Interactive Transcript
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This is an MRI of the brain,
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an eleven-year-old child with headache.
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At first glance,
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we're not seeing any big mass,
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we're not seeing any mass effect.
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We're not seeing any midline shift.
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We're not seeing any signs of hydrocephalus.
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So at first approximation,
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we're not seeing anything majorly abnormal.
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If we look closely at the thalamus,
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we're seeing some subtle hyperintense signal
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in the thalami, bilaterally patchy.
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Now, the thalamus is gray matter,
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but it actually is so heavily myelinated,
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because there are so many connections coming to
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and from the thalamus that it actually,
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typically, in a myelinated individual,
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has signal that looks very
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similar to white matter.
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See this white matter here
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of the optic radiations,
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this dark signal on T2-weighted imaging,
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that's typically what the thalamus looks like.
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Here we're seeing these heterogeneous
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bright areas.
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That brings about a classic differential of
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things with bilateral thalamic abnormalities.
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Now,
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there's acute disseminated encephalomyelitis,
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for instance,
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and other acute demyelinating disorders,
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such as anti-MOG antibodies.
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Those won't usually present with
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headaches as an outpatient.
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Those are going to be more acute presentations
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with neurologic deficits.
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There is bithalamic gliomas.
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Now, a bilateral thalamic glioma is usually not
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going to be this patchy area of infiltration.
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It will typically be expansile,
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and when it goes across,
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it will be crossed through the mass intermedia
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or the interthalamic adhesion.
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So, I don't think that this
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is a bithalamic glioma.
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There's something called an artery
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of percheron infarction,
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which is related to a stroke from basilar perforators.
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And in some individuals,
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a single trunk of the basilar perforator
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supplies the medial aspect of both thalami.
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Well,
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an artery percheron infarction will first of all
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be the medial aspect of both thalami,
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not this patchy involvement of the
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whole thalamus bilaterally.
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And it will also show diffusion restriction.
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So that's not what this is.
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Now, you can also get a venous infarction
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and venous congestion from thrombosis
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of the vein of Galen and internal cerebral veins.
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Well, on this T2-weighted image,
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we're seeing normal T2 flow voids in the
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posterior aspect of the internal cerebral veins
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in the vein of Galen.
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We're also not seeing any signal abnormality
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on diffusion-weighted imaging.
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And additionally,
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that's also an abnormality that would
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typically be the medial thalamus,
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and it would also be an abnormality that would
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occur as more of an acute presentation,
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not an outpatient for headaches.
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Now, there's also Wernicke's encephalopathy.
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Wernicke's encephalopathy is a bilateral
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thalamic abnormality,
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medial thalami that you don't want to miss.
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You want to be aware it,
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you want it to come to your mind.
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Well, that also is going to present more in the
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acute setting. Now, in an acute setting,
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if you see bilateral thalamic abnormalities,
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even if you may think it's ADEM,
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there's very few entities where
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giving Thiamine replacement,
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which is the treatment for Wernicke's encephalopathy,
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there's very few entities
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where that would hurt.
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So, if I see a patient with an acute abnormality,
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where there's bilateral thalamic abnormalities,
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I'll often sort of suggest,
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is there a contraindication to Thiamine?
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That's my way of saying, well,
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it may not be Wernicke's,
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but in the off chance that it is,
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it wouldn't hurt.
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There's another bilateral thalamic abnormality
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that comes up in differentials,
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that's often discussed on board exams.
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That's Creutzfeldt-Jakob disease.
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Now, that's very rare
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and that's even more rare in children.
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So, that's not something I'm worried
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about in an adolescent,
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but that is at least something to be aware of
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or thinking about with bilateral
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thalamic abnormalities.
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The other entity with bilateral thalamic
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abnormalities is neurofibromatosis type 1.
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Now, we're not seeing a lot of other abnormalities
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of NF 1 here, except if we look closely,
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we see signal abnormality in
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the right globus pallidus.
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So, we're not seeing other definite abnormalities.
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But it turns out that this child with
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headaches actually had neurofibromatosis type 1.
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Just a very subtle clinical case of it.
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So, in general,
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most of the patients with neurofibromatosis type 1
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that get MRI,
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we know in the beginning that that's
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what their diagnosis is.
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But every now and then, there's going to be
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a patient where they get an MRI,
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and we don't know that that's
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what the diagnosis is.
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And this is one of those examples.
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