Abstract:A wide range of neurological signs and symptoms have been associated with SARS-CoV-2 infection. In the present report, we described two Italian patients diagnosed with diaphragmatic myoclonus after COVID-19. In both cases, mild lymphocytosis at cerebrospinal fluid analysis and no structural brain changes were reported. The pathophysiological origin of the myoclonus in the two cases was different. In case 1, electroencephalogram did not reveal any cortical correlates and brain imaging of the spine was unremarka… 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 ] …”
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 ] …”
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.
“…Including our case report, there were 51 cases of myoclonus or ataxia associated with COVID-19 identified. Of these, 23.5% (12/51) of cases had myoclonus and ataxia [ 9 – 16 ], 35.3% (18/51) of cases had myoclonus without ataxia [ 17 – 23 ], and 41.2% (21/51) of cases had ataxia without myoclonus [ 24 – 40 ]. Demographic information and COVID-19 characteristics are summarized in Table 1 and neurological features, investigations, treatments, and outcomes are summarized in Table 2 .…”
Section: Resultsmentioning
confidence: 99%
“…In the 21 cases with a clear time of onset for myoclonus, the median latency between COVID-19 symptoms and myoclonus was 13 days (IQR 11–21), with a minimum of 7 days and a maximum of 48 days. All cases, except one case of focal diaphragmatic myoclonus [ 17 ], described multifocal or generalized myoclonus, often involving a combination of the face, upper extremities, and lower extremities. Negative myoclonus was reported in four cases [ 22 , 23 ].…”
Background
Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic in December 2019, neurological manifestations have been recognized as potential complications. Relatively rare movement disorders associated with COVID-19 are increasingly reported in case reports or case series. Here, we present a case and systematic review of myoclonus and cerebellar ataxia associated with COVID-19.
Methods
A systematic review was performed according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guideline using the PubMed and Ovid MEDLINE databases, from November 1, 2019 to December 6, 2020.
Results
51 cases of myoclonus or ataxia associated with COVID-19, including our case, were identified from 32 publications. The mean age was 59.6 years, ranging from 26 to 88 years, and 21.6% were female. Myoclonus was multifocal or generalized and had an acute onset, usually within 1 month of COVID-19 symptoms. Myoclonus occurred in isolation (46.7%), or with ataxia (40.0%) or cognitive changes (30.0%). Most cases improved within 2 months, and treatment included anti-epileptic medications or immunotherapy. Ataxia had an acute onset, usually within 1 month of COVID-19 symptoms, but could be an initial symptom. Concurrent neurological symptoms included cognitive changes (45.5%), myoclonus (36.4%), or a Miller Fisher syndrome variant (21.2%). Most cases improved within 2 months, either spontaneously or with immunotherapy.
Conclusions
This systematic review highlights myoclonus and ataxia as rare and treatable post-infectious or para-infectious, immune-mediated phenomena associated with COVID-19. The natural history is unknown and future investigation is needed to further characterize these movement disorders and COVID-19.
Supplementary Information
The online version contains supplementary material available at 10.1007/s00415-021-10458-0.
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