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Hello and welcome to Noon Conference, hosted by MRI Online

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to learn alongside top radiologists from around the world.

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0:29

Today we are honored to welcome Dr. Maria Cortez

0:32

for a lecture entitled Acute Encephalitis.

0:35

Dr. Cortez completed her radiology residency at Funes Santa

0:40

Fe in Bogota, Columbia.

0:42

She completed her diagnostic radiology neuroradiology

0:45

fellowship at the University of British Columbia

0:48

and continued with a three year fellowship in

0:51

Neurointerventional Radiology at the Montreal Neurological

0:54

Institute in the hospital

0:55

and McGill University in Montreal, Canada.

0:59

She stayed on staff

1:00

as a staff NEUROINTERVENTIONAL radiologist,

1:02

combining a clinical and interventional radiology practice.

1:07

At the end of the lecture, please join Dr. Cortez in a q

1:10

and a session where she will address questions you

1:12

may have on today's topic.

1:13

Please remember to use the q

1:15

and a feature to submit your questions so we can get to

1:17

as many as we can before our time is up.

1:20

With that, we are ready to begin today's lecture. Dr.

1:23

Cortes, please take it from here.

1:26

Hello everyone. Um, my name is Maria Cortes

1:28

and I'm presenting today on acute encephalitis.

1:31

I would like to start by thanking Dr. David Sem

1:35

and the team at, uh, modality for organizing

1:38

and coordinating this presentation.

1:43

I don't have anything to disclose, so today

1:48

I will be presenting you with a brief on definitions

1:52

and epidemiology, and then we will

1:55

get a little bit deeper into viral

1:57

encephalitis, the most common cause.

1:59

Uh, we will see some cases

2:01

to illustrate their main imaging findings.

2:04

And finally, I wanted to discuss, uh,

2:07

briefly about autoimmune encephalitis.

2:11

The term acute encephalitis is very broad and very vague.

2:16

It includes any acute inflammation of the brain

2:19

that presents, uh, as an acute mental change.

2:24

Two thirds of these cases usually have a viral infection

2:27

as the underlying cause,

2:29

but we know that also bacteria fgi parasites can cause it.

2:34

Although infections are the most common found cause there is

2:38

a large group of acute encephalitis cases that are treated

2:41

but never have a final diagnosis.

2:45

This raises the question,

2:46

if we couldn't find the actual cause,

2:49

or maybe they were not infectious at all

2:51

and they were autoimmune types, even more, we have learned

2:55

that at least 50% of all cases

2:58

with known cause are immune-mediated diseases.

3:04

To add to the confusion between these two, uh, situations,

3:08

autoimmune diseases

3:09

or infections diseases, we know

3:10

that there is well-established correlation

3:12

of autoimmune diseases, um, that are chronic

3:17

and they could present with an acute encephalitis picture.

3:21

So here you have a list of those,

3:23

and as this field of autoimmune encephalitis is becoming

3:26

more and more approachable to us, the people we witness,

3:30

how our criteria for diagnosis is widening.

3:33

So we have more inclusion criteria to use the term

3:37

acute encephalitis

3:38

and the demographics that we use as a tool

3:41

to make differential diagnosis is becoming less

3:44

and less significant.

3:46

Because autoimmune diseases are worldwide distributed,

3:49

they're not dependent on external factors,

3:51

they're not dependent on any vectors or different climates.

3:56

As radiologists, we might have

3:58

to start reshaping our mindset

4:01

and considering that maybe we are trying to insist too much

4:05

and using imaging findings to differentiate diseases

4:09

that are quite different, outcomes are very different

4:13

and they share basic, uh, uh, pathological,

4:19

uh, process undergoing.

4:22

Let me expand a little bit what I'm trying

4:24

to say here on this slide.

4:26

I took some pictures from the internet to illustrate

4:28

what it looks like in the brain when you have an acute

4:32

inflammatory process.

4:33

Regardless the cost. So the first step is

4:36

that neutro files will proliferate

4:39

and they're the earliest responders in acute inflammation.

4:42

They kind of activate the general immune response

4:45

by signaling diverse cell types, including

4:48

endothelial cells, mesenchymal stem cells,

4:51

lymphocytes, and microglia.

4:53

On the following histology slides I'm showing here, I wanted

4:57

to illustrate, and I took these images from a great article

5:00

on brainstem encephalitis, how the proliferation, first

5:05

of all is mostly around, um, uh,

5:09

vessels, uh, small vessels,

5:12

and also is, um, mainly, um,

5:18

populated by lymphocytes that we have here.

5:21

In this, uh, slide is a C3 three staining

5:24

that shows lymphocytic infiltration.

5:27

So from here, there is a no return point

5:31

where the microglia once activated

5:34

and being a resident, macrophage

5:36

of the central nervous system, will lead things to,

5:39

uh, permanent damage.

5:41

And they can do that

5:42

because they exhibit an antigen presentation

5:45

and they can trigger phagocytosis.

5:48

It means that this moment is a very important signaling

5:52

moment for the tissue that can go back to normal

5:55

or into a permanent damage.

5:57

Here in this, uh, this is from a different patient with aem

6:00

where we can see with looks sofast staining many areas

6:04

of de myelination and permanent damage.

6:07

More recently, we learned

6:09

that neutrophils are extravasated from blood vessels

6:12

and they can reenter the blood streams several times

6:15

and trouble in different organs.

6:17

So this is gonna lead to amplification

6:19

of the molecular profile

6:21

and also can promote a continued inflammatory

6:24

inflammation process.

6:27

What I'm trying to say here is that as in tumors,

6:30

there is a signal that some cells trigger

6:35

and will lead the process into very different outcomes

6:39

for the patients, even if they started at similar points.

6:43

And here I have a, uh, an example to illustrate this.

6:47

In the upper panel, you see a 73-year-old patient

6:50

who was diagnosed with a viral encephalitis

6:54

Epstein bar virus.

6:56

And in the lower panel, we, you have a 29-year-old patient

6:59

with an an MDA encephalitis.

7:01

We'll hear more about it later on.

7:05

What happens to these patients is quite interesting.

7:07

In four months, the patient

7:08

who received antiviral treatment responded

7:11

and has a very minimal residual lesion,

7:14

and the patient is clinically back to her baseline

7:17

and discharged home.

7:19

For the younger patient, the situation is quite different.

7:21

The patient starts having, uh, showing some signals or,

7:25

or some signs of permanent damage

7:27

with enlargement of the ventricles.

7:28

And we see that after 10 months,

7:30

this patient is cognitively impaired

7:32

and her life is never gonna go back to normal.

7:35

So at some point in this disease, both started

7:39

with the same inflammatory process, there is a signal

7:43

that makes them go into very different pathways.

7:46

If we as radiologists could help clinicians to define

7:51

that moment, hopefully with imaging, um,

7:54

we could help these patients to be treated faster.

7:58

So that's the point about these confusing situations.

8:02

Let's go back to our clinical route into acute encephalitis.

8:06

There are clinical criteria that, uh, is established

8:09

to diagnose acute or to suspect acute encephalitis.

8:13

The required criteria includes any alter mental status, loss

8:17

of consciousness, liturgy,

8:19

or personality change in less than 24 hours.

8:22

There are variable criteria that are included.

8:25

Um, and that's new seizures, new deficits,

8:29

neurological deficits, white blood cell count.

8:31

That is increased suspicious MRI that, uh, for encephalitis

8:36

or acute abnormalities in EEG.

8:39

And there are also criteria

8:40

to suspect acute autoimmune encephalitis.

8:44

The time span from symptoms onset is a little bit more lax

8:49

for the autoimmune type.

