Palilalia as a prominent feature of anti-NMDA receptor encephalitis in a woman with COVID-19

McHattie, Andrew W; Coebergh, Jan; Khan, Faraan; Morgante, Francesca

doi:10.1007/s00415-021-10542-5

Cited by 24 publications

(20 citation statements)

References 7 publications

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“…We did not quantify CSF anti-SARS-CoV-2 IgG and in the absence of paired serology, this would limit our ability to comment on CNS compartmentalization. Given recent literature also demonstrating that autoantibodies may be present in the CSF of patients with COVID-19 [ [44] , [45] , [46] , [47] , [48] , [49] ], further studies are required to determine whether compartmentalized anti-SARS-CoV-2 antibodies are present and if so, whether the presence of antibodies is associated with intrathecal inflammatory responses or blood brain barrier disruption despite absent pleocytosis or elevated protein.…”

Section: Discussionmentioning

confidence: 99%

Intrathecal inflammatory responses in the absence of SARS-CoV-2 nucleic acid in the CSF of COVID-19 hospitalized patients

Normandin

Holroyd

Collens

et al. 2021

Journal of the Neurological Sciences

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Objective Little is known about CSF profiles in patients with acute COVID-19 infection and neurological symptoms. Here, CSF was tested for SARS-CoV-2 RNA and inflammatory cytokines and chemokines and compared to controls and patients with known neurotropic pathogens. Methods CSF from twenty-seven consecutive patients with COVID-19 and neurological symptoms was assayed for SARS-CoV-2 RNA using quantitative reverse transcription PCR (RT-qPCR) and unbiased metagenomic sequencing. Assays for blood brain barrier (BBB) breakdown (CSF:serum albumin ratio (Q-Alb)), and proinflammatory cytokines and chemokines (IL-6, IL-8, IL-15, IL-16, monocyte chemoattractant protein −1 (MCP-1) and monocyte inhibitory protein – 1β (MIP-1β)) were performed in 23 patients and compared to CSF from patients with HIV-1 (16 virally suppressed, 5 unsuppressed), West Nile virus (WNV) ( n = 4) and 16 healthy controls (HC). Results Median CSF cell count for COVID-19 patients was 1 white blood cell/μL; two patients were infected with a second pathogen ( Neisseria , Cryptococcus neoformans ). No CSF samples had detectable SARS-CoV-2 RNA by either detection method. In patients with COVID-19 only, CSF IL-6, IL-8, IL-15, and MIP-1β levels were higher than HC and suppressed HIV (corrected- p < 0.05). MCP-1 and MIP-1β levels were higher, while IL-6, IL-8, IL-15 were similar in COVID-19 compared to WNV patients. Q-Alb correlated with all proinflammatory markers, with IL-6, IL-8, and MIP-1β ( r ≥ 0.6, p < 0.01) demonstrating the strongest associations. Conclusions Lack of SARS-CoV-2 RNA in CSF is consistent with pre-existing literature. Evidence of intrathecal proinflammatory markers in a subset of COVID-19 patients with BBB breakdown despite minimal CSF pleocytosis is atypical for neurotropic pathogens.

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Section: Discussionmentioning

confidence: 99%

Intrathecal inflammatory responses in the absence of SARS-CoV-2 nucleic acid in the CSF of COVID-19 hospitalized patients

Normandin

Holroyd

Collens

et al. 2021

Journal of the Neurological Sciences

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“…All patients had positive GluN1 antibodies in the CSF. Only patients 1–4 showed pronounced respiratory symptoms including low O 2 saturation, bilateral milk glass opacities on chest x-ray and patchy bibasilar consolidation on chest computed tomography (CT) imaging [ 10 – 12 ], and severe hypoxemia with bilateral infiltrations [ 13 ]. Patients 2, 3 and 5–8 developed epileptic seizures during the course [ 11 , 12 , 14 – 16 , 18 ].…”

