Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 16 de 16
Filter
2.
Front Cardiovasc Med ; 8: 649922, 2021.
Article in English | MEDLINE | ID: covidwho-1186796

ABSTRACT

Since the early days of the pandemic, there have been several reports of cerebrovascular complications during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Numerous studies proposed a role for SARS-CoV-2 in igniting stroke. In this review, we focused on the pathoetiology of stroke among the infected patients. We pictured the results of the SARS-CoV-2 invasion to the central nervous system (CNS) via neuronal and hematogenous routes, in addition to viral infection in peripheral tissues with extensive crosstalk with the CNS. SARS-CoV-2 infection results in pro-inflammatory cytokine and chemokine release and activation of the immune system, COVID-19-associated coagulopathy, endotheliitis and vasculitis, hypoxia, imbalance in the renin-angiotensin system, and cardiovascular complications that all may lead to the incidence of stroke. Critically ill patients, those with pre-existing comorbidities and patients taking certain medications, such as drugs with elevated risk for arrhythmia or thrombophilia, are more susceptible to a stroke after SARS-CoV-2 infection. By providing a pictorial narrative review, we illustrated these associations in detail to broaden the scope of our understanding of stroke in SARS-CoV-2-infected patients. We also discussed the role of antiplatelets and anticoagulants for stroke prevention and the need for a personalized approach among patients with SARS-CoV-2 infection.

3.
J Clin Neurol ; 17(2): 155-163, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1175631

ABSTRACT

Coronavirus disease 2019 (COVID-19) can reportedly manifest as an acute stroke, with most cases presenting as large vessel ischemic stroke in patients with or without comorbidities. The exact pathomechanism of stroke in COVID-19 remains ambiguous. The findings of previous studies indicate that the most likely underlying mechanisms are cerebrovascular pathological conditions following viral infection, inflammation-induced endothelial dysfunction, and hypercoagulability. Acute endothelial damage due to inflammation triggers a coagulation cascade, thrombosis propagation, and destabilization of atherosclerosis plaques, leading to large-vessel occlusion and plaque ulceration with concomitant thromboemboli, and manifests as ischemic stroke. Another possible mechanism is the downregulation of angiotensin-converting enzyme 2 as the target action of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). Acute stroke management protocols need to be modified during the COVID-19 pandemic in order to adequately manage stroke patients with COVID-19.

4.
J Med Case Rep ; 15(1): 148, 2021 Mar 22.
Article in English | MEDLINE | ID: covidwho-1147316

ABSTRACT

BACKGROUND: A significant portion of critically ill patients with coronavirus disease 2019 (COVID-19) are at high risk of developing intensive care unit (ICU)-acquired swallowing dysfunction (neurogenic dysphagia) as a consequence of requiring prolonged mechanical ventilation. Pharyngeal electrical stimulation (PES) is a simple and safe treatment for neurogenic dysphagia. It has been shown that PES can restore safe swallowing in orally intubated or tracheotomized ICU patients with neurogenic dysphagia following severe stroke. We report the case of a patient with severe neurogenic post-extubation dysphagia (PED) due to prolonged intubation and severe general muscle weakness related to COVID-19, which was successfully treated using PES. CASE PRESENTATION: A 71-year-old Caucasian female patient with confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection developed neurogenic dysphagia following prolonged intubation in the ICU. To avoid aerosol-generating procedures, her swallowing function was evaluated non-instrumentally as recommended by recently published international guidelines in response to the COVID-19 pandemic. Her swallowing function was markedly impaired and PES therapy was recommended. PES led to a rapid improvement of the PED, as evaluated by bedside swallowing assessments using the Gugging Swallowing Screen (GUSS) and Dysphagia Severity Rating Scale (DSRS), and diet screening using the Functional Oral Intake Scale (FOIS). The improved swallowing, as reflected by these measures, allowed this patient to transfer from the ICU to a non-intensive medical department 5 days after completing PES treatment. CONCLUSIONS: PES treatment contributed to the restoration of a safe swallowing function in this critically ill patient with COVID-19 and ICU-acquired swallowing dysfunction. Early clinical bedside swallowing assessment and dysphagia intervention in COVID-19 patients is crucial to optimize their full recovery. PES may contribute to a safe and earlier ICU discharge of patients with ICU-acquired swallowing dysfunction. Earlier ICU discharge and reduced rates of re-intubation following PES can help alleviate some of the pressure on ICU bed capacity, which is critical in times of a health emergency such as the ongoing COVID-19 pandemic.


