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Asymmetric flaccid paralysis A neuromuscular presentation of West Nile virus infection.

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ORIGINAL ARTICLES
Asymmetric Flaccid Paralysis:
A Neuromuscular Presentation of
West Nile Virus Infection
Jun Li, MD, PhD,1 Jeffrey A. Loeb, MD,1,2 Michael E. Shy, MD,1,2 Aashit K. Shah, MD,1
Alex C. Tselis, MD,1 William J. Kupski, MD,3 and Richard A. Lewis, MD1
The neuromuscular aspects of West Nile virus (WNV) infection have not been characterized in detail. We have studied
a group of six patients with proven WNV infection. All cases presented with acute, severe, asymmetric, or monolimb
weakness, with minimal or no sensory disturbance after a mild flu-like prodrome. Four cases also had facial weakness.
Three of our cases had no encephalitic signs or symptoms despite cerebrospinal fluid pleocytosis. Electrophysiological
studies showed severe denervation in paralyzed limb muscles, suggesting either motor neuron or multiple ventral nerve
root damage. This localization is supported further by the finding of abnormal signal intensity confined to the anterior
horns on a lumbar spine magnetic resonance imaging. Muscle biopsies from three patients showed scattered necrotic
fibers, implicating mild direct or indirect muscle damage from the WNV infection. In summary, we describe a group of
patients with acute segmental flaccid paralysis with minimal or no encephalitic or sensory signs. We have localized the
abnormality to either the spinal motor neurons or their ventral nerve roots. It will be important for physicians to
consider WNV infection in patients with acute asymmetric paralysis with or without encephalitic symptoms.
Ann Neurol 2003;53:703–710
West Nile virus (WNV) is a RNA virus that belongs to
the flavivirus family taxonomically.1 The dramatic outbreak of WNV infection in New York City in 1999
heralded the virus reaching North America.2 Since
then, WNV has rapidly spread across the United
States. There were only 142 cases with 18 deaths between 1999 and 2001. However, during the summer
of 2002, the incidence of WNV infection drastically
increased to a total of 3,052 cases with 153 deaths to
date.3 Ten percent of patients with WNV infection
from Israel and New York City presented with acute,
bilateral flaccid paralysis.2,4 The findings from their
electromyography and nerve conduction studies were
not described in detail but were interpreted as axonal
motor neuropathy, imitating Guillain–Barré syndrome.2 There also have been a few case reports describing patients with WNV infection and a “poliolike” syndrome.5–7
During this past summer (2002), Michigan had a
significant number of cases of WNV infection. In this
report, we describe a group of WNV-infected patients
presenting with a peculiar acute segmental flaccid pa-
ralysis. We provide detailed electrophysiological and
neuroimaging evidence that this disorder is localized to
the anterior horn motor neurons and/or ventral roots
of the spinal cord.
From the 1Department of Neurology, 2Center for Molecular Medicine and Genetics, and 3Department of Pathology, Wayne State
University School of Medicine, Detroit, MI.
Address correspondence to Dr Li, Department of Neurology,
Wayne State University, 4201 St. Antoine, UHC-8D, Detroit, MI
48201. E-mail: junli@med.wayne.edu
Patients and Methods
Six patients, four men and two women, were examined,
ranging in age from 27 to 63 years old. Workup included
magnetic resonance imaging (MRI) of the brain and spine,
lumbar puncture, electrophysiology, and muscle /nerve biopsy. Four of these patients had positive IgM antibodies to
WNV by enzyme-linked immunosorbent assay (ELISA) test
of their cerebrospinal fluid (CSF), performed in the Department of Health of the State of Michigan. The remaining two
cases had positive IgM antibodies in the serum with positive
neutralizing antibody test, which is also confirmatory.
Results
Case Reports
Laboratory and neuroimaging results for all cases are
listed in Table 1.
Received Nov 21, 2002, and in revised form Feb 19, 2003. Accepted for publication Mar 7, 2003.
© 2003 Wiley-Liss, Inc.
703
Table 1. Laboratory and Neuroimaging Results
Patient No.
