Interactive Transcript
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So imaging, uh, neuroimaging of 2023.
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Still the most important technique is the structural MRI.
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We cannot interpret physiologic
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or any other fancier imaging technique without actually
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seeing what the tumor looks like on structural imaging.
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But we also do physiology based MRI to assess
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where their vascularity their metabolism.
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And another very important, uh, type of technique
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that we use is this hybrid imaging called PET ct or PET mr.
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And many institutions are beginning to use this technique
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to look at is this a recurrent tumor
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or is this a radiation necrosis?
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So today I'm only going to highlight couple
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of the structural and couple of physiologic MRI.
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And as I said
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before, structural MRI post con precon, T one,
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T two flare multimodality multiplanar imaging.
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This is the bread and butter of what we do,
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and this will never go away,
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but we put additional test to look
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for hyper vascularity, whether there are leaky VAs, uh,
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permeability and whether there is a hyper cellularity
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or where there's high choline metabolism.
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So physiologic, MRI gives us a lot of insight into
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very non-invasive way of gland, um,
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glancing at their tumor biology.
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It's not as good as obviously actually looking at pathology,
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but it's a really powerful non-invasive tool.
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And this is what we do at UCSF
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and it's pretty standard at most institution.
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Pre post T one, T two FSC flare and DWI
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and a D, C, uh, D uh, a DC and DW.
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This is a must. And we also do, uh, SWI
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and a SL profusion imaging.
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SWI is becoming more
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and more important in brain tumor imaging
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because we use this primarily to look for areas
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of blood products, especially after radiation therapy.
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And we use this for assessing where the, the extent of micro
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and macro hemorrhages
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and also vascular lesions that are, uh,
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mimicking brain tumors
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and primarily in the brain tumor arena.
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We use this to assess for the extent of radiotherapy, uh,
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related injuries.
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So here three different patients
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with susceptibility weighted imaging.
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You could see this patient as literally innumerable punctate
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dots of susceptibility or micro hemorrhage.
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This is a patient who received whole brain radiotherapy
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for medulloblastoma 15 years prior.
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Here's a patient with very peculiar looking branching
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pattern of SWI.
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This is a person with a ven neuritis.
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This whole thing was removed.
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Removed, and it's not glioblastoma.
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This is a ven neuritis or veins that are partially thrombo.
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And this is a patient with hyper, um, very clear,
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large vascular mass.
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And that's cavernous malformation. So SWI, very helpful.
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Here's an example that we saw at tumor
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where a patient had a, a re enhancing,
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very aggressive looking, right brachi
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and pontus mass in the posterior fossa.
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But if you look at patients, SWI, there are
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new innumerable punctate micro hemorrhages.
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This is a telltale sign
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that patient probably had a radiation therapy.
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And lo and behold, we got the history
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after the fact that patient had a nasopharyngeal carcinoma
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and a pit tumor that were radiated twice before.
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Uh, we did not have the radiation field,
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but with that history
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and with that SWI appearance,
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we feel very comfortable calling this radiation necrosis.
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And patient was treated for steroids to control some
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of the edema related mass effect
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and pay this lesion slowly, uh, disappeared.
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DWI very important sequence.
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We use this to, uh, assess work,
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acute infarc abscess, cellular tumor,
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and, uh, actively demyelinating lesion.
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So here are three different patients.
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Here's the DWI imaging without even looking
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at structural imaging.
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When you see this homogeneous in, uh, reduced diffusion
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with an irregular mass like this,
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this is a intracranial abscess until proven otherwise.
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Here's a patient, you can barely make it out.
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The lesion on DWI kind of disappears.
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This is what diffuse glioma looks like on a diffusion.
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Here's a patient with two lesions, have a leading edge,
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reduced diffusion.
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This is pretty classic for non neoplastic,
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usually inflammatory, uh,
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actively demyelinating type of lesion.
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And this young, uh, patient was biopsied
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and that's a tumor effective demyelinating lesion.
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So diffusion is a must sequence when you're interpreting a
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brain brain mass.
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Here's another example.
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This patient came to us
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with a preoperative diagnosis from elsewhere, right?
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Frontal glioblastoma. I think that's not a bad diagnosis.
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There's a lots of mass effect.
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There's edema crossing the corpus callosum
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with central necrosis ri of enhancement.
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But once you see the DWI
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and a DC, you know that there's
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homogeneous reduced diffusion within the necrotic tumor.
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So that is a very unusual appearance of a glioblastoma.
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So this is more classic appearance for biogenic abscess.
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And indeed pathology proved that this is biogenic abscess.
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Our surgeons going in knew
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That this was going to be a puss 'cause we told them
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and they end up just doing a little bur hole
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and sucking that pus out.
