Transition of COVID-19 to endemic phase and emergence of COVID-19 related neuropathic pain

Abstract

Coronavirus disease 2019 (COVID-19) has caused several million deaths since it was first reported in December 2019 [1]. From the beginning of the COVID-19 pandemic, the main concern has been related to its acute respiratory involvement which may need ICU hospitalization and could lead to death. Since peaking in January 2022, new cases have continued to decline around the world. Gradually, extrapulmonary manifestations and post-COVID-19 syndrome have attracted more attention [2]. One of these is pain, one of the most common symptoms in the acute phase even after recovery from COVID-19.Acute pain during COVID-19 does not seem significantly different from most viral diseases, and myalgia and headache are the main symptoms, while anosmia and ageusia occurs more frequently [3]. Many of these have been managed with symptomatic treatments such as painkillers and anti-inflammatory drugs, but some patients suffer from pain that lasts more than four weeks, which is regarded as one of the post-COVID-19 syndromes [4]. In fact, symptoms in the acute phase, such as headache, anosmia and ageusia, could be recognized as a neurological manifestation.

The Effect of COVID-19 Vaccine Acceptance, Intention, and/or Hesitancy and Its Association with Our Health and/or Important Areas of Functioning

“…Moreover, COVID-19 vaccination opens the way for us to function socially and occupationally, especially as the COVID-19 vaccine process is ongoing. Furthermore, as some countries are trying to declare COVID-19 as endemic [ 41 , 42 , 43 ], some scholars are discussing whether we should treat the COVID-19 vaccine as a flu vaccine. In addition, informational fatigue and misinformation continue to be a challenge.…”

Evaluation and follow-up of pain, fatigue, and quality of life in COVID-19 patients

“…The current literature supports the premise that pain in COVID-19 patients is due, at least in part, to the neurotropism of SARS-CoV-2. Pain can be caused by the interaction of the virus with the angiotensin-converting enzyme isoform 2 receptors in spinal neurons and microglia, by immune system-mediated inflammation, or by viral damage [ 9 ].…”