A previously healthy 42-year-old man presented with difficulty speaking, cognitive deficits, ataxia, and progressive disabling jerks in upper and lower limbs, leading to falls (see Supplementary video-). Neurological examination demonstrated spontaneous, action-induced, and tactile-sensitive myoclonus on the face, upper extremities, and lower extremities. He had dysmetria and dysdiadochokinesia with superimposed action-induced myoclonus in the upper and lower extremities. Myoclonus prevented him from standing independently, and he had a wide-based gait. The rest of the neurological examination was normal. Laboratory tests including renal function, liver function, ammonium, urea, and CO2 were normal, except for the nasopharyngeal RT-PCR test for SARS-CoV-2, which was positive. Computed tomography (CT) of the head and brain magnetic resonance imaging (MRI) were normal. Electroencephalogram (EEG) and electromyography (EMG) were performed but did not reveal any abnormalities. Given these findings and the positive SARS-CoV-2 PCR, myoclonus was considered postinfectious. No other symptoms such as fever, myalgia, cough, fatigue, hyposmia, or hypogeusia were present. Cerebrospinal fluid (CSF) analysis was unremarkable, RT-PCR test for SARS-CoV-2 and autoantibodies were negative. He was treated with methylprednisolone 1000 mg IV daily for five days, bringing about a partial resolution of myoclonus. Complete recovery was observed on a follow-up session one month later.
A previously healthy 52-year-old man presented with progressive imbalance and generalized jerks (see Supplementary video-). A week before, he had experienced myalgia and tested positive for SARS-CoV-2. Upon admission, he had generalized stimulus-sensitive myoclonus affecting his face, hands, and legs, confining him to a wheelchair. Other neurological findings, including eye movements, muscle tone, and deep tendon reflexes, were normal. He did not have any coughing, fever, dyspnea, and O2 saturation was more than 97% without nasal O2. Ground-glass opacities suggestive of SARS-CoV-2 infection were detected on chest CT. Laboratory studies showed no increase in inflammatory markers in peripheral blood; CRP and white blood cell count were normal. Brain CT and MRI were normal. Results from CSF evaluations, including autoantibody investigations, were unremarkable. The cerebellar syndrome improved after high-dose IV methylprednisolone (1 gr/day for five days); on a follow-up session after three weeks, the patient could walk independently.