Test
1
2
Brain MRI
Normal
Normal
Spine MRI
Normal
Normal
CSF (day)
Cell and
differentiation
Day 20
RBC 22,
Nuc 61
L 84%
171
77
220
⫹ In CSF
Day 1
RBC 10,
Nuc 32
L 85%
96
84
17,808
⫹ In CSF
protein
Glucose
CK
WNV IgM ab
a
3
4
Not done; head CT:
a 1cm mass in
pituitary
Not done
Not done;
head CT:
normal
Not done
Day 25
RBC 1140, Nuc15
L 90%
Day 2
RBC 14,
Nuc 425
L 24%
83
72
28
⫹ In serum
145
80
—
⫹ In CSF
5
6
Normal
Normal
Stenosis at C3-7,
intact cord;
T/L/S spine
MRI: normal
Day 9
RBC 33, Nuc 4
L 81%
Abnormal signal
intensity at
anterior horn
of C/L cord
Day 7
BC 10, Nuc
150 L 24%
193
67
—
⫹ In serum
52
66
141
⫹ In CSF and
serum
Days after onset of symptoms.
MRI ⫽ magnetic resonance imaging; C/L ⫽ cervical/lumbar; CT ⫽ computed tomography; CSF ⫽ cerebrospinal fluid; L ⫽ lymphocytes;
RBC ⫽ red blood cell; T/L/S ⫽ thoracic/lumbar/sacral; WNV ⫽ West Nile virus.
PATIENT 1. A 36-year-old woman was healthy until 1
week before presentation when she developed mild
“flu-like” symptoms, including headache, malaise, and
gastrointestinal upset. One day before admission, she
noted lower back pain. On the morning that she came
to the hospital, she awoke to find her left leg paralyzed.
At no time did she have confusion, neck stiffness, or
other meningoencephalitic symptoms or signs. She denied bowel and bladder dysfunction or muscle pain.
Examination showed a temperature of 38.2°C and a
flaccid left leg without movement except for minimal
ankle dorsal and plantar flexion. There was minimally
reduced sensation to pinprick in the leg and absent left
knee and ankle deep tendon reflexes. All other reflexes
were well preserved, and the rest of her examination
was normal.
She received a course of intravenous immunoglobulin treatment (1gm/kg/day for 2 days) with no significant improvement. After 5 months, there had been no
improvement of her motor deficit.
PATIENT 2. Six days before admission, this 45-year-old
man fell on the steps of his front porch and found that
his left leg was weak. He struggled to stand up and was
able to walk only a few blocks. The weakness in this
leg progressed over the next hour to the point that he
could no longer walk or even support himself. He had
significant diarrhea 1 day before admission. He had
one incident of bowel incontinence, but it was unclear
whether the incontinence was from diarrhea or secondary to sphincter dysfunction. He denied muscle pain.
There was no fever, headache, or neck stiffness. The
day after admission, he was noted to be confused.
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His examination on day 2 showed a temperature of
36.6°C, disorientation to time and place, and mild
nystagmus on lateral gaze to the right and bilateral facial weakness including frontalis muscles. Muscle examination showed 2/5 strength in the left leg and 4/5
strength in the right leg. Sensory examination was normal for vibration and equivocal to pinprick in the left
leg. Deep tendon reflexes were absent in the left knee
and ankle, but normal in other limbs.
His mental status returned to normal over 4 days,
but his weakness persisted.
A 27-year-old man with a history of alcohol abuse presented with diarrhea, vomiting, and generalized fatigue approximately 2 weeks before admission. Six days before admission, he fell while climbing
stairs. The next morning, he awoke with right arm paralysis. Within 2 to 3 days, the left arm also became
mildly weak. He denied sensory disturbance, muscle
pain, and bowel and bladder dysfunction. There was
no alteration of mental status. He did not have headache, fever, or neck stiffness.
His examination showed a normal temperature and
mental status. There was neck flexor and bilateral facial
weakness including frontalis muscles, 0/5 strength in
the right arm and 4/5 in the left arm. There was minimal weakness of both legs. Sensory examination was
normal. Deep tendon reflexes were normal in the left
arm but were reduced in all other limbs.
He received a course of intravenous immunoglobulin
(1gm/kg/day for 2 days), which did not alter his motor
deficit. A telephone interview 2 months later suggested
that his arm weakness persisted.
PATIENT 3.
