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 31-year-old Spanish-speaking male with no significant past medical history presented to the emergency department (ED) with progressively worsening weakness, numbness, and difficulty walking. Approximately two months prior to presentation, he woke up and noticed some numbness in his right hand. One month later he noticed double vision. He started wearing an eye patch over one eye to help with symptoms of diplopia. He then started experiencing numbness in his right leg as well as left facial weakness with dysarthria. About a week later, his symptoms progressed to numbness on the left upper and lower extremity, which prompted a visit to an outside hospital. His workup was reportedly normal including a magnetic resonance imaging (MRI) of the brain and lumbar puncture. His weakness and bilateral paresthesias progressed to the point that he was unable to ambulate, which prompted his current visit. The patient denied any trauma, headache, neck stiffness, loss of vision, fever, cough, or any other infectious symptoms. He denied any recent travel, sick contacts, or contacts with similar complaints.\nOn presentation to the ED his vital signs were within normal limits, and with the exception of a malar facial rash and abnormal neurologic exam, his physical exam was unremarkable. On neurologic exam, he was awake, alert, and oriented appropriately. On primary gaze there was left-eye adduction and cranial nerve VI palsy bilaterally with extraocular movements and vertical nystagmus. He had a unilateral, lower motor neuron cranial nerve VII palsy with left upper and lower hemifacial weakness, and also cranial nerve XII dysfunction with tongue deviation to the left. Overall his motor bulk was normal and strength was 5/5 in flexor and extensor groups of all four extremities. His sensation was intact to light touch and pinprick in all extremities. He had significant dysmetria with finger-nose-finger and heel-to-shin bilaterally, slightly worse on the left with decreased amplitude and discoordination on finger tapping and other rapidly alternating movements bilaterally. All upper extremity reflexes were intact; however, he had no patellar or Achilles reflexes; he had downgoing plantar reflex on the left. and mute plantar reflex on the right. He was unable to stand or test gait secondary to significant ataxia.\nThe patient was admitted and underwent an extensive workup including infectious, autoimmune, paraneoplastic, metabolic, and neurologic testing. MRI of his brain and lumbar spine were unremarkable. A computed tomography of his chest looking for neoplasm revealed a consolidation in his left lower lobe that prompted SARS-CoV-2 polymerase chain reaction testing and returned positive. Cerebrospinal fluid (CSF) studies revealed the presence of anti-ganglioside – GQ1b (Anti-GQ1b) immunoglobulin G antibodies (1:100), with lymphocytic predominance without albuminocytologic dissociation, and he subsequently was found to have positive immunoglobulin G (IgG) antibodies to COVID–19.\nThe patient was treated with convalescent plasma, tocilizumab, and intravenous immunoglobulin, in addition to extensive physical and occupational therapy. He had some mild subjective improvement in vision and coordination as well as return of patellar reflexes bilaterally; however, he required maximum assistance to ambulate on transfer to rehab facility.