Interactive Transcript
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This was a very valuable teaching case in an
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individual who presented to the emergency room with
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a two-week history of a left-sided Horner syndrome.
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I was reading this case with the fellow,
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and it was a patient that had quite a
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bit of pathology on the flare scan.
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What we noticed was that there were multiple white
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matter lesions that were identified in the
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periventricular and subcortical region in a pattern
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that was suggestive of multiple sclerosis.
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The patient did not have a history
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of multiple sclerosis.
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So as I was going over this case with the fellow,
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I said, well,
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we should be very careful about demyelinating
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plaques near the hypothalamus,
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which might account for the patient's Horner
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syndrome or around the third nerve nucleus.
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And we were going over the anatomy of the third
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nerve nucleus in the periaqueductal region
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and looking for demyelinating plaques.
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And I was waxing poetic about MS and how
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it could cause a Horner syndrome.
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The next study was the cervical spine
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and the cervical spine examination.
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I was again talking about how the neurons that lead
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to Horner syndrome may extend into the cervical
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spinal cord, and in particular,
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you wanted to be careful about the C7-T1
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level. So we looked at the cervical spinal cord.
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We saw that there was a little bit of expansion of
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the spinal cord here at the C7 level and then
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went on to the axial scans looking for demyelinating
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plaques. And as you can see,
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there's some bright signal intensity that occurs in
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the midline of this patient and then off to the
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right side in the lateral aspect of the spinal cord
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and then proceeding down even into
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the lower cervical spine.
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We were looking at the C7-T1 level and wondering
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whether there was a demyelinating plaque at the C7-T1
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level on the left side that could account
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for the patient's Horner syndrome.
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Here's the first rib identifying the C7-T1 level
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on the left side. So I was saying, well,
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we have multiple sclerosis,
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we have demyelinating plaques,
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we have something potentially in the periaqueductal
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region. We have something down to C7-T1 level.
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All of these could cause a Horner syndrome.
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But the patient also had an MRA.
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So on the raw data of the MRA,
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I was commenting to the fellow that we should be
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careful to look for an aneurysm which may occur
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at the posterior communicating artery,
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which might affect the third cranial nerve.
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And we sort of spent a lot of time looking at the
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posterior communicating artery and wondering whether
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there was a little bit of an aplasia here.
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So in the end, we read this out as a new
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diagnosis of multiple sclerosis
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with demyelinating plaques,
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which could potentially explain a Horner syndrome,
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and recommended that they look at the
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different first-order, second-order,
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and third-order neurons for the determination of
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the type of Horner syndrome.
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The next day,
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I got a phone call from the neurologist,
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and he said, "That was very excellent work.
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I'm wondering, however,
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whether this patient had a dissection of the
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internal carotid artery on the left side,
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which might be present on the imaging.
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And as I went back over the case, sure enough,
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here's the internal carotid artery,
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and here is a bright signal intensity wall hematoma
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of a left internal carotid artery dissection as
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a source of the patient's Horner syndrome.
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In fact, what I missed on the MRA,
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and which is clearly obvious now,
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is here you can see the internal carotid artery and
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the bright signal intensity wall hematoma accounting
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for the patient's Horner syndrome.
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So, of the different causes of Horner syndrome,
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we got the demyelination in the periacoductal
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region, we got the demyelination in the C7-T1 level.
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We looked for the aneurysm at the posterior communicating artery,
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but the classic diagnosis is a carotid dissection,
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which we missed. So did an addendum on the report.
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Fortunately,
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the complication of the carotid dissection,
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which is flipping a clot up intracranially
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leading to a stroke, did not happen.
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This patient was placed on the antiplatelet drugs
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Aspirin and Plavix to prevent potential thrombus
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formation and did well in the hospital.
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And my mistake
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did not account for any complication.
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But this is an example, I think,
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of a great case of what is called a satisfaction of
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search error, a cognitive error in interpretation.
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We looked for various pathologies.
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We found various pathologies,
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including the demyelination,
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the new diagnosis of multiple sclerosis,
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and the possible aneurysm, and we gave up.
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At that point,
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instead of continuing to look for additional
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pathology where the carotid artery dissection
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would have been discovered.
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