Neurological emergencies associated with COVID-19: stroke and beyond

Abstract

Novel coronavirus disease (COVID-19) was declared a global pandemic on March 1, 2020. Neurological manifestations are now being reported worldwide, including emergent presentation with acute neurological changes as well as a comorbidity in hospitalized patients. There is limited knowledge on the neurologic manifestations of COVID-19 at present, with a wide array of neurological complications reported, ranging from ischemic stroke to acute demyelination and encephalitis. We report five cases of COVID-19 presenting to the ER with acute neurological symptoms, over the course of 1 month. This includes two cases of ischemic stroke, one with large-vessel occlusion and one with embolic infarcts. The remainders of the cases include acute tumefactive demyelination, isolated cytotoxic edema of the corpus callosum with subarachnoid hemorrhage, and posterior reversible encephalopathy syndrome (PRES).

Keywords: COVID-19; Hypercoagulable; MRI; Neurological; Neurotropism.

Fig. 1

Ischemic stroke with large vessel occlusion: Non-contrast head (a) shows moderate size acute infarct in the left MCA territory. Cerebral blood volume (CBV) map (b) shows corresponding acute infarct core with Time to Peak (TTP) map (c) showing large area of ischemic penumbra. CT and catheter angiogram images depicting the left MCA thrombotic occlusion (d, e) with significant revascularization post mechanical thrombectomy (f)

Fig. 2

Ischemic stroke with embolic infarcts: Chest CT images (a,b) reveal multi-focal consolidative and ground-glass pulmonary opacities, along with areas of crazy paving suggesting acute lung injury. Multiple diffusion-weighted images (c–e) show acute punctate embolic infarcts (arrows)

Fig. 3

Acute tumefactive demyelination: Sagittal T1 (a), sagittal T2-FLAIR (b), axial T2-FLAIR (c), diffusion-weighted image (d), axial (e), and coronal (f) post-contrast images reveal extensive foci of demyelination in the supratentorial brain with marked involvement of the corpus callosum and pericallosal white matter. Many of these lesions show restricted diffusion and patchy enhancement (arrows)

Fig. 4

Cytotoxic lesion of the corpus callosum: Multiple CT head images reveal edema with hypodensity involving the posterior body and splenium of corpus callosum (white arrows). Minimal subarachnoid hemorrhage seen along right parietal convexity (black arrow)

Fig. 5

Posterior reversible encephalopathy syndrome (PRES): axial T2-FLAIR images (a,b) and axial T2-spine echo image (c) reveals near-symmetric areas of subcortical signal changes with edema and sulcal effacement in the occipital lobes. Apparent diffusion coefficient (ADC) maps (d) show increased signal representing facilitated diffusion as seen in vasogenic edema