PMC:7546130 / 6606-11824 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7546130","sourcedb":"PMC","sourceid":"7546130","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7546130","text":"Discussion\nWe present a patient with pulmonary COVID-19 infection who developed neurological symptoms characterized by severely impaired consciousness, with multiple DWI areas of restricted diffusion and scattered SWI hypointensities at brain MRI and CSF positivity for SARS-CoV-2 RNA.\nNeurological complications following COVID-19 infection are not uncommon [2], and various putative mechanisms for brain involvement have been suggested [3]. Our patient presented MRI signs of brain vascular injury, characterized by the coexistence of acute ischemic areas and scattered microbleeds or alternatively microthrombi. The underlying mechanisms, which include direct and indirect penetration of the virus to the central nervous system and systemic cardiorespiratory complications [4], are yet to be elucidated, and a direct correlation with SARS-CoV-2 infection remains uncertain, but we tried to make some observations.\nFirst, the multiple supratentorial ischemic lesions seen on DWI, with corpus callosum involvement, do not depict a territorial distribution, inconsistent with COVID-19-associated large vessel occlusion [5]. Instead, they might reflect diffuse local thrombosis or, less likely, embolism. In this setting, high D-dimer values may reflect thrombus formation, but they can also act as acute-phase enhancer of the inflammatory cascade and stimulates monocyte synthesis and release of proinflammatory cytokines, which can contribute to the occurrence of stroke [6]. We cannot ascertain a specific correlation of the DWI findings with SARS-CoV2 infection in our patient. Nevertheless, similar MRI findings of bilateral supratentorial and corpus callosum DWI lesions have been described in COVID-19 patients with similar clinical manifestations [2].\nThe SWI hypointense foci in our patient are also of difficult interpretation. In fact, SWI hypointensities in the corpus callosum and in the cortical/iuxtacortical regions of COVID-19 patients with neurological impairment have been reported [7], but their pathological correlate is not univocal, as they could represent microbleeds or microthrombi. In one pathology study, microhemorrages were detected on brain tissue at the location of SWI hypointensities [8]. Though a coagulopathic disorder has been reported in COVID-19 patients, diffuse, mostly peripherally distributed brain microbleeds can also be the expression of critical illness in ICU patients [9].\nAcute necrotizing encephalopathy (ANE) [2], with similar bithalamic SWI hypointensities, has been reported in COVID-19 patients, but the MRI picture we describe is different, because no signs of edema and necrosis were evident.\nOur patient did not develop any EEG abnormalities typically related to meningoencephalitis, hypoxic encephalopathy, or renal failure, such as epileptiform focal abnormalities and lateralized or generalized periodic discharges. Accordingly, post-contrast MRI showed a lack of parenchymal and meningeal enhancement, and no MRI signs of encephalitis were present.\nThe meaning of SARS-CoV-2 RNA positivity in the CSF of our patient is unclear. A direct effect of the virus, with normal proteins and no pleocytosis in the CSF, is questionable. Viral neurotropism has been largely theorized, and virus particles have been observed to cross the capillary endothelium of the brain blood barrier (BBB) [10], but direct implication of SARS-CoV-2 in neurological manifestations is controversial, and viral RNA in the CSF of patients with neurological complications is only rarely detected [11]. In a recent study including 31 patients with neurological manifestations, none had CSF viral positivity, but many had signs of disturbance of the blood brain barrier (BBB) integrity [12]. Our patient showed signs of mild damage of the BBB as well, which might also be a possible consequence of systemic inflammation, in a patient with multiple organ failure. Therefore, an indirect mechanism of neurovascular unit breakdown, resulting in a passage of the virus in the CSF through the damaged BBB, cannot be excluded. Contamination or artifact could also be a possibility [11].\nIn COVID-19 pneumonia, the extensive microvascular damage seems to be related to a macrophage activation syndrome (MAS)-like mechanism [13], which induces a coagulopathic cascade with subsequent local microthrombosis and microbleeding in the lungs. A similar mechanism could be responsible for central nervous system manifestations, but supporting data are scarce.\nWe consider this case an example of neurological manifestations possibly related to COVID-19, characterized by vascular damage predominantly involving microvessels. The absence of pathological confirmation represents a major limitation, but similar MRI patterns [2] and recent pathological correlations seem to support a microangiopathic substrate [8]. Different mechanisms including a systemic procoagulative status and systemic and local inflammatory processes involving the endothelium, most likely via the ACE2 receptor, and eventual immune-mediated vascular injury could be considered [11]. Clinicians should be aware of the possible severe neurological complications in COVID-19 patients and of the role of MRI in their 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