Could The Fbromyalgia Syndrome Be Triggered Or Enhanced By COVID‑19? Part 1
Sep 28, 2023
Abstract
Fibromyalgia (FM) is a complex disease with an uncertain etiology and intricate pathophysiology. Although its genesis is not fully explained, potential environmental factors, such as viral infections might trigger FM or worsen patients' clinical outcomes. The SARS-CoV-2 virus may affect central and peripheral nervous systems, leading to musculoskeletal, neurological, and psychological disturbances. These symptoms might persist at least 12 months beyond the recovery, often referred to as post-COVID syndrome, which resembles FM syndrome. In this sense, we argued the potential consequences of COVID-19 exclusively on FM syndrome. First, we have described post-COVID syndrome and its painful symptoms. Afterward, we argued whether FM syndrome could be triggered or enhanced by COVID-19 infection or by numerous and persistent stressors imposed daily by the pandemic setting (isolation, uncertainty, depression, mental stress, generalized anxiety, and fear of the virus). In addition, we have demonstrated similarities between pathophysiological mechanisms and cardinal symptoms of FM and COVID-19, speculating that SARS-CoV-2 might represent a critical mediator of FM or an exacerbator of its symptoms once both syndromes share similar mechanisms and complaints. Therefore, pharmacologic and non-pharmacological approaches commonly used to treat FM could serve as strategic therapies to attenuate painful and neurological manifestations of post-COVID syndrome. Although it is still theoretical, clinicians and researchers should be alert of patients who develop symptoms similar to FM or those who had their FM symptoms increased post-COVID to manage them better.
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Graphical Abstract
Keywords SARS-CoV-2 · Post-COVID syndrome · Musculoskeletal pain · Fatigue · Myalgia · Chronic pain
Abbreviations
ACR American College of Rheumatology
BBB Blood-brain barrier
CNS Central nervous system
COVID-19 Coronavirus disease 19
DRG Dorsal root ganglia
FM Fibromyalgia
FDA Food and Drug Administration
GABA Gamma-aminobutyric acid
HIV Human immunodeficiency virus
ICU Intensive care units
IFN Interferon
IL Interleukin
JAK Janus kinase
NLRP3 NLR Family pyrin domain containing 3
NSAIDs Nonsteroidal anti-inflammatory drugs
PNS Peripheral nervous system
SNRIs Serotonin and noradrenaline reuptake inhibitors
SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2
STAT Signal transducer and activator of the transcription
TNF-α Tumour necrosis factor-alpha
Introduction
Fibromyalgia (FM) is a common but intricate illness with unknown etiology. It is classified as neoplastic pain, which arises from the altered function of pain-related sensory pathways in the nervous system, causing increased sensitivity (Fitzcharles et al. 2021). There are many potential triggering factors for FM, such as genetic predisposition, inactivity, obesity, stressful life events, and environmental factors (Häuser et al. 2015; Sarzi-Puttini et al. 2020). The latter includes several infections of viral or bacterial origin that culminate in long febrile disorder, particularly if accompanied by long bed rest (Buskila et al. 2008; Häuser et al. 2015). Although the pathogenesis of FM is not fully understood, it is believed that abnormal host response due to the direct microorganism invasion or immunological process may be implicated in the development and chronicity of pain in chronic fatigue syndromes (Komarov and Lipkin 2021). Besides, physical or mental stress related to infection is also a known factor associated with worsening FM pain (Häuser et al. 2015; Sarzi-Puttini et al. 2020). In light of the above, there is a growing idea that coronavirus disease (COVID) may impact the development or exacerbate FM syndrome.
The global pandemic of COVID-19 has exhibited devastating potential, causing high morbidity and mortality rates worldwide (WHO 2023). Fortunately, due to the recent development of vaccines, the infection and mortality rates have decreased and are better controlled. Patients with COVID-19 experience acute symptoms during the early illness, with acute respiratory distress being the most problematic (Mahmudpour et al. 2020; Krynytska et al. 2021). However, musculoskeletal, neurological, and psychological disturbances might persist after recovery from COVID-19 (Carfì et al. 2020; Huang et al. 2021b; Nalbandian et al. 2021).
