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1.
CNS Neurol Disord Drug Targets ; 21(3): 210-216, 2022.
Article in English | MEDLINE | ID: covidwho-1592276

ABSTRACT

The coronavirus, also known as SARS-CoV-2 (Severe Acute Respiratory Syndrome Corona Virus-19), with its rapid rate of transmission, has progressed with a great impact on respiratory function and mortality worldwide. The nasal cavity is the promising gateway of SARS-CoV-2 to reach the brain via systemic circulatory distribution. Recent reports have revealed that the loss of involuntary process of breathing control into the brainstem that results in death is a signal of neurological involvement. Early neurological symptoms, like loss of smell, convulsions, and ataxia, are the clues of the involvement of the central nervous system that makes the entry of SARS-CoV-2 further fatal and life-threatening, requiring artificial respiration and emergency admission in hospitals. Studies performed on patients infected with SARS-CoV-2 has revealed three-stage involvement of the Central Nervous System (CNS) in the progression of SARS-CoV-2 infection: Direct involvement of CNS with headache, ataxia, dizziness, altered or impaired consciousness, acute stroke or seizures as major symptoms, peripheral involvement with impaired taste, smell, vision, and altered nociception, and skeletal muscle impairment that includes skeletal muscle disorders leading to acute paralysis in a particular area of the body. In the previous era, most studied and researched viruses were beta coronavirus and mouse hepatitis virus, which were studied for acute and chronic encephalitis and Multiple Sclerosis (MS). Although the early symptoms of SARS-CoV are respiratory pathogenesis, the differential diagnosis should always be considered for neurological perspective to stop the mortalities.


Subject(s)
Brain/metabolism , COVID-19/metabolism , Nervous System Diseases/metabolism , Nervous System Diseases/virology , SARS-CoV-2/metabolism , Animals , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , Brain/drug effects , COVID-19/drug therapy , Humans , Nervous System Diseases/drug therapy , SARS-CoV-2/drug effects
2.
Molecules ; 26(17)2021 Sep 06.
Article in English | MEDLINE | ID: covidwho-1390161

ABSTRACT

Phenolic acids comprise a class of phytochemical compounds that can be extracted from various plant sources and are well known for their antioxidant and anti-inflammatory properties. A few of the most common naturally occurring phenolic acids (i.e., caffeic, carnosic, ferulic, gallic, p-coumaric, rosmarinic, vanillic) have been identified as ingredients of edible botanicals (thyme, oregano, rosemary, sage, mint, etc.). Over the last decade, clinical research has focused on a number of in vitro (in human cells) and in vivo (animal) studies aimed at exploring the health protective effects of phenolic acids against the most severe human diseases. In this review paper, the authors first report on the main structural features of phenolic acids, their most important natural sources and their extraction techniques. Subsequently, the main target of this analysis is to provide an overview of the most recent clinical studies on phenolic acids that investigate their health effects against a range of severe pathologic conditions (e.g., cancer, cardiovascular diseases, hepatotoxicity, neurotoxicity, and viral infections-including coronaviruses-based ones).


Subject(s)
Anti-Inflammatory Agents/pharmacology , Antioxidants/pharmacology , Cinnamates/pharmacology , Hydroxybenzoates/pharmacology , Plant Extracts/pharmacology , Anti-Inflammatory Agents/therapeutic use , Antioxidants/therapeutic use , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/drug therapy , Cinnamates/therapeutic use , Clinical Trials as Topic , Coronavirus Infections/diagnosis , Coronavirus Infections/drug therapy , Humans , Hydroxybenzoates/therapeutic use , Liver Diseases/diagnosis , Liver Diseases/drug therapy , Neoplasms/diagnosis , Neoplasms/drug therapy , Nervous System Diseases/diagnosis , Nervous System Diseases/drug therapy , Plant Extracts/therapeutic use , Severity of Illness Index , Treatment Outcome
3.
J Neurosci ; 41(25): 5338-5349, 2021 06 23.
Article in English | MEDLINE | ID: covidwho-1282334