8:51

So it's a subacute onset.

8:53

What is could be included of alter mental status,

8:56

short memory loss or psychiatric symptoms.

8:59

This is important for us

9:00

because, for a reason that we don't know exactly

9:04

why autoimmune encephalitis present more often

9:07

with psychiatry, uh, uh, presentations.

9:12

The variable criteria is very similar

9:14

to any acute clinical case.

9:16

White blood cell count, uh, should be included.

9:19

Proteins two new seizures, new deficits,

9:22

oligoclonal bands elevated,

9:25

and any abnormality in MRI suggestive

9:27

of limbic encephalitis.

9:29

So let's get more into epidemiology on the most common, uh,

9:34

source, which are the viral infections.

9:38

It occurs, uh, for the viral, um, infections

9:42

that is more often in the very young or the very early,

9:46

and the incidence is about 3.5 to 7.5 per 100,000 people.

9:51

Vaccination has changed these numbers, uh, especially

9:55

for months and until, until recently for melis.

9:59

But now we know that there is an outbreak of melis,

10:01

so eventually it's gonna get, again,

10:03

under control with the vaccination.

10:05

So that also has helped

10:06

to change the numbers we have available.

10:09

There is also, um, higher numbers of, let's say Epstein

10:14

bbar virus or cy cytomegalovirus encephalitis

10:18

that are more prevalent in certain populations like

10:21

immunosuppressed patients, HIV post-transplant cases.

10:25

Geography can also alter the prevalence.

10:28

As we know in hot humid weathers, there are more mosquitoes

10:32

and they can be vectors for certain types of infections.

10:36

We know that in North America we have predominant, uh,

10:39

tick-borne encephalitis cases.

10:42

So that's another geographic, uh, uh, reason

10:45

for high incidence of encephalitis in certain countries.

10:49

And here we have a more wide spectrum of

10:52

what are the most common types.

10:54

This was, um, done by a group, uh,

10:57

who did an excellent review, uh, is, uh, a website

11:01

of a group called International Encephalitis International.

11:06

It was published in 2023

11:07

and shows a very meticulous analysis of

11:10

what is the most common cause of infectious

11:13

cases in industrialized patients.

11:15

They show us how, uh, herpes is the most common type

11:20

of encephalitis followed by varicella zoster.

11:24

The mortality for viral infections

11:26

as per report is 1.4 per 100,000 cases.

11:33

And getting now into the more common type,

11:35

we should start talking about herpes simplex encephalitis.

11:39

Herpes is basically the most common cause of fatal,

11:43

sporadic necrotizing viral encephalitis.

11:46

And in that group, the type one of the, uh,

11:49

herpes virus is the one more, uh, associated to the disease,

11:53

95% or over of cases.

11:56

The incidence is two cases per million per year.

11:59

They're associated with high mortality and morbidity.

12:01

They are not treated promptly, so it's very important

12:04

that we help to recognize them right away.

12:07

The process of infection is caused by gaining access

12:10

through the nassif NAL mucosa, um,

12:12

that reaches the brain along the branches

12:14

of the trigeminal nerve.

12:16

The viral gene remains late latent until something happens,

12:21

and that could be trauma, stress, immunosuppression,

12:25

or sometimes it's just spontaneously.

12:27

Once the virus is activated,

12:29

the inflammation spreads locally from the ganglion terminals

12:32

to the base of the skull and to the dur adjacent brain.

12:35

This is explaining the symptoms

12:38

of presentation in these cases.

12:40

So the clinical picture for a patient with acute herpes

12:44

herpes, uh, encephalitis is frontal and temporal meningitis.

12:49

It can extend to the tissue itself

12:51

and can, uh, give more symptoms related

12:54

to the same localization, confusion, comma seizures,

12:58

personality changes, anno or gustatory hallucinations.

13:03

Uh, in the long term, these patients can suffer from

13:05

amnesia, dementia, epilepsy,

13:08

and in the very initial phase,

13:10

this is the only findings we're gonna, um, have available

13:15

to diagnose the disease aside from the clinical and MRI

13:18

because the CSF can be negative.

13:21

Let's see an example of this disease.

13:22

So here we have a 64-year-old patient alcohol, uh,

13:27

addicted patient, alcoholic, uh, found by his wife,

13:31

very confused, shaking,

13:32

and with decreased level of consciousness.

13:35

We seen the MRI in, um, coronal flare, an area

13:39

of very subtle signal abnormality in the

13:41

mesial temporal lobe.

13:43

This was not evident in the CT scan.

13:46

We see with more slices in coronal

13:48

and axial views of flare

13:49

that definitely there is asymmetry in the signal abnormality

13:53

of the meial temporal lobe

13:55

that shows some restricted diffusion in DWI and a DC map

14:00

and has no enhancement with gadolinium.

14:04

Part of the workup is the clinical presentation,

14:08

the MRI findings,

14:09

and a little bit later in the disease,

14:12

the CSF can start showing cytosis early

14:15

during the disease is gonna be neutrophils

14:17

and more, uh, later on it's gonna be more lymphocytes,

14:21

elevated protein that is gonna be a sign of brain necrosis.

14:25

Glucose should be normal

14:27

and in cases of herpes, PCR is gonna be elevated.

14:30

Let's see, another example,

14:32

more dramatic than the previous one, where we see a swelling

14:35

of the meial and posterior inferior frontal lobes.

14:39

This was a 66-year-old patient who presented

14:42

with muscle weakness and fever urinary incontinence

14:45

and mental status change on this patient.

14:49

We start seeing also some signal changes in the

14:51

contralateral brain

14:53

and te uh, brain temporal and frontal lobes.

14:56

And we see some patchy restricted diffusion areas in DWI.

15:00

If you notice the gradient recall, echo images

15:04

show some focal hyperintensities

15:06

of the mesial temporal lobe.

15:07

This is indication of hemorrhage

15:10

that can be noticed in our imaging, but a little bit later

15:14

after the acute onset.

15:16

So 48 hours or later we could start seeing contralateral

15:20

involvement or hemorrhagic transformation.

15:23

The differential diagnosis for something.

15:24

So, um, swallow like this could be stroke if it is

15:29

only one lobe and one closer to a vascular territory,

15:33

but also can be a status epilepticus or postictal edema.

15:38

In those cases, in the postictal edema, the uh,

15:41

involvement is more widespread of all the cortex

15:46

and it can extend to the entire hemispheric, uh,

15:49

site that is involved.

15:50

So that would be our key

15:52

to differentiate it from only seizures.

15:54

Another example to show you 83-year-old patient

15:57

with fever and new seizures.

16:00

Um, in this case, we see a swelling, again,

16:03

of the temporal lobe, uh, cortex and the frontal area.

16:07

But we see also an interesting feature,

16:10

the missial temporal lobe.

16:12

Uh, the missial thalamus is showing some signal abnormality.

16:16

Again, we have some patchy restricted diffusion.

16:19

And again, there is no evidence of enhancement.

16:22

So that's another feature that could be interesting for us

16:25

and is that there's no, uh, avid enhancement

16:28

of the territory that is involved.

16:32

A last case to illustrate her big simplex, uh,

16:35

related encephalitis.

16:36

A 55-year-old patient with, um, fever that was found

16:40

by her husband speaking very slowly with headache

16:43

and rapidly became stuporous.

16:46

The CT scan, as you see, shows very subtle hypodensity

16:49

of the meial temporal lobe in MRI.

16:52

We can confirm that this indeed a real finding

16:55

and we see some swelling already of the meial area.

16:58

We see involvement of the meial thalamus.

17:01

We can see also Apache against, uh, um,

17:05

restricted diffusion and DWI and no enhancement with galin.

