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1.
Front Immunol ; 12: 674922, 2021.
Article in English | MEDLINE | ID: covidwho-1607886

ABSTRACT

Since December 2019, the world has been facing an outbreak of a new disease called coronavirus disease 2019 (COVID-19). The COVID-19 pandemic is caused by a novel beta-coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The SARS-CoV-2 infection mainly affects the respiratory system. Recently, there have been some reports of extra-respiratory symptoms such as neurological manifestations in COVID-19. According to the increasing reports of Guillain-Barré syndrome following COVID-19, we mainly focused on SARS-CoV-2 infection and Guillain-Barré syndrome in this review. We tried to explain the possibility of a relationship between SARS-CoV-2 infection and Guillain-Barré syndrome and potential pathogenic mechanisms based on current and past knowledge.


Subject(s)
COVID-19/complications , Guillain-Barre Syndrome/etiology , SARS-CoV-2/pathogenicity , COVID-19/epidemiology , COVID-19/immunology , COVID-19/pathology , Guillain-Barre Syndrome/epidemiology , Guillain-Barre Syndrome/immunology , Guillain-Barre Syndrome/pathology , Humans , Nervous System Diseases/epidemiology , Nervous System Diseases/etiology , Nervous System Diseases/immunology , Nervous System Diseases/pathology , Virulence
2.
Neurol Neuroimmunol Neuroinflamm ; 9(1)2022 01.
Article in English | MEDLINE | ID: covidwho-1596607

ABSTRACT

BACKGROUND AND OBJECTIVES: To investigate whether children receiving immunosuppressive therapies for neuroimmunologic disorders had (1) increased susceptibility to SARS-CoV2 infection or to develop more severe forms of COVID-19; (2) increased relapses or autoimmune complications if infected; and (3) changes in health care delivery during the pandemic. METHODS: Patients with and without immunosuppressive treatment were recruited to participate in a retrospective survey evaluating the period from March 14, 2020, to March 30, 2021. Demographics, clinical features, type of immunosuppressive treatment, suspected or confirmed COVID-19 in the patients or cohabitants, and changes in care delivery were recorded. RESULTS: One hundred fifty-three children were included: 84 (55%) female, median age 13 years (interquartile range [8-16] years), 79 (52%) on immunosuppressive treatment. COVID-19 was suspected or confirmed in 17 (11%) (all mild), with a frequency similar in patients with and without immunosuppressive treatment (11/79 [14%] vs 6/74 [8%], p = 0.3085). The frequency of neurologic relapses was similar in patients with (18%) and without (21%) COVID-19. Factors associated with COVID-19 included having cohabitants with COVID-19 (p < 0.001) and lower blood levels of vitamin D (p = 0.039). Return to face-to-face schooling or mask type did not influence the risk of infection, although 43(28%) children had contact with a classmate with COVID-19. Clinic visits changed from face to face to remote for 120 (79%) patients; 110 (92%) were satisfied with the change. DISCUSSION: In this cohort of children with neuroimmunologic disorders, the frequency of COVID-19 was low and not affected by immunosuppressive therapies. The main risk factors for developing COVID-19 were having cohabitants with COVID-19 and low vitamin D levels.


Subject(s)
COVID-19/complications , COVID-19/immunology , Immunocompromised Host , Immunosuppressive Agents/adverse effects , Nervous System Diseases/complications , Nervous System Diseases/immunology , SARS-CoV-2/immunology , Adolescent , COVID-19/prevention & control , COVID-19/virology , Child , Delivery of Health Care/organization & administration , Delivery of Health Care/statistics & numerical data , Female , Humans , Immunosuppressive Agents/therapeutic use , Male , Masks/statistics & numerical data , Masks/virology , Nervous System Diseases/virology , Pandemics , Recurrence , Retrospective Studies , Vitamin D/blood
3.
Front Immunol ; 12: 704110, 2021.
Article in English | MEDLINE | ID: covidwho-1376699

ABSTRACT

Patients diagnosed with malignancy, neurological and immunological disorders, i.e., fragile patients, have been excluded from COVID-19 vaccine trials. However, this population may present immune response abnormalities, and relative reduced vaccine responsiveness. Here we review the limited current evidence on the immune responses to vaccination of patients with different underlying diseases. To address open questions we present the VAX4FRAIL study aimed at assessing immune responses to vaccination in a large transdisease cohort of patients with cancer, neurological and rheumatological diseases.


