The emergence of SARS-CoV-2 has profoundly impacted global society and various aspects of
human life. While the pandemic has resulted in disruptions and challenges, it has also accelerated
scientific research on viruses and immunology, leading to remarkable progress in vaccine technology and
immunization strategies. This review examines the impact of SARS-CoV-2 on pre-existing neuromuscular
disorders, and neuromuscular events following SARS-CoV-2 infection, including immune-mediated and
critical illness status-related disorders. Furthermore, the review discusses the relationship between SARSCoV-
2 vaccination and neuromuscular complications. The findings highlight the need for further research
and understanding to improve patient outcomes.

The emergence of SARS-CoV-2 over the past three years has undeniably reshaped the global landscape and profoundly affected various aspects of human life. The consequential measures, such as social distancing and restriction lockdown, have disrupted daily routines and prompted a significant societal shift. Nevertheless, amidst these challenging circumstances, the pandemic accelerates scientific research on viruses and immunology. Moreover, the urgency to develop effective vaccines against SARS- CoV-2 has propelled remarkable progress in vaccine technology and immunization strategies. The unexpected benefits arising from the global ordeal with SARS-CoV-2 should not be overlooked. This review focused on the impact of SARS-CoV-2 and vaccines against SARS- CoV-2 on neuromuscular disorders. 

The temporal relationship between neuromuscular disorders and SARS-CoV-2 infection can be described in three patterns. Firstly, in a pre-existing neuromuscular disorder, SARS- Co V-2 infection may trigger an exacerbation during the course(1,2). Secondly, a monophasic neuromuscular disorder can appear in a naïve individual, such as Guillain Barré syndrome (GBS), immune-mediated myositis, critical illness polyneuropathy (CIP), or critical illness myopathy (CIM). Thirdly, a new neuromuscular disorder appears in a susceptible individual or a subclinical disorder has accelerated to a clinical status.

The impact of SARS-CoV-2 in patients with existing neuromuscular disorders

Patients with neuromuscular disorders comprised a group of rare diseases, most often of genetic or autoimmune origin. They are considered at a high risk of developing severe complications with SARS-CoV-2 as they can be under immune therapy or subject to cardiac   or respiratory insufficiency. In the early pandemic, French Health Care Network for Rare Neuromuscular Diseases published a prevalence of symptomatic SARS-CoV-2 estimated at 0.0017(2). The hospitalization rate in medical and intensive care units (ICU) was 0.27 and 0.14. SARS- CoV-2 caused worsening symptoms and death in 31% and 11% of this group of patients. Among the 58% of infected patients who received home care, SARS-CoV-2 showed no impact on their neuromuscular disorders. The risk factors for worse outcomes in SARS-CoV-2 infection included comorbid hypertension, diabetes, and severe disease status before the infection, which were identical to that of general populations(3,4).

To particularly consider the effects of immune therapy, myasthenia gravis (MG) might be at a greater risk of worse outcomes than otherwise healthy people because of an immunocompromised state related to immunotherapy and possible respiratory and bulbar muscular weakness. However, discontinuing immunotherapy increases the risk of relapse as well. Although the SARS-CoV-2 infection rate in MG patients was equivalent to that of the general population(5), infection is a well-known trigger of symptom exacerbation for MG. The need for data to answer the critical question was quickly recognized, and a registry was created to capture high-quality information on SARS- CoV-2 Associated Risks and Effects in Myasthenia Gravis (CARE-MG). The preliminary data by December 2020 showed that worsening MG requiring rescue therapy (e.g., intravenous immunoglobulin, plasma exchange, or steroids) in the setting of SARS-CoV-2 was reported in 40% of patients. Complete recovery or discharge to home was reported in 43% of patients, whereas 24% of patients died due to SARS-CoV-2(6). Subsequent retrospective studies and systematic reviews suggested that SARS-CoV- 2-infected MG patients were frequently hospitalized and had a higher mortality rate than the general population with SARS-CoV-2(7-11). In addition, patients with a pre- existing diagnosis of MG who were hospitalized for SARS-CoV-2 infection had severe disease courses(12). However, there are systematic reviews that disapprove this notion(13).