ABSTRACT

Clinical reports suggest that the coronavirus disease-19 (COVID-19) pandemic caused by severe acute respiratory syndrome (SARS)-coronavirus-2 (CoV-2) has not only taken millions of lives, but has also created a major crisis of neurologic complications that persist even after recovery from the disease. Autopsies of patients confirm the presence of the coronaviruses in the CNS, especially in the brain. The invasion and transmission of SARS-CoV-2 in the CNS is not clearly defined, but, because the endocytic pathway has become an important target for the development of therapeutic strategies for COVID-19, it is necessary to understand endocytic processes in the CNS. In addition, mitochondria and mechanistic target of rapamycin (mTOR) signaling pathways play a critical role in the antiviral immune response, and may also be critical for endocytic activity. Furthermore, dysfunctions of mitochondria and mTOR signaling pathways have been associated with some high-risk conditions such as diabetes and immunodeficiency for developing severe complications observed in COVID-19 patients. However, the role of these pathways in SARS-CoV-2 infection and spread are largely unknown. In this review, we discuss the potential mechanisms of SARS-CoV-2 entry into the CNS and how mitochondria and mTOR pathways might regulate endocytic vesicle-mitochondria interactions and dynamics during SARS-CoV-2 infection. The mechanisms that plausibly account for severe neurologic complications with COVID-19 and potential treatments with Food and Drug Administration-approved drugs targeting mitochondria and the mTOR pathways are also addressed.


Subject(s)
COVID-19/complications , Nervous System Diseases/virology , Neurons/virology , Animals , COVID-19/drug therapy , COVID-19/metabolism , COVID-19/pathology , COVID-19/virology , Humans , Mitochondria/metabolism , Mitochondria/virology , Nervous System Diseases/drug therapy , Nervous System Diseases/metabolism , Nervous System Diseases/pathology , Neurons/metabolism , SARS-CoV-2/pathogenicity , TOR Serine-Threonine Kinases/metabolism
4.
Mol Neurobiol ; 58(9): 4694-4715, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1281328

ABSTRACT

The unremitting coronavirus disease 2019 (COVID-19) pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) marked a year-long phase of public health adversaries and has severely compromised healthcare globally. Early evidence of COVID-19 noted its impact on the pulmonary and cardiovascular functions, while multiple studies in recent time shed light on its substantial neurological complications, though a comprehensive understanding of the cause(s), the mechanism(s), and their neuropathological outcomes is scarce. In the present review, we conferred evidence of neurological complications in COVID-19 patients and shed light on the SARS-CoV-2 infection routes including the hematogenous, direct/neuronal, lymphatic tissue or cerebrospinal fluid, or infiltration through infected immune cells, while the underlying mechanism of SARS-CoV-2 invasion to the central nervous system (CNS) was also discussed. In an up-to-date manner, we further reviewed the impact of COVID-19 in developing diverse neurologic manifestations associated with CNS, peripheral nervous system (PNS), skeletal muscle, and also pre-existing neurological diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy, and myasthenia gravis. Furthermore, we discussed the involvement of key factors including age, sex, comorbidity, and disease severity in exacerbating the neurologic manifestations in COVID-19 patients. An outlook of present therapeutic strategies and state of existing challenges in COVID-19 management was also accessed. Conclusively, the present report provides a comprehensive review of COVID-19-related neurological complications and emphasizes the need for their early clinical management in the ongoing COVID-19 pandemic.


Subject(s)
COVID-19/complications , Nervous System Diseases/etiology , Pandemics , SARS-CoV-2/pathogenicity , Adult , Age Factors , Aged , Aged, 80 and over , Autoimmune Diseases of the Nervous System/epidemiology , Autoimmune Diseases of the Nervous System/etiology , COVID-19/epidemiology , COVID-19/immunology , COVID-19/virology , Central Nervous System/virology , Child , Comorbidity , Female , Humans , Immune System/virology , Inflammation , Male , Middle Aged , Models, Biological , Muscular Diseases/etiology , Nervous System Diseases/drug therapy , Nervous System Diseases/epidemiology , Nervous System Diseases/physiopathology , Neurodegenerative Diseases/complications , Neurons/virology , Organ Specificity , Sex Factors , Viremia/chemically induced , Viremia/immunology , Virus Internalization
5.
Sci Rep ; 11(1): 12414, 2021 06 14.
Article in English | MEDLINE | ID: covidwho-1268007

