CLINICAL PEARL Fibrocartilaginous embolism myelopathy is a stroke syndrome, characterized by rapidly progressive paraplegia (hours to 2-3 days) following an episode of back pain (mostly after a minor trauma).1 CSF studies are normal and MRI shows T2 hyperintensity in the spinal cord with associated swelling, diffusion restriction, and often presence of Schmorl's nodes at the level of injury.1 CASE REPORT A 25-year-old man with no significant past medical history and an active lifestyle presented to the hospital with a complaint of bilateral lower extremity numbness and weakness. Three days prior, the patient slipped while getting out of his truck and fell into a split position. Immediately afterwards he felt a sudden pain in his left groin with associated paraesthesia and weakness initially in his left thigh. Within several hours, the weakness and paraesthesia spread over the entire left leg and 24 hours later to the right leg. He also felt his bladder was full and lost control of his flatulence.The patient was a well-developed man in mild distress with normal vital signs. On neurologic examination, mental status and cranial nerves were normal. Manual motor testing of his upper extremities was unremarkable. Testing of his lower extremities revealed increased tone bilaterally. In the right lower extremity his iliopsoas was 4/5, hamstrings were 4ϩ/5, quadriceps were 4ϩ/5, tibialis anterior was 5/5, and gastrocnemius was 5/5. In the left lower extremity, his iliopsoas was 1/5, hamstrings were 4Ϫ/5, quadriceps were 4Ϫ/5, tibialis anterior was 4/5, and gastrocnemius was 4ϩ/5. Muscle bulk was normal. Rectal sphincter tone was diminished. He had no adventitial movements. Deep tendon reflexes were 2ϩ/4 in the upper extremities and 4ϩ/4 in the lower extremities bilaterally, with several beats of ankle clonus and bilateral extensor response in the toes. Sensory examination revealed intact vibration, proprioception, and pain and temperature sensation in the upper extremities bilaterally. There was an L1 sensory level involving pinprick and temperature testing. Proprioception and vibration were intact. Light touch elicited dysesthesias in the left lower extremity. Coordination was intact. The patient was able to sit up with assistance but was not able to bear any weight on his legs.The patient was admitted to a telemetry unit and had a thoracolumbar spine MRI, which showed a hyperintense T2 signal in the central and left posterior aspect of the cord from T9 through T11, slightly greater in the craniocaudal dimension. There were Schmorl's nodes at the inferior T10, superior T11, inferior T11, and superior T12 end plates (figure). Axial and sagittal MRI T1 pre-and post-gadolinium images did not show any evidence of enhancement at the level corresponding to the T2 hyperintensity. A lumbar puncture revealed an opening pressure of 29 cm of water with CSF analysis showing leukocytes 2/L, erythrocytes 4/L, glucose 63 mg/dL, and protein 44 mg/dL. CSF Lyme antibody was negative. CSF myelin basic protein was elevated at 307 ng/mL. CS...

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This case report describes a 41-year-old previously healthy male who presented with stuttering transient ischemic symptoms and radiographic evidence of a left common carotid artery thrombus as well as acute and subacute ischemic infarcts in the left middle cerebral artery territory. An exhaustive stroke work-up did not provide a plausible etiology for his symptoms. His complete blood count and iron studies, however, revealed evidence of severe iron-deficiency anemia without reactive thrombocytosis. His stool guaiac test was positive. He was discharged home on oral antithrombotic agents and aggressive iron replacement therapy with a plan for repeat vascular imaging in 3 months and a colonoscopy. This case report suggests that severe iron-deficiency anemia with or without reactive thrombocytosis should be viewed as a possible hematologic condition associated with thrombotic tendencies and a risk factor for ischemic stroke, especially in young adults. Aggressive iron supplementation and short-term antithrombotic therapy with follow-up vascular imaging are a reasonable treatment for these patients.

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Rationale: It is recommended that patients with Rheumatic diseases that are at high risk of developing active infections be screened for Tuberculosis, Hepatitis B, and Hepatitis C before receiving second-line immunosuppressive therapies. With the emergence 2019 novel coronavirus (SARS-CoV-2), expanded guidelines have not been proposed for screening in these patients before starting advanced therapy. Patient concerns: We present an unique circumstance whereas a patient with a 5 year history of inflammatory muscle disease, diagnosed by clinical history and muscle biopsy with elevated creatine kinase levels, suffered a hypoxemic cardiopulmonary arrest due to asymptomatic SARS-CoV-2 after receiving advanced immunosuppressive therapy. Diagnoses: The patient presented with an acute exacerbation of inflammatory muscle disease with dysphagia, muscle weakness, and elevated creatine kinase. Interventions: After no improvement with intravenous immunoglobulin the patient received mycophenolate and plasma exchange therapy. Outcomes: Subsequently the patient suffered a fatal hypoxemic cardiopulmonary arrest. Polymerase chain reaction test was positive for SARS-CoV-2 RNA. Lessons: We conclude that rheumatic patients, asymptomatic for SARS-CoV-2 infection, be screened and tested before initiating second-line immunosuppressive treatment.

An occlusion of the artery of Percheron (AOP) is a rare clinical condition that remains a diagnostic challenge for physicians given its variable presentation. This infarction is a result of an anatomical variant of a single vessel arising from the posterior cerebral artery. Occlusion of the AOP results in variable levels of alteration of consciousness, vertical gaze palsy, and memory impairment. Unfortunately, due to this variable presentation these strokes are often missed. We report a case of a 71 year-old-female who presented with sudden onset of unresponsiveness who was subsequently diagnosed with bilateral thalamic infarction with midbrain involvement secondary to AOP occlusion. Delayed diagnosis can result in poor neurologic outcomes as demonstrated in this case making it imperative to bring further awareness to this clinical syndrome.