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INTRODUCTION: Work-related traumatic brain injury is a frequent cause of chronic morbidity, mortality, and high treatment costs. Its causes are highly environmentally determined and were affected by COVID-19 pandemic lockdowns. OBJECTIVE: We aimed to describe traumatic brain injury (TBI) epidemiology in working population and evaluate its modifications during the COVID-19 pandemic. METHODS: We performed a 2-year retrospective epidemiological analysis of TBI patients hospitalized in a tertiary work-related hospital before and during the COVID-19 pandemic. RESULTS: In the prepandemic period, TBI patients were predominantly men, with a bimodal age distribution. Crash accidents were the leading work-related traumatic brain injury cause. During COVID-19 pandemic lockdowns, there was a positive correlation between street traffic and TBI rate, presenting increased motor crash accidents as a cause of TBI. CONCLUSIONS: These results are relevant for planning and focalization of resources for TBI prevention.

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We report a 50-year-old woman with a history of celiac disease, who presented with lumbar pain and progressive flaccid tetraparesis 48 hours after the inoculation of the first dose of CoronaVac inactivated SARS-CoV-2 vaccine. CSF was normal and electrodiagnostic studies showed an axonal motor polyneuropathy. No other triggers were identified, and other etiologies were ruled out. The presentation was compatible with the AMAN (Acute Motor Axonal Neuropathy) subtype of GBS, and intravenous immunoglobulin halted the progression of symptoms. Intensive neurorehabilitation was performed. The patient was discharged five weeks after admission, walking with poles and climbing stairs with minimal assistance. To date no cases of inactivated SARSCoV-2 vaccine related GBS have been reported. Thus, description of its clinical presentation is relevant. We discuss the current evidence relating GBS with vaccines, highlighting that vaccine associated GBS is a controversial entity and causality must be interpreted cautiously given the actual COVID-19 pandemic context.

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We report a 50-year-old woman with a history of celiac disease, who presented with lumbar pain and progressive flaccid tetraparesis 48 hours after the inoculation of the first dose of CoronaVac inactivated SARS-CoV-2 vaccine. CSF was normal and electrodiagnostic studies showed an axonal motor polyneuropathy. No other triggers were identified, and other etiologies were ruled out. The presentation was compatible with the AMAN (Acute Motor Axonal Neuropathy) subtype of GBS, and intravenous immunoglobulin halted the progression of symptoms. Intensive neurorehabilitation was performed. The patient was discharged five weeks after admission, walking with poles and climbing stairs with minimal assistance. To date no cases of inactivated SARSCoV-2 vaccine related GBS have been reported. Thus, description of its clinical presentation is relevant. We discuss the current evidence relating GBS with vaccines, highlighting that vaccine associated GBS is a controversial entity and causality must be interpreted cautiously given the actual COVID-19 pandemic context.

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Resumen La hipoacusia unilateral es una alteración prevalente e importante en la población infantil que puede llevar a un deterioro del procesamiento auditivo. Cualquier patología que cause hipoacusia asimétrica (conductiva o sensorioneural) durante ventanas críticas del desarrollo cerebral, puede dar lugar a déficits del procesamiento auditivo que podrían persistir incluso después de la rehabilitación audiológica. Este proceso fisiopatológico se ha denominado "ambliaudia" y los niños que la presentan tienen un mayor riesgo de sufrir retraso en el desarrollo del lenguaje, así como de padecer dificultades académicas, sociales y cognitivas. Por esto, la ambliaudia se presenta como un desafío en audiología, siendo necesario comprender los mecanismos neurobiológicos que la subyacen. Entender de mejor manera cuáles son las consecuencias que tiene la pérdida auditiva asimétrica sobre el desarrollo del sistema nervioso podría ser clave para guiar de mejor forma las intervenciones terapéuticas. En este artículo se revisan trabajos en humanos y en modelos animales que describen las consecuencias neurobiológicas de la deprivación auditiva unilateral durante el desarrollo del sistema nervioso y su posible aplicación a la práctica clínica.

