Association Between #Neonatal #Neuroimaging and #Clinical Outcomes in #Zika-Exposed #Infants From #Rio de Janeiro, #Brazil (JAMA Netw Open., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

JAMA Netw Open. 2019 Jul 3;2(7):e198124. doi: 10.1001/jamanetworkopen.2019.8124.

Association Between Neonatal Neuroimaging and Clinical Outcomes in Zika-Exposed Infants From Rio de Janeiro, Brazil.

Pool KL1, Adachi K1, Karnezis S1, Salamon N1, Romero T1, Nielsen-Saines K1, Pone S2, Boechat M2, Aibe M2, Gomes da Silva T2, Ribeiro CTM2, Boechat MI1, Brasil P2, Zin A2, Tsui I1, Gaw SL3, Daltro P4, Ribeiro BG4, Fazecas T4, Hygino da Cruz LC4, Nogueira R4, Vasconcelos Z2, Pereira JP Jr2, Saad Salles T2, Barbosa CN2, Chen W5, Foo SS5, Jung J5, Moreira ME2, Pone M2.

Author information: 1 David Geffen School of Medicine, University of California, Los Angeles. 2 Fundação Oswaldo Cruz, Rio de Janeiro, Brazil. 3 University of California San Francisco School of Medicine. 4 Clinica de Diagnostico por Imagem CDPI, Rio de Janeiro, Brazil. 5 University of Southern California School of Medicine, Los Angeles.

 

Abstract

IMPORTANCE:

Congenital Zika virus (ZIKV) infection may present with a spectrum of clinical and neuroradiographic findings.

OBJECTIVE:

To determine whether neuroimaging findings for infants with a history of ZIKV exposure are associated with infant clinical outcomes and gestational age at antenatal ZIKV infection.

DESIGN, SETTING, AND PARTICIPANTS:

This cohort study retrospectively reviewed neuroimaging results (computed tomography and/or magnetic resonance imaging scans) of 110 ZIKV-exposed infants from a maternity and children’s hospital in Rio de Janeiro, Brazil, following the 2015 to 2016 ZIKV epidemic. Neuroimaging from March 1, 2016, to June 30, 2017, was evaluated to determine whether findings were associated with clinical outcomes and the timing of maternal ZIKV infection. Data were analyzed from July 1, 2017, to August 30, 2018.

EXPOSURES:

Neuroimaging (computed tomography and/or magnetic resonance imaging) was performed on ZIKV-exposed infants after birth. Blood and/or urine specimens from mothers and infants were tested for ZIKV by polymerase chain reaction assay.

MAIN OUTCOMES AND MEASURES:

Neuroimaging studies were evaluated for structural abnormalities and other forms of brain injury.

RESULTS:

A total of 110 infants with a mean (SD) gestational age of 38.4 (2.1) weeks had neuroimaging and clinical outcome data reviewed. Of these, 71 (65%) had abnormal neuroimaging findings, with the majority (96%) classified as having severe ZIKV infection at birth. The most common neuroimaging abnormalities were structural abnormalities including brain calcifications, especially at the cortico-subcortical white matter junction, cortex malformations, ventriculomegaly, and reduced brain volumes, followed by brainstem hypoplasia, cerebellar hypoplasia, and corpus callosum abnormalities. Frequency of abnormal imaging was higher in infants with specific clinical findings as opposed to those without them; these findings included fetal brain disruption sequence (100% vs 35%), microcephaly (100% vs 30%), congenital contractures (100% vs 58%), ophthalmologic abnormalities (95% vs 44%), hearing abnormalities (100% vs 58%), and neurologic symptoms (94% vs 10%). Four of 39 infants (10%) without initial evidence of severe ZIKV infection and normal findings on neurologic evaluation at birth had abnormal neuroimaging findings. Neuroimaging abnormalities differed by trimester of maternal ZIKV infection, with 63% of infants born to mothers infected in the first trimester, 13% of infants born to mothers infected in the second trimester, and 1% of infants born to mothers infected in the third trimester exhibiting neuroimaging abnormalities. The odds of abnormal neuroimaging were 7.9 times greater for infants with first trimester ZIKV exposure compared with other trimesters combined (odds ratio, 7.9; 95% CI, 3.0-20.4; P < .001).

CONCLUSIONS AND RELEVANCE:

Neuroimaging abnormalities of computed tomography and/or magnetic resonance imaging scans were common in ZIKV-exposed infants. While neuroimaging abnormalities were seen in 10% of infants without clinically severe ZIKV, most occurred almost exclusively among those with clinically severe ZIKV, especially among those with a history of ZIKV exposure in the first trimester.

PMID: 31365112 DOI: 10.1001/jamanetworkopen.2019.8124

Keywords: Zika Virus; Zika Congenital Infection; Zika Congenital Syndrome; Neurology; Neuroimaging.

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#Congenital #Zika Syndrome: The Main Cause of #Death and Correspondence Between #Brain #CT and Postmortem #Histological Section Findings From the Same Individuals (Top Magn Reson Imaging, abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Top Magn Reson Imaging. 2019 Feb;28(1):29-33. doi: 10.1097/RMR.0000000000000194.

Congenital Zika Syndrome: The Main Cause of Death and Correspondence Between Brain CT and Postmortem Histological Section Findings From the Same Individuals.

de Fatima Viana Vasco Aragão M1,2, van der Linden V3, Petribu NC3, Valenca MM4, Parizel PM5,6, de Mello RJV4.

Author information: 1 Multimagem, Recife, Brazil. 2 Catholic University of Pernambuco, Recife, Brazil. 3 Barão de Lucena Hospital, Recife, Brazil. 4 Federal University of Pernambuco, Recife, Brazil. 5 Royal Perth Hospital (RPH), Perth, WA, Australia. 6 University of Western Australia (UWA) Medical School, Perth, WA, Australia.

 

Abstract

In the present case series, the cause of death of infants diagnosed with congenital Zika syndrome (CZS) was lung disease (pneumonia and sepsis with massive pulmonary aspiration), probably secondary to dysphagia and reflux. The main findings in infants with a confirmed diagnosis of CZS who died were as follows: (1) calcification and hypoplasia of the lentiform nuclei, hypoplasia of the caudate nuclei, and calcification at the cortical-subcortical junction was noted in all cases (100%) and calcification of the caudate nuclei was noted in 66.7% of cases; (2) calcification in the brainstem and along the lateral wall of the lateral ventricles was noted in only the case with arthrogryposis (33.3%); and (3) lesions in the posterior fossa (hypoplasia of the brainstem and cerebellum) were noted in two cases (66.7%), including the case with arthrogryposis. The findings concerning calcifications and brain malformations obtained from non-contrast computed tomography (CT) demonstrated good agreement with findings obtained from the postmortem pathological analysis; however, CT failed to detect discontinuity of the pia mater with heterotopia, invasion of the cerebral tissue into the subarachnoid space, and discontinuity of the ependyma in the lateral ventricles with gliosis; this last feature was only imaged in the most severe case of extreme microcephaly with a simplified gyral pattern. Only histopathology showed grouped calcifications associated with scattered calcifications suggestive of the neuron morphology.

PMID: 30817678 DOI: 10.1097/RMR.0000000000000194 [Indexed for MEDLINE]

Keywords: Congenital Zika Syndrome; Zika Virus; Microcephaly; Histopathology; Neurology; Neuroimaging.

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