Subject(s)
COVID-19/therapy , Deglutition Disorders/therapy , Electric Stimulation Therapy/methods , Intubation, Intratracheal/adverse effects , Pharynx , Recovery of Function , Aged , Deglutition Disorders/etiology , Deglutition Disorders/physiopathology , Female , Humans , Respiration, Artificial , SARS-CoV-2 , Severity of Illness Index , Treatment Outcome
5.
Stem Cells ; 39(7): 904-912, 2021 07.
Article in English | MEDLINE | ID: covidwho-1126519

ABSTRACT

We have shown previously that transplanted bone marrow mononuclear cells (BM-MNC), which are a cell fraction rich in hematopoietic stem cells, can activate cerebral endothelial cells via gap junction-mediated cell-cell interaction. In the present study, we investigated such cell-cell interaction between mesenchymal stem cells (MSC) and cerebral endothelial cells. In contrast to BM-MNC, for MSC we observed suppression of vascular endothelial growth factor uptake into endothelial cells and transfer of glucose from endothelial cells to MSC in vitro. The transfer of such a small molecule from MSC to vascular endothelium was subsequently confirmed in vivo and was followed by suppressed activation of macrophage/microglia in stroke mice. The suppressive effect was absent by blockade of gap junction at MSC. Furthermore, gap junction-mediated cell-cell interaction was observed between circulating white blood cells and MSC. Our findings indicate that gap junction-mediated cell-cell interaction is one of the major pathways for MSC-mediated suppression of inflammation in the brain following stroke and provides a novel strategy to maintain the blood-brain barrier in injured brain. Furthermore, our current results have the potential to provide a novel insight for other ongoing clinical trials that make use of MSC transplantation aiming to suppress excess inflammation, as well as other diseases such as COVID-19 (coronavirus disease 2019).


Subject(s)
Cell Communication , Gap Junctions , Human Umbilical Vein Endothelial Cells/metabolism , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells , Stroke , Allografts , Animals , COVID-19/metabolism , COVID-19/pathology , Gap Junctions/metabolism , Gap Junctions/pathology , Human Umbilical Vein Endothelial Cells/pathology , Humans , Mesenchymal Stem Cells/metabolism , Mesenchymal Stem Cells/pathology , Mice , SARS-CoV-2/metabolism , Stroke/metabolism , Stroke/pathology , Stroke/therapy
6.
Front Neurol ; 12: 626780, 2021.
Article in English | MEDLINE | ID: covidwho-1110313

