| Identifier |
Pharmacologic_testing_for_Horners |
| Title |
Horner's Pharmacological Testing |
| Creator |
Andrew G. Lee, MD; Aleena Karediya |
| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (AK) Class of 2022, Baylor College of Medicine, Houston, Texas |
| Subject |
Neuroanatomy; Pathology; Horner's Syndrome; Signs and Symptoms |
| Description |
Dr. Lee lectures medical students on Horner's syndrome and its pharmacologic evaluation. |
| Transcript |
We're going to be talking about Horner's syndrome and specifically we're going to be covering the pharmacologic evaluation. This is mostly for your test's purposes because in the real world, we have moved away from pharmacologic testing and just imaging the entire sympathetic axis. So just by way of review, the sympathetics of the eye is a three-order neuron arc starting from the hypothalamus and descending posteriolaterally down the brainstem all the way to down the spinal cord to the C8/T2 level, the ciliospinal center of Budge. This exits from the spinal cord, arches over the apex of the lung, and in that location a tumor called a Pancoast tumor can produce Horner's syndrome. Then it rises up the sympathetic chain passing without synapse to the inferior middle cervical ganglion to synapse in the ganglia of the second order neuron which is called superior cervical ganglion-that is usually at the level of the jaw. Then, onto the internal carotid artery, it goes up and back into the head and in the internal carotid artery to the cavernous sinus, a short little piece on sixth , and then the subdivision one through the superior orbital fissure to the target. The sixth nerve is particularly interesting because six and Horner's syndrome is known as the Parkinson's sign. That is a very good cavernous sinus sign. So we know we have a three door arc: the central preganglionic primary, the secondary pre ganglionic, and the third on our postganglionic. So when we're dealing with Horner's syndrome we're usually dealing with an anisocoria and assuming it's unilateral we have a little pupil and a big pupil. So the first thing we want to do is make sure that the big pupil reacts to light and also that the little pupil reacts to light. So if the light reaction is good, then we know that we're either dealing with a physiological anisocoria or Horner's. So the way that we're going to determine that is look in the dark. In the dark, a normal pupil will dilate, so the anisocoria will be greater in the dark than in Horner's syndrome because the normal pupil will be dilating the smaller pupil (the miotic pupil will dilate as well) and there'll be a dilation lag-that is, there'll be a lag in the time for the dilation of the Horner's pupil and 10 seconds vs. 15 seconds vs. 20 seconds. The pharmacological testing of the sympathetic pathway depends on the use of sympathomimetics. We have various sympathomimetics that bind directly to the receptor, and indirect sympathomimetics which do not bind directly to the receptor. They work by indirectly stimulating release or inhibiting the reuptake of norepinephrine at the junction. So the most common indirect sympathomimetics that we have are cocaine, which works by inhibiting the reuptake of norepinephrine of the junction and hydroxy amphetamine so these two drops are used in the determination of both the Horner's syndrome and localization. So if we put cocaine into an eye that has been innervated from a sympathetic lesion at the Horner's syndrome it won't dilate as much as if we put it in the normal pupil. And we need to put it the drop in both eyes so that we can use the other eye as a control. So if we have a post cocaine drop anisocoria that's greater than about point 8 millimeters you can have some high sensitivity and specificity that this patient has a Horner's syndrome on the side of this molecule. Cocaine therefore can only tell us if we have a Horner's syndrome or not, it doesn't tell you whether you're in the first the second or the third neuron. in contrast, hydroxy amphetamine which is also an indirect acting sympathomimetic but it acts in a different mechanism it stimulates the release of norepinephrine at the junction and therefore is a test of the integrity of the third-order drive so if we put hydroxy amphetamine into a patient who has already had a cocaine test proving that it's a Horner's and it does dilate as well then we know the problem is in that third ordered neuron. If however we have a cocaine test that's positive and the hydroxy amphetamine dilates the pupil equally in both eyes then we know we're dealing with a pre ganglionic Horner's syndrome, either first-order or second-order neuron borders. The hydroxy amphetamine test however cannot differentiate between a first-order neuron and a second-order neuron there is no test with drops that you can determine that because the drops are working at the eye and so we can only test the integrity of the third-order neuron and that means we can only tell the difference between a pre ganglionic and a postganglionic using hydroxy amphetamine. You cannot tell first versus a second that has to be done with clinical testing or age. Now we have a different indirect acting sympathomimetic that we used to confirm the Horner's syndrome and that drug is a lot easier to get and to use than the controlled substances cocaine and amphetamines that drug is called Apraclonidine. Apraclonidine is a direct acting sympathomimetic that has differential effects on the alpha 2 and the alpha 1 pathway. As you know the alpha 2 is a presynaptic feedback control mechanism on the sympathetic innervation and alpha 1 is the postsynaptic and so just like the drug clonidine which is used for hypertension even though this drug clonidine is a sympathomimetic, its alpha-2 effect allows it to be used this an antihypertensive. Likewise, apraclonidine has an alpha-2 effect, and even though is it is sympathomimetic in normal people, apraclonidine will either do nothing, which causes slight constriction of the pupil. Under conditions of the Horner's syndrome, however, we have denervation, supersensitivity and upregulation of the postsynaptic receptor, in this case alpha-1, so apraclonidine will dilate a Horner's pupil and constrict slightly the normal eye or do nothing and that often produces a reversal of the anisocoria. It is this reversal of the