512

Miller Fisher's Syndrome

James W. Teener,

^ Department of Neurology, University of Michigan Health System, Address for correspondence James W. Teener, MD, Department of
Ann Arbor, Michigan Neurology, University of Michigan Health System, 1C327 UH EMG LAB
SPC 5036, 1500 E. Medical Center Dr., Ann Arbor, Ml 48109-5036
Semin Neurol 2012;32:512-516. {e-mail: jteener@med.umich.edu).

Abstract Miller Fisher's syndrome is a rare variant of Guillain-Barré's syndrome characterized by

Keywords the acute development of ataxia, ophthalmoparesis, and areflexia. Most patients have a
- Miller Fisher's measureable antibody in serum directed against the GQ1 b ganglioside. This antibody is
syndrome also present in the serum of patients with other forms of Guillain-Barré's syndrome who
•- Guillain-Barré's have prominent ataxia or ophthalmoplegia as part of their clinical presentation. Miller
syndrome Fisher's syndrome generally is self-limited and has an excellent prognosis.
- Bickerstaff's
brainstem
encephalitis
"- ganglioside
antibodies
- GQIb antibody
- ataxia
"- ophthalmoparesis

Guillain-Barré's syndrome (GBS) is currently recognized to be
a group of immune-mediated acute neuropathies. --Table 1
lists the recognized subtypes of GBS, including Miller Fisher's
syndrome, the focus of this review. Although the occurrence
of the clinical triad of the acute onset of ophthalmoplegia,
ataxia, and areflexia was first described by Collier in 1932, the
clinical syndrome came to be recognized as variant of GBS
following the description of three cases by Charles Miller
Fisher in 1956.^-^ The disorder is known as Miller Fisher's
syndrome. This is a rare disorder. The worldwide incidence of
GBS is estimated at 1 to 2 in 100,000, and Miller Fisher's
syndrome represents a small fraction of that total. It has a
higher incidence in Asia, estimated at 15 to 25% of GBS
compared with 1 to 7% in the West. There is a slight male
predominance, and Miller Fisher's syndrome can occur in all
age groups.
Typical Miller Fisher's Syndrome Case
A 49-year-old man presented to the emergency department
for evaluation of double vision and "wobbly gait." He first
noted mild difficulties with balance 5 days prior to presenta-
tion, but blamed the symptoms on "getting old and working
too hard." On questioning, he admits his gait difficulties have
worsened slightly each day. He first noted diplopia when
distant road signs were seen as double on the day prior to
presentation. His double vision is now continuous, and
objects appear skewed, that is separated diagonally in his
visual field. He reports that he is nauseated and finds it
difficult to tolerate the double vision. He reports no definite
weakness, but has considerable difficulty walking without
holding on to someone. He reports no numbness, tingling or
sensory loss in his limbs, trunk, or face. He has a very limited
past medical history. He takes simvastatin for moderate
elevation in serum cholesterol, but no other medications.
He has not been hospitalized. He reports no recent fevers or
sweats, but does recall a bout of mild diarrhea two weeks
prior to presentation. He is an engineer for a major auto
company, and frequently travels to their plants in Mexico. He
has a 15 pack-year smoking history, but has not smoked for
9 years. He does not abuse alcohol or illicit drugs. There is no
pertinent family history.
' On examination, he appears uncomfortable, but not acute-
ly ill. He tends to keep his eyes closed. General medical

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Table 1 Culllain-Barré's syndrome subtypes
CBS Subtype
Acute inflammatory demyelinating polyneuropathy (AIDP)
Acute motor and sensory axonal neuropathy (AMSAN)
Acute motor axonal neuropathy (AMAN)
Miller Fisher's syndrome''
Acute pandysautonomia^
Acute sensory ataxic neuropathy^
Pharyngeal-cervical-brachial weakness''
^These may occur along with typical AIDP, but can occur in isolation as distinct clinical syndromes.
examination is unremarkable. He is fully alert with a normal
mental status examination. His eyes are dysconjugate, with
markedly restricted abduction of the left eye, and modest
restriction of movement of both eyes in all other directions.
