sARS-cOv-2

Hello everybody.

This is Stephen Zuckerman in baton rouge Louisiana and I'm

going to give a presentation about the neurological manifestation of

covid infections.

I'm taking this information from a review article published in

the most recent continuum and it was written by a

doctor nath who was head of virology at the NIH.

No other corona viruses have caused neurological effects.

But the severe acute respiratory syndrome criminalized too with all

of its mutations is more adept at replicating and adapting

to humans.

Now, when the pandemic first started, it seemed to me

like neurologists were sort of reaching for neurological complications so

they could be considered important in this horrible worldwide pandemic.

But actually I was proven wrong and the nervous system

is certainly part of the multi organ system involvement of

this horrible condition.

In fact no part of the nervous system is immune.

That's my little dad pun from the potential effects of

covid and these can occur even without any respiratory involvement.

So let's take a look at what could cause or

be caused by the coronavirus infection.

And not only can we divide the different parts of

the nervous system, central peripheral neuromuscular et cetera.

They have different time courses in relationship two when the

infection occurs.

So there are power infectious syndromes and those are listed

here and there are post infectious syndromes which for the

most part are immune mediated.

So we're going to go over the individual ones and

see what sense we can make out of this.

So the power infectious syndromes occur during Vira mia.

So it's an acute infection and these neurological processes occur

while the virus is still in the patient's system.

And it's estimated about 13% of hospitalized patients.

How these, even though as we'll talk about later, that

number seems incredibly low depending on your definition of nervous

system involvement I guess.

So let's talk about some of the power infectious complications,

one of which is an AS miA.

That's the one that may herald the disease.

And the path of physiology involves the sustenance, ocular or

support cells of the nasal mucosa which are rich in

the angiotensin converting enzyme to receptors just like the rest

of the respiratory system.

And so it activates macrophages.

And there is diffuse inflammation which affects the olfactory bulb.

As it turns out, there's no actual direct viral involvement

of the olfactory vole.

Now when you can't smell which is what a nausea

means. Of course you also can't taste because you depend

on your smell in order to taste.

Well most of these people actually resolve some people don't

get their full smell back and that's called parasomnia which

also impairs of course their taste.

Um So we see macrophages but no viruses in the

olfactory bulb And it's estimated about 40-60% of people with

covid infections develop an AS mia.

Next very common, relatively speaking involvement is that of a

stroke. And about probably up to 5% of hospitalized COVID

patients may suffer from a stroke.

And the reason for that is we have to invoke

dr vishal because thrombosis is of course depends on his

triad. So there is vascular endothelial injury, there are alterations

in the constitution of blood which make it hyper co

arguable and the patient themselves or himself or herself don't

move around too much.

And so there was clear cut stasis.

So as a result of these processes the vascular injury,

the hyper kogel ability and the alteration in blood flow.

One ends up getting a lot of thrombosis which can

either be strokes or venous thrombosis.

Now the SARS covid can get to the vascular areas

either hematology nicely of course or via neuronal propagation.

I either is the vagal nerve and there are viral

particles that have been found in the Gi tract and

also they may travel retrograde axonal transport by the olfactory

bulb. Now the diagram on the right shows how there

are a stew inhibitors in the end of helium which

then caused the inflammation and endothelial itis, if that's a

word, I don't know, I'm gonna look that up.

Um And these changes can result not only in thrombosis

but in alteration in the blood brain barrier such that

proteins can seep through to the brain as well as

blood. So not only does one see ischemic infarct, but

there is hemorrhage that is possible as well.

And so people who have risk factors such as vascular

disease probably have a higher percentage probability of developing strokes,

but people who are otherwise healthy with no known risk

factors can present with strokes.

And those strokes can be multiple, multiple arterial inclusions.

There can be a intracranial venous thrombosis, leading to raising

your cranial pressure in pseudo tumor cerebro.

I has been described as a complication of covid as

well as these micro hemorrhages.

