Introduction: Respiratory viral illnesses are associated with diverse neurological complications, including acute transverse myelitis (ATM). Among the respiratory viral pathogens, the Coronaviridae family and its genera coronaviruses have been implicated as having neurotropic and neuroinvasive capabilities in human hosts.1 Despite previous strains of coronaviruses exhibiting neurotropic and neuroinvasive capabilities, little is known about the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its involvement with the central nervous system (CNS). The current pandemic has highlighted the diverse clinical presentation of SARS-CoV-2 including a possible link to CNS manifestation with disease processes such as Guillain-Barré syndrome and cerebrovascular disease. It is critical to shed light on the varied neurological manifestation of SARS-CoV-2 to ensure clinicians do not overlook at-risk patient populations and are able to provide targeted therapies appropriately. Case Report: While there are currently no published reports on post-infectious ATM secondary to SARS-CoV-2, there is one report of parainfectious ATM attributed to SARS-CoV-2 in pre-print. Here, we present a case of infectious ATM attributed to SARS-CoV-2 in a 24-year-old male who presented with bilateral lower-extremity weakness and overflow urinary incontinence after confirmed SARS-CoV-2 infection. Magnetic resonance imaging revealed non-enhancing T2-weighted hyperintense signal abnormalities spanning from the seventh through the twelfth thoracic level consistent with acute myelitis. Conclusion: The patient underwent further workup and treatment with intravenous corticosteroids with improvement of symptoms and a discharge diagnosis of ATM secondary to SARS-CoV-2.

Mitochondria may be a principle source of oxidative stress causing MI/R injury. Coenzyme Q10 (CoQ10) is essential for electron transport in normal mitochondria, has antioxidant properties but its bioavailability is likely reduced due to oxidative stress during MI/R. Coenzyme Q1 (CoQ1) is a derivative of CoQ10, but is a more potent antioxidant than CoQ10 due to a shorter isoprene chain. We hypothesize that CoQ1 will exhibit better cardioprotective effects during MI/R. CoQ1 (MW=250 g/mol; 20 μM, n=4) and CoQ10 (MW=863 g/mol; 20 μM, n=5) were given at reperfusion in isolated rat hearts subjected to I (30 min)/R (45 min). We found that MI/R hearts (n=7) and MI/R+DMSO hearts (n=4) (1% DMSO was used to solubilize CoQ1 and CoQ10) exhibited significantly compromised cardiac contractile/diastolic pressures and coronary flow during reperfusion compared to those of sham hearts (n=5). By contrast, the final left ventricular developed pressure was significantly improved by CoQ1 treatment (53.5±5.5 mmHg), but not CoQ10 treatment (38.4±8.6 mmHg), when compared to that in MI/R hearts (33.6±6.2 mmHg) and MI/R+DMSO hearts (36.4±9.7 mmHg) (p<0.05). Similarly, the final peak of the first derivative of left ventricular pressure was significantly higher in CoQ1 treatment (1180.2±103.0 mmHg/s), but not CoQ10 treatment (770.6±120.1 mmHg/s), when compared to that in MI/R hearts (700.6±134.7 mmHg/s) and MI/R+DMSO hearts (and 741.5±168.6 mmHg/s) (p<0.05). CoQ1 and CoQ10 treated hearts showed no improvement on diastolic pressure and coronary flow compared to the controls. Moreover, infarct size was reduced by CoQ1 treatment (25±3%) and CoQ10 treatment (29±4%) compared to that in untreated MI/R (44±6%) and MI/R+DMSO (32±4%). In summary, our preliminary results indicate that CoQ1 was more effective than CoQ10 in restoring post‐reperfused cardiac contractile function, but not infarct size during MI/R.Support or Funding InformationThis study was supported by Division of Research, the Center for Chronic Disorders of Aging, and Department of Bio‐Medical Sciences at Philadelphia College of Osteopathic Medicine.

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