There is no nystagmus. There is no ptosis, and the pupils are
equal and normally reactive. The degree of ocular misalign-
ment does not appear to fluctuate. Facial strength and
sensation are normal. The palate elevates normally, and the
tongue appears normal as well. Hearing is intact. Limb tone,
bulk, and strength are normal. Rapid alternating movements
of the hands and feet are slowed. He is quite imprecise when
performing the knee-heel-shin maneuver. Vibratory and
temperature perception are normal in the hands and feet,
but proprioception is impaired. He cannot walk or even stand
unassisted despite appearing to have sufficient strength to do
so. Refiexes are absent. Plantar responses are fiexor.
In the emergency department, urgent brain magnetic
resonance imaging (MRI) reveals no areas of restricted diffu-
sion or other signal abnormalities. Computed tomography
angiogram (CTA) reveals no vascular stenosis in the anterior
or posterior circulation. He is admitted to the neurology
service. A lumbar puncture demonstrates an elevated cere-
brospinal fiuid (CSF) protein concentration at approximately
twice the upper limit of normal, without pleocytosis. Routine
sensory and motor nerve conduction studies in the right arm
and leg were normal. Needle electromyogram (EMC) exami-
nation of the rüght arm, leg, and face muscles also was normal.
A diagnosis of Miller Fisher's syndrome was suspected, and
the patient was treated with supportive care. An eye patch
eliminated diplopia. He was trained to use a walker, which
allowed safe ambulation for short distances. Several sérologie
studies were obtained, including normal thyroid-stimulating
hormone (TSH), normal antinuclear antibody (ANA), negative
rapid plasma reagin (RPR), normal acetylcholine receptor,
and anti-muscle-specific receptor tyrosine kinase (MuSK)
antibody titers, and a normal Lyme titer. A measurement of
anti-CQl b antibodies in serum was ordered, and the resulting
markedly elevated titer returned 5 days after the patient was
discharged. He returned for an outpatient follow-up visit
1 week after discharge and reported persistent diplopia,
but his gait was steadier. He was still unable to walk without
assistance. At his second follow-visit, approximately 6 weeks
after symptom onset, he reported diplopia only on left gaze
Miller Fisher's Syndrome Teener 513
Also known as
"Classic" CBS
Axonal CBS
Chinese paralytic syndrome
and no gait unsteadiness. He remained arefiexic At 6 months
following symptom onset, he felt entirely well, and deep
tendon reflexes had returned to normal.
Clinical Features
Classic Miller Fisher's syndrome is defined by the acute onset
of ophthalmoparesis, ataxia, and areflexia. These features
may also be present with signs and symptoms indicative of
more widespread neuropathy. Patients with otherwise typi-
cal acute inflammatory demyelinating polyneuropathy
(AIDP), and less commonly other forms of CBS, may develop
some degree of ophthalmoparesis and ataxia. Antibodies
directed against the CQlb ganglioside are often present in
patients with classic Miller Fisher's syndrome, and when
ophthalmoparesis is present in patients with AIDP. The role
of such antibodies is discussed in detail below. Drowsiness
may sometimes be present. This finding highlights the appar-
ent relationship between Miller Fisher's syndrome and Bick-
erstaffs brainstem encephalitis, which is discussed further
below.
Ophthalmoparesis is an early finding, often leading to
diplopia, which is a frequent presenting symptom in Miller
Fisher's syndrome. The presence of ophthalmoparesis in
Miller Fisher's syndrome or accompanying AIDP is highly
associated with the presence of antibodies to CQlb ganglio-
side. The clinical syndrome of acute isolated ophthalmopa-
resis has been described in patients with antibodies to CQ.lb.
