LAUSR

SARS-CoV-2 has a proven neurotropic potential and can cause various neurological complications [1]. Involuntary movements represent a rare manifestation of COVID-19. We present a case report of COVID-19-associated chorea. This is to the best of our knowledge the first such case to be reported in a Polish population. A 77-year-old woman was admitted to the University Hospital due to involuntary movements of acute onset. Two weeks before, she had received her first dose of COVID-19 mRNA vaccine. Soon afterwards, she had a close contact with a SARSCoV-2-infected person. Five days before admission, she developed disturbances in attention, consciousness, and cognition — she was hyperactive, occasionally delusional, and slight involuntary movements of the face appeared. On the next day, infection symptoms (i.e. cough, fever) also appeared. Her neurological condition worsened and fluctuated — involuntary movements spread to the limbs and a confusional state progressed. On admission, a routine COVID-19 antigen test from nasopharyngeal swab had been performed, confirming SARS-CoV-2 infection. The patient had a history of arterial hypertension, diabetes mellitus, hypothyroidism, and urinary incontinence, and had three malignancies in remission (skin melanoma, thyroid and colon cancer). According to her family, for several months before her current deterioration she had required some help with everyday activities and had experienced slight problems with cognition. She did not take any medication with known potential to induce chorea (Tab. 1). In neurological examination on admission, psychomotor slowing, orofacial dyskinesia and involuntary chorea-type movements of the trunk and all limbs (more pronounced on the left) were observed. Non-contrast computed tomography (CT), CT angiography and perfusion CT of the brain were performed, showing no relevant abnormalities. Chest high-resolution CT revealed bilateral pneumonia (Fig. 1A). Head magnetic resonance imaging (MRI) (Fig. 1B) demonstrated marked features of cerebral small vessel disease — diffuse white matter hyperintensities, cortical and subcortical atrophy — with no acute ischaemic or contrast-enhancing lesions, nor oedema of the basal ganglia. Cerebrospinal fluid (CSF) and serum tests were unremarkable except for elevated serum inflammation markers (CRP 79.60 mg/dL) and mild dyselectrolytemia (Na+ 134 mmol/L, K+ 3.03 mmol/L, Ca2+ 2.09 mmol/L). Neuroinfection, hypoxic-ischaemic encephalopathy, metabolic, hormonal and autoimmune systemic diseases, paraneoplastic syndrome and prion disease were excluded. Antistreptolisin-O level was not elevated. Laboratory test results are summarised in Table 1. Electroencephalography (EEG) could not be performed on the COVID-19 ward. A preliminary diagnosis of non-infectious encephalitis was made. Empirical treatment with steroids (methyloprednisolone 1 g i.v. per day for five days), symptomatic with diazepam and antiviral treatment with remdesivir (200 mg i.v. on day 1, and 100 mg i.v. for the following four days)