So when one evaluates a patient in the hospital we'll

talk about a little bit keep in mind that strokes

are very much a possibility to contribute to neurological declines.

Now talking still in the very me a phase, there

are certain immune mediated conditions or syndromes that have been

defined or described.

Now there is a leuco encephalopathy and this may simply

be from hypoxic ischemic cerebral injury.

It's not necessarily an immune mediated process.

But in a patient in the ICU, he was not

responding well who has had severe respiratory involvement.

Certainly this is a consideration that needs evaluation.

Unlike that condition, however, there is one called acute necrotizing

hemorrhagic encephalitis.

I love that name and it is characteristic by bilateral,

equally symmetrical the lamb IQ involvement as well as hemorrhage,

hence the name.

And this condition is certainly found to be mediated by

cytokines. So within the brain macrophages um can produce cytokines

and as a result there is actually a treatment for

that doesn't respond to steroids.

But plasma exchange and I?

Ve have been shown to be effective in helping some

of these patients out and whether or not um all

patients respond is unclear, but it is certainly worth an

attempt Now, of course the virus itself is not neurotrophic.

So mingle encephalitis does not occur as a result of

direct viral involvement of the brain or meninges.

But rather these more immune mediated processes, one of which

doesn't even have a name, but it has an incredible

list of central nervous system involvement, including coma, but you

get movement disorder, several attacks etcetera, etcetera.

Uh and again, this is related to cytokine release.

This sort of harkens back to the old days of

neurology when they had no clue what was going on.

And they simply describe the condition in regards to the

neurological localization and manifestations and they didn't really understand the

path of physiology.

Unlike here where they we do understand a lot more

about the immune system and again this has responded like

the previous syndrome, two cortical steroids or are big.

Alright, so that takes care of the power infectious phase.

Now after that, our weight before I go through that,

I'm sorry.

Um so a lot of patients who have this acute

illness will develop an encephalopathy.

And so how to sort out whether that encephalopathy is

simply metabolic.

Obviously we'll see if there increase create innings or liver

functions are sufficient to cause altered mental status, whether their

respiratory status in and of itself is sufficient to cause

they're altered mental status.

Um but if it's thought that there is more confusion

or delirium or even seizures or comatose beyond what that

can be explained by a metabolic process, derangement.

You'd have to consider whether there was a stroke.

And so an MRI scan looking for strokes are are

one of the other rarer conditions and even consider obtaining

spinal fluid to see whether there is some sort of

immune mediated process.

We would check their Olivo clonal bands there, I.

G. Synthesis rate and ultimately we would want to see

if it would be possible to check a cell site

commentary to see whether this is a T cell mediated

process or B cell or even obtain a side akin

panel to help direct which part of the immune system

needs further either control or boosting.

So um medications can obviously cause a role and this

is the most common manifestation of a neurological process and

when it occurs when there is a delirium or altered

mental status, it certainly prolongs the hospitalization as well as

affecting the overall prognosis of that patient.

In the at least 2/3 of people who developed an

encephalopathy when they are discharged, no longer regain um functional

ah activity.

They are not independent, They can't perform activities of daily

living and so as a clear cut um bad prognostic

indicator. Now we can move out of the power infectious

and let's go to the post viral syndromes that have

been recognized and these may occur in any part of

the nervous system.

So we'll talk about the peripheral nervous system, central and

neuro muscular in the peripheral nervous system.

After they resolve the acute infection, they may develop diffuse

weakness and they may have either characteristic or classical type

dim illuminating gingham beret or have an axonal Gamber.

And even the so called Miller fisher variant of Dion

bar A has been described as you all, of course.

Remember, Miller fisher is characterized by a triad of optima

plea J ataxia and he reflects you and accordingly there

are cranial neuropathy, these ridiculous sympathies and flexible these which

have been described after the acute infectious processes over similarly.

sARS-cOv-2

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