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Osmotic demyelination is a term that is used to

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encompass both central pontine myelinolysis,

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as well as extrapontine myelinolysis.

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While this classically affects the central

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aspect of the pons, it may, in fact,

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affect white matter tracts in the splenium of

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the corpus callosum or in the connecting

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fibers between the basal ganglia,

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or else within the brain's white matter tracts.

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And this is classically described as

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rapid correction of hyponatremia.

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There's a spike in central pontine myelinolysis

0:37

in July when new interns join the force and want

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to impress their attendings by how rapidly

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they can correct the sodium

0:47

when patients come into the emergency room

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or as an admission with low sodium.

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It's said that you should correct the sodium in

0:55

the same pace at which the low sodium

0:59

has developed.

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So if, for example,

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a patient is fasting for six days and takes

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their normal sodium value of 145 down to 116,

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you should correct it over

1:11

the same amount of time,

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six days to get it back to normal,

1:15

shouldn't be precipitous, for example.

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These are two different patients with central

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pontine myelinolysis, osmotic demyelination.

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Remember that osmotic demyelination can occur

1:27

with different electrolytes, classically sodium,

1:30

but may also be affected by potassium.

1:33

So the patient on the left is a patient

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with a T2-weighted scan

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in which there is abnormal signal intensity

1:41

in the central aspect of the pons,

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but it is sparing the corticospinal tracts.

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So, here is the bright signal intensity

1:48

on T2-weighted imaging

1:50

in the central aspect of the pons.

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And curiously,

1:53

we see these two areas in the central portion

1:57

of the central aspect of the pons,

1:59

and those are the corticospinal tract.

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This is relatively pathognomonic for

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central pontine myelinolysis,

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but it doesn't occur all the time.

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So it's specific, but not necessarily sensitive.

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The patient to the right shows

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T2-weighted abnormal signal intensity,

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and then we have the ADC map on the far right.

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You notice that there is dark

2:25

signal on the ADC map.

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So this is an example of restricted diffusion

2:31

occurring without it being on an ischemic basis.

2:34

This is on a demyelination basis that

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you see this restricted diffusion.

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This is one of the examples of restricted

2:42

diffusion that can completely reverse.

2:44

So this does not imply irreversible

2:46

damage to the pons.

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This implies a process that is

2:50

causing cytotoxic edema.

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So you'll see this as bright on the

2:54

DWI and dark on the ADC map.

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In this case, we noticed that

3:00

sort of that triangular,

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if you will,

3:03

appearance to the involvement of the pons.

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And in this case,

3:07

without sparing of the corticospinal tracts.

3:12

Central pontine myelinolysis, by and large,

3:15

does not enhance.

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However,

3:17

in the cases that were shown,

3:19

you saw a patient who had mild enhancement

3:22

of the white matter of the central pons

3:26

in the previous case that was demonstrated.

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This is a non-hemorrhagic process,

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but it may or may not have restricted diffusion.

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Let me show an example of extrapontine myelinolysis.

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Another example of osmotic demyelination.

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So, actually, these are two different patients,

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one on the top and one on the bottom left.

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So, here we have a patient who seems to have

3:56

relatively diffuse white matter disease,

3:59

which is including the basal ganglia.

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Here we have our putamen and Globus Palladus.

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We're at the edge of the thalamus here.

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And these are gray matter structures that are

4:10

affected by extrapontine myelinolysis.

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But within that category of what we

4:17

would call osmotic demyelination.

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This is another case from Johns Hopkins.

4:25

Again, relatively diffuse involvement

4:27

of Globus Palladus, putamen,

4:29

as well as thalamus, bilaterally,

4:32

as well as the white matter of the external

4:34

capsule and internal capsule.

4:37

Another example of osmotic demyelination in

4:40

a patient who had too rapid correction of

4:42

hyponatremia and hypokalemia,

4:45

low potassium,

4:47

who had a rip roaring case of

4:50

extrapontine myelinolysis.

4:53

This is a third case from the literature of a

4:57

patient who also had diffuse involvement of deep

5:01

gray matter, as well as the white matter tracts

5:03

connecting them in an example of

5:05

extra pontine myelinolysis.

5:08

This is a disease entity that we usually say has

5:11

a prognosis that's quite variable.

5:14

Sometimes you have a patient with extrapontein

5:17

myelinolysis who remains in coma and may

5:20

actually be locked in because of the central

5:23

aspect of the pon's involvement

5:25

and irreversible damage.

5:27

One third of patients have mild deficits upon

5:32

correction of the extra pontine myelinolysis

5:35

or central pontimyelysis osmotic demyelination,

5:38

and one third recover completely.

5:40

So, quite variable prognosis in

5:45

osmotic demyelination.