The n e w e ng l a n d j o u r na l of m e dic i n e
Case Records of the Massachusetts General Hospital
From the Departments of Neurology
(H.M.R., N.V.), Radiology (H.B.H.), and
Pathology (J.A.B.), Massachusetts Gen‑
eral Hospital, and the Departments of
Neurology (H.M.R., N.V.), Radiology
(H.B.H.), and Pathology (J.A.B.), Harvard
Medical School — both in Boston.
N Engl J Med 2018;379:1862-8.
DOI: 10.1056/NEJMcpc1810387
Copyright © 2018 Massachusetts Medical Society.
1862
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Founded by Richard C. Cabot
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Virginia M. Pierce, M.D., David M. Dudzinski, M.D., Meridale V. Baggett, M.D.,
Dennis C. Sgroi, M.D., Jo‑Anne O. Shepard, M.D., Associate Editors
Alyssa Y. Castillo, M.D., Case Records Editorial Fellow
Emily K. McDonald, Sally H. Ebeling, Production Editors
Case 34-2018: A 58-Year-Old Woman with
Paresthesia and Weakness of the Left Foot
and Abdominal Wall
Haatem M. Reda, M.D., H. Benjamin Harvey, M.D., J.D.,
Nagagopal Venna, M.D., and John A. Branda, M.D.​​
Pr e sen tat ion of C a se
Dr. Amrit Misra (Neurology): A 58-year-old woman was seen in the outpatient neurol-
ogy clinic of this hospital in early autumn because of hypoesthesia, paresthesia, and
weakness.
The patient had been well until 10 weeks before this presentation, when back
pain developed between the shoulder blades. The pain resolved during the next
2 weeks, without an intervention. Six weeks before this presentation, numbness
developed in a bandlike distribution around her trunk, with involvement of the
area between the shoulder blades and the area under the breasts.
Five weeks before this presentation, the numbness extended to the upper abdo-
men. The patient was unable to sit up from the supine position without using her
arms, and she had abdominal distention. Four weeks before this presentation,
paresthesia developed in the third, fourth, and fifth fingers of the left hand and
the fourth and fifth fingers of the right hand. The patient was seen at a clinic at
another hospital, and magnetic resonance imaging (MRI) of the spine was scheduled.
However, 2 weeks before this presentation, the numbness extended to the genital
area and urinary incontinence developed, prompting the patient to present to the
emergency department of this hospital for evaluation.
In the emergency department, the patient reported no fevers, night sweats,
change in weight, arm weakness, leg weakness, or change in gait. She had a his-
tory of hypertension, hypothyroidism, and symptomatic spinal stenosis, for which
she had undergone L4–L5 decompression and bilateral medial facetectomy 6 years
before this presentation. She had also undergone open reduction and internal
fixation of left tibial and fibular fractures that had resulted from a fall, as well as
excision of a foreign body that had punctured the right thenar.
Three months before this presentation, the patient had noted an area of non-
pruritic, nonpainful erythema (measuring 8 cm in diameter) on the left gluteal
fold, surrounding what she had thought to be an insect bite. Fever did not develop,
n engl j med 379;19 nejm.org  November 8, 2018
The New England Journal of Medicine
 Case Records of the Massachuset ts Gener al Hospital
and the erythema resolved during the subsequent
4 weeks. The patient’s only medication was levo-
thyroxine, and she was allergic to penicillin. She
drank alcohol rarely, had smoked tobacco in the
past, and did not use illicit drugs. She was mar-
ried and lived with her husband in a wooded
area in northeastern Connecticut. She worked
in health care. There was no family history of
neurologic disease.
