exacerbates
nausea and vomiting in pregnancy,
resulting in inadequate absorption of
nutrients and erratic blood glucose
control. Patients with gastroparesis
may benefit from treatment with
metoclopramide or erythromycin, both
FDA category B medications in preg-
nancy. Total parenteral nutrition may be
necessary in cases of severe gastro-
paresis with nausea and vomiting. Di-
minished counter-regulatory response
to hypoglycemia may be present.33 This
www.ContinuumJournal.com 109
 Peripheral Neuropathies in Pregnancy
KEY POINTS
h Deficiency of B vitamins
should be considered
as a cause of
polyneuropathy in
pregnancy, particularly
in women with
hyperemesis gravidarum.
h In women presenting
with polyneuropathy
postpartum, a detailed
history of emesis, diet,
and supplementation
during pregnancy is
essential.
110 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
may result in inadequate release of
glucagon, norepinephrine, epineph-
rine, and cortisol, which would typi-
cally restore normoglycemia.34 Patients
should be assessed for this and edu-
cated on strategies to minimize the
occurrence of hypoglycemia.33
Cardiac autonomic neuropathy is
estimated to affect 11% to 33% of young
adults with diabetes mellitus and de-
pends on the quality of glycemic control.
It may be accompanied by left ventricu-
lar hypertrophy and diastolic dysfunc-
tion. Cardiac autonomic neuropathy
manifests as exercise intolerance, ortho-
static hypotension, cardiac arrhythmias,
silent myocardial ischemia, or intrao-
perative cardiovascular lability and in-
creased cardiac events.33 Hypotension
may worsen as a result of blunting of
the normal compensatory response of
increased heart rate. Volume expan-
sion in pregnancy, however, may also
reduce baseline orthostasis. Obstetric
anesthetists should be aware of the
possibility of labile blood pressures in
response to general anesthesia.32
Neuropathy due to Nutritional
Deficiency
When evaluating pregnant or postpartum
patients with symptoms of poly-
neuropathy, it is important to consider
nutritional etiologies. Nausea and
vomiting are common and affect 50%
of pregnancies. In approximately 0.3%
to 1% of pregnant women, these
symptoms are severe and meet criteria
for hyperemesis gravidarum. In these
settings, women are at risk for
polyneuropathy related to nutritional
deficiency, particularly thiamine (vita-
min B1), pyridoxine (vitamin B6), and
cobalamin (vitamin B12).35 This is a
point well illustrated by Case 5-2.
Polyneuropathy due to nutritional
deficiency typically follows a length-
dependent, axonal, and sensory greater
than motor pattern. In thiamine defi-
ciency, patients may have ophthal-
moparesis or nystagmus or other
features of Wernicke encephalopathy.
Vitamin B12 deficiency can be manifested
by myelopathy (including posterior col-
umn and corticospinal tract abnormali-
ties). Neuropathy due to B12 deficiency
may also manifest as a large fiber sensory
neuropathy or small fiber neuropathy
with normal nerve conduction studies.36
In addition to low serum B12 levels,
assessing for increased methylmalonic
acid and homocysteine levels increases
the diagnostic yield. B6 supplementation
has sometimes been used to treat
nausea and vomiting in pregnant wom-
en. Therefore, both B6 toxicity and B6
deficiency should be considered poten-
tial causes of polyneuropathy in this
group. B6 intoxication manifests as a
sensory neuropathy or neuronopathy;
strength is preserved, although signifi-
cant sensory ataxia may be present.
Serum B6 and whole blood thiamine
can be reliably measured. In patients
with presumed thiamine deficiency, one
should emergently provide thiamine
re p l a c e m e n t t o t r e a t p o ss i b l e
Wernicke encephalopathy and not
delay treatment while the results of
the blood level are pending.
HEREDITARY DISORDERS OF
PERIPHERAL NERVE
Charcot-Marie-Tooth Disease
Hereditary motor and sensory neuropa-
thies, which is a term used interchange-
ably with Charcot-Marie-Tooth disease
(CMT), are the most common inherited
polyneuropathies. Symptoms often be-
gin in the first to third decades and
progress slowly. Symmetric distal limb
weakness, pes cavus, sensory loss with-
out positive sensory symptoms, and
imbalance are typical. Significant genetic
and phenotypic variability exists. In some
forms of CMT, postural tremor, dyspho-
nia from vocal cord paralysis, respiratory
insufficiency, pupillary dysfunction, or
February 2014
 KEY POINT

Case 5-2 h Treatment of

Charcot-Marie-Tooth
A 30-year-old woman was seen 3 months postpartum for numbness and
disease is heavily
painful paresthesia in her distal lower extremities, which started during
focused on adaptive
the second trimester of pregnancy. Pregnancy was complicated by
equipment. Functional
hyperemesis gravidarum and 30-pound weight loss. Physical examination
needs or abilities may
was notable for loss of pinprick and light touch sensation distal to the
change during
ankles with intact vibration, proprioception, and strength. Deep tendon
pregnancy or postpartum,
reflexes were brisk throughout. Plantar responses were flexor. EMG and
and reassessment
nerve conduction studies, including autonomic testing of R-R interval
is warranted.
variability with deep breathing and posture, were normal. Laboratory
evaluation demonstrated normal whole blood thiamine, vitamin E, vitamin
B6, copper, erythrocyte sedimentation rate, extractable nuclear antigens,
angiotensin-converting enzyme, antinuclear antibody, serum protein
electrophoresis, and thyroid function testing. Hemoglobin A1C and 2-hour
glucose tolerance testing were normal. Zinc levels were mildly low.
Vitamin B12 was 199 pg/mL and had decreased from 600 pg/mL 2 months
earlier. Methylmalonic acid was elevated due to B12 deficiency. HIV and
hepatitis C testing had previously been negative. She was treated for
small fiber neuropathy in association with B12 deficiency with oral B12
supplementation. Follow-up B12 and methylmalonic acid levels were
normal, and the patient’s symptoms greatly improved.
Comment. This patient was diagnosed with small fiber neuropathy due
to B12 deficiency. While B12 deficiency typically causes a myeloneuropathy
with findings of a large fiber sensory and motor axonal neuropathy, it may
also cause small fiber neuropathy. Routine electrodiagnostic studies are
normal in small fiber neuropathy. In this case, B12 deficiency developed
due to hyperemesis gravidarum. In her evaluation, it was important to
exclude other significant nutritional deficiencies and other non-nutritional,
common causes of small fiber neuropathy. She was not breast-feeding,
and gabapentin was successfully used for symptomatic relief. In the
postpartum period, breast-feeding status may influence the clinician’s
decision to treat symptomatically and the choice of medications.

