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This is a nine year old child

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with tubersclerosis complex

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with a fairly severe imaging phenotype.

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Now, I say fairly severe imaging phenotype because

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it doesn't correlate one to one with their

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clinical phenotype. But oftentimes,

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when we see this many areas of dysplasia,

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notice that this area here on the right,

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parietal and occipital lobe,

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almost looks like confluent involvement of dysplasia.

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The higher the lesion burden,

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the more likely they are to have seizures.

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The more likely they are to have complex

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seizures that are difficult to manage.

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Multiple types of seizures and

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lower intellectual capacity.

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The dysplasia is just multifocal.

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We almost can't identify the individual morphology.

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Can see this on the FLAIR image,

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just very confluent. This is fairly severe.

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Now, despite that,

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the patient ended up having a focal lesion resection,

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or called a topectomy,

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where they resected this in the

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hopes of seizure control.

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And again,

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it doesn't mean that you

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have to cure seizures.

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If a patient goes from,

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you know,

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20 seizures a day to 3 seizures a week,

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that's still very profound.

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So, just because not all the seizures

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are coming from one location,

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if a majority of them are,

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they still may end up going for surgery,

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because it still may benefit the patient

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and their caregivers significantly.

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This patient has multiple subependymal nodules.

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We can see here on T2,

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they're somewhat hypointense.

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On susceptibility weighted imaging,

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a lot of them are hypointense.

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And on post contrast imaging,

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many of them enhance.

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So there's multiple nodules,

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none of which look like they're

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a centimeter in size,

1:55

none of which look like there's impending

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impingement of the phramina of Monroe.

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This one here looks like

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a conglomeration of nodules.

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It measures 11 mm,

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but it's probably not one nodule.

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And even if this tripled in size,

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we would not expect there to be

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any impingement of CSF flow.

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There's moderate prominence

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of the lateral ventricles,

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likely somewhat on an x vacuolar basis due to

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decreased cerebral white matter volume.

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So, this patient definitely

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does not seem to be at immediate risk for

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a sega obstructing their csf flow.

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One other thing we notice in this patient,

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we can see actually dysplasia of

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the left cerebellar hemisphere.

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The right cerebellar hemisphere is

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probably not completely normal.

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But while we think of tuberculosis complex

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as predominantly being a cerebral

2:48

hemispheric involvement,

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they can have abnormal development

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of the cerebellar hemispheres.

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So, this is a patient with tuberculosis as complex,

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a fairly severe burden of dysplasia,

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as well as left cerebellar dysplasia.