SARS-CoV-2 infection associated with diplopia and anti-acetylcholine receptor antibodies

Dear Editor:

A novel coronavirus, SARS-CoV-2, was detected in Wuhan, China, in December 2019 and the associated disease, known as COVID-19, has quickly become a pandemic. Several reports suggest that SARS-CoV-2 may infect the central nervous system, causing neurological alterations.¹ Some authors have reported cases of encephalopathy,² acute necrotising haemorrhagic encephalopathy,³ meningoencephalitis,⁴ headache, myalgia, neuropathic pain, hyposmia, ageusia, ataxia, epileptic seizures, and cerebrovascular events.⁵ To our knowledge, no peripheral nervous system alterations other than those mentioned above have been reported to date. We present the case of a 48-year-old man with paranoid schizophrenia, under treatment with aripiprazole; inverse psoriasis; and no other relevant medical history. The patient came to the emergency department due to a 5-day history of binocular diplopia, which was more marked at long distance and with lateral gaze, with a tendency to improvement. He also reported presenting high fever, dry cough, dyspnoea, and myalgia 15 days previously; he self-isolated in view of the current epidemiological situation. Fever resolved 5 days prior to the consultation, but diplopia appeared; the remaining symptoms had improved. The physical examination revealed expiratory wheezing. The neurological examination revealed isochoric, reactive pupils; normal confrontation visual field test results; horizontal diplopia with gaze to the right; and no observable eye movement restriction. Results were normal for all other areas. A blood analysis detected high levels of acute-phase reactants (fibrinogen 885 mg/dL, CRP 8.8 mg/dL, d-dimer 1095 ng/mL). The patient was admitted to the internal medicine department due to suspected COVID-19. PCR testing was negative for SARS-CoV-2 in nasopharyngeal exudate but positive in sputum. A chest radiography showed right lower lobe opacification and lingula consolidation; these findings were confirmed by a chest CT scan and linked to the infection (Figs. 1 and 2). More detailed analyses showed normal kidney, liver, and thyroid function; vitamin B₁₂ and folate levels within normal ranges; and normal lipid profile, blood count, and coagulation profile. Autoimmune tests yielded negative results except for antinuclear antibodies (1:320, homogeneous pattern) and acetylcholine receptor antibodies (1.10 nmol/L; positive: >0.20 nmol/L). Serology tests were negative. Diplopia resolved the day after hospital admission. A head CT scan showed no space-occupying lesions, vascular alterations, or any other abnormal findings. The patient's general condition improved and he was discharged 2 days after admission; he was instructed to continue treatment with hydroxychloroquine and azithromycin. Our patient developed diplopia associated with acetylcholine receptor antibodies in the context of microbiologically confirmed SARS-CoV-2 infection; symptoms resolved completely within days. He had no cardiovascular risk factors and neuroimaging studies revealed no vascular or space-occupying lesions that may otherwise explain his symptoms. We suggest 2 possible explanations for our case. First, the patient had latent myasthenia gravis, which was precipitated by SARS-CoV-2 infection; and second, SARS-CoV-2 infection was the main cause of the patient's symptoms, triggering an autoimmune response, with tropism to the neuromuscular junction as a result of molecular mimicry.⁶ Clinical and serological follow-up of our patient is necessary to evaluate his progression and detect any changes. Patients with COVID-19 must be screened for symptoms of muscle fatigability. This information is essential to direct further testing, with a view to determining whether myasthenia gravis is a possible complication of SARS-CoV-2 infection. This may open new lines of research into COVID-19.

Figure 1.

Chest radiography showing right lower lobe opacification and left lingula consolidation.

Figure 2.

Chest CT scan revealing ground-glass parenchymal opacification in the upper lobe of the left lung.