Staring Down the Barrel of a Gun: A Potential Pain Pandemic Following COVID-19 Infection.
Thacker, M and Mansfield, M (2020). Staring Down the Barrel of a Gun: A Potential Pain Pandemic Following COVID-19 Infection. Pain and Rehabilitation. 2020 (49), pp. 1-8.
|Authors||Thacker, M and Mansfield, M|
In December 2019 several people presented with an acute atypical respiratory disease in Wuhan, China. Soon after, several new cases of infection were reported across mainland China and then spread rapidly across the globe. Following extensive research, it was established that a novel (to humans) coronavirus was responsible, the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2, 2019-nCoV); the virus was named due to its high homology (~80%) to Severe Acute Respiratory Syndrome (SARS-CoV), which caused acute respiratory distress syndrome (ARDS) and high mortality during 2002–2003 (25, 36). The human disease caused by this virus was given the name Coronavirus disease 19 (abbreviated to COVID-19) and eventually a global pandemic was declared by The World Health Organization (WHO). COVID-19 has had, and is still having, a massive impact, being reported in approximately 200 countries and territories and infecting a huge number of people worldwide. As of June 12th 2020, 7.27 million people world-wide have had a confirmed diagnosis of COVID-19, which includes 293 000 confirmed cases and 41 481 deaths in the United Kingdom (UK), with these figures continue continuing to grow.
Coronaviruses have been identified in several non-human mammalian species, including rats, mice, cattle, swine, cats, dogs, rabbits and horses and, notably for this infection, bats. In these species (36), Coronavirus infection often causes devastating respiratory or enteric diseases (25,36). Several coronaviruses have been identified since the mid-1960s. Prior to the SARS-CoV outbreak in the early 2000s, coronaviruses were only thought to cause mild, self-limiting respiratory infections in humans, commonly referred to as “colds”. These viruses are endemic among the human populations, causing 15–30 % of respiratory tract infections each year (25,36). Whilst rare, it is known that these viruses can cause lower respiratory tract infections (25,36).
The majority of people with SARS-CoV-2 virus who become symptomatic, report a typical presentation of fever, dry cough and dyspnoea consistent with the primary viral effects on the respiratory system (24). The developed respiratory symptoms of Covid-19 are extremely heterogeneous, ranging from minimal to significant hypoxia and in severe cases the development of Adult Respiratory Distress Syndrome (ARDS) (26). In addition, there is increasing evidence that other organ systems may be either primarily or subsequently involved, including renal, cardiac, hepatic and the nervous systems (15,21,22,24). Several symptoms associated with COVID-19 including, headache, dizziness, generalized weakness and fatigue as well as vomiting and loss of taste and/or smell have been linked to alterations within the Central Nervous System (CNS) (25). It has been suggested that about 88% among severely affected patients (those requiring respiratory support) display neurologic manifestations including acute cerebrovascular disease and impaired consciousness (23,31,32) and there is now an agreement that the headache reported by around 8% of infected individuals is of neural origin (22,29,36,39).
The exact pathophysiological mechanisms operating outside of the pulmonary system in COVID-19 are currently undetermined but are thought to involve an interplay between the primary actions of the virus and the body’s defensive systems with a particular emphasis on the immune system (15,22,31,38). COVID-19 leads to a fast activation of innate immune cells following viral contact and the magnitude of this response has been shown to be greater in those patients who develop more severe disease/symptoms (15,21,31,38). Indicators of immune facilitation in COVID-19 include an increase in the number of circulating neutrophil and a marked lymphocytopenia that mostly targets all the sub-types (effector, memory and regulatory) of CD4+ T cells (38,40). These changes are consistent with neuro-immune alterations that have been observed following somatic injury/inflammation and associated with nociception (8,17,19,20,35). It is this nervous system-immune system interaction and their potential involvement in the development of clinical pain that caught our attention in the early phase of COVID-19.
Here we outline our hypothesis that those who have been infected with SARS-CoV-2 and developed symptoms may have an increased propensity to develop a clinically significant pain state/s due to the associated neuro-immune interactions. These interactions and the subsequent neuro-inflammation produce a series of neuroplastic responses within the nervous system that are well established as important mechanisms in the generation and maintenance of several clinical pain states (8,17,19,20,35). A full exposition of neuroimmune interactions in both pain and COVID-19 are beyond the scope of this extended editorial so here we briefly highlight several important features of COVID-19 infection that mirror neuroimmune mechanisms associated with the development and maintenance of pain. We aim to demonstrate our concern that we are potentially on the brink of a POST COVID-19 “pain pandemic” as a result of the neuroinvasive potential of the SARS-CoV-2 virus (see also 40 & 41).
|Journal||Pain and Rehabilitation|
|Journal citation||2020 (49), pp. 1-8|
|Publisher||The Physiological Pain Association|
|01 Jul 2020|
|Publication process dates|
|Accepted||10 Jul 2020|
|Deposited||13 Aug 2020|
|Accepted author manuscript|
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|License: CC BY|
|File access level: Open|
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