Neurological Diseases Define the Cytokine Profile in CFS during SARS-CoV-2 Infection in Highly Ill Patients.

Neuroinflammation is critical in developing and progressing neurological diseases. The underlying pro-inflammatory cytokine expression combined with additional mechanisms in the neuropathology, such as oxidative stress, brain-blood barrier damage, and endothelial dysfunction, could contribute to the susceptibility to developing severe COVID-19. The physiopathology of SARS-CoV-2 and other human coronaviruses (H-CoVs) has not been completely understood; however, they have all been linked to a disproportionated response of the immune system, particularly an exacerbated cytokine production and the dysregulation of total cell counts. In this article, based on the compilation of studies reported by our working group regarding COVID-19 and neurological diseases, we propose that the inflammation observed in the central nervous system, through a CSF analysis, could be conditioned by neurological disease(s) and enhanced by COVID-19. Therefore, it is necessary to determine the cytokine profile in different neurological disorders to propose adequate treatments and avoid severe forms of the disease in these patients.

Blood-brain Barrier Damage is Pivotal for SARS-CoV-2 Infection to the Central Nervous System.

Transsynaptic transport is the most accepted proposal to explain the SARS-CoV-2 infection of the CNS. Nevertheless, emerging evidence shows that neurons do not express the SARS-CoV-2 receptor ACE2, which highlights the importance of the blood-brain barrier (BBB) in preventing virus entry to the brain. In this study, we examine the presence of SARS-CoV-2 messenger ribonucleic acid (mRNA) and the cytokine profile in cerebrospinal fluids (CSF) from two patients with a brain tumor and COVID-19. To determine the BBB damage, we evaluate the Q- albumin index, which is an indirect parameter to assess the permeability of this structure. The Q-albumin index of the patient with an intraventricular brain tumor suggests that the BBB is undamaged, preventing the passage of SARS-CoV-2 and pro-inflammatory molecules. The development of brain tumors that disrupt the BBB (measured by the Q-albumin index), in this case, a petroclival meningioma (Case 1), allows the free passage of the SARS-CoV-2 virus and probably lets the free transit of pro-inflammatory molecules to the CNS, which leads to a possible activation of the microglia (astrogliosis) and an exacerbated immune response represented by IL-13, IFN-γ, and IL-2 trying to inhibit both the infection and the carcinogenic process.

Incidence of neurosurgical pathology of the spine in population of Mexico City.

BACKGROUND: Spine pathologies have been increased in the past years worldwide being important cause of disability which represents significant economic losses. OBJECTIVE: The objective of the study was to establish the incidence of spinal neurosurgical pathology in a national reference hospital in Mexico City (General Hospital of Mexico "Dr. Eduardo Liceaga"). MATERIALS AND METHODS: A descriptive, observational, retrospective, and cross-sectional study was carried out, using the database of all patients that were undergoing spinal surgery from January 2015 to January 2020. Measures of central tendency and percentages, demographic variables, diagnosis, and affected segment were assessed. RESULTS: A total of 341 cases were analyzed, the group of patients with degenerative disease represents the main cause of care followed by neoplasms; trauma and special cases of congenital type and reoperations were the less frequent pathologies between the groups. In general, the most affected age group was 51-60 years. CONCLUSIONS: Within the study population, a wide range of diseases that affect the spine were treated, ranging from degenerative diseases, neoplasms, trauma, congenital, and infectious diseases.

ANTECEDENTES: La incidencia de enfermedades de la columna ha ido en incremento en los últimos años a nivel mundial, las cuales representan una importante causa de incapacidad laboral e importantes pérdidas económicas. OBJETIVO: Establecer la incidencia de enfermedades neuroquirúrgicas de la columna en un hospital nacional de referencia de la Ciudad de México (Hospital General de México "Dr. Eduardo Liceaga"). MATERIALES Y MÉTODOS: Se llevó a cabo un estudio descriptivo, observacional, retrospectivo y transversal utilizando la base de datos de los pacientes que se sometieron a una cirugía de columna de enero del 2015 a enero del 2020. Se evaluaron medidas de tendencia central y porcentajes, variables demográficas, diagnóstico y segmento afectado. RESULTADOS: Se analizaron un total de 341 casos, la enfermedad degenerativa representa la principal causa de atención seguida de las neoplasias y los traumatismos; los casos especiales de tipo congénito y las reintervenciones fueron las patologías menos frecuentes. El grupo de edad más afectado fue de entre 51 a 60 años. CONCLUSIONES: Dentro de la población de estudio se trataron una amplia gama de enfermedades que afectan a la columna, que van desde enfermedades degenerativas, neoplasias, traumatismos, enfermedades congénitas e infecciosas.

High Levels of IL-8 and MCP-1 in Cerebrospinal Fluid of COVID-19 Patients with Cerebrovascular Disease.

The coronavirus family has tropism for the Central Nervous System (CNS), however, there is no solid evidence demonstrating that the neurological effects of COVID-19 result from direct viral infection or systemic inflammation. The goals of this study were to examine the cytokine profile and the presence of SARS-CoV-2 messenger ribonucleic acid (mRNA) in cerebrospinal fluids (CSF) from two patients with cerebrovascular disease and COVID-19. Although the SARS-CoV-2 mRNA was not detected in CSF of both patients, we found abnormally high levels of numerous proinflammatory cytokines and chemokines, especially IL-8 and MCP-1. Since these chemokines mediate activation and recruitment of neutrophils, monocytes, and macrophages, it is feasible that cerebrovascular disease related-neuroinflammation found in both patients results from an exacerbated inflammatory response instead of SARS-CoV-2 direct invasion to CNS. These results suggest that neuroinflammation plays a key role in cerebrovascular disease and COVID-19.