key: cord-0762977-cx2bk0z0 authors: Porta-Etessam, Jesús; Yus, Miguel; García, Nuria González; Valcarcel, Andrea; Barrado-Cuchillo, Julia; Pérez-Somarriba, Juncal title: Brain inflammatory thrombogenic vasculopathy related with SARS-CoV-2 infection date: 2020-08-03 journal: Neurologia DOI: 10.1016/j.nrl.2020.07.012 sha: dd39769495e859198e9354b46983314985a6b3f2 doc_id: 762977 cord_uid: cx2bk0z0 nan The SARS-CoV-2 virus was first identified in December 2019 in the city of Wuhan, China. This novel betacoronaviridae has been related with several neurological symptoms and complication, as anosmia, headache, seizure and stroke (1) . The relationship with stroke could be explained by coagulopathy and endothelial dysfunction and there is a theoretical risk for large-vessel stroke (2) . We report a 70years-old man with subacute encephalopathy due to a multiple brain acute vascular lesions presumably related with CoviD-19 vasculopathy. We present a 70-year-old man with a diagnosis of Bence-Jones light chain disease that was admitted to hospital at the end of March complained about fever and cough. The temperature was 38ºC (100.4ºF). Neurological examination at admission was unremarkable. A chest X-ray was performed, showing new bilateral infiltrates and PCR for SARS-CoV-2 was positive. The patient was started with hydroxychloroquine and support oxygentherapy for 7 days. Ten days later, the patient experienced began with an episode of subacute disorientation and conduct disorder, without any neurological focal symptomatology. We perform a An unenhanced cranial CT that showed showing multiple low attenuate hypodense brain and cerebellar lesions, and a brain MRI with angiographic sequence acquired a week later confirmed confirms multiple supra and infratentorial subacute ischemic lesions, without large and medium vessel occlusion or stenosis (fig 1a y 1b) . An extended study that included transthoracic and transesophageal echocardiography, antiphospholidip antibodies, supra aortic arteries study was normal. Therefore, it was decided to start anticoagulant treatment, with a good evolution until the resolution of the clinical situation. Discussion We present a patient with Bence-Jones light chain disease and CoviD19 that developed an encephalopathy due to multivascular acute lesions. We hypothesize that the lesions could be related with a SARS-CoV-2 induce rain vasculopathy. Is well known, that the ACE2 receptor allows the virus that causes COVID-19 to infect and destroy our cells (3). Brain capillary express ACE2 receptor (4). This could induce an inflammatory thrombogenic vasculopathy. This catastrophic microvascular injury syndrome mediated by activation of complement pathways and the associated procoagulant state could explain this findings (5) . The microvascular injury could be also related with the high incidence of Post-intensive Care Syndrome in CoviD-19 (6). We propose that every patient with encephalopathy, acute neurological non focal symptoms or post-intensivecare syndrome should be studied to rule out a microvascular damage. showing several subacute small infarcts (arrows), with high signal in both T2 and DWI images, contrast enhancement, and decreased ADC values in some of them. Acute cerebrovascular disease following COVID-19: a single center, retrospective, observational study Large-Vessel Stroke as a Presenting Feature of Covid-19 in the Young A review on the cleavage priming of the spike protein on coronavirus by angiotensin-converting enzyme-2 and furin Effect of angiotensin II type 2 receptor on stroke, cognitive impairment and neurodegenerative diseases Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases