RESUMO
In early 2021, Brazil saw a dramatic recurrence in Covid-19 cases associated to the spread of a novel variant of the SARS-CoV-2 virus, the P1 variant. In light of previous reports showing that this variant is more transmissible and more likely to infect people who had recovered from previous infection, a retrospective analysis was conducted to assess if the early 2021 Covid-19 wave in Brazil was associated with an increase in the number of individuals presenting with a more severe clinical course. Fifty-one thousand and fourteen individuals who underwent telemedicine consultations were divided into two groups: patients seen on or before January 31, 2021, and on or after February 1, 2021. These dates were chosen based on the spread of the P1 variant in Brazil. Referral to the emergency department (ED) was used as a marker of a more severe course of the disease. No differences were seen in the proportion of patients referred to the ED in each group nor in the odds ratio of being referred to the ED from the 1st of February 2021 (OR=0.909; 95%CI: 0.81-1.01). Considering the entire cohort, age had an impact on the odds of being referred to the ED, with individuals older than 59 years showing twice the risk of the remaining population and those less than 19 years showing a lower risk.
RESUMO
Introducción. Las enfermedades neurodegenerativas, incluyendo los accidentes cerebrovasculares, los traumatismos cerebrales o las lesiones de la médula espinal, tienen una elevada incidencia en todo el mundo. Se pueden identificar dos patrones lesivos claros tras estos episodios destructivos: un daño primario, consecuencia temprana del episodio patológico primario, y una degeneración neuronal secundaria (DNS), un grupo de episodios patológicos que inducen la degeneración tardía en células que no están afectadas por el daño primario o que sólo lo están parcialmente. Este mecanismo patológico es un importante factor que contribuye a los déficit funcionales y es el objetivo de enfoques terapéuticos. Hay varios factores implicados en la etiología de la DNS, incluyendo la excitotoxicidad, la inflamación y el estrés oxidativo. Objetivo. Revisar los principales mecanismos que subyacen en la DNS tras los trastornos neuronales agudos. Desarrollo. Se tratan los hallazgos más recientes sobre el proceso desencadenante de la DNS, así como su importancia para la degeneración de las vías de la sustancia blanca. Conclusiones. La caracterización de los episodios que subyacen en la DNS es de gran importancia para el desarrollo de nuevos enfoques terapéuticos suficientemente eficaces para disminuir los déficit funcionales y contribuir a la mejora de la calidad de vida de quienes padecen enfermedades neurológicas. Para una mejor eficacia neuroprotectora de la sustancia gris y de la sustancia blanca, estos enfoques terapéuticos deben validarse en modelos experimentales, tanto de enfermedades cerebrales como de la médula espinal, que simulen eficazmente los trastornos neuronales (AU)
Introduction. Acute neurodegenerative diseases, including stroke and traumatic brain and spinal cord injury, possess an elevated worldwide incidence. Two distinct lesive patterns can be identified after these destructive events: primary damage, an early consequence of the primary pathological event, and secondary neural degeneration (SND), a group of pathological events inducing late degeneration in cells not or even only partially affected by the primary damage. This pathological mechanism is an important contributing factor for functional deficits and target for therapeutic approaches. Several factors are involved on the SND etiology, including excitotoxicity, inflammation, and oxidative stress. Aim. To review the main mechanisms underlying the SND occurring after acute neural disorders. Development. The more recent findings about the eliciting processes of SND degeneration are discussed, as well as their significance to degeneration of white matter tracts. Conclusions. The characterization of the events underlying SND is of fundamental importance for the development of new therapeutic approaches effective enough to decrease the functional deficits, contributing to the improvement of the quality of life of people suffering neurological diseases. These therapeutic approaches must be validated in experimental models of both brain and spinal cord diseases, which effectively simulate human neural disorders protecting both gray and white matters for a better neuroprotective efficacy (AU)
