Abstract:The common presenting symptoms of fever, fatigue, and mild respiratory symptoms like dry cough, are associated with COVID-19, however, patients can also develop neurological manifestations like headache, anosmia, hyposmia, dysgeusia, meningitis, encephalitis, and acute cerebrovascular accidents during the disease. Although very rare, these neurological manifestations are sometimes the sole initial presenting complaint of COVID-19. This case report discusses patients where the initial presenting symptoms seemed… Show more
“…CSF pleocytosis may be indicative of infection, inflammation or other CNS injury [ 247 ]. There were 29/409 patients (7%) who had a CSF WBC count of 21–100 cells/μL, all of whom had symptoms that localized to the CNS; 10 (34%) of these patients had CSF RBC counts provided, all of whom had a CSF RBC count of <300 cells/μL; Naz et al described a patient with headache and indicated that CSF was consistent with viral meningitis, but the CSF WBC count was unclear, as it was noted that he had 90 lymphocytes and 10 neutrophils (no units provided so we were unsure if these were percentages or numbers of cells), so we classified these findings as “increased WBC.” [ 10 , [27] , [28] , [29] , 44 , 75 , 79 , [127] , [128] , [129] , 140 , 145 , 154 , 160 , 161 , 170 , 173 , 183 , 184 , 187 , 198 , 205 , 208 , 216 ] Fig. 3 Cerebrospinal fluid white blood cell count results.…”
Section: Resultsmentioning
confidence: 99%
“…There were 29/409 patients (7%) who had a CSF WBC count of 21-100 cells/μL, all of whom had symptoms that localized to the CNS; 10 (34%) of these patients had CSF RBC counts provided, all of whom had a CSF RBC count of <300 cells/μL; Naz et al described a patient with headache and indicated that CSF was consistent with viral meningitis, but the CSF WBC count was unclear, as it was noted that he had 90 lymphocytes and 10 neutrophils (no units provided so we were unsure if these were percentages or numbers of cells), so we classified these findings as "increased WBC." [10,[27][28][29]44,75,79,[127][128][129]140,145,154,160,161,170,173,183,184,187,198,205,208,216] The CSF WBC count was >100 cells/μL for 8/409 patients (2%). Although Abdel-Mannan et al noted that two patients with encephalopathy had a CSF WBC count of 8,000 cells/μL and 2,000 cells/μL in a table, they indicated in the text that CSF was acellular; we attempted to reach the authors for clarification, but were unsuccessful, so we classified these two patients as having "normal WBC") [31,75,127,130,171,199,222,241,245].…”
We sought to review the literature on cerebrospinal fluid (CSF) testing in patients with COVID-19 for evidence of viral neuroinvasion by SARS-CoV-2. Methods: We performed a systematic review of Medline and Embase between December 1, 2019 and November 18, 2020 to identify case reports or series of patients who had COVID-19 diagnosed based on positive SARS-CoV-2 polymerase chain reaction (PCR) or serologic testing and had CSF testing due to a neurologic symptom. Results: We identified 242 relevant documents which included 430 patients with COVID-19 who had acute neurological symptoms prompting CSF testing. Of those, 321 (75%) patients had symptoms that localized to the central nervous system (CNS). Of 304 patients whose CSF was tested for SARS-CoV-2 PCR, there were 17 (6%) whose test was positive, all of whom had symptoms that localized to the central nervous system (CNS). The majority (13/17, 76%) of these patients were admitted to the hospital because of neurological symptoms. Of 58 patients whose CSF was tested for SARS-CoV-2 antibody, 7 (12%) had positive antibodies with evidence of intrathecal synthesis, all of whom had symptoms that localized to the CNS. Of 132 patients who had oligoclonal bands evaluated, 3 (2%) had evidence of intrathecal antibody synthesis. Of 77 patients tested for autoimmune antibodies in the CSF, 4 (5%) had positive findings. Conclusion: Detection of SARS-CoV-2 in CSF via PCR or evaluation for intrathecal antibody synthesis appears to be rare. Most neurological complications associated with SARS-CoV-2 are unlikely to be related to direct viral neuroinvasion.