Subject(s)
COVID-19 Vaccines/administration & dosage , Adult , COVID-19 Vaccines/immunology , Clinical Protocols , Humans , Immune System Diseases/immunology , Immunocompromised Host/immunology , Neoplasms/immunology , Nervous System Diseases/immunology , Patient Selection , Prospective Studies
4.
J Neuroimmunol ; 358: 577658, 2021 09 15.
Article in English | MEDLINE | ID: covidwho-1322224

ABSTRACT

Several neurological symptoms and complications have been described in association with COVID-19, such as anosmia, ageusia, encephalitis and Guillain-Barré syndrome. Here, we review the literature describing SARS-CoV-2-induced neurological manifestations and provide a comprehensive discussion of proposed mechanisms underlying the neurological pathophysiology. First, we analyse the neuroinvasiveness potential of the coronavirus family based on previous SARS-CoV-1 studies. Then, we describe the current evidence on COVID-19-induced nervous tissue damage, including processes behind brain vasculopathy and cytokine storm. We also discuss in detail anosmia and Guillain-Barré syndrome. Finally, we provide a summarised timeline of the main findings in the field. Future perspectives are presented, and suggestions of further investigations to clarify how SARS-COV-2 can affect the CNS.


Subject(s)
Brain/immunology , COVID-19/complications , COVID-19/immunology , Nervous System Diseases/etiology , Nervous System Diseases/immunology , SARS-CoV-2/immunology , Animals , Brain/pathology , COVID-19/diagnosis , Humans , Nervous System Diseases/diagnosis
5.
J Immunother Cancer ; 9(7)2021 07.
Article in English | MEDLINE | ID: covidwho-1318086

ABSTRACT

Expanding the US Food and Drug Administration-approved indications for immune checkpoint inhibitors in patients with cancer has resulted in therapeutic success and immune-related adverse events (irAEs). Neurologic irAEs (irAE-Ns) have an incidence of 1%-12% and a high fatality rate relative to other irAEs. Lack of standardized disease definitions and accurate phenotyping leads to syndrome misclassification and impedes development of evidence-based treatments and translational research. The objective of this study was to develop consensus guidance for an approach to irAE-Ns including disease definitions and severity grading. A working group of four neurologists drafted irAE-N consensus guidance and definitions, which were reviewed by the multidisciplinary Neuro irAE Disease Definition Panel including oncologists and irAE experts. A modified Delphi consensus process was used, with two rounds of anonymous ratings by panelists and two meetings to discuss areas of controversy. Panelists rated content for usability, appropriateness and accuracy on 9-point scales in electronic surveys and provided free text comments. Aggregated survey responses were incorporated into revised definitions. Consensus was based on numeric ratings using the RAND/University of California Los Angeles (UCLA) Appropriateness Method with prespecified definitions. 27 panelists from 15 academic medical centers voted on a total of 53 rating scales (6 general guidance, 24 central and 18 peripheral nervous system disease definition components, 3 severity criteria and 2 clinical trial adjudication statements); of these, 77% (41/53) received first round consensus. After revisions, all items received second round consensus. Consensus definitions were achieved for seven core disorders: irMeningitis, irEncephalitis, irDemyelinating disease, irVasculitis, irNeuropathy, irNeuromuscular junction disorders and irMyopathy. For each disorder, six descriptors of diagnostic components are used: disease subtype, diagnostic certainty, severity, autoantibody association, exacerbation of pre-existing disease or de novo presentation, and presence or absence of concurrent irAE(s). These disease definitions standardize irAE-N classification. Diagnostic certainty is not always directly linked to certainty to treat as an irAE-N (ie, one might treat events in the probable or possible category). Given consensus on accuracy and usability from a representative panel group, we anticipate that the definitions will be used broadly across clinical and research settings.