In one interesting study looking at 100 patients with isolated
sixth nerve palsy, in whom no diabetes, tumor, vascular
disease, or recent trauma was present, 25% of patients had
CQlb antibodies.^ Pupillary abnormalities, indicative of in-
ternal ophthalmoparesis, are common in Miller Fisher's
syndrome. Findings may include pupillary asymmetry, slug-
gish reactivity to light, and light-near dissociation.^"^
The ataxia in Miller Fisher's syndrome is often very severe.
Patients are unable to ambulate independently, despite nor-
mal strength. Ataxia is occasionally seen in isolation, and in a
manner similar to isolated ophthalmoparesis, is associated
with antibodies to CQlb ganglioside. There is evidence of
both central and peripheral mechanisms of ataxia in Miller
Fisher's syndrome. Proprioception is severely impaired, and
muscle spindle afferent fibers appear to be particularly
Seminars in Neurology Vol.32 No. 5/2012
514 Miller Fisher's Syndrome Teener
involved^ Antibodies directed against cerebellar antigens
have also been described in patients with Miller Fisher's
syndrome.^
Areflexia is the least specific sign in the classic triad of
Miller Fisher's syndrome because it is a typical finding in AIDP
and other acute neuropathies. It is also the sign that is most
likely to be absent in patients with otherwise typical Miller
Fisher's syndrome. One report indicates that 18% of patients
with Miller Fisher's syndrome have intact reflexes.^ The
areflexia appears to be due to peripheral nerve dysfunction,
and most patients with areflexia in Miller Fisher's syndrome
have abnormalities on sensory nerve conduction studies.^*^
Diagnosis
The diagnosis of Miller Fisher's syndrome is made based upon
recognition of the triad of signs, and may be supported by
laboratory studies. An elevation in cerebrospinal fluid (CSF)
protein concentration is a classic finding in AIDP, and is often
seen in Miller Fisher's syndrome. An increased CSF protein
concentration may not be present early in the presentation,
and may not develop at all in some cases. It appears that
increased CSF protein concentration is more common when
there is more peripheral nerve involvement, that is. in
"overlap syndromes" between pure Miller Fisher's syndrome
and CBS.^^'^^The measurementofanti-CQ.lb antibodies isa
more sensitive test for Miller Fisher's syndrome than identi-
fication of an increased CSF protein concentration. The path-
ogenic role of antibodies reactive to CQlb ganglioside is
discussed in detail below. Such antibodies can be detected
in at least 85% of patients with Miller Fisher's syndrome.^ ^
Miller Fisher's syndrome is not typically associated with
any abnormalities on brain imaging. Many patients with
Miller Fisher's syndrome do undergo brain imaging, particu-
larly if the triad of symptoms is not fully present, and the vast
majority have normal brain MRI studies. Oculomotor abnor-
malities and ataxia raise the possibility of lesions in the
brainstem and/or cerebellum, and many practitioners are
reassured by the absence of ischémie, inflammatory, or
mass lesions in the posterior fossa. In rare instances, patients
with Miller Fisher's syndrome may have faint enhancement
or increased T2 signal of cranial or spinal nerve roots, and
isolated reports of increased T2 signal in the brainstem or
cerebellum exist.^^"^^
Electrodiagnostic studies (nerve conduction studies and
EMC), which play a large role in confirming the diagnosis of
Table 2 Antiganglioside antibodies associated with GBS subtypes
GBS Subtype
AMAN
Miller Fisher's syndrome
Acute sensory ataxic neuropathy
Bickerstaff's brainstem encephalitis
Pharyngeal-cervical-brachial weakness
Abbreviations: CBS, Guiltain-Barré's syndrome; AMAN, motor axonal neuropathy.
Seminars in Neurology Vol. 32 No. 5/2012
AIDP and other forms of CBS. have a more limited role in
Miller Fisher's syndrome. In true Miller Fisher's syndrome,
routine studies may be normal. Mild abnormalities in sensory
nerve conduction studies are often seen. Blink reflex studies
may also be abnormal.^^ In patients with the most common
overlap syndromes, nerve conduction studies may reveal
changes typical of AIDP.