On examination, the temperature was 36.6°C,
the blood pressure 144/75 mm Hg, the heart rate
84 beats per minute, and the respiratory rate 18
breaths per minute. The weight was 74.8 kg, and
the body-mass index (the weight in kilograms
divided by the square of the height in meters)
25.8. There was decreased sensation on the pos-
terior and anterior trunk and abdomen. The ab-
domen was distended. The remainder of the gen-
eral medical examination was normal. The blood
glucose level was 291 mg per deciliter (16.2 mmol
per liter; reference range, 70 to 110 mg per deci-
liter [3.9 to 6.1 mmol per liter]). The blood elec-
trolyte levels were normal, as were the results of
tests of renal and liver function, the complete
blood count, and the differential count. Imaging
studies were obtained.
Dr. H. Benjamin Harvey: MRI of the cervical,
thoracic, and lumbar spine, performed without
the administration of contrast material, revealed
no spinal cord compression, cord signal abnor-
mality, or epidural collection. There were multi-
level degenerative changes of the spine, as well
as postsurgical changes related to remote L4–L5
decompression, without associated high-grade
spinal-canal stenosis or nerve-root impingement.
The nerve roots of the conus medullaris and
cauda equina appeared to be normal, and there
was no evidence of thickening or clumping of
the nerve roots.
Dr. Misra: The patient chose to seek neuro-
logic evaluation for her symptoms, and 2 weeks
later, she was seen in the outpatient neurology
clinic of this hospital. She reported stable pares-
thesia of the hands, ongoing numbness of the
trunk and abdomen, new numbness of the upper
anterior legs, and a 5-day history of difficulty
lifting the front part of her left foot when she
walked. She also reported difficulty taking a deep
breath and coughing.
On examination, the temperature was 36.4°C,
the blood pressure 106/67 mm Hg, the heart rate
77 beats per minute, and the respiratory rate 16
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breaths per minute. The patient’s mental status
was normal, as were the results of testing of the
2nd through 12th cranial nerves. Strength was
4/5 during flexion of the left wrist, 5/5 while the
patient was gripping the examiner’s fingers, 4/5
during dorsiflexion of the left foot, and 4/5 dur-
ing extension of the left toes; strength was other-
wise 5/5. When the patient attempted to walk on
her heels, she was unable to keep her left fore-
foot from touching the floor. Diaphragmatic ex-
cursion, as measured by percussion along the
posterior chest at the end of inspiration and expi-
ration, was symmetric. There was diminished
tone in the bilateral rectus abdominis muscles,
with associated abdominal distention. The patient
was unable to rise from the supine position with-
out assistance from the examiner. There was
diminished sensation in response to light touch
and pinprick in a bandlike distribution around
the T6 dermatome spanning to the T12 derma-
tome. Deep-tendon reflexes were absent at the
biceps on the left side and at the ankles bilater-
ally. The remainder of the neurologic and medi-
cal examination was normal.
Laboratory testing revealed a glycated hemo-
globin level of 11.8% (reference range, <5.7), an
erythrocyte sedimentation rate of 25 mm per
hour (reference range, <30), and normal levels of
thyrotropin, creatine kinase, vitamin D, vitamin
B12, and folate.
Dr. Harvey: Chest radiographs obtained in the
inspiratory and expiratory views showed no evi-
dence of parenchymal opacity, pleural effusion,
or lymphadenopathy. Hemidiaphragmatic move-
ment between inspiration and expiration was
present bilaterally. On MRI of the thoracic and
lumbar spine without contrast enhancement, the
findings were stable, as compared with the pre-
vious study. On MRI of the thoracic spine with
contrast enhancement, there was no evidence of
abnormal cord or meningeal enhancement (Fig. 1).
Dr. Misra: A diagnostic test was performed.
Differ en t i a l Di agnosis
Dr. Haatem M. Reda: The first step in evaluating a
patient with a potential neurologic problem is to
define the syndrome — that is, the neuroana-
tomical localization combined with a specific
temporal profile. Over a 10-week period, this
patient had back pain followed by weakness in
muscles of the abdominal and thoracic walls,
1863
 The n e w e ng l a n d j o u r na l of m e dic i n e

A B C

Figure 1. MRI of the Thoracic Spine.