Most patients who recovered from COVID-19 carry a burden of sequelae after infection, which impacts their daily quality of life (Nalbandian et al. 2021; Elkan et al. 2021). Thus, it is essential to elucidate better the pandemic's aftermath and COVID-19 on the population. Some studies point out that FM syndrome and other chronic painful conditions might be triggered or exacerbated by COVID-19 or due to the numerous and persistent stressors imposed daily by the pandemic setting (Clauw et al. 2020; Kemp et al. 2020; Attal et al. 2021). Furthermore, the COVID-caused widespread pain and symptoms associated with nervous system sensitization support the hypothesis that the syndrome that appears months after infection resembles features of a neoplastic origin condition (Kosek et al. 2021; Goodman et al. 2021; Fernández-de-las-Peñas et al. 2022).
Based on this, we reported on painful, musculoskeletal, and neurological symptoms caused by COVID-19, mainly in a recovery situation. We also argued the potential consequences of COVID-19 exclusively on FM syndrome, which might include: (i) COVID-19 as a trigger of FM syndrome; (ii) COVID-19 as an enhancer of FM syndrome; (iii) similar mechanisms between FM syndrome and COVID-19; (iv) potential FM treatments for post-COVID syndrome; and (v) therapies to inflammation, given the robust inflammation triggered by the infection. Although our review is quite speculative, our goal is to alert clinicians and researchers about the similarities between post-COVID syndrome and FM symptoms, to better treat this group of patients.
COVID‑19 symptoms and their relation with chronic pain
As the pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) occurs, the number of patients recovered from COVID-19 grows worldwide (WHO 2023). Although many individuals remain asymptomatic throughout the infection of SARS-CoV-2, about 32%–85% of infected patients have a non-severe disease, and 15%–31% face a severe illness (Wiersinga et al. 2020a; Guan et al. 2020; Carfì et al. 2020; Tuzun et al. 2021). Severe illness usually occurs in vulnerable people, leading to a considerable rate of morbidity and mortality (Wiersinga et al. 2020a; Zamorano Cuervo and Grandvaux 2020). The most common clinical manifestations at the onset of illness have included signs of a typical cold, such as sore throat, nasal congestion, rhinorrhea (approx. 7%), dry cough (50%–86%), fever (60%–90%), dyspnoea (approx. 65%) or shortness of breath (53%–80%), anorexia (approx. 30%), and gastrointestinal symptoms (e.g., diarrhea (15%–39%)) (Liguori et al. 2020; Wiersinga et al. 2020a; Wang et al. 2020; Guan et al. 2020; Mao et al. 2020; Landewé et al. 2020; Carfì et al. 2020).
SARS-CoV-2 may also infect skeletal muscle (Disser et al. 2020; Santos et al. 2022), causing musculoskeletal and pain-related symptoms (Mao et al. 2020). Among these symptoms are fatigue (38%–85%), weakness (approx. 25%), mild to moderate body pain resembling a pattern compatible with local or generalized myalgia (15%–68%), arthralgia (15%–55%; primarily notable at the wrist, ankle, and knee joints), chest pain (approx. 40%), back pain (approx. 20%), and abdominal pain (2%–5%) (Liguori et al. 2020; Nalleballe et al. 2020; Wang et al. 2020; Guan et al. 2020; Mao et al. 2020; Landewé et al. 2020; Carfì et al. 2020; Wiersinga et al. 2020b; Rowbotham and Arendt-Nielsen 2021; Kayaaslan et al. 2021). Thus, muscle involvement in COVID-19 appears to be a triangle of myalgia, physical fatigue, and muscle weakness (Tuzun et al. 2021). However, musculoskeletal symptoms do not seem to be associated with the severity of COVID-19 (Schett et al. 2020). They may have a longer duration when compared to other viral infections, being unresponsive to conventional analgesics(Kucuk et al. 2020).
More than one-third of patients with COVID-19 have experienced various neurologic manifestations due to the neuroinvasive potential of SARS-CoV-2 (Josephson and Kamel 2020; Shiers et al. 2020), which has affected both central and peripheral nervous systems (Nalleballe et al. 2020; Mao et al. 2020). Altered mental status, confusion, delirium, dizziness, nausea, vomiting, seizures, and headache (4–45%) were the most common manifestations related to the central nervous system (CNS) (Nalleballe et al. 2020; Mao et al. 2020; Josephson and Kamel 2020; Harapan and Yoo 2021). Neuralgias (e.g., burning pain, numbness, or paraesthesia), polyneuropathy, and sensory problems, such as allodynia (i.e., abnormal tenderness to light touch or pressure) (Nalleballe et al. 2020; Aksan et al. 2020; Gheita et al. 2021), dysgeusia (i.e., taste impairment; approx. 5%) and anosmia (i.e., smell impairment; approx. 5%) were the most frequent symptoms reported by patients and related to the peripheral nervous system (PNS) (Nalleballe et al. 2020; Wiersinga et al. 2020a; Mao et al. 2020; Tancheva et al. 2020; Rowbotham and Arendt-Nielsen 2021). Psychological disturbances were also present from the early phases of the disease. They included sleep impairment, anxiety, mood disorders such as depression, memory problems, suicidal ideation, and post-traumatic stress disorder (Valiuddin et al. 2020; Liguori et al. 2021).