17:11

So with these examples, we can't, um, have a,

17:14

a few key points for us to remember that in herpes simplex

17:19

encephalitis, the, uh, abnormalities are mostly to chew

17:22

and flare signal abnormality.

17:25

We could see some restricted diffusion.

17:27

Remember, it's mostly patchy.

17:28

It's not a very, uh, smooth and increased signal.

17:32

We could see after 4, 8, 4, 8 hours

17:35

hemorrhage of those areas.

17:37

And involvement of the contralateral brain

17:39

for the type one virus is more typical

17:42

to see frontal and temporal.

17:44

And for the less common one,

17:45

we could see diffuse brain involvement.

17:48

Both are highly lethal if they're not treated promptly.

17:53

I made this table inspired on, um, what I found in,

17:56

in an art, an excellent, uh, article for the, uh,

18:00

ram from a col medical college in India, Ram Chandra

18:03

Medical College that gave me this idea.

18:06

And I have a few cases

18:08

to illustrate different viral encephalitis.

18:11

And I included here one that is very unusual to present.

18:16

The Epstein virus encephalitis is unusual

18:20

because this is predominantly affecting patients who had,

18:24

uh, transplants or patients who are very immunosuppressed

18:27

or have maybe HIV.

18:30

So this immunocompetent patient I'm showing you,

18:33

was a, a rare case.

18:35

This patient at the age of 73 was brought

18:38

to the emergency room with a, a picture of, um,

18:42

hemiparesis on the left.

18:43

He antibody and loss of consciousness.

18:46

The CT scan was requested to rule out a stroke,

18:49

and as you can see, there's no typical

18:51

picture for a stroke here.

18:53

What we see is internal capsule

18:55

and thalamic hypodensity that it might be extending

18:57

to the bones, uh, to the mid brain and bones.

19:01

The MRI is more clear in demonstrating those findings

19:05

that is extensive signal abnormality and flare,

19:08

and we see how it's involving basal, uh,

19:12

thala thalamus internal capsule,

19:14

and a little bit of the right cerebellum.

19:17

There is only focal restricted diffusion documented in,

19:20

in the right side of the midbrain and the pons.

19:23

And there was no enhancement associated to this finding.

19:27

This is the case I, uh, showed you earlier

19:29

during the presentation.

19:30

And the, uh, diagnosis was a stem bar virus.

19:34

As I said, this is more typical for, uh, children

19:37

or, uh, patients who had, um, stem cell transplants

19:41

or solid organ transplant or are infected with HIV.

19:46

It's being, uh,

19:47

has been reported in immunocompetent patients too,

19:50

but is a rare presentation, has a good prognosis with, um,

19:56

timely, uh, antiviral treatment.

19:58

And it covers

20:00

or is very similar in presentation in imaging to

20:04

what we should expect to see in zoster, uh,

20:06

virus encephalitis.

20:08

I don't have an example of that,

20:10

but you will see there is a lot

20:11

of over imposition in the findings.

20:14

Also, um, zoster, uh, occurs in patients

20:18

who are immunosuppressed

20:20

and can be, uh, involving, um, roots

20:24

of the ophthalmic, uh, pathway.

20:26

So it can over, um, impose an imaging only.

20:30

But in clinical presentation for the clinicians,

20:32

it's a little bit more clear that is some sort

20:34

of shingles kind of, uh, presentation.

20:38

The patients with Epstein virus, as I said,

20:40

have good prognosis if they're treated promptly

20:42

as it happened with this patient four months later,

20:45

she was completely recovered and was discharged home.

20:49

Another example that I wanted to show you

20:51

because it has very different presentation from the most

20:54

common type that is the herpes inflex encephalitis is HIV

20:59

related encephalitis.

21:00

We're used to seeing HIV many opportunistic infections,

21:04

and we pretty much always think of that,

21:06

but see this case, uh,

21:08

to see if I can change your mind about it.

21:11

So this 36-year-old patient immigrated to Canada.

21:14

She had a complex medical history of HIV

21:17

and at the time of examination, she had a very low CD four

21:21

of 28 only.

21:22

She presented to the emergency room with severe headache

21:25

and, um, uh, fluctuating a state of, uh, um, consciousness.

21:30

The CT scan didn't show anything very specific,

21:33

but the MRI showed very subtle signal abnormalities in the

21:37

pre ventricular white matter, uh, some in the car nucleus.

21:43

There was no atrophy at the time of this examination.

21:46

And we were able to compare

21:48

with previous exams the patient had in their home country.

21:52

And there was no signal abnormality reported on these areas.

21:55

There was no restricted diffusion

21:57

for this signal changes only noted in flare and T two,

22:01

and there was no enhancement.

22:03

The patient had previous history of crypto cocus neoformans

22:07

that was treated, uh, at least 10 weeks prior

22:10

to this clinical presentation.

22:12

And in the past, she also suffered from malaria.

22:14

She had many reasons to have an, uh,

22:17

opportunistic infection,

22:18

but as you can see here, there's nothing

22:20

that is telling us this is the case early in the disease.

22:24

This is how encephalitis related to HIV could present

22:28

with wide matter lesions that are bilateral

22:31

and more, uh, advanced.

22:33

In the encephalitis is described

22:36

that we could see meial frontal atrophy,

22:39

which it was not evident for this patient,

22:42

but I found it was an interesting, um, case

22:45

to include in the differential diagnosis with this imaging.

22:49

I would encourage you to include PML

22:51

because patients with HIV are prone to have that infection.

22:54

However, PML, we should expect to see lesions

22:58

that are involving white matter in the posterior foss,

23:01

especially in the middle cerebellar peronial.

23:04

Or it can involve, uh, subcortical areas in territories

23:08

of u fibers in in the, uh, brain,

23:12

um, hemispheres.

23:15

So we have seen now 2D uh, very different presentations

23:19

of acute viral encephalitis, remembering

23:21

that the most common one is the herpes

23:24

that affects more frontal and temporal lobes.

23:27

Um, and, uh, they present

23:29

with very patchy restricted diffusion

23:31

and no enhancement moving on into other types

23:35

of encephalitis that are not that common in North America.

23:38

But we should be aware of it

23:40

because we have people traveling from where they are more,

23:43

um, common is Japanese encephalitis.

23:46

So let me show you a case of a a 64-year-old patient

23:50

who arrived from the Philippines, not feeling very well.

23:54

He spent six months traveling to different areas

23:56

of the country and had confusion, fever, and conjunctivitis.

24:00

The patient was known for hypertension and lipidemia.

24:04

The CT scan was really not very specific.

24:07

Some patchy hypodensities of the, uh,

24:09

white matter is the only thing we could comment on on these

24:12

images, but the MRI was quite, uh, uh, abnormal.

24:16

So we see very extensive white matter disease here

24:20

that is debatable if he had that

24:23

before from his dyslipidemia and hypertension

24:26

and his comorbidities.

24:28

What is not, uh, fitting with that is the very symmetrical

24:33

and impressive bilateral thalamic involvement.

24:36

Uh, it's not extensive to the brainstem, um, um,

24:40

but it's quite, uh, abnormal.

24:43

There was no restricted diffusion with DWI

24:46

and no enhancement.

24:48

So Japanese encephalitis is transmitted to the human, uh,

24:52

by a mosquito that is, uh, one of, in the, uh, family

24:56

of the kyx, uh, mosquito families

24:59

is very predominant inia with at least 68,000 cases,

25:04

um, per year.

25:06

Fortunately, it's very common

25:08

that people can get the disease and flu-like symptoms,

25:11

but it's not common

25:12

that they get the severity of the disease.

25:14

Unfortunately, who get sick from this

25:18

has very high mortality of 30%.