Abstract Unilateral hearing loss is a prevalent and important disorder in children that can lead to an impairment of auditory processing. Any pathology that causes asymmetric (conductive or sensorineural) hearing loss during critical brain development windows can lead to hearing deficits that may persist even after audiological rehabilitation. This pathophysiological process has been referred to as amblyaudia, and children are at greater risk of experiencing language developmental delays as well as academic, social and cognitive impairments. For this reason, amblyaudia presents itself as a challenge in audiology, and it has become necessary to understand its neurobiological mechanisms. A better understanding of the consequences of asymmetric hearing loss on the development of the nervous system may be key to better guiding therapeutic interventions. This article reviews studies performed in humans and animal models that describe the neurobiological consequences of unilateral hearing deprivation during the development of the nervous system and its possible applications to clinical practice.

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In the last decades, there has been an increase in life expectancy in the world, with the consequent modification in the proportion of adults over 60 years. This is accompanied by an increase in pathologies for which aging is the main risk factor, such as dementia and hearing loss, which profoundly affect the quality of life of individuals and their family and impact health system costs. Given the lack of disease-modifying treatments for dementia, the study of mechanisms to prevent its occurrence has become a world priority. In the year 2017, the Lancet "Commission for dementia prevention, intervention, and care" proposed a model, in which hearing loss emerged as a new modifiable risk factor for the development of dementia. This result undoubtedly has important consequences for the understanding the multifactorial nature of dementia, our daily clinical practice and public policies aimed at its prevention and treatment. In this article, we review the current evidence supporting the association between dementia and hearing loss, discussing the available strategies for prevention, detection and treatment of hearing loss and its possible impact on the natural course of dementia. A flow chart for the clinical management of different subgroups of patients is proposed.

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In the last decades, there has been an increase in life expectancy in the world, with the consequent modification in the proportion of adults over 60 years. This is accompanied by an increase in pathologies for which aging is the main risk factor, such as dementia and hearing loss, which profoundly affect the quality of life of individuals and their family and impact health system costs. Given the lack of disease-modifying treatments for dementia, the study of mechanisms to prevent its occurrence has become a world priority. In the year 2017, the Lancet "Commission for dementia prevention, intervention, and care" proposed a model, in which hearing loss emerged as a new modifiable risk factor for the development of dementia. This result undoubtedly has important consequences for the understanding the multifactorial nature of dementia, our daily clinical practice and public policies aimed at its prevention and treatment. In this article, we review the current evidence supporting the association between dementia and hearing loss, discussing the available strategies for prevention, detection and treatment of hearing loss and its possible impact on the natural course of dementia. A flow chart for the clinical management of different subgroups of patients is proposed.

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An important unresolved question about neural processing is the mechanism by which distant brain areas coordinate their activities and relate their local processing to global neural events. A potential candidate for the local-global integration are slow rhythms such as respiration. In this study, we asked if there are modulations of local cortical processing that are phase-locked to (peripheral) sensory-motor exploratory rhythms. We studied rats on an elevated platform where they would spontaneously display exploratory and rest behaviors. Concurrent with behavior, we monitored whisking through electromyography and the respiratory rhythm from the olfactory bulb (OB) local field potential (LFP). We also recorded LFPs from dorsal hippocampus, primary motor cortex, primary somatosensory cortex, and primary visual cortex. We defined exploration as simultaneous whisking and sniffing above 5 Hz and found that this activity peaked at ~8 Hz. We considered rest as the absence of whisking and sniffing, and in this case, respiration occurred at ~3 Hz. We found a consistent shift across all areas toward these rhythm peaks accompanying behavioral changes. We also found, across areas, that LFP gamma (70-100 Hz) amplitude could phase-lock to the animal's OB respiratory rhythm, a finding indicative of respiration-locked changes in local processing. In a subset of animals, we also recorded the hippocampal theta activity and found that occurred at frequencies overlapped with respiration but was not spectrally coherent with it, suggesting a different oscillator. Our results are consistent with the notion of respiration as a binder or integrator of activity between brain regions.

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