Correction: Castelan-Ramírez et al. Schwann Cell Autophagy and Necrosis as Mechanisms of Cell Death by . 2020, , 458.

In the original publication [...

Clinical profile of patients with surgical brain abscesses and etiology in a reference hospital.

Introduction: The annual incidence of brain abscesses is 1-2% in developed countries and up to 8% in developing countries. Our aim was to describe the profile and etiological agents of patients with surgical brain infections according to their nosological diagnosis on admission, and to analyze whether the initial diagnosis influenced the neurological deficit at discharge.

Methodology: This was an observational study with convenience sampling.

Central Nervous System Tuberculosis in a Murine Model: Neurotropic Strains or a New Pathway of Infection?

Tuberculosis (TB) of the central nervous system (CNS) is a lethal and incapacitating disease. Several studies have been performed to understand the mechanism of bacterial arrival to CNS, however, it remains unclear. Although the interaction of the host, the pathogen, and the environment trigger the course of the disease, in TB the characteristics of these factors seem to be more relevant in the genesis of the clinical features of each patient.

The role of TNF receptors as mediators of chronic vasculitis in possible milder forms of the CNS tuberculosis.

Introduction: Central nervous system (CNS) tuberculosis (TB) is the most severe form of TB due to its high mortality and functional sequelae. There are several differential diagnoses for TB; and, it can also cause secondary conditions, such as vasculitis.

Methodology: 155 biopsies, corresponding to 155 different patients out of 5,386 registered biopsies from 2008-2013, met the criteria of unknown etiology vasculitis and evidence of cerebral vascular disease.

Effect of Systemic Inflammation in the CNS: A Silent History of Neuronal Damage.

Central nervous system (CNS) infections including meningitis and encephalitis, resulting from the blood-borne spread of specific microorganisms, provoke nervous tissue damage due to the inflammatory process. Moreover, different pathologies such as sepsis can generate systemic inflammation. Bacterial lipopolysaccharide (LPS) induces the release of inflammatory mediators and damage molecules, which are then released into the bloodstream and can interact with structures such as the CNS, thus modifying the blood-brain barrier's (BBB´s) and blood-cerebrospinal fluid barrier´s (BCSFB´s) function and inducing aseptic neuroinflammation.