The clinical triad of ataxia, areflexia, and ophthalmoplegia was first described by Collier in 1932 as a variant of the Guillain-Barré syndrome (GBS) (1). In 1956, Charles Miller Fisher reported 3 patients with this disorder, postulated that it represented a distinct clinical variant of GBS with a good prognosis (2), and pointed out that more invasive techniques such as cerebral angiography, previously used in evaluating such patients, were not necessary (3). The disorder became known as the Miller Fisher syndrome or simply “Fisher's syndrome” in 1957, when Smith and Walsh (4) used the term in describing 2 additional patients with facial weakness and paresthesias. (Because Miller is Fisher's middle name, we will follow their lead in this review and refer to the condition as Fisher syndrome [FS]).
Although most published reviews define FS strictly as an acute monophasic illness featuring the clinical triad of ophthalmoplegia, ataxia, and areflexia, it can present with 2 or even 1 of these features. It can also present with features that overlap Bickerstaff brainstem encephalitis (BBE), a syndrome characterized by ophthalmoplegia, ataxia, impaired consciousness, and hyperreflexia (5), and with features typical of GBS, in which limb weakness is the most prominent finding, sometimes accompanied by sensory loss and nonocular motor cranial neuropathies (6). These disorders can all develop after an antecedent infection and share a characteristic elevation of cerebrospinal fluid (CSF) protein.
The identification of the GQ1b autoantibody, present in most patients with FS, has further transformed thinking about the nosologic position of this syndrome. FS is now widely regarded as belonging to a spectrum of acute inflammatory polyneuropathies that includes BBE, anti-GQ1b-positive acute ophthalmoparesis without ataxia (AO), ataxic GBS, and GBS with ophthalmoplegia (7,8) (Table 1). The ability to test for the presence of the anti-GQ1b antibody has made the diagnosis of FS more consistent and has allowed for a greater appreciation of FS-related disorders.
The marked variability in the clinical presentation of FS has blurred the lines between FS in its purest form and related clinical syndromes that defy classification (Table 2). In this article we review the demographics as well as the neuro-ophthalmic and systemic symptoms and signs, ancillary tests, natural history, and treatment options for disorders that can together be grouped as the Fisher variant of GBS.
INCIDENCE AND DEMOGRAPHICS
The worldwide incidence of GBS is 1-2 per 100,000 per year (9), with FS as a percentage of such cases varying depending on geography. Whereas FS has been reported at a rate of 1%-7% of GBS in countries in the Western hemisphere (10-15), it is much more common in Asia, comprising 18%-19% of cases of GBS studied in Taiwan (16,17) and 25% of GBS in Japan (18). Men are somewhat more often affected than women, making up 60% and 68% of those with FS in 2 large series (18,19). Male predominance is also found in related disorders such as AO and BBE (19-21). FS has been described in people of all ages, including infants (22), although it is less common in children than in adults (23). A retrospective study of 466 patients with FS reported a median age of onset of 44 years with a bimodal age distribution peaking between 30 and 39 years and 50 and 59 years (19). There is dispute about a seasonal predilection for FS, with studies showing a rise in new cases in the spring (20,24-27), winter (17), summer, and fall (20).
The variability in seasonal occurrence of FS may be related to the typically postinfectious nature of this disorder. Prodromal upper respiratory symptoms are experienced more commonly than gastrointestinal symptoms (18,28). The median time from onset of prodromal to neurologic manifestations was 8 days in 1 large series (18).
Campylobacter jejuni is the most commonly identified agent causing antecedent infection in patients with acute FS and those with GBS and related disorders, followed by Haemophilus influenzae. However, in most patients, no definite infectious association has been detected (29). In 1 large study, 21% of patients with FS had positive titers for C. jejuni, 8% for H. influenzae, 4% for cytomegalovirus, and 3% for Mycoplasma pneumoniae (19). Less common antecedent infectious agents associated with FS are Epstein-Barr virus (30), group A streptococcus (31), Coxiella burnetii (32), Pasteurella multocida (33), Helicobacter pylori (34), Aspergillus species (35), and varicella zoster (36). FS also has been reported after inoculation with the influenza vaccine (37) and after vaccination with Pneumovax (38). An association does not allow a causal relationship to be inferred (39,40).