ABSTRACT

Background: Post-stroke aphasia is a chronic condition that impacts people's daily functioning and communication for many years after a stroke. Even though these individuals require sustained rehabilitation, they face extra burdens to access care due to shortages in qualified clinicians, insurance limitations and geographic access. There is a need to research alternative means to access intervention remotely, such as in the case of this study using a digital therapeutic. Objective: To assess the feasibility and clinical efficacy of a virtual speech, language, and cognitive digital therapeutic for individuals with post-stroke aphasia relative to standard of care. Methods: Thirty two participants completed the study (experimental: average age 59.8 years, 7 female, 10 male, average education: 15.8 years, time post-stroke: 53 months, 15 right handed, 2 left handed; control: average age 64.2 years, 7 female, 8 male, average education: 15.3 years, time post-stroke: 36.1 months, 14 right handed, 1 left handed). Patients in the experimental group received 10 weeks of treatment using a digital therapeutic, Constant Therapy-Research (CT-R), for speech, language, and cognitive therapy, which provides evidence-based, targeted therapy with immediate feedback for users that adjusts therapy difficulty based on their performance. Patients in the control group completed standard of care (SOC) speech-language pathology workbook pages. Results: This study provides Class II evidence that with the starting baseline WAB-AQ score, adjusted by -0.69 for every year of age, and by 0.122 for every month since stroke, participants in the CT-R group had WAB-AQ scores 6.43 higher than the workbook group at the end of treatment. Additionally, secondary outcome measures included the WAB-Language Quotient, WAB-Cognitive Quotient, Brief Test of Adult Cognition by Telephone (BTACT), and Stroke and Aphasia Quality of Life Scale 39 (SAQOL-39), with significant changes in BTACT verbal fluency subtest and the SAQOL-39 communication and energy scores for both groups. Conclusions: Overall, this study demonstrates the feasibility of a fully virtual trial for patients with post-stroke aphasia, especially given the ongoing COVID19 pandemic, as well as a safe, tolerable, and efficacious digital therapeutic for language/cognitive rehabilitation. Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT04488029.

7.
Brain Behav Immun ; 94: 458-462, 2021 05.
Article in English | MEDLINE | ID: covidwho-1091937

ABSTRACT

BACKGROUND: The newly emerged severe acute respiratory syndrome coronavirus (SARS-CoV-2) has caused a worldwide pandemic of human respiratory disease. Angiotensin-converting enzyme (ACE) 2 is the key receptor on lung epithelial cells to facilitate initial binding and infection of SARS-CoV-2. The binding to ACE2 is mediated via the spike glycoprotein present on the viral surface. Recent clinical data have demonstrated that patients with previous episodes of brain injuries are a high-risk group for SARS-CoV-2 infection. An explanation for this finding is currently lacking. Sterile tissue injuries including stroke induce the release of several inflammatory mediators that might modulate the expression levels of signaling proteins in distant organs. Whether systemic inflammation following brain injury can specifically modulate ACE2 expression in different vital tissues has not been investigated. METHODS: For the induction of brain stroke, mice were subjected to a surgical procedure for transient interruption of blood flow in the middle cerebral artery for 45 min and sacrificed after 1 and 3 days for analysis of brain, lung, heart, and kidney tissues. Gene expression and protein levels of ACE2, ACE, IL-6 and IL1ß were measured by quantitative PCR and Western blot, respectively. The level of soluble ACE2 in plasma and bronchial alveolar lavage (BAL) was measured using an immunoassay. Immune cell populations in lymphoid organs were analyzed by flow cytometry. Post-stroke pneumonia in mice was examined by bacterial cultures from lung homogenates and whole blood. RESULTS: Strikingly, 1 day after surgery, we observed a substantial increase in the protein levels of ACE2 in the lungs of stroke mice compared to sham-operated mice. However, the protein levels of ACE2 were found unchanged in the heart, kidney, and brain of these animals. In addition, we found increased transcriptional levels of alveolar ACE2 after stroke. The increased expression of ACE2 was significantly associated with the severity of behavioral deficits after stroke. The higher protein levels of alveolar ACE2 persisted until 3 days of stroke. Interestingly, we found reduced levels of soluble ACE2 in plasma but not in BAL in stroke-operated mice compared to sham mice. Furthermore, stroke-induced parenchymal and systemic inflammation was evident with the increased expression of IL-6 and IL-1ß. Reduced numbers of T-lymphocytes were present in the blood and spleen as an indicator of sterile tissue injury-induced immunosuppression. CONCLUSIONS: We demonstrate specific augmented alveolar ACE2 levels and inflammation in murine lungs after experimental stroke. These pre-clinical findings suggest that patients with brain injuries may have increased binding affinity to SARS-CoV-2 in their lungs which might explain why stroke is a risk factor for higher susceptibility to develop COVID-19.


