Peripheral nerve conduction in Miller Fisher syndrome.

Guiloff, R J

doi:10.1136/jnnp.40.8.801

Cited by 60 publications

(26 citation statements)

References 17 publications

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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: 36%

“…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%

“…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%

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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: 36%

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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“…Several studies have shown evidence of electrodiagnostic abnormalities in FS [2,3,12,13]. Predominant sensory potential amplitude changes were the consistent findings in most studies.…”

Section: Introductionmentioning

confidence: 59%

Sensory Conduction Study in Fisher Syndrome: Patterns of Abnormalities and Their Clinical Correlation

Lyu

Chang²,

Chu³

et al. 2013

Eur Neurol

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Objective: To report sensory conduction findings in patients with typical Fisher syndrome (FS) and to determine if a specific pattern of sensory conduction abnormalities was present in such patients. Methods: We retrospectively reviewed results of sensory conduction studies of 55 FS patients and compared them with those obtained from 83 age- and sex-matched healthy volunteers. Results: Mean median and ulnar sensory nerve action potential (SNAP) amplitudes were lower in FS patients than in normal subjects, whereas sural SNAP amplitudes were not different between the two groups. Abnormal median/ulnar sensory responses (reduced SNAP amplitude or absent response) were more frequently observed than abnormal sural response. Normal sensory conduction results were found in 31 (56%) patients. Of the 24 (44%) patients with abnormal sensory findings, 18 (33%) had a sural-sparing pattern of abnormalities. Patients with impaired sensation had lower median and ulnar SNAP amplitudes than those without. Conclusions: Abnormal median and ulnar sensory responses were the most frequent sensory findings in FS. Findings of the sural-sparing pattern of abnormalities suggest distal sensory nerve involvement in these patients.

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“…The days listed in the nerve conduction studies (NCSs) column indicate the timing of the NCSs from the onset of FS. Abbreviations: URI: upper respiratory infection case series indicate that demyelinating processes cause the decreased amplitudes of SNAPs observed in patients with FS (11)(12)(13)(14), whereas the results from two large case series suggest that axonal neuropathy or dorsal root ganglionopathy are responsible (8,10). Therefore, the question of whether decreases in SNAP amplitudes result from a demyelinating process or an axonal mechanism remains controversial.…”

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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Peripheral nerve conduction in Miller Fisher syndrome.

Cited by 60 publications

References 17 publications

Miller Fisher Syndrome: A Hospital-Based Retrospective Study

Miller Fisher Syndrome: A Hospital-Based Retrospective Study

Sensory Conduction Study in Fisher Syndrome: Patterns of Abnormalities and Their Clinical Correlation

Demyelinating Features in Sensory Nerve Conduction in Fisher Syndrome

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