Little is known about the pathogenesis of cerebral sinovenous thrombosis (CSVT) in the
neonate. Although thrombophilia has been described as increasing the risk of CSVT in
adults, it remains controversial in pediatric patients, and prospective case–control
studies regarding neonatal CSVT are lacking. From 2008 to 2017, all 26 consecutive newborn
infants ≥35 weeks of gestation diagnosed with neonatal CSVT, and their mothers, were
tested for factor V Leiden (FV) G1691A, FII G20210A, and methylenetetrahydrofolate
reductase C677T (MTHFR C677T) mutations. Eighty-five mother–infant pairs were recruited as
controls. All infants except 1 with CSVT were suspected due to clinical symptoms, mainly
seizures (22/25). Magnetic resonance imaging was performed in 24/26 infants. Heterozygous
FV G1691A, FII G20210A, and homozygous MTHFR C677T mutations were present in 1/26, 3/26,
and 3/20 infants with CSVT, respectively. FII (odds ratio: 10.96; 95% confidence interval
[CI]: 1.09-110.35) and male sex (3.93; 95% CI: 1.43-10.76) were associated with CSVT. When
FII G20210A analysis was adjusted for sex, the OR for FII G20210A was 6.70 (95% CI:
0.65-69.22). No differences were found for FV G1691A or homozygous MTHFR mutations between
neonates with CSVT and their mothers, compared to controls.
Objective The study aimed to describe the cases of neurological disease related to the outbreak of enterovirus (EV) in three regions in Northern Spain during 2016.
Materials and Methods Multicenter retrospective observational study. Clinical, radiological, and microbiological data were analyzed from patients younger than 15 years with confirmed EV-associated neurological disease admitted to 10 hospitals of Asturias, Cantabria, and Castile and Leon between January 1 and December 31, 2016.
Results Fifty-five patients were included. Median age was 24 months (interquartile range = 18.5 months). Fifteen patients were classified as aseptic meningitis (27.3%). In total, 37 cases presented brainstem encephalitis (67.3%), 25 of them due to EV-A71 with excellent prognosis (84.6% asymptomatic 2 months following the onset). Three cases of acute flaccid myelitis (5.5%) by EV-D68 were reported and presented persistent paresis 2 months following the onset. Microbiological diagnosis by reverse transcriptase polymerase chain reaction was performed in all cases, finding EV in cerebrospinal fluid in meningitis, but not in brainstem encephalitis and acute flaccid myelitis, where EV was found in respiratory or rectal samples. Step therapy was administrated with intravenous immunoglobulin (IVIG; 32.7%), methylprednisolone (10%), and plasmapheresis (3.6%). Four patients received fluoxetine (7.3%). Twenty patients needed to be admitted to pediatric intensive care unit (36.4%).
Conclusion Clinical, microbiological, and radiological diagnosis is essential in outbreaks of EV neurological disease, taking into account that it can be difficult to identify EV-A71 and EV-D68 in CSF, requiring throat or rectal samples. There is not specific treatment to these conditions and the efficacy and understanding of the mechanism of action of immune-modulatory treatment (IVIG, corticosteroids, and plasmapheresis) is limited.
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