Abstract
BackgroundThe SARS-Coronavirus-2 (SARS-CoV-2) invades the respiratory system, causing acute and sometimes severe pulmonary symptoms, but turned out to also act multisystematically with substantial impact on the brain. A growing number of studies suggests a diverse spectrum of neurological manifestations. To investigate the spectrum of symptoms, we here describe the neurological manifestations and complications of patients with proven SARS-CoV-2 infection who have been hospitalized at the RWTH University Hospital Aachen, Germany.MethodsBetween March and September 2020, we evaluated common symptoms, clinical characteristics, laboratory (including cerebrospinal fluid (CSF) analysis), radiological, and electroencephalography (EEG) data from 53 patients admitted with a positive SARS-CoV-2 polymerase chain reaction (PCR). We used the Montreal Cognitive Assessment Test (MoCA) to screen for cognitive impairment, when feasible. We compared critically ill and non-critically ill patients categorized according to the presence of Acute Respiratory Distress Syndrome (ARDS).ResultsMajor clinical neurological features of hospitalized COVID-19 patients were coordination deficits (74%), cognitive impairment (61.5%), paresis (47%), abnormal reflex status (45%), sensory abnormalities (45%), general muscle weakness and pain (32%), hyposmia (26%), and headache (21%). Patients with ARDS were more severely affected than non-ADRS patients. 29.6% of patients with ARDS presented with subarachnoid bleedings, and 11.1% showed ischemic stroke associated with SARS-CoV-2 infection. Cognitive deficits mainly affected executive functions, attention, language, and delayed memory recall. We obtained cerebrospinal fluid (CSF) by lumbar puncture in nine of the 53 patients, none of which had a positive SARS-CoV-2 PCR.ConclusionsIn line with previous findings, our results provide evidence for a range of SARS-CoV-2-associated neurological manifestations. 26% of patients reported hyposmia, emphasizing the neuro-invasive potential of SARS-CoV-2, which can enter the olfactory bulb. It can therefore be speculated that neurological manifestations may be caused by direct invasion of the virus in the CNS; however, PCR did not reveal positive intrathecal SARS-CoV-2. Therefore, we hypothesize it is more likely that the para-infectious severe pro-inflammatory impact of COVID-19 is responsible for the neurological deficits including cognitive impairment. Future studies with comprehensive longitudinal assessment of neurological deficits are required to determine potential long-term complications of COVID-19.
Highlights
The SARS-Coronavirus-2 (SARS-CoV-2) invades the respiratory system, causing acute and sometimes severe pulmonary symptoms, but turned out to act multisystematically with substantial impact on the brain
We present data from a single-center prospective study of 53 in-house COVID-19 patients hospitalized at the RWTH University Hospital Aachen in Germany, which were referred to the Department of Neurology between March and September 2020
The frequent occurrence of neurological symptoms changed this view throughout the initial weeks. (iii) The University Hospital Aachen being reference center, COVID-19 patients were transferred but their critical status did not allow for in-depth neurological examination or neurological imaging. (iv) Of the patients treated in the Intensive Care Units (ICU), 44% died [10]
Summary
The SARS-Coronavirus-2 (SARS-CoV-2) invades the respiratory system, causing acute and sometimes severe pulmonary symptoms, but turned out to act multisystematically with substantial impact on the brain. Corona Virus Disease 2019 (COVID-19) primarily affects the pulmonary system, neurological pathological manifestations in patients infected with SARS-CoV-2 have been reported already in early stages of the pandemic [1]. The detection of viral particles and genomic sequences of SARS-CoV-1 in lymphocytes and monocytes implicates a hematogenous way as a possible mechanism of viral entry into the CNS [5, 6]. Another way of CNS invasion might be SARS-CoV-2 interaction with Angiotensin-converting enzyme 2 (ACE2) receptors which are expressed in lung and intestinal epithelium but are found in the endothelial cells of the blood-brain barrier (BBB) [7]. In addition to the effects induced by the virus itself, other mechanisms including indirect effects of SARS-CoV-2 infection such as massive cytokine release, hypercoagulopathy and the organ damage it triggers, or sepsis itself have been described as possible mechanisms responsible for sequelae [2]
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