SARS-CoV-2, a novel pathogen causing COVID-19, had been reported to cause many extra-respiratory presentations. We would like to report a possible neuromuscular manifestation of SARS-CoV-2 infection.
The patient is a 51-year-old Taiwanese lady with the history of hypertension and obesity (body mass index 34.9.) There was no past history of neuromuscular disorders. She had been travelling with a tour group in Europe before the admission, and was noted to have fever (38.2 °C) upon arriving in Taiwan. PCR for SARS-CoV-2 returned positive, and she was subsequently hospitalized on March 15th, 2020.
On admission, her consciousness and physical examination were normal. Chest Roentgenogram revealed increased infiltration and consolidation in the right lung field. She had progressive dyspnea and was intubated on March 18th. During the admission, rosuvastatin 5 mg/day was administered from March 20th to April 1st, and cisatracurium 8 mg/h was administered from March 24th to April 7th. Other medications included azithromycin, meropenem, lopinavir/ritonavir, hydroxychloroquine, baricitinib and sedative agents. She was extubated on April 9th without complication. The PCR for SARS-CoV-2 became negative since April 6th.
The patient remained quadriplegic in the following days. Gradual improvements of muscle power occurred since April 17th, with symmetrical weakness over the limbs (proximal limbs medical research council grading 2/5, distal limbs 3/5). Improvements occurred gradually, and she was able to walk with support of caregiver on May 1st. Myalgia was not reported throughout the whole course.
On examination, the upper limbs were normoreflexic and the lower limbs were hyporeflexic, with slightly diffuse hypotonia. There were no observable fasciculation or significant atrophic change. The pinprick sensation was intact, and the vibratory sensation was mildly decreased in the ankles.
The creatine kinase (CK) level became elevated since April 2nd, which peaked on the next day (2949 U/L) and returned to normal range on April 12th. Another episode of CK elevation occurred from April 16th to 20th, with maximum of 4294 U/L (supplementary table 1). Autoimmune workup and antisynthetase antibodies returned negative. Nerve conduction study on May 4th revealed asymmetrical axonal injury in lower limbs (supplementary table 2) while 3 Hz repetitive stimulating test of trapezius muscle revealed no decremental responses. Needle electromyography (Fig. 1 ) revealed early recruitment and small-amplitude polyphasic waves in the biceps brachii, rectus femoris, and tibialis anterior muscles. Increased spontaneous activities including fibrillations, positive waves, and fasciculations were found in the biceps brachii and tibialis anterior muscles. The findings are compatible with myopathy. Follow-up in late May 2020 revealed normal serum CK level along with full muscle power.
Figure 1.
Findings of electromyography in a patient with SARS-CoV-2 (COVID-19) infection. (A) Volitional motor unit compound potential (MUAP) of biceps brachii revealed polyphasic waves with decreased amplitude of MUAP. (B) Spontaneous activities of biceps brachii revealed increased insertion activities along with presence of fibrillations. (C) Volitional MUAP of rectus femoris revealed polyphasic waves.
Few reports had been published on the detailed description of neurological manifestation of COVID-19. Focusing on neuromuscular manifestation, there had been a few reported cases indicating that infection by SARS-CoV-2 may have a correlation with Guillian-Barre syndrome1 , 2 and Miller Fisher syndrome.3 Skeletal muscle damage has not been well documented and reported patients with COVID-19. The preceding elevation of CRP before each episode of hyperCKemia strongly indicated an inflammatory pathology for the myopathy observed. Inflammatory myopathy should be considered as a cause for persistent respiratory failure and weakness in patients with COVID-19.
Study funding
None.
Declaration of Competing Interest
The authors have nothing to disclose.
Acknowledgment
We thank the medical, nursing, and support staff of Units 2 A and 7 B for taking care of the patient.
Footnotes
Supplementary data to this article can be found online at https://doi.org/10.1016/j.jfma.2020.07.042.
Appendix A. Supplementary data
The following is the Supplementary data to this article:
References
- 1.Toscano G., Palmerini F., Ravaglia S., Ruiz L., Invernizzi P., Cuzzoni M.G. Guillain-Barré Syndrome Associated with SARS-CoV-2. N Engl J Med. 2020;382(26):2574–2576. doi: 10.1056/NEJMc2009191. Epub 2020 Apr 17. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Alberti P., Beretta S., Piatti M., Karantzoulis A., Piatti M.L., Santoro P. Guillain-Barré syndrome related to COVID-19 infection. Neurol Neuroimmunol Neuroinflamm. 2020;7:e741. doi: 10.1212/NXI.0000000000000741. published 2020 April 19. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Gutiérrez-Ortiz C., Méndez A., Rodrigo-Rey S., Pedro-Murillo E.S., Bermejo-Guerrero L., Gordo-Mañas R. Miller Fisher Syndrome and polyneuritis cranialis in COVID-19. Neurology. 2020;95(5):e601–e605. doi: 10.1212/WNL.0000000000009619. published April 17, 2020. [DOI] [PubMed] [Google Scholar]
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