ABSTRACT

Primary aim was to assess prevalence and severity of potential and real drug-drug interactions (DDIs) among therapies for COVID-19 and concomitant medications in hospitalized patients with confirmed SARS-CoV-2 infection. The secondary aim was to analyze factors associated with rDDIs. An observational single center cohort study conducted at a tertiary hospital in Spain from March 1st to April 30th. rDDIs refer to interaction with concomitant drugs prescribed during hospital stay whereas potential DDIs (pDDIs) refer to those with domiciliary medication. DDIs checked with The University of Liverpool resource. Concomitant medications were categorized according to the Anatomical Therapeutic Chemical classification system. Binomial logistic regression was carried out to identify factors associated with rDDIs. A total of 174 patients were analyzed. DDIs were detected in 152 patients (87.4%) with a total of 417 rDDIs between COVID19-related drugs and involved hospital concomitant medication (60 different drugs) while pDDIs were detected in 105 patients (72.9%) with a total of 553 pDDIs. From all 417 rDDIs, 43.2% (n = 180) were associated with lopinavir/ritonavir and 52.9% (n = 221) with hydroxychloroquine, both of them the most prescribed (106 and 165 patients, respectively). The main mechanism of interaction observed was QTc prolongation. Clinically relevant rDDIs were identified among 81.1% (n = 338) ('potential interactions') and 14.6% (n = 61) (contraindicated) of the patients. Charlson index (OR 1.34, 95% IC 1.02-1.76) and number of drugs prescribed during admission (OR 1.42, 95% IC 1.12-1.81) were independently associated with rDDIs. Prevalence of patients with real and pDDIs was high, especially those clinically relevant. Both comorbidities and polypharmacy were found as risk factors independently associated with DDIs development.


Subject(s)
COVID-19/drug therapy , Drug Interactions , Hydroxychloroquine/chemistry , Lopinavir/chemistry , Ritonavir/chemistry , Aged , Analgesics/chemistry , Analgesics/therapeutic use , COVID-19/pathology , COVID-19/virology , Cardiovascular Diseases/drug therapy , Cohort Studies , Diuretics/chemistry , Diuretics/therapeutic use , Female , Humans , Hydroxychloroquine/therapeutic use , Lopinavir/therapeutic use , Male , Middle Aged , Nervous System Diseases/drug therapy , Polypharmacy , Risk Factors , Ritonavir/therapeutic use , SARS-CoV-2/isolation & purification , Severity of Illness Index , Spain
6.
Int J Mol Sci ; 22(8)2021 Apr 15.
Article in English | MEDLINE | ID: covidwho-1186972

ABSTRACT

COVID-19 is a severe respiratory disease caused by the newly identified human coronavirus (HCoV) Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). The virus was discovered in December 2019, and in March 2020, the disease was declared a global pandemic by the World Health Organization (WHO) due to a high number of cases. Although SARS-CoV-2 primarily affects the respiratory system, several studies have reported neurological complications in COVID-19 patients. Headache, dizziness, loss of taste and smell, encephalitis, encephalopathy, and cerebrovascular diseases are the most common neurological complications that are associated with COVID-19. In addition, seizures, neuromuscular junctions' disorders, and Guillain-Barré syndrome were reported as complications of COVID-19, as well as neurodegenerative and demyelinating disorders. However, the management of these conditions remains a challenge. In this review, we discuss the prevalence, pathogenesis, and mechanisms of these neurological sequelae that are secondary to SARS-CoV-2 infection. We aim to update neurologists and healthcare workers on the possible neurological complications associated with COVID-19 and the management of these disease conditions.


Subject(s)
COVID-19/complications , Nervous System Diseases/drug therapy , Nervous System Diseases/etiology , Central Nervous System/drug effects , Central Nervous System/virology , Cerebrovascular Disorders/drug therapy , Cerebrovascular Disorders/etiology , Cerebrovascular Disorders/virology , Humans , Nervous System Diseases/epidemiology , Nervous System Diseases/virology , Prevalence , SARS-CoV-2/metabolism
7.
Brain ; 143(10): 3104-3120, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-1066271

