Cerebral Microbleeds Assessment and Quantification in COVID-19 Patients With Neurological Manifestations.

It is increasingly acknowledged that Coronavirus Disease 2019 (COVID-19) can have neurological manifestations, and cerebral microbleeds (CMBs) have been observed in this setting. The aim of this study was to characterize CMBs patterns on susceptibility-weighted imaging (SWI) in hospitalized patients with COVID-19 with neurological manifestations. CMBs volume was quantified and correlated with clinical and laboratory parameters. The study included patients who were hospitalized due to COVID-19, exhibited neurological manifestations, and underwent a brain MRI between March and May 2020. Neurological, clinical, and biochemical variables were reported. The MRI was acquired using a 3T scanner, with a standardized protocol including SWI. Patients were divided based on radiological evidence of CMBs or their absence. The CMBs burden was also assessed with a semi-automatic SWI processing procedure specifically developed for the purpose of this study. Odds ratios (OR) for CMBs were calculated using age, sex, clinical, and laboratory data by logistic regression analysis. Of the 1,760 patients with COVID-19 admitted to the ASST Papa Giovanni XXIII Hospital between 1 March and 31 May 2020, 116 exhibited neurological symptoms requiring neuroimaging evaluation. Of these, 63 patients underwent brain MRI and were therefore included in the study. A total of 14 patients had radiological evidence of CMBs (CMBs+ group). CMBs+ patients had a higher prevalence of CSF inflammation (p = 0.020), a higher white blood cell count (p = 0.020), and lower lymphocytes (p = 0.010); the D-dimer (p = 0.026), LDH (p = 0.004), procalcitonin (p = 0.002), and CRP concentration (p < 0.001) were higher than in the CMBs- group. In multivariable logistic regression analysis, CRP (OR = 1.16, p = 0.011) indicated an association with CMBs. Estimated CMBs volume was higher in females than in males and decreased with age (Rho = -0.38; p = 0.18); it was positively associated with CRP (Rho = 0.36; p = 0.22), and negatively associated with lymphocytes (Rho = -0.52; p = 0.07). CMBs are a frequent imaging finding in hospitalized patients with COVID-19 with neurological manifestations and seem to be related to pro-inflammatory status.

Corpus Callosum in COVID-19 Cytokinopathy

Objective: Report a COVID-19 related encephalopathy from selective white matter involvement of corpus callosum. Background: 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 39.2deg;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 hypoinflated with mild bibasilar airspace opacities. A NCCT head obtained for a stroke alert, revealed a hypodense corpus collosum. She was admitted to the ICU with worsening hypoxia, kidney injury, metabolic acidosis, and alteration of consciousness. She received tocilizumab, steroids, remdesivir and convalescent plasma exchange for a severe COVID-19 infection. After extubation she developed a dysexecutive syndrome. Design/Methods: Case report Results: 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. Conclusions: Like prior coronaviridae, severe acute respiratory syndrome coronavirus 2 (SARSCoV-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.

Susceptibility-weighted imaging reveals cerebral microvascular injury in severe COVID-19.

We evaluated the incidence, distribution, and histopathologic correlates of microvascular brain lesions in patients with severe COVID-19. Sixteen consecutive patients admitted to the intensive care unit with severe COVID-19 undergoing brain MRI for evaluation of coma or neurologic deficits were retrospectively identified. Eleven patients had punctate susceptibility-weighted imaging (SWI) lesions in the subcortical and deep white matter, eight patients had >10 SWI lesions, and four patients had lesions involving the corpus callosum. The distribution of SWI lesions was similar to that seen in patients with hypoxic respiratory failure, sepsis, and disseminated intravascular coagulation. Brain autopsy in one patient revealed that SWI lesions corresponded to widespread microvascular injury, characterized by perivascular and parenchymal petechial hemorrhages and microscopic ischemic lesions. Collectively, these radiologic and histopathologic findings add to growing evidence that patients with severe COVID-19 are at risk for multifocal microvascular hemorrhagic and ischemic lesions in the subcortical and deep white matter.