Monophasic neuromuscular event after SARS-CoV-2 infection

The neuromuscular manifestations after SARS-CoV-2 infection are commonly mentioned in patients without neuromuscular disorders(14). In a prospective multicenter observational study that included 4491 hospitalized severe SARS-CoV-2 infected patients, the prevalence of neuropathy and myopathy is around 0.8% and 0.5%. Many of the cases of neuropathy and myopathy were attributed to critical illness. Furthermore, there was a significant association between the severity of illness markers (intubation, SOFA scores, acute renal failure) and the occurrence of neurologic disorders, suggesting that critical illness itself may have contributed to neurologic complications(14).

Neuromuscular events not attributed to the critical illness status also can be found in this pandemic, such  as newly developed MG provoked by SARS-CoV-2 infection(15-17), GBS after infection(17-24), and myositis concurrently or subsequently to the SARS-CoV-2 infection(25-28).

Immune-mediated monophasic event: focusing on myopathy

Muscular symptoms are commonly seen in viral infections, such as influenza, coxsackie virus B, Epstein-Barr virus (EBV), and coronal virus(29,30). In several pandemic coronavirus events, including SARS- CoV-1, Middle East respiratory syndrome coronavirus (MERS), and the recent SARS-CoV-2 pandemic, various proportions of patients (ranging from 30%-70%) reported muscular symptoms, including myalgia and weakness(31-35). In 2003, there was an outbreak of SARS-CoV-1 in Hong Kong and Taiwan(36). The report from Hong Kong showed that creatine kinase (CK) levels and lactate dehydrogenase (LDH) were elevated in 32.1% and 71% of patients, respectively. None of the patients with elevated CK levels had abnormal values for CK-MB or troponin T, indicating that the source of CK was unlikely to be cardiac muscle(36). A postmortem case series showed focal myofiber necrosis with macrophage infiltration.

Regenerative fibers were scanty. In situ hybridization, viral cultures, and examination for viral particles under electron microscopy (EM) revealed negative results(37). The authors suggested that focal myofiber necrosis is possibly immune-mediated. However, because of the lack of staining for major histocompatibility complex-1 (MHC-I) or myxovirus resistance protein A (MxA), and the small case numbers of muscle pathology, the report could not conclude pathomechanism of SARS-related myopathy. Critical illness myopathy and superimposed steroid myopathy may also play an important role in SARS-CoV-1.

MERS outbroke ten years ago. The muscle pathology in the postmortem study showed atrophic and myopathic myofibre changes, splitting of the muscle fibers, and lymphohistiocytic inflammatory infiltration consisting of CD68+ macrophages, CD4+, and CD8+ lymphocytes. The numbers of inflammatory cells were more abundant  in atrophic myofibres. Ultrastructural EM study identified MERS-CoV particles in macrophages infiltrating the muscle but not in the muscle fibers(38).

In this SARS-CoV-2 pandemic, a cross-sectional study analyzed 73435 infected patients and found an increased hazard ratio and excess burden in muscle weakness(39). Early studies suggested that roughly 30% - 60% of infected patients experienced myalgia(40-43), and the combination of myalgia and increased levels of CK was more pronounced in critically ill patients demanding intensive care support than in mildly affected individuals (44-46) and was associated with higher mortality rates(46,47).

The possibility that the virus invades skeletal muscle has been considered because muscle expresses angiotensin-converting enzyme 2, a cell surface receptor utilized by SARS-CoV-1 and SARS-CoV-2 for host cell entry(48). In one study that examined the diaphragm muscle obtained from 26 consecutive autopsies of critically ill COVID-19–infected patients who died, SARS-CoV-2 RNA was found in the muscle in 4 cases (15.4%)(49). At the same time, several case reports included biopsies that advocated a dermatomyositis-like phenotype(27,50-52).  A negative SARS-CoV-2 IHC staining in muscle was reported in two independent postmortem studies which argued against this hypothesis(41,53). In these two histopathology studies, patients with myositis had CD68+, CD4+, and/or CD8+ histiocytes and T cells in the muscles.

