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Supplemental Digital Content is available in the text., Background: Cardiac involvement among hospitalized patients with severe coronavirus disease 2019 (COVID-19) is common and associated with adverse outcomes. This study aimed to determine the prevalence and clinical implications of COVID-19 cardiac involvement in young competitive athletes. Methods: In this prospective, multicenter, observational cohort study with data from 42 colleges and universities, we assessed the prevalence, clinical characteristics, and outcomes of COVID-19 cardiac involvement among collegiate athletes in the United States. Data were collected from September 1, 2020, to December 31, 2020. The primary outcome was the prevalence of definite, probable, or possible COVID-19 cardiac involvement based on imaging definitions adapted from the Updated Lake Louise Imaging Criteria. Secondary outcomes included the diagnostic yield of cardiac testing, predictors for cardiac involvement, and adverse cardiovascular events or hospitalizations. Results: Among 19 378 athletes tested for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, 3018 (mean age, 20 years [SD, 1 year]; 32% female) tested positive and underwent cardiac evaluation. A total of 2820 athletes underwent at least 1 element of cardiac triad testing (12-lead ECG, troponin, transthoracic echocardiography) followed by cardiac magnetic resonance imaging (CMR) if clinically indicated. In contrast, primary screening CMR was performed in 198 athletes. Abnormal findings suggestive of SARS-CoV-2 cardiac involvement were detected by ECG (21 of 2999 [0.7%]), cardiac troponin (24 of 2719 [0.9%]), and transthoracic echocardiography (24 of 2556 [0.9%]). Definite, probable, or possible SARS-CoV-2 cardiac involvement was identified in 21 of 3018 (0.7%) athletes, including 15 of 2820 (0.5%) who underwent clinically indicated CMR (n=119) and 6 of 198 (3.0%) who underwent primary screening CMR. Accordingly, the diagnostic yield of CMR for SARS-CoV-2 cardiac involvement was 4.2 times higher for a clinically indicated CMR (15 of 119 [12.6%]) versus a primary screening CMR (6 of 198 [3.0%]). After adjustment for race and sex, predictors of SARS-CoV-2 cardiac involvement included cardiopulmonary symptoms (odds ratio, 3.1 [95% CI, 1.2, 7.7]) or at least 1 abnormal triad test result (odds ratio, 37.4 [95% CI, 13.3, 105.3]). Five (0.2%) athletes required hospitalization for noncardiac complications of COVID-19. During clinical surveillance (median follow-up, 113 days [interquartile range=90 146]), there was 1 (0.03%) adverse cardiac event, likely unrelated to SARS-CoV-2 infection. Conclusions: SARS-CoV-2 infection among young competitive athletes is associated with a low prevalence of cardiac involvement and a low risk of clinical events in short-term follow-up.

Consider demyelinating disease in the differential diagnosis of cranial nerve III palsy, particularly in a younger patient without typical microvascular risk factors.

A previously healthy 72-year-old man presented with 1 year of progressive ataxia and slurred speech. There was no notable family history and no history of alcohol abuse or neurotropic drug use. Examination showed bilateral hypometric saccades, a 2–3 Hz palatal tremor with face and neck involvement, and truncal ataxia (video at [Neurology.org/cp][1]). There was no pendular nystagmus. MRI brain 6 months after the onset of symptoms showed high signal abnormality in the inferior olivary nuclei of the anterior medulla and mild superior vermal atrophy (figure, A and B). His clinical presentation and neuroimaging were consistent with a diagnosis of progressive ataxia and palatal tremor (PAPT), a rare idiopathic neurodegenerative disease with bulbar features, palatal tremor, and cerebellar ataxia. PAPT imaging features include a typical hypertrophic olivary appearance on MRI, sometimes with cerebellar degeneration.1,2 [1]: http://cp.neurology.org/lookup/doi/10.1212/CPJ.0000000000000298

A previously healthy 39-year-old woman presented with 3 weeks of progressive leg numbness. Examination showed mild bilateral iliopsoas weakness and patchy leg numbness. She was admitted, and spinal MRI revealed T2 enhancing thoracic lesions, nonenhancing cervical cord lesions (figure, A), and subtle pial and cauda equina enhancement (figure, B). Brain MRI revealed multiple periventricular T2 hyperintensities (figure, C). Since the diagnosis of multiple sclerosis (MS) was considered likely, lumbar puncture (LP) was deferred and she received 5 days of IV methylprednisolone. One week later, she developed increasing right-sided hearing loss and vertigo with right cochlear enhancement (figure, D). Two weeks later, a morbilliform and vesicular flank and trunk rash appeared (figure, E and F). She was readmitted and treated with IV acyclovir for presumed disseminated varicella zoster virus (VZV). LP revealed a lymphocytic pleocytosis (90 leukocytes, 100% lymphocytes) and elevated protein (150 mg/dL). Oligoclonal bands were positive, and neuromyelitis optica and human T-cell lymphotropic virus–1 antibodies were negative. A PCR encephalitis panel was positive for herpes simplex virus (HSV)–2 and negative for VZV and HSV-1. Skin biopsy viral culture and PCR were positive for HSV. Three weeks after rash onset, the patient developed worsening leg numbness, received 5 more days of IV methylprednisolone, and soon after developed severe ataxia and weakness. Repeat MRI revealed new pontine lesions atypical for MS, punctate lesions following a vascular distribution, and new enhancing spinal cord lesions (figure, G and H). Repeat LP revealed a decreasing leukocyte count (17 leukocytes) and rising protein (298 mg/dL). CSF HSV-2 PCR was now negative, yet quantitative ELISA revealed positive HSV-2 immunoglobulin G (IgG) (8.83 antibody index [AI]) and negative HSV-1 IgG (0.3 [reference range 0.9 AI]). CSF HSV-1 and HSV-2 immunoglobulin M (IgM) (1.15) and IgG titers were elevated (27.93 [reference range 0.9 AI]). A unifying diagnosis of HSV-2 encephalomyelitis was made. The patient was treated with plasmapheresis, followed by IV immunoglobulin (IVIG), concurrently with 6 weeks of IV acyclovir. A follow-up LP 3 weeks after treatment initiation demonstrated decreasing HSV IgM (0.22 AI) and IgG (7.96 AI) titers, pleocytosis (6 leukocytes), and protein (111 mg/dL), consistent with declining inflammation. Monthly follow-up imaging showed interval resolution of spinal enhancement and no new lesions, commensurate with resolving sensory symptoms and ataxia.