Hearing brain evaluated using near-infrared spectroscopy in congenital toxoplasmosis

Ana Lívia Libardi Bertachini,Rickson Coelho Mesquita,Gabriela Cintra Januario,Gláucia Manzan Queiroz Andrade,Marco Aurélio Romano Silva,Sergio Luiz Novi,Luciana Macedo De Resende,Débora Marques De Miranda

doi:10.1038/s41598-021-89481-0

Ana Lívia Libardi Bertachini, Rickson Coelho Mesquita + Show 6 more

Open Access

https://doi.org/10.1038/s41598-021-89481-0

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Abstract

Congenital toxoplasmosis (CT) is a known cause of hearing loss directly caused by Toxoplasma gondii. Hearing loss might result from sensory, neural, or sensorineural lesions. Early treated infants rarely develop hearing loss, but retinochoroidal lesions, intracranial calcifications and hydrocephalus are common. In this study, we aimed to evaluate the brain evoked hemodynamic responses of CT and healthy infants during four auditory stimuli: mother infant directed speech, researcher infant directed speech, mother reading and researcher recorded. Children underwent Transitionally Evoked Otoacoustic Emission Auditory Testing and Automated Brainstem Auditory Response tests with normal auditory results, but with a tendency for greater latencies in the CT group compared to the control group. We assessed brain hemodynamics with functional near-infrared spectroscopy (fNIRS) measurements from 61 infants, and we present fNIRS results as frequency maps of activation and deactivation for each stimulus. By evaluating infants in the three first months of life, we observed an individual heterogeneous brain activation pattern in response to all auditory stimuli for both groups. Each channel was activated or deactivated in less than 30% of children for all stimuli. There is a need of prospective studies to evaluate if the neurologic or auditory changes course with compromise of children outcomes.

Highlights

Congenital toxoplasmosis (CT) is a known cause of hearing loss directly caused by Toxoplasma gondii
The latency of wave V in the right ear showed a significant difference between groups with a tendency for greater latencies in the CT group compared to the control group
Most newborns with Congenital toxoplasmosis are a symptomatic[9], and early treatment seems effective to minimize neurological sequelae, allowing a better brain development and growth[7,8,9]

Summary

Introduction

Congenital toxoplasmosis (CT) is a known cause of hearing loss directly caused by Toxoplasma gondii. Hearing loss might result from sensory, neural, or sensorineural lesions. Treated infants rarely develop hearing loss, but retinochoroidal lesions, intracranial calcifications and hydrocephalus are common. By evaluating infants in the three first months of life, we observed an individual heterogeneous brain activation pattern in response to all auditory stimuli for both groups. T gondii infection was confirmed in 190 cases, and about 80% had retinochoroidal lesions, 20% intracranial calcifications, 6% hydrocephalus, 5% microcephaly[2] and 4% sensorioneural hearing loss[10]. The prevalence of sensorineural hearing loss (SNHL) in children who received appropriate treatment in the first year of life is rare, whereas it can reach 28% in children without effective treatment[11]. In the presence of hearing impairment, especially the retrocochlear, there is an increased risk for changes in auditory processing and language development, and performance. As a white matter disorder, CT might compromise development due to impairments in auditory and language processing

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