“…The neurological involvement in this case was not discovered until Day 26 postinfection, which highlights the importance of clinical values, such as NLR, lymphocyte-to-CRP ratio (LCRPR), and lymphocyte-to-platelet ratio (LPR), as prognostic indicators of severe inflammation and possible neurological complications. Other studies have shown that COVID-19-induced severe inflammation and inflammatory infiltrates consisting of T cells, macrophages, and neutrophils contribute to the rupture of atheromatous plaques in patients with pre-existing atheromatous disease due to the production of proteolytic enzymes and endothelial cell disruption [99][100][101]. Although the use of protease inhibitors in these patients may be beneficial, they should be carefully used as they may promote SARS-CoV-2-induced hypercoagulation.…”
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.
“…The neurological involvement in this case was not discovered until Day 26 postinfection, which highlights the importance of clinical values, such as NLR, lymphocyte-to-CRP ratio (LCRPR), and lymphocyte-to-platelet ratio (LPR), as prognostic indicators of severe inflammation and possible neurological complications. Other studies have shown that COVID-19-induced severe inflammation and inflammatory infiltrates consisting of T cells, macrophages, and neutrophils contribute to the rupture of atheromatous plaques in patients with pre-existing atheromatous disease due to the production of proteolytic enzymes and endothelial cell disruption [99][100][101]. Although the use of protease inhibitors in these patients may be beneficial, they should be carefully used as they may promote SARS-CoV-2-induced hypercoagulation.…”
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.
“…COVID-19 inflammation induces a prothrombotic milieu among patients who are at risk of vascular events and those with the pre-existing atheromatous disease. Among patients with coronary disease, evidence suggests that virally induced inflammatory infiltrates such as T cells, macrophages, and neutrophils populate the atheromatous plaque leading to a cascade of events including vascular permeability, endothelial disruption, and exposure of prothrombotic elements such as collagen, tissue factor, and platelet adhesion molecules, which all play a role in thrombogenesis (68). Furthermore, it is known that carotid artery plaques with features of a thin fibrous cap, large core lipid, intraplaque bleeding, and the abundance of monocyte-derived macrophages and activated smooth muscle cells cause instability and vulnerability to plaque rupture (69).…”
Section: Inflammation-induced Plaque Progression and Vulnerabilitymentioning
Clinical reports of neurological manifestations associated with severe coronavirus disease 2019 (COVID-19), such as acute ischemic stroke (AIS), encephalopathy, seizures, headaches, acute necrotizing encephalitis, cerebral microbleeds, posterior reversible leukoencephalopathy syndrome, hemophagocytic lymphohistiocytosis, peripheral neuropathy, cranial nerve palsies, transverse myelitis, and demyelinating disorders, are increasing rapidly. However, there are comparatively few studies investigating the potential impact of immunological responses secondary to hypoxia, oxidative stress, and excessive platelet-induced aggregation on the brain. This scoping review has focused on the pathophysiological mechanisms associated with peripheral and consequential neural (central) inflammation leading to COVID-19-related ischemic strokes. It also highlights the common biological processes shared between AIS and COVID-19 infection and the importance of the recognition that severe respiratory dysfunction and neurological impairments associated with COVID and chronic inflammation [post-COVID-19 neurological syndrome (PCNS)] may significantly impact recovery and ability to benefit from neurorehabilitation. This study provides a comprehensive review of the pathobiology of COVID-19 and ischemic stroke. It also affirms that the immunological contribution to the pathophysiology of COVID-19 is predictive of the neurological sequelae particularly ischemic stroke, which makes it the expectation rather than the exception. This work is of fundamental significance to the neurorehabilitation community given the increasing number of COVID-related ischemic strokes, the current limited knowledge regarding the risk of reinfection, and recent reports of a PCNS. It further highlights the need for global collaboration and research into new pathobiology-based neurorehabilitation treatment strategies and more integrated evidence-based care.
“…The COVID-19-induced severe inflammation and inflammatory infiltrate consisting of T cells, macrophages and neutrophils contribute to the rupture of atheromatous plaques in patients with pre-existing atheromatous disease due to the production of proteolytic enzymes and endothelial cell disruption [60].…”
The systematic online search of articles utilizing the search terms ”Coronavirus, SARS-COV-2 and Neurological complications”, published between January 2019 and September 2021, was performed.
Neurological manifestations are prevalent during infection with the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). There is a clear association between cerebrovascular disease and coronavirus disease 2019 (COVID-19). But today, whether this association is causal or incidental is still unknown. This systemic review presents the possible pathophysiological mechanisms linking COVID-19 and cerebrovascular disease, describes the most often neurological complications and their prognosis, discusses several clinical and laboratory characteristics.
A systematic literature search was conducted, and relevant information was abstracted. Angiotensin-converting enzyme-2 receptor dysregulation, uncontrollable immune storm with inflammation, coagulopathy, complications due to critical illness and prolonged hospitalization can all contribute as potential etiological and pathogenic mechanisms leading to diverse cerebrovascular clinical manifestations.
Acute ischemic stroke, intracerebral haemorrhage, and cerebral venous sinus thrombosis have been described in case reports and cohorts of COVID-19 patients, with a prevalence ranging between 0.5 % and 5.0 %. SARS-CoV-2-positive stroke patients have higher mortality rates, worse functional outcomes at discharge and longer duration of hospitalization as compared with SARS-CoV-2-negative stroke patients. Understanding of the specific demographic, clinical, laboratory and radiological characteristics may be used as ‘red flags’ in recognizing COVID-19-related acute neurological complications.
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