Subject(s)
Drug-Related Side Effects and Adverse Reactions/diagnosis , Immune Checkpoint Inhibitors/adverse effects , Immunotherapy/adverse effects , Nervous System Diseases/diagnosis , Practice Guidelines as Topic , Consensus , Humans , Nervous System Diseases/chemically induced , Nervous System Diseases/immunology , Neurologists/statistics & numerical data , Oncologists/statistics & numerical data , Patient Care Team/organization & administration , Patient Care Team/statistics & numerical data
6.
Curr Opin Neurol ; 34(3): 417-422, 2021 06 01.
Article in English | MEDLINE | ID: covidwho-1183108

ABSTRACT

PURPOSE OF REVIEW: Over the course of the coronavirus disease (COVID-19) pandemic, it has become increasingly clear that there is a high prevalence of neurological complications in people infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). RECENT FINDINGS: Studies of central nervous system (CNS) tissue in brain model systems and from adults with acute SARS-CoV-2 infection have begun to uncover potential mechanisms for neurological damage during COVID-19. These studies suggest that direct viral invasion of the CNS occurs in a subset of cases but does not frequently cause overt viral meningoencephalitis. Vascular abnormalities including microvascular thrombi and endothelial activation, as well as parainfectious processes, including CNS specific immune responses, may contribute to neurological symptoms during acute SARS-CoV-2 infection. SUMMARY: Neuroimmune perturbations and vascular inflammation observed in people with COVID-19 may warrant investigation of immune-modulating interventions to ameliorate neurological complications associated with acute SARS-CoV-2 infection. These therapies may also impact the trajectory of potential long-term complications of COVID-19.


Subject(s)
COVID-19/complications , Nervous System Diseases/etiology , Nervous System Diseases/pathology , Humans , Immunotherapy , Nervous System Diseases/immunology , Nervous System Diseases/therapy , Vasculitis/etiology , Vasculitis/immunology
8.
Viruses ; 13(3)2021 03 17.
Article in English | MEDLINE | ID: covidwho-1138761

ABSTRACT

In December 2019, a novel coronavirus known as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, the capital of Hubei, China. The virus infection, coronavirus disease 2019 (COVID-19), represents a global concern, as almost all countries around the world are affected. Clinical reports have confirmed several neurological manifestations in COVID-19 patients such as headaches, vomiting, and nausea, indicating the involvement of the central nervous system (CNS) and peripheral nervous system (PNS). Neuroinvasion of coronaviruses is not a new phenomenon, as it has been demonstrated by previous autopsies of severe acute respiratory syndrome coronavirus (SARS-CoV) patients who experienced similar neurologic symptoms. The hypothalamus is a complex structure that is composed of many nuclei and diverse neuronal cell groups. It is characterized by intricate intrahypothalamic circuits that orchestrate a finely tuned communication within the CNS and with the PNS. Hypothalamic circuits are critical for maintaining homeostatic challenges including immune responses to viral infections. The present article reviews the possible routes and mechanisms of neuroinvasion of SARS-CoV-2, with a specific focus on the role of the hypothalamic circuits in mediating the neurological symptoms noted during COVID-19 infection.


Subject(s)
COVID-19/complications , Hypothalamus/virology , Nervous System Diseases/virology , SARS-CoV-2/physiology , Animals , COVID-19/immunology , COVID-19/virology , Humans , Hypothalamus/immunology , Nervous System Diseases/etiology , Nervous System Diseases/immunology , SARS-CoV-2/genetics
9.
J Immunoassay Immunochem ; 41(6): 960-975, 2020 Nov 01.
Article in English | MEDLINE | ID: covidwho-1104705

