Polyneuritis cranialis—subtype of Guillain–Barré syndrome?

Wakerley, Benjamin R; Yuki, Nobuhiro

doi:10.1038/nrneurol.2015.115

Cited by 19 publications

(24 citation statements)

References 8 publications

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“…GBS spectrum disorders exist, such as Miller Fisher syndrome (MFS) and other variants. Polyneuritis cranialis, characterized by manifestations isolated to cranial nerves without limb involvement (as seen in our patient), could be considered a GBS/MFS interface disorder . The neurological abnormalities in the patient described were restricted to cranial nerves, which only developed several weeks after the initial ulceroglandular infection.…”

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confidence: 52%

Polyneuritis cranialis after acute tularemia infection: A case study

et al. 2019

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A 60-year-old man was referred for multiple cranial neuropathies. Six weeks earlier, a minor left finger laceration was exposed to rabbit blood. Two days later, he developed flulike symptoms and lymphadenopathy. The wound became swollen, and expressed pus was sent for culture. He started an empirical course of cephalexin, but, when the culture was positive for Francisella tularensis, he was initiated on a 20-day course of doxycycline.Over the subsequent 2 weeks he developed worsening cough, dry heaves, and conjunctivitis. He was admitted to a local hospital 1 month only present in 50% and 75% of GBS patients within the first and third week of symptoms, respectively. 10 GBS spectrum disorders exist, such as Miller Fisher syndrome (MFS) and other variants. Polyneuritis cranialis, characterized by manifestations isolated to cranial nerves without limb involvement (as seen in our patient), could be considered a GBS/MFS interface disorder. 11The neurological abnormalities in the patient described were restricted to cranial nerves, which only developed several weeks after the initial ulceroglandular infection. This, along with unremarkable CSF and MRI results, supported an immune-mediated mechanism rather than damage due to direct F tularensis infection. Accordingly, rather than additional antibiotic therapy, he was treated with IVIg with subsequent clinical and electrodiagnostic improvement. The presence of low-titer P/Q-type calcium channel antibodies is of uncertain significance, possibly supporting an autoimmune mechanism.In conclusion, polyneuritis cranialis may be a rare immunemediated manifestation of ulceroglandular tularemia.

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confidence: 52%

Polyneuritis cranialis after acute tularemia infection: A case study

et al. 2019

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“…Diagnosis of GBS relies on the results of clinical, electrophysiological, and cerebrospinal fluid (CSF) examinations (classically albuminocytological dissociation) [ 57 – 59 ]. The clinical spectrum of GBS encompasses a classic sensorimotor form, Miller Fisher syndrome (MFS), bilateral facial palsy with paraesthesia, pure motor, pure sensory, paraparetic, pharyngeal–cervical–brachial variants, polyneuritis cranialis (GBS–MFS overlap), and Bickerstaff brainstem encephalitis [ 57 – 60 ]. As regard electrophysiological features, three main subtypes are recognized: AIDP, acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN) [ 57 , 58 , 61 ].…”

Section: Introductionmentioning

confidence: 99%

Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases

et al. 2020

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Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain-Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11-max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.

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“…Wakerley et al analyzed 15 historical cases of PNC attributed to GBS and proposed that PNC can only be diagnosed in patients with general features of GBS who present with ocular and pharyngeal weakness in the absence of limb weakness or ataxia, with facial palsy being present or not ( 39 ). The authors further argued that it was an oculopharyngeal type of GBS that lay at the borderland between GBS and MFS ( 4 ). ABPp syndrome and PNC had something in common in terms of diagnostic criteria; some patients with ABPp syndrome in our study, for example, ABP plus ophthalmoplegia, can also be diagnosed as PNC.…”

Section: Discussionmentioning

confidence: 99%

“…It may appear with cervical–brachial weakness, when it has been referred to as PCB weakness, or occur in isolation ( 2 ), although very rarely, which has been termed incomplete PCB as a localized form of GBS at this time; additionally, ABP has also been described as a transitional symptom that either overlaps with other regional variants of GBS or evolves into generalized GBS ( 3 ). However, some GBS cases presenting with ABP in combination with other neurological symptoms, such as cranial nerve paralysis and ataxia, do not satisfy the criteria for any subtype of GBS, MFS, and their variants; polyneuritis cranialis (PNC), an oculopharyngeal subtype of GBS proposed by Wakerley et al ( 4 ), cannot completely explain these cases either because ataxia is not allowed in PNC. In this context, Kim et al put forward the concept of acute bulbar palsy plus (ABPp) syndrome, which is categorized to be a type of GBS manifesting with ABP plus other cranial symptoms or additional signs such as ataxia but in the absence of neck or limb weakness ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

Case Report: Acute Bulbar Palsy Plus Syndrome: A Guillain-Barré Syndrome Variant More Prone to Be a Subtype Than Overlap of Distinct Subtypes

Cao

Chu

et al. 2020

Front. Neurol.

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Objective: Acute bulbar palsy plus (ABPp) syndrome is a rare regional variant of Guillain-Barré syndrome (GBS) characterized by acute bulbar palsy combined with other cranial symptoms or ataxia without limb and neck weakness. We aim to investigate characteristics of ABPp syndrome and analyze its nosological position within the GBS spectrum.Methods: A patient with ABPp syndrome was reported, and previous case reports of patients who met the criteria for ABPp syndrome from the literature were reviewed.Results: A total of 28 patients were included in our study. Median age was 32 years. Most of the patients (78.6%) were from Asia, and 75.0% had preceding infection. The main accompanying symptoms were ophthalmoplegia (85.7%), facial palsy (60.7%), and ataxia (50.0%). There existed asymmetric weakness in the form of unilateral facial palsy (32.1%) and ptosis (3.6%). Approximately half of the patients had albuminocytological dissociation. All the tested patients were seropositive for antiganglioside antibodies, of which the two most common were immunoglobulin G (IgG) anti-GT1a (77.3%) and anti-GQ1b (59.1%) antibodies. Over one-third of the patients who underwent electrophysiological assessment showed subclinical neuropathy beyond cranial nerves. The outcome was generally favorable as 89.3% of patients made full recovery within 5 months.Conclusion: The hitherto largest case series of ABPp syndrome advances our understanding of this disease. Serologically, the presence of IgG anti-GT1a and anti-GQ1b antibodies predicts and contributes to the disease. Phenotypically, ABPp syndrome is more prone to be a separate subtype of GBS than overlap of distinct subtypes and has the potential to complement current diagnostic framework of GBS.

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Polyneuritis cranialis—subtype of Guillain–Barré syndrome?

Cited by 19 publications

References 8 publications

Polyneuritis cranialis after acute tularemia infection: A case study

Polyneuritis cranialis after acute tularemia infection: A case study

Guillain–Barré syndrome spectrum associated with COVID-19: an up-to-date systematic review of 73 cases

Case Report: Acute Bulbar Palsy Plus Syndrome: A Guillain-Barré Syndrome Variant More Prone to Be a Subtype Than Overlap of Distinct Subtypes

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