Interactive Transcript
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Let's quickly review where we are in the
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assessment of intradural intramedullary lesions.
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We started off by saying that the most common
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etiology for a cord lesion is spondylomyelopathy,
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that is, cervical spinal stenosis or thoracic spinal
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stenosis leading to cord injury.
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Let me just comment about the etiology of the
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cord injury with spondylomyelopathy.
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It's kind of unclear where the cord injury is
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from direct traumatic compression by the
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degenerative change by stretch injury in which
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the cord is fixed by the spinal stenosis and
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then through the activity of the neck,
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you stretch that cord and injure it on
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that basis, or a vascular etiology.
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Even among the vascular etiologies,
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some people say that it is a venous outflow
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ischemic injury to the spinal cord as opposed to
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an arterial injury to the spinal cord from
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compression of the anterior and posterior spinal
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arteries or the small arteries in the spinal cord.
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However, it's pretty uncommon for us to see a spinal
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cord infarct from spinal stenosis.
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That would be very unusual.
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The second category that we talked
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about were neoplastic lesions,
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and we went through various histologies.
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We then just saw multiple cases of demyelinating
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disorders, and I want to review that quickly.
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So the most common of the demyelinating disorders
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in the spinal cord will be multiple sclerosis,
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this far outweighs neuromyelitis optica.
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So cord lesions associated with multiple sclerosis,
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which is the most common demyelinating disorder in adults,
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occur in about one-third to one-half of cases.
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throughout the lifetime of the patient.
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And the initial evaluation of the patient with
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multiple sclerosis usually does include brain,
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cervical, and thoracic spine.
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Please do not recommend evaluation of the lumbar
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spine since MS does not affect the nerve roots.
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For multiple sclerosis,
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we are mostly focusing on our STIR and T2
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weighted images because demyelinating plaques
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in the cord, just like in the brain,
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may or may not show contrast enhancement.
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When we see demyelination in the spinal
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cord with short segment lesions,
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we usually recommend to check the brain,
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in those cases, to exclude periventricular,
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subcortical, or infratentorial lesions,
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which are the other manifestations of
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dissemination in space by McDonald criteria.
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Here is our patient who has upper extremity
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weakness and has a stereotypical lesion
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associated with multiple sclerosis, that is,
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a short segment lesion
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that is located in the posterior
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aspect of the spinal cord.
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MS does favor the posterior columns.
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which may or may not be associated
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with contrast enhancement.
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And on the axial scan, we see that it is a
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small lesion as favoring, in this case,
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the posterior aspect of the spinal cord.
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There likely is another lesion down below.
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Multiple sclerosis of the cervical spinal cord.
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We would recommend getting an MRI of
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the brain and the MRI of the brain.
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We see that this patient has periventricular
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lesions, as well as a lesion in the left internal
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capsule. And more importantly,
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we see a small lesion in the subcortical white
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matter which is showing contrast enhancement.
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Therefore, dissemination in time.
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In the lower spinal cord, we see additional
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lesions that are not expanding the spinal cord
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and likely would not show contrast enhancement.
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Transverse myelitis is a manifestation
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of neuromyelitis optica.
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Transverse myelitis should be considered
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a diagnosis clinically,
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but not a specific pathologic diagnosis.
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Transverse myelitis may be caused by any number
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of abnormalities, including neuromyelitis optica,
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but also
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infectious etiologies, as well as ischemic etiologies.
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Why is this case not multiple sclerosis?
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It does not show small lesions,
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short segment lesions.
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It's a longitudinally extensive transverse
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myelitis. By longitudinally extensive,
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we usually say it spans greater than three segments.
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In this case, it's going from cervical even
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into the thoracic spine.
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This might be a manifestation of neuromyelitis optica.
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The next step would be to scan the orbits as
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well as the brain to identify whether or not the
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patient has optic neuritis and the stereotypical
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NMO brain lesions at the area postrema of the
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brainstem or along the hypothalamus and
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favoring the periaqueductal and posterior
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fossa structures over the supratentorial structures.
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Here is an example of a patient who
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who has NMO, Neuromyelitis Optica Spectrum disorder,
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NMOSD, we see a patient who has a long segment
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lesion in the spinal cord, going over multiple levels
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That shows contrast enhancement along the left
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lateral aspect of the lesion, with a relatively
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subtle lesion on the T2-weighted scan.
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And in addition, has a bright optic nerve, which is showing
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contrast enhancement,
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compare that with the normal optic nerve on the left side.
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When we have a patient who has transverse
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myelitis and we find no etiologies, remember that
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we have to think about demyelinating disorders,
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ischemic disorders, infectious disorders.
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I should mention autoimmune and
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collagen vascular disorders.
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So things like scleroderma or lupus can cause
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transverse myelitis, as well as vasculitis.
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When all those get ruled out,
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we come to the diagnosis of
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Idiopathic Acquired Transverse Myelitis.
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You'll see the acronym IATM
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for Idiopathic Acquired Transverse Myelitis.
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This may be the first manifestation of multiple
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sclerosis in what's called clinically isolated
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syndrome. Or it may occur in and of itself.
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Approximately 30% to 40% of patients
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who present with IATM, ultimately
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down the line, will carry the diagnosis of multiple sclerosis.
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But you can have it just as an isolated
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abnormality, similar to optic neuritis, which
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may occur in an isolated fashion.
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Enhancement with IATM is variable,
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but usually it's not very avid enhancement.
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