25:21

And the sequela is, uh, very important in our patient.

25:25

Unfortunately, uh, you know,

25:27

the patient passed away from this infection,

25:29

so it was a severe case of encephalitis.

25:33

The virus itself is a flave die, um,

25:38

family virus.

25:40

And as I said, the human as a host is an unusual, uh,

25:44

host is primary, uh,

25:47

infecting birds and mammals.

25:50

So it's very unlucky that we get the disease very unlucky

25:53

that we become symptomatic

25:55

and we have the aggressive, uh, way of the presentation.

26:00

The most common finding for this type

26:02

of encephalitis is the central involvement.

26:05

Bilateral thalamus, ma brainstem in general.

26:09

They say basal ganglia, para thalamic.

26:12

It could become hemorrhagic, especially at thalamus,

26:16

and unusually could be extra basal ganglia involvement.

26:20

Um, in the cortical, uh, hemispheres has been described,

26:24

but for you to remember

26:25

as a key is the bi thalamic involvement as one

26:29

of the distinctive features of this type of encephalitis.

26:33

And in the same family, we have

26:35

what we could see more often in North America.

26:37

So the West Nile virus encephalitis that is not transmitted

26:42

by a mosquito, but it's transmitted by a tick.

26:46

Um, it's unusual for us to see it, uh,

26:49

as a severe form of the disease.

26:51

Many people get the flu-like symptoms,

26:54

and it's only one out of 150 infected people who could have

26:59

or develop a severe form of the disease like encephalitis.

27:03

It could be fatal sometimes,

27:04

and the findings are a bit variable.

27:06

In imaging, we could expect to see something similar

27:10

as I showed you in the Japanese, uh, encephalitis version.

27:15

But I, as in this case, we had an unusual presentation.

27:18

This patient, 60-year-old patient presented

27:21

with acute right antibody spasticity, confusion

27:24

and behavioral changes.

27:25

And the MRI, what we found, um, was hyperintensities

27:30

that were involving the, uh, cardio nucleus

27:34

and pre ventricular white matter, the thalamus,

27:37

we could confirm that, uh,

27:38

the restricted diffusion we saw nearby the cardiac nucleus

27:41

and per ventricular white matter was most likely hemorrhage

27:45

with gradient echo.

27:46

And the patient also had some other foci of hemorrhage.

27:50

The patient was not known for any other comorbidities,

27:53

and we presume they were all related to the same picture

27:57

of the acute, uh, west Nile virus encephalitis.

28:01

The most common feature for this kind

28:04

of disease could be a normal MRI,

28:06

so we should not exclude it from our differential diagnosis

28:09

if there are no, uh, findings,

28:12

and as I said, it could be in some cases very, uh,

28:16

aggressive and can end up in, uh, t outcomes.

28:21

I included also here, uh, encephalitis

28:24

that are not really viral.

28:26

Uh, initially prior were in,

28:30

were presumed similar to viruses,

28:33

but now we know that they're not.

28:36

They lack really, uh, nucleic acid,

28:38

so there cannot be called virus.

28:41

However, they share infectiousness

28:43

and they share some, um, uh, features with viruses that, um,

28:48

could be overlapping for the two diseases for us in imaging.

28:53

Unfortunately, prior infections can look like a viral

28:57

infection, and that's what I thought was important for us

29:00

as radiologists to keep in mind when we're diagnosing a

29:03

patient with acute, uh,

29:05

or relatively acute symptoms, especially like these two

29:08

that we have here from our local institution that were, uh,

29:13

quite difficult to diagnose.

29:15

The first patient is a 60

29:17

or 60-year-old patient who, uh, had history of hypertension

29:21

and dyslipidemia

29:22

and presented with a weak history of episodes

29:25

of disco coordination on the right side of the body.

29:28

The patient couldn't go downstairs,

29:30

the patient couldn't brush his teeth.

29:33

He, uh, stopped playing the piano.

29:36

The CT scan was unremarkable.

29:38

But the MRI, uh,

29:40

looking at it very carefully demonstrated some signal

29:43

changes in the cortex in flare in different areas

29:47

of the brain, mainly in the parietal cortex

29:50

and some, um, incipient restricted diffusion.

29:53

That was the only finding.

29:54

And the patient was rapidly progressing into not being able

29:58

to move and was, uh, bed reading

30:00

and eventually passed away in, uh, the following month.

30:06

The CJD disease

30:07

or Chris Jacob disease is the most common of the prior type

30:11

of diseases that can involve the brain.

30:13

We have other types like, uh, called kru,

30:17

and there are other syndromes, uh, described like, uh,

30:22

gerstman, uh, sheerman, uh, sorry, str schenker syndrome.

30:27

Difficult to remember.

30:29

Those are, um, immune

30:32

or hereditary related diseases.

30:34

The most common type is like the one I'm showing you here

30:38

is APOPO type.

30:40

They're also familiar, um, hereditary.

30:44

And, um, there is another variant.

30:48

So 98% of chances that if you see something sim

30:52

that makes you think of a ion disease is gonna be CJD.

30:56

So it's, uh, worth to mention it

30:58

as the differential diagnosis.

31:01

The clinical symptoms include rapidly progressing dementia.

31:05

In imaging, we're gonna witness some, uh, atrophy

31:09

that is progressing very rapidly.

31:11

These patients have sometimes psychiatric symptoms

31:15

and myoclonic jerks

31:17

and sensory, uh, changes all progressing very rapidly,

31:22

and unfortunately is there's no cure

31:24

or any, uh, treatment for them.

31:27

It has been described in the imaging

31:29

that they could show some, uh, putamen

31:34

or pul sign hyperintensity in the posterior aspect

31:37

of the thalamus or the hockey stick sign, also as a, a sign

31:42

of involvement of the thalami,

31:44

but they can involve other basal ganglia.

31:46

And I have another case to illustrate this.

31:48

A 57-year-old patient who had, uh, full three months prior

31:53

to presentation At the time of presentation, the patient had

31:57

dizziness, changing behavior.

31:59

She was elaborating ideas

32:01

and was not able to walk, uh, by herself anymore.

32:05

The MRI and flare demonstrated signal abnormality

32:08

of the gut nucleus and lengthy form nucleus.

32:11

Very subtle, uh, findings.

32:12

So the clinical information is quite important

32:15

for the neuroradiologist when we're interpreting this.

32:18

The diffusion was quite striking with areas

32:21

of restricted diffusion in those areas that helped us

32:23

to go back to the team

32:25

and mentioned we think this could be CJD

32:27

and, um, uh, effectively it was the case.

32:32

The neurologist also rely a lot on the EEG findings in CJD

32:36

since, uh, these patients, although one of these patients,

32:40

and I don't remember which of the two was, had normal eeg,

32:43

but typically they rely, uh, on

32:46

that when the patient presents pre periodic sharp wave

32:49

complexes that are typical for them, uh, as indicative

32:54

of CJD infection.

32:57

And lastly, I included transfusing encephalitis,

33:01

which is not an acute presentation,

33:03

but sometimes surprises you.

33:05

Um, it's a disease

33:06

that I involves mostly younger people from

33:10

14 months to 14 years.

33:12

Uh, patients can present with seizures,

33:14

and initially the MRIs could be negative.

33:18

This patient came to us at the age of 21 with,

33:22

uh, recurrent seizures.

33:24

Seizures that were controlled for a long time, um, uh,

33:29

became, uh, recurrent and uncontrollable.

33:32

So the MRI findings on this patient, we had access

33:35

to previous images where there was no finding,

33:39

and we were able to, um, document

33:42

that the patient was having a progressive cortical

33:45

and subcortical abnormality only on the left,

33:49

on the right hemisphere, there was progressive atrophy

33:53

and there was some signal changes as well.

