Interactive Transcript
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This is a 13-month-old child
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with tuberous sclerosis complex
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receiving an MRI for routine surveillance.
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And we can see on this FLAIR image,
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multiple subependymal nodules.
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You can see better on the T2-weighted imaging,
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the relatively confluent areas of dysplasia
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in the right parietal lobe,
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an additional conglomeration of
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relatively confluent dysplasia
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in the left frontal pole.
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Several other areas,
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you can see this gyrus is rather enlarged,
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doesn't maintain the normal typical morphology
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of the sulcation pattern expected there.
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So, one thing that was noted is this lesion here
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and this caught people's attention.
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But if we look closely,
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we're not seeing a correlate on T2-weighted imaging.
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While some of these nodules enhance,
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there is nothing enhancing in this location
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in the anterior body of the
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left lateral ventricle.
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And I'm not seeing anything on STIR either,
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except I'm seeing a slightly ill-defined
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area of hypointense signal.
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So, this is a fake out.
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This is not a subependymal giant astrocytoma.
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This is something that we can see in many
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MRIs of the brain,
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and our eyes may end up ignoring it,
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or sometimes maybe we may get concerned.
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This is a CSF pulsation flow void.
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CSF is coming through
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the foramen of Monroe.
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And at the time that the inversion pulse know
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the signal of water here, between the time
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of that inversion pulse and the readout,
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this fluid comes in with protons that
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had not received the inversion pulse.
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And so, we're seeing this bright signal here
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and we're seeing a subtle little, you know,
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flow anomaly here, flow void really
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to CSF pulsation.
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So, this is normal.
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This is a physiologic finding.
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This is not a subependymal giant cell astrocytoma.
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This is just a good example that even in
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patients with a known disease process,
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those scans are prone to all the normal
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artifacts that we see in other imaging
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sequences in other patients.
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So, we see another CSF pulsation
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flow void in the fourth ventricle here.
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But so, this is a patient with
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tuberous sclerosis complex,
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moderately severe burden of dysplasia,
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multiple subependymal nodules and a CSF
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pulsation flow void that could
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be mistaken for a sega.
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