Due to the large portion of the population who have survived COVID-19, there is immense concern about the long-term sequelae. Although we have lived with it for more than three years, the lineup and incidence of long-term or persistent COVID-19-related symptoms are still unclear. Nevertheless, it is believed that people who have been infected with SARS-CoV-2 and recovered carry a burden of sequelae, regardless of their virus immunity (Scherlinger et al. 2021). As time passes, it has been possible to observe that the musculoskeletal, neurological, and psychological disorders that occur during the acute phase of the infection may persist beyond the recovery time. The terminology for this phenomenon is still evolving, and there is no standard clinical terminology, although it is often referred to as a post-COVID-19 syndrome (Fig. 1) (Carfì et al. 2020; Tancheva et al. 2020; Nalbandian et al. 2021; Kayaaslan et al. 2021). In this sense, a high proportion (70–90%) of individuals still complain about at least one symptom after recovery, including fatigue (76%), dyspnea (43.4%), arthralgia (27.3%), chest pain (21.7%), headache (10%), or myalgia (5%–8%) (Carfì et al. 2020; Nasserie et al. 2021; Elkan et al. 2021; Scherlinger et al. 2021; Moghimi et al. 2021; Kayaaslan et al. 2021).
Altered psychological parameters of post-COVID patients have encompassed stress, cognitive dysfunction (67.5%), including memory and concentration impairment (approx. 9%), depression or anxiety (approx. 7%), and sleep impairment and insomnia (29.4%) (Nasserie et al. 2021; Elkan et al. 2021; Moghimi et al. 2021). Furthermore, restraints imposed by lockdown during the pandemic of COVID-19 have altered the social environment where people live and work, contributing to the worsening of these parameters (Varga et al. 2021).
It is clear that COVID-19 is associated with painful symptoms, and even those who face a non-severe disease may require strong analgesics for their pain management (Kemp et al. 2020). In the face of a high-severity pandemic (such as COVID-19), keeping patients alive is of absolute importance, and pain assessment may not be a priority. However, if patients' pain is undertreated and underestimated, it can become chronic and strongly interfere with their post-COVID lives (Kemp et al. 2020; Fernández-de-las-Peñas et al. 2021a, 2023). Although studies report days of hospitalization as a risk factor for the development of postCOVID-19 musculoskeletal pain symptoms (Kemp et al. 2019; Fernández-de-las-Peñas et al. 2021b, a), the chronic pain and persistent poor health after COVID-19 may not necessarily be associated with respiratory complications, initial disease severity, or the need for hospital care (Logue et al. 2021; Townsend et al. 2021). Thus, the health consequences of COVID-19 extend far beyond acute infection, even among those who experience mild illness (Logue et al. 2021).
In this sense, a subset of patients who faced non-severe COVID-19 disease has reported persistent painful symptoms, which included fatigue/muscle weakness (70.6%), trouble with mobility (7%), headaches (68%), and myalgias (55%) (Graham et al. 2021; Nehme et al. 2021; Moghimi et al. 2021). Moreover, it has been shown that painful symptoms might persist for 7–12 months, ranging from one to five complaints (Huang et al. 2021b; Nehme et al. 2021; Fernández-de-las-Peñas et al. 2023). Some symptoms, such as myalgia, arthralgia, and fatigue, appear early in the infection and persist. While other symptoms, such as paraesthesia (60%), burning (43%), and musculoskeletal pain (40%), are rarely reported at the onset of infection but emerge and become prevalent for at least 6–12 months (Scherlinger et al. 2021; Fernández-de-las-Peñas et al. 2023).
