Monica Falleni (Italy)
Pathology and Medical Genetics Unit ASST Santi Paolo & Carlo and Department of Health Sciences, University of Milan, MilanAuthor Of 1 Presentation
BRAINSTEM INVOLVEMENT IN COVID-19: A NEUROPATHOLOGICAL AND NEUROPHYSIOLOGICAL STUDY
- Tommaso Bocci (Italy)
Abstract
Background and Aims:
Whilst respiratory failure in COVID-19 arises from severe interstitial lung involvement, SARS-CoV-2 likely spreads also through the nervous system in a prion-like way, possibly reaching respiratory centers in the brainstem. Here, we evaluated neuropathologically, neurophysiologically and clinically the brainstem involvement in COVID-19.
Methods:
Neuropathological data were acquired from two patients died for COVID-19 and two patients COVID-19 negative; neuronal damage and the number of corpora amylacea (CA)/mm2 were assessed. The expression of the “nuclear protein” of SARS-Cov-2 was also evaluated. To clarify whether neuropathological findings had a functional correlate, we studied the blink reflex (BR) in 11 COVID-19 patients, admitted to our Intensive Care Unit (ICU), and compared data both with healthy subjects and non COVID-19 ICU patients. BR assesses a ponto-medullary circuitry partly involving the reticular formation (RF) close to the respiratory nuclei; RF itself modulates the activity of the respiratory centers. An extensive neurological examination, comprising the corneal and glabellar reflexes, was also performed.
Results:
Autopsies showed a high percentage of neuronal damage and a higher number of CA in the medulla oblongata of COVID-19 patients; immunohistochemistry revealed the presence of SARS-Cov-2 virus in the brainstem (Figure 1). Neurophysiologically, the medullary RII component of the BR was selectively impaired in COVID-19 and, clinically, the glabellar reflex severely impaired or absent.
Conclusions:
Our findings provide the neuropathological, neurophysiological and clinical evidence of SARS-Cov-2-related brainstem involvement, suggesting a neurogenic component of respiratory failure.