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  1. Uncini A, Shahrizaila N, Kuwabara S
    J Neurol Neurosurg Psychiatry, 2017 03;88(3):266-271.
    PMID: 27799296 DOI: 10.1136/jnnp-2016-314310
    In 2016, we have seen a rapid emergence of Zika virus-associated Guillain-Barré syndrome (GBS) since its first description in a French-Polynesian patient in 2014. Current evidence estimates the incidence of GBS at 24 cases per 100 000 persons infected by Zika virus. This will result in a sharp rise in the number of GBS cases worldwide with the anticipated global spread of Zika virus. A better understanding of the pathogenesis of Zika-associated GBS is crucial to prepare us for the current epidemic. In this review, we evaluate the existing literature on GBS in association with Zika and other flavivirus to better define its clinical subtypes and electrophysiological characteristics, demonstrating a demyelinating subtype of GBS in most cases. We also recommend measures that will help reduce the gaps in knowledge that currently exist.
    Matched MeSH terms: Guillain-Barre Syndrome/classification
  2. Hiew FL, Ramlan R, Viswanathan S, Puvanarajah S
    Clin Neurol Neurosurg, 2017 Jul;158:114-118.
    PMID: 28514704 DOI: 10.1016/j.clineuro.2017.05.006
    OBJECTIVES: This study aimed to evaluate the clinical and electrophysiological characteristics of various distinctive classical and localised Guillain-Barré syndrome (GBS) subtypes.

    PATIENTS AND METHODS: Clinical characteristics and electrophysiological data of sixty-one consecutive patients admitted between 2012 and 2015 were systematically analysed and reclassified according to the new GBS clinical classification. Neurophysiology was evaluated with Hadden et al.'s vs recently proposed Rajabally et al.'s criteria. Functional severity and clinical outcome of various GBS subtypes were ascertained.

    RESULTS: All patients initially identified as GBS or related disorders can be sub-classified into having classical GBS (41, 67%), classic Miller-Fisher Syndrome (MFS) (6, 10%), Pharyngeal-cervical-brachial (PCB) (3, 5%), paraparetic GBS (4, 7%), bifacial weakness with paresthesia (3, 5%), acute ophthalmoparesis (AO) (1, 2%) and overlap syndrome (3, 5%): one (2%) with GBS/Bickerstaff brainstem encephalitis overlap and 2 (3%) with GBS/MFS overlap. Greater proportion of axonal classical GBS (67% vs 55%, p=0.372) seen with Rajabally et al.'s criteria and a predominantly axonal form of paraparetic variant (75%) independent of electrodiagnostic criteria were more representative of Asian GBS cohort. Classical GBS patients had lowest admission and discharge Medical Research Council Sum Score (MRCSS), greater functional disability and longest length of in-patient stay. Twenty (20/21, 95%) patients who needed mechanical ventilation had classical GBS. Patients required repeated dose of intravenous immunoglobulin (5/6, 3%) or plasma exchange (4/4, 100%) more frequently had axonal form of classical GBS.

    CONCLUSION: Phenotype recognition based on new GBS clinical classification, supported by electrodiagnostic study permits more precise clinical subtypes determination and outcome prognostication.

    Matched MeSH terms: Guillain-Barre Syndrome/classification*
  3. Shahrizaila N, Kokubun N, Sawai S, Umapathi T, Chan YC, Kuwabara S, et al.
    Neurology, 2014 Jul 8;83(2):118-24.
    PMID: 24920848 DOI: 10.1212/WNL.0000000000000577
    To comprehensively investigate the relationship between antibodies to single glycolipids and their complexes and Guillain-Barré syndrome subtypes and clinical features.
    Matched MeSH terms: Guillain-Barre Syndrome/classification
  4. Tan CY, Sekiguchi Y, Goh KJ, Kuwabara S, Shahrizaila N
    Clin Neurophysiol, 2020 01;131(1):63-69.
    PMID: 31751842 DOI: 10.1016/j.clinph.2019.09.025
    OBJECTIVE: We aimed to develop a model that can predict the probabilities of acute inflammatory demyelinating polyneuropathy (AIDP) based on nerve conduction studies (NCS) done within eight weeks.

    METHODS: The derivation cohort included 90 Malaysian GBS patients with two sets of NCS performed early (1-20days) and late (3-8 weeks). Potential predictors of AIDP were considered in univariate and multivariate logistic regression models to develop a predictive model. The model was externally validated in 102 Japanese GBS patients.

    RESULTS: Median motor conduction velocity (MCV), ulnar distal motor latency (DML) and abnormal ulnar/normal sural pattern were independently associated with AIDP at both timepoints (median MCV: p = 0.038, p = 0.014; ulnar DML: p = 0.002, p = 0.003; sural sparing: p = 0.033, p = 0.009). There was good discrimination of AIDP (area under the curve (AUC) 0.86-0.89) and this was valid in the validation cohort (AUC 0.74-0.94). Scores ranged from 0 to 6, and corresponded to AIDP probabilities of 15-98% at early NCS and 6-100% at late NCS.

    CONCLUSION: The probabilities of AIDP could be reliably predicted based on median MCV, ulnar DML and ulnar/sural sparing pattern that were determined at early and late stages of GBS.

    SIGNIFICANCE: A simple and valid model was developed which can accurately predict the probability of AIDP.

    Matched MeSH terms: Guillain-Barre Syndrome/classification
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