scoliosis may be manifest.37 Classification
of the CMT variant as axonal or demye-
linating, combined with any available
clues regarding pattern of inheritance,
directs genetic testing. Inheritance is
mainly autosomal dominant, although
X-linked and autosomal recessive forms
exist. Life expectancy is normal. Patients
rarely (approximately 5%) become
wheelchair dependent. Care is focused
on maintaining function and mobility.
Important areas for discussion re-
garding pregnancy for women with
CMT, as with other preexisting periph-
eral neuropathic disorders, are outlined
(Table 5-3).10 Retrospective data on
pregnancy outcomes in CMT are gener-
ally favorable. In the most recent review,
which included 33 patients undergoing a
total of 63 pregnancies, pregnancy out-
comes were good. No increase in the
rate of miscarriage, pregnancy complica-
tions, preterm delivery, delivery by ce-
sarean delivery or instrumentation,
abnormal presentation, or adverse neo-
natal outcome was documented.38 This
study did not replicate prior data on
increased risk of presentation abnor-
malities, instrumentation, cesarean deliv-
ery, or postpartum bleeding. As with
prior studies, however, transient wors-
ening of CMT symptoms was reported
in approximately 32% of pregnancies,
and persistent worsening in an additional

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 Peripheral Neuropathies in Pregnancy

KEY POINT
h Pregnancy outcomes are
typically favorable in
Charcot-Marie-Tooth
disease. Transient
worsening of
Charcot-Marie-Tooth
disease occurs in
approximately 30%
of pregnancies, while
persistent worsening is
seen in an additional
22% of pregnancies.
TABLE 5-3 Key Considerations for Pregnancy in Women With
Preexisting Neuropathya
b Will the course of maternal disease change with pregnancy?
b Will treatment need to be adjusted, and, if so, how?
b What are the potential effects of therapy on the fetus?
b Will there be complications during labor and delivery?
b Are there additional implications for the fetus?
a
Data from Guidon AC, Massey EW, Neurol Clin.10 www.sciencedirect.com/science/article/pii/
S0733861912000199.

22% of pregnancies.38 Worsening may be
more common with earlier-onset disease.
Deterioration in one pregnancy generally
predicts deterioration in subsequent
pregnancies. Women with CMT who are
ambulatory before pregnancy, however,
typically remain ambulatory. Case reports
have documented safe use of regional
anesthesia during delivery.39
The authors recommend optimiz-
ing functional status before pregnancy
and reevaluating patients for any
new needs during pregnancy and post-
partum. It is important to address the
generally good pregnancy outcomes
and to allow the opportunity for genetic
counseling. Carrier and prenatal testing
and preimplantation genetic diagnosis
are available for some forms of
CMT. Fatigue and excessive daytime
sleepiness are common in CMT.
Physicians should be mindful of poten-
tial worsening of baseline fatigue in
pregnant and postpartum patients with
CMT.37 The authors recommend that
patients work with physical and occu-
pational therapists to anticipate the
challenges of holding, feeding, and
carrying the newborn.
Hereditary Neuropathy With
Liability to Pressure Palsies
Hereditary neuropathy with liability to
pressure palsies (HNPP) is an autosomal
dominant disorder, which is allelic to
CMT1A: 85% to 90% of cases are due to a
PMP22 gene deletion and 10% to a
PMP22 point mutation. It is a multifocal
demyelinating neuropathy that presents
as recurrent painless mononeuro-
pathies. These mononeuropathies occur
at typical sites of compression (eg,
fibular neuropathy at the knee, ulnar
neuropathy at the elbow) and with
everyday activities such as leg crossing,
squatting, or leaning on an elbow.37
Although HNPP mononeuropathies gen-
erally recover spontaneously, fixed defi-
cits may occur. Women with HNPP may
develop such neuropathies during preg-
nancy or delivery: axillary and fibular
neuropathies have been reported.40,41
Women with HNPP should take partic-
ular precautions to avoid compression.
A personal or family history of multiple
prior compression neuropathies prompts
consideration of HNPP. EMG/NCS is
utilized to confirm the mononeuropathy
and site of compression.
CONCLUSION
Although rare, acquired peripheral
neuropathic disorders in pregnancy
are seen in practice. Neurologists can
greatly assist the patient and often
the rest of the medical team by
facilitating localization of the problem,
treatment, symptom management,
and appropriate counseling. Diagnos-
tic evaluation and treatment may be

112 www.ContinuumJournal.com February 2014

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influenced in key ways by pregnancy
and consideration of fetal outcomes.
For neurologists who see women with
preexisting disorders, an early and
open dialogue about pregnancy can
allow for anticipatory guidance and
planning. Current data in this field are
limited, and additional study of pe-
ripheral neuropathies in pregnancy is
needed.
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February 2014