Subject(s)
COVID-19 , Stroke , Animals , Humans , Lung , Mice , Peptidyl-Dipeptidase A/genetics , SARS-CoV-2
8.
Brain Behav Immun ; 91: 649-667, 2021 01.
Article in English | MEDLINE | ID: covidwho-1064858

ABSTRACT

For the last two decades, researchers have placed hopes in a new era in which a combination of reperfusion and neuroprotection would revolutionize the treatment of stroke. Nevertheless, despite the thousands of papers available in the literature showing positive results in preclinical stroke models, randomized clinical trials have failed to show efficacy. It seems clear now that the existing data obtained in preclinical research have depicted an incomplete picture of stroke pathophysiology. In order to ameliorate bench-to-bed translation, in this review we first describe the main actors on stroke inflammatory and immune responses based on the available preclinical data, highlighting the fact that the link between leukocyte infiltration, lesion volume and neurological outcome remains unclear. We then describe what is known on neuroinflammation and immune responses in stroke patients, and summarize the results of the clinical trials on immunomodulatory drugs. In order to understand the gap between clinical trials and preclinical results on stroke, we discuss in detail the experimental results that served as the basis for the summarized clinical trials on immunomodulatory drugs, focusing on (i) experimental stroke models, (ii) the timing and selection of outcome measuring, (iii) alternative entry routes for leukocytes into the ischemic region, and (iv) factors affecting stroke outcome such as gender differences, ageing, comorbidities like hypertension and diabetes, obesity, tobacco, alcohol consumption and previous infections like Covid-19. We can do better for stroke treatment, especially when targeting inflammation following stroke. We need to re-think the design of stroke experimental setups, notably by (i) using clinically relevant models of stroke, (ii) including both radiological and neurological outcomes, (iii) performing long-term follow-up studies, (iv) conducting large-scale preclinical stroke trials, and (v) including stroke comorbidities in preclinical research.


Subject(s)
Stroke Rehabilitation/methods , Stroke/immunology , Stroke/physiopathology , Animals , Brain Ischemia/drug therapy , Comorbidity , Disease Models, Animal , Humans , Immunity/immunology , Immunity/physiology , Inflammation/immunology , Neuroprotection/immunology , Neuroprotection/physiology , Outcome Assessment, Health Care , Reperfusion/methods , Reperfusion/trends
9.
J Cereb Blood Flow Metab ; 41(6): 1179-1192, 2021 06.
Article in English | MEDLINE | ID: covidwho-1061015

ABSTRACT

Cerebrovascular events have emerged as a central feature of the clinical syndrome associated with Sars-CoV-2 infection. This increase in infection-related strokes is marked by atypical presentations including stroke in younger patients and a high rate of hemorrhagic transformation after ischemia. A variety of pathogenic mechanisms may underlie this connection. Efforts to identify synergism in the pathophysiology underlying stroke and Sars-CoV-2 infection can inform the understanding of both conditions in novel ways. In this review, the molecular cascades connected to Sars-CoV-2 infection are placed in the context of the cerebral vasculature and in relationship to pathways known to be associated with stroke. Cytokine-mediated promotion of systemic hypercoagulability is suggested while direct Sars-CoV-2 infection of cerebral endothelial cells may also contribute. Endotheliopathy resulting from direct Sars-CoV-2 infection of the cerebral vasculature can modulate ACE2/AT1R/MasR signaling pathways, trigger direct viral activation of the complement cascade, and activate feed-forward cytokine cascades that impact the blood-brain barrier. All of these pathways are already implicated as independent mechanisms driving stroke and cerebrovascular injury irrespective of Sars-CoV-2. Recognizing the overlap of molecular pathways triggered by Sars-CoV-2 infection with those implicated in the pathogenesis of stroke provides an opportunity to identify future therapeutics targeting both Sars-CoV-2 and stroke thereby reducing the impact of the global pandemic.