Upregulated MHC-1 in the early phase of the disease of non-necrotic/non-regenerating muscle fibers was evident in all patients with myositis or necrotizing myopathy. Concomitant upregulation of MHC-II on myofibers in later stages indicated the involvement of skeletal muscle in the immune response against SARS-CoV-2. Type 2 fiber atrophy was observed in all patients. Compared with cardiac muscle, inflammatory changes were more pronounced in skeletal muscles than in cardiac muscles. Abnormal MxA immunostaining was presented in the capillaries, indicating a type I interferon signature, rather than sarcolemma. In all cases, IHC stainings for SARS- CoV-2 nucleocapsid and antibodies against SARS-CoV-2 spike protein were negative. No viral particles were found by EM.

Critical illness status-related monophasic event

Patients with SARS-CoV-2 infection who develop severe respiratory failure, need ventilation assistance, experience prolonged ICU stay, and suffer from long-term immobility tend to develop CIP or CIM(42,54,55). According to the PANDEMIC registry in Germany, 20% of SARS- COV-2-positive ICU patients developed neuromuscular disorders(56). CIP/CIM accounted for 86.25% of all neuromuscular disorders(56). Although the mortality rate was 50% of intubated patients with CIP/CIM(43), CIP/CIM had the lowest influence on mortality (OR: 0.21, 95% CI 0.08-0.58) compared to acute ischemic stroke (OR: 3.89, 95% CI 1.85-8.17)(56).

The development of CIP/CIM in patients with SARS- CoV-2 is multifactorial(44-46). The characteristic finding in CIM is the loss of myosin, the motor protein responsible for initiating muscle contraction(57,58). Myosin is especially vulnerable to high-dose corticosteroids. Contrary to CIM, decreased levels of local axonal survival factors, increased vascular permeability, and voltage-gated sodium channel dysfunction(59) can finally result in CIP(60). Although evidence of direct SARS-CoV-2 invasion to the skeletal muscle is inconclusive(49,51,61,62), an indirect inflammatory process combined with patients’ comorbidities, high- dose steroids, and use of neuromuscular blocking agents appears to be a more plausible explanation(63).

Another study in Italy included 44 patients diagnosed with acute respiratory distress syndrome (ARDS) (23 patients were SARS-CoV-2 positive)(64). The mortality rate was 33% in the entire CIP/CIM cohort, regardless of the SARS-CoV-2 status(64). CIP/CIM was diagnosed in 65% of SARS-CoV-2-positive patients and 71% of SARS- CoV-2-negative patients(64). The comorbidities, CK levels, LDH levels, length of ICU stay, and the outcome at ICU discharge between the groups with or without SARS- CoV-2 were not statistically different(64). Therefore, early recognition of CIP/CIM followed by an individualized management strategy is essential to improve ICU discharge outcomes(65-67).

Newly developed chronic neuromuscular disorders after SARS-CoV-2 infection

Jacob et al. summarized the influence of clinically major viruses on different kinds of neuromuscular disorders. In the acute setting, most of the virus families are found to be associated with GBS(68). In the chronic status, SARS-CoV-2 and influenza viruses are closely linked to myopathic conditions. SARS- CoV-2 virus, Zika virus, and West Nile virus also share similar associations with MG(68). For the rest of the viruses, chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is associated with EBV and Hepatitis B virus. Motor neuron disorders are related to the human immunodeficiency virus, human T-lymphotropic virus, enteroviruses, and Coxsackievirus B3 virus(68). In line with the hypothesis of autoimmunity secondary to viral infection, newly developed chronic neuromuscular disorders will become an important issue for neuromuscular specialists.

