The eyes of Long COVID patients show significant nerve damage.
They display notable nerve degradation.
Their corneal nerve fibers are sparser, branching is stunted, and the nerve lengths are curtailed.
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The complex network of corneal nerves in the human eye is like a spiderweb.
Within the elegant structure of this web, each silken thread represents a delicate neural pathway, connected to maintain stability and harmony.
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This web is specifically designed to optimize its function – catching insects – just as the corneal nerves are designed to relay sensory information efficiently.
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Now, picture this masterpiece under siege by a tempest—SARS-CoV-2.
Each gust of wind and drop of rain symbolizing the virus's assaults on our systems.
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Yet, this storm's most insidious challenge isn't just the overpowering wind or torrential rain, but the barrage of debris it carries—twigs, leaves, and foreign particles, all disrupting the web's meticulous design.
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This debris is reminiscent of the inflammatory dendritic cells that proliferate in the corneas of Long COVID patients.
Dendritic cells, under typical physiological conditions, play sentinel roles in our immune responses.
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However, in the eyes of those enduring Long COVID, these cells undergo a transformation.
They proliferate in excessive numbers, their morphology shifts, and they become hyperactive.
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Just as debris might clog and tear at the spiderweb, these altered dendritic cells disturb the corneal neural landscape.
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They can initiate cascades of inflammatory reactions, leading to the degradation of nerve fibers, manifesting as reduced corneal nerve density, stunted branching, and abbreviated nerve lengths.
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Post-storm, the spider attempts to repair.
However, some parts of the web develop abnormalities: knots and clumps in place of the former sleek strands.
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These are analogous to the microneuromas detected in Long COVID patients.
While they are a result of the body’s attempts to heal, they don’t fully restore the original structure or function.
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In this damaged state, the web’s overall efficiency and structural integrity are compromised.
The aftereffects of SARS-CoV-2 aren't subtle.
Plainly put, the virus throws a wrench into the machinery of our eyes, causing inflammation and obvious nerve damage.
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Long COVID's grip on the nervous system doesn't just let go.
Long covid is a wildfire scorching healthcare funds 🔥🧵
In a healthcare landscape already marred by pandemics and chronic diseases, LC is the cataclysmic firestorm that makes everything else look like a campfire.
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SARS-CoV-2 isn’t a fire that emergency services can contain.
It’s a blazing inferno that devours everything in its path.
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From 2020 to 2023, LC’s spread led to a relentless increase in healthcare use across all categories:
Upon SARS-CoV-2 interaction, the brain’s protective pathways cascade towards self-destruction.
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Imagine the brain as a grand orchestra, finely tuned and synchronized to produce harmonious melodies that represent cognitive functions and emotions.
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SARS-CoV-2 acts like an insidious conductor with a malevolent score.
When it begins to wave its baton, the composition starts changing.
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SARS-CoV-2’s insidious invasion leaves a trail of neural devastation and vascular chaos 🧵
The aftermath of an infection is not just an extended bout of the initial symptoms.
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The central nervous system shows signs of distress post infection.
Neuroinflammation is a state where the brain’s defense mechanisms start attacking its own cells.
It has been significantly higher in individuals with PASC compared to healthy controls.
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Key regions of the brain, including the midcingulate and anterior cingulate cortex, corpus callosum, thalamus, basal ganglia, and areas surrounding the ventricles, have become inflamed battlegrounds.
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