Subject(s)
COVID-19/pathology , Cerebrovascular Disorders/etiology , Stroke/etiology , Angiotensin-Converting Enzyme 2/metabolism , Blood-Brain Barrier/metabolism , COVID-19/complications , COVID-19/virology , Cerebrovascular Disorders/metabolism , Complement Activation , Humans , Renin-Angiotensin System , Spike Glycoprotein, Coronavirus/metabolism , Stroke/metabolism , Virus Internalization
10.
World Neurosurg ; 145: 356-359, 2021 01.
Article in English | MEDLINE | ID: covidwho-850856

ABSTRACT

BACKGROUND: During the coronavirus disease 2019 (COVID-19) pandemic, a rapid screening method for COVID-19 detection is needed to decide the appropriate strategy to treat stroke patients. In acute ischemic stroke treatment, the efficacy and safety of emergent carotid artery stenting (eCAS) for hyperacute ischemic stroke (hAIS) due to internal carotid artery stenosis (ICS) have not been sufficiently established. CASE DESCRIPTION: A 71-year-old man with hAIS caused by severe ICS was treated via intravenous alteplase infusion. The patient underwent screening for COVID-19 by the loop-mediated isothermal amplification (LAMP) assay shortly after arrival at our institution. The LAMP result was obtained within 90 minutes, during intravenous alteplase infusion, and turned out to be negative. The symptom of hemiplegia worsened during alteplase infusion, and he, therefore, underwent eCAS after administration of aspirin (200 mg). Recanalization was achieved successfully by eCAS, and dual antiplatelet therapy and argatroban were administrated following eCAS. Hemorrhagic complications or restenosis/occlusion of the carotid artery were not observed. He was discharged without neurologic deficits 15 days following eCAS. Because of the rapid negative diagnosis for COVID-19 using the LAMP method, eCAS could be performed following standard procedures, along with infectious defense, without delay. CONCLUSIONS: This case report suggests that eCAS for hAIS due to ICS following intravenous alteplase can be an effective treatment, along with appropriate antiplatelet medication and management in select patients. During the COVID-19 pandemic, the LAMP assay for COVID-19 detection might be a suitable diagnostic strategy preceding stroke treatment because of the rapid turnaround time.


Subject(s)
COVID-19/diagnosis , Carotid Stenosis/surgery , Fibrinolytic Agents/therapeutic use , Ischemic Stroke/drug therapy , Ischemic Stroke/surgery , Molecular Diagnostic Techniques , Nucleic Acid Amplification Techniques , Stents , Tissue Plasminogen Activator/therapeutic use , Aged , Arginine/analogs & derivatives , Arginine/therapeutic use , Carotid Stenosis/complications , Carotid Stenosis/diagnostic imaging , Combined Modality Therapy , Hemiplegia/etiology , Humans , Ischemic Stroke/etiology , Magnetic Resonance Imaging , Male , Pipecolic Acids/therapeutic use , Platelet Aggregation Inhibitors/therapeutic use , Sulfonamides/therapeutic use , Tomography, X-Ray Computed , Treatment Outcome
11.
Heart ; 107(2): 113-119, 2021 01.
Article in English | MEDLINE | ID: covidwho-808650

ABSTRACT

OBJECTIVE: To describe the place and causes of acute cardiovascular death during the COVID-19 pandemic. METHODS: Retrospective cohort of adult (age ≥18 years) acute cardiovascular deaths (n=5 87 225) in England and Wales, from 1 January 2014 to 30 June 2020. The exposure was the COVID-19 pandemic (from onset of the first COVID-19 death in England, 2 March 2020). The main outcome was acute cardiovascular events directly contributing to death. RESULTS: After 2 March 2020, there were 28 969 acute cardiovascular deaths of which 5.1% related to COVID-19, and an excess acute cardiovascular mortality of 2085 (+8%). Deaths in the community accounted for nearly half of all deaths during this period. Death at home had the greatest excess acute cardiovascular deaths (2279, +35%), followed by deaths at care homes and hospices (1095, +32%) and in hospital (50, +0%). The most frequent cause of acute cardiovascular death during this period was stroke (10 318, 35.6%), followed by acute coronary syndrome (ACS) (7 098, 24.5%), heart failure (6 770, 23.4%), pulmonary embolism (2 689, 9.3%) and cardiac arrest (1 328, 4.6%). The greatest cause of excess cardiovascular death in care homes and hospices was stroke (715, +39%), compared with ACS (768, +41%) at home and cardiogenic shock (55, +15%) in hospital. CONCLUSIONS AND RELEVANCE: The COVID-19 pandemic has resulted in an inflation in acute cardiovascular deaths, nearly half of which occurred in the community and most did not relate to COVID-19 infection suggesting there were delays to seeking help or likely the result of undiagnosed COVID-19.