PATIENT 4. A 48-year-old man with a previous medical
history of diabetes and non-Hodgkin’s lymphoma (cyclophosphamide, hydroxydaunomycin, vincristine, and
prednisone chemotherapy completed 2 years earlier) developed diarrhea, vomiting, and abdominal cramps and
generalized fatigue 4 days before admission. On the day
of admission, he acutely became unable to walk and developed a flaccid left arm. He denied any sensory disturbance, muscle pain, and bowel and bladder incontinence. He became disorientated soon after admission
but improved the following week. He denied fever,
headache, or neck stiffness before admission.
His examination showed a low-grade fever (38.3°C)
and disorientation to time and place. There was bilateral facial weakness including frontalis muscles, 0/5
strength in the left arm, 4/5 in the right arm, and 3/5
in both legs. Sensory examination was unremarkable.
Deep tendon reflexes were normal in the right arm but
otherwise reduced throughout.
By telephone interview 1 month later, the patient
reported that his leg strength improved enabling him
to walk with a walker; however, his arm weakness remained the same.
PATIENT 5. A 63-year-old healthy man awoke 6 days
before admission with pain in the middle of his back
and found that his left leg was weak and that he was
unable to walk. There were no sensory symptoms,
muscle pain, or bowel and bladder dysfunction. He denied fever, malaise, gastrointestinal discomfort, headache, neck stiffness, and confusion.
His examination showed normal temperature, mental status, and cranial nerve function. His left leg was
flaccid except for minimal flexion of the knee and ankle joints. The strength of the right leg was mildly reduced (4/5), but strength in upper limbs was normal.
Pinprick, light touch, and vibration modalities were
symmetrically reduced in the distal legs and feet, with
noticeable hammertoes and high-arch feet. Deep tendon reflexes were normal in all joints but were absent
in both ankles. The tone of the anal sphincter was normal.
By telephone interview 5 months later, the patient
reported that his leg weakness remained the same.
A 51-year-old healthy woman developed
“flu-like” symptoms 1 week before hospitalization.
Two days after admission, her right leg became paralyzed. Her left arm also became weak. The weakness
quickly spread to the left leg and right arm but was less
severe. She was bed-bound. She had diffuse back muscle aching, but no other sensory disturbance. The patient denied bowel and bladder incontinence. She had
a fever of 38.8° C and a stiff neck upon admission.
The patient was not evaluated by us until 5 months
after the onset of her symptoms. At this time, she had
PATIENT 6.
normal cranial nerve function, severe weakness (1–2/5)
in the right leg, and mild to moderate weakness (3–
4/5) in her other limbs. Sensory examination was normal. Deep tendon reflexes were brisk in all joints with
down-going toes.
Her strength has improved over 5 months from being bed-bound to ambulating with a wheeled walker.
Highlights of Laboratory Findings
Four patients had positive IgM antibodies to WNV detected by ELISA on the CSF. These patients were considered confirmed cases of WNV. Patients 4 and 5 had
positive IgM antibodies in the serum with positive
neutralizing antibody test, which was also confirmatory.8 No ELISA test was conducted on the CSF of
Patients 4 and 5. Patient 2 had a markedly elevated
creatine kinase level. Because the patient fell 6 days before presentation, the creatine kinase level could be related to muscle injury, but the creatine kinase level elevation persisted for more than 12 days, making a
traumatic cause less likely. CSF examination showed
protein elevation and pleocytosis with lymphocytic predominance in four patients (see Table 1). Patient 4 had
76% neutrophils initially but converted to 93% lymphocytes in the second CSF examination collected 4
days later.
MRI studies in Patients 1 and 2 did not show abnormalities in the brain or spinal cord. Cervical MRI
in Patient 5 showed degenerative changes causing stenosis at C3 to C7, but the cord was normal. The spine
MRI of Patient 6, performed 3 days after the onset of
weakness, was remarkable for showing focal abnormal
signal intensity within the anterior horns on T2weighted images (see Fig 1). The level of abnormal
MRI findings corresponded to the weakness. No abnormal signals were found in roots, nor were roots enhanced after injection of contrast.
Routine blood counts were normal in three patients,
but one had increased leukocytes (Patient 3) and two
had reduced platelets (Patients 3 and 4). Sedimentation
rates were only performed in Patients 1 and 3 and were
markedly elevated.