Many patients with Miller Fisher's syndrome report a
prodromal illness, with upper respiratory symptoms de-
scribed more commonly than gastrointestinal symptoms. In
both Miller Fisher's syndrome and GBS, Campylobacter jejuni
is the most commonly identified organism causing an ante-
cedent infection. Haemophiius inßuenzae, cytomegalovirus.
f\/iycoplasma pneumoniae are also identified in a small per-
centage of cases.^^
Miller Fisher's syndrome may also develop in the setting of
various neoplastic or autoimmune disorders. There are re-
ports of Miller Fisher's syndrome developing in patients with
myasthenia gravis, lupus. Still's disease, autoimmune thyroid
disease, lung cancer. Hodgkin's and non-Hodgkin's lympho-
ma, leukemia, and acquired immunodeficiency syndrome.^^
It should be noted that such associations with both infections
and immune disorders do not necessarily imply causality.
Pathogenesis
There is growing recognition that antibodies directed against
gangliosides play a significant role in the pathogenesis of
many acute autoimmune neuropathies. This is particularly
true of Miller Fisher's syndrome. -Table 2 lists the antigan-
glioside antibodies most closely linked with various GBS
subtypes. Gangliosides are sialic acid-bearing glycoproteins
present on neuronal cell membranes. They seem to cluster in
areas of the cell membrane known as lipid rafts, with their
oligosaccharides exposed on the cell surface. The ganglioside
GQIb is richly present at the paranodal myelin in cranial
nerves III. IV. VI and in the dorsal root ganglia.^^ This
localization is likely responsible for the unique clinical triad
of Miller Fisher's syndrome, ophthalmoparesis, ataxia, and
arefiexia. Approximately 80 to 90% of Miller Fisher's syn-
drome patients have antibodies against GQ.1 b. The antibodies
are also present in several closely related disorders, including
CBS with ophthalmoparesis, isolated acute ophthalmopare-
sis. ataxia without ophthalmoparesis, and Bickerstaffs brain-
stem encephalitis. Such antibodies are not detected in sera
from patients with many other neurologic disorders. The
Associated antiganglioside antibodies
GM-l.CDla, GTIb
GQIb
GDlb
CQlb
GTla. GQIb

GQlb and GDlb gangliosides are also highly present in
muscle spindles.^^ Measurement of anti-GQlb titers often
allows diagnosis of Miller Fisher's syndrome and these related
disorders, and differentiates these syndromes from other
disorders on the differential diagnosis, including multiple
sclerosis and myasthenia gravis.
The trigger for the development of antiganglioside anti-
bodies appears to frequently be an infection. Campylobacter
jejuni infection seems to be the most common infection
preceding several variants of GBS, particularly acute motor
axonal neuropathy and Miller Fisher's syndrome. This rela-
tionship has been extensively studied, and it is apparent that
certain serotypes of C jejuni express surface lipo-oligosac-
charide molecules that share tetrasaccharide moieties with
various gangliosides, including GM-1 and GQl b.^^ This allows
for what has come to be known as "molecular mimicry,"
where the body may mount an immune response to an
epitope on an infectious agent that then also recognizes
and attacks self-antigens on nerve.
Bickerstaffs brainstem encephalitis is characterized by
ataxia, ophthalmoparesis, impaired consciousness, and hy-
perreflexia. Patients may also have nonocular cranial mono-
neuropathies and have features similar to GBS with limb
weakness and sensory loss. Many authorities feel that Bick-
erstaffs brainstem encephalitis lays on a continuum with
Miller Fisher's and related disorders that include the acute
onset of ataxia and ophthalmoparesis. The presence of symp-
toms such as somnolence or even coma, and hyperreflexia
suggests that anti-GQlb antibodies have pathologic effects in
the central nervous system as well as in the cranial and
peripheral nerves. Recent studies have demonstrated that
anti-GQl b antibodies bind to and inhibit the calcium currents
of cerebellar granule cells.
