PMC:7253233 / 2662-4238 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7253233","sourcedb":"PMC","sourceid":"7253233","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7253233","text":"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged first in Wuhan, China, in 2019 and spread rapidly worldwide as a pandemic of the twenty-first century. The symptoms and disease manifestations caused by SARS-CoV-2 were named Coronavirus disease 2019 (COVID-19) by the World Health Organization [1]. The neurological manifestations of this disease are not well known, and there is growing evidence that the disease has effects on the central nervous system (CNS) as detailed in retrospective reports from several centers worldwide. An initial retrospective case series from Wuhan, China, showed that neurological manifestations are present in patients with COVID-19 disease [2]. In that series, 45.5% of patients with COVID-19 disease who had severe systemic disease burden also suffered from acute cerebrovascular disease, acute encephalopathy, and skeletal muscle symptoms. These patients also had higher levels of inflammatory markers and greater evidence of multi-organ failure. However, the study did not elucidate how many patients with encephalopathy were monitored and treated for acute symptomatic seizures. Another series of patients were reported in Strasbourg, France, with neurological features of encephalopathy and corticospinal tract signs. Only a small proportion of the patients (8 out of 64) had electroencephalography performed, which demonstrated diffuse slowing consistent with encephalopathy [3]. 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