33:55

This is typical for

33:57

what transfusing encephalitis has been described for.

34:01

It's not clear if there is a viral infection

34:03

that triggers this process initially.

34:06

Some theories also include that these patients have some,

34:09

uh, toxicity to glutamate,

34:12

and that is what triggers the whole, uh, process.

34:16

So just to remember that it is, uh,

34:18

involving only one hemisphere.

34:20

It can be accompanied by, uh, signal changes.

34:24

The important thing to remember is

34:26

that it's not only the cortex,

34:28

but the sub cortical white matter

34:30

that get affected on these patients.

34:33

There are descriptions

34:34

of basal ganglia involvement in a few, uh, patients.

34:38

Um, but that's, as you know, these are,

34:41

this is a rare disease.

34:43

So the most typical one is the cortical, uh, presentation.

34:46

So here we have seen then kind of a review

34:49

of different types of viral encephalitis.

34:52

Always, um, remember that it's frontal

34:55

and temporal, um, the most common

34:58

involvement in the most common viral, um,

35:01

source for this disease.

35:04

And that, uh, initially, you know,

35:06

it's only signal changes were we're gonna, uh,

35:09

witness later on the disease hemorrhagic transformation

35:13

and later on, uh, volume loss.

35:17

So, um, there are other less common viral, uh, infections

35:21

that I have to mention, um, in our presentation today.

35:25

I don't have examples of them to show you.

35:28

And also, I'm missing here something that I guess we have

35:31

to start getting used to mention,

35:33

and is the, uh, uh, start, uh, to

35:38

or covid, uh, virus as, um, part

35:43

of the group of causes for viral encephalitis.

35:46

In the few reports we have available, we, uh, could see

35:50

that 2.2% of patients with covid presenting

35:55

with neurological neurological symptoms had, um, exams

36:00

that were positive for infection encephalitis, uh, related

36:04

to the, uh, the, uh, covid virus.

36:08

The patients presented mostly with seizures,

36:11

confusion, and headache.

36:13

And the series reported.

36:14

There is, uh, an interesting

36:16

and complete meta-analysis of, uh, all the cases reported

36:20

as, um, encephalitis related to, uh, covid disease

36:26

that, uh, mentions that, um, the, uh,

36:30

cases where it's difficult to understand

36:33

what was the presentation they included 72% of patients

36:38

with positive MRI findings,

36:40

but is looking at the report of each series

36:45

is not really clear

36:46

that the patients were having acute encephalitis symptoms.

36:50

Uh, they were just abnormal MRIs.

36:53

So I don't think we have a precise description of

36:56

how covid involvement of the brain should look like.

37:00

So this is work in progress,

37:01

and I'm sure we're gonna get more reports,

37:04

uh, to learn from this.

37:05

Um, so this is helping us to close

37:09

the most common presentation for viral for, uh,

37:12

in acute encephalitis, which is the infectious disease.

37:15

And I decided to explore a little bit more on autoimmune

37:18

encephalitis because I find

37:20

that it is getting very confusing for us when we try

37:23

to separate the two diseases.

37:25

Uh, autoimmune encephalitis is also a cause of acute, um,

37:30

alter mental status.

37:32

We don't usually mention it in our

37:35

differential diagnosis initially.

37:37

We kind of use it more as in any patients

37:40

who have the clinical symptoms as an exclusion diagnosis.

37:44

So maybe it's the time for us to start

37:46

changing our approach to them.

37:50

Uh, we don't know exactly how often they are

37:53

because it's difficult to document them,

37:55

and many infectious diseases can become an

37:58

autoimmune encephalitis case.

38:00

So those are things that we need to,

38:02

uh, probably work on that.

38:04

So, uh, maybe, um, by reviewing this topic,

38:08

we could start the movement of changing

38:10

and not saying it's an exclusion diagnosis,

38:13

but maybe should be included in the list

38:15

of differential diagnosis.

38:17

Let's review what we know about autoimmune encephalitis.

38:20

So historically, we say other two types per neoplastic

38:24

and no per neoplastic.

38:26

This is what we learn all from textbooks

38:28

and basic knowledge.

38:30

So this is a way to understand them,

38:31

and it made a lot of sense

38:33

because the per neoplastic, uh, type, um,

38:38

was something different in presentation.

38:41

Um, uh, let's say, let's say for each patient,

38:46

the paraneoplastic ones were understood as if a tumor

38:50

was sharing some antigens with native neuronal cells,

38:55

and there was a cross reaction to the brain.

38:57

And so that was leading to a,

38:59

an antibody mediated attack on previously immune privileged

39:04

neuronal structures.

39:06

And it was usually T-cell mediated response.

39:08

Whereas in non-par neoplastic cases, we had antibody, uh,

39:13

uh, a reaction triggered by B cells.

39:17

The course of encephalitis history is important

39:21

for our learning here.

39:22

So this was, uh, a disease

39:24

that was described since a long time ago, 1968, at least.

39:28

This concept was brought up as our antibodies, uh,

39:32

explaining limbic encephalitis.

39:35

And, uh, followed following this description,

39:39

more work published was helping to shape more

39:42

and more that there was onco neural antibodies that, uh,

39:46

would be mentioned in the context of an encephalitis

39:50

and would be the cause for it.

39:53

It took till, uh, 2010 when the first report,

39:57

official report came up about LGI, uh, one antibodies

40:03

explaining a case of encephalitis

40:05

and then bringing up the possibility that there was

40:08

a non-par neoplastic form of this disease.

40:11

So thanks to this, uh, group of publishers, we had like new,

40:16

uh, light towards, okay, so there is diseases that are,

40:20

have nothing to do with tumors, so

40:22

how can we understand what's happening?

40:24

And this created a big change.

40:26

So from para neoplastic

40:28

and non-plastic, we went into group one and group two,

40:32

and the difference was made based on the location

40:35

of the antigens that would be, um, sick

40:40

by the an, uh, antibodies.

40:43

If the antigens were surfaced, antibodies,

40:46

then the disease would in entail a

40:49

different response to treatment.

40:51

And the, um, the, the, uh, best diagram I found, um,

40:56

to explain that, to understand that myself was published by

41:01

vore, um, um,

41:03

and a group of, uh, neurologists in Italy

41:08

who had this amazing, uh, simple diagram to show us

41:12

that when the antigens are in the surface of the cell, the,

41:16

uh, antibodies that are seeking these antigens location

41:21

are pathogenic antibodies.

41:23

And it makes sense that these diseases diagnosed timely,

41:27

will respond rapidly to treatment

41:29

because the, uh, the, uh,

41:32

problem is in the surface on the cell.

41:34

Whereas when the antigens are inside the cell,

41:38

it's more difficult for any treatment to reach out

41:41

and to wash out those antibodies.

41:44

This explains that if the, uh, complex of antibody

41:48

is reachable, any IV plex

41:50

or exchange, that is what the treatments are about, could,

41:54

is easily wash all the disease.

41:58

There's an exemption for the group

42:00

of diseases included in the, uh, group of surface antigens,

42:04

and is the cases of NMDA,

42:07

which is the most common type we're gonna see in this group,

42:11

um, where, um, there is a high association to, um,

42:17

teratoma in women, 60%.

42:19

We're gonna find 45 in a, in a few reports, uh,

42:23

but it can go high to 60% of, um, ovarian teratoma.

42:27

And depending on the age, elderly patients

42:31

or older women could have, um, carcinomas of the, uh,

42:36

of the ovaries also, um, kind

42:39

of triggering this autoimmune response.

