Guillain–Barré syndrome and Fisher syndrome: Case definitions and guidelines for collection, analysis, and presentation of immunization safety data

Sejvar, James J.; Kohl, Katrin; Gidudu, Jane; Amato, Anthony A.; Bakshi, Nandini; Baxter, Roger; Burwen, Dale R.; Cornblath, David R.; Cleerbout, Jan; Edwards, Kathryn M.; Heininger, Ulrich; Hughes, Richard; Khuri‐Bulos, Najwa; Korinthenberg, Rudolf; Law, Barbara; Munro, Ursula; Maltezou, Helena C.; Nell, Patricia; Oleske, James M.; Sparks, Robert; Velentgas, Priscilla; Vermeer, Patricia; Wiznitzer, Max

doi:10.1016/j.vaccine.2010.06.003

Cited by 554 publications

(517 citation statements)

References 78 publications

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“…Persons with negative results for Zika virus by RT-PCR in all specimens tested are considered to have presumptive recent infection with a single arbovirus when results are positive for that virus by IgM ELISA, and presumptive flavivirus infection if they test positive for both Zika virus and dengue virus by IgM ELISA. Neurologic diagnosis for GBS cases with evidence of arboviral infection was confirmed by chart review using the Brighton Collaboration criteria, a set of standardized diagnostic criteria based on clinical presentation, CSF laboratory results, and electrophysiologic findings (6). Chart reviews are performed after hospital discharge, >28 days after onset of neurologic signs for persons who remain hospitalized, or death.…”

Section: Epidemiologic Surveillance For Gbsmentioning

confidence: 99%

Guillain-Barré Syndrome During Ongoing Zika Virus Transmission — Puerto Rico, January 1–July 31, 2016

Dirlikov¹,

Major²,

Mayshack³

et al. 2016

MMWR Morb. Mortal. Wkly. Rep.

113

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Section: Epidemiologic Surveillance For Gbsmentioning

confidence: 99%

Guillain-Barré Syndrome During Ongoing Zika Virus Transmission — Puerto Rico, January 1–July 31, 2016

Dirlikov¹,

Major²,

Mayshack³

et al. 2016

MMWR Morb. Mortal. Wkly. Rep.

113

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“…The GBS group included 88 patients who received examinations and treatments at the Research Center of Neurology (Moscow, Russia). GBS was diagnosed according to criteria of the Brighton Collaboration GBS Working Group (29). The form of GBS was determined according to the neurophysiological classifications of GBS (30).…”

Section: Patientsmentioning

confidence: 99%

The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

Ziganshin

Ivanova

Lomakin

et al. 2016

Molecular & Cellular Proteomics

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Acute inflammatory demyelinating polyneuropathy (AIDP) -the main form of Guillain-Barre syndrome-is a rare and severe disorder of the peripheral nervous system with an unknown etiology. One of the hallmarks of the AIDP pathogenesis is a significantly elevated cerebrospinal fluid (CSF) protein level. In this paper CSF peptidome and proteome in AIDP were analyzed and compared with multiple sclerosis and control patients. A total protein concentration increase was shown to be because of even changes in all proteins rather than some specific response, supporting the hypothesis of protein leakage from blood through the blood-nerve barrier. The elevated CSF protein level in AIDP was complemented by activization of protein degradation and much higher peptidome diversity. Because of the studies of the acute motor axonal form, Guillain-Barre syndrome as a whole is thought to be associated with autoimmune response against neurospecific molecules. Thus, in AIDP, autoantibodies against cell adhesion proteins localized at Ranvier's nodes were suggested as possible targets in AIDP. Indeed, AIDP CSF peptidome analysis revealed cell adhesion proteins degradation, however no reliable dependence on the corresponding autoantibodies levels was found. Proteome analysis revealed overrepresentation of Gene Ontology groups related to responses to bacteria and virus infections, which were earlier suggested as possible AIDP triggers. Immunoglobulin blood serum analysis against most common neuronal viruses did not reveal any specific pathogen; however, AIDP patients were more immunopositive in average and often had polyinfections. Cytokine analysis of both AIDP CSF and blood did not show a systemic adaptive immune response or general inflammation, whereas innate immunity cytokines were up-regulated. To supplement the widely-accepted though still unproven autoimmunity-based AIDP mechanism we propose a hypothesis of the primary peripheral nervous system damaging initiated as an innate immunity-associated local inflammation following neurotropic viruses egress, whereas the autoantibody production might be an optional complementary secondary process. Molecular & Cellular

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“…Historically, patients with these symptoms have been referred to as having 'poly neuritis crani alis' , a descriptive term that has been used in other cases of multiple cranial neuro pathy regardless of aetiology. A case of poly neuritis cranialis (or isolated multiple cranial neuro pathy) that was attributable to GBS was reported alongside diagnostic cri teria for GBS and MFS established in 1990, 4 but this term has not appeared in more recent definitions 5,6 and has thus avoided nosological consideration. 1 In a recent review, we examined the clin ical features of 15 historical cases of poly neuritis cranialis attributed to GBS.…”

mentioning

confidence: 99%

Polyneuritis cranialis—subtype of Guillain–Barré syndrome?

Wakerley

Yuki

2015

Nat Rev Neurol

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Guillain–Barré syndrome and Fisher syndrome: Case definitions and guidelines for collection, analysis, and presentation of immunization safety data

Cited by 554 publications

References 78 publications

Guillain-Barré Syndrome During Ongoing Zika Virus Transmission — Puerto Rico, January 1–July 31, 2016

Guillain-Barré Syndrome During Ongoing Zika Virus Transmission — Puerto Rico, January 1–July 31, 2016

The Pathogenesis of the Demyelinating Form of Guillain-Barre Syndrome (GBS): Proteo-peptidomic and Immunological Profiling of Physiological Fluids

Polyneuritis cranialis—subtype of Guillain–Barré syndrome?

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