MRI of the thoracic spine was performed 1 week after the patient was evaluated in the emergency department.
­Sagittal images of the thoracic spine were obtained along the midline. A T2-weighted image (Panel A), a T1-weighted
image without contrast enhancement (Panel B), and a fat-saturated, T1-weighted image with contrast enhancement
(Panel C) show no specific evidence of cord signal abnormality, high-grade spinal stenosis, or abnormal enhancement,
with allowance for expected vascularity along the cord surface.

reduced truncal sensation with involvement of
the genitals, multifocal areflexic weakness in the
arms and legs, and probable urinary overflow
incontinence. Localization of the process will
allow us to develop an initial differential diag-
nosis that can then be logically narrowed.
Localization
This patient’s initial symptom was pain between
the shoulder blades. Pain is the least specific
symptom, but it localizes the lesion somewhere
in the peripheral nervous system, with few excep-
tions. Injury of spinal sensory nerve roots com-
monly causes back pain that radiates to the axilla
or flank.
A key component of this patient’s neuromus-
cular evaluation was examination of the abdom-
inal-wall muscles, which allow flexion of the
trunk and forceful exhalation and prevent the
abdominal contents from protruding. We are not
told whether she had Beevor’s sign (deflection of
the umbilicus away from a weak segment of the
rectus abdominis muscle on activation of the
abdominal-wall muscles). However, we know that
she was unable to sit up from the supine posi-
tion and had abdominal distention that was re-
lated to diminished abdominal-wall muscle tone.
The presence of concurrent numbness rules out
a myopathy, so I suspect the weakness of the
abdominal-wall muscles localizes to the lower
thoracic or upper lumbar nerve roots.
The patient reported difficulty taking a deep
breath and coughing, which could be a sign of
diaphragmatic weakness from dysfunction of the
upper cervical cord or brain stem. However, she
did not have weakness on neck flexion or oro-
pharyngeal dysphagia, and diaphragmatic excur-
sion was normal on examination. Another po-
tential cause of this patient’s difficulty taking a
deep breath is weakness of the external intercos-
tal muscles, which assist in expansion of the
chest cavity during inspiration and are innervated
by thoracic segmental nerve roots.1
Let us now consider the patient’s sensory
symptoms. Reduced truncal sensation implies
dysfunction of the sensory tracts in the spinal
cord, sensory nerve roots, dorsal-root ganglia, or
segmental nerves at the affected levels. This pa-
tient’s sensory loss had a bandlike or suspended
distribution, meaning that it had superior and
inferior boundaries. The presence of a suspend-
ed sensory level could be consistent with a small
central cord lesion or syrinx with interruption of
decussating spinothalamic-tract fibers in the ven-

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 Case Records of the Massachuset ts Gener al Hospital

tral commissure. Central cord lesions can cause of diabetic radiculopathy are often bilateral but
pain, and if they are large enough, they can affect are usually asymmetric and limited to one seg-
the anterior horns, resulting in areflexic segmen- ment (cervical, thoracic, or lumbosacral).2 Over-
tal weakness. However, several features of this all, I think diabetic thoracic polyradiculopathy is
patient’s presentation argue against a central unlikely in this case.
