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Previously, we discussed the entity of optic neuritis and

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recognized that it can occur as an isolated entity,

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or with systemic disorders, such as multiple sclerosis,

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or neuromyelitis optica spectrum disorder.

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On these images, we have the normal optic nerve seen in

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sagittal plane, representing dark signal intensity like the

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white matter and outlined with the optic nerve sheath

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and the CSF within the optic nerve sheath.

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And we note that there's a relative absence of enhancement

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of the optic nerve sheath, other than little scant areas.

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On the coronal image,

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we note the bright signal intensity in the optic nerve

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on the left side at the optic canal.

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Once again, identify the anterior clinoid process as the

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marker for the optic canal, and this is also seen on a

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sagittal reconstruction as the optic nerve goes through

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the optic canal to enter the intracranial space.

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Note that at the junction of the anterior clinoid process

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and the intracranial space, we see the difference between

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the abnormal signal and a normal pre chiasmal optic nerve.

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This area at the optic canal shows contrast enhancement

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on the fat-suppressed T1-weighted scan.

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And this is again noted on the coronal image with the

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bright signal intensity optic nerve on the left,

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compared with the normal signal intensity on the right side,

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and the contrast-enhancing optic nerve versus the non-

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enhancing optic nerve on the right side.

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There are some institutions that prefer to perform fat-suppressed

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and CSF signal intensity-suppressed scans through the orbit.

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So, this is what is known as your

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fat-suppressed FLAIR imaging.

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What is the benefit to the fat-suppressed FLAIR imaging?

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By FLAIR imaging, we have CSF suppression.

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So you note that the subarachnoid space on this coronal

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FLAIR imaging is dark in signal intensity.

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We also have performed fat suppression.

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So, we see that the signal intensity of the orbital fat is

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also dark, as is the subcutaneous fat.

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In some instances, this may allow you to identify the bright

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signal intensity optic nerve,

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versus optic nerve sheath pathology, which would normally

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be darkened signal intensity because of

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the CSF suppression of the FLAIR scan.

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This is a technique that you may experiment with.

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We do not routinely perform it.

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We use the T2-weighted fat-suppressed imaging only.

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We describe the entity of neuromyelitis optica as one in

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which the patient has long segment high signal intensity

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disease within the spine for neuromyelitis optica.

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And in this case,

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we have both high signal intensity within the spinal cord,

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as well as an area where there is spinal

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cord atrophy from previous injury.

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And as you can see on the post-gadolinium scan,

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there is faint enhancement of the entire long segment of

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this spinal cord, associated with neuromyelitis optica.

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And this is also seen on the axial scans with the bright

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signal intensity on T2-weighted scan and the faint

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areas of contrast enhancement on

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post-gad T1-weighted imaging.

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Another example of demyelination in the spinal

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cord associated with optic nerve pathology.

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So here we have, once again, high signal intensity in the

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spinal cord with slight expansion of the spinal

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cord, absence of contrast enhancement,

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but we do see the high signal intensity in the right optic

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nerve, associated with contrast enhancement of the optic nerve.

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As I stated previously, with neuromyelitis optica,

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you don't have to have concurrent activity of transverse

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myelitis with optic neuritis to make the diagnosis.

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It is now considered a polyphasic disorder.