Biography
Interests
Ghaydaa Shehata, A.
Department of Neurology and Psychiatry, Assuit University Hospitals, Assuit, Egypt
*Correspondence to: Dr. Ghaydaa Shehata, A., Department of Neurology and Psychiatry, Assuit University Hospitals, Assuit, Egypt.
Copyright © 2020 Dr. Ghaydaa Shehata, A. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
A New detected virus called COVID-19 reported by World Health Organization (WHO) as
pandemic at March 2020 COVID-19 is affected mainly by respiratory illness, but it can also affect
the brain. Neurological manifestations are recorded COVID-19 pandemics but are not effectively
addressed how to deal and treat them.
In this review, I try to discuss the postulated neuronal mechanisms of the coronavirus infection
sequelae. After made midlines about this topic, I discuss prevalence, pathogenesis, and then put a
proposal on how to deal with muscle disease, neuromuscular junctions’ disorders.
This review aims to educate and update the neurologists and health team who work with patients with muscle and neuromuscular junctions’ disease among suspected cases of COVID-19 about the
possible neurological presentations.
Introduction
At the end of 2019, at Wuhan, China new strain virus of CORONA group spread all over the world called
COVID-19 [1,2]. This virus mainly affected respiratory system. However, about 36.4% (78/214) of patients
with COVID-19 developed many neurological symptoms [3]. The affection of CNS occurred in severe cases
rather than mild or moderate [4-9]. In general for more studies and researches in the past decades revealed
coronaviruses had capacity to go beyond the respiratory system to enter the nervous system and establish
persistent brain damage [4-9].
My aim in this review is to update according to my knowledge, the neurologists working with suspected cases of COVID-19 or with patents without respiratory symptoms about the possible muscle or neuromuscular. Also, I try to put a proposal to how to deal and treat patients with neurological disorders and COVID-19.
I searched Medline, Egyptian Knowledge Bank, Scopus, Elsevier, PubMed, and Google Scholar. I collected
data published between Jan 1, 2019, and June 25, 2020, using keywords ‘‘COVID-19”, ‘‘Coronavirus”,
‘‘pandemic”, ‘‘SARS COV-2”, management’s strategy of neurological ‘‘neurology”, ‘‘neurological”, “muscle
disease” myasthenia gravis” myositis” myalgia. My Search limited only to the English language.
How COVID-19 Affect Muscle and Neuromuscular
As previously known, Coronaviruses are not invading neurons primary. They invade respiratory epithelium
first [3]. Then they invade CNS by a different mechanism. The coronaviruses invaded the nervous system
either by direct or indirect pathways. In addition, it has a chronic phase in the affection of CNS. Affection
of muscles and neuromuscular occur from indirect and chronic pathways.
Prevalence of Neurological Disorders With COVID-19
One large study involved 214 confirmed COVID-19 cases. It revealed (36.4%) had neurological
manifestations, including (24.8%) with the central nervous system (CNS)and (8.9%) with the peripheral
nervous system (PNS). Also, (10.7%) with skeletal muscle affections, gustatory [5,14-17].
In a large study in china, fatigue occurred in 26%-51% of patients with COVID-19 in China, 36% of them had myalgia and increased creatine kinase (CK) was present in 33% of patients [18,19]. Myositis and rhabodomyolysis occurred In the last era of MERSA and SARS Viral affection [4,18].
How to Deal With Some Neurological Disorders During Pandemic
Delly et al., reported the first known case of myasthenia gravis (MG )crises with COVID-19 [20]. Viral
infections in general include Coronavirus have been reported to affect upon autoimmunity through
augmentation of T cell signaling causing a pro-inflammatory environment due to a hyper-reactive antiviral
immune response. Also, epitope spreading and also fever has an effect on neuromuscular junction function
[21]. The scientists suggest the shared component between COVID-19 and MG crises are dysregulation
of cytokine which promotes the increase of pro-inflammatory cytokines and chemokines that attack organ
systems, particularly the lungs which can result in ARDS [20-22].
