The Epidemiology of Guillain-Barré Syndrome in Children under 15 Years Old in Southwest Iran

Background: Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy, which has become the most common cause of acute flaccid paralysis. An accurate estimation of GBS occurrence would be useful for investigating the potential causal relationships between risk factors and GBS. The aim of the study was to analyze the incidence, annual time trend, and some epidemiological aspects of GBS in children in the Southwest of Iran. Methods: This was a retrospective study conducted by the Department of Pediatrics of Ahvaz Jundishapur University of Medical Sciences from January 2006 to December 2015. We extracted data from the national database of Acute Flaccid Paralysis Surveillance System. Results: A total of 184 subjects with GBS were assessed. The mean age of subjects was 5.43 ± 4.07 years. The average annual incidence rate of GBS was 1.51 per 100,000 children under 15 years old (95% CI: 1.29-1.73). There was no significant statistical difference in GBS incidence rate between girls and boys (p = 0.376). The highest and lowest proportions of the GBS occurrences were in autumn (32.2%) and summer (14.7%), respectively. Conclusions: The findings indicated that the annual incidence rate of GBS in this study was similar to those in other studies in this area.

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Zika virus infection causes temporary paralysis in adult mice with motor neuron synaptic retraction and evidence for proximal peripheral neuropathy

Scientific Reports ◽

10.1038/s41598-019-55717-3 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

John D. Morrey ◽

Alexandre L. R. Oliveira ◽

Hong Wang ◽

Katherine Zukor ◽

Mateus Vidigal de Castro ◽

...

Keyword(s):

Peripheral Neuropathy ◽

Virus Infection ◽

Motor Neurons ◽

Zika Virus ◽

Acute Flaccid Paralysis ◽

Flaccid Paralysis ◽

Guillain Barre Syndrome ◽

Zika Virus Infection ◽

Guillain Barré Syndrome ◽

Guillain Barré

AbstractClinical evidence is mounting that Zika virus can contribute to Guillain-Barré syndrome which causes temporary paralysis, yet the mechanism is unknown. We investigated the mechanism of temporary acute flaccid paralysis caused by Zika virus infection in aged interferon αβ-receptor knockout mice used for their susceptibility to infection. Twenty-five to thirty-five percent of mice infected subcutaneously with Zika virus developed motor deficits including acute flaccid paralysis that peaked 8-10 days after viral challenge. These mice recovered within a week. Despite Zika virus infection in the spinal cord, motor neurons were not destroyed. We examined ultrastructures of motor neurons and synapses by transmission electron microscopy. The percent coverage of motor neurons by boutons was reduced by 20%; more specifically, flattened-vesicle boutons were reduced by 46%, and were normalized in recovering mice. Using electromyographic procedures employed in people to help diagnose Guillain-Barré syndrome, we determined that nerve conduction velocities between the sciatic notch and the gastrocnemius muscle were unchanged in paralyzed mice. However, F-wave latencies were increased in paralyzed mice, which suggests that neuropathy may exist between the sciatic notch to the nerve rootlets. Reversible synaptic retraction may be a previously unrecognized cofactor along with peripheral neuropathy for the development of Guillain-Barré syndrome during Zika virus outbreaks.

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