cord lesion. Central cord lesions typically result
in contiguous deficits, whereas this patient had Multiple Mononeuropathies
noncontiguous numbness involving the lower Although the syndrome of multiple mononeu-
cervical, lower thoracic, and sacral segments, ropathies (mononeuritis multiplex) is not a poly-
without involvement of upper cervical and lower radiculopathy, it must be considered in this pa-
lumbar segments. In addition, numbness of the tient with painful, multifocal sensory loss, given
genital area argues against a central cord lesion, the importance of early recognition of an under-
because spinothalamic-tract fibers that originate lying systemic or peripheral nervous system vas-
in the sacral segment are located laterally within culitis.3 However, in patients with multiple mono-
the tracts and are typically spared. The patient neuropathies, symptoms develop in a haphazard
also had urinary incontinence, a symptom that peripheral-nerve distribution, and this patient’s
would not be expected to occur with small cen- symptoms were more radicular. In addition, this
tral cord lesions or syringomyelia. Finally, she did patient had predominantly truncal symptoms,
not have myelopathic signs, such as spastic para- which would be unusual in multiple mononeu-
paresis, hyperreflexia, or crossed sensory signs ropathies, because it most often affects the long
that would suggest a large cord lesion. nerves in the arms and legs, given their rela-
A suspended sensory level can also result from tively high susceptibility to vasculitis-associated
spinal sensory nerve-root or ganglion dysfunc- ischemia.
tion. A sensory ganglionopathy can be ruled out
because the patient also had weakness. Overall, Inflammatory Polyneuropathy
her syndrome is most consistent with a subacute Another important consideration in this patient
polyradiculopathy or polyradiculoneuropathy, with is multifocal acquired demyelinating sensory and
initial involvement of the mid and lower thoracic motor neuropathy (MADSAM), a variant of chron-
segments, followed by involvement of the lower ic inflammatory demyelinating polyradiculoneu-
cervical, upper thoracic, lumbar, and sacral seg- ropathy4 that causes pain, multifocal sensory loss,
ments. and areflexic weakness in a radicular or periph-
eral-nerve distribution. MADSAM most common-
Differential Diagnosis of Polyradiculopathy ly involves long nerves, although cranial nerves
Diabetic Polyradiculopathy may also be affected. However, this patient’s
There are several disorders that cause or mimic predominantly truncal presentation would be
subacute polyradiculopathy or polyradiculoneu- unusual with this diagnosis.
ropathy with potentially normal findings on
imaging of the spine, as described in this patient. Cancer
Among the most common of these disorders is Leptomeningeal carcinomatosis or lymphomato-
diabetic thoracic polyradiculopathy, which is the sis is a diagnostic consideration in this patient.
pathophysiological equivalent of diabetic cervical Spinal and cranial nerve roots may be damaged
or lumbosacral radiculoplexus neuropathy. One as they pass through diseased meninges. How-
quarter of cases of acute-to-subacute thoracic ever, this syndrome is rarely part of the initial
polyradiculopathy coincide with a new diagnosis presentation of cancer, and this patient did not
of diabetes mellitus, which fits with this patient’s have other signs or symptoms suggestive of ad-
newly discovered elevated blood glucose and gly- vanced cancer. In addition, she did not have
cated hemoglobin levels. However, patients with findings suggestive of leptomeningeal disease
diabetic polyradiculopathy typically have a pro- on MRI. Although cerebrospinal fluid (CSF)
drome of constitutional symptoms that include analysis or meningeal biopsy would be neces-
weight loss and malaise, as well as symptoms of sary to rule out this diagnosis, I suspect that
autonomic failure, and such symptoms were not other possible causes of her illness are more
seen in this patient. In addition, the symptoms likely.

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 The n e w e ng l a n d j o u r na l
Neurosarcoidosis
Neurosarcoidosis has protean manifestations,
which can include thoracic polyradiculopathy.
Sarcoidosis has a predilection for involvement of
sensory nerve roots and ganglia but most com-
monly affects cranial nerve roots and the optic
nerves. Patients with neurosarcoidosis often have
systemic disease and abnormal findings on neuro-
imaging, features that were not seen in this pa-
tient. Although neurosarcoidosis cannot be ruled
out, I will consider other possible causes of this
patient’s presentation.
Infection
Could this patient have herpes zoster? Reactiva-
tion of latent varicella–zoster virus arises in the
dorsal-root ganglia and spreads centrifugally to
the skin along sensory nerves or vasa nervorum.
