Dysregulation in immune responses has been reported in association with hyperinflammation in COVID-19 patients, NLR has been linked to the severity of the patient's clinical status, and an increase in NLR is reported to be an independent risk factor for in-hospital mortality. Pain is a frequently seen symptom at the onset of viral infections and throughout the course of the disease. Although the pain mechanisms triggered by viral pathogens are not yet entirely understood, pain is thought to arise as a result of direct activation of nociceptor neurons by pathogens and their interaction with molecular ligands. Toll-like receptor 7 (TLR7), a pathogen recognition receptor that plays an important role in immune responses to viruses by binding to viral RNA, is known to be involved in pain development in different RNA virus infections. Park et al. showed that extracellular micro RNAs activate nociceptive neurons via the TLR7 pathway. Although these mechanisms have been demonstrated for different viral infections, the viral pathogenesis leading to pain in COVID-19 is still unclear. The purpose of this study was to investigate the prevalence of headache and muscular pain in patients diagnosed with COVID-19 and to determine the relationship between these symptoms and inflammatory parameters.
The neutrophil-lymphocyte ratio (NLR) used to demonstrate inflammatory status in recent years can be calculated by dividing the absolute neutrophil count by the absolute lymphocyte count at routine blood tests.