How COVID-19 Can Affect and Damage the Brain

Just maybe this earlier research answers the question:

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.

 What that means is your doctor needs EXACT PROTOCOLS that prevent your need to be hospitalized as soon as you are diagnosed with COVID-19.

YOUR DOCTOR'S RESPONSIBILITY!

I'm not medically trained but due to the research I'm reading I'm doing heparin.

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

But this research below suggests not due to bleeding risks. I'll take that risk since I've been on warfarin, aspirin and had Lovenox shots. 

COVID-Related Strokes Especially Severe, Result in Worse Outcomes

The paragraph from there:

"On the other hand, in most patients with COVID-19 associated ischaemic stroke, very early anti-coagulation is probably not warranted as a strategy to prevent inpatient stroke recurrence, as this outcome is too uncommon to justify the increased risk of secondary haemorrhage," according to the group.(So you wait until the clots are severe before you do anti-coagulation. OK, not for me.)

You doctor better know the EXACT PROTOCOL to prevent these complications.

Do not tough it out at home.

 

The latest here:

 How COVID-19 Can Affect and Damage the Brain

On December 1, 2020, the number of COVID-19 cases worldwide totaled over 63.6 million, with 13.6 million cases within the United States. Of this total, nearly 1.5 million deaths were attributed to COVID-19, with over 269,000 of the deaths occurring in the U.S.1

COVID-19 had primarily been thought to be a respiratory disease. In recent months, however, growing evidence shows that the disease may likely be a disease of the epithelium of the lungs, or the lining of the respiratory tract, and the endothelium, the lining of arteries and veins throughout the body.2

Because of this, complications of COVID-19 tend to strike some organ systems more frequently than others.  Respiratory, cardiovascular, renal, gastrointestinal, and neurological systems appear to be the most commonly impacted. Infection can present a loss of the sense of smell (anosmia) or taste (ageusia), Guillain-Barre syndrome, encephalopathy, encephalitis, and acute cerebrovascular disease.3,4

While extensive longstanding research has not been conducted due to relative inexperience with the virus, information is emerging that strongly suggests the risk of neurologic damage. One study compared the rate of acute ischemic stroke in individuals with COVID-19 to a group of people with influenza, a known stroke trigger. The research found the likelihood of stroke with COVID-19 infection (1.6% of people) to be substantially higher than for influenza (0.2%). 3

Another study examined the risk of developing cerebrovascular disease with COVID-19 infection, which refers to disorders that affect the blood vessels and blood supply to the brain. The categories of cerebrovascular disease examined included cerebral ischemia, intracerebral hemorrhage, and leukoencephalopathy of the posterior reversible encephalopathy type. In total, 1.4% of 1,683 cases developed neurological complications over 50 days.2 Neurological injuries included arterial dissections, subarachnoid hemorrhage, microbleeds, and single or multiple hematomas -severe injuries that resulted in high rates of death or significant disability.

The study found that the injuries tended to occur in the vascular areas that serve the brainstem and posterior (back) portions of the brain. Blood clotting in these areas can be exceedingly significant and impact the arteries feeding blood to the brain.5

There is also emerging evidence that individuals with pre-existing neurological injury are at greater risk for developing neurological complications in the event of COVID-19 infection. A case report of post-COVID-19 autoimmune encephalitis, an inflammation of the brain and spinal cord, found potentially significant long-term neurological symptoms and consequences if undiagnosed or improperly treated. These included non-fluent aphasia, oculomotor dysfunction, myoclonus of the tongue and limbs, echolalia, perseveration, and hallucinations.6

Recovery patterns post-COVID-19 show symptoms persistence at the time of follow-up visit to range from 5% to more than 50% for neurological symptoms ranging from myalgia, vertigo, lack of appetite, headache, loss of taste, loss of smell, and fatigue.7

For the time being, it is reasonable to exercise caution in prediction about recovery from neurological deficits that accompany COVID-19 infection. There is evidence of recovery in some symptoms, such as the loss of taste or smell and significant long-term deficits associated with other complications such as stroke. However, we remain in the earliest stages in regards to understanding the near- and longer-term neurological consequences of COVID-19 infection.  Recovery and symptom severity in the presence of newer interventions that impact viral replication rates and address inflammatory processes may be different, and hopefully better, than the currently available data.