Miller Fisher syndrome

Sauron, B; Bouché, P; Cathala, H.P.; Chain, François; Castaigne, P

doi:10.1212/wnl.34.7.953

Cited by 80 publications

(45 citation statements)

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“…These findings suggest a block of conduction in the spinal roots, limb girdle plexuses or proximal segments of the nerves. Several reports had the consensus that sensory changes predominated with significant loss of amplitudes and mild motor and sensory conduction slowing [21, 22, 25, 26, 29]. In our study, this phenomenon was not observed.…”

Section: Discussioncontrasting

confidence: 43%

“…The results have been controversial. Although some studies revealed no evidence of affection of the peripheral nerves [9, 11, 12, 13], most studies revealed peripheral nerve involvement such as abnormalities in distal motor latencies, motor conduction velocities, sensory conduction velocities, F wave latencies and H reflexes [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34]. Three out of our 10 patients had abnormal electrophysiological findings.…”

Section: Discussionmentioning

confidence: 99%

“…Many of the ocular motor signs, such as symmetrical ophthalmoplegia, Parinaud’s syndrome, convergence spasm, preserved Bell’s phenomenon despite upward paresis and internuclear ophthalmoplegia have been considered to be due to central nervous system lesions. Others regard it absolutely as a variant of GBS based on the findings of preceding illness, hyporeflexia or areflexia, albuminocytological dissociation in the CSF, similar electrophysiological results as GBS and favorable outcome [20, 22, 24, 25, 26, 27, 29, 30, 31, 33]. The ataxia in MFS was mostly attributed to be cerebellar in type [18].…”

Section: Discussionmentioning

confidence: 99%

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Miller Fisher Syndrome: A Hospital-Based Retrospective Study

Yuan

Wang²,

Tsai³

2000

Eur Neurol

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Miller Fisher syndrome (MFS), characterized as ataxia, areflexia and ophthalmoplegia, is generally considered as a variant of Guillain-Barré syndrome (GBS). However, some investigators believed that the syndrome could be explained by a central origin. To obtain more information about MFS for comparison with GBS, we conducted a retrospective study by analyzing the clinical data of MFS patients admitted to our hospital over a period of 11 years. The calibrated male/female ratio was 1.65. A seasonal clustering in winter was noted. The percentage of MFS among GBS was especially high (18%, 11/60) in Taiwan when compared with other series. Involvement of limb muscle strength, autonomic function and cranial nerves, except ocular motor nerves, was rarely found in our patients. When MFS is accompanied by limb weakness, it might represent a transitional form between MFS and GBS. Bulbar palsy and dysautonomia might predict a relatively poor prognosis. To obtain more reliable information, lumbar puncture should be done 1 week after disease onset, and electrophysiological tests should be done serially in every MFS patient. Eighty percent (80%, 4/5) of our patients were positive for IgG anti-GQ_1b antibody activity. In our study, there is more evidence indicating that MFS is a peripheral nervous system disorder; however, no definite conclusion could be made as to whether MFS is exclusively a peripheral or central nervous system disorder. We think MFS is an immune-mediated clinical entity which mainly involves the peripheral nervous system with rare involvement of other parts of the central nervous system.

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Section: Discussioncontrasting

confidence: 43%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Miller Fisher Syndrome: A Hospital-Based Retrospective Study

Yuan

Wang²,

Tsai³

2000

Eur Neurol

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“…The MFS is seen in two patients who had ataxia, areflexia, and ophthalmoplegia affecting 3, 4, and 6 cranial nerve. (10) The Polyneuropathy of Diphtheria Mimics GB Syndrome. However, there are few differences.…”

Section: Localization Of Lesion In the Nervesmentioning

confidence: 99%

A Clinical Study of Multiple Cranial Neuropathies (Mcn)

G¹,

Ramesh²,

Suma³

et al. 2016

jemds

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BACKGROUNDCranial neuropathies are frequently seen by neurologist. The causes are many and evaluation presents a unique challenge for the diagnostician. The differential diagnosis is broad and includes infections, inflammatory conditions, cavernous sinus lesions, and many life-threatening processes like neoplastic meningitis A knowledge of the anatomy of the cranial nerves and their involvement in pathologic processes is therefore one of the corner stones of neurologic diagnosis. Just as with any other neurologic presentation, the first step in the evaluation requires correct localization. Processes affecting multiple cranial nerves may involve intramedullary structures of the brainstem as well as their extramedullary course. The majority of the literature regarding aetiologies of multiple cranial neuropathies consists of case reports or small case series with very few reported large series. The largest reported series to date of multiple cranial neuropathies was that of Keane.

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“…In contrast, sensory nerve conduction studies (SNCSs) show decreased amplitudes of sensory nerve action potentials (SNAPs) in 70-90% of Caucasian patients with FS (8)(9)(10). Earlier reports from a small M none dysesthesia present none none positive day 10 2 28 M URI ataxia present none none negative day 7 3 23 M diarrhea diplopia absent none none not done day 16 4 68 M URI diplopia present none none positive day 17 5 36 F URI diplopia absent none none positive day 4 6 34 M diarrhea diplopia present none none positive day 4 hypesthesia group (group H, n = 4) 7 38 M URI diplopia present hypesthesia none negative day 11 8 21 F none diplopia present hypesthesia none positive day 5 9 38 F URI diplopia present hypesthesia hypesthesia positive day 14 10 68 M URI ataxia present hypesthesia hypesthesia positive day 4 The patients were divided into the following Two groups: those without hypesthesia (cases 1-6) and those with hypesthesia (cases 7-10).…”

Section: Introductionmentioning

confidence: 99%

Demyelinating Features in Sensory Nerve Conduction in Fisher Syndrome

et al. 2012

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Objective A significant number of patients with Fisher syndrome (FS) exhibit sensory symptoms in addition to the classical triad of opthalmoplegia, ataxia and areflexia. Previous studies have shown the amplitudes of sensory nerve action potentials (SNAPs) to decrease in patients with FS, thus implying the presence of an axonal pathology in the sensory nerves. Methods We included ten consecutive patients with FS who were divided into the following two groups: those with hypesthesia (group H) and those without hypesthesia (group NS). The parameters obtained from nerve conduction studies (amplitudes of compound muscle action potentials, motor conduction velocities, amplitudes/duration of SNAPs and sensory conduction velocities) were retrospectively compared between the two groups. In addition, follow-up sensory nerve conduction studies were conducted in one representative patient from each group. Results Of the 10 patients with FS, four (40%) showed hypesthesia and eight (80%) showed distal paresthesia. The amplitudes of the SNAPs of both the median and sural nerves were lower in group H than in group NS. Moreover, the duration of the sural SNAPs was longer in group H than in group NS. Desynchronization of SNAPs in the acute phase was observed during follow-up in both patients who underwent followup studies. Conclusion The prolonged duration of SNAPs in group H and the desynchronization of SNAPs in the two patients who underwent follow-up studies suggest the presence of a concomitant demyelinating process in the sensory nerves.

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Miller Fisher syndrome

Cited by 80 publications

References 0 publications

Miller Fisher Syndrome: A Hospital-Based Retrospective Study

Miller Fisher Syndrome: A Hospital-Based Retrospective Study

A Clinical Study of Multiple Cranial Neuropathies (Mcn)

Demyelinating Features in Sensory Nerve Conduction in Fisher Syndrome

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