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In the discussion of carotid dissection,

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I mentioned that one of the symptom complexes

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that we should consider is the Horner syndrome.

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The classic description of the Horner syndrome is miosis,

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ptosis, and facial anhidrosis.

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Miosis means that the pupil of the eye is smaller

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on the side of the affected Horner syndrome.

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So if we look at this gentleman,

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what you see is the pupil of the eye on the unaffected

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side is larger than the pupil on the abnormal side.

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Next thing that we notice is that where the lid lies.

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So the lid here is crossing at, you know,

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maybe nine thirty and two thirty on the iris.

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Compare that to the normal side,

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where you have it at like 1 o'clock and 11 o'clock .

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So this eyelid is lower,

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accounting for what we call Ptosis.

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Now, facial anhidrosis refers to the absence of sweating.

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So if we take this person over here,

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we notice that the eyelid is lower.

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So there's Ptosis.

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We notice that the pupil is smaller on the left side,

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and you see that the patient is sweating on the left side,

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the normal side. But on this side,

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there is no sweating.

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So these three symptoms are the classic

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symptoms of a Horner syndrome,

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and the clinical evaluation of the patient certainly

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trumps the imaging evaluation of the patient.

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So let's talk about the imaging evaluation of the patient.

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Let's talk about the imaging evaluation of the patient

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with Horner syndrome. As I mentioned,

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carotid dissection is one of the etiologies of a Horner syndrome.

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However,

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additional abdominalities that can account for a Horner

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syndrome extend from the intracranial compartment,

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particularly the hypothalamus,

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and go down into the cervical spine, and

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then back around into the carotid sheath.

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And these are the different order neurons

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that are associated with a Horner syndrome.

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So although we recommend a CTA, it's true that other pathology,

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either in the brain or in the cervical spine,

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may lead to a Horner syndrome.

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And for that,

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we would require a brain and a cervical spine MRI scan.

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Finally, at the lung apex, in this case,

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you see a Pancoast tumor.

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You may have a tumor that will affect the C7, T1,

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C8 ganglion region that can

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also lead to a Horner syndrome.

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So here is the diagram of the pathology and the

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neurons that can affect the Horner syndrome.

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We're going to start here

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in the posterolateral thalamus.

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And the first order neuron will go down through

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the brain stem into the cervical spine where

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it will cross here at the C8 T1 level.

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The second neuron is from this ganglion here

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at the C8 T1 level, will extend across

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and over the lung apex in the lower neck.

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And then we'll have a communication here

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at the superior cervical ganglion.

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Notice where the superior cervical ganglion is.

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It's just above the carotid bifurcation and it's in close

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association with the sympathetic nervous system

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plexus that surrounds the carotid artery.

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This is usually occurring at about the C4 level.

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So from the C4 level superiorly, you see that we go

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back up along the carotid artery and into the sympathetic nervous

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system plexus that leads to the pupil which will account for

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the Ptosis and Miosis, and I guess not the anhidrosis,

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which would occur right here at the superior cervical ganglion.

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So you can have disease in the hypothalamus, in the brain stem,

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in the cervical spine, at the lung apex, and then up and around

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the carotid sheath, that can lead to a Horner's syndrome.

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Here is an example of a vascular study with arteriogram, showing

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a patient who has dissection of the internal carotid artery

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with fibromuscular dysplasia and irregularity of that internal

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carotid artery, accounting for the Horner syndrome dissection.