ABSTRACT

Preliminary clinical data indicate that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with neurological and neuropsychiatric illness. Responding to this, a weekly virtual coronavirus disease 19 (COVID-19) neurology multi-disciplinary meeting was established at the National Hospital, Queen Square, in early March 2020 in order to discuss and begin to understand neurological presentations in patients with suspected COVID-19-related neurological disorders. Detailed clinical and paraclinical data were collected from cases where the diagnosis of COVID-19 was confirmed through RNA PCR, or where the diagnosis was probable/possible according to World Health Organization criteria. Of 43 patients, 29 were SARS-CoV-2 PCR positive and definite, eight probable and six possible. Five major categories emerged: (i) encephalopathies (n = 10) with delirium/psychosis and no distinct MRI or CSF abnormalities, and with 9/10 making a full or partial recovery with supportive care only; (ii) inflammatory CNS syndromes (n = 12) including encephalitis (n = 2, para- or post-infectious), acute disseminated encephalomyelitis (n = 9), with haemorrhage in five, necrosis in one, and myelitis in two, and isolated myelitis (n = 1). Of these, 10 were treated with corticosteroids, and three of these patients also received intravenous immunoglobulin; one made a full recovery, 10 of 12 made a partial recovery, and one patient died; (iii) ischaemic strokes (n = 8) associated with a pro-thrombotic state (four with pulmonary thromboembolism), one of whom died; (iv) peripheral neurological disorders (n = 8), seven with Guillain-Barré syndrome, one with brachial plexopathy, six of eight making a partial and ongoing recovery; and (v) five patients with miscellaneous central disorders who did not fit these categories. SARS-CoV-2 infection is associated with a wide spectrum of neurological syndromes affecting the whole neuraxis, including the cerebral vasculature and, in some cases, responding to immunotherapies. The high incidence of acute disseminated encephalomyelitis, particularly with haemorrhagic change, is striking. This complication was not related to the severity of the respiratory COVID-19 disease. Early recognition, investigation and management of COVID-19-related neurological disease is challenging. Further clinical, neuroradiological, biomarker and neuropathological studies are essential to determine the underlying pathobiological mechanisms that will guide treatment. Longitudinal follow-up studies will be necessary to ascertain the long-term neurological and neuropsychological consequences of this pandemic.


Subject(s)
Coronavirus Infections , Nervous System Diseases , Pandemics , Pneumonia, Viral , Adolescent , Adrenal Cortex Hormones/therapeutic use , Adult , Aged , Aged, 80 and over , Betacoronavirus/pathogenicity , COVID-19 , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Drug Utilization/statistics & numerical data , Female , Humans , Immunoglobulins, Intravenous/therapeutic use , London/epidemiology , Magnetic Resonance Imaging , Male , Middle Aged , Nervous System Diseases/cerebrospinal fluid , Nervous System Diseases/diagnostic imaging , Nervous System Diseases/drug therapy , Nervous System Diseases/epidemiology , Pneumonia, Viral/drug therapy , Pneumonia, Viral/epidemiology , Retrospective Studies , SARS-CoV-2 , Young Adult
8.
Eur J Pharmacol ; 889: 173629, 2020 Dec 15.
Article in English | MEDLINE | ID: covidwho-1023556

ABSTRACT

The absence of a specific treatment for SARS-CoV-2 infection led to an intense global effort in order to find new therapeutic interventions and improve patient outcomes. One important feature of COVID-19 pathophysiology is the activation of immune cells, with consequent massive production and release of inflammatory mediators that may cause impairment of several organ functions, including the brain. In addition to its classical role as a neurotransmitter, serotonin (5-hydroxytryptamine, 5-HT) has immunomodulatory properties, downregulating the inflammatory response by central and peripheral mechanisms. In this review, we describe the roles of 5-HT in the regulation of systemic inflammation and the potential benefits of the use of specific serotonin reuptake inhibitors as a coadjutant therapy to attenuate neurological complications of COVID-19.


Subject(s)
COVID-19/drug therapy , Inflammation/drug therapy , Nervous System Diseases/drug therapy , Neuroprotective Agents/therapeutic use , Serotonin Uptake Inhibitors/therapeutic use , Animals , COVID-19/complications , Humans , Inflammation/complications , Nervous System Diseases/complications , Neuroprotective Agents/pharmacology , Pandemics , SARS-CoV-2 , Serotonin Uptake Inhibitors/pharmacology
10.
Eur Rev Med Pharmacol Sci ; 24(19): 10267-10278, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-890962

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) uses Angiotensin- converting enzyme 2 (ACE2) receptors to infect host cells which may lead to coronavirus disease (COVID-19). Given the presence of ACE2 receptors in the brain and the critical role of the renin-angiotensin system (RAS) in brain functions, special attention to brain microcirculation and neuronal inflammation is warranted during COVID-19 treatment. Neurological complications reported among COVID-19 patients range from mild dizziness, headache, hypogeusia, hyposmia to severe like encephalopathy, stroke, Guillain-Barre Syndrome (GBS), CNS demyelination, infarcts, microhemorrhages and nerve root enhancement. The pathophysiology of these complications is likely via direct viral infection of the CNS and PNS tissue or through indirect effects including post- viral autoimmune response, neurological consequences of sepsis, hyperpyrexia, hypoxia and hypercoagulability among critically ill COVID-19 patients. Further, decreased deformability of red blood cells (RBC) may be contributing to inflammatory conditions and hypoxia in COVID-19 patients. Haptoglobin, hemopexin, heme oxygenase-1 and acetaminophen may be used to maintain the integrity of the RBC membrane.


