A 51 year old man presented to the Emergency Department (ED) with acute onset left sided peripheral facial palsy and a complete right sided homonymous hemianopsia.\nThe patient was a Caucasian male of normal BMI with no prior history of hypertension, hypercholesterolemia, diabetes, smoking and or heart disease. He had been in good health until March 2020 when he returned from a group holiday to Austria. The patient started feeling unwell with a fever and was diagnosed with coronavirus disease (COVID-19) along with several members of the group that he had travelled with. A nasopharyngeal PCR swab confirmed the presence of SARS-CoV-2 RNA on the 22nd of March 2020. The patient was admitted the hospital on the 29th of March 2020 after increasing shortness of breath and onset of diarrhea and vomiting. The patient was febrile but had no oxygen requirement and was therefore diagnosed with mild COVID-19. He was admitted for observation, managed conservatively, and was discharged home 3 days later on the 1st of April 2020 after showing clinical improvement.\nThe patient was readmitted 2 days later on the 3rd of April 2020 with increasing shortness of breath. Clinically, pulmonary embolism (PE) was suspected with no signs of hemodynamic compromise. The diagnosis was confirmed by a CT Pulmonary Angiography (CTPA) (Fig. ) which demonstrated multiple bilateral subsegmental PE with no signs of right sided heart strain. The CTPA also demonstrated bilateral ground glass and consolidation in the lungs in keeping with COVID-19 infection (Fig. ). The CT examination was performed using the Siemens® Somatom Definition Flash using GE Healthcare® Omnipaque intravenous contrast and a standardized CTPA protocol. The patient had a D-dimer > 4.0 mg/L (normal range 0.2–0.6 mg/L). The Chest CT performed during the CTPA also shows the radiological extent of the COVID-19 illness in the lungs (Fig. ). The patient was started on Low Molecular Weight Heparin (LMWH) with bridging to direct oral anticoagulation (DOAC) on a dose of 20 mg Rivaroxaban OD. The patient continued DOAC treatment for a total of three months until the beginning of July 2020.\nOn the 26th of February 2021, approximately 11 months after being diagnosed with COVID-19, the patient contacted the emergency medical services due to acute onset visual field disturbances. The ambulance arrived on scene minutes after the onset of symptoms. A preliminary examination by the paramedics revealed as right sided visual field defect and a left sided facial palsy. The patient had a heart rate of 70 beats per minute and blood pressure of 147/89 mm Hg. The prehospital oxygen saturation was 98 % whilst breathing room air. Based on their initial findings, the paramedics suspected a stroke, and the patient was blue lighted to the ED.\nOn admission to the ED the patient was taken directly to the CT lab. The patient had a temperature of 35.5 ℃, ECG showing normal sinus rhythm, blood glucose of 5.8 mmol/L, a blood pressure of 157/99 mmHg and an oxygen saturation of 99 % on room air. A rapid neurological examination revealed a left sided peripheral facial palsy, right sided homonymous upper quadrantopia. A National Institutes of Health Stroke Scale (NIHSS) exam revealed a score of 3.\nA CT scan was performed including a pre- and intra- cerebral angiography. A subsequent cerebral perfusion scan was also performed. The CT examination was performed using the Siemens® Somatom Definition Flash using GE Healthcare® Omnipaque intravenous contrast and standardized protocols for angiography and perfusion.\nThe plain CT showed no signs of hemorrhage and based on the clinical suspicion of stroke the decision to treat with intravenous thrombolysis was made. Alteplase was administered at a dose of 0.9 mg/kg as per guidelines. The CT angiography three occluded intracerebral vessels, occlusions of the P2 and P3 segments of the left posterior cerebral artery (Fig. ) and an occlusion of the left superior cerebellar artery. The CT perfusion scan show increased time to drain (TTD) and reduced cerebral blood flow (CBF) in the afore mentioned occluded vascular territories (Fig. ).\nThe patient was admitted to the stroke unit and showed neurological improvement after Alteplase administration. The following day the patient had a NIHSS of 0.\nDuring hospital admission examinations were performed to determine ischemic stroke etiology. Ultrasound of the pre- and intra- cerebral vessels showed no significant stenoses or occlusions. Five day in-hospital cardiac rhythm monitoring showed sinus rhythm without any signs of atrial fibrillation and or other arrythmia. The patient underwent a Trans- Thoracic Echocardiography (TTE) which was normal and a Trans- Esophageal Echocardiography (TEE) where a patent foramen ovale was detected (PFO). The right to left shunting was visualized on color doppler and whilst using contrast (Fig. ). A blood work up during admission showed a normal ESR, normal levels of Immunoglobulin G and M, normal levels of Protein C and S and normal Factor Xa activity. Immunological assays did not detect the presence of rheumatoid factor, ANCA, ANA, anti-CCP antibodies. Furthermore, no factor V Leiden mutation was detected nor the presence of Lupus anticoagulant. The only abnormal finding was an elevated D-dimer of 1.2 mg/L (normal range 0.2–0.6 mg/L). A full body CT was performed including a CTPA and a CT venography of the lower extremities. The full body CT showed no signs of malignancy. The CTPA showed no evidence of pulmonary embolus and the CT venography of the lower extremities ruled out deep vein thrombosis (DVT).\nThe patient was discharged with a NIHSS of 0 following an Embolic Stroke of Unknown Source (ESUS). The patient is currently being treated with 20 mg Rivaroxaban OD, and atranscatheter closure of his PFO has been scheduled.