SARS-CoV-2 Vaccinations and neuromuscular disorders

Thanks to the emergence of SARS-CoV-2, vaccines have been developed rapidly, leading to a swift accumulation of information regarding neuromuscular complications associated with vaccination. The most common neuromuscular disorders, GBS, brachial neuritis (BN), and MG, are summarized below.

Guillain-Barré syndrome

GBS is one of the most common neurological complications following SARS-CoV-2 vaccines. However, the incidence of SARS-CoV-2 vaccine-induced GBS is smaller than GBS in general (0.81 to 1.91 cases per 100,000 person-years)(69-72). In addition, SARS-CoV-2 vaccine-induced GBS is less frequent than SARS-CoV-2 infection-induced GBS(73-76). Compared with influenza vaccines, SARS-CoV-2 vaccines appeared to have fewer cases of neurological complications, including GBS(77). A retrospective study in the United States demonstrated that the GBS reporting rate was 3.29 per one million doses in Ad26.COV.2.S (Janssen), 0.29 in BNT162b2 (Pfizer- BioNTech), and 0.35 in mRNA-1273 (Moderna)(78). In Mexico, the overall incidence was 1.19 per one million doses, in which the incidence was 3.86 per one million doses in Ad26.COV2-S and 1.92 in BNT162b2(79). In the United Kingdom, the prospective surveillance study showed that 67 out of 70 patients with vaccine-induced GBS had received ChAdOx1 (Oxford-AstraZeneca), while the remaining three patients had received BNT162b2(80).   A case of ChAdOx1-induced GBS was also reported in a Taiwanese study(81). In South Korea, the prospective study showed overall incidence was 1.42 per million doses, in which the incidence of GBS was 4.49 per million doses from vector-based vaccines and 0.80 from mRNA-based vaccines(82). Based on the aforementioned studies, mRNA- based vaccines were least likely to induce GBS. Recurrent GBS due to vaccine is rare, and the exact incidence related to the SARS-CoV-2 vaccine remains uncertain(83-86).

Among the SARS-CoV-2 vaccination-related GBS, sensorimotor and pure motor variants were the most common clinical presentations, followed by cranial nerve involvement, paraparesis, and Miller-Fisher syndrome(78-80,82,87-89). Demyelination was the predominant electrodiagnostic finding(79,80,82,90,91). The presence of antiganglioside antibodies was extremely rare(74,80,82). About 13% to 30% of vaccine-induced GBS required mechanical ventilation(79,82,92), and the mortality rate ranged from 2% to 9%(80,82,91,93). Most patients responded to the conventional treatment, but the total recovery rate was generally low(79,80,92,94,95).

Brachial neuritis

The clinical presentation of BN, also known as neuralgic amyotrophy or Parsonage-Turner syndrome, is the sudden onset of severe unilateral pain over the shoulder girdle followed by weakness and muscle atrophy in the following weeks(96). Hypoesthesia or paresthesia is usually present over the involved nerves(96). Several cases of BN have been reported after receiving vaccinations against SARS-CoV-2(97-115). BN was more likely to develop in patients who received mRNA-based vaccines than adenovirus vector-based vaccines, and the risk was similar to those who received the influenza vaccine(97,98,116). The time from the vaccination to symptom onset varies greatly, but two weeks on average, regardless of the vaccine type(97,98,100,103,104). BN mostly occurs at the location where patients received the injection(97,102). Some studies observed that patients with BN may have enhancement of brachial plexus and/or cervical lymphadenopathy on the Magnetic Resonance Imaging study(97,110,112-114,116). Prior study revealed that complete remission of BN was roughly 60% in one year and up to 90% in three years(117,118). Twenty- five percent of SARS-CoV-2 vaccine-induced BN had remission within two months(97).

