Losing one’s sense of smell and taste is now well-established as an early sign of SARS-CoV-2 infection – to this point (and my chagrin), I must attest to the fact that I have not experienced these symptoms every morning to get clearance to enter my building at work. Unfortunately, a case study from France has revealed that other, more disturbing neurological symptoms may precede respiratory symptom onset.
Writing in the Journal of Neurology, Forestier et al. describe the case of a 55-year old man who presented to clinic with a headache and fever of 100.7° F (Forestier et al., 2020). Blood work revealed a slight increase in C-reactive protein, but lymphocyte count, renal and hepatic function, natremia, and troponin were normal. Chest radiograph was normal and the patient did not have respiratory symptoms. However, in the evening the patient experienced dizziness and pre-fainting episodes. On day 1, the patient was tested for SARS-CoV-2, influenza, and upper respiratory bacterial infections but all came back negative. On day 3, a brain MRI was performed to evaluate his neurological symptoms and revealed cytotoxic lesions within the corpus callosum. At this point, the patient also was found to have ground glass opacities on chest CT scan, but did not have upper respiratory symptoms. Lumbar puncture revealed a normal CSF profile. On day 7, the patient’s respiratory function deteriorated – a chest CT scan revealed “bilateral pulmonary lesions with arising crazy-paving pattern.” The patient required mechanical ventilation and had to be intubated. SARS-CoV-2 RNA was detected from nasopharyngeal swab by RT-PCR on day 7. 17 days later, the patient was successfully extubated and 3 days after that, a follow-up MRI revealed complete regression of the corpus callosum lesion.
It is unclear what the etiology was of the observed corpus callosum lesion, but the authors believe it was cytotoxic in nature. The authors don’t offer an explanation on etiology, but they do mention that cytotoxic lesions of the corpus callosum are infection-associated and involve cell-cytokine interactions. If SARS-CoV-2 infects the brain relatively early in some patients, it may trigger the release of cytokines in the CNS from many different cell types, including microglia, astrocytes, endothelial cells, pericytes, and perhaps invading lymphocytes – however, no one has published anything on this topic yet in the context of COVID-19. It is also possible that patients may develop reversible demyelinating lesions in context of SARS-CoV-2 infection, in a manner reminiscent of acute demyelinating encephalomyelitis (ADEM) that may clear with treatment of the underlying infection. More research on neurological manifestations of COVID-19 will help to delineate types of CNS lesions that could be observed during the initiation stages of the infection.
References
Forestier, G., de Beaurepaire, I., Bornet, G., & Boulouis, G. (2020). Cytotoxic lesion of the corpus callosum as presenting neuroradiological manifestation of COVID-2019 infection. Journal of Neurology, 1-3.
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