Neurological manifestations of coronavirus infections - a systematic review.

To optimize diagnostic workup of the current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, we systematically reviewed neurological and neuroradiological manifestations of SARS-CoV-2 and all other known human coronavirus species (HCoV). Which lessons can we learn? We identified relevant publications (until 26 July 2020) using systematic searches in PubMed, Web of Science, and Ovid EMBASE with predefined search strings. A total of 4571 unique publications were retrieved, out of which 378 publications were selected for in-depth analysis by two raters, including a total of 17549 (out of which were 14418 SARS-CoV-2) patients. Neurological complications and associated neuroradiological manifestations are prevalent for all HCoVs (HCoV-229E, HKU1, NL63, OC43, Middle East respiratory syndrome (MERS)-CoV, SARS-CoV-1, and SARS-CoV-2). Moreover there are similarities in symptomatology across different HCoVs, particularly between SARS-CoV-1 and SARS-CoV-2. Common neurological manifestations include fatigue, headache, and smell/taste disorders. Additionally, clinicians need to be attentive for at least five classes of neurological complications: (1) Cerebrovascular disorders including ischemic stroke and macro/micro-hemorrhages, (2) encephalopathies, (3) para-/postinfectious immune-mediated complications such as Guillain-Barré syndrome and acute disseminated encephalomyelitis, (4) (meningo-)encephalitis, potentially with concomitant seizures, and (5) neuropsychiatric complications such as psychosis and mood disorders. Our systematic review highlights the need for vigilance regarding neurological complications in patients infected by SARS-CoV-2 and other HCoVs, especially since some complications may result in chronic disability. Neuroimaging protocols should be designed to specifically screen for these complications. Therefore, we propose practical imaging guidelines to facilitate the diagnostic workup and monitoring of patients infected with HCoVs.

Nervous System Involvement in Coronavirus Disease 2019: Results from a Retrospective Consecutive Neuroimaging Cohort.

Background Neurologic complications in coronavirus disease 2019 (COVID-19) have been described, but the understanding of their pathophysiologic causes and neuroanatomical correlates remains limited. Purpose To report on the frequency and type of neuroradiological findings in COVID-19. Materials and Methods In this retrospective study, all consecutive adult hospitalized patients with polymerase chain reaction positivity for severe acute respiratory syndrome coronavirus 2 and who underwent neuroimaging at Karolinska University Hospital between March 2 and May 24, 2020, were included. All examinations were systematically re-evaluated by 12 readers. Summary descriptive statistics were calculated. Results A total of 185 patients with COVID-19 (62 years ± 14 [standard deviation]; 138 men) underwent neuroimaging. In total, 222 brain CT, 47 brain MRI, and seven spinal MRI examinations were performed. Intra-axial susceptibility abnormalities were the most common finding (29 of 39; 74%, 95% CI: 58, 87) in patients who underwent brain MRI, often with an ovoid shape suggestive of microvascular pathology and with a predilection for the corpus callosum (23 of 39; 59%; 95% CI: 42, 74) and juxtacortical areas (14 of 39; 36%; 95% CI: 21, 53). Ischemic and macrohemorrhagic manifestations were also observed, but vascular imaging did not demonstrate overt abnormalities. Dynamic susceptibility contrast perfusion MRI in 19 patients did not reveal consistent asymmetries between hemispheres or regions. Many patients (18 of 41; 44%; 95% CI: 28, 60) had leukoencephalopathy and one patient had a cytotoxic lesion of the corpus callosum. Other findings included olfactory bulb signal abnormalities (seven of 37; 19%), prominent optic nerve subarachnoid spaces (20 of 36; 56%), and enhancement of the parenchyma (three of 20; 15%), leptomeninges (three of 20; 15%), cranial nerves (two of 20; 10%), and spinal nerves (two of four; 50%). At MRI follow-up, regression of leukoencephalopathy and progressive leptomeningeal enhancement was observed in one patient each, respectively, which is suggestive of dynamic processes. Conclusion Patients with coronavirus disease 2019 had a wide spectrum of vascular and inflammatory involvement of both the central and peripheral nervous system. © RSNA, 2020 Online supplemental material is available for this article.

Early and late outcome prediction of death in the emergency room setting by point-of-care and laboratory assays of cardiac troponin I.

BACKGROUND: Point-of-care (POC) assays of cardiac troponins are common in the emergency department setting. The question raised was as follows: What is the clinical impact of the results of POC assays of cardiac troponins as compared with sensitive laboratory assays? METHODS: Patients admitted consecutively to the emergency department (N = 1,069) and on whom cardiac troponins were requested as part of their clinical work-up were included. Cardiac troponin I (cTnI) was measured by the POC assays-i-Stat (Abbott Diagnostics, Abbott Park, IL) and Stratus CS (Siemens Healthcare Diagnostics, Deerfield, IL)-and by the laboratory assays-Access AccuTnI (Beckman Coulter, Fullerton, CA) and Architect cTnI (Abbott Diagnostics). Results were related to early (14 days) and late outcome (median 3.3 months, range 0.1-35) as to death. RESULTS: The laboratory assays identified more patients (P < .001) with elevated levels than the two POC assays (39%-74% vs 20%-27%). Adopting the 99th percentiles upper reference limit, the Access AccuTnI identified 88% and Architect cTnI identified 81% of all patients who died of cardiovascular disease as compared with 50% and 54% for i-Stat and Stratus CS, respectively (P < .001). Negative predictive values for the laboratory assays were 97% as compared with 89% to 93% for the POC assays. Negative likelihood ratios were 0.25 (CI 0.15-0.041) and 0.59 to 0.68 (CI 0.47-0.79), respectively. CONCLUSIONS: The current POC cTnI assays are less sensitive for outcome prediction of patients with myocardial injury. The clinical judgment of the patient with suspected myocardial ischemia should not solely rely on results from POC assays. If a clinical suspicion of myocardial injury remains despite negative cTnI results with the POC assays, such results should be complemented by results from sensitive laboratory assays.