Subject(s)
Brain/physiopathology , COVID-19/physiopathology , Erythrocytes/pathology , Hemolysis , Nervous System Diseases/physiopathology , Brain/blood supply , COVID-19/complications , Erythrocytes/drug effects , Hemolysis/drug effects , Humans , Models, Neurological , Molecular Targeted Therapy/methods , Nervous System Diseases/complications , Nervous System Diseases/drug therapy , Pandemics , SARS-CoV-2
11.
Mol Neurobiol ; 58(1): 106-117, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-746880

ABSTRACT

The SARS-CoV-2 virus that is the cause of coronavirus disease 2019 (COVID-19) affects not only peripheral organs such as the lungs and blood vessels, but also the central nervous system (CNS)-as seen by effects on smell, taste, seizures, stroke, neuropathological findings and possibly, loss of control of respiration resulting in silent hypoxemia. COVID-19 induces an inflammatory response and, in severe cases, a cytokine storm that can damage the CNS. Antimalarials have unique properties that distinguish them from other anti-inflammatory drugs. (A) They are very lipophilic, which enhances their ability to cross the blood-brain barrier (BBB). Hence, they have the potential to act not only in the periphery but also in the CNS, and could be a useful addition to our limited armamentarium against the SARS-CoV-2 virus. (B) They are non-selective inhibitors of phospholipase A2 isoforms, including cytosolic phospholipase A2 (cPLA2). The latter is not only activated by cytokines but itself generates arachidonic acid, which is metabolized by cyclooxygenase (COX) to pro-inflammatory eicosanoids. Free radicals are produced in this process, which can lead to oxidative damage to the CNS. There are at least 4 ways that antimalarials could be useful in combating COVID-19. (1) They inhibit PLA2. (2) They are basic molecules capable of affecting the pH of lysosomes and inhibiting the activity of lysosomal enzymes. (3) They may affect the expression and Fe2+/H+ symporter activity of iron transporters such as divalent metal transporter 1 (DMT1), hence reducing iron accumulation in tissues and iron-catalysed free radical formation. (4) They could affect viral replication. The latter may be related to their effect on inhibition of PLA2 isoforms. Inhibition of cPLA2 impairs an early step of coronavirus replication in cell culture. In addition, a secretory PLA2 (sPLA2) isoform, PLA2G2D, has been shown to be essential for the lethality of SARS-CoV in mice. It is important to take note of what ongoing clinical trials on chloroquine and hydroxychloroquine can eventually tell us about the use of antimalarials and other anti-inflammatory agents, not only for the treatment of COVID-19, but also for neurovascular disorders such as stroke and vascular dementia.


Subject(s)
Antimalarials/therapeutic use , COVID-19/complications , COVID-19/drug therapy , Nervous System Diseases/drug therapy , Nervous System Diseases/etiology , SARS-CoV-2 , Animals , Antimalarials/metabolism , Blood-Brain Barrier/drug effects , Blood-Brain Barrier/metabolism , COVID-19/metabolism , Humans , Nervous System Diseases/metabolism , Treatment Outcome
12.
Nature ; 585(7826): 614-619, 2020 09.
Article in English | MEDLINE | ID: covidwho-744380

ABSTRACT

Tropane alkaloids from nightshade plants are neurotransmitter inhibitors that are used for treating neuromuscular disorders and are classified as essential medicines by the World Health Organization1,2. Challenges in global supplies have resulted in frequent shortages of these drugs3,4. Further vulnerabilities in supply chains have been revealed by events such as the Australian wildfires5 and the COVID-19 pandemic6. Rapidly deployable production strategies that are robust to environmental and socioeconomic upheaval7,8 are needed. Here we engineered baker's yeast to produce the medicinal alkaloids hyoscyamine and scopolamine, starting from simple sugars and amino acids. We combined functional genomics to identify a missing pathway enzyme, protein engineering to enable the functional expression of an acyltransferase via trafficking to the vacuole, heterologous transporters to facilitate intracellular routing, and strain optimization to improve titres. Our integrated system positions more than twenty proteins adapted from yeast, bacteria, plants and animals across six sub-cellular locations to recapitulate the spatial organization of tropane alkaloid biosynthesis in plants. Microbial biosynthesis platforms can facilitate the discovery of tropane alkaloid derivatives as new therapeutic agents for neurological disease and, once scaled, enable robust and agile supply of these essential medicines.