Subject(s)
Acute Coronary Syndrome , COVID-19 , Cause of Death , Mortality/trends , Stroke , Acute Coronary Syndrome/etiology , Acute Coronary Syndrome/mortality , Adult , Aged , Aged, 80 and over , COVID-19/diagnosis , COVID-19/epidemiology , Causality , England/epidemiology , Female , Hospitalization/statistics & numerical data , Humans , Male , Middle Aged , Outcome and Process Assessment, Health Care , Residence Characteristics/statistics & numerical data , Retrospective Studies , SARS-CoV-2/isolation & purification , Stroke/etiology , Stroke/mortality
12.
J Stroke Cerebrovasc Dis ; 29(11): 105314, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-753197

ABSTRACT

BACKGROUND AND PURPOSE: Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection is associated with stroke. The role of sex on stroke outcome has not been investigated. To objective of this paper is to describe the characteristics of a diverse cohort of acute stroke patients with COVID-19 disease and determine the role of sex on outcome. METHODS: This is a retrospective study of patients with acute stroke and SARS-CoV-2 infection admitted between March 15 to May 15, 2020 to one of the six participating comprehensive stroke centers. Baseline characteristics, stroke subtype, workup, treatment and outcome are presented as total number and percentage or median and interquartile range. Outcome at discharge was determined by the modified Rankin Scale Score (mRS). Variables and outcomes were compared for males and females using univariate and multivariate analysis. RESULTS: The study included 83 patients, 47% of which were Black, 28% Hispanics/Latinos, and 16% whites. Median age was 64 years. Approximately 89% had at least one preexisting vascular risk factor (VRF). The most common complications were respiratory failure (59%) and septic shock (34%). Compared with females, a higher proportion of males experienced severe SARS-CoV-2 symptoms requiring ICU hospitalization (73% vs. 49%; p = 0.04). When divided by stroke subtype, there were 77% ischemic, 19% intracerebral hemorrhage and 3% subarachnoid hemorrhage. The most common ischemic stroke etiologies were cryptogenic (39%) and cardioembolic (27%). Compared with females, males had higher mortality (38% vs. 13%; p = 0.02) and were less likely to be discharged home (12% vs. 33%; p = 0.04). After adjustment for age, race/ethnicity, and number of VRFs, mRS was higher in males than in females (OR = 1.47, 95% CI = 1.03-2.09). CONCLUSION: In this cohort of SARS-CoV-2 stroke patients, most had clinical evidence of coronavirus infection on admission and preexisting VRFs. Severe in-hospital complications and worse outcomes after ischemic strokes were higher in males, than females.


Subject(s)
Brain Ischemia/epidemiology , Coronavirus Infections/epidemiology , Health Status Disparities , Intracranial Hemorrhages/epidemiology , Pneumonia, Viral/epidemiology , Stroke/epidemiology , Aged , Aged, 80 and over , Brain Ischemia/diagnosis , Brain Ischemia/therapy , COVID-19 , Chicago/epidemiology , Coronavirus Infections/diagnosis , Coronavirus Infections/therapy , Female , Humans , Intracranial Hemorrhages/diagnosis , Intracranial Hemorrhages/therapy , Male , Middle Aged , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/therapy , Prognosis , Retrospective Studies , Risk Assessment , Risk Factors , Sex Factors , Stroke/diagnosis , Stroke/therapy , Time Factors
13.
Stroke ; 51(10): 3156-3168, 2020 10.
Article in English | MEDLINE | ID: covidwho-748838

