Before that SARS-CoV-2 emerged at a global scale, other coronaviruses have been proven to invade the brainstem in mice and humans. SARS-CoV-2 might spread cell-to-cell in a prion-like way, along the vagus nerve, reaching respiratory centers in the brainstem, possibly adding a neurogenic component to the respiratory failure. To test this hypothesis, the authors assessed neurophysiologically and clinically the brainstem in COVID-19 patients admitted to the ICU. The blink reflex (BR) was assessed in 11 severe COVID-19 patients (9 males, mean age 55.2 ± 7.1 years, range 48–70). Whereas all the COVID-19 patients had normal pontine RI latencies (p = 0.1), in two of them the second response (RII) was absent and in the remaining cases markedly abnormal, both the ipsilateral (latency: p < 0.0001; amplitude: p < 0.0001; duration: p < 0.0001) and the contralateral response (latency: p = 0.0014; amplitude: p < 0.0001; duration: p < 0.0001). Among COVID-19 patients, four had an absent glabellar reflex (score = 0), while the others had a markedly impaired reflex (score = 1). The corneal reflex was present in eight COVID-19 patients out of 11, and reduced in the remaining three. Non-COVID patients showed normal glabellar and corneal reflexes. The authors concluded that their findings provide the neurophysiological and clinical evidence of SARS-CoV-2 -related brainstem involvement in severe COVID-19 patients, especially at the medullary level.
Bocci, T., Bulfamante, G., Campiglio, L. et al. Brainstem clinical and neurophysiological involvement in COVID-19. J Neurol (2021). https://doi.org/10.1007/s00415-021-10474-0