A 72-y-old nonsmoking man with a single episode of transient global amnesia 10 y previously presented with progressive diffuse arthralgia and a sore throat (day 0). Two days afterward, his general practitioner started josamycin for 4 d. On day 8, the patient exhibited an episode of fever (38°C–38.5°C) without rhinorrhea, cough, or dyspnea, leading to the prescription of azithromycin. He never experienced anosmia or ageusia. On day 12, chest CT showed peripheral bilateral ground-glass lesions and consolidative opacities suggestive of SARS-CoV-2 infection. The symptoms improved gradually. On day 17, he started to develop bilateral upper-limb action tremor. The next day, the tremor worsened, involving the lower limbs and trunk, making walking and sitting impossible and leading to his admission to the hospital.\nNeurologic examination showed a cerebellar syndrome (action tremor, ataxia, dysarthria, and upper-limb dysmetria) associated with spontaneous diffuse myoclonus, mostly affecting the proximal limbs and worsening with movement, also stimulus-sensitive. The remainder of the neurologic examination showed normal findings, including ocular motility and deep tendon reflexes. His body temperature, oxygen saturation, respiratory rate, and lung auscultation were normal. A moderate biologic inflammatory syndrome was present, with increased fibrinogen (7.07 g/L; reference level, 1.90–4.30 g/L) and C-reactive protein (14 mg/L; reference level, 0.0–5.0 mg/L).\nThe first nasopharyngeal swab test for SARS-CoV-2 was positive (day 18), as was the serology afterward (strongly positive for IgM and IgG). The next swab tests, quantitative reverse-transcription polymerase chain reaction testing of nasopharyngeal or oropharyngeal swabs, were negative (days 21, 22, 26, and 27).\nElectroencephalography showed symmetric diffuse background slowing, reactive to stimulation, without interictal paroxysm and, notably, no correlation of the myoclonus on back-averaging. Brain MRI with gadolinium contrast injection had normal results (). Brain PET with 18F-FDG showed putaminal and cerebellum hypermetabolism associated with diffuse cortical hypometabolism, confirmed by whole-brain voxel-based SPM quantification (). Slight lung and hilar lymph node hypermetabolism was noticed, matching postinfectious pseudonodular retractile consolidation on CT, without a straightforward argument for neoplasia.\nCerebrospinal fluid (CSF) testing showed normal cell counts (4 × 106/L), a mildly elevated protein level (49 mg/dL), negative reverse-transcription polymerase chain reaction, and no oligoclonal banding. Nerve tissue immunostaining with the serum and CSF revealed the presence of autoantibodies directed against the nuclei of Purkinje cells, striatal neurons, and hippocampal neurons, as illustrated with the CSF in . This immunostaining did not evoke any previously described targets for autoimmune encephalitis. The titer of the IgG isotype autoantibodies in the serum was extremely high (1/25,000) but was 1/96 in the CSF. The same intensity and reactivity in serum and CSF were observed at the same IgG concentration, ruling out intrathecal autoantibody synthesis in concordance with the absence of CSF-specific IgG oligoclonal banding. Dot blot assays against onconeural antigens and cell-based assays against membrane antigens had negative results. Finally, the patient was negative for antinuclear, antiphospholipid, and antipolynuclear autoantibodies and other tissue autoantibodies.\nBecause of the suspected autoimmune nature of the encephalitis, we promptly started immunomodulatory treatment: at first, beginning on day 23, we used intravenous immunoglobulins (0.4 g/kg/d for 5 d); tolerance was good, but there was no significant clinical improvement. We then decided to treat the patient with intravenous methylprednisolone (1 g/d for 5 d) beginning on day 30. To help reduce myoclonus, we introduced oral drops of clonazepam (0.3 mg 3 times a day), but the treatment was stopped because of drowsiness. Clinically, the patient improved considerably after the methylprednisolone treatment, leading to cessation of myoclonus and upper-limb dysmetria and allowing him to walk without assistance. He was discharged from the hospital on day 37. We did not observe any signs of SARS-CoV-2 reactivation.