ABSTRACT
Background: Coronavirus disease 2019 (COVID-19) typically causes breathing issues that can range from flu symptoms to extreme pneumonia, but it can also impair extra respiratory systems and cause multisystemic failure, including neurological complications. Case Presentation: A 55-year-old male with acute progressive symmetrical ascending quadriparesis complaints was admitted to the hospital. Twelve days prior to hospitalization, the patient with taste disruption, myalgia, fever, and polymerase chain reaction with reverse transcription was confirmed to have been positive for COVID-19 infection. The neurophysiological findings were consistent with the diagnosis of Guillain-Barré syndrome (GBS). Conclusion: COVID-19 activates inflammatory cells and creates a number of inflammatory cytokines and eventually produces immune-mediated processes. Both cell and humoral-dependent pathways of GBS pathogenesis are believed to be related. The peripheral nervous system, myelin, axons, and in some cases, both immune-mediated attacks are believed to be the cause of molecular expression. COVID-19 is believed to induce antibody formation against particular gangliosides. Further study is needed to understand the role of GBS caused by infection with COVID-19.
ABSTRACT
BACKGROUND: Neuroinflammation has an important role in the pathophysiology of migraine, which is a complex neuro-glio-vascular disorder. The main aim of this review is to highlight findings of cortical spreading depolarization (CSD)-induced neuroinflammatory signaling in brain parenchyma from the inflammasome perspective. In addition, we discuss the limited data of the contribution of inflammasomes to other aspects of migraine pathophysiology, foremost the activation of the trigeminovascular system and thereby the generation of migraine pain. MAIN BODY: Inflammasomes are signaling multiprotein complexes and key components of the innate immune system. Their activation causes the production of inflammatory cytokines that can stimulate trigeminal neurons and are thus relevant to the generation of migraine pain. The contribution of inflammasome activation to pain signaling has attracted considerable attention in recent years. Nucleotide-binding domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) is the best characterized inflammasome and there is emerging evidence of its role in a variety of inflammatory pain conditions, including migraine. In this review, we discuss, from an inflammasome point of view, cortical spreading depolarization (CSD)-induced neuroinflammatory signaling in brain parenchyma, the connection with genetic factors that make the brain vulnerable to CSD, and the relation of the inflammasome with diseases that are co-morbid with migraine, including stroke, epilepsy, and the possible links with COVID-19 infection. CONCLUSION: Neuroinflammatory pathways, specifically those involving inflammasome proteins, seem promising candidates as treatment targets, and perhaps even biomarkers, in migraine.