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
).
Table 1
Main differences of Guillain Barre syndrome, before and after zika
Before Zika
After Zika
Abbreviations: AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute
motor axonal neuropathy.
Predominant neuroconduction pattern
AMAN
AIDP
Etiological agents
Campylobacter
jejuni
Cytomegalovirus
Haemophilus
influenzae
Epstein–Barrvirus
Mycoplasma
pneumoniae
ZikaDengueChikungunyaEnterovirusHerpesHepatitis A-E
Campylobacter jejuni
Treatment
Intravenousimmunoglobulin orplasmapheresis
Intravenousimmunoglobulin orplasmapheresis
Prognosis
Bad, because of the predominant axonal involvementAccording to the promptness of treatment
initiation
Good 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.