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1.
BMC Infect Dis ; 22(1): 640, 2022 Jul 23.
Article in English | MEDLINE | ID: covidwho-1957048

ABSTRACT

BACKGROUND: We report the first case of COVID-19 associated acute necrotizing encephalopathy (ANE) without pulmonary disease in a patient with an extremely high interleukin-6 (IL-6) level and Ran Binding Protein 2 (RANBP2) mutation. CASE PRESENTATION: A 29-year-old woman recently immunized with inactivated viral vaccine-BBIBP32-CorV (Sinopharm) presented with alteration of consciousness. Her body temperature was 37° Celsius, blood pressure 42/31 mmHg, heart rate 130 bpm, respiratory rate 20 per minute, and oxygen saturation 98%. Respiratory examination was unremarkable. Neurological examination revealed stupor but preserved brainstem reflexes. Non-contrast computerized tomography of the brain showed symmetrical hypodense lesions involving bilateral thalami and cerebellar hemispheres characteristic of ANE. No pulmonary infiltration was found on chest radiograph. SARS-CoV-2 was detected by PCR; whole genome sequencing later confirmed the Delta variant. RANBP2 gene analysis revealed heterozygous Thr585Met mutation. Serum IL-6 was 7390 pg/mL. Urine examination showed pyelonephritis. Her clinical course was complicated by seizure, septic shock, acute kidney injury, and acute hepatic failure. She later developed coma and passed away in 6 days. CONCLUSIONS: ANE is caused by cytokine storm leading to necrosis and hemorrhage of the brain. IL-6 was deemed as a prognostic factor and a potential treatment target of ANE in previous studies. RANBP2 missense mutation strongly predisposes this condition by affecting mitochondrial function, viral entry, cytokine signaling, immune response, and blood-brain barrier maintenance. Also, inactivated vaccine has been reported to precipitate massive production of cytokines by antibody dependent enhancement (ADE). The true incidence of COVID-19 associated ANE is not known as were the predictors of its development. We proposed these potential two factors (RANBP2 mutation and ADE) that could participate in the pathogenesis of ANE in COVID-19 apart from SARS-CoV2 infection by itself. Further study is needed to confirm this hypothesis, specifically in the post-vaccination period. Role of RANBP2 mutation and its application in COVID-19 and ANE should be further elaborated.


Subject(s)
Brain Diseases , COVID-19 , Leukoencephalitis, Acute Hemorrhagic , Adult , Brain Diseases/complications , Female , Humans , Interleukin-6/genetics , Leukoencephalitis, Acute Hemorrhagic/diagnosis , Leukoencephalitis, Acute Hemorrhagic/genetics , Molecular Chaperones , Mutation , Nuclear Pore Complex Proteins , RNA, Viral , SARS-CoV-2/genetics , Vaccines, Inactivated/therapeutic use
3.
J Neurol ; 269(5): 2293-2300, 2022 May.
Article in English | MEDLINE | ID: covidwho-1604983

ABSTRACT

Numerous reports support the possible occurrence of acute disseminated encephalomyelitis (ADEM) following COVID-19. Herein, we report a case of ADEM in a 53-year-old man 2 weeks after SARS-CoV-2 infection. We reviewed the reports of adult cases of ADEM and its variant acute necrotizing hemorrhagic leukoencephalitis (ANHLE) to check for possible prognostic factors and clinical/epidemiological peculiarities. We performed a descriptive analysis of clinical and cerebrospinal fluid data. Ordinal logistic regressions were performed to check the effect of clinical variables and treatments on ADEM/ANHLE outcomes. We also compared ADEM and ANHLE patients. We identified a total of 20 ADEM (9 females, median age 53.5 years) and 23 ANHLE (11 females, median age 55 years). Encephalopathy was present in 80% of ADEM and 91.3% of ANHLE patients. We found that the absence of encephalopathy predicts a better clinical outcome in ADEM (OR 0.027, 95% CI 0.001-0.611, p = 0.023), also when correcting for the other variables (OR 0.032, 95% CI 0.001-0.995, p = 0.05). Conversely, we identified no significant prognostic factor in ANHLE patients. ANHLE patients showed a trend towards a worse clinical outcome (lower proportion of good/complete recovery, 4.5% vs 16.7%) and higher mortality (36.4% vs 11.1%) as compared to ADEM. Compared to pre-pandemic ADEM, we observed a higher median age of people with post-COVID-19 ADEM and ANHLE, a shorter interval between infection and neurological symptoms, and a worse prognosis both in terms of high morbidity and mortality. Despite being affected by the retrospective nature of the study, these observations provide new insights into ADEM/ANHLE following SARS-CoV-2 infection.


Subject(s)
Brain Diseases , COVID-19 , Encephalomyelitis, Acute Disseminated , Leukoencephalitis, Acute Hemorrhagic , Adult , COVID-19/complications , Encephalomyelitis, Acute Disseminated/etiology , Female , Humans , Leukoencephalitis, Acute Hemorrhagic/diagnostic imaging , Leukoencephalitis, Acute Hemorrhagic/epidemiology , Leukoencephalitis, Acute Hemorrhagic/etiology , Male , Middle Aged , Prognosis , Retrospective Studies , SARS-CoV-2
5.
Neurol Neuroimmunol Neuroinflamm ; 8(6)2021 11.
Article in English | MEDLINE | ID: covidwho-1376615

ABSTRACT

BACKGROUND AND OBJECTIVES: Since the onset of the COVID-19 pandemic, a growing number of reports have described cases of acute disseminated encephalomyelitis (ADEM) and acute hemorrhagic leukoencephalitis (AHLE) following infection with COVID-19. Given their relatively rare occurrence, the primary objective of this systematic review was to synthesize their clinical features, response to treatments, and clinical outcomes to better understand the nature of this neurologic consequence of COVID-19 infection. METHODS: Patients with a history of COVID-19 infection were included if their reports provided adequate detail to confirm a diagnosis of ADEM or AHLE by virtue of clinical features, radiographic abnormalities, and histopathologic findings. Cases purported to be secondary to vaccination against COVID-19 or occurring in the context of a preexisting relapsing CNS demyelinating disease were excluded. Case reports and series were identified via PubMed on May 17, 2021, and 4 additional cases from the authors' hospital files supplemented the systematic review of the literature. Summary statistics were used to describe variables using a complete case analysis approach. RESULTS: Forty-six patients (28 men, median age 49.5 years, 1/3 >50 years old) were analyzed, derived from 26 case reports or series originating from 8 countries alongside 4 patient cases from the authors' hospital files. COVID-19 infection was laboratory confirmed in 91% of cases, and infection severity necessitated intensive care in 67%. ADEM occurred in 31 cases, whereas AHLE occurred in 15, with a median presenting nadir modified Rankin Scale score of 5 (bedridden). Anti-MOG seropositivity was rare (1/15 patients tested). Noninflammatory CSF was present in 30%. Hemorrhage on brain MRI was identified in 42%. Seventy percent received immunomodulatory treatments, most commonly steroids, IV immunoglobulins, or plasmapheresis. The final mRS score was ≥4 in 64% of patients with adequate follow-up information, including 32% who died. DISCUSSION: In contrast to ADEM cases from the prepandemic era, reported post-COVID-19 ADEM and AHLE cases were often advanced in age at onset, experienced severe antecedent infection, displayed an unusually high rate of hemorrhage on neuroimaging, and routinely had poor neurologic outcomes, including a high mortality rate. Findings are limited by nonstandardized reporting of cases, truncated follow-up information, and presumed publication bias.


Subject(s)
COVID-19/complications , Encephalomyelitis, Acute Disseminated/etiology , Brain/diagnostic imaging , Brain/pathology , Encephalomyelitis, Acute Disseminated/mortality , Encephalomyelitis, Acute Disseminated/physiopathology , Encephalomyelitis, Acute Disseminated/therapy , Glucocorticoids/therapeutic use , Humans , Immunoglobulins, Intravenous/therapeutic use , Immunologic Factors/therapeutic use , Intensive Care Units , Leukoencephalitis, Acute Hemorrhagic/etiology , Leukoencephalitis, Acute Hemorrhagic/mortality , Leukoencephalitis, Acute Hemorrhagic/physiopathology , Leukoencephalitis, Acute Hemorrhagic/therapy , Magnetic Resonance Imaging , Plasmapheresis , SARS-CoV-2 , Severity of Illness Index
6.
Neurol India ; 69(2): 260-271, 2021.
Article in English | MEDLINE | ID: covidwho-1290494

ABSTRACT

BACKGROUND: A variety of neuroimaging abnormalities in COVID-19 have been described. OBJECTIVES: In this article, we reviewed the varied neuroimaging patterns in patients with COVID-19-associated neurological complications. METHODS: We searched PubMed, Google Scholar, Scopus and preprint databases (medRxiv and bioRxiv). The search terms we used were "COVID -19 and encephalitis, encephalopathy, neuroimaging or neuroradiology" and "SARS-CoV-2 and encephalitis, encephalopathy, neuroimaging or neuroradiology". RESULTS: Neuroimaging abnormalities are common in old age and patients with comorbidities. Neuroimaging abnormalities are largely vascular in origin. COVID-19-associated coagulopathy results in large vessel occlusion and cerebral venous thrombosis. COVID-19-associated intracerebral hemorrhage resembles anticoagulant associated intracerebral hemorrhage. On neuroimaging, hypoxic-ischemic damage along with hyperimmune reaction against the SARS-COV-2 virus manifests as small vessel disease. Small vessel disease appears as diffuse leukoencephalopathy and widespread microbleeds, and subcortical white matter hyperintensities. Occasionally, gray matter hyperintensity, similar to those observed seen in autoimmune encephalitis, has been noted. In many cases, white matter lesions similar to that in acute disseminated encephalomyelitis have been described. Acute disseminated encephalomyelitis in COVID-19 seems to be a parainfectious event and autoimmune in origin. Many cases of acute necrotizing encephalitis resulting in extensive damage to thalamus and brain stem have been described; cytokine storm has been considered a pathogenic mechanism behind this. None of the neuroimaging abnormalities can provide a clue to the possible pathogenic mechanism. CONCLUSIONS: Periventricular white-matter MR hyperintensity, microbleeds, arterial and venous infarcts, and hemorrhages are apparently distinctive neuroimaging abnormalities in patients with COVID-19.


Subject(s)
COVID-19/complications , COVID-19/diagnostic imaging , Nervous System Diseases/complications , Nervous System Diseases/diagnostic imaging , Neuroimaging , SARS-CoV-2/pathogenicity , Cytokine Release Syndrome , Humans , Leukoencephalitis, Acute Hemorrhagic
8.
Neuroradiology ; 63(5): 653-661, 2021 May.
Article in English | MEDLINE | ID: covidwho-1084384

ABSTRACT

PURPOSE: Acute hemorrhagic leukoencephalitis (AHLE) is a rare and severe form of acute disseminated encephalomyelitis (ADEM). Only a few reports of AHLE in coronavirus disease 2019 (COVID-19) patients have been described to date. We report a case of COVID-19-related AHLE along with a literature review describing salient clinical and imaging characteristics. METHODS: A literature search was performed on Medline (2020-present), PubMed, Cochrane Library, CINAHL, and Google scholar on 28 January 2021 for all articles published using MeSH terms "COVID-19" or "SARS-CoV-2" with "Acute hemorrhagic leukoencephalitis" or "Acute hemorrhagic encephalitis." Relevant case reports and case series describing clinical and imaging features of AHLE associated with SARS-CoV-2 infection were included, data compiled, and critically reviewed. RESULTS: Acute onset encephalopathy and rapidly deteriorating neurological status is the common clinical presentation in AHLE. CSF analysis reveals elevated proteins and lymphocytic pleocytosis. Typical neuroimaging features include multifocal, variable-sized, poorly defined cerebral white matter lesions with cortical sparing. Involvement of the brainstem, cerebellar peduncles, and deep grey matter can also occur, although rarely. Lesions are hyperintense on T2-weighted (T2W) and fluid-attenuated inversion recovery (FLAIR) images, hypointense on T1W images, and show microhemorrhages, variable diffusion restriction, and post-contrast enhancement. Extensive microhemorrhages, brainstem involvement, and gross hemorrhage often portend a poor prognosis. CONCLUSION: Heightened awareness about the clinical and imaging presentation of COVID-19-related AHLE can positively alter the outcome in a select few by enabling early diagnosis and aggressive management.


Subject(s)
COVID-19/complications , Leukoencephalitis, Acute Hemorrhagic/diagnostic imaging , Leukoencephalitis, Acute Hemorrhagic/virology , Fatal Outcome , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Pneumonia, Viral/complications , Pneumonia, Viral/virology , SARS-CoV-2 , Tomography, X-Ray Computed
9.
Neurology ; 95(10): 445-449, 2020 09 08.
Article in English | MEDLINE | ID: covidwho-999777

ABSTRACT

Here, we report a case of COVID-19-related acute necrotizing encephalopathy where SARS-CoV-2 RNA was found in CSF 19 days after symptom onset after testing negative twice. Although monocytes and protein levels in CSF were only marginally increased, and our patient never experienced a hyperinflammatory state, her neurologic function deteriorated into coma. MRI of the brain showed pathologic signal symmetrically in central thalami, subinsular regions, medial temporal lobes, and brain stem. Extremely high concentrations of the neuronal injury markers neurofilament light and tau, as well as an astrocytic activation marker, glial fibrillary acidic protein, were measured in CSF. Neuronal rescue proteins and other pathways were elevated in the in-depth proteomics analysis. The patient received IV immunoglobulins and plasma exchange. Her neurologic status improved, and she was extubated 4 weeks after symptom onset. This case report highlights the neurotropism of SARS-CoV-2 in selected patients and emphasizes the importance of repeated lumbar punctures and CSF analyses in patients with suspected COVID-19 and neurologic symptoms.


Subject(s)
Brain/diagnostic imaging , Coronavirus Infections/cerebrospinal fluid , Leukoencephalitis, Acute Hemorrhagic/cerebrospinal fluid , Pneumonia, Viral/cerebrospinal fluid , RNA, Viral/cerebrospinal fluid , Acyclovir/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus/genetics , COVID-19 , Coronavirus Infections/diagnostic imaging , Coronavirus Infections/physiopathology , Coronavirus Infections/therapy , Female , Glial Fibrillary Acidic Protein/cerebrospinal fluid , Humans , Immunoglobulins, Intravenous/therapeutic use , Immunologic Factors/therapeutic use , Interleukin-6/cerebrospinal fluid , Leukoencephalitis, Acute Hemorrhagic/diagnostic imaging , Leukoencephalitis, Acute Hemorrhagic/physiopathology , Leukoencephalitis, Acute Hemorrhagic/therapy , Magnetic Resonance Imaging , Middle Aged , Neurofilament Proteins/cerebrospinal fluid , Pandemics , Plasma Exchange , Pneumonia, Viral/diagnostic imaging , Pneumonia, Viral/physiopathology , Pneumonia, Viral/therapy , Real-Time Polymerase Chain Reaction , SARS-CoV-2 , Tomography, X-Ray Computed , Viral Tropism , tau Proteins/cerebrospinal fluid
12.
West J Emerg Med ; 21(6): 45-51, 2020 Oct 06.
Article in English | MEDLINE | ID: covidwho-869246

ABSTRACT

Severe acute respiratory syndrome coronavirus 2, the source of COVID-19, causes numerous clinical findings including respiratory and gastrointestinal findings. Evidence is now growing for increasing neurological symptoms. This is thought to be from direct in-situ effects in the olfactory bulb caused by the virus. Angiotensin-converting enzyme 2 receptors likely serve as a key receptor for cell entry for most coronaviridae as they are present in multiple organ tissues in the body, notably neurons, and in type 2 alveolar cells in the lung. Hematogenous spread to the nervous system has been described, with viral transmission along neuronal synapses in a retrograde fashion. The penetration of the virus to the central nervous system (CNS) allows for the resulting intracranial cytokine storm, which can result in a myriad of CNS complications. There have been reported cases of associated cerebrovascular accidents with large vessel occlusions, cerebral venous sinus thrombosis, posterior reversible encephalopathy syndrome, meningoencephalitis, acute necrotizing encephalopathy, epilepsy, and myasthenia gravis. Peripheral nervous system effects such as hyposmia, hypogeusia, ophthalmoparesis, Guillain-Barré syndrome, and motor peripheral neuropathy have also been reported. In this review, we update the clinical manifestations of COVID-19 concentrating on the neurological associations that have been described, including broad ranges in both central and peripheral nervous systems.


