Dear Editors,
We read with great interest the article by Studart-Neto et al.[1], which presented the importance of recognizing neurological conditions that can
worsen the prognosis of SARS-CoV-2 infection. We acknowledge the notable work demonstrating
that knowledge in neurology is relevant for better treatment and follow-up of the
disease.
We aim to reveal the importance of early recognition of symptoms and signs of neuromuscular
disorders (NMD) in young COVID-19 patients, in whom the disease has a greater possibility
of progressing into respiratory failure. Since it is not an expected outcome in this
age group, we present two cases in which COVID-19 triggered disease decompensation
and we suggest considering NMD in diagnosing young patients with unexpected respiratory
failure due to SARS-CoV-2 infection.
The first case is a 23-year-old man who complained of weakness, associated with fatigue,
muscle pain, and history of falls. Weakness was first attributed to obesity. In 7
months, he lost 40 kg with restrictive diet; with no improvement of his weakness.
Electromyography (EMG) suggested myopathy as the primary diagnosis. He denied ocular
symptoms so far and was due for a muscle biopsy when he experienced marked worsening
of weakness, dysphagia, and dysphonia. The rt-PCR of nasopharyngeal secretion returned
positive for SARS-CoV-2; he was then transferred to our unit. Upon admission, mild
ptosis was observed ([Figure 1]). He underwent orotracheal intubation due to hypercapnic respiratory failure.
Figure 1 Patient 1 face - right before the intubation, with a mild ptosis.
The patient had normal creatine phosphokinase (CPK) levels. Mild improvement was observed
after the intramuscular neostigmine test. Another EMG examination was performed, revealing
a decrement greater than 10% at 3-Hz repetitive stimulation in the ulnar nerve ([Figure 2]) and no evidence of myopathic motor unit potentials, although this can be a feature
encountered in EMG of myasthenic patients. The anti-acetylcholine receptor antibody
was positive. Pyridostigmine therapy was then started. He received 6-mg dexamethasone
for 5 days to treat COVID-19. His complications included pneumonia, and treatment
involved the use of meropenem, polymyxin, daptomycin, vancomycin, ertapenem, tigecycline,
linezolid, tazocin, ceftriaxone, and amikacin, which can be considered triggers for
myasthenic crisis. Ventilatory status improvement was noted; however, a tracheostomy
was required. After 36 days, he was transferred to the neurology ward. Dysphagia,
dyspnea, and generalized fatigue were further noted; hence, intravenous immunoglobulin
(IVIg) was administered and azathioprine started. Significant clinical improvement
was observed 2 weeks later.
Figure 2 Repetitive stimulation with 11% decrement between 1 and 4 motor potentials; ulnar
nerve - right side.
The second case is a 14-year-old girl who has been followed by psychiatry clinics
for initial symptoms of depression for 3 months, evolving with hallucination, loss
of self-care and appetite within the last month. She was under treatment with sertraline
and risperidone when she developed generalized weakness and apathy. Following a diarrheic
episode for 1 week, her laboratory tests showed high glutamic oxaloacetic transaminase
and positive IgG serology for SARS-CoV-2. She received no specific treatment for SARS-CoV-2
infection. Previous drugs were replaced by lithium and mirtazapine, with no improvement
in symptoms. She was then admitted to the psychiatry unit.
A neurological consultation was requested due to a CPK of 5000. On the first physical
examination, she was apathetic and had proximal weakness with hyporeflexia and no
sensory symptoms. Her consciousness rapidly deteriorated. Blood gas analysis showed
PCO2>100; she underwent an orotracheal intubation. EMG showed a myopathic pattern
([Figure 3]), without significant decrement during the 3-Hz stimulation test. Lithemia was within
normal values (0.66 mmol/L). Her rheumatologic panel showed positive antinuclear antibodies
(ANA), SSB, SSA, and Antineutrophil cytoplasmic antibodies (P-ANCA) antibodies and
low C3 complement levels. She was diagnosed with systemic lupus erythematosus, with
psychosis as clinical criteria and low C3 complement levels and positive anti-Smith
antibody as immunological criteria, according to the 2019 American College of Rheumatology
Classification Criteria for Systemic Lupus Erythematosus. Therefore, she was treated
with IVIg, followed by cyclophosphamide; significant improvement was observed, and
the patient was extubated. During the 2-month follow-up, only mild weakness was noted.
Figure 3 Myopathic potentials; tibial anterior muscle - right side.
Neuromuscular junction and myopathic disorders are difficult to diagnose owing to
their nonspecific symptoms and the necessity of specific exams to confirm the diagnosis[2]. During the pandemic of a respiratory virus, NMD patients are more vulnerable to
infection due to thoracic musculature weakness, difficulty in mobilizing secretions,
and the use of immunosuppressive medications[3]. SARS-CoV-2 infection can lead to neuromuscular manifestations, such as myasthenia
gravis[4],[5], and previous myasthenia gravis can worsen the course of COVID-19 infection[6].
A recent national paper described the clinical course of hospitalized patients with
previous myasthenia gravis infected by COVID-19, highlighting elevated rates of mechanical
ventilation and multiple antibiotics used, such as the case described[6]. Moreover, SARS-CoV-2 can exacerbate previous NMD that were not diagnosed due to
misdiagnosis as fatigue or other psychiatric disorders, as reported in these cases[4]. We aimed to emphasize the importance of investigating NMD diagnosis during a pandemic
as early detection and treatment can provide patients a better prognosis.