42:41

So that's kind of the exception to the term of

42:44

non paraneoplastic.

42:45

But as we understand now, not easy

42:48

to separate them completely.

42:50

So in the group one where we have the, uh, antigens

42:54

inside the cell, and we have a more clear

42:58

cross reaction from two more cells to this antigens

43:03

in the brain, the best representative is the anti

43:07

hue encephalitis.

43:09

This has been described for a long time,

43:11

and we have a group of diseases, uh, that are all, you know,

43:16

uh, related to this anti glutamic

43:18

and the carboxylase, uh, encephalitis, anti rye anti,

43:24

I don't think as radiologists, unfortunately,

43:27

all this differentiation changes our approach

43:31

to the imaging in these cases.

43:33

But I thought it was important for us to understand, uh,

43:37

at least that when we are dealing with the ones

43:40

that have surface antigens, our

43:43

help in diagnosing them faster is important.

43:46

The second most common disease, uh, from this group of, uh,

43:51

non-tumor related all the time encephalitis, uh,

43:56

from NMDA, is the moga, uh, encephalitis.

43:59

And we're gonna see a few cases to illustrate this.

44:04

So the first one I wanted

44:05

to show you is an anti-MOC encephalitis.

44:08

This is a very interesting case.

44:10

A patient who was diagnosed with MS in 2007 when she was 21,

44:15

and presents at the age of 31, 10 years later

44:19

with multiple relapses

44:20

and focal to generalize seizure activity, which she didn't,

44:25

um, have before.

44:26

The EEG was showing a temporal, uh,

44:30

low area lesion.

44:32

So the MRI, uh, showed new lesions she didn't have

44:36

before at the temporal lobe, very hazy margins,

44:40

and there was no edema, no mass effect.

44:43

So more like a tumor effecti type

44:45

of demyelinating lesion could be interpreted.

44:49

In this case, there was no enhancement

44:51

and no restricted diffusion to this lesion.

44:55

So, um, after many tests

44:57

and investigations, the patient was confirmed

45:00

as having an anti Moog, uh, positive disease.

45:04

MOOG stands for myelin Oleg Cyte

45:08

glycoprotein, and it's a protein

45:11

that is exclusively expressed on the surface of

45:15

oligodendrocytes and is believed that, um,

45:18

it's also like a marker for mature myelin

45:21

because it's only found later, uh, uh, in the,

45:26

uh, development of the, uh, oligodendrocytes.

45:30

So it's an important marker of normal cells.

45:35

Let's say the, um,

45:38

Antioch has been identified as an auto antigen

45:42

and auto antibody target in the myelinating disease.

45:46

And at the beginning, when all the work was done for this,

45:50

which was around 2016, when the

45:55

publisher publishers starting presenting cases

45:58

of anti-MOC encephalitis, there was the issue

46:02

that this could be, um, the cause of ms.

46:06

So there was a lot of confusion with the two diseases,

46:09

and for us in imaging, it's gonna be, uh,

46:12

a little bit difficult to differentiate them.

46:14

So with more development of knowledge of the disease,

46:18

we have learned that an Moog antibody diseases are a

46:23

complete separate entity from ms.

46:26

Although the markers, uh, the lack

46:29

of markers in MS makes it more difficult

46:32

to differentiate anti Moog, um,

46:36

than in the case of, uh, anti aquaporin for,

46:42

uh, cases, which is, would be the overlapping

46:47

disease for us in imaging.

46:50

So anti-MOC can also involve the optic nerves

46:54

as it happens in the NMO spectrum diseases,

46:59

uh, most commonly involves both optic nerves simultaneously.

47:04

This is what, um, you can find in some of the reports.

47:09

It can present as an a encephalitis

47:12

or alike, uh, disease

47:15

with poorly demarcated t tissue and flare lesions.

47:20

Um, that also can involve the brainstem,

47:23

can involve the spinal cord, so it can also present

47:27

with long extensive transverse myelitis.

47:31

And, um, can give also the presentation

47:34

of unilateral cortical encephalitis.

47:38

Uh, these patients can present with headache, fever,

47:41

seizures, and encephalopathy that make the differentiation,

47:45

uh, very difficult from an viral type of, uh, encephalitis.

47:50

So the test, uh, um, the disease can be confirmed

47:55

by serum tests

47:56

or CSF, um, IgG antibodies

48:01

and for the clinicians is clearly, uh, standard.

48:04

The way to confirm it

48:05

for us in imaging is gonna be a little bit more difficult,

48:08

especially in cases like this, where we have patient

48:11

with already demyelinating, uh, disease.

48:14

Here, it's just to show you

48:15

that there's no enhancement in the same case.

48:18

And I got inspiration from a very good paper, uh,

48:22

published about all different autoimmune diseases

48:26

to just have a summary of what is important

48:29

for us from the imaging point of view

48:31

for diagnosing anti-MOC encephalitis,

48:34

and is to remember that it can overlap in findings with, in

48:38

with the anti aquaporin for, um, diseases,

48:43

and is included in the spectrum of NO spectrum

48:47

of diseases with optic neuritis, transverse myelitis, um,

48:52

and brainstem encephalitis alike presentations

48:56

or unilateral cortical encephalitis.

49:00

The, um, their there, very interesting reports trying

49:05

to analyze in imaging.

49:08

How specific is, uh, for us, you know,

49:12

certain findings to guide us towards more anti-MOC than,

49:16

uh, NO or they call it IQP four.

49:20

Not anymore, anymore because it's a confusing term.

49:23

And the only one

49:24

that has shown a statistical significance is the presence

49:28

of cortical weight matter

49:30

or juxta cortical white matter lesions.

49:32

So that's something for us that could be useful.

49:35

If we have a patient that looks like NO

49:37

or anti mo, um, just try

49:41

to find cortical lesions

49:42

or subcortical lesions that, that will, uh,

49:45

shift the balance more towards anti-MOC

49:48

antibody um, disease.

49:51

Another example of this type of, um,

49:54

autoimmune presentation is this case, 37-year-old patient

49:58

with headache and fever presented with, um, bilateral, uh,

50:03

flacid, uh, leg weakness.

50:05

Patient was found by the ambulance, uh, naked

50:10

in her home, completely confused.

50:12

The MRI findings demonstrated some signal abnormalities

50:16

that are not very specific as you see in flare.

50:19

We see some, uh, dolike, uh, lesions in the thalamus

50:23

and in the midbrain.

50:25

And the patient, um, uh, had, um,

50:29

also some, um, intermediate signal in diffusion

50:34

in the same location, some restricted diffusion,

50:37

which some people argue that it could be more favorable

50:40

of an acute demyelinating plaque.

50:43

Um, but we cannot use that

50:46

as a path pathognomonic sign.

50:49

And the patient had some, uh, spinal cord abnormalities

50:52

that are also, uh, all, uh, giving us, you know,

50:57

similar findings to any demyelinating disease.

51:01

So this is just to remind us that the, uh,

51:04

investigation on these patients should include a complete

51:07

cord imaging that if we can diagnose the long, uh,

51:11

lesions, it would help us to shape more the, uh,

51:15

differential diagnosis.

51:18

Um, another type of autoimmune disease,

51:21

and the most common one is the anti NMDA that stands

51:26

for NMA spartic acid receptor encephalitis.

51:30

This patient, uh, has a very complex history.

51:33

In 2020, um, this previously healthy patient presented

51:37

with a picture of subacute me encephalitis.

51:40

She had fever headache.

51:42

Um, they were questioned about diplopia

51:44

and altered mental status.

51:47

The initial MRI was almost normal, except

51:50

for very subtle signal abnormalities in the motor cortex

51:54

with some restricted diffusion, uh, signal in DWI,

51:59

but not clearly restricted in a DC map.