ABSTRACT

In December 2019, an outbreak of pandemic severe respiratory distress syndrome coronavirus disease 2019 (COVID-19) initially occurred in China, has spread the world resulted in serious threats to human public health. Uncommon neurological manifestations with pathophysiological symptoms were observed in infected patients including headache, seizures, and neuroimmunological disorders. Regardless of whether these neurological symptoms are direct or indirect casual infection relationship, this novel viral infection has a relevant impact on the neuroimmune system that requires a neurologist's careful assessment. Recently, the use of immunotherapy has been emerged in fighting against COVID-19 infection despite the uncertain efficiency in managing COVID-19 related disorders or even its proven failure by increasing its severity. Herein, the author is addressing the first approaches in using immunotherapies in controlling COVID-19 viral impact on the brain by highlighting their role in decreasing or increasing infection risks among subjects. This point of view review article supports the use of immunotherapies in managing COVID-19 neurological disorders but in optimal timing and duration to ensure the maximum therapeutic outcome by reducing morbidity and mortality rate. Based on recently published data, the current review article highlights the beneficial effects and drawbacks of using immunotherapies to combat COVID-19 and its neurological symptoms.


Subject(s)
COVID-19/immunology , COVID-19/therapy , Cytokine Release Syndrome/virology , Immunotherapy/methods , Nervous System Diseases/immunology , Nervous System Diseases/therapy , Brain/pathology , COVID-19/complications , Cladribine/therapeutic use , Cytokine Release Syndrome/therapy , Cytokines/immunology , Glucocorticoids/therapeutic use , Headache/virology , Humans , Immunoglobulins, Intravenous/therapeutic use , Interferon-beta/immunology , Interleukin-6/immunology , Nervous System Diseases/virology , Pandemics
10.
Horm Mol Biol Clin Investig ; 42(1): 69-75, 2021 Feb 23.
Article in English | MEDLINE | ID: covidwho-1094095

ABSTRACT

COVID-19 caused by SARS CoV2 (The novel corona virus) has already taken lives of many people across the globe even more than anyone could have imagined. This outbreak occurred in China and since then it is expanding its devastating effects by leaps and bounds. Initially it appeared to be an outbreak of pneumonia but soon it was found to be much more than that and the infectivity was found to be very high. This is the reason that it has taken whole globe in its trap and become a pandemic in such a short span of time. Death is occurring because it is a new virus and human body has no specific antibodies for it. Presently there is no approved vaccine so everyone is susceptible but people with co-morbidities appear to be in more risk and the best way for protection is social distancing and increasing one's natural immunity by taking healthy diet and exercise. When a person is infected the clinical presentation ranges from asymptomatic to severe ARDS, sudden onset of anosmia, headache, cough may be the initial symptoms. This review is focused on immunopathology and effect of COVID-19 on neurological disorders and also the neurological manifestations and the treatment.


Subject(s)
COVID-19/complications , COVID-19/epidemiology , Nervous System Diseases , Pandemics , COVID-19/immunology , COVID-19/therapy , Comorbidity , Humans , Immune System/physiology , Nervous System Diseases/complications , Nervous System Diseases/epidemiology , Nervous System Diseases/immunology , Nervous System Diseases/therapy , Neuroimmunomodulation/physiology , SARS-CoV-2/immunology , SARS-CoV-2/physiology
11.
Rev Neurosci ; 32(4): 427-442, 2021 06 25.
Article in English | MEDLINE | ID: covidwho-1069660

ABSTRACT

As the coronavirus disease 2019 (COVID-19) pandemic continues to be a multidimensional threat to humanity, more evidence of neurological involvement associated with it has emerged. Neuroimmune interaction may prove to be important not only in the pathogenesis of neurological manifestations but also to prevent systemic hyperinflammation. In this review, we summarize reports of COVID-19 cases with neurological involvement, followed by discussion of possible routes of entry, immune responses against coronavirus infection in the central nervous system and mechanisms of nerve degeneration due to viral infection and immune responses. Possible mechanisms for neuroprotection and virus-associated neurological consequences are also discussed.


