Neurological complications have emerged as a significant cause of morbidity and mortality in the ongoing COVID-19 pandemic. In this focused review, we summarize evidence of the neuroinvasiveness, neurotropism and neurovirulence of the novel beta coronavirus SARS-CoV-2. Potential means of neuroinvasion include hematogenous spread, neuronal retrograde transport from the vagus or olfactory nerves and the transcribrial route. Pathologic studies suggest direct neuroinvasion via hematogenous spread and retrograde transport by the olfactory nerve, while retrograde transport through the vagus and olfactory nerves remains hypothetical. Experimental evidence confirms that angiotensin converting enzyme 2 (ACE2) is the main receptor for SARS-CoV2, suggesting this ACE2 as a target of neurotropism. Direct evidence of detection of the virus in cerebral spinal fluid or post-mortem brain tissue is sparse. There is a paucity of reported post-mortem neuropathological examinations in victims of COVID-19, highlighting the importance of accruing additional cases. The potential for long-term neurological consequences of COVID-19 signals the importance of continued surveillance for neuroimmune disorders and neurodegenerative in those infected by SARS-CoV-2.

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