ABSTRACT

Understanding the relationship between infection and stroke has taken on new urgency in the era of the coronavirus disease 2019 (COVID-19) pandemic. This association is not a new concept, as several infections have long been recognized to contribute to stroke risk. The association of infection and stroke is also bidirectional. Although infection can lead to stroke, stroke also induces immune suppression which increases risk of infection. Apart from their short-term effects, emerging evidence suggests that poststroke immune changes may also adversely affect long-term cognitive outcomes in patients with stroke, increasing the risk of poststroke neurodegeneration and dementia. Infections at the time of stroke may also increase immune dysregulation after the stroke, further exacerbating the risk of cognitive decline. This review will cover the role of acute infections, including respiratory infections such as COVID-19, as a trigger for stroke; the role of infectious burden, or the cumulative number of infections throughout life, as a contributor to long-term risk of atherosclerotic disease and stroke; immune dysregulation after stroke and its effect on the risk of stroke-associated infection; and the impact of infection at the time of a stroke on the immune reaction to brain injury and subsequent long-term cognitive and functional outcomes. Finally, we will present a model to conceptualize the many relationships among chronic and acute infections and their short- and long-term neurological consequences. This model will suggest several directions for future research.


Subject(s)
Atherosclerosis/epidemiology , Infections/epidemiology , Stroke/epidemiology , Arrhythmias, Cardiac/epidemiology , Arrhythmias, Cardiac/physiopathology , Atherosclerosis/immunology , Atherosclerosis/physiopathology , Bacteremia/epidemiology , Bacteremia/immunology , Bacteremia/physiopathology , Betacoronavirus , COVID-19 , Chronic Disease , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Cytomegalovirus Infections/epidemiology , Cytomegalovirus Infections/immunology , Cytomegalovirus Infections/physiopathology , Endothelium/physiopathology , HIV Infections/epidemiology , HIV Infections/immunology , HIV Infections/physiopathology , Humans , Immunocompromised Host/immunology , Infections/immunology , Infections/physiopathology , Inflammation/immunology , Influenza, Human/epidemiology , Influenza, Human/immunology , Influenza, Human/physiopathology , Pandemics , Platelet Activation , Platelet Aggregation , Pneumonia/epidemiology , Pneumonia/immunology , Pneumonia/physiopathology , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , Prognosis , Risk Factors , SARS-CoV-2 , Stroke/immunology , Thrombosis/epidemiology , Thrombosis/immunology , Varicella Zoster Virus Infection/epidemiology , Varicella Zoster Virus Infection/immunology , Varicella Zoster Virus Infection/physiopathology
14.
Cureus ; 12(8): e10025, 2020 Aug 25.
Article in English | MEDLINE | ID: covidwho-736866

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a respiratory pathogen with remarkable properties of multisystem involvement and numerous complications. The coronavirus disease of 2019 (COVID-19) presenting as stroke is becoming more common. Herein, we describe an unusual case of COVID-19 in a patient who initially presented with myalgia, fatigue, loss of taste and smell, and non-specific memory impairment. Two months after infection with SARS-CoV-2, the patient presented with acute onset of right-sided weakness, sensory loss, and worsening cognitive impairment. Reverse transcription-polymerase chain reaction was performed to detect the SARS-CoV-2 virus, and the results were positive at the time of initial infection as well as during the current admission. Neuroimaging suggested a subacute ischemic infarct in the middle cerebral artery. The patient was re-tested for SARS-CoV-2 and found to be positive, but the cycle threshold was high (40.4) along with a positive test for immunoglobulin-G (IgG) for SARS-CoV-2. This report highlights a unique case of stroke-related to COVID-19 infection in a middle-aged woman with otherwise mild symptomatic illness. The patient had a chronic ischemic stroke with delayed presentation two months after the initial symptomatic viral infection. This case underscores the importance of neurological assessment as well as timely evaluation of patients presenting with COVID-19 and any neurological concerns to recognize stroke as a complication of COVID-19 promptly.

