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This patient presented with

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left eye blurred vision.

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This was the first neurologic

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symptom of the patient.

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For orbital imaging,

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we rely most heavily on coronal sequences with

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T1-weighted scans to look for masses,

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T2-weighted scans to look at the optic nerve

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and postgadolinium-enhanced scans

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to characterize the lesion.

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On this T2-weighted scan,

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one can see that the left optic nerve

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is brighter in signal intensity

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than the right optic nerve.

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Let's look at the right optic nerve.

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What you see is fat-suppressed

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fat dark in signal intensity.

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Then you see the edge

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with the fat,

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which is the edge of the optic nerve sheath.

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Between the optic nerve and the optic

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nerve sheath, we have bright CSF.

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And then centrally,

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we have the optic nerve itself,

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which, because it's a white matter tract,

1:23

has the same signal intensity as the

1:26

white matter of the frontal lobe.

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Now, on the left side,

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we have an indistinct optic

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nerve sheath complex.

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It all looks like the same signal intensity with

1:38

no distinction between CSF and the optic nerve.

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And that's because the optic nerve here

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is bright in signal intensity,

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brighter than the white matter.

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This is abnormal.

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If we look on the corresponding postgad fatsat

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T1-weight scan to the far right,

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we see that indeed,

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this optic nerve is enhancing compared to

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the non-enhancing right optic nerve.

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Let me just magnify this even further.

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So here we have an enlarged optic nerve sheath

2:19

complex with a bright optic nerve.

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And on the post gadolinium-enhanced scan,

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again,

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you can see that that optic nerve

2:32

is showing contrast enhancement.

2:34

These are the image characteristics of optic

2:38

neuritis. Is there a differential diagnosis?

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There's always a differential diagnosis,

2:42

and it doesn't tell us what the etiology

2:44

of the optic neuritis is.

2:46

There are viral optic neuritis.

2:48

There's autoimmune optic neuritis,

2:50

there's infectious inflammatory optic neuritis.

2:53

There's all different varieties

2:55

of optic neuritis,

2:56

including collagen vascular disease we could

2:59

even have. And this. Ischemic optic neuropathy,

3:01

which actually is the most common cause of optic

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neuropathy is small vessel ischemic

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disease in the elderly.

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However,

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in a young patient

3:12

with an enhancing and enlarged optic nerve,

3:17

we would raise the possibility of autoimmune

3:21

idiopathic optic neuritis.

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This patient had a single symptom

3:27

just left optic neuritis. So therefore,

3:30

this patient could be said to have clinically

3:33

isolated syndrome, a single neurologic event.

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What one wants to do in that situation is to

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scan the patient's brain to see whether

3:45

there are any demyelinating plaques,

3:48

which could suggest that this patient

3:51

will progress to multiple sclerosis.

3:55

In point of fact,

3:58

this patient does indeed have some

4:01

subcortical white matter lesions

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that are seen here

4:09

in the frontal lobes. Now,

4:12

this is a nonspecific pattern and doesn't yet

4:14

fulfill McDonald criteria unless and until we

4:18

also have periventricular white matter lesions,

4:21

juxtacortical white matter lesions,

4:24

or

4:25

spinal cord lesions. If, on the other hand,

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we're using the magnums criteria and we have

4:32

optic neuritis and juxtaportical

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white matter lesions,

4:37

we would have fulfilled the magnums

4:40

criteria for multiple sclerosis.

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Given that the patient only has

4:44

a solitary neurologic event,

4:46

this would still be called clinically

4:48

isolated syndrome.

4:49

But by virtue of the white matter

4:51

lesions in the brain,

4:53

it would have a higher rate of conversion over

4:56

the course of time to a final ultimate

4:58

diagnosis of multiple sclerosis.