An observational study by researchers was performed to understand the role that SARS-CoV-2 infection could play in causing post-COVID-19-parkinsonism (even to the point of creating a modern pandemic of post-infectious parkinsonism) has gained significant traction since the virus first emerged. 

One year later, however, there have been only five published cases of parkinsonism occurring in the setting of COVID-19. Although the clinical features of one of these cases are highly suggestive of a parainfectious/inflammatory etiology,4 many of the other presentations may merely represent an infectious stressor unmasking prodromal Parkinson’s disease (PD). The researchers presented an alternative cause of parkinsonism following SARS-CoV-2 infection.

Fever, dyspnea, and cough were observed in a 46-year-old patient. He was diagnosed with COVID-19 and quickly became hypoxemic, requiring intubation and ventilation due to acute respiratory distress syndrome. His respiratory function deteriorated and he became hypotensive, necessitating pressor assistance. His stay in the intensive care unit (ICU) was made more difficult by acute renal failure, which necessitated dialysis and disseminated intravascular coagulation (DIC). He had severe hypophonia and bradykinesia when he was finally extubated. He still has severe residual parkinsonism a year later, which is unresponsive to levodopa (450 mg/day). Yawning, severe hypophonia, hypomimia, asymmetric rigidity and bradykinesia, gait freezing, and postural instability were all found throughout the examination. With an impaired Luria test, he displayed a positive grab reflex.


Disseminated cerebral microhemorrhages, unlike the alterations seen in the patient, are a well-known complication of critical disease. Microhemorrhages have been identified in the basal ganglia (but not the dentate nuclei) in post-mortem COVID-19 studies as a result of SARS-CoV-2-induced endothelins. A recent neuropathological investigation of 41 COVID-19 patients demonstrated hypoxic/ischemic abnormalities in all of their brains, with several of them hemorrhagic. In 22% of the cases, these findings were prominent. Microglial nodules and neuronophagia were also seen in a number of locations, including the deep cerebellar nuclei. There was no evidence of direct SARS-CoV-2 infection.

The study revealed an interesting, however poorly understood, alternate source of COVID-19-associated parkinsonism, as opposed to the revelation of pre-existing PD or a form of post-infectious parkinsonism that has yet to be demonstrated. Given the degree of respiratory compromise and “silent hypoxia” that may accompany COVID-19, as well as possible virus-specific endothelium pathways, this could be a substantial, if not more important, cause of parkinsonism that deserves more thorough observation and research.