Subject(s)
Alkaloids/biosynthesis , Alkaloids/supply & distribution , Hyoscyamine/biosynthesis , Saccharomyces cerevisiae/metabolism , Scopolamine/metabolism , Acyltransferases/genetics , Acyltransferases/metabolism , Animals , Atropa belladonna/enzymology , Atropine Derivatives/metabolism , Biological Transport , Datura/enzymology , Glucosides/biosynthesis , Glucosides/metabolism , Hyoscyamine/supply & distribution , Lactates/metabolism , Ligases/genetics , Ligases/metabolism , Models, Molecular , Nervous System Diseases/drug therapy , Oxidoreductases/genetics , Oxidoreductases/metabolism , Protein Engineering , Saccharomyces cerevisiae/genetics , Scopolamine/supply & distribution , Vacuoles/metabolism
14.
J Neuroophthalmol ; 40(3): 305-314, 2020 09.
Article in English | MEDLINE | ID: covidwho-682845

ABSTRACT

The initiation and continuation of immune-based therapies to treat and prevent complications of inflammatory neuro-ophthalmologic disorders during the 2019 novel coronavirus (COVID-19) pandemic is the subject of considerable debate. In each case, a treatment decision must be reached based on best clinical practices for the disorder, patient comorbidities, the current state of knowledge about the pathogenesis and infectivity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the utilization of hospital and community resources. Unfortunately, the evidence needed to standardize the decision-making process for each neuro-ophthalmologic disorder is currently absent and is likely to require months or years to develop based on the accrual of robust international data sets. In this article, we review the current understanding of SARS-CoV-2 and COVID-19 complications to provide a framework for approaching the treatment of inflammatory neuro-ophthalmic disorders during the COVID-19 viral pandemic.


Subject(s)
Betacoronavirus , Coronavirus Infections/epidemiology , Eye Diseases/drug therapy , Inflammation/drug therapy , Nervous System Diseases/drug therapy , Pandemics , Pneumonia, Viral/epidemiology , COVID-19 , Coronavirus Infections/immunology , Giant Cell Arteritis/drug therapy , Humans , Immunomodulation , Immunosuppressive Agents/therapeutic use , Myasthenia Gravis/drug therapy , Optic Neuritis/drug therapy , Pneumonia, Viral/immunology , SARS-CoV-2
15.
Neurocrit Care ; 32(3): 667-671, 2020 06.
Article in English | MEDLINE | ID: covidwho-133453

ABSTRACT

The magnitude of the COVID-19 pandemic will result in substantial neurological disease, whether through direct infection (rare), para-infectious complications (less rare), or critical illness more generally (common). Here, we raise the importance of stringent diagnosis and data collection regarding neurological complications of COVID-19; we urge caution in the over-diagnosis of neurological disease where it does not exist, but equally strongly encourage the concerted surveillance for such conditions. Additional to the direct neurological complications of COVID-19 infection, neurological patients are at risk of harm from both structural limitations (such as number of intensive care beds), and a hesitancy to treat with certain necessary medications given risk of nosocomial COVID-19 infection. We therefore also outline the specific management of patients with neuroinflammatory diseases in the context of the pandemic. This article describes the implications of COVID-19 on neurological disease and advertises the Neurocritical Care Society's international data collection collaborative that seeks to align data elements.


Subject(s)
Coronavirus Infections/physiopathology , Nervous System Diseases/physiopathology , Pneumonia, Viral/physiopathology , Betacoronavirus , COVID-19 , Cognitive Dysfunction/etiology , Coronavirus Infections/complications , Critical Care , Critical Illness , Cross Infection/prevention & control , Data Collection , Encephalomyelitis, Acute Disseminated/etiology , Guillain-Barre Syndrome/etiology , Humans , Immunosuppressive Agents/adverse effects , Infection Control , International Cooperation , Myelitis, Transverse/etiology , Nervous System Diseases/drug therapy , Nervous System Diseases/etiology , Pandemics , Pneumonia, Viral/complications , SARS-CoV-2
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