The persistence of painful symptoms might also be related to hospital procedures (e.g., routine procedures in the intensive care unit (ICU)) or medications (e.g., antiretroviral drugs, neuromuscular blockers, and corticosteroids) (Kemp et al. 2020; Heesakkers et al. 2022). Furthermore, it is also important to note that the pain may cause rapid and shallow breathing, increasing the respiratory workload and oxygen consumption. In this way, the pain can negatively affect the course of the disease in patients with COVID-19 who have respiratory failure (Pektas et al. 2021). Several studies have reported the persistence of at least one symptom in previously hospitalized patients, which can persist at least 6 (68%) and 12 (49%) months after infection (Huang et al. 2021b; Nasserie et al. 2021).
It is essential to highlight that COVID-19 may not only be related to trigger pain but also exacerbate the pain of patients who live with chronic pain, such as FM. Worsening of pre-existing pain might be associated with COVID-related physical or mental conditions (Clauw et al. 2020), social threats, discontinuation of therapy or reduced access to treatments, and hospitalization (Attal et al. 2021; Fernándezde-las-Peñas et al. 2023). Indeed, the patients living with chronic pain infected by COVID-19 reported that no new symptoms appeared, but clearly, their painful symptoms (e.g., intensity, duration, location, or frequency) worsened after hospitalization (Fernández-de-las-Peñas et al. 2023). Likewise, patients with chronic neuropathic pain exposed to SARS-CoV-2 appear to exacerbate their pain and deteriorate their neurological condition (Attal et al. 2021). Based on these data, we hypothesize that COVID-19 can also exacerbate symptoms of FM syndrome.
During the pandemic, people not infected with COVID-19 were also impacted. Evidence supports that painful symptoms can have been triggered or exacerbated during the worldwide lockdown, probably associated with emotional and social factors (such as fear, catastrophism, social alarm, and posttraumatic stress disorder) (Clauw et al. 2020; Karos et al. 2020; Meulders et al. 2022). Persistent and excessive stress can also lead to severe mental health consequences, triggering anxiety, depression, and sleep disorders, which are comorbidities frequently reported in chronic pain states (Choy 2015; Clauw et al. 2020; Karos et al. 2020).
Remarkably, the COVID-19 pandemic or the aftermath of restraints imposed by the lockdown during the pandemic could potentially increase the prevalence of chronic pain after a SARS-CoV-2 infection (Clauw et al. 2020). The widespread pain and symptoms associated with nervous system sensitization support the hypothesis that post-COVID syndrome resembles features of a neoplastic condition (Kosek et al. 2021; Goodman et al. 2021; Fernández-delas-Peñas et al. 2023). Thus, our concern is mainly given to FM syndrome, a chronic pain condition of neoplastic origin. These approaches make us wonder: could the FM syndrome be impacted by COVID-19? To clarify this hypothesis, we focused our review on how symptoms of FM could be triggered or exacerbated by SARS-CoV-2.
Could fibromyalgia syndrome be impacted by COVID‑19?
Fibromyalgia syndrome
FM is classified as chronic primary pain, considered the third most frequent musculoskeletal condition, affecting 2–3% of the world population (Treede et al. 2019; Sarzi-Puttini et al. 2020). This condition is characterized by polysymptomatology once it results from the interplay between many predisposing, triggering, and sustaining factors (Häuser et al. 2015; Sarzi-Puttini et al. 2020). Thus, the term FM includes a pathway of multiple somatic, psychological, and social contributions, and consequently, the severity and complaints of FM vary from patient to patient (Sarzi-Puttini et al. 2020).
The clinical manifestations of FM are mainly characterized by pain, fatigue, and sleep disturbances, which are currently considered diagnostic criteria (Häuser et al. 2015, 2017; Sarzi-Puttini et al. 2020). Patients with FM present with chronic widespread pain with a variable anatomical location that affects the entire body (Häuser et al. 2017; Sarzi-Puttini et al. 2020), spontaneous pain in the muscles or joints (Napadow et al. 2010), headache (Littlejohn and Guymer 2018), and a variety of sensory symptoms (Clauw 2014; Larson et al. 2014; Littlejohn and Guymer 2018). Furthermore, chronic widespread pain is the unanimous complaint among patients with FM, and fatigue is achieved by 70% of patients (Choy 2015). This fatigue might be physical or mental, varying from mild to severe tiredness (SarziPuttini et al. 2020), morning stiffness (Häuser et al. 2015), muscle pain and weakness (Park et al. 2000), or restricted gait (Littlejohn and Guymer 2018). Sleep problems are also preponderant in patients with FM since approximately 90% of patients have insomnia or frequent awakenings (SarziPuttini et al. 2020). Although the quality and duration of sleep are sometimes unchanged, patients with FM often report insufficient rest (Choy 2015; Sarzi-Puttini et al. 2020).
