A 48-year-old man with a history of asymptomatic HIV infection, with normal CD-4 count and undetectable viral load, for which he received treatment with antiviral therapy (dolutegravir, abacavir, lamivudine) was referred to the outpatient clinic of the Radboud University Medical Centre because of the onset of jerky movements that had emerged after the resolution of symptoms related to COVID-19. His only other medication was pantoprazole. On day 1, this patient developed a fever and a concomitant headache but with minimal cough. On day 7, the general practitioner treated him with amoxicillin for 5 days. Symptoms gradually resolved except for persistent fatigue. On day 13, he developed involuntary jerky movements and clumsiness of his trunk and limbs during the course of several hours. The jerks were present at rest but worsened with movement, causing considerable disability. Gait had become insecure. Following the initial subacute onset, his complaints did not progress any further. A nasopharyngeal swab tested positive for SARS-CoV-2 by polymerase chain reaction (PCR on day 16). PCR was not repeated.\nNeurological examination on day 20 revealed a normal consciousness with fully intact cognitive functions. Eye movements showed saccadic intrusions and hypermetric saccades, but no opsoclonus. There was facial jerking. Examination of the cranial nerves was otherwise unremarkable. There were generalized myoclonic jerks of the trunk and limbs, particularly involving the hands, which were present at rest but that clearly worsened both posturally and with action (). The myoclonus was not stimulus sensitive to touch, and there was no startle response to a loud acoustic stimulus. Except for some lapses in the legs upon rising from a chair, there was no convincing negative myoclonus. Motor examination further revealed clear cerebellar ataxia of the arms and legs (hypermetria) and an ataxic gait (). There was no paresis or sensory deficit. Deep tendon reflexes were normal, and plantar responses were unremarkable.\nAn extensive laboratory work-up, including thyroid function test and celiac disease screening, cranial magnetic resonance imaging (MRI) with gadolinium, and extensive cerebrospinal fluid (CSF) analysis, revealed no abnormalities (Table ). PCR for SARS-CoV-2 in CSF on day 35 was negative. SARS-CoV-2 serology on day 62 was positive.\nNo immunotherapy was given, but symptomatic treatment with levetiracetam was initiated, which alleviated the myoclonus within several days. Functional disability also diminished considerably. Repeat neurological examination several weeks later (day 62) showed that both the myoclonus and the ataxia had improved, but recovery was not yet complete ().
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.