Abstract Details

A 26-year-old African American female tested positive for SARS - COV 2 in April 2020.  Her medical morbidities included uncontrolled type 1 DM (on insulin), obesity, and CKD stage III (diabetic nephropathy).

She presented with fever, headache, dyspnea, myalgia, nausea, and loss of appetite. She was tachypneic, tachycardic, hypertensive, had a temperature of 39.2° C and saturating 98% at room air. Pertinent lab values included a glucose of 212 mg/dl, creatinine of 2.7 mg/dl, BUN of 34 mg/dl, and lipase 771 IU/L. CRP was 66.9 mg/L, with a normocytic anemia of 7.9 gm/dl, ferritin 1784 ng/ml, fibrinogen of 651 mg/dl and a peak D-dimer of 10,180 ng/ml. CXR was hypo-inflated with mild bibasilar airspace opacities. 

Report a COVID-19 related encephalopathy from selective white matter involvement of corpus callosum.

A contrast enhanced MR brain confirmed an expansile T2 hyperintense signal along the complete length of corpus callosum associated with restriction of diffusion, and T1 prolongation. There was no superimposed susceptibility or pathologic enhancement. No large vessel occlusions were identifiable from gradient echo (GRE), turbo spin echo (TSE), susceptibility weighted imaging (SWI) and post contrast MR sequences. A repeat MRI brain post discharge demonstrated an improving leukoencephalopathy by virtue of normalizing ADC values.

Like prior coronaviridae, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) affects the brain over a spectrum of injury. Until we clarify direct neurotropism of SARS-CoV-2; this case is supportive of a cytokine mediated excitotoxic injury concomitant with the severity of disease.