Patients with FM often present with other clinical symptoms non-pain-related (Choy 2015; Häuser et al. 2015; Sarzi-Puttini et al. 2020) that include cognitive dysfunction, mostly concentration problems or memory deficits (SarziPuttini et al. 2020), anxiety (60%) or mood disturbances, such as depression (14–36%) (Choy 2015; Sarzi-Puttini et al. 2020), and variable gastrointestinal symptoms (Clauw 2015). Moreover, most symptoms of FM can be aggravated by physical or mental stress during the syndrome (Häuser et al. 2017), which leaves us intrigued if a pandemic situation could trigger or exacerbate the FM symptoms.
The FM pathophysiology is not fully understood, although it covers several pathological characteristics. The CNS plays a critical role in FM symptomatology, once altered pain processing (termed central sensitization henceforth), dysfunctional descending pain modulation, and structural and functional changes in the brain (Choy 2015; Häuser et al. 2015). However, FM has been also associated with abnormalities in peripheral systems. At least in a subset of patients with FM, the inflammatory process has been demonstrated, with altered levels of inflammatory and immunoregulatory cytokines, neuropeptides release, and neurogenic inflammation (Littlejohn 2015; Littlejohn and Guymer 2018), inflammatory cells increase (Theoharides et al. 2019), and NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activation (Cordero et al. 2014). Additionally, mitochondrial dysfunction has been observed in the blood, muscle, and skin biopsies of some patients with FM (Cordero et al. 2012b; Scherlinger et al. 2021). The imbalance of nutritional components, such as essential minerals and vitamins, also might play a critical role in FM (Bjørklund et al. 2018).
Even though several other mechanisms besides those punctuated here had been related to the pathophysiology of FM, we highlighted only the similar pathophysiological features between COVID-19 and FM. We focus on mechanisms that can help explain the development of similar symptomatology between these two conditions.
Could fibromyalgia syndrome be triggered by COVID‑19?
The persistent symptoms post-COVID are becoming increasingly apparent over time and are known as post-COVID syndrome (Carfì et al. 2020; Nalbandian et al. 2021). Similarities between post-COVID syndrome and FM syndrome raise the hypothesis that SARS-CoV-2 infection could trigger the development of FM once potential environmental factors generate it (Häuser et al. 2015; SarziPuttini et al. 2020). Indeed, at least 30% of patients identify a preceding physical or psychological trigger of their syndrome (Fitzcharles et al. 2021). Some viral infections have been linked to the development of FM, including infection induced by the hepatitis C virus, human immunodeficiency virus (HIV), parvovirus, or Epstein–Barr virus (Buskila et al. 2008). The observation that such infectious agents are associated with FM syndrome suggests that abnormal host response to infection may be implicated (Komarov and Lipkin 2021). Thus, the hypothesis that SARS-CoV-2 and its sequelae might play a role in the development of FM is encouraged.
Of note, clinical features of the FM syndrome, such as musculoskeletal pain, fatigue, sleep impairment, depression, and anxiety have been reported in one-third of patients with symptoms of the post-COVID syndrome (as presented in Table 1) (Sarzi-Puttini et al. 2020; Nalbandian et al. 2021; Fernández-de-las-Peñas et al. 2023). Based on this, web-centred research uncovered more than 600 patients who developed post-COVID syndrome (Ursini et al. 2021). Of them, about 30% of patients met the 2011 American College of Rheumatology (ACR) criteria for diagnosis of FM (Wolfe et al. 2010) at a mean of 6 months after their recovery from COVID-19. Therefore, they were referred to as post-COVID FM (Ursini et al. 2021).
The comorbidity of obesity and male gender also seem to be risk factors for developing the post-COVID FM-like syndrome in this subgroup of interviewed patients (Ursini et al. 2021). The authors have suggested that patients who developed severe COVID-19 (with hospital admission and oxygen therapy need) are more suggestive of developing a post-COVID FM-like syndrome (Ursini et al. 2021). However, in another study, 56.7% of patients (17/30) who showed mild and moderate symptoms during COVID-19 were positive for FM-like symptoms 6 months after the infection (Scherlinger et al. 2021). Thus, the severity of the symptoms during the disease course seems not to be an essential factor for developing a post-COVID FM-like syndrome.