Subject(s)
COVID-19/complications , SARS-CoV-2 , Bell Palsy/virology , Delirium/virology , Guillain-Barre Syndrome/virology , Humans , Leukoencephalitis, Acute Hemorrhagic/virology , Myelitis/virology , Parkinson Disease/complications , Sinus Thrombosis, Intracranial/virology , Stroke/virology
16.
Headache ; 60(8): 1806-1811, 2020 09.
Article in English | MEDLINE | ID: covidwho-642109

ABSTRACT

OBJECTIVE: To summarize for the trainee audience the possible mechanisms of headache in patients with COVID-19 as well as to outline the impact of the pandemic on patients with headache disorders and headache medicine in clinical practice. BACKGROUND: COVID-19 is a global pandemic caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2, of which a large subset of patients features neurological symptoms, commonly headache. The virus is highly contagious and is, therefore, changing clinical practice by forcing limitations on in-person visits and procedural treatments, more quickly shifting toward the widespread adaptation of telemedicine services. DESIGN/RESULTS: We review what is currently known about the pathophysiology of COVID-19 and how it relates to possible mechanisms of headache, including indirect, potential direct, and secondary causes. Alternative options for the treatment of patients with headache disorders and the use of telemedicine are also explored. CONCLUSIONS: Limited information exists regarding the mechanisms and timing of headache in patients with COVID-19, though causes relate to plausible direct viral invasion of the nervous system as well as the cytokine release syndrome. Though headache care in the COVID-19 era requires alterations, the improved preventive treatment options now available and evidence for feasibility and safety of telemedicine well positions clinicians to take care of such patients, especially in the COVID-19 epicenter of New York City.


Subject(s)
COVID-19/complications , Education, Medical, Continuing , Headache Disorders, Secondary/etiology , Neurology/education , Pandemics , SARS-CoV-2/pathogenicity , Aged, 80 and over , Anosmia/etiology , Anosmia/virology , COVID-19/epidemiology , COVID-19/physiopathology , COVID-19/prevention & control , Comorbidity , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/physiopathology , Headache/epidemiology , Headache Disorders, Secondary/physiopathology , Humans , Inflammation Mediators/metabolism , Leukoencephalitis, Acute Hemorrhagic/etiology , Migraine Disorders/complications , Migraine Disorders/prevention & control , Migraine Disorders/therapy , New York City/epidemiology , Physical Distancing , SARS-CoV-2/isolation & purification , SARS-CoV-2/physiology , Telemedicine
17.
Neurol India ; 68(3): 560-572, 2020.
Article in English | MEDLINE | ID: covidwho-640338

ABSTRACT

COVID-19, in most patients, presents with mild flu-like illness. Elderly patients with comorbidities, like hypertension, diabetes, or lung and cardiac disease, are more likely to have severe disease and deaths. Neurological complications are frequently reported in severely or critically ill patients with comorbidities. In COVID-19, both central and peripheral nervous systems can be affected. The SARS-CoV-2 virus causes the disease COVID-19 and has the potential to invade the brain. The SARS-CoV-2 virus enters the brain either via a hematogenous route or olfactory system. Angiotensin-converting enzyme two receptors, present on endothelial cells of cerebral vessels, are a possible viral entry point. The most severe neurological manifestations, altered sensorium (agitation, delirium, and coma), are because of hypoxic and metabolic abnormalities. Characteristic cytokine storm incites severe metabolic changes and multiple organ failure. Profound coagulopathies may manifest with ischemic or hemorrhagic stroke. Rarely, SARS-CoV-2 virus encephalitis or pictures like acute disseminated encephalomyelitis or acute necrotizing encephalopathy have been reported. Nonspecific headache is a commonly experienced neurological symptom. A new type of headache "personal protection equipment-related headache" has been described. Complete or partial anosmia and ageusia are common peripheral nervous system manifestations. Recently, many cases of Guillain-Barré syndrome in COVID-19 patients have been observed, and a postinfectious immune-mediated inflammatory process was held responsible for this. Guillain-Barré syndrome does respond to intravenous immunoglobulin. Myalgia/fatigue is also common, and elevated creatine kinase levels indicate muscle injury. Most of the reports about neurological complications are currently from China. COVID-19 pandemic is spreading to other parts of the world; the spectrum of neurological complications is likely to widen further.


