COVID-19 and Parkinsonism: A Critical Appraisal

• Published in: Biomolecules (Basel, Switzerland) Vol. 12; no. 7; p. 970
• Main Authors: Cavallieri, Francesco, Fioravanti, Valentina, Bove, Francesco, Del Prete, Eleonora, Meoni, Sara, Grisanti, Sara, Zedde, Marialuisa, Pascarella, Rosario, Moro, Elena, Valzania, Franco
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 11-07-2022; MDPI
• Subjects: Antipsychotics; Basal ganglia; Brain diseases; Brain injury; Central nervous system diseases; Coronaviruses; COVID-19; Dopamine receptors; Encephalitis; Encephalopathy; extrapyramidal; Hypoxia; Infections; Inflammation; Invasiveness; Medical imaging; Movement disorders; Neurodegenerative diseases; Neuroimaging; Parkinson's disease; parkinsonism; Patients; Review; SARS-CoV-2; Severe acute respiratory syndrome coronavirus 2; Structure-function relationships; Synuclein; Systematic review; Traumatic brain injury; Variables; Viral infections
• ISSN: 2218-273X; 2218-273X
• DOI: 10.3390/biom12070970

A few cases of parkinsonism linked to COVID-19 infection have been reported so far, raising the possibility of a post-viral parkinsonian syndrome. The objective of this review is to summarize the clinical, biological, and neuroimaging features of published cases describing COVID-19-related parkinsonism and to discuss the possible pathophysiological mechanisms. A comprehensive literature search was performed using NCBI’s PubMed database and standardized search terms. Thirteen cases of COVID-19-related parkinsonism were included (7 males; mean age: 51 years ± 14.51, range 31–73). Patients were classified based on the possible mechanisms of post-COVID-19 parkinsonism: extensive inflammation or hypoxic brain injury within the context of encephalopathy (n = 5); unmasking of underlying still non-symptomatic Parkinson’s Disease (PD) (n = 5), and structural and functional basal ganglia damage (n = 3). The various clinical scenarios show different outcomes and responses to dopaminergic treatment. Different mechanisms may play a role, including vascular damage, neuroinflammation, SARS-CoV-2 neuroinvasive potential, and the impact of SARS-CoV-2 on α-synuclein. Our results confirm that the appearance of parkinsonism during or immediately after COVID-19 infection represents a very rare event. Future long-term observational studies are needed to evaluate the possible role of SARS-CoV-2 infection as a trigger for the development of PD in the long term.