Among patients affected by the virus COVID-19, physicians have observed ventilation disorders. It is relevant to assess neurological involvement, including the role of diaphragmatic function. Its possible impairment could be related to the systemic inflammatory response and disease progression that both typify COVID-19 infection. We distinguished two groups (severe group (SG) and mild group (MG)) according to the severity of respiratory symptomatology. We performed neurophysiological and sonography studies to evaluate the diaphragmatic function. Regarding the sonography variables, we identified statistically significant differences in the right mean diaphragmatic thickness along with the expiration, showing 1.56 mm (SEM: 0.11) in the SG vs 1.92 mm (SEM: 0.19) in the MG (p = 0.042). The contractibility of both hemidiaphragms was 15% lower in the severe group, though this difference is not statistically significant. In our examination of the neurophysiological variables, in the amplitude responses, we observed a greater difference between responses from both phrenic nerves as follows: the raw differences in amplitude were 0.40 μV (SEM: 0.14) in the SG vs 0.35 μV (SEM: 0.19) in the MG and the percentage difference was 25.92% (SEM: 7.22) in the SG vs 16.28% (SEM: 4.38%) in the MG. Although diaphragmatic dysfunction is difficult to detect, our combined functional and morphological approach with phrenic electroneurograms and chest ultrasounds could improve diagnostic sensitivity. We suggest that diaphragmatic dysfunction could play a relevant role in respiratory disturbance in hospitalised patients with severe COVID-19.

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Myasthenia gravis is a neuromuscular disease that causes weakness in skeletal muscles because of the presence of acetylcholine receptor antibodies. These antibodies produce a compromise in the end-plate potential, reducing the safety factor for effective synaptic transmission. Clinically, this manifests as muscle weakness and, in severe cases, respiratory failure. There is widespread knowledge about the association between small cell lung carcinoma and Lambert-Eaton myasthenic syndrome, but not with other neuromuscular disorders, such as myasthenia gravis. We present a patient with small cell lung carcinoma who presented weakness affecting the proximal muscles over the last three years, and electromyography findings suggesting myasthenia gravis. After this electrodiagnosis, analytical tests showed an increase in anti-acetylcholine receptor antibodies. Given these findings, we can affirm that neurophysiological tests provide a significant value in diagnosing myasthenia gravis, as anti-acetylcholine receptor antibodies were negative at the moment of the electromyography's performance. Likewise, it is essential to consider a paraneoplastic syndrome in this type of carcinoma.