15.
Eur J Neurol ; 27(11): 2308-2311, 2020 11.
Article in English | MEDLINE | ID: covidwho-697171

ABSTRACT

BACKGROUND AND PURPOSE: Ischaemic stroke has been described in association with COVID-19. Several pathophysiological mechanisms have been suggested, i.e. prothrombotic state, cardiac injury etc. It was sought to assess the potential association between ischaemic stroke associated with SARS-CoV-2 infection and underlying atherosclerotic lesions. METHODS: A retrospective analysis of stroke related to large vessel occlusion was conducted amongst patients with SARS-CoV-2 infection and underlying mild atherosclerotic disease, between 19 March and 19 April 2020 in six different stroke centers in the Île-de France area, France. RESULTS: The median age was 52 years, median body mass index was 29.5 kg/m2 . All patients displayed previous vascular risk factors such as high blood pressure, diabetes, dyslipidemia or body mass index > 25. The delay between the first respiratory symptoms of COVID-19 and stroke was 11.5 days. At baseline, all had tandem occlusions, i.e. intracerebral and extracerebral thrombus assessed with computed tomography or magnetic resonance imaging. Cases displayed a large thrombus in the cervical carotid artery with underlying mild non-stenosing atheroma, after an etiological workup based on angio-computed tomography or magnetic resonance imaging and/or cervical echography. CONCLUSION: Our study should alert clinicians to scrutinize any new onset of ischaemic stroke during COVID-19 infection, mainly in patients with vascular risk factors or underlying atherosclerotic lesions.


Subject(s)
Atherosclerosis/complications , COVID-19/complications , Intracranial Thrombosis/etiology , Ischemic Stroke/etiology , Arterial Occlusive Diseases/etiology , Atherosclerosis/diagnostic imaging , COVID-19/diagnostic imaging , Carotid Artery Diseases/diagnostic imaging , Carotid Artery Diseases/etiology , Female , Humans , Intracranial Thrombosis/complications , Intracranial Thrombosis/diagnostic imaging , Ischemic Stroke/diagnostic imaging , Magnetic Resonance Imaging , Male , Middle Aged , Retrospective Studies , Risk Factors , Tomography, X-Ray Computed
16.
Eur J Case Rep Intern Med ; 7(6): 001736, 2020.
Article in English | MEDLINE | ID: covidwho-594977

ABSTRACT

INTRODUCTION: A strong association between stroke and atrial fibrillation (AF) has been demonstrated. Anticoagulation for the prevention of stroke in high-risk patients has the benefit of improving the life expectancy, quality of life, autonomy and social functioning of the patient. The COVID-19 pandemic poses challenges for stroke patients because of the association between SARS-CoV-2 infection and thromboembolic risk. CASE DESCRIPTION: We describe the case of an 84-year-old female patient admitted due to an embolic stroke and non-anticoagulated AF. Her admission symptoms were sensory-motor aphasia and severe right limb paresis with an NIHSS score of 24. The diagnosis of embolic stroke (namely, total anterior circulation infarct; TACI) was made. Her stroke was extensive so she was not started on anticoagulation. During hospitalization, new embolic events occurred and a concomitant diagnosis of COVID-19 was made with progressive respiratory dysfunction followed by multiorgan failure. The patient died despite appropriate treatment. DISCUSSION: The prognosis of elderly patients with cardioembolic stroke depends on anticoagulation administration. The NIHSS score on admission of our patient meant anticoagulation therapy was not appropriate. The diagnosis of COVID-19 contributed to the patient's death. LEARNING POINTS: Anticoagulation should be considered in stroke patients with total infarction and atrial fibrillation.There is an association between COVID-19 and thromboembolic stroke.Elderly patients with stroke and COVID-19 are at higher risk of death.

SELECTION OF CITATIONS
SEARCH DETAIL