Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 4 de 4
Journal of Stroke Medicine ; : 25166085221089731, 2022.
Article in English | Sage | ID: covidwho-1785139


Background and Purpose:Severe acute respiratory syndrome coronavirus 2 (SARS-COV2) infection induces a prothrombotic state frequently associated with arterial ischemic strokes. Cerebral venous sinus thrombosis (CVST) is also reported with corona virus disease-19 (COVID-19) but a large cohort study is lacking. Our aim was to study the characteristics, treatment response, and outcomes of CVST occurring in association with COVID-19 (COVID-CVST) and the causal relationship with COVID-19.Methods:Data of 34 patients admitted in COVID facility and suffering from CVST and SARS-COV2 infection was studied with respect to their clinic-radiological and lab features, predisposing factors, treatment, and outcome.Observations and Results:15 patients with CVST were detected positive for COVID but remained asymptomatic for the same. 14 patients had CVST along with symptoms of COVID, whereas 5 had CVST after recovery from COVID, at an average of 18 days after COVID-19. 4 patients were on aspirin as prophylaxis against thrombo-embolic events. The number of males exceeded females (22:12), conventional risk factors were seen in only 8 patients (postpartum state-3, alcohol abuse-2 and anemia-3), whereas the majority (26/34) showed none of them. The mean serum homocysteine level was normal and antiphospholipid antibody was tested normal in the assessed subjects. D-dimer and C reactive protein were elevated in all. 4 symptomatic patients who suffered from severe pneumonia died because of systemic complications.Conclusion:COVID-19 predisposes to CVST and the outcome is related to the severity of COVID pneumonia. CVST related to COVID occurs during or after a few weeks of COVID pneumonia and can also be seen in asymptomatic SARS-COV2 infection. COVID-19 can occur independently or in association with traditional thrombotic risk factors which increase the risk and severity of CVST in COVID. If recognized early, CVST associated with COVID can usually be treated effectively to achieve a very good outcome.

Ann Indian Acad Neurol ; 25(1): 7-10, 2022.
Article in English | MEDLINE | ID: covidwho-1726287


During the second wave of COVID-19 pandemic, there is a sudden increase in number of cases mucormycosis infection in India. This communication by the Tropical Neurology subsection expert group of the Indian Academy of Neurology (IAN) describes the clinical and diagnostic features, treatment of the disease and gives recommendations about the ways forward.

J Neurol Sci ; 414: 116884, 2020 07 15.
Article in English | MEDLINE | ID: covidwho-197833


A comprehensive review of the neurological disorders reported during the current COVID-19 pandemic demonstrates that infection with SARS-CoV-2 affects the central nervous system (CNS), the peripheral nervous system (PNS) and the muscle. CNS manifestations include: headache and decreased responsiveness considered initial indicators of potential neurological involvement; anosmia, hyposmia, hypogeusia, and dysgeusia are frequent early symptoms of coronavirus infection. Respiratory failure, the lethal manifestation of COVID-19, responsible for 264,679 deaths worldwide, is probably neurogenic in origin and may result from the viral invasion of cranial nerve I, progressing into rhinencephalon and brainstem respiratory centers. Cerebrovascular disease, in particular large-vessel ischemic strokes, and less frequently cerebral venous thrombosis, intracerebral hemorrhage and subarachnoid hemorrhage, usually occur as part of a thrombotic state induced by viral attachment to ACE2 receptors in endothelium causing widespread endotheliitis, coagulopathy, arterial and venous thromboses. Acute hemorrhagic necrotizing encephalopathy is associated to the cytokine storm. A frontal hypoperfusion syndrome has been identified. There are isolated reports of seizures, encephalopathy, meningitis, encephalitis, and myelitis. The neurological diseases affecting the PNS and muscle in COVID-19 are less frequent and include Guillain-Barré syndrome; Miller Fisher syndrome; polyneuritis cranialis; and rare instances of viral myopathy with rhabdomyolysis. The main conclusion of this review is the pressing need to define the neurology of COVID-19, its frequency, manifestations, neuropathology and pathogenesis. On behalf of the World Federation of Neurology we invite national and regional neurological associations to create local databases to report cases with neurological manifestations observed during the on-going pandemic. International neuroepidemiological collaboration may help define the natural history of this worldwide problem.

Betacoronavirus , Cerebrovascular Disorders/etiology , Coronavirus Infections/complications , Nervous System Diseases/etiology , Neuromuscular Diseases/etiology , Pandemics , Pneumonia, Viral/complications , Registries , Adult , Angiotensin-Converting Enzyme 2 , Animals , COVID-19 , Cerebrovascular Disorders/physiopathology , Communicable Diseases, Emerging/epidemiology , Communicable Diseases, Emerging/virology , Coronaviridae/pathogenicity , Coronaviridae/physiology , Coronaviridae/ultrastructure , Coronavirus Infections/epidemiology , Coronavirus Infections/physiopathology , Coronavirus Infections/veterinary , Coronavirus Infections/virology , Cytokine Release Syndrome/etiology , Cytokine Release Syndrome/physiopathology , Endothelium, Vascular/pathology , Endothelium, Vascular/virology , Humans , Models, Animal , Nervous System Diseases/physiopathology , Neuromuscular Diseases/physiopathology , Organ Specificity , Peptidyl-Dipeptidase A/physiology , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Thrombophilia/etiology , Thrombophilia/physiopathology , Viral Tropism