ABSTRACT
The global pandemic of novel coronavirus disease 2019 (COVID-19) has taken the entire human race by surprise and led to an unprecedented number of mortalities worldwide so far. Current clinical studies have interpreted that angiotensin-converting enzyme 2 (ACE2) is the host receptor for severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). In addition, ACE2 is the major component of the renin-angiotensin system. ACE2 deteriorates angiotensin II, a peptide that is responsible for the promotion of stroke. The downregulation of ACE2 further activates an immunological cascade. Thus, researchers need to explore and examine the possible links between COVID-19 and ischemic stroke (IS). Human ACE2 expression level and pattern in various tissues might be decisive for the vulnerability, symptoms, and treatment outcomes of the SARS-CoV-2 infection. The swift increase in the knowledge of SARS-CoV-2 has given creditable evidence that SARS-CoV-2 infected patients also encounter neurological deficits. As the SARS-CoV-2 binds to ACE2, it will hamper the activity of ACE2 in providing neuroprotection, especially in the case of stroke patients. Due to the downregulation of ACE2, the inflammatory response is activated in the ischemic penumbra. The COVID-19 pandemic has affected people with various pre-existing diseases, including IS, in such a way that these patients need special care and attention for their survival. Several clinical trials are currently ongoing worldwide as well as many other projects are in different stages of conceptualization and planning to facilitate the effective management of stroke patients with COVID-19 infection.
Subject(s)
Betacoronavirus , Brain Ischemia/etiology , Coronavirus Infections/physiopathology , Pandemics , Pneumonia, Viral/physiopathology , Renin-Angiotensin System/physiology , Stroke/etiology , Angiotensin-Converting Enzyme 2 , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Betacoronavirus/pathogenicity , Betacoronavirus/physiology , Blood-Brain Barrier , Brain Ischemia/epidemiology , Brain Ischemia/immunology , Brain Ischemia/physiopathology , COVID-19 , Chemotaxis, Leukocyte , Comorbidity , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Cytokines/physiology , Encephalitis, Viral/complications , Encephalitis, Viral/physiopathology , Hemodynamics , Humans , Inflammation , Models, Immunological , Models, Neurological , Multiple Organ Failure/etiology , Multiple Organ Failure/physiopathology , Nervous System Diseases/epidemiology , Nervous System Diseases/etiology , Peptidyl-Dipeptidase A/physiology , Pneumonia, Viral/complications , Pneumonia, Viral/epidemiology , Receptors, Virus/physiology , Risk , SARS-CoV-2 , Stroke/epidemiology , Stroke/immunology , Stroke/physiopathologyABSTRACT
We report a 20-year-old female with SARS-CoV-2 encephalitis who presented with 4 days of upper respiratory symptoms, fevers and sudden acute altered mental status. An extensive work up led to the most likely cause for the neurologic decompensation to be viewed as SARS-CoV-2 symptomology.
Subject(s)
Coronavirus Infections/complications , Encephalitis, Viral/complications , Pneumonia, Viral/complications , Betacoronavirus/genetics , Betacoronavirus/isolation & purification , COVID-19 , Coronavirus Infections/diagnosis , Coronavirus Infections/therapy , Encephalitis, Viral/diagnosis , Encephalitis, Viral/therapy , Female , Humans , Mental Disorders/diagnosis , Mental Disorders/etiology , Mental Disorders/therapy , Nasopharynx/virology , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/therapy , SARS-CoV-2 , Treatment Outcome , Young AdultABSTRACT
A pandemic due to novel coronavirus arose in mid-December 2019 in Wuhan, China, and in 3 months' time swept the world. The disease has been referred to as COVID-19, and the causative agent has been labelled SARS-CoV-2 due to its genetic similarities to the virus (SARS-CoV-1) responsible for the severe acute respiratory syndrome (SARS) epidemic nearly 20 years earlier. The spike proteins of both viruses dictate tissue tropism using the angiotensin-converting enzyme type 2 (ACE-2) receptor to bind to cells. The ACE-2 receptor can be found in nervous system tissue and endothelial cells among the tissues of many other organs.Neurological complications have been observed with COVID-19. Myalgia and headache are relatively common, but serious neurological disease appears to be rare. No part of the neuraxis is spared. The neurological disorders occurring with COVID-19 may have many pathophysiological underpinnings. Some appear to be the consequence of direct viral invasion of the nervous system tissue, others arise as a postviral autoimmune process, and still others are the result of metabolic and systemic complications due to the associated critical illness. This review addresses the preliminary observations regarding the neurological disorders reported with COVID-19 to date and describes some of the disorders that are anticipated from prior experience with similar coronaviruses.