ABSTRACT
Congenital Zika virus infection can cause microcephaly and severe brain abnormalities (1). Congenital Zika syndrome comprises a spectrum of clinical features (2); however, as is the case with most newly recognized teratogens, the earliest documented clinical presentation is expected to be the most severe. Initial descriptions of the effects of in utero Zika virus infection centered prominently on the finding of congenital microcephaly (3). To assess the possibility of clinical presentations that do not include congenital microcephaly, a retrospective assessment of 13 infants from the Brazilian states of Pernambuco and Ceará with normal head size at birth and laboratory evidence of congenital Zika virus infection was conducted. All infants had brain abnormalities on neuroimaging consistent with congenital Zika syndrome, including decreased brain volume, ventriculomegaly, subcortical calcifications, and cortical malformations. The earliest evaluation occurred on the second day of life. Among all infants, head growth was documented to have decelerated as early as 5 months of age, and 11 infants had microcephaly. These findings provide evidence that among infants with prenatal exposure to Zika virus, the absence of microcephaly at birth does not exclude congenital Zika virus infection or the presence of Zika-related brain and other abnormalities. These findings support the recommendation for comprehensive medical and developmental follow-up of infants exposed to Zika virus prenatally. Early neuroimaging might identify brain abnormalities related to congenital Zika infection even among infants with a normal head circumference (4).
Subject(s)
Microcephaly/epidemiology , Zika Virus Infection/congenital , Zika Virus Infection/diagnosis , Zika Virus/isolation & purification , Brazil/epidemiology , Female , Humans , Infant , Infant, Newborn , Male , Pregnancy , Pregnancy Complications, Infectious , Retrospective StudiesABSTRACT
INTRODUCTION: This article aims to describe a patient with Parinaud syndrome due to neurotuberculosis confirmed by cerebrospinal fluid analysis. CASE REPORT: Initially, patient sought medical care, performed a chest x-ray and later a chest CT scan, with a probable diagnosis of miliary tuberculosis. In addition, she presented binocular diplopia worse at right lateral gaze, paresis of vertical gaze, light near-dissociation and convergent retraction nystagmus and presence of mycobacterium tuberculosis on PCR Xpert MTB/RIF. The treatment of miliary tuberculosis was interrupted due to pharmacodermia, but after diagnosis of neurotuberculosis, it was restarted with isoniazid, pyrazinamide and ethambutol with partial visual symptoms improvement. DISCUSSION: This case demonstrates the importance of pursuing diagnosis through more accurate techniques, especially in a patient with previous treatment pharmacoderma, whose absence of proper diagnosis and treatment would be extremely deleterious.