Myasthenia gravis

Pre-existing MG with SARS-CoV-2 vaccines

Vaccinated MG patients were less likely to have COVID-19 infection (hazard ratio, 0.43; 95% CI 0.30 – 0.60)(119). Overall, SARS-CoV-2 vaccines are safe for MG patients(120). The exacerbations of MG due to vaccination were reported. In a cohort of 113 MG patients who received three doses of the BioNTech SARS-CoV-2 vaccine in Italy, only 8 (7.1%) had an exacerbation(121).  In another cohort of 160 MG patients in Israel, 150 MG patients had received BNT162b2 mRNA vaccines, and 8 (5.3%) had confirmed exacerbation after vaccination(122). Among them, the exacerbation occurred mostly after the second dose (53.8%), and the time from vaccination to symptom onset varied greatly (0.5 to 30 days)(122). In a cohort with 343 MG patients in Japan, only 3 (0.87%) patients reported exacerbation(123).

MG-related immunotherapies and SARS-CoV-2 vaccines

Immunosuppressive therapies may interfere with the effect of SARS-CoV-2 vaccines, especially for cell- depleting agents. Spike-IgG positivity was seen in 88.77% of patients after vaccination(124). However, patients receiving combined therapy had a lower seroconversion ratio and T-cell responses(124-127). In two case reports when one patient receiving mycophenolate and prednisolone and the other one receiving mycophenolate, eculizumab, and prednisolone, both patients had undetectable SARS- CoV-2 antibody levels after two doses of vaccines(128,129). Temporarily discontinuing mycophenolate or eculizumab before the next dose increased the efficacy of vaccines(128-130). In a small prospective study, Damato et al. observed that spike-IgG seroconversion only occurred in one of three patients with rituximab therapy after SARS- CoV-2 vaccination(131).

New onset MG and SARS-CoV-2 vaccines

Case reports on the new onset MG associated with SARS-CoV-2 vaccination have increased since 2020(132- 146). In these reports, 83% of the patients were male, and 58% were > 60 years old at onset (ranging from 28  to  91 years old). The median time of symptom onset was six days (ranging from 1 to 28 days). Among all vaccine types, 50% received BNT162b2, 29% with AstraZeneca, 17% with mRNA1273, and 4% with Covishield vaccines. Most patients (54%) had initial symptoms after the first dose of the vaccine. The distribution of ocular type MG and generalized type MG was both 42%, followed by oculo-bulbar type (16%). These findings were comparable to a literature review conducted by Virgilio et al(136). The exact causality between SARS-CoV-2 vaccination and MG is still under debate(147). A plausible explanation may be the combination of molecular mimicry between the acetylcholine receptor and vaccine antigen and the bystander effect from T-cell activation(146). Although these patients were responsive to standard treatment, whether this new onset MG follows similar long-term clinical courses will be an interesting topic in the post-COVID-19 era.

CONCLUSION

In individuals with neuromuscular disorders, the infection can trigger exacerbation in pre-existing conditions, particularly in patients with MG who are immunocompromised related to immunotherapy and possible respiratory and bulbar muscular weakness. The outcome severity depends on comorbidities and disease status before the infection. The SARS-CoV-2 infection also leads to immune-mediated neuromuscular events such as GBS and myositis. SARS-CoV-2-related myositis is currently thought of as a type I interferon-mediated myopathy. The incidence of CIP/CIM in SARS-CoV-2- positive patients who had ARDS was similar to patients with ARDS secondary to other causes. Moreover, SARS- CoV-2 may cause the development of new neuromuscular disorders in susceptible individuals which warrants more research on the subsequent clinical course.

Regarding the association between SARS-CoV-2 vaccinations and neuromuscular complications, the incidence of vaccine-induced GBS is lower than SARS- CoV-2-related GBS. The incidence of SARS-CoV-2 vaccine-induced BN is also lower than BN indued by influenza vaccine. Overall, this review underscores the importance of ongoing scientific investigation and clinical management to optimize outcomes for patients with neuromuscular disorders in the context of SARS-CoV-2.

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