Subject(s)
Ageusia/physiopathology , Coronavirus Infections/physiopathology , Cytokine Release Syndrome/immunology , Encephalitis/physiopathology , Guillain-Barre Syndrome/physiopathology , Headache/physiopathology , Olfaction Disorders/physiopathology , Pneumonia, Viral/physiopathology , Stroke/physiopathology , Ageusia/etiology , Betacoronavirus , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/etiology , Blood-Brain Barrier , Brain Ischemia/blood , Brain Ischemia/etiology , Brain Ischemia/immunology , Brain Ischemia/physiopathology , COVID-19 , Coma/etiology , Coma/physiopathology , Coronavirus Infections/blood , Coronavirus Infections/complications , Coronavirus Infections/immunology , Delirium/etiology , Delirium/physiopathology , Encephalitis/etiology , Encephalitis/immunology , Encephalomyelitis, Acute Disseminated/etiology , Encephalomyelitis, Acute Disseminated/immunology , Encephalomyelitis, Acute Disseminated/physiopathology , Fatigue/etiology , Fatigue/physiopathology , Guillain-Barre Syndrome/etiology , Headache/etiology , Humans , Intracranial Hemorrhages/blood , Intracranial Hemorrhages/etiology , Intracranial Hemorrhages/physiopathology , Leukoencephalitis, Acute Hemorrhagic/etiology , Leukoencephalitis, Acute Hemorrhagic/immunology , Leukoencephalitis, Acute Hemorrhagic/physiopathology , Myalgia/etiology , Myalgia/physiopathology , Olfaction Disorders/etiology , Pandemics , Personal Protective Equipment/adverse effects , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , SARS-CoV-2 , Stroke/blood , Stroke/etiology , Stroke/immunology
19.
Neurology ; 95(10): 454-457, 2020 09 08.
Article in English | MEDLINE | ID: covidwho-616669
20.
Ann Neurol ; 88(1): 1-11, 2020 07.
Article in English | MEDLINE | ID: covidwho-584154

ABSTRACT

In less than 6 months, the severe acute respiratory syndrome-coronavirus type 2 (SARS-CoV-2) has spread worldwide infecting nearly 6 million people and killing over 350,000. Initially thought to be restricted to the respiratory system, we now understand that coronavirus disease 2019 (COVID-19) also involves multiple other organs, including the central and peripheral nervous system. The number of recognized neurologic manifestations of SARS-CoV-2 infection is rapidly accumulating. These may result from a variety of mechanisms, including virus-induced hyperinflammatory and hypercoagulable states, direct virus infection of the central nervous system (CNS), and postinfectious immune mediated processes. Example of COVID-19 CNS disease include encephalopathy, encephalitis, acute disseminated encephalomyelitis, meningitis, ischemic and hemorrhagic stroke, venous sinus thrombosis, and endothelialitis. In the peripheral nervous system, COVID-19 is associated with dysfunction of smell and taste, muscle injury, the Guillain-Barre syndrome, and its variants. Due to its worldwide distribution and multifactorial pathogenic mechanisms, COVID-19 poses a global threat to the entire nervous system. Although our understanding of SARS-CoV-2 neuropathogenesis is still incomplete and our knowledge is evolving rapidly, we hope that this review will provide a useful framework and help neurologists in understanding the many neurologic facets of COVID-19. ANN NEUROL 2020;88:1-11 ANN NEUROL 2020;88:1-11.


Subject(s)
Betacoronavirus , Coronavirus Infections/physiopathology , Nervous System Diseases/physiopathology , Pneumonia, Viral/physiopathology , Brain Diseases/etiology , Brain Diseases/physiopathology , Brain Ischemia/etiology , Brain Ischemia/physiopathology , COVID-19 , Coronavirus Infections/complications , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/physiopathology , Encephalitis/etiology , Encephalitis/physiopathology , Encephalomyelitis, Acute Disseminated/etiology , Encephalomyelitis, Acute Disseminated/physiopathology , Guillain-Barre Syndrome/etiology , Guillain-Barre Syndrome/physiopathology , Humans , Inflammation , Intracranial Hemorrhages/etiology , Intracranial Hemorrhages/physiopathology , Leukoencephalitis, Acute Hemorrhagic/etiology , Leukoencephalitis, Acute Hemorrhagic/physiopathology , Meningitis, Viral/etiology , Meningitis, Viral/physiopathology , Nervous System Diseases/etiology , Olfaction Disorders/etiology , Olfaction Disorders/physiopathology , Pandemics , Pneumonia, Viral/complications , SARS-CoV-2 , Sinus Thrombosis, Intracranial/etiology , Sinus Thrombosis, Intracranial/physiopathology , Stroke/etiology , Stroke/physiopathology , Thrombophilia/etiology , Thrombophilia/physiopathology
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