52:03

Two years later, the patient has, uh, a follow-up

52:07

because of recurrent seizures,

52:09

and you see how progressive disease was for her

52:12

with cortical and subcortical lesions

52:14

that were enhancing in multiple locations.

52:17

So the picture here changed dramatically for us.

52:21

Um, the, uh, patient underwent all, uh,

52:26

investigation for, uh, maybe, uh,

52:29

overate teratoma that was negative.

52:31

And because her epileptic, epileptic disease was out

52:35

of control, she ended up in a prophylactic of ectomy, um,

52:40

that didn't improve much the condition.

52:42

And unfortunately, this is the most recent MRI we have on

52:45

her, where you can, uh, see how much, uh,

52:48

brain loss she had, um, very prominent ventricular system

52:53

as a compensatory phenomenon.

52:56

The anti NMDA is by far the most common

52:59

of the autoimmune diseases.

53:01

Uh, we're gonna encounter the patients course with a lot

53:05

of psychiatric symptoms, uh, presentation.

53:08

And in the long term, uh, this patient improved in

53:12

and some of her, uh, initial presentation,

53:16

but remain severely depressed.

53:18

And so that's something for us to remember

53:21

that autoimmune diseases occur with more, uh,

53:24

psychiatric symptoms.

53:26

One of the explanations I found for that is that

53:28

because they tend

53:29

to be more often localized in the temporal lobe

53:32

as limbic encephalitis do, that's the explanation.

53:36

But as you can see, the presentation is quite variable.

53:38

It's not necessarily limbic encephalitis.

53:40

So I'm not so sure about theory, uh, for that.

53:45

Um, the, uh, the, uh, correlation with, uh,

53:50

ovarian teratoma important in young females.

53:52

So we should always, uh, include that in our recommendations

53:56

to do a full investigation for these patients.

53:59

The, uh, the classical presentation is young women,

54:03

and we're gonna see it in our summary, uh, uh,

54:07

summary information here.

54:09

That is mostly female, very young patients.

54:13

And, uh, the presentation more often in MRI,

54:17

unfortunately, is a normal exam as we have in this, uh,

54:22

second case I wanted to show you.

54:24

30-year-old patient with one month history

54:26

of paranoid ideas, insomnia, and disorganized behavior.

54:30

Patient was being treated for psychosis.

54:33

Her MRI was completely normal,

54:35

and the patient, um, was fully investigated,

54:38

had a small lesion, um,

54:41

in her CT abdomen at the one of the ovaries, and was removed

54:46

and confirmed as a teratoma.

54:47

This patient had a better, uh, outcome with improvement

54:51

of her symptoms, however, remained depressed

54:54

and is under treatment for, uh, depression and anxiety,

54:57

but cognitively, she's spared.

55:00

So the, uh, an MDA, uh, receptor,

55:05

I try to understand.

55:06

Okay, so why so, um, severe this disease is

55:10

because the receptor is widely distributed in our brain,

55:14

is a, is a common site, let's say.

55:18

Um, it's a receptor of glutamate,

55:20

and glutamate is the primary excitatory neurotransmitter

55:24

in our brain.

55:26

So it explains how the, uh, implication is

55:30

so severe when, uh, any antibody targets, uh, that,

55:35

uh, location.

55:37

So here we have a summary

55:38

of possible autoimmune encephalitis

55:41

and their presentation in MRIs.

55:44

Many of these diseases, if not 80% of them, will present

55:48

as a limbic encephalitis.

55:50

So it's important for us to keep it in mind.

55:52

Um, and the other important thing here in la, darker blue,

55:58

I, I'm showing you the ones that are non perine neoplastic,

56:01

the ones that are the group two that, uh, are associated to,

56:05

uh, surface antigens

56:07

where the antibody antibodies are not pathogenic.

56:11

Uh, they're newer

56:12

and newer, uh, information published about them, um,

56:16

about the, uh, voltage, um,

56:21

gated, uh, potassium channel encephalitis.

56:26

We have like a new name

56:28

and is the one called anti LGI I one.

56:32

Um, here we have an example of that disease that,

56:35

as you can see, presented as a limbic encephalitis,

56:38

typical involvement of the mesial temporal lobes, um,

56:42

very subtle, uh, signal change in the diffusion

56:45

and no enhancement.

56:47

Um, this one, uh, was a 64-year-old patient who presented

56:51

with rapidly cognitive changes and decline,

56:54

and, uh, presented

56:56

with acute seizures to the emergency room.

56:59

So it, these cases, these patients, um,

57:04

could be very responsive to acute, um, uh, treatment

57:08

with IV flex or corticosteroids.

57:11

And it's quite difficult for the clinicians to decide what

57:13

to do because also looks like a viral encephalitis.

57:17

So therefore, my point that we have to use any,

57:22

any subtle, uh, information that can help us

57:26

to guide the clinician towards, uh, more prompt, uh,

57:29

treatment for the appropriate disease.

57:32

And the, uh, summary for, uh, that type of encephalitis,

57:37

just to remind you

57:38

that there's only one feature in the clinical information

57:41

that can help us, and is the fact

57:43

that these patients present with a very specific type

57:46

of encephalitis in the LGI one, uh, uh, disease,

57:51

and is, uh, described as, um,

57:56

uh, facial, facial brachial dystonic seizures.

58:00

So it is a, it is a type of jerking movement

58:03

that involve a spasm of the face and the same side arm,

58:08

and it's very specific in the clinical presentation

58:10

and can help us a lot to guide.

58:13

Okay, this could be an autoimmune type of encephalitis.

58:16

It has limbic encephalite, uh, typical findings in MRI

58:20

for limbic encephalitis,

58:21

but it, it can guide us a little bit better than the simply,

58:25

uh, you know, non-specific imaging findings.

58:28

Also that is more common in males and in the middle age.

58:32

So those are simple features that I hope, uh, can help us

58:36

to decide in the, uh, in the, uh, situation.

58:41

So this was a very difficult, uh, topic to put together

58:46

because it's, it's complex and all over imposing.

58:50

I hope, um, that, um, as me at the end

58:54

of the preparing this, um, you can conclude

58:58

that it's important for us to start trying

59:00

to include in our differential diagnosis autoimmune

59:04

encephalitis as one of the options

59:05

and try to get, um,

59:08

more information from the clinicians about

59:11

psychiatric symptoms in the patient

59:13

and not very acute presentation, which also can help us

59:17

to guide better our differential diagnosis in imaging.

59:21

Unfortunately, um, if it is a temporal

59:23

and missile frontal involvement, we're gonna be, uh, in di

59:28

situation to go towards infectious versus autoimmune.

59:32

But, um, we saw that, you know, uh, with some extra help

59:37

and discussion with the clinicians, uh, we could be of help.

59:42

Uh, with this. I'm finishing my presentation.

59:44

I thank you all for your patience and time,

59:48

and I'm happy to discuss any questions you have.

59:53

We have a question about how can West Nile jars

59:56

or Japanese encephalitis be differentiated from postviral,

60:01

acute necrotizing encephalopathy

60:03

as all have bilateral thalamic lesions

60:06

with central cavitation?

60:08

Yeah, I don't think we, we can really, uh,

60:11

do a differentiation.

60:13

Um, I guess again, we, you have to rely on

60:16

what the clinical, um, information is for the patient

60:20

and also depends where you are in the world.

60:22

Uh, uh, for us, Japanese encephalitis was, uh, first case,

60:27

uh, is very unusual for us to see it here.

60:30

It wouldn't be the case for a West Nile.

