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This is a 52-year-old who was in a motor vehicle

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collision and started seizing

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in the emergency room.

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They instituted antiepileptic drug therapy,

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and after a CT scan, sent a patient for an MRI,

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the CT scan was relatively normal.

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So let's look at the MRI.

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We have the FLAIR, the T2, and the ADC map.

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As we scroll through the images,

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looking initially at a haste T2-weighted scan,

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because the patient was moving.

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We see a relatively normal-looking FLAIR scan

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until we get to the top of the corpus callosum,

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where there appears to be abnormal

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signal intensity.

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This is also seen in the splenium

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of the corpus callosum,

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better seen on the T2-weighted scan

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than the FLAIR scan.

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If we divert our eyes to the ADC map,

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we see a similar area as previously described on

0:55

the most recent case of low signal intensity

0:59

on the ADC map, reflecting cytotoxic edema.

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Where we to look at the diffusion

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weighted images,

1:07

we would expect to see the bright signal

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intensity within the splenium

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of the corpus callosum.

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Now, at first blush,

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this may look just like the previous case in

1:19

which we saw the focal area of splenium

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demyelination associated with the institution

1:25

of antiepileptic drugs.

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However,

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we have to deal with the top of the corpus callosum

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that we are seeing here,

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where there appears to be abnormal signal

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intensity as well on the diffusion

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weighted scan.

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The other thing for those who have sharp eyes,

1:41

is that on the T2-weighted scan,

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we see a blood fluid level within the occipital

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pole of the left lateral ventricle,

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which is also seen on the B zero map of the

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diffusion-weighted scan.

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At the same time,

1:57

you notice that there is quite a bit of edema in

2:00

the scalp reflecting the patient's trauma.

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At this juncture,

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it's good to refer to the susceptibility

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weighted images,

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and on these susceptibility weighted images,

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we again see the dark signal intensity of the

2:14

blood products in the occipital horn

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of the left lateral ventricle,

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as well as other areas of dark signal intensity

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within the white matter of the occipital

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lobe and the periventricular zone.

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And as we extend higher to the

2:28

top of the corpus callosum,

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we now see very dark signal intensity

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at the top of the corpus callosum.

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So, these focal areas of low signal intensity are

2:39

what I'm referring to at the

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top of the corpus callosum.

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And you see that there is some blood products

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also noted elsewhere in the brain and

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or in the subarachnoid space.

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There's probably some blood in the subarachnoid

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space along the medial aspect of

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the right parietal lobe.

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So this is not secondary to

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the patient's institution of antiepileptic therapy.

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This is splenium demyelination,

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splenium tear on the basis of trauma.

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So while it's true that the patient had

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institution of the antiepileptic drugs

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for the seizure in the emergency room,

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this is more likely because of the presence of

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hemorrhage to represent traumatic splenium

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injury as opposed to demyelination on

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the basis of antiepileptic drug.

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So as you scroll this susceptibility weighted scan,

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you see additional areas of hemorrhage

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in the subarachnoid space,

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as well as at the gray white junction

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on the SWI scan.

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So the SWI scan was very instrumental in

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identifying the source of the splenium

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demyelination and splenium

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injury in this patient.

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A lookalike for splenium demyelination secondary

3:53

to institution or withdrawal

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of antiepileptic drugs.