Interactive Transcript
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Let's have a look at an 82-year-old who is
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severely Parkinsonian,
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but also has severe dementia.
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I don't have the information as to how long this
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has been going on or which process has dominated.
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However,
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the degree of atrophy as we scroll
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up and down is profound.
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Now, atrophy does occur
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at the end stage of Parkinson's disease.
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So unless you have a time course,
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it makes it difficult.
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But with such profound atrophy,
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you would at least have to consider the diagnosis
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of Lewy Body Disease as a cause of a Parkinsonian
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syndrome rather than classic isolated
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Parkinson's disease.
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There's quite a bit of overlap between the two.
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Let's blow up the brain a little bit so we can
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get a better feel for the arrangement of the
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substantia nigra, which is cut off laterally
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as you would see with classic PD.
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And there is bleeding between the substantia
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nigra and the red nucleus.
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There's not a good crisp, linear, high signal,
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compacta zone, yet the atrophy is profound.
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So let's scroll up and down.
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You should also be struck in this 82-year-old by
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the relative paucity of vascular disease, which
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wouldn't be a very good explanation for the
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patient's clinical symptoms of dementia and
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Parkinsonian-like symptoms, including tremor.
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So the differential lies between Lewy Body Dementia
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and Parkinson's disease.
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This patient has proven, unfortunately,
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at post LBD.
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And one of the tip-offs to the diagnosis is
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the involvement of the temporal lobe.
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Now, it is said in the literature that temporal lobe
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involvement is more severe step by step
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or in other words, time versus time,
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five years of Parkinson's disease
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versus five years of LBD.
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More atrophy in the entorhinal cortex in ALZ.
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But compared with Parkinson's disease,
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Lewy Body Dementia has more atrophy in the
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entorhinal cortex and temporal lobe compared with PD.
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So for temporal lobe involvement,
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it goes ALZ, LBD, PD, in that order.
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This patient has what I would call moderate
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to severe temporal lobe atrophy.
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So let's talk about Lewy Body Dementia,
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which was described by Frederic Lewy in 1912.
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These patients have spherical neuronal inclusions
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that are intracellular.
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And in fact,
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they're intracytoplasmic staining
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with ubiquitous antibodies.
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Whereas PD patients have extraneural inclusions,
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interstitial inclusions that include
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Lewy body-like lesions as well.
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So they both have Lewy bodies.
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One is intracellular, the other is extracellular.
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The Lewy Bodies and Lewy Body Dementia
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contain neurofilament proteins
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and ubiquitin proteins,
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and it accounts for 15% of all dementias.
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Some say that it's the second most
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common dementia after ALZ,
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although others might argue that frontal
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lobar dementia is slightly more common.
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The posterior cingulum tends to be preserved
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especially on specked in LBD,
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whereas the Myoinositol or Mi peak in spec is
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elevated in ALZ.
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Not so much in Lewy body disease.
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A couple of final take-home points.
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Clearly, there is imaging overlap between PD,
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Parkinson's Disease and dementia with Lewy bodies.
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They both get dementia,
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but in Parkinson's disease,
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motor symptoms predate cognitive symptoms
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most of the time, in fact,
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more than 90% of the time by approximately
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twelve months.
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Another differentiating feature
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that you could use PET for,
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especially amyloid staining PET,
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is that beta amyloid is found
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in dementia with Lewy bodies,
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but not in classic Parkinson's disease.
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In Alzheimer's disease,
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and in Lewy Body dementia,
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they both may have amyloid uptake on PET scanning
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using agents like the Pittsburgh agent and others.
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So in summary,
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cognitive decline early on,
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favor DLB,
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cognitive decline 12 months or more later,
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favor Parkinson's disease,
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amyloid staining favors dementia
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with Lewy bodies or ALZ
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over Parkinson's disease.
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