LAUSR

A 67-year-old man was admitted to the Emergency Department because of the acute onset of dyspnea, fever, anosmia and ageusia. Chest CT showed bilateral interstitial pneumonia and nasopharyngeal swab was positive for SARS-CoV-2. Due to worsening of his respiratory function, he was immediately treated with tocilizumab with subsequent symptoms improvement and hospital discharge after 5 days. Four months later, he was seen in the neurology outpatient clinic because of new progressive impaired finger dexterity and mild resting tremor at the right hand, and nightmares characterized by vocal sounds and limbs’ movements. Before COVID-19 infection, no Parkinson’s Disease (PD) prodromal symptoms were ever noted by the patient and his family. Neurological examination (NE) showed mild resting tremor in the right hand, slight bilateral bradykinesia and rigidity, and reduction of right arm swing during gait (MDS-UPDRS-III: 12/132). Brain MRI showed mild microvascular changes (Fig. 1A) whereas single-photon emission computed tomography (SPECT) with Ioflupane I123 injection (DaTscanTM) showed a mild bilateral reduction in presynaptic dopaminergic uptake (Fig. 1B). A diagnosis of probable PD was made [1]. An extensive genetic testing for mutations in common hotspots of the leucine-rich repeat kinase 2 (LRRK2) gene and full gene sequencing of glucocerebrosidase (GBA) variants revealed the presence of an heterozygous variant in the GBA gene (NM_000157.3:c.1223C > T-p.(Thr408Met); [T369M]). A 45-year-old previously healthy male was seen at the outpatient neurological clinic with the chief complaint of resting tremor at the left leg since approximately 1 month. Four months earlier, he presented with fever, anosmia and ageusia that lasted for 20 days. He was diagnosed with mild COVID-19 infection after a positive nasopharyngeal swab for SARS-CoV-2. NE revealed mild resting tremor at his left leg and slight bradykinesia at his left hand (MDS-UPDRSIII: 4/132). Brain MRI was unremarkable (Fig. 1C) but SPECT DaTscanTM revealed decreased dopamine transporter density in both putamens (Fig. 1D). A diagnosis of probable PD was made [1]. The medical history was negative for PD prodromal symptoms. An extensive genetic testing for mutations in 68 genes related to PD revealed the presence of a heterozygous variant in the PRKN gene (chr6:162683546–1 62683807NM_004562; exons:3). A few cases of parkinsonism linked to COVID-19 infection have been reported so far [2–4]. Onset was acute or subacute in all of them (10–32 days after COVID-19 diagnosis) raising the possibility of a postor para-infectious parkinsonian syndrome [2–5]. However, the presence of decreased DaTscanTM uptake in all of the reported cases, which would be unlikely to occur within a short period of time, supports a possible conversion from prodromal to symptomatic PD promoted by the COVID-19 infection Francesco Cavallieri and Valentina Fioravanti equally contributed to the manuscript.