Subject(s)
COVID-19/complications , Central Nervous System/virology , Nervous System Diseases/complications , SARS-CoV-2/pathogenicity , COVID-19/immunology , Central Nervous System/immunology , Humans , Immunity/immunology , Nervous System Diseases/immunology , Neuroprotection/immunology , SARS-CoV-2/immunology
12.
Immunity ; 54(1): 164-175.e6, 2021 01 12.
Article in English | MEDLINE | ID: covidwho-1065205

ABSTRACT

Patients suffering from Coronavirus disease 2019 (COVID-19) can develop neurological sequelae, such as headache and neuroinflammatory or cerebrovascular disease. These conditions-termed here as Neuro-COVID-are more frequent in patients with severe COVID-19. To understand the etiology of these neurological sequelae, we utilized single-cell sequencing and examined the immune cell profiles from the cerebrospinal fluid (CSF) of Neuro-COVID patients compared with patients with non-inflammatory and autoimmune neurological diseases or with viral encephalitis. The CSF of Neuro-COVID patients exhibited an expansion of dedifferentiated monocytes and of exhausted CD4+ T cells. Neuro-COVID CSF leukocytes featured an enriched interferon signature; however, this was less pronounced than in viral encephalitis. Repertoire analysis revealed broad clonal T cell expansion and curtailed interferon response in severe compared with mild Neuro-COVID patients. Collectively, our findings document the CSF immune compartment in Neuro-COVID patients and suggest compromised antiviral responses in this setting.


Subject(s)
COVID-19/immunology , Monocytes/immunology , Nervous System Diseases/immunology , T-Lymphocytes/immunology , COVID-19/cerebrospinal fluid , COVID-19/complications , COVID-19/pathology , Cell Differentiation , Cerebrospinal Fluid/immunology , Encephalitis, Viral/cerebrospinal fluid , Encephalitis, Viral/immunology , Gene Expression Profiling , Humans , Interferons/genetics , Interferons/immunology , Leukocytes/immunology , Lymphocyte Activation , Nervous System Diseases/cerebrospinal fluid , Nervous System Diseases/etiology , Nervous System Diseases/pathology , Receptors, Antigen, T-Cell/genetics , Receptors, Antigen, T-Cell/metabolism , SARS-CoV-2/immunology , Single-Cell Analysis
13.
J Mol Neurosci ; 71(11): 2192-2209, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1037256

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic is an issue of global significance that has taken the lives of many across the world. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus responsible for its pathogenesis. The pulmonary manifestations of COVID-19 have been well described in the literature. Initially, it was thought to be limited to the respiratory system; however, we now recognize that COVID-19 also affects several other organs, including the nervous system. Two similar human coronaviruses (CoV) that cause severe acute respiratory syndrome (SARS-CoV-1) and Middle East respiratory syndrome (MERS-CoV) are also known to cause disease in the nervous system. The neurological manifestations of SARS-CoV-2 infection are growing rapidly, as evidenced by several reports. There are several mechanisms responsible for such manifestations in the nervous system. For instance, post-infectious immune-mediated processes, direct virus infection of the central nervous system (CNS), and virus-induced hyperinflammatory and hypercoagulable states are commonly involved. Guillain-Barré syndrome (GBS) and its variants, dysfunction of taste and smell, and muscle injury are numerous examples of COVID-19 PNS (peripheral nervous system) disease. Likewise, hemorrhagic and ischemic stroke, encephalitis, meningitis, encephalopathy acute disseminated encephalomyelitis, endothelialitis, and venous sinus thrombosis are some instances of COVID-19 CNS disease. Due to multifactorial and complicated pathogenic mechanisms, COVID-19 poses a large-scale threat to the whole nervous system. A complete understanding of SARS-CoV-2 neurological impairments is still lacking, but our knowledge base is rapidly expanding. Therefore, we anticipate that this comprehensive review will provide valuable insights and facilitate the work of neuroscientists in unfolding different neurological dimensions of COVID-19 and other CoV associated abnormalities.


Subject(s)
COVID-19/complications , Nervous System Diseases/etiology , Pandemics , SARS-CoV-2/pathogenicity , Adolescent , Adult , Angiotensin-Converting Enzyme 2/physiology , Asymptomatic Infections , Autoimmune Diseases of the Nervous System/etiology , Blood-Brain Barrier , COVID-19/immunology , COVID-19/physiopathology , Cerebrovascular Disorders/etiology , Child , Communicable Diseases, Emerging , Coronavirus Infections/complications , Humans , Hypoxia/etiology , Hypoxia/physiopathology , Nervous System/virology , Nervous System Diseases/immunology , Nervous System Diseases/physiopathology , Organ Specificity , Receptors, Virus/physiology , Severe Acute Respiratory Syndrome/complications , Synapses/virology , Viral Tropism , Young Adult
17.
J Infect Dis ; 222(9): 1439-1443, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-817413

