Acute Bulbar Palsy-Plus Variant of Guillain-Barré Syndrome in a 3-Year-Old Girl

Dukkipati, Saihari S.; Zhou, Daniel J.; Powers, Andria M.; Piccione, E; Koh, Sookyong

doi:10.1177/2329048x221115476

Cited by 3 publications

(2 citation statements)

References 20 publications

(27 reference statements)

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“…Kim et al [3] and Cao et al [9] proposed the diagnostic criteria of ABPp syndrome as follows: (1) prominent ABP, absence of neck and limb weakness; (2) other cranial involvements or gait ataxia or both; (3) compliance with the illness pattern of general GBS; and (4) absence of identified alternative diagnosis. According to the presentation of our patient here, we summarized the GBS patients with ABP and facial paralysis reported previously, which fit the diagnosis of ABPp syndrome (Table 2) [3,[10][11][12][13][14][15][16][17][18][19][20][21][22][23]. The literature search showed twenty-three patients previously, eighteen adults (age: 20y-67y) and five children (age: 10 m-13y).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, eighteen patients of the 23 cases (Table 2) [3,[10][11][12][13][14][15][16][17][18][19][20][21][22][23] underwent serological assay, and antiganglioside antibodies were identified in 88.9% patients (16/18 cases). IgG anti-GT1a antibody (11, 68.8%) was the most frequent, followed by IgG anti-GQ1b (10/16, 62.5%), IgM anti-GT1a (4/16), IgM anti-GQ1b (2/16), IgG anti-GM1b (2/16), IgM anti-GM1b (2/16), IgG anti-GM2 (1/16), IgG anti-GM3 (1/16), IgG anti-GD1a (1/16), IgM anti-GD1a (1/16), IgG anti-GT1b(1/16).…”

Section: Table 1 Nerve Conduction Studymentioning

confidence: 99%

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A case of variant of GBS with positive serum ganglioside GD3 IgG antibody

Xue,

Song,

Zhao

et al. 2024

Ital J Pediatr

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Background Acute bulbar palsy-plus (ABPp) syndrome is an unusual variant of Guillain-Barré syndrome (GBS). Anti-GT1a and anti-GQ1b antibodies have been reported in patients with ABPp, but without reports related to GD3 antibodies. Methods Clinical data of a patient diagnosed as ABPp syndrome were reviewed clinically. And we summarized the GBS patients with ABP and facial paralysis reported in the literature. Results We reported a 13-year-old girl presented with asymmetric bifacial weakness, bulbar palsy and transient limb numbness, and had positive serum IgG anti-GD3 antibody. Through reviewing the GBS patients with ABP and facial paralysis reported previously, we found that facial palsy could be unilateral or bilateral. The bilateral facial palsy could present successively or simultaneously, and could be symmetrical or asymmetrical. Other common symptoms included ophthalmoplegia, sensory abnormality and ataxia. IgG anti-GT1a and IgG anti-GQ1b antibodies were the most frequent. Most of the patients had full recovery within two weeks to one year of follow-up. Conclusions We reported a patient with asymmetric bifacial palsy and bulbar palsy, which seemed to fit the diagnosis of ABPp syndrome. This was the first report of ABPp variant of GBS with positive serum ganglioside GD3 IgG antibody.

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Section: Discussionmentioning

confidence: 99%

Section: Table 1 Nerve Conduction Studymentioning

confidence: 99%

A case of variant of GBS with positive serum ganglioside GD3 IgG antibody

Xue,

Song,

Zhao

et al. 2024

Ital J Pediatr

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Influenza virus vaccine

2022

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Triggers of Guillain–Barré Syndrome: Campylobacter jejuni Predominates

Finsterer¹

2022

IJMS

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Guillain–Barré syndrome (GBS) is a rare immune-mediated acute polyradiculo-neuropathy that typically develops after a previous gastrointestinal or respiratory infection. This narrative overview aims to summarise and discuss current knowledge and previous evidence regarding triggers and pathophysiology of GBS. A systematic search of the literature was carried out using suitable search terms. The most common subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). The most common triggers of GBS, in three quarters of cases, are previous infections. The most common infectious agents that cause GBS include Campylobacter jejuni (C. jejuni), Mycoplasma pneumoniae, and cytomegalovirus. C. jejuni is responsible for about a third of GBS cases. GBS due to C. jejuni is usually more severe than that due to other causes. Clinical presentation of GBS is highly dependent on the structure of pathogenic lipo-oligosaccharides (LOS) that trigger the innate immune system via Toll-like-receptor (TLR)-4 signalling. AIDP is due to demyelination, whereas in AMAN, structures of the axolemma are affected in the nodal or inter-nodal space. In conclusion, GBS is a neuro-immunological disorder caused by autoantibodies against components of the myelin sheath or axolemma. Molecular mimicry between surface structures of pathogens and components of myelin or the axon is one scenario that may explain the pathophysiology of GBS.

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Acute Bulbar Palsy-Plus Variant of Guillain-Barré Syndrome in a 3-Year-Old Girl

Cited by 3 publications

References 20 publications

A case of variant of GBS with positive serum ganglioside GD3 IgG antibody

A case of variant of GBS with positive serum ganglioside GD3 IgG antibody

Influenza virus vaccine

Triggers of Guillain–Barré Syndrome: Campylobacter jejuni Predominates

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