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This is a 51-year-old gentleman who

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was engaged in a six-day fast

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and presented to the emergency room

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with lightheadedness.

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He was subsequently transferred

0:15

to Johns Hopkins for treatment of hyponatremia.

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The MR scan shows a FLAIR image that is

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remarkable for abnormal signal intensity

0:32

within the pons,

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and to a lesser extent,

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the deep white matter of the corona

0:39

radiata and centrum semiovale.

0:41

And this is seen also on the T2-weighted scan.

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Again, we tend to emphasize

0:47

the T2-weighted scan for posterior fossa

0:50

and brain stem abnormalities.

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And you can see this lesion fairly well

0:54

on the FLAIR,

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as well as the T2-weighted scan.

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In looking at the ADC map,

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we note that the patient does not show evidence

1:06

of restricted diffusion.

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In point of fact,

1:10

this area is a little bit brighter in

1:11

signal intensity within the pons.

1:13

The patient had administration of gadolinium,

1:16

as well as an MRA.

1:18

The MRA was unremarkable.

1:19

They were looking for vertebra

1:21

basilar artery insufficiency,

1:24

and both the intracranial and neck MRA

1:26

looked fine.

1:27

On the post-gadolinium-enhanced scans,

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you can see that there is this unusual

1:34

triangular-shaped area of enhancement

1:39

in the central aspect of the pons.

1:41

And this is what I'm referring to here.

1:44

It's sort of almost got a

1:45

little triangular shape,

1:47

which corresponds to the signal intensity

1:49

abnormality seen on the FLAIR

1:52

and on the T2-weighted scans.

1:55

In looking at the history,

1:58

turns out that the patient had been treated for

2:02

hyponatremia associated with the fasting

2:08

at the outside hospital,

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and the sodium had been taken from 124

2:13

to 144 in the course of 24 hours.

2:17

That's a little bit too rapid for

2:20

the correction of hyponatremia,

2:22

and this leads to the diagnosis

2:24

of osmotic demyelination.

2:27

I use the term osmotic demyelination rather than

2:30

central pontine myelinolysis,

2:32

because we now understand

2:34

that there are many different

2:35

manifestations of osmotic demyelination,

2:38

which include extra pontine myelinolysis.

2:42

Curiously,

2:43

extra pontine myelinolysis may affect the fibers

2:47

that connect the gray matter

2:49

of the basal ganglia.

2:51

So it may actually look like a deep gray matter

2:54

lesion when we're dealing with extra pontine myelinolysis.

2:58

So, although the common vernacular

3:00

is CPM or Central Pontine Myelinolysis,

3:05

the term that is favored is

3:08

osmotic demyelination,

3:09

which is due to any number of corrections

3:13

of abnormal electrolytes.

3:14

We think about it with regard to sodium,

3:16

but also potassium.

3:18

Dysmetabolism can also lead

3:20

to osmotic demyelination.

3:23

There are different patterns of osmotic

3:25

demyelination that can occur.

3:27

This one is one of the classic forms with

3:31

the central aspect of the pons.

3:33

But I've also seen osmotic demyelination,

3:36

which involves the entirety of the central

3:39

aspect of the pons but spares

3:42

the corticospinal tract.