Electrophysiology
Motor nerve conduction studies showed severely reduced amplitudes of compound muscle action potentials in symptomatic limbs (Table 2). Nerve conduction velocities (CVs) in these limbs were relatively
preserved. All patients whose CVs were mildly reduced
also had very low amplitudes of their compound muscle action potential, making it probable that the decreased CVs were caused by severe axonal loss. Sensory
nerve conduction studies were normal except for Patients 4 and 5 who had a history of diabetes and
hammertoes/high-arch feet (possibly a pre-existing neuropathy), respectively. Patient 1 had a conspicuous
Li et al: Segmental Flaccid Paralysis
705
weak limbs and the corresponding paraspinal muscles
(Table 3). Taken together, the pattern of striking denervation in muscles of the paralyzed limbs and corresponding paraspinal muscles with relative sparing of
sensation localizes the lesions to the anterior horn motor neurons and/or their ventral nerve roots. The localization was further corroborated by the aforementioned
MRI abnormalities at the anterior horns. Thus, anterior horn cell damage is a plausible explanation for the
weakness in most, if not all, patients. Interestingly,
needle electromyogram showed myopathic changes in
two to three muscles of Patients 3 and 6, whereas other
clinically affected muscles had neurogenic alterations.
This finding may be consistent with the findings of the
three muscle biopsies (Fig 2) with abnormalities described below.
Muscle and Nerve Histology
We performed nerve and muscle biopsies on four patients (see Fig 2). Muscle biopsies of Patients 1 and 2
showed scattered necrotic muscle fibers, which were invaded by macrophages. In Patient 5, inflammatory cells
were found around small vessels (Fig 3). Because of the
small size of the vessels, we could not be certain if vessel walls were necrotized. The muscle biopsy of Patient
3 was normal. The sural nerve biopsy from Patient 1
showed only occasional degenerated axons with scattered ovoids. Nerve biopsy of Patient 2 was normal.
In an attempt to provide evidence of direct invasion
of muscle by WNV, we performed immunohistochemistry on the biopsied muscle from Patient 2 with polyclonal antibodies against Japanese encephalitis serocomplex flavivirus, an antibody that also labels other
flaviviruses including WNV. The muscle did not show
reactivity with these antibodies.
Fig 1. Abnormal magnetic resonance imaging (MRI) signal
intensity at the anterior horns of spinal cord. (A) A sagittal
T2-weighted MRI of the lumbar spinal cord. Abnormal signal
intensity (arrows) is conspicuous within the cord. (B) A transverse view of the cord at the midlumbar level. Abnormal signal intensity (arrows) is confined to the anterior horns.
asymmetry of sural and superficial peroneal nerve responses in the symptomatic left leg. Needle electromyogram showed severe denervation in muscles of
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Discussion
We have identified several WNV cases presenting with
predominantly motor deficits at the level of the anterior horn motor neurons and/or their ventral roots.
This acute segmental flaccid paralysis has several
unique features compared with other neurological presentations related to WNV infection.2,5–7 These patients have a primarily neuromuscular disorder with
minimal or no viral prodrome. The weakness was
markedly asymmetric or involved only a single limb
and progressed over minutes or hours to paralysis.
There was conspicuous denervation by needle electromyogram and minimal or no sensory involvement by
nerve conduction study. Three patients (1, 3, and 5)
had no clinical meningoencephalitic signs or symptoms, although they did have pleocytosis in their CSF.
Three patients had no fever upon presentation. Unlike
other reports to date,2,5,6 most of our patients were not
elderly or immunosuppressed.