In trial to put protocol Guidance for the management of myasthenia gravis (MG) and Lambert-Eaton myasthenic syndrome (LEMS) during the COVID-19 pandemic, we studied different reports and different case reports [20,21,23-26] to conclude the following:
1. The MG expert pane suggests that decisions to manage every patient should be individualized according
to the severity of illness and liability to get infections with COVID-19
2. More protections with extraordinary measures should be taken by the patients and their families as more
distance, postpone blood tests if not necessary and used telemedicine and social applications for routine
follow up.
3. MG/LEMS patients should take their treatment as there is no scientific evidence to suggest that
Pyridostigmine or 3,4 Diaminopyridine increases the risk of infection
4. MG on immunosuppressive therapy should not stop it as that carries a potential for increased disease
activity and/or MG exacerbation or crisis.
5. It is currently no evidence to suggest that the intravenous immunoglobulin (IVIG) or therapeutic plasma
exchange (PLEX or TPE) increase the risk of getting infected with COVID-19? In which, IVIG uses
pooled normal IgG that works through numerous mechanisms, which include: blocking both cytokine production and pathologically activated the differentiation of Th1, Th17, and Tfh subsets, overwhelming
the neonatal Fc receptor which in turn causes a reduction in endogenous and exogenous IgG leading to
reduction of AChR antibodies, neutralization of autoantibodies by anti-idiotypic antibodies and inhibition
of complement activation.
6. Hydroxychloroquine is reported to worsen MG as the combined use of hydroxychloroquine and
azithromycin, a macrolide that aggravates MG, may have caused the worsening of MG, which may lead to
the use an additional dose of IVIG.
7. However, the doctor should take care from the potential complication of IVIG is thrombosis and widespread
thrombosis has also been reported in critically ill COVID-19 patients. Therefore, careful administration of
IVIG is required in MG patients.
8. Delay initiation a B-cell depleting therapy4 (e.g., rituximab) as increasing the risk of worsening myasthenia
or crisis and the risk of contracting the viral infection, until the peak of the outbreak is over.
Fatigue occurred in 26%-51% of patients with COVID-19 in China [27], 36% had myalgia and elevated
creatine kinase (CK) found in 33% of patients. There are no reports of EMG or muscle biopsy. Myositis
due to virus infections reported during MERS [28] and SARS [29]. Also, myositis reported in patients with
acute renal failure during SARS, and two reports of muscle involved during COVID [27,30]. Neuromuscular
complications that may be directly or indirectly related to coronavirus infection include Risk of infection -
causing a new myositis or critical illness myopathy.
In addition, the risk of exacerbating to unmasking previously unrecognized MG, myositis, muscular dystrophies, congenital myopathies, mitochondrial myopathies, metabolic myopathies. The risk of COVID-19 affection increased with the usage of immunosuppressant/immunomodulating therapies in patients with autoimmune neuromuscular disorders. Hydroxychloroquine and chloroquine can cause toxic neuropathy and myopathy [23].
As regard treatment guideline for patients with autoimmune muscular disorder Gudion and Amato, recommended Patients with NMD already on corticosteroids require doses adjustment according to stress. Other immunosuppression is stopped or continued based on the patient’s clinical status from COVID-19 and the severity of their illness.
Chloroquine and hydroxychloroquine used as a possible treatment for COVID-19. They are associated with potential neuromuscular side effects. Unfortunately, patients taking chloroquine or hydroxychloroquine develop slowly progressive, painless, proximal weakness and atrophy in the legs more than the arms [23].
Myalgia and fatigue have been commonly reported during the infection process. fatigue recorded in 26%-
51%, and 36% had myalgia [13]. Some patients showed fatigue, muscle soreness, and elevated muscle
enzyme levels, which may be related to the inflammation and muscle damage caused by the virus.
Conclusion
There is a clear emerging group of neurological manifestations during and after SARS-CoV-2 infection.
The COVID-19 pandemic is still affecting many people all over the world. Muscle and neuromuscular
disorders occur due to indirect, or as chronic. Available treatment options might potentially lead to a wave
of muscles and myasthenia gravis sequelae. Now we are facing unknown possible neurological complications
of COVID-19. So, many types of researches should be developed to postulate this pointing.
Financial Disclosure and Conflict of Interest
The study had no external funding source. The author declare that I have not received any grants for this
work. No ghost, guest or gift writing or personal relationships that could have appeared to influence the
work reported in this paper. Also, I have not fund support.
Bibliography
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