ABSTRACT

BACKGROUND: During the coronavirus disease 2019 (COVID-19) pandemic, we detected a new immunofluorescence (IF) pattern in serum autoantibody (autoAb) screening of laboratory-confirmed COVID-19 patients. METHODS: The IF pattern was composed of liver and gastric mucosa staining on rat kidney/liver/stomach sections. RESULTS: We describe 12 patients positive for the cross-reactive antibody, compared with a negative group of 43 hospitalized COVID-19 patients, finding association with either neurologic or thrombotic complications. In sequential pre- and post-COVID-19 serum samples, we confirmed autoAb seroconversion. CONCLUSIONS: Our data indicate that autoAb screening in COVID-19 patients may be easily performed by IF and alert for autoreactive-mediated complications such as thrombotic or neurologic events.


Subject(s)
Autoantibodies/blood , Betacoronavirus , Coronavirus Infections/immunology , Nervous System Diseases/immunology , Pneumonia, Viral/immunology , Thrombosis/immunology , Adult , Age Factors , Aged , Aged, 80 and over , Animals , COVID-19 , Case-Control Studies , Coronavirus Infections/blood , Coronavirus Infections/complications , Cross Reactions/immunology , Female , Ferritins/blood , Fluorescent Antibody Technique, Indirect , Humans , Male , Middle Aged , Nervous System Diseases/virology , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Rats , SARS-CoV-2 , Seroconversion , Serologic Tests , Thrombosis/virology , Young Adult
18.
Fluids Barriers CNS ; 17(1): 55, 2020 Sep 10.
Article in English | MEDLINE | ID: covidwho-755214

ABSTRACT

Human coronaviruses are highly pathogenic viruses that pose a serious threat to human health. Examples include the severe acute respiratory syndrome outbreak of 2003 (SARS-CoV-1), the Middle East Respiratory Syndrome (MERS-CoV) outbreak of 2012, and the current SARS-CoV-2 (COVID-19) pandemic. Herein, we review the neurological manifestations of coronaviruses and discuss the potential pathogenic role of blood-brain barrier dysfunction. We present the hypothesis that pre-existing vascular damage (due to aging, cardiovascular disease, diabetes, hypertension or other conditions) facilitates infiltration of the virus into the central nervous system (CNS), increasing neuro-inflammation and the likelihood of neurological symptoms. We also discuss the role of a neuroinflammatory cytokine profile in both blood-brain barrier dysfunction and macrovascular disease (e.g. ischemic stroke and thromboembolism). Future studies are needed to better understand the involvement of the microvasculature in coronavirus neuropathology, and to test the diagnostic potential of minimally-invasive screening tools (e.g. serum biomarkers, fluorescein retinal angiography and dynamic-contrast MRI).


Subject(s)
Blood-Brain Barrier/physiopathology , Coronavirus Infections/physiopathology , Inflammation/physiopathology , Microvessels/physiopathology , Nervous System Diseases/physiopathology , Pneumonia, Viral/physiopathology , Betacoronavirus , Blood-Brain Barrier/immunology , Blood-Brain Barrier/virology , COVID-19 , Cardiovascular Diseases/physiopathology , Coronavirus Infections/immunology , Cytokines/immunology , Diabetes Mellitus/physiopathology , Encephalitis/immunology , Encephalitis/physiopathology , Humans , Inflammation/immunology , Microvessels/immunology , Nervous System Diseases/immunology , Pandemics , Pneumonia, Viral/immunology , SARS-CoV-2 , Seizures/immunology , Seizures/physiopathology , Stroke/immunology , Stroke/physiopathology , Thromboembolism/immunology , Thromboembolism/physiopathology
19.
Mol Neurobiol ; 57(12): 5263-5275, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-738570