The pathogenesis of acute segmental flaccid paralysis
Table 2. Eletrophysiology
1a
(day 5)
Nerves
Norms
R
L
Lower extremity nerve conduction studies
Peroneal
DML
⬍5.5msec
5.4
6.0
CV
⬎41m/sec 47
49
Amp
⬎3mv
4.3
0.5
F
⬍56msec
55
NR
Tibial
DML
⬍6.0msec
5.0
7.0
CV
⬎41m/sec 46
45
Amp
⬎4mv
5.0
1.0
F
⬍58msec
57
NR
Sural
Lat
⬍4.5msec
3.8
4.2
CV
⬎35m/sec 47
45
Amp
⬎6␮V
17
11
Sup per
Lat
⬍4msec
3.6
4.2
CV
⬎35m/sec 54
41
Amp
⬎5␮V
21
9
Upper extremity nerve conduction studies
Median motor
DML
⬍4.5msec
3.6 —
CV
⬎50m/sec 57
Amp
⬎4mv
9.3
F
⬍32msec
30
Ulnar motor
DML
⬍3.5msec
3.0 —
CV
⬎50m/sec 57
Amp
⬎6mv
10
F
⬍32msec
28
Medi sen
Lat
⬍3.5msec
3.2 —
CV
⬎45m/sec 56
Amp
⬎20␮V
35
Ulnar sen
Lat
⬍3.5msec
3.5 —
CV
⬎45m/sec 50
Amp
⬎10␮V
35
2
(day 10)
3
(day 7)
R
L
R
5.4
38
2.6
NR
NR
—
4b
(day 11)
L
R
3.9
43
3.2
50
—
—
—
5.5
46
11
53
—
3.9
44
9.3
3.8
47
12
4.6
37
21
—
—
—
5b
(day 6)
6
(5 mo)
L
R
L
R
L
8.0
33
0.1
—
NR
NR
NR
NR
7.0
29
0.3
NR
—
5.9
36
2.0
65
6.5
37
6.5
66
6.4
39
3.0
54
—
—
NR
3.5
40
8.5
NR
4.1
35
7
5.1
36
10
—
—
—
NR
NR
—
—
—
6.0
44
2.0
39
4.6
47
4.0
32
5.0
45
2.0
NR
3.9
50
4.5
34
5.0
52
5.4
—
4.0
52
8.0
31
4.0
51
6.0
29
—
—
5.2
44
1.0
36
3.3
51
3.0
31
3.7
45
4.0
NR
3.3
50
4.6
36
3.1
57
7.6
31
2.8
56
8.0
28
—
—
4.3
42
41
3.4
56
39
4.0
48
11
4.1
44
9.2
2.9
48
23
3.5
50
26
3.8
47
29
—
—
4.4
41
52
3.4
50
50
3.9
45
7.0
3.8
47
11
—
3.3
54
17
3.5
54
27
6.5
38
0.6
NR
a
Days after onset of weakness.
Patient 4 received prior cyclophosphamide, hydroxydaunomycin, vincristine, prednisone chemotherapy and has a history of diabetes, which
may contribute to the conduction abnormalities. Patient had evidence of pes cavus suggesting a possible pre-existing neuropathy.
b
DML ⫽ distal motor latency; CV ⫽ conduction velocity; L ⫽ left; R ⫽ right.
is unknown currently but probably involves the anterior horn motor neurons or their ventral nerve roots.
Although the clinical presentation of acute segmental
flaccid paralysis is rather unique, because WNV is a
flavivirus, it is not surprising that the anterior horn region is affected.1 All flaviviruses of the Japanese and
tick-borne encephalitis complex, including WNV, are
known to affect lower motor neurons.8 –18 Of interest
is that several the flaviviruses causes prominent facial,
neck, and shoulder girdle weakness, best typified by
Russian spring summer tick borne encephalitis.19 It
therefore is reasonable to speculate that the paralysis of
the patients described from Mississippi5 and Georgia6
as well as our cases are caused by anterior horn cell
lesions, similar to that seen in acute poliomyelitis. One
of our patients had an MRI showing abnormal signal
intensity confined to the anterior horns, further supporting a role for spinal motor neurons in the pathogenesis of the disease. However, a potential involvement of ventral nerve roots and distal motor nerve
fibers, as well, cannot be excluded. The rapidity of the
paralysis also raises the possibility that damage to the
anterior horn may be of vascular origin secondary to
the meningeal inflammation. This is supported by inflammatory changes around vessels seen in the muscle
biopsy of Patient 5 (see Fig 3). Interestingly, similar
Li et al: Segmental Flaccid Paralysis
707
Table 3. Needle EMG
Patient
Muscle
Fibs/⫹ Waves
Motor Unit
Case 1
L leg
L lumbar paraspinal
R leg
L leg
L lumbar paraspinal
R leg
L deltoid and biceps
L triceps
L abductor pollicis brevis
L cervical paraspinal
R arm
L leg
L orbicularis oris
L arm
L leg
L cervical paraspinal
R leg
L leg
R leg
L arm
L leg
R arm
R leg
R lumbar paraspinal
0/1⫹
2⫹/1⫹
0/0
2⫹/3⫹
0/1⫹
0/1⫹
2⫹/3⫹
2⫹/1⫹
2⫹/1⫹
0/1⫹
2⫹/3⫹
1⫹/0
2⫹/4⫹
2⫹/2–3⫹
0/0–1⫹
1⫹
1⫹/1⫹
0
0
3⫹
1⫹
3⫹/4⫹
2⫹
N
3⫹
N
N
N
3⫹
N
1⫹ amp/dur 2⫹ poly
N
N
2⫹
1⫹
2⫹
1⫹
N
N
1 ⫹ Polyphasic
N⫺ 2⫹ polyphasic
N⫺ 1⫹ polyphasic
3–4⫹
N
3⫹
2⫹
NA
Unable to assess
1 Polyphasic
N
Polyphasic
Polyphasic
Polyphasic
NA
2 4⫹
2 2–3⫹
2⫹
2–3⫹
3–4⫹
Patient 2
Patient 3
Patient 4
Patient 5
Patient 6
Recruitment
Fig 2. Muscle and nerve biopsies: (upper left) Left lateral gastrocnemius muscle biopsy from Patient 1 shows scattered acutely necrotic myofibers (arrows) in early stage of phagocytosis. Frozen section, hematoxylin and eosin stain, ⫻250 original magnification.