Patients with herpes zoster often have severe
dermatomal pain and sensory deficits; a segmen-
tal rash is common but not always present. In
some cases, patients with herpes zoster have
segmental weakness of the arms, legs, or thoracic-
wall muscles. However, although patients with
sensory herpes zoster may have symptoms with-
out a herpetic rash, this is almost never the case
in patients with segmental zoster paresis. In ad-
dition, the disease is almost always limited to
one or very few segments.5
Patients who have Lyme meningoradiculitis
typically present 2 to 18 weeks after infection,
during the early disseminated phase, with pain,
sensory loss, and areflexic weakness. Over half
of patients with Lyme meningoradiculitis pres-
ent with seventh cranial nerve palsy — a mani-
festation of Lyme disease that many recognize
— but any cranial or spinal nerve root may be
involved. Several clues in this patient’s history
point us toward this diagnosis. First, she was
living in a wooded area in a region of the coun-
try where Lyme disease is endemic. Second, she
presented in early autumn, and approximately
3 months earlier, she had had a small, uniformly
erythematous, painless, nonpruritic rash that was
consistent with the hallmark skin lesion of early
Lyme disease, erythema migrans. Although the
classic rash of Lyme disease is described as hav-
ing an area of central clearing (bull’s eye), in
many cases, it does not. Third, the location of
the patient’s rash on the left gluteal fold is a
common site of tick bites; other locations include
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of m e dic i n e
the axillae, hairline, groin, and beltline.6 Given
the seasonal timing of this patient’s presentation,
the history of a rash consistent with erythema
migrans, and her clinical syndrome of polyradic-
ulopathy, I suspect that this patient had Lyme
meningoradiculitis in the context of early dis-
seminated Lyme disease. The next step in the
diagnosis would be serum and CSF analysis for
antibodies against Borrelia burgdorferi.
Dr. Meridale V. Baggett (Medicine): Dr. Misra,
what was your clinical impression when you
evaluated this patient, and how did you pursue a
diagnosis?
Dr. Misra: We thought this patient’s presenta-
tion was most consistent with an infectious poly-
radiculopathy; her recent rash and associated
risk factors for Lyme disease made Lyme radicu-
lopathy our leading diagnosis. A lumbar punc-
ture was performed, and CSF analysis revealed a
glucose level of 115 mg per deciliter (6.4 mmol
per liter; reference range, 50 to 75 mg per deci-
liter [2.8 to 4.2 mmol per liter]), a total protein
level of 128 mg per deciliter (reference range, 5 to
55), and a nucleated-cell count of 46 per cubic
millimeter (reference range, 0 to 5). We requested
CSF and serum serologic testing for Lyme dis-
ease to establish the diagnosis.
Cl inic a l Di agnosis
Lyme radiculopathy.
Dr . H a atem M. R eda’s Di agnosis
Lyme meningoradiculitis in the context of early
disseminated Lyme disease.
Pathol o gic a l Discussion
Dr. John A. Branda: The laboratory tests that were
performed to support the diagnosis were serum
antibody tests for Lyme borreliosis. A first-tier
enzyme-linked immunosorbent assay (ELISA) was
reactive, prompting the performance of second-
tier IgM and IgG immunoblot assays. The serum
IgM immunoblot assay showed 1 of 3 specific
bands (the 39-kDa band), which is a negative
outcome according to Centers for Disease Con-
trol and Prevention (CDC) criteria.7 The serum
IgG immunoblot assay showed 9 of 10 specific
bands, which is a positive outcome according
 Case Records of the Massachuset ts Gener al Hospital
to CDC criteria.7 The tests indicated an expanded
B. burgdorferi antibody response with a switch of
immunoglobulin class from IgM to IgG; these
results are associated with B. burgdorferi infection
of at least 1 or 2 months’ duration, and they cor-
relate well with the patient’s clinical history. In
addition to serum antibody testing, CSF IgM and
IgG immunoblot assays for B. burgdorferi and CSF
polymerase-chain-reaction (PCR) assays for B. burg-
dorferi, B. mayonii, B. garinii, and B. afzelii were
performed.