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And patient did great.
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Here's a young woman that I showed a little bit earlier.
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This, uh, young woman was diagnosed with stroke at an
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outside hospital and you could see why, why?
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Because there is actual homogeneously reduced diffusion
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and it's very dark on a DC,
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but I think most of you would also notice that
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that shape is not a good, good, uh, shape
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for a territorial infarct.
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But nonetheless, patient was fine.
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The workup was negative, was transferred to our hospital
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and patient underwent surgery.
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And this is ahy hypercellular,
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unfortunately what's called a molecular
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glioblastoma perfusion.
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We use it to look for hyper vascularity
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hypervascular tumors.
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We also use perfusion for, to detect recurrent tumor
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assessed for glioma grade and sometimes postictal changes.
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Here's a patient who came to us
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with a homogeneously enhancing right cerebellar mass.
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And you could see that DWI is not reduced.
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There's a little bit of a rim
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of susceptibility, but not much else.
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So the question is, is this a metastasis or something else?
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Patient did undergo whole body workup and there was no mass.
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And if you add a SL perfusion, you could see
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that the whole lesion is very, very vascular
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in the cerebellum.
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And this is pretty classic appearance for
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a heman neoblastoma.
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And that's indeed what it was on pathology.
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Here's a person who's been coming to us for, um,
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serial imaging after patient had a subtotal resection.
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But you could see here that we don't know
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where the recurrent tumor here is.
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Patient had a seizure, they controlled the seizure.
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So after they controlled the seizure,
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we brought the patient back and did a profusion imaging
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and you could see that there is a clear unmistakable lump
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of hyper vascularity associated with
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non mass like flare here.
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So our neurosurgical colleagues went in
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and resected this, uh, hyperperfusion area.
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And the whole thing was a live recurrent diffuse glioma,
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IDH wild type spectroscopy.
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We use this tool now as a problem solving tool.
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Here is a normal single voxel spectroscopy, normal
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NAA creatine and colon.
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This is what you wanna see.
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And we've done many, many spectroscopy studies,
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both two DA single voxel, 2D and 3D.
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But I still find this single voxel very powerful.
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And here's an example of some of our patients, um,
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that we did on spectroscopy.
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Oh, by the way, a single voxel only requires about less than
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three minute of imaging.
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So it's a really powerful tool
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that does not take up much in terms of additional imaging.
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And we've now kind of developed four different types of
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spectroscopic appearance of an abnormal lesion.
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So what we call the proliferative, where there's high,
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high choline hypoxic profile where there is clear lactate,
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peak infectious profile where we see amino acids, alanine
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and acetate, and the necrotic pattern
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where we see predominantly very high lipid and lactate.
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And here's an example of how we use this single voxel
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two minute of additional imaging.
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So this patient came to us with a left frontal glioblastoma
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as the preoperative diagnosis
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does look like glioblastoma was central necrosis.
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But once you get DWI, you know that inside of
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that reen enhancing lesion,
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there is a clear reduced diffusion that looks like pus.
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So we brought the patient down
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and with a single voxel spectroscopy using te
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of 35 milliseconds and 2 88 milliseconds,
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and we saw all the metabolites
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that classically seen in biogenic abscess such
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as amino acid, lactate acetate,
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and the choline, which is not a tumor marker, it's a, uh,
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membrane turnover marker is very, very low.
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So our confidence putting the together with the diffusion
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that this is going to be a genic abscess was near 100%.
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And our neurosurgical colleagues just did a very small bur
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hole and sucked out the fluid.
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And lo and behold, there is that yellowish purine material
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and this is a path proven biogenic abscess.
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So let me now, uh,
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focus more on the brain tumors based on the molecular
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genetics, and I'm going to start with three different types
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of pediatric tumors
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and go on to adult tumors using the, uh, imaging techniques
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that I just described to you.
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So pediatric brain tumors in the WHO scheme from 2016
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to 2021, many different, um,
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classification changes have been made.
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The first is these two tumor types,
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one medulloblastoma, the other appendamoma,
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and you could see that without
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knowing anything about the tumor.
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So here's post con T one.
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You could see that the, this patient has a tumor
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that is relatively homogeneously reduced and diffusion.
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So this is going to be some type
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of a cellular tumor patient.
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On the other hand, this tumor both are
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midline enhancing lesion.
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You could see that DWI is not
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Reduced.
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So DWI is single most helpful sequence
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after looking at post contrast imaging.
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So we already know this patient has a hypervascular,
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a hypercellular tumor, and that's a me neuroblastoma.
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And this patient on the right, this is a patient
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with APPENDAMOMA
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and DWI is really the first step towards
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honing down into the molecular
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or biologic feature of their tumors.