Strikingly, one case report published in April 2021 also demonstrated the strong relationship between FM symptoms and post-COVID syndrome (Gheita et al. 2021). Three female patients with no previous history of FM or any other rheumatic disease complained of persistent symptoms after recovery from COVID-19, such as generalized musculoskeletal pain, allodynia, fatigue, anxiety, depression, paraesthesia, and non-restorative sleep. General examination and several laboratory investigations, including an autoimmune profile and radiological investigation, were all normal. However, all women met the 2010 ACR criteria for a diagnosis of FM (Wolfe et al. 2010; Gheita et al. 2021). The standard clinical treatments of FM, including non-pharmacological and pharmacological management, were prescribed to them, such as physical exercise and therapies approved by the Food and Drug Administration (FDA), including duloxetine ((serotonin and norepinephrine reuptake inhibitor (SNRI)) and gabapentin (gabapentinoid). All women reported improved well-being and mood after the onset of treatment, which contributed to confirming the diagnosis of a post-COVID FM-like syndrome (Gheita et al. 2021).
Another case published in 2020 reported a woman diagnosed with COVID-19 without a history of any previous painful condition but with some associated comorbidities (Aksan et al. 2020). The patient presented with pain symptoms very similar to the complaints reported by patients with FM (Häuser et al. 2017), which included: (i) constant neck and back pain (resembling generalized pain), (ii) a burning quality (resembling a neuropathic-like FM pain), which was (iii) exacerbated by light touch and heat (resembling mechanical and thermal hypersensitivity). This patient presented with bilateral and generalized pain, which was not a pattern for viral neuropathic pain. Furthermore, the onset of the pain coincided with her SARS-CoV-2 infection, and there was no other likely explanation for the symptoms. Sleep problems, which are observed in many patients with FM, were also reported. The patient's treatment with acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs), and opioids did not alleviate her pain. It makes us hypothesize that this patient was going through a post-COVID FM-like syndrome once these usual treatment approaches are ineffective for patients with FM. On the other hand, gabapentinoids, a class of drugs recommended for the treatment of FM, attenuated the painful hypersensitivity and improved the sleep quality of this patient.
The studies published so far speculate that the development of FM might be occasioned in a subgroup of patients after SARS-CoV-2 infection (Gheita et al. 2021; Ursini et al. 2021). However, it is currently unknown what factors contribute to it. Potential processes have been suggested for the pathophysiology of post-COVID syndrome (Nalbandian et al. 2021). These processes might also be linked to the development of FM syndrome after the viral infection. Substantial mechanisms that may contribute to the trigger of an FM-like syndrome after COVID-19 are: (i) pathophysiologic changes caused by SARS-CoV-2 itself, mainly neuropsychiatric sequelae such as chronic malaise, diffuse myalgia, depressive and anxiety symptoms, non-restorative sleep, and cognitive impairment (Abdullahi et al. 2020; Nalbandian et al. 2021) and (ii) SARS-CoV-2 cell-to-cell inflammatory mechanisms (ie, cytokine storms) which might provoke hyperexcitability of PNS and CNS (Fernández-de-las-Peñas et al. 2023). Furthermore, the (iii) sequelae of post-critical illness are indirect processes responsible for worsening the physical, cognitive, and psychiatric domains after COVID-19. They can be caused by posttraumatic stress disorder, prolonged bed rest, ICU admission, and the necessity of sedation and ventilation (Häuser et al. 2015; Inoue et al. 2019; Hosey and Needham 2020; Heesakkers et al. 2022).
The co-existence of comorbidities or immunosuppressive diseases is a known factor for anticipating or developing chronic pain (Clauw et al. 2020; Kemp et al. 2020) and increasing severity and mortality related to COVID-19 (Nalbandian et al. 2021). Thus, it can also be suggested that the presence of these parameters might support the advancement of FM-like symptoms after COVID-19 (Nalbandian et al. 2021). However, more studies are necessary to understand the direct and indirect mechanisms of the pathophysiology of the FM-like syndrome triggered after COVID-19.
Although the long-term effects of the post-COVID syndrome and its similarity with FM syndrome remain actively debated, acknowledging the post-COVID FM-like syndrome is still a challenge. Moghimi et al. (2021), for example, proposed a diagnostic criterion for the neurological post-acute sequelae of SARS-CoV-2 infection. Among the proposed criteria, 60% of them (25 of 42 reported symptoms) match the criteria for FM diagnosis. The early recognition of the development of an FM-like syndrome after COVID-19 could lead to prompt and targeted treatment and, thus, mitigate the potential impact of chronic pain on health and the social environment.