60:32

Um, but it seems that West Nile is, um, has less,

60:37

uh, diffuse involvement of the thalamus

60:40

as we see in Japanese, uh, encephalitis.

60:43

So a more diffused basal ganglia, more uniform

60:46

and symmetrical, I think will favor more the Japanese type.

60:50

But that's not scientific, uh, scientifically proven.

60:54

Uh, just based on what I read

60:57

and I can tell you, was this diagnosis

61:00

of CJD made a time of imaging?

61:02

Yes. So this was not like, uh, the patient passed away

61:07

and they came to tell us like we saw the imaging,

61:09

but I have to tell you

61:11

that we have very close relationship with the neurologists.

61:15

They, when they have a case,

61:17

they come and discuss it with us.

61:18

So that helped me. That was the, uh, the reason to,

61:22

um, to find it.

61:24

Uh, so it's the clinical information like rapid progressive

61:27

changes, um, and you start being paranoid

61:31

and looking at that flare carefully,

61:33

and the diffusion sometimes reusing encephalitis presents

61:38

with acute presentation that show hemispheric brain swelling

61:41

with diffusion restriction.

61:43

That's a very good, uh, comment in this situation.

61:45

How can it be differentiated from other causes?

61:48

I guess it's just the hemisphere one hemisphere involvement

61:52

and that you have cortical involvement as well.

61:54

It's not only frontal and temporal,

61:56

but it's kind of a more diffused,

61:58

and it's not only cortical,

62:00

but it's also subcortical signal changes with

62:03

which if you had, um, like, um, a swelling from al

62:09

activity that is more the cortex, um, in,

62:13

in trans mucin, it would be also sub cortical signal changes

62:17

as we saw in our case.

62:19

Um, uh, what common viral

62:24

causes encephalitis?

62:26

What common viral?

62:27

Um, common viral is

62:31

herpetic encephalitis.

62:33

That's the most common of all viruses.

62:35

Um, uh, Dr.

62:40

Shaima sometimes, um, sorry, it's just

62:44

that they kind of go back to the, they jump

62:48

brain on fire is a book of movie of autoimmune encephalitis,

62:51

presents a young women, thanks for the talk,

62:54

which age group is high risk for both types of encephalitis.

62:59

So, um, viral encephalitis

63:04

is more common in the very young or the very elderly.

63:08

Those are the two populations at risk.

63:11

Autoimmune disease,

63:12

I would say is more common in young females.

63:17

If you look at all the comparison of the, uh,

63:20

published cases, it seems like really between 20

63:25

and 40 is where you have that window

63:28

for the most common ones.

63:31

If we're talking about the non-plastic ones, right?

63:34

The ones that are NMDA or anti mog, which is bad

63:39

because MS happens in that same population.

63:42

NMOD disorder spectrum happens on that population.

63:46

So that is not very helpful.

63:48

The ones that could be more per neoplastic than you

63:51

expect to see more.

63:52

Um, the, uh, fifth

63:55

or sixth decade, uh, population involved.

64:00

Can mitochondrial disease

64:01

with multiple cortical first be differentiated

64:04

from encephalitis?

64:05

I guess the presentation would be quite different.

64:08

Um, and the fact that you don't have, uh, very

64:14

restricted diffusion signal in DWI.

64:17

So in a strokes, you see very strong restricted diffusion.

64:20

In encephalitis, it's more patchy.

64:22

It's never like, uh, bright as we see in,

64:27

in a stroke or in an abscess type of case.

64:31

So that would be my way to differentiate it,

64:34

a spectroscopy in autoimmune.

64:36

That's a very interesting, um, uh, question.

64:39

Um, we have in a couple of the cases,

64:43

I showed a spectroscopy

64:45

because we were routinely obtaining MRS

64:49

and didn't show really great, um, help

64:54

because in both, let's say in demyelinating disease

64:58

and autoimmune, you're gonna have a lot of inflammation, um,

65:03

explaining deletions.

65:05

So lactate is gonna be increased,

65:08

lipids are gonna be increased glutamate,

65:11

it's gonna be increased in both diseases.

65:14

So there's doesn't seem to be very useful.

65:17

I think it would be probably more useful if you're thinking

65:20

of another, uh, differential diagnosis.

65:24

Like if you are not sure if it is a tumor versus, uh, kind

65:29

of an inflammatory lesion in that case,

65:31

then probably there would be room for the MRS.

65:36

I don't have any experience

65:37

with perfusion on these patients.

65:40

I'm curious to know the extent

65:41

of the damage COVID-19 have caused of the brain's

65:44

and long-term effect on the same.

65:46

Agree with that, uh, comment.

65:48

I don't think we can really say, uh, what is gonna be like

65:53

in encephalitis by covid

65:54

because there's a lot of overlapping,

65:56

and I, I was thinking all the long covid, uh, cases,

66:00

maybe they are just autoimmune encephalitis

66:03

and we haven't been able to demonstrate it

66:05

and their MRIs are negative.

66:07

Um, I saw MRIs that were reporting hemorrhage

66:12

edema, all sorts of findings

66:14

that we're not really following a pattern.

66:17

So, uh, I don't think

66:21

we have a picture clear about covid, um, for that.

66:24

But it should be included in textbooks as of now,

66:27

at least in the group of viruses that can, uh,

66:30

cause encephalitis for acute encephalitis.

66:35

Uh, so depending what drug,

66:37

which drug is most commonly used is one of the questions.

66:40

So depends if it is a viral.

66:43

And here in our institution, regardless,

66:45

all patients get antiviral treatment while we

66:48

figure out what it is.

66:50

So they all get acyclovir right away.

66:54

And if they don't respond and we repeat the MRI

66:57

and we start, you know, seeing more pattern

67:00

of something else, then they get the IV flex

67:03

and solum role, uh, for treatment.

67:06

But they don't do it until they're not sure.

67:08

It's not a, an infectious type, how

67:13

to differentiate between infarct

67:15

and encephalitis if it shows restricted

67:18

diffusion without history.

67:20

Um, so I would use the signal

67:23

intensity in restricted diffusion.

67:26

Um, it should be more homogeneous, more vascular territory.

67:29

Um, and a clear restricted what I,

67:32

the cases I showed you were very weak, patchy signals.

67:36

It was not, um, like the typical one we see in a stroke,

67:42

how could we explain on contrast enhancement and,

67:45

and the, uh, IUs lesion?

67:47

Um, that's a very good point

67:48

because there must be some disruption

67:51

of the blood brain barrier in acute encephalitis.

67:54

Um, I didn't find any explanation for that.

67:59

We all read on this reviews that, uh,

68:03

there is variable enhancement,

68:05

but what we have seen in the cases

68:08

that enhance is very fine peripheral enhancement

68:12

or patchy ponte,

68:13

but not like an extensive enhancement as we see, um,

68:17

in other diseases that are

68:20

maybe causing the same histological process.

68:23

So I don't have a scientific answer, uh, for that.

68:28

So I haven't used any perfusion as I said,

68:34

um, for MRI.

68:37

And, um, um,

68:43

I have a question for, from Dr.

68:45

Hasek Lu, um, uh, a comment. Thank you and hello to you too.

68:50

Um, so I think with this we can

68:55

conclude and you know, I'm happy to

69:00

in the future, uh,

69:01

or by email answer any other questions you guys have.

69:09

Oh, thank you so much

69:10

for sharing your lecture today with us, Dr. Cortez.

69:12

And thank you so much for taking the time

69:14

to answer so many questions. Uh, it was really great.

69:18

Well, thanks to you and, uh,

69:19

have a good afternoon. Thank you again.

69:22

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69:23

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69:26

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69:35

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69:39

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69:42

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