zerebraler Infarkt bei Covid 19 Infektion

Neurological

complications in pediatric patients with SARS-CoV-2 infection: a systematic review of the literature. MRI DWI: lesion in the left subcortical white matter

Neurological

complications in pediatric patients with SARS-CoV-2 infection: a systematic review of the literature. MRI DWI: lesion of the splenium of corpus callosum (transversal section)

Neurological

complications in pediatric patients with SARS-CoV-2 infection: a systematic review of the literature. MRI DWI: lesion of the splenium of corpus callosum (sagittal section)

Central

nervous system complications associated with SARS-CoV-2 infection: integrative concepts of pathophysiology and case reports. COVID-19 related stroke and posterior reversible encephalopathy syndrome. a Ischemic and hemorrhagic infarcts. A 73-year-old female presented with respiratory difficulty related to COVID-19 necessitating intubation. Following extubation and cessation of sedation, she remained persistently somnolent and was noted to have weakness of all extremities. Initial NIHSS was 12. Past medical history was notable for coronary artery disease, congestive heart failure, hypertension, and diabetes mellitus. Laboratory findings were notable for slightly elevated CRP (1.2 mg/dl) and significant elevation of ferritin (754 ng/ml) and D-Dimer (4184 ng/ml). Axial FlAIR MR images (1, 2, 3) demonstrate multifocal areas of signal abnormalities involving both cerebellar hemispheres, right occipital lobe, and right frontal lobe, with a hemorrhagic component (mostly involving right frontal region). Smaller foci of signal abnormality were present in the parietal cortices and centrum semiovale. Axial DWI (4, 5, 6) display multifocal areas of diffusion restriction consistent with acute ischemia. Hypercoagulopathy is the likely etiology of strokes. The patient had been on clopidogrel and low dose enoxaparin (DVT prophylaxis) before her stroke. Her neurological condition improved substantially with only minimal residual left hemiparesis and mild ataxia were noted at the first follow-up visit, which was several weeks after hospital discharge. b Posterior reversible encephalopathy syndrome (PRES). A 43-year-old SARS-CoV-2-positive female presented with respiratory distress that progressed rapidly to ARDS. Serological findings were notable for elevation of CRP (32 mg/dl), ferritin (259 ng/ml), and D-Dimer (7643 ng/ml). Post-extubation, she remained lethargic despite discontinuation of sedatives. She was slightly hypotensive to normotensive. The neurological exam showed lethargy, dysconjugate gaze, and triplegia. CSF analysis was entirely normal. Oligoclonal bands were absent. IgG index 0.8 (normal < 0.7). Notably, the neurological recovery was slow and concurrent with the return of serum inflammatory markers to normal levels. T2W MR images (1, 2) demonstrate bilateral parietal, and to a lesser extent frontal lobe, signal hyperintensities consistent with vasogenic edema. There is no corresponding high signal intensity on DWI (3, 4) or low signal intensity on ADC (5, 6) to suggest diffusion restriction. The findings are suggestive of PRES associated with high circulating markers of inflammation and coagulation pathways activation. The patient exhibited a slow, but steady, recovery concurrent with the reduction of serum levels of the inflammatory markers. This recovery was further enhanced by a 3-day course of intravenous pulse methylprednisolone (1000 mg/day). She was discharged home with only mild cognitive and motor impairment

Central

nervous system complications associated with SARS-CoV-2 infection: integrative concepts of pathophysiology and case reports. Strokes and concurrent subacute inflammatory necrotizing response. An 84-year-old SARS-CoV-2-positive female presented solely with rapidly progressive encephalopathy and neurological decline associated with mild left sided hemiparesis and left sided-visuospatial neglect. There were no concurrent respiratory or any other systemic symptoms. Serological findings were remarkable for CRP of 5.89 mg/dl, ferritin of 383 ng/dl, and D-Dimer of 852 ng/dl, and positive anticardiolipin IgM antibodies of 32.CSF analysis revealed elevated protein (153 mg/dl), normal glucose, and a cell count of three nucleated cells. Computed tomography (CT) scan (1, 2) shows prominent vasogenic edema nearly involving the entire right temporal lobe (green arrow), watershed subacute-chronic ischemic infarction of the right anterior frontal (red arrow), and old cystic encephalomalacia of the left parietal (blue arrow). 3D CT angiogram (3) shows normal flow through the right middle cerebral artery without evidence of large vessel occlusion or high grade stenosis. Axial T1-(4) and T1-weighted post-gadolinium [axial (5) and sagittal (6)] MR images show diffuse gyral cortical enhancement with subcortical areas of necrosis involving right temporal lobe (green arrow). Axial FLAIR (7) and axial T2W (8) MR images reveal signal hyperintensities with gyral swelling nearly involving the entire right temporal lobe and insula (green arrow) associated with petechial hemorrhage, best seen on the gradient echo image (9). In addition, there are subacute-chronic infarct of the right anterior lateral frontal lobe (red arrow) and a wedge-shaped old cystic encephalomalacia of the left parietal lobe (blue arrow). Following treatment with tocilizumab 560 mg (4 mg/kg), the patient exhibited significant improvement of the mental status and left hemiparesis and was subsequently discharged home. Hypercoagulopathy is the likely etiology of the right frontal and left parietal strokes. The appearance of the concurrent right temporal lobe and insula abnormalities is highly suggestive of an independent subacute inflammatory-necrotizing, rather than ischemic, process. This is supported by the findings of completely patent right middle cerebral artery, diffuse gyral swelling and enhancement with concurrent prominent subcortical vasogenic edema and necrosis, and significantly elevated CSF protein. Although the precise mechanisms underlying vasogenic edema and necrosis remain unclear, we suggest that localized hyper-inflammation provoked by exuberant innate immune response (CNS cytokine response) might be pathogenetically relevant. Direct viral neuroinvasion and involvement of the neurovascular endothelial cells were subsequently excluded by the brain biopsy from the right temporal necrotizing lesion