Acute ophthalmoparesis associated with IgG anti-GQ1b antibody subsequent to Streptococcus pyogenes infection

Kikuchi, Masahiro; Tagawa, Yoshiyuki; Saotome, Shunichi; Nonoyama, Tomohito; Hoshino, Hisao; Yuki, Nobuhiro

doi:10.1016/s1090-3798(97)80011-6

Cited by 7 publications

(8 citation statements)

References 5 publications

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“…However, we failed to find any study of nerve conduction in SC. There is one recently published case report describing acute ophthalmoparesis associated with IgG anti‐GQ1b antibody, but this condition occurred not in the context of SC or RF, rather in association with Streptococcus pyogenes infection 5. Our results (normal mean and standard deviation of all neurophysiological parameters investigated) suggest that the peripheral nerve is not the site of significant pathological state in this condition.…”

Section: Discussionsupporting

confidence: 44%

“…Recent studies suggest that the spectrum of disorders associated with Streptococcus ‐induced cross‐reactive antibodies may be wider than previously recognized, possibly including clinical syndromes such as Tourette syndrome, obsessive–compulsive disorder, and ophthalmoparesis 1, 4, 5. We recently described6 a series of patients with acute disseminated encephalomyelitis associated with antibodies induced by β‐hemolytic streptococci, which cross‐react with basal ganglia antigens.…”

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confidence: 99%

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Nerve conduction study in Sydenham's chorea

Cardoso¹,

Dornas²,

Cunningham³

et al. 2005

Movement Disorders

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Sydenham's chorea (SC) is a late complication of group A beta-hemolytic streptococci infection presumably caused by an abnormal autoimmune reaction. Despite rare case reports of peripheral neuropathy associated with streptococcal infection, there is no investigation of peripheral nerve in SC. We performed nerve conduction studies in a cohort of patients with SC. The neurophysiology investigation comprised measurement of amplitude and sensory conduction velocity of median, ulnar, and sural nerves; amplitude and motor conduction velocity; and F-wave latency of median, ulnar, fibular, and tibial nerves. Twenty-six patients entered the study (12 females, 14 males; mean age 12.8 +/- 3.6 years). Thirteen subjects had absent or decreased deep reflexes. All investigated neurophysiological parameters fell within the normal range for our population. We failed to find neurophysiological evidence of peripheral nerve involvement in patients with a history of SC. Our findings suggest that the possible autoimmune dysfunction in SC patients is not targeted against epitopes present in peripheral nerves.

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Section: Discussionsupporting

confidence: 44%

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confidence: 99%

Nerve conduction study in Sydenham's chorea

Cardoso¹,

Dornas²,

Cunningham³

et al. 2005

Movement Disorders

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“…17,18 Since anti-GQ1b antibodies are directly implicated in the pathogenesis of ophthalmoplegia in AO and MFS, removal of anti-GQ1b antibodies seems reasonable and useful for treating anti-GQ1b antibody syndrome. However, in view of the good prognosis of AO even in patients without treatments and no randomized controlled study for the efficacy of each treatment option, therapeutic intervention in AO requires further validation.…”

Section: Resultsmentioning

confidence: 99%

Acute ophthalmoplegia (without ataxia) associated with anti-GQ1b antibody

Sh¹,

Gh²,

Js³

et al. 2008

Neurology

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“…The illnesses of the other seven (4%) were unclassified. Among the patients included in this study, illustrative cases of acute ophthalmoparesis,23MFS,10 BBE,24 and MFS/GBS25 have been reported previously. An illustrative case of BBE/GBS is described below.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, established treatments for GBS (plasmapheresis and intravenous immunoglobulin) may be more readily introduced as treatments for BBE and acute ophthalmoparesis, as well as for MFS. Some patients with BBE and acute ophthalmoparesis have responded favourably to plasmapheresis and intravenous immunoglobulin8 23 24 42 Recent studies by Buchwald et al 43 and Plomp et al 44 show that anti-GQ1b IgG, at least, is a pathophysiological mediator of motor symptoms in MFS and related disorders. This is theoretical evidence that removal of the autoantibody is efficacious treatment for patients with anti-GQ1b IgG.…”

Section: Discussionmentioning

confidence: 99%

Anti-GQ1b IgG antibody syndrome: clinical and immunological range

Odaka

2001

Journal of Neurology, Neurosurgery &Amp; Psychiatry

327

226

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Objectives-To clarify the nosological relation among Miller Fisher syndrome (MFS), Guillain-Barré syndrome (GBS) with ophthalmoplegia, BickerstaV's brain stem encephalitis (BBE), and acute ophthalmoparesis without ataxia. Serum samples from patients with each condition often have anti-GQ1b IgG antibody. Methods-Information on antecedent illness, initial symptoms, neurological signs during the illness, and CSF findings were reviewed in 194 patients with anti-GQ1b IgG. It was determined whether overlapping MFS and GBS (MFS/GBS), as well as overlapping BBE and GBS (BBE/GBS), is explained by the combined action of antiGQ1b IgG and anti-GM1 or anti-GD1a IgG, serological markers of GBS. Results-Based on the diagnostic criteria, all the patients with acute ophthalmoparesis, MFS, MFS/GBS, BBE/GBS, and BBE had external ophthalmoplegia; all the patients with MFS, MFS/GBS, or GBS had hyporeflexia or areflexia; and all those with MFS and BBE showed ataxia. Tendon reflexes were decreased or absent in 91% of those with BBE/GBS, 67% of those with BBE, and 53% of those with acute ophthalmoparesis. Ataxia was present in 68% of the patients with MFS/GBS and 45% of those with BBE/ GBS. Antecedent illness caused by upper respiratory tract infection had occurred in 60% to 80% of these patients, and CSF albuminocytological dissociation in 25% to 75%. Anti-GM1 or anti-GD1a IgG was present in 50% of those with GBS, 35% of those with MFS/GBS, 27% of those with BBE/GBS, 16% of those with MFS, and 8% of those with BBE. Conclusions-These findings together with the common autoantibody (antiGQ1b IgG) suggest that a common autoimmune mechanism functions in the pathogenesis of these illnesses. In a larger study, it was confirmed clinically that MFS, GBS, BBE, and acute ophthalmoparesis are closely related, forming a continuous range. This is supported by the immunological findings. The term "anti-GQ1b IgG antibody syndrome" is not intended to be used as a clinical diagnosis, but recognition of this syndrome is useful for understanding the aetiological relation among the various illnesses and for introducing the established treatments of GBS for use with other conditions. (J Neurol Neurosurg Psychiatry 2001;70:50-55)

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Acute ophthalmoparesis associated with IgG anti-GQ1b antibody subsequent to Streptococcus pyogenes infection

Cited by 7 publications

References 5 publications

Nerve conduction study in Sydenham's chorea

Nerve conduction study in Sydenham's chorea

Acute ophthalmoplegia (without ataxia) associated with anti-GQ1b antibody

Anti-GQ1b IgG antibody syndrome: clinical and immunological range

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