(upper right) Muscle biopsy from Patient 1. Detail of a necrotic fiber (arrow). Note absence of inflammation or endomysial fibrosis
in surrounding muscle. Frozen section, hematoxylin and eosin stain, ⫻500 original magnification. (lower left) Left vastus lateralis
muscle biopsy from Patient 2 shows scattered basophilic regenerating fibers (arrows) in distribution similar to Patient 1. Note absence of inflammation or fibrosis. Frozen section, hematoxylin and eosin stain, ⫻250 original magnification. (lower right) Crosssection of sural nerve biopsy from Patient 1 shows several degenerating fibers (arrows). Overall fiber density appears normal. No
inflammation is noted. Plastic embedded section, toluidine blue stain, ⫻500 original magnification.
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Fig 3. Inflammatory changes in muscle biopsy. Left rectus femoris muscle biopsy from Patient 5 includes intramuscular nerve twig
showing inflammation of small endoneurial and perineurial blood vessels (long arrows) and scattered degenerating myelinated nerve
fibers (short arrows). There were perivascular cuffs of mononuclear inflammatory cells around the vessels, and some of the inflammatory cells may have infiltrated the vessel wells. Because the small size of the vessel, we could not be certain whether vessel walls
were necrotized. Frozen section, hematoxylin and eosin stain, ⫻500 original magnification.
inflammatory changes have been described in other flavivirus infections.20
The histological findings from muscle biopsies are
intriguing. Scattered, necrotic muscle fibers are an unlikely explanation for the severe paralysis observed. The
presence of these necrotic muscle fibers raises the possibility of viral invasion of muscle. However, immunohistochemistry did not detect WNV on biopsied muscle. Because the immunohistochemistry was performed
in only one case, the possibility of direct viral invasion
to muscles cannot be completely excluded at this time.
We observed prolonged distal motor latencies and
F-wave latencies in at least two patients (see Table 2),
implying that there may be a demyelinating component. However, this slowing might be exaggerated by
the low amplitudes of the compound muscle action
potential and ventral nerve root damage. Moreover, the
inflammatory infiltration identified in the terminal
twigs of motor nerves (see Fig 3) may contribute to the
prolongation of distal motor latencies. Interestingly,
there was a recent case report documenting an acute
inflammatory demyelinating polyneuropathy–like presentation in a WNV infection patient with CVs of approximately 20 to 30 meter/second.21 These are well
below the CVs we observed. In addition, monolimb
involvement and conspicuous asymmetry of weakness
make it unlikely that these cases were variants of Guillain–Barré syndrome, such as acute motor axonal neuropathy.22
In summary, acute segmental flaccid paralysis may
be a more common presentation of WNV than previously considered and can occur in the presence of, or
absence of, clinical signs of meningoencephalitis or systemic viremia. It therefore will require a high index of
suspicion to consider this diagnosis. The acute onset of
paralysis without significant sensory loss in one or two
motor regions should make one consider WNV infection, especially in an epidemic area.
We thank Dr W.-J. Shieh for immunohistochemistry study on biopsied muscles and B. True and Dr J. Garbern for preparation of
photomicrographs.
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