Abstract
BackgroundThe Zika virus (ZIKV) has been associated with Guillain-Barré syndrome (GBS) in epidemiological studies. Whether ZIKV-associated GBS is related to a specific clinical or electrophysiological phenotype has not been established. To this end, we performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS.MethodsWe searched Pubmed, EMBASE and LILACS, and included all papers, reports or bulletins with full text in English, Spanish or Portuguese, reporting original data of patients with GBS and a suspected, probable or confirmed recent ZIKV infection. Data were extracted according to a predefined protocol, and pooled proportions were calculated.ResultsThirty-five studies were included (13 single case reports and 22 case series, case-control or cohort studies), reporting on a total of 601 GBS patients with a suspected, probable or confirmed ZIKV infection. Data from 21 studies and 587 cases were available to be summarized. ZIKV infection was confirmed in 21%, probable in 22% and suspected in 57% of cases. ZIKV PCR was positive in 30% (95%CI 15–47) of tested patients. The most common clinical features were: limb weakness 97% (95%CI 93–99), diminished/absent reflexes 96% (95%CI 88–100), sensory symptoms 82% (95%CI 76–88), and facial palsy 51% (95%CI 44–58). Median time between infectious and neurological symptoms was 5–12 days. Most cases had a demyelinating electrophysiological subtype and half of cases were admitted to the Intensive Care Unit (ICU). Heterogeneity between studies was moderate to substantial for most variables.ConclusionsThe clinical phenotype of GBS associated with ZIKV infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating ICU admittance. Time between infectious and neurological symptoms and negative PCR in most cases suggests a post-infectious disease mechanism. Heterogeneity between studies was considerable and results may be subject to reporting bias. This study was registered on the international Prospective Register of Systematic Reviews (CRD42018081959).
Highlights
Guillain-Barresyndrome (GBS) is the most common cause of acute flaccid paralysis worldwide, with an incidence rate of approximately 1 per 100,000 person-years.[1]
The clinical phenotype of GBS associated with Zika virus (ZIKV) infection reported in literature is generally a sensorimotor demyelinating GBS with frequent facial palsy and a severe disease course often necessitating Intensive Care Unit (ICU) admittance
Our study shows that published cases with ZIKV-related GBS generally have both sensory and motor symptoms, facial palsy, demyelination on electrophysiological examination, and a severe disease course that often necessitates ICU admittance
Summary
Guillain-Barresyndrome (GBS) is the most common cause of acute flaccid paralysis worldwide, with an incidence rate of approximately 1 per 100,000 person-years.[1]. The classic form of GBS is characterized by a rapidly progressive and symmetrical weakness of the limbs, with sensory symptoms and reduced or absent tendon reflexes.[4] Cranial nerve involvement is frequent, with facial and bulbar muscles most often affected.[5] Electrophysiological studies help to confirm the diagnosis of GBS, and can indicate different subtypes, including acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor and sensory axonal neuropathy (AMSAN).[4] The majority of patients will lose the ability to walk during the acute phase of the disease and about 25% of patients need to be mechanically ventilated at the Intensive Care Unit (ICU).[6] Clinical presentation and severity of GBS can vary extensively between patients This variability is thought to be, in part, caused by differences in the type of preceding infections. We performed a systematic review and meta-analysis of all published studies on ZIKV-related GBS
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