You don't want this to happen so get treatment immediately upon diagnosis.
You see a doctor immediately and get anti-coagulation going. You don't wait until it gets severe before you see a doctor. I'm going to demand heparin. Don't tough it out at home. The damage in the brain seems to occur from a different source than microclots.
How the Coronavirus Attacks the Brain
From this comes this statement:
A new study offers the first clear evidence that, in some people, the coronavirus invades brain cells, hijacking them to make copies of itself. The virus also seems to suck up all of the oxygen nearby, starving neighboring cells to death.
Why I'm getting heparin. Heparin binds to cells at a site adjacent to ACE2, the portal for SARS-CoV-2 infection, and "potently" blocks the virus, which could open up therapy options.
Anticoagulation Again Shown to Improve Survival in COVID-19 Patients;-Mortality risk about 50% lower
Stroke occurs frequently in COVID-19, leads to ‘devastating consequences’ for patients
I'm not medically trained so I know nothing, don't listen to me.
The latest here:
Large and Small Cerebral Vessel Involvement in Severe COVID-19
Abstract
Background and Purpose:
Case series indicating cerebrovascular disorders in coronavirus disease 2019 (COVID-19) have been published. Comprehensive workups, including clinical characteristics, laboratory, electroencephalography, neuroimaging, and cerebrospinal fluid findings, are needed to understand the mechanisms.
Methods:
We evaluated 32 consecutive critically ill patients with COVID-19 treated at a tertiary care center from March 9 to April 3, 2020, for concomitant severe central nervous system involvement. Patients identified underwent computed tomography, magnetic resonance imaging, electroencephalography, cerebrospinal fluid analysis, and autopsy in case of death.
Results:
Of 32 critically ill patients(You have to prevent getting critically ill. YOUR DOCTOR'S RESPONSIBILITY) with COVID-19, 8 (25%) had severe central nervous system involvement. Two presented with lacunar ischemic stroke in the early phase and 6 with prolonged impaired consciousness after termination of analgosedation. In all but one with delayed wake-up, neuroimaging or autopsy showed multiple cerebral microbleeds, in 3 with additional subarachnoid hemorrhage and in 2 with additional small ischemic lesions. In 3 patients, intracranial vessel wall sequence magnetic resonance imaging was performed for the first time to our knowledge. All showed contrast enhancement of vessel walls in large cerebral arteries, suggesting vascular wall pathologies with an inflammatory component. Reverse transcription-polymerase chain reactions for SARS-CoV-2 in cerebrospinal fluid were all negative. No intrathecal SARS-CoV-2-specific IgG synthesis was detectable.
Conclusions:
Different mechanisms of cerebrovascular disorders might be involved in COVID-19. Acute ischemic stroke might occur early. In a later phase, microinfarctions and vessel wall contrast enhancement occur, indicating small and large cerebral vessels involvement. Central nervous system disorders associated with COVID-19 may lead to long-term disabilities. Mechanisms should be urgently investigated to develop neuroprotective strategies.
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