ABSTRACT

Similar to its predecessors, coronavirus disease 2019 (COVID-19) exhibits neurotrophic properties, which lead to progression of neurologic sequelae. Besides direct viral invasion to the central nervous system (CNS), indirect CNS involvement through viral-mediated immune response is plausible. Aberrant immune pathways such as extreme release of cytokines (cytokine storm), autoimmunity mediated by cross-reactivity between CNS components and viral particles, and microglial activation propagate CNS damage in these patients. Here, we review the currently available evidence to discuss the plausible immunologic pathways that may contribute to the development of COVID-19 neurological complications, namely Alzheimer's disease, Parkinson's disease, stroke, multiple sclerosis, Guillain-Barre syndrome, seizure, and brainstem involvement.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Nervous System Diseases/etiology , Pandemics , Pneumonia, Viral/complications , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus/immunology , Betacoronavirus/pathogenicity , Brain Stem/physiopathology , Brain Stem/virology , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/immunology , Cytopathogenic Effect, Viral , Disease Outbreaks , Guillain-Barre Syndrome/etiology , Guillain-Barre Syndrome/immunology , Humans , Mice , Multiple Sclerosis/etiology , Multiple Sclerosis/immunology , Nerve Tissue Proteins/physiology , Nervous System Diseases/immunology , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/immunology , Neuroglia/pathology , Neuroglia/virology , Neurons/pathology , Neurons/virology , Peptidyl-Dipeptidase A/physiology , Pneumonia, Viral/immunology , Receptors, Virus/physiology , Respiratory Insufficiency/etiology , Respiratory Insufficiency/physiopathology , SARS-CoV-2 , Seizures/etiology , Seizures/immunology , Severe Acute Respiratory Syndrome/complications , Severe Acute Respiratory Syndrome/epidemiology , Stroke/etiology , Stroke/immunology
20.
J Neurol ; 268(3): 751-757, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-688846

ABSTRACT

BACKGROUND: Evidence of immune-mediated neurological syndromes associated with the severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection is limited. We therefore investigated clinical, serological and CSF features of coronavirus disease 2019 (COVID-19) patients with neurological manifestations. METHODS: Consecutive COVID-19 patients with neurological manifestations other than isolated anosmia and/or non-severe headache, and with no previous neurological or psychiatric disorders were prospectively included. Neurological examination was performed in all patients and lumbar puncture with CSF examination was performed when not contraindicated. Serum anti-gangliosides antibodies were tested when clinically indicated. RESULTS: Of the 349 COVID-19 admitted to our center between March 23rd and April 24th 2020, 15 patients (4.3%) had neurological manifestations and fulfilled the study inclusion/exclusion criteria. CSF examination was available in 13 patients and showed lymphocytic pleocytosis in 2 patients: 1 with anti-contactin-associated protein 2 (anti-Caspr2) antibody encephalitis and 1 with meningo-polyradiculitis. Increased serum titer of anti-GD1b antibodies was found in three patients and was associated with variable clinical presentations, including cranial neuropathy with meningo-polyradiculitis, brainstem encephalitis and delirium. CSF PCR for SARS-CoV-2 was negative in all patients. CONCLUSIONS: In SARS-Cov-2 infected patients with neurological manifestations, CSF pleocytosis is associated with para- or post-infectious encephalitis and polyradiculitis. Anti-GD1b and anti-Caspr2 autoantibodies can be identified in certain cases, raising the question of SARS-CoV-2-induced secondary autoimmunity.


Subject(s)
COVID-19/complications , Nervous System Diseases/etiology , Nervous System Diseases/immunology , Adult , Aged , Aged, 80 and over , Antibodies/cerebrospinal fluid , COVID-19/cerebrospinal fluid , Delirium/etiology , Delirium/psychology , Encephalitis/etiology , Encephalitis/psychology , Female , Gangliosides/immunology , Humans , Leukocytosis/cerebrospinal fluid , Male , Membrane Proteins/cerebrospinal fluid , Middle Aged , Nerve Tissue Proteins/cerebrospinal fluid , Nervous System Diseases/cerebrospinal fluid , Neurologic Examination , Radiculopathy/etiology , Radiculopathy/psychology , Spinal Puncture
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