Section: Resultsmentioning

confidence: 99%

“…Patients 1 and 5–8 exhibited motor failures or dysarthria [ 10 , 14 – 16 , 18 ]. Cases 4 and 8 had increased levels of C-reactive protein (CRP) and patients 3, 4 and 8 had decreased lymphocytes [ 12 , 13 , 16 ]. Increased interleukin-6 (IL-6) levels were found in blood and CSF in one subject (patient 5) [ 14 ] and only in CSF in another (patient 1) [ 10 ].…”

Section: Resultsmentioning

confidence: 99%

“…Patient 2 had ovarian teratoma as an associated malignancy and potential alternative trigger of disease [ 11 ]. EEG recordings from patients 1, 4, 5 and 8 showed a slowdown, and one of these (patient 5) showed an extreme delta brush-like pattern, typical for the diagnosis [ 10 , 13 , 14 , 16 ]. In five patients, imaging examinations of the brain appeared normal but patient 4 showed hyperintensities on fluid-attenuated inversion recovery (FLAIR) images in left amygdala, left anterior putamen with negligible effects in the right amygdala [ 13 ].…”

Section: Resultsmentioning

confidence: 99%

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Molecular mimicry of NMDA receptors may contribute to neuropsychiatric symptoms in severe COVID-19 cases

Vasilevska

Guest

Bernstein

et al. 2021

J Neuroinflammation

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Approximately 30% of individuals with severe SARS-CoV-2 infections also develop neurological and psychiatric complaints. In rare cases, the occurrence of autoimmune encephalitis has been reported after SARS-CoV-2 infection. In this systematic review, we have identified eight SARS-CoV-2-associated cases of anti-NMDA receptor encephalitis. All had cerebrospinal fluid antibodies against the NMDA receptor and a recent onset of working memory deficits, altered mental status, or psychiatric symptoms, such as confusion, agitation, auditory hallucination, catatonia and speech dysfunction. All patients received high-dose steroid and immunoglobulin therapeutics and conditions improved in each case. These findings suggest that clinical attention should be paid to warning signs of autoimmune encephalitis in severe COVID-19 cases. If characteristic features of autoimmune encephalitis are present, autoantibody diagnostics should be performed and confirmed cases should be treated with immunotherapy to minimize neurological impairments.

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“…This mimicry may lead to the generation of IgG antibodies against the NMDAR subunits after SARS-CoV-2 infection. Recent case reports describing the development of NMDAR encephalitis in temporal association with SARS-CoV-2 positivity support this hypothesis (46)(47)(48)(49)(50)(51). Activation of TH17 cells in COVID-19 sufferers may be a facilitating factor, as this has generally been associated with the occurrence of autoimmune diseases.…”

Section: Biological Mechanisms Of Mental Disorders In the Context Of Covid-19mentioning

confidence: 94%

Potential Cross-Links of Inflammation With Schizophreniform and Affective Symptoms: A Review and Outlook on Autoimmune Encephalitis and COVID-19

et al. 2021

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Based on current implications of the SARS-CoV-2 pandemic with regards to mental health, we show that biological links exist between inflammation and mental illness in addition to psychoreactive effects. We describe key principles of the biological interaction of the immune system and the mind, as well as the possible routes of viral entry into the brain. In addition, we provide a stepwise scheme for the diagnosis and therapy of autoimmune-encephalitis with schizophrenia-like symptomatology as a general guide for clinical practice and in the specialized scenario of infections, such as those caused by the SARS-CoV-2 virus.

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Palilalia as a prominent feature of anti-NMDA receptor encephalitis in a woman with COVID-19

Cited by 24 publications

References 7 publications

Intrathecal inflammatory responses in the absence of SARS-CoV-2 nucleic acid in the CSF of COVID-19 hospitalized patients

Intrathecal inflammatory responses in the absence of SARS-CoV-2 nucleic acid in the CSF of COVID-19 hospitalized patients

Molecular mimicry of NMDA receptors may contribute to neuropsychiatric symptoms in severe COVID-19 cases

Potential Cross-Links of Inflammation With Schizophreniform and Affective Symptoms: A Review and Outlook on Autoimmune Encephalitis and COVID-19

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