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.
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.