“…CSF pleocytosis may be indicative of infection, inflammation or other CNS injury [ 247 ]. There were 29/409 patients (7%) who had a CSF WBC count of 21–100 cells/μL, all of whom had symptoms that localized to the CNS; 10 (34%) of these patients had CSF RBC counts provided, all of whom had a CSF RBC count of <300 cells/μL; Naz et al described a patient with headache and indicated that CSF was consistent with viral meningitis, but the CSF WBC count was unclear, as it was noted that he had 90 lymphocytes and 10 neutrophils (no units provided so we were unsure if these were percentages or numbers of cells), so we classified these findings as “increased WBC.” [ 10 , [27] , [28] , [29] , 44 , 75 , 79 , [127] , [128] , [129] , 140 , 145 , 154 , 160 , 161 , 170 , 173 , 183 , 184 , 187 , 198 , 205 , 208 , 216 ] Fig. 3 Cerebrospinal fluid white blood cell count results.…”
Section: Resultsmentioning
confidence: 99%
“…There were 29/409 patients (7%) who had a CSF WBC count of 21-100 cells/μL, all of whom had symptoms that localized to the CNS; 10 (34%) of these patients had CSF RBC counts provided, all of whom had a CSF RBC count of <300 cells/μL; Naz et al described a patient with headache and indicated that CSF was consistent with viral meningitis, but the CSF WBC count was unclear, as it was noted that he had 90 lymphocytes and 10 neutrophils (no units provided so we were unsure if these were percentages or numbers of cells), so we classified these findings as "increased WBC." [10,[27][28][29]44,75,79,[127][128][129]140,145,154,160,161,170,173,183,184,187,198,205,208,216] The CSF WBC count was >100 cells/μL for 8/409 patients (2%). Although Abdel-Mannan et al noted that two patients with encephalopathy had a CSF WBC count of 8,000 cells/μL and 2,000 cells/μL in a table, they indicated in the text that CSF was acellular; we attempted to reach the authors for clarification, but were unsuccessful, so we classified these two patients as having "normal WBC") [31,75,127,130,171,199,222,241,245].…”
We sought to review the literature on cerebrospinal fluid (CSF) testing in patients with COVID-19 for evidence of viral neuroinvasion by SARS-CoV-2. Methods: We performed a systematic review of Medline and Embase between December 1, 2019 and November 18, 2020 to identify case reports or series of patients who had COVID-19 diagnosed based on positive SARS-CoV-2 polymerase chain reaction (PCR) or serologic testing and had CSF testing due to a neurologic symptom. Results: We identified 242 relevant documents which included 430 patients with COVID-19 who had acute neurological symptoms prompting CSF testing. Of those, 321 (75%) patients had symptoms that localized to the central nervous system (CNS). Of 304 patients whose CSF was tested for SARS-CoV-2 PCR, there were 17 (6%) whose test was positive, all of whom had symptoms that localized to the central nervous system (CNS). The majority (13/17, 76%) of these patients were admitted to the hospital because of neurological symptoms. Of 58 patients whose CSF was tested for SARS-CoV-2 antibody, 7 (12%) had positive antibodies with evidence of intrathecal synthesis, all of whom had symptoms that localized to the CNS. Of 132 patients who had oligoclonal bands evaluated, 3 (2%) had evidence of intrathecal antibody synthesis. Of 77 patients tested for autoimmune antibodies in the CSF, 4 (5%) had positive findings. Conclusion: Detection of SARS-CoV-2 in CSF via PCR or evaluation for intrathecal antibody synthesis appears to be rare. Most neurological complications associated with SARS-CoV-2 are unlikely to be related to direct viral neuroinvasion.
“…Loss of smell and taste are the most common peripheral nervous system symptoms which were consistently presented early during infection, emerging from 0 to 3 days of confirmation (Naz et al, 2020). Most patients recover after 1 to 3 weeks, as reported by a study done in an Egyptian hospital (n=65), where more than 80% patients experienced partial or complete loss of smell and taste (Al-Zaidi & Badr, 2020).…”
Ever since the first reported case series on SARS-CoV-2-induced neurological manifestation in Wuhan, China in April 2020, various studies reporting similar as well as diverse symptoms of COVID-19 infection relating to the nervous system were published. Since then, scientists started to uncover the mechanism as well as pathophysiological impacts it has on the current understanding of the disease. SARS-CoV-2 binds to the ACE2 receptor which is present in certain parts of the body which are responsible for regulating blood pressure and inflammation in a healthy system. Presence of the receptor in the nasal and oral cavity, brain, and blood allows entry of the virus into the body and cause neurological complications. The peripheral and central nervous system could also be invaded directly in the neurogenic or hematogenous pathways, or indirectly through overstimulation of the immune system by cytokines which may lead to autoimmune diseases. Other neurological implications such as hypoxia, anosmia, dysgeusia, meningitis, encephalitis, and seizures are important symptoms presented clinically in COVID-19 patients with or without the common symptoms of the disease. Further, patients with higher severity of the SARS-CoV-2 infection are also at risk of retaining some neurological complications in the long-run. Treatment of such severe hyperinflammatory conditions will also be discussed, as well as the risks they may pose to the progression of the disease. For this review, articles pertaining information on the neurological manifestation of SARS-CoV-2 infection were gathered from PubMed and Google Scholar using the search keywords "SARS-CoV-2", "COVID-19", and "neurological dysfunction". The findings of the search were filtered, and relevant information were included.
“…Обращают на себя внимание случаи развития нейроковида, в том числе тяжелых форм (менингит, энцефалит, миелит), без предшествующих типичных респираторных проявлений [161][162][163]. Это порождает вопросы о том, что же в этих случаях служит входными воротами для инфекции, каким образом возбудитель может преодолевать гематоэнцефалический барьер при гематогенной диссеминации первично респираторной инфекции?…”
COVID-19 usually manifests by respiratory symptoms. However, it would be an erroneous simplification to consider it as a local respiratory disease. The nervous system and intestines are often involved even in patients with mild infection, although the risk of dissemination of the infectious process and the development of severe systemic disease is mainly associated with lung damage. The addition of infectious thrombotic microvasculitis (endothelitis) to bronchopneumonia-alveolitis not only forms a substrate for respiratory failure, but also increases a risk of viruses entry into the bloodstream. Viral sepsis develops, whereas inflammatory thrombosis damages new areas of the vascular bed. These mechanisms or direct viral invasion can result in involvement of many tissues and organs in the pathological process. This review examines the molecular, cellular and clinical manifestations and complications of the new coronavirus disease.
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