A common infectious etiology links FS with related disorders. In one study of 21 patients with AO, 81% experienced symptoms of antecedent infection, with 57% having symptoms of an upper respiratory tract infection (41). C. jejuni was isolated from 1 of those patients (41). In another series, 96% of 53 patients with BBE reported prior infectious symptoms, again mostly respiratory (19). Kimoto et al (42) reported on the spectrum of neurologic disorders that occurs subsequent to C. jejuni enteritis, including, in descending order of frequency, GBS, FS, muscle stretch reflex-preserved GBS, FS/GBS overlap, acute oropharyngeal palsy, BBE, BBE/GBS overlap, AO, and ataxic GBS. They correlated these groups with genotypic variations and proposed that the conditions were on a continuum.
FS occasionally develops spontaneously in patients with various autoimmune, neoplastic, or infectious diseases such as myasthenia gravis (43-45), systemic lupus erythematosus (46,47), Still disease (48), thyroid disease (49,50), Hodgkin disease (51), lung cancer (52), leptomeningeal signet-ring cell carcinomatosis (53), Burkitt lymphoma (54), chronic lymphocytic leukemia (55), and AIDS (56). It has also been reported in patients after treatment with several medications, including tacrolimus (57), the antiretroviral agent stavudine (24,58), and tumor necrosis factor antagonists (59,60). These associations may be fortuitous.
In its purest form, FS is a triad of acute ophthalmoplegia, ataxia, and areflexia, although even the initial descriptions of the condition include patients with additional findings such as mild limb weakness or drowsiness (2).
The initial symptom in FS is typically diplopia (65%), followed by gait disturbance (32%) (19). These symptoms were described as occurring simultaneously in 14% of patients with FS (19). Dysesthesias are also commonly reported, occurring in 14% of patients with FS in 2 large studies (18,19). Less common presenting symptoms are blepharoptosis, mild limb weakness (19), dysphagia, photophobia (18), blurred vision, dizziness, headache, and facial weakness (16). One man with FS and positive serum anti-GQ1b autoantibodies presented with a severe and persistent headache that the authors postulated was due to antibody-mediated effects on the trigeminovascular pain pathway (61).
Ophthalmoplegia seems to be the most prevalent and consistent finding in FS and related disorders during the acute phase of the illness (19) and can manifest as various combinations of deficits (21) (Fig. 1). Ophthalmoplegia is closely tied to the presence of anti-GQ1b antibodies, although these antibodies also can be found in patients with no eye movement abnormalities (8,62). Most patients with FS exhibit bilateral, relatively symmetrical ophthalmoplegia, but the condition also can be unilateral (41,63-65). Up to one third of patients have complete external ophthalmoplegia (18). A review of 31 patients with complete bilateral ophthalmoplegia during a 34-year period (66) revealed that FS was the most common cause and, together with GBS, was responsible for 58% of such cases.
The ophthalmoplegia seen in FS is similar to that described in AO (21). A study that compared the findings in 11 anti-GQ1b antibody-positive patients with AO to the findings in 20 anti-GQ1b antibody-positive patients with other disorders including FS concluded that the patterns of ophthalmoplegia were similar in these groups. Abduction deficit was the most common finding, occurring in 73% (21). The association of acute ophthalmoparesis with the anti-GQ1b antibody was identified in 1993, when Chiba et al (67) described 5 patients with isolated ophthalmoparesis, 4 of whom had had a common cold as a prodrome, the fifth having had diarrhea. All had evidence of mild bilateral sixth cranial nerve palsy, and the condition was designated “atypical FS.” Interestingly, 2 patients in that study who were negative for anti-GQ1b antibody (1 with typical FS and 1 with GBS with ophthalmoplegia) had isolated complete unilateral sixth cranial nerve palsy, suggesting that a different mechanism and pattern of ophthalmoplegia might be present in anti-GQ1b antibody-negative patients (67).