Treatment
Fortunately, Miller Fisher syndrome is almost always a self-
limited disorder with an excellent outcome. There are a
limited number of controlled trials of treatment of Miller
Fisher's syndrome. Some trials are complicated by the inclu-
sion of patients with more typical GBS with ophthalmopa-
resis and/or ataxia. There are also few treatment trials in
Bickerstaffs brainstem encephalitis. A Cochrane Review has
been published regarding the treatment of Miller Fisher's
syndrome, Bickerstaffs brainstem encephalitis, and related
disorders.^^ »-Table 3 summarizes the results of the Cochrane
Review.
Table 3 Summary of results of Cochrane Review on the treatment of Miller Fisher's syndrome and Bickerstaffs brainstem
encephalitis
Disorder
No treatment
Miller Fisher's syndrome 60-100%
Limited Miller Fisher's syndrome 100% normal at 6 months regardless of treatment
Bickerstaffs brainstem encephalitis 66% of all patients normal with no clear treatment benefit
Abbreviation: IVIC, intravenous immunoglobulin.
Miller Fisher's Syndrome Teener 515
Because the natural history of these disorders is favorable,
it is difficult to demonstrate a treatment benefit. One might
expect treatment to hasten recovery, and that appears to be
the case for intravenous immunoglobulin (IVIG). In an animal
model, IVIG has been demonstrated to reduce binding of anti-
GQl b antibodies and limit the pathologic effects of the anti-
bodies.^'' Mori et al reported that patients began to recover
earlier following IVIG treatment in comparison to no treat-
ment. Plasma exchange did not appear to hasten recovery.^^
In the largest reported series of Bickerstaffs brainstem
encephalitis, most patients had a favorable outcome regard-
less of therapy.^^ Several different therapies were reported,
including combinations of plasmapheresis with corticoste-
roids, IVIG, and corticosteroids alone, which of course dilutes
the ability to detect differences between any single therapy
and the natural history of the disease. In »-Table 3, limited
Miller Fisher's syndrome refers to isolated acute ophthalmo-
plegia associated with the presence of anti-GQlb antibodies.
Prognosis was uniformly good in this small group, some of
whom were not treated and some of whom were treated
with IVIG.
There is insufficient data to recommend any treatment for
Miller Fisher's syndrome or Bickerstaffs brainstem encepha-
litis. Because the natural history suggests a good outcome, the
decision to offer any treatment must be carefully weighed
against the risks of the proposed treatment. Many patients
have an overlap syndrome with varying features indicative of
AIDP or another subtype of GBS with prominent neuropathy,
with the additional features of ophthalmoparesis or ataxia.
These patients should be treated as if they have typical GBS.
There is considerable evidence that both IVIG and plasma-
pheresis improve the course of GBS, but corticosteroids do not
have a role in treatment of GBS at this ^^
Conclusion
Miller Fisher's syndrome is a rare subtype of GBS character-
ized by the acute development of ataxia, ophthalmoparesis,
and areflexia. The triad may be present in isolation or may
occur along with features of more typical GBS. Patients with
Miller Fisher's syndrome or otherwise typical GBS with some
features of Miller Fisher's syndrome are likely to have anti-
bodies directed against GQlb ganglioside detectable in se-
rum. Bickerstaffs brainstem encephalitis is an even rarer,
related condition in which impaired consciousness and hy-
perreflexia accompany ataxia and ophthalmoparesis. Anti-
bodies against GQlb ganglioside are present in Bickerstaffs
% Complete clinical recovery at 6 months
IVIC Plasma exchange
89% 66-96%
Seminars in Neurology Vol.32 No. 5/2012
516 Miller Fisher's Syndrome Teener
brainstem encephalitis as well as Miller Fisher's syndrome.
Both of these conditions are typically self-limited and no
treatment is necessary, unless there are features of an overlap
syndrome w'\t\\ AIDP or other neuropathic subtypes of GBS. In
that case, treatment with IVIG or plasmapheresis is indicated.
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