Neurologic and otologic findings in Fisher's syndrome

Minoda, Ryousei; Uno, Kengo; Toriya, Takafumi; Eura, Masao; Noguchi, Satoshi; Masuyama, Keisuke

doi:10.1016/s0385-8146(98)00050-9

Cited by 12 publications

(8 citation statements)

References 10 publications

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“…38 In addition, spontaneous downbeat nystagmus, periodic alternating nystagmus, GEN, central positional nystagmus, ocular flutter, and saccadic dysmetria have been described in anti-GQ1b antibody syndromes. 10,33,39 Our observations demonstrate that SN, canal paresis, and positive HITs, which are typical findings of AUPV, may be observed when associated with anti-GQ1b antibodies.…”

Section: Discussionmentioning

confidence: 52%

“…32 Indeed, canal paresis can be observed in patients with FS without ophthalmoparesis. 33 Furthermore, the typical features of AUPV may be observed in association with positive serum anti-GQ1b antibody. 8 Abnormal HITs 34 and canal paresis 35 mostly indicate peripheral vestibulopathy, whereas internuclear ophthalmoplegia, 36 one-and-a-half syndrome, 37 or dissociated horizontal nystagmus suggest central involvements.…”

Section: Discussionmentioning

confidence: 99%

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Clinical Features and Neurotologic Findings in Patients With Acute Unilateral Peripheral Vestibulopathy Associated With Antiganglioside Antibody

Kim,

Park,

Lee

et al. 2023

Neurology

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Background and Objectives: Anecdotal studies have reported the presence of anti-ganglioside antibodies in acute unilateral peripheral vestibulopathy (AUPV). This study aimed to determine the prevalence, clinical characteristics, and neurotologic findings of AUPV associated with anti-ganglioside antibodies. Methods: Serum anti-gangliosides were measured in consecutive patients with AUPV according to the Bárány Society criteria during the acute and recovery phases, in a referral-based university hospital in South Korea from September 2019 to January 2023. Clinical characteristics and neurotologic findings were compared between those with and without anti-ganglioside antibodies. The results of video-oculography, video head-impulse and bithermal caloric tests, and other neurotologic evaluations including ocular and cervical vestibular-evoked myogenic potentials, subjective visual vertical were compared between the two. MRIs dedicated to the inner ear were also conducted when considered necessary. Results: One hundred and five patients (mean age±standard deviation [SD] = 60±13 years, 57 male) were included for analyses. During the acute phase, 12 patients (12/105, 11%) were tested positive for serum anti-ganglioside antibodies, including anti-GQ1b IgG (n=5) or IgM (n=4), anti-GM1 IgM (n=3), and anti-GD1a IgG (n=1, including one with a positive anti-GQ1b antibody). Patients with anti-ganglioside antibodies showed lesser intensity of spontaneous nystagmus (median [interquartile range (IQR)] = 1.8 [1.2–2.1] vs. 3.4 [1.5–9.5], p=0.003), a lesser degree of canal paresis (30 [17–47] vs. 58 [34–79], p=0.028), and gain asymmetry of the vestibulo-ocular reflex (VOR) for the horizontal semicircular canal (HC) during head impulse tests (HITs) (0.07 [-0.04–0.61] vs. 0.36 [0.18–0.47], p=0.032) than those without antibodies. Negative conversion of antibodies and vestibular recovery were observed in most patients (6/8, 75%). Among 30 AUPV patients with 4-hour delayed 3D-FLAIR dedicated to the inner ear, gadolinium enhancement was observed in 18 (18/30, 60%), either in the vestibule (n=9), semicircular canal (n=6), or vestibular nerve (n=5). The positivity rates based on specific antibodies could not be determined due to limited sample sizes. Discussion: The association between anti-ganglioside antibodies and AUPV suggests an immune-mediated mechanism in acute vestibular failure and extends the clinical spectrum of anti-ganglioside antibody syndrome.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Clinical Features and Neurotologic Findings in Patients With Acute Unilateral Peripheral Vestibulopathy Associated With Antiganglioside Antibody

Kim,

Park,

Lee

et al. 2023

Neurology

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“…Patients can also have central ocular motor signs such as impaired smooth pursuit and vestibulo-ocular reflex cancellation, and sometimes even present with impaired vestibuloocular responses with otherwise normal eye movements. 9 Patients can have gaze-evoked, dissociated abducting, convergence retraction, or rebound nystagmus. Other cranial nerves may be affected, particularly the seventh nerve with subsequent facial palsy.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Sixth Nerve Palsy and Nasal Voice in Two Sisters as a Variant of Guillan–Barré Syndrome

Pellegrini¹,

Wang

Romeo

et al. 2018

Neuro-Ophthalmology

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A 6-year-old girl with acute pharyngitis presented with complaints of hypernasal speech and double vision. Examination revealed a bilateral abduction deficit associated with soft palate palsy causing rhinolalia aperta. Cerebrospinal fluid analysis showed albuminocytologic dissociation. Her sister also suffered from the same disorder, albeit milder, 1 month before. After treatment with intravenous immunoglobulin and steroids, the patient made a full recovery. After the case report, a brief discussion of Miller Fisher syndrome, Guillan-Barré syndrome, and their variants is made. This case highlights that bilateral sixth nerve palsy and rhinolalia aperta in the absence of ataxia should still raise suspicion for these autoimmune conditions that may rarely and atypically present in siblings.

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“…The complete recovery observed 8 months later is another argument to link this vestibular dysfunction to the acute relapse of MFS. Vestibular testing has very rarely been reported in MFS: Minoda et al [12] reported a unilateral diminished response to caloric testing without severe restriction of eye movements, in 3 patients among a cohort of 14 MFS patients.…”

Section: Discussionmentioning

confidence: 99%

Recurrent Miller Fisher Syndrome with Vestibular Involvement

Vermeersch¹,

Boschi²,

Deggouj

et al. 2011

Eur Neurol

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We describe a patient who had four relapses of Miller Fisher syndrome over a period of 20 years. The classical triad – ophthalmoparesis, ataxia and areflexia – was present during the first two attacks; ataxia was not observed during the third episode. The final recurrence was characterized by signs suggestive of a central involvement of the oculomotor pathways, subclinical slowing of the visual-evoked potentials, and peripheral vestibular hyporeactivity. Brain imaging was normal, but high levels of anti-GQ1b IgG antibodies were detectable during the second relapse and persisted after the fourth recurrence despite complete clinical recovery.

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Neurologic and otologic findings in Fisher's syndrome

Cited by 12 publications

References 10 publications

Clinical Features and Neurotologic Findings in Patients With Acute Unilateral Peripheral Vestibulopathy Associated With Antiganglioside Antibody

Clinical Features and Neurotologic Findings in Patients With Acute Unilateral Peripheral Vestibulopathy Associated With Antiganglioside Antibody

Bilateral Sixth Nerve Palsy and Nasal Voice in Two Sisters as a Variant of Guillan–Barré Syndrome

Recurrent Miller Fisher Syndrome with Vestibular Involvement

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