Yuki et al (68) described 8 anti-GQ1b antibody-positive patients with ophthalmoplegia and no ataxia and termed the condition simply “acute ophthalmoparesis.” Two had horizontal and vertical gaze palsies; the other 6 had bilateral sixth cranial nerve palsies. Yuki et al (41) subsequently summarized the findings in 21 other patients with AO, most of whom had bilateral, horizontal, mostly abduction deficits. In this group, gaze deficits were bilateral in 76%. Both horizontal and vertical movements were affected in 48%, and 52% had gaze deficits limited to the horizontal plane. Bilateral abduction deficit was the most common pattern, occurring in 33% of patients. Other case series have confirmed that the most characteristic pattern of AO is an initial bilateral sixth cranial nerve palsy followed by third cranial nerve palsy with internal ophthalmoplegia (8,69), a pattern present in 48% of the 21 patients reported by Yuki et al (41). No studies have determined definitively the frequency of the anti-GQ1b antibody in patients with isolated ophthalmoparesis. However, in a study of 100 patients with isolated sixth cranial nerve palsies, when traditional etiologies such as diabetes mellitus, vascular disorders, trauma, or tumor were excluded, the anti-GQ1b antibody was present in the sera of 25%, indicating that some cases may be related to FS (70).
“Brainstem” Ocular Motor Deficits
Clinical findings suggestive of brainstem ocular motor deficits have been described in some patients with otherwise typical FS, suggesting the possibility of central nervous system (CNS) involvement (71,72). In a study of 50 patients with typical FS (18), 2 exhibited preservation of the Bell phenomenon despite paralysis of voluntary upgaze; 2 had gaze-evoked, horizontal, dissociated nystagmus; 1 showed preservation of convergence despite adduction palsy; and 1 had an internuclear ophthalmoplegia. Other forms of apparently CNS ocular motor dysfunction reported in patients with otherwise typical FS include dorsal midbrain syndrome with eyelid retraction (2), convergence spasm, divergence paralysis (73,74), saccadic dysmetria (75), defective vestibulo-ocular reflex despite recovery of upgaze, central vestibular nystagmus, and relative preservation of optokinetic nystagmus and preservation of the vestibulo-ocular reflex despite an otherwise complete ophthalmoplegia (76).
Internal ophthalmoplegia is quite common in FS and related syndromes, with the pupillary constriction to light and near stimulation ranging from slow to absent (21,77). Light-near dissociation may be present (78-80). All 3 patients initially reported by Fisher exhibited a sluggish pupillary constriction to light (2), and in the series of 50 patients with FS reported by Mori et al (18), mydriasis was present in 42%-about half of whom had anisocoria-and the pupillary constriction to light was sluggish in 42%. Of 11 patients with FS in a study linking FS to anti-GQ1b antibody positivity, 64% had absent or sluggish pupillary reflexes (81). Most of these findings were bilateral.
With regard to disorders that share the anti-GQ1B antibody, the incidence of internal ophthalmoplegia is highest in patients with FS exhibiting limb weakness (52%), followed by BBE (42%) and typical FS (37%) (8). Pupillary abnormalities seem to occur less commonly in patients with AO, as evidenced by the lack of pupillary defects in the study by Yuki et al (68) of 21 patients with AO and 7% involvement in the series of 15 patients reported by Odaka et al (8). Nevertheless, in 1 study of 11 patients with AO, about half had internal ophthalmoplegia (21). Patients with anti-GQ1b antibody positivity have also been reported to have internal ophthalmoplegia as the prominent feature with little or no external ophthalmoplegia (79,82,83). Many of these patients demonstrate denervation supersensitivity to cholinergic agents, suggesting ciliary ganglion or short ciliary nerve involvement (78,79).
Ataxia is often the initial presenting symptom in FS and can be quite severe, causing a gait disturbance so profound that, in 1 large series, 30% of affected persons could not walk independently (18). Ataxia in FS is associated with the anti-GQ1b antibody. This autoantibody also can be found in patients who have a variant of ataxia without ophthalmoplegia (84,85). One study showed that anti-GQ1b antibody-positive patients had more cerebellar-type severe ataxia than patients with FS who were antibody-negative (81). The autoantibodies seen in the ataxic forms of GBS also exhibit the same fine specificity patterns for other gangliosides as those seen in FS, further evidence that the 2 disorders are related (86).
The pathogenesis of the ataxia in FS is not completely understood. Both peripheral and central mechanisms have been implicated. Early studies showed a correlation between abnormalities in muscle fiber afferents and severity of ataxia, suggesting impaired proprioception as the mechanism (87,88). Indeed, postural sway analysis reveals selective dysfunction of proprioception in patients with FS (85,89) and BBE (19). Thus, dysfunction of muscle spindle afferent fibers may be responsible for the ataxia, at least in some patients (18,89,90). However, the presence of anti-cerebellar antibodies in the sera of patients with FS has led other investigators to suggest that the ataxia in such patients is cerebellar in origin (91,92). Additional research is needed to elucidate fully the pathophysiology of ataxia in FS and related syndromes.
Deep tendon areflexia is part of the classically described FS triad, although it is also part of typical GBS (6). The loss of reflexes was initially thought to be present in almost all patients with FS. However, reflexes are intact more often than originally believed (93). For example, in a series of 581 patients with FS and BBE who presented with acute ophthalmoplegia and ataxia, Ito et al (19) found that of the 528 patients with intact consciousness, 12% had normal or even accentuated deep tendon reflexes (19). In a review of 13 Korean patients with ophthalmoplegia and ataxia and anti-GQ1b antibody-positivity, 4 (31%) had normal reflexes (21). A 1992 review of the published reports of FS (23) concluded that 18.4% of patients had intact reflexes. Electrophysiologic studies support peripheral nerve dysfunction as the cause of reduced deep tendon reflexes (94,95).
Other findings often reported in patients with FS and related syndromes include various patterns of blepharoptosis, occurring in up to 58% of patients (18,23,41), and eyelid nystagmus (96). Dysesthesias can occur in 45% of patients during the acute phase of illness (19). Facial and bulbar palsies were described in 32% and 26%, respectively, in 1 large study (18). Limb weakness is a prominent and distinguishing feature of GBS as opposed to FS, but a mild decrease in muscle strength is commonly seen in FS (18). Several case reports have described bilateral and, less commonly, unilateral optic neuritis in FS (97-102). Headache is reported in FS and was present in 2 of Fisher's original patients (2). Pain in FS can occur periocularly and in the back and extremities (103,104). In a study by Koga et al (103), pain was described by 22% of 27 patients, half of whom localized the discomfort to the periocular region, and was more common in children and young adults. Micturition disturbances were present in 16% of patients with FS in 1 large case series (18), and urinary retention also has been reported (17,105). Angle-closure glaucoma developed in a patient with FS in whom pupillary dysfunction occurred in the setting of a congenitally narrow anterior chamber angle (106). One patient with FS had unilateral absence of corneal sensation (107). Autonomic neuropathy can occur in FS but is less severe and less frequent than in GBS or BBE (105). In 1 study of cardiovascular autonomic function (108), subclinical autonomic dysfunction was identified in most patients with FS.
A rise in protein concentration in the cerebrospinal fluid (CSF) in 1 of Fisher's original patients was the key piece of evidence that led the author to believe that the condition bore a close relationship to a “GBS type of polyneuropathy” (2). Elevation of CSF protein with minimal or no cellular reaction or “cytoalbuminous dissociation,” may be absent at the time of initial symptoms, becoming prominent over the next weeks (109). It seems to occur more frequently in the overlap syndrome of BBE/GBS than in FS and occurs even less frequently in AO (8,41). However, it is difficult to compare CSF findings among these variants because the finding of elevated CSF protein depends on when in the course of the disease the specimen is collected, information that is not consistently reported.
The discovery of the frequent presence of the anti-GQ1b antibody in the acute-phase sera of patients with FS has helped clinicians understand the broader spectrum of FS and related disorders (7). This antibody was first reported in FS in 1992 by Chiba et al (7), who described 6 patients. This report and subsequent studies (109) have affirmed that this antibody, which cross-reacts with the GT1a ganglioside, is present in more than 85% of patients with FS. It is absent in normal control subjects and is found less often in patients with GBS without ophthalmoplegia (67,81,110,111). This autoantibody is also found in FS-related diseases such as GBS with ophthalmoplegia (67), AO (68), BBE (21,112), and ataxic GBS without ophthalmoplegia (86). Clinically, the presence of the anti-GQ1b antibody correlates with the presence of ophthalmoplegia (41) and ataxia (84) but has been reported in the absence of both (62). Odaka et al (8) described clinical similarities and variations among the diseases that constitute the “anti-GQ1b syndrome” and proposed this as further evidence that that they are part of a clinically continuous range of illnesses.
The GQ1b ganglioside is a cell surface component that is concentrated in the paranodal regions of the human third, fourth, and sixth cranial nerves. It contains polysaccharides identical to the lipopolysaccharides (LPS) contained in the outer membranes of certain bacteria and may thus be the target of an immune response initiated against epitopes shared by these nerve fibers and various infectious agents (41). In 1994, Yuki et al (113) found that monoclonal antibodies to the GQ1b ganglioside reacted to LPS fractions from C. jejuni isolated from patients with FS. These investigators proposed that, through the mechanism of molecular mimicry, they were not only a marker for the disease, but actually played a role in its pathophysiology. Anti-GQ1b/GT1a antibodies also bind to LPS from FS-related H. influenzae strains, suggesting a common pathogenesis (29). The finding of these antibodies in the sera of patients with isolated internal ophthalmoplegia suggests that these epitopes may also be present in the ciliary ganglia (41,67,79,114).
Anti-GQ1b antibodies affect the neuromuscular junction, inducing axon and Schwann cell degeneration through complement-mediated pathways (115-119). Ganglioside complexes containing GQ1b have also been investigated as other possible targets for autoantibodies (120,121) whose specificity may be associated with the clinical features of GBS and FS (90). In addition, reactivity to minor gangliosides has been shown to be present in FS and related disorders and may prove to be helpful in their diagnosis and treatment (122).
In comparing the prevalence of CSF protein elevation with that of serum anti-GQ1b antibodies in the diagnosis of FS, Nishimoto et al (109) demonstrated that in the 1st week after onset of symptoms, anti-GQ1b antibodies were almost always present, whereas elevated CSF protein was found in only 25% of patients. They concluded that CSF findings are not as sensitive as the anti-GQ1b antibody assay in diagnosing FS in the early stage of the disorder. In addition, anti-GQlb antibody titers have been shown to correlate with clinical severity of the disease, particularly ophthalmoplegia (123) and also demonstrate a relationship to disease course because they decline with clinical recovery (81,109).
NEUROIMAGING AND PATHOLOGIC STUDIES
Results of neuroimaging are usually unremarkable in patients with FS. However, in 1 large study (19), 1% of patients with FS had MRI abnormalities in the midbrain, cerebellum, or middle cerebellar peduncle. Other individual case reports have described MRI lesions in the brainstem (124-127); fourth (128), sixth (129), and seventh cranial nerves (130,131); spinocerebellar tracts in the region of the lower medulla (132); lumbosacral roots (131); cauda equina (133); and posterior columns (134) of patients with FS. In general, lesions seen on MRI in patients with FS appear as hyperintense abnormalities on T2 images or, more commonly, as enhancing areas on postcontrast T1 images (127,130,135-138). Similar imaging abnormalities have been described in patients with GBS, although much less frequently (24).
A small number of necropsy studies have shown inflammatory brainstem lesions (23,139-141) as well as demyelination of peripheral nerves (142). In 1 patient with recurrent FS, demyelination and axonal impairment of the intra-axial portion of the third cranial nerve were present and associated with mild retrograde degeneration in the third, fifth, sixth, and seventh cranial nerve nuclei (143).
Most patients with FS recover spontaneously and completely within 2-3 months of disease onset. In 1 study (18), the median time from onset of neurologic symptoms to beginning of recovery in 28 untreated patients was 12 days for ataxia and 15 days for ophthalmoplegia. The median time to full recovery was 1 month for ataxia and 3 months for ophthalmoplegia. At 6 months after illness onset, no patients had substantial disability. The recovery rate was unrelated to patient age, sex, evidence of prior infection, disability at illness peak, or latency to peak (18).
Although FS is typically regarded as a monophasic illness, recurrences have been reported (99,144-158). Patients may present differently during subsequent episodes (150). Chronic ophthalmoplegia associated with persistently high titers of anti-GQ1b antibody has been reported (159). Rarely, the disease can progress, and patients develop features similar to GBS, requiring more significant supportive care and mechanical ventilation (22,160-166). In a recent series, 1% of patients with FS required assisted ventilation compared with 34% of those with BBE (19). However, patients with FS who develop quadriparesis, often considered to have a “FS/GBS overlap,” are more likely to require mechanical ventilation than patients with typical GBS (167). Other serious complications in FS include coma (168), ballism (164,169), cardiomyopathy from dysautonomia (170), lactic acidosis (58), corticobulbar dysfunction (24,171), and life-threatening hyponatremia from inappropriate secretion of antidiuretic hormone (SIADH) (172). Death in FS is rare (142).
Although no randomized, controlled clinical trials of treatment for FS have been performed (173), a retrospective analysis of 92 consecutive patients showed that treatment with intravenous immune globulin (IVIg) had no effect on overall outcome, presumably because patients with FS typically show good spontaneous recovery (174). Plasmapheresis has also been used in selected patients with FS but without definite clinical benefit (175-185). As in all conditions in which spontaneous resolution is the rule, the risks of treatment in patients with FS must be balanced with the high likelihood of spontaneous recovery (186-190).
FS seems to represent a collection of manifestations derived from a spectrum of disorders that include GBS, BBE, and AO. The factors that determine which patients develop FS and which develop the related disorders remain unknown. The anti-GQ1b antibody is much more commonly associated with FS than with its related disorders, although patients with each of the disorders may have no serologic evidence of the antibody. When an infectious process caused by C. jejuni precedes the development of 1 of these conditions, the serotype of the responsible strain seems to influence the clinical presentation and the severity of the condition (29,191)
Host susceptibility probably also plays a role in phenotypic expression (192). Because the GQ1b antibody is found in sites unaffected by FS, its location in the body cannot be the only reason certain tissues are preferentially affected (114,115,193). For example, the antibody may have more access to certain structures through a compromised blood-brain barrier, perhaps leading to conditions more consistent with the CNS manifestations seen in BBE (85,89). Other factors may include the degree to which these gangliosides play a role in neural functioning or the “level of immunologic tolerance to microbial glycans that mimic self gangliosides” (119).
Although the full immunologic cascade leading to FS has yet to be elucidated, the frequent finding of the GQ1b autoantibody is of great diagnostic value. Research into the molecular targets involved in the development of FS has already led to rational therapeutic studies in which monoclonal antibodies have shown success in treating murine models of the disorder (194,195). These investigations may ultimately clarify our understanding of the pathogenesis of FS and related disorders and lead to insights that will aid in treating more severe and generalized neuropathies.
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