Literature DB >> 31602158

Guillain-Barré Syndrome, Before and After Zika.

Luis Del Carpio-Orantes1, Jesús Salvador Sánchez-Díaz1.   

Abstract

Entities:  

Year:  2019        PMID: 31602158      PMCID: PMC6785321          DOI: 10.1055/s-0039-1697564

Source DB:  PubMed          Journal:  J Neurosci Rural Pract        ISSN: 0976-3155


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After the invasion of the Zika virus to American lands following the route of dissemination left by Chikungunya in 2015, an increase in acute neurological syndromes was noted, among them the so-called Guillain-Barré syndrome, which is characterized as the main current cause of flaccid paralysis as well as being an acute demyelinating polyneuropathy. After the outbreak of Zika in the Americas, incidences as high as 400 and 800% of the expected cases were reported, mainly in South America and the Caribbean. Prior to this colonization by arboviruses hitherto unknown in America, Guillain-Barré syndrome was considered an entity with a low global incidence in the range of 0.6 to 4 cases per 100,000 inhabitants. It usually without distinction of gender and in two predominant age groups: 15 to 34 years and 60 to 74 years. Regarding the etiological agents, the main ones identified previously were Campylobacter jejuni (20-50%), Cytomegalovirus (5-22%), Haemophilus influenzae (2-13%), Epstein-Barr virus (10%), and Mycoplasma pneumoniae (5%). In addition to infectious agents, other related conditions are surgeries, vaccines, and injuries. The predominant neuroconduction pattern was axonal (acute motor axonal neuropathy or acute motor sensory axonal neuropathy) both in America and in Europe and some Asian regions, which conferred poor functional and vital prognosis. 1 2 3 After the arrival of Zika and after declaring a neurotropic virus due to the high incidence of cases of microcephaly (now called congenital syndrome due to Zika) and Guillain-Barré syndrome, according to a bibliometric study, the overall incidence of these cases due to recent Zika infection (from South America to Mexico) was 42%, although the incidence of Zika was very variable even in the same geographical area, being from 0 to 100%; the estimated prevalence according to a meta-analysis was 1.23%. In contrast, the most frequent neuroconduction pattern was acute inflammatory demyelinating polyneuropathy, which, according to bibliographic records, has a better functional and vital prognosis, recovering more quickly and in many cases without sequelae ( Table 1 ).

Main differences of Guillain Barre syndrome, before and after zika

Before ZikaAfter Zika
Abbreviations: AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy.
Predominant neuroconduction patternAMANAIDP
Etiological agents Campylobacter jejuni Cytomegalovirus Haemophilus influenzae Epstein–Barrvirus Mycoplasma pneumoniae ZikaDengueChikungunyaEnterovirusHerpesHepatitis A-E Campylobacter jejuni
TreatmentIntravenousimmunoglobulin orplasmapheresisIntravenousimmunoglobulin orplasmapheresis
PrognosisBad, because of the predominant axonal involvementAccording to the promptness of treatment initiationGood most of the time, according to the promptness of treatment initiation
In a more delimited way, in Mexico, the incidence of cases associated with Zika was very low (5.8%); in contrast, other neurotropic infectious agents were identified: dengue, chikungunya, herpes, enterovirus, hepatitis B and even more relevant, the identification of Campylobacter cases that in contrast to common campylo-bacteriosis, these were not always presented with diarrheal or enteral syndrome, hypothesizing that probably the neurological syndrome was the primary manifestation of this infection. Despite all the documentary work done so far, the full causal relationship between Zika and Guillain-Barré is not clear, nor has it been possible to clarify why the incidences of the syndrome increased so exponentially in several latitudes of the American continent. 4 5 Following the information obtained in a global way, the following points of good practice are recommended for a better diagnosis and treatment of patients affected by Guillain-Barré syndrome: All acute neurological symptoms that meet the clinical criteria of Asbury-Cornblath (asymmetric paralysis and areflexia) should be treated as Guillain-Barré syndrome until proven otherwise. Take into account that there are atypical variants such as Miller-Fisher syndrome, pharyngo-cervical-brachial weakness, facial diplegia, Bickerstaff encephalitis, among others. Any case of Guillain-Barré syndrome should be protocolized according to Brighton criteria, trying to perform a diagnostic protocol that includes cerebrospinal fluid analysis, neuroimaging studies, and nerve neuroconduction An infectious protocol should be performed that includes viral and bacterial agents with proven neurotropism, integrating endemic or tropical zones, serologies, and molecular studies of dengue, Zika, and chikungunya. Likewise, the importance of identifying the causative agents is that some active infections are susceptible to specific treatment (herpes, Cytomegalovirus, hepatitis, campylobacter , influenza, and human immunodeficiency virus) For a better serological scrutiny of arboviruses, it is recommended to use reverse transcription polymerase chain reaction techniques from day 0 to 7 and later immunoglobulin M determination; in regions where there are infections by other arboviruses and there may be immunological cross-reactions between arboviruses (dengue, Zika, mayaro, chikungunya, oropouche, and yellow fever), it is recommended to perform the neutralization technique by plate reduction to elucidate which is the arboviral agent involved Pharmacological treatment should be initiated as soon as the suspicion of Guillain-Barré syndrome is established, with intravenous immunoglobulin or plasmapheresis, the main lines of treatment. In the same way, concomitant therapies such as physical therapies and neuromuscular rehabilitation. The functional and vital prognosis of the patient depends on the promptness of the diagnosis and the establishment of the treatment Use scales of functionality such as Hugues, medical research council, Erasmus (EGOS-EGRIS), to define the degree of affectation and its recovery after the treatment provided Remember that the management of these patients must be multidisciplinary for a better resolution.
  4 in total

1.  [Emerging Arboviroses in Mexico: chikunguña and zika].

Authors:  Luis del Carpio-Orantes
Journal:  Rev Med Inst Mex Seguro Soc       Date:  2016 May-Jun

2.  [Zika, a neurotropic virus?].

Authors:  Luis Del Carpio-Orantes
Journal:  Rev Med Inst Mex Seguro Soc       Date:  2016 Jul-Aug

Review 3.  Zika virus: - a review of the main aspects of this type of arbovirosis.

Authors:  Ítala Keane Rodrigues Dias; Cicera Luciana da Silva Sobreira; Rosa Maria Grangeiro Martins; Kelly Fernanda Silva Santana; Maria do Socorro Vieira Lopes; Emanuella Silva Joventino; Maria Corina Amaral Viana
Journal:  Rev Soc Bras Med Trop       Date:  2018 May-Jun       Impact factor: 1.581

Review 4.  Prevalence of Guillain-Barré syndrome among Zika virus infected cases: a systematic review and meta-analysis.

Authors:  Ludovica Barbi; Antonio Victor Campos Coelho; Luiz Cláudio Arraes de Alencar; Sergio Crovella
Journal:  Braz J Infect Dis       Date:  2018-03-12       Impact factor: 3.257

  4 in total
  1 in total

1.  Guillain-Barré syndrome, from the search for Zika to the discovery of asymptomatic campylobacteriosis as a risk factor for neurological syndromes in Veracruz, Mexico.

Authors:  Luis Del Carpio-Orantes
Journal:  Brain Circ       Date:  2022-09-21
  1 in total

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