When a patient is seropositive and has a char-
acteristic clinical syndrome for Lyme neurobor-
reliosis, as in this case, CSF tests for Lyme dis-
ease are unnecessary to establish a diagnosis.
When Lyme neuroborreliosis with central nervous
system involvement is suspected, detection of
intrathecal B. burgdorferi antibody production can
support the diagnosis, but its absence does not
rule out the diagnosis. The best method for the
detection of intrathecal B. burgdorferi antibody
production is determination of the CSF–serum
antibody index with quantitative ELISAs or simi-
lar assays, rather than immunoblot assays. Sub-
stantial differences between results on serum
and CSF immunoblot assays are not reliably
present when there is intrathecal B. burgdorferi
antibody production.8 In this patient, the CSF
IgG immunoblot assay showed 5 specific bands
and the CSF IgM immunoblot assay showed no
bands. Although more bands were present on
the respective serum immunoblot assays, the dif-
ferences between these results do not refute intra-
thecal antibody production and are noncontribu-
tory. Direct detection of the infectious agent with
CSF PCR assays is usually not possible.9,10 CSF
PCR assays for Lyme-related borrelia are not rec-
ommended, and a negative assay (which was
present in this case) does not influence diagnos-
tic considerations, because sensitivity of the as-
say is poor. On the basis of the patient’s clinical
features and seroreactivity, the final diagnosis
was Lyme meningoradiculitis.
Discussion of M a nagemen t
Dr. Nagagopal Venna: It is not uncommon during
the summer and fall months in New England
to make a diagnosis of Lyme polyradiculitis or
meningoradiculitis in a patient who presents with
a syndrome of subacute, multifocal, painful ra-
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diculitis. The syndrome typically affects the arms
and legs in an asymmetric fashion and is often
associated with cranial nerve palsies. In contrast,
this patient’s symptoms primarily involved the
trunk, whereas involvement of the arms and legs
was less prominent. Such a presentation can
lead to several diagnostic challenges. Visceral
causes of pain are often appropriately investi-
gated first, and neurologic causes are not con-
sidered unless the patient also has paresthesias,
which serve as a clue of a neurologic cause of the
pain. Moreover, the sensory and strength exami-
nation of the trunk and abdomen is often over-
looked and not performed. In this patient, exami-
nation of skin sensation on the abdominal and
chest walls and testing of abdominal-wall mus-
cle strength were instrumental in arriving at the
correct diagnosis. Lyme disease has a predilection
for involvement of the thoracic nerve roots in
some patients. The basis for this is not known,
but there is a suggestion that localization might
be related to the site of inoculation of infection.
After the diagnosis was confirmed, the patient
received a 3-week course of intravenous ceftri-
axone. Her diabetes was treated with a sliding
scale of insulin initially, followed by metformin.
The absence of distal symmetric sensory periph-
eral neuropathy and the rapid development of
asymmetric polyradiculopathy accompanied by
CSF pleocytosis made the diagnosis of diabetic
polyradiculopathy improbable. The patient’s pain
diminished over a 4-week period. When we saw
her in the clinic 4 months after the initiation of
treatment with ceftriaxone, her sensation and
strength of the abdominal wall had increased
such that she could contract the rectus abdomi-
nis muscles while standing, but she continued
to have difficulty sitting up from the supine
position. The weakness of the left foot had di-
minished, but she still had difficulty walking
on the heel.
Fina l Di agnosis
Lyme meningoradiculitis.
This case was presented at Neurology Grand Rounds.
Dr. Branda reports receiving grant support from Immunetics,
bioMerieux, and Alere, consulting fees from T2 Biosystems, and
grant support and consulting fees from DiaSorin. No other po-
tential conflict of interest relevant to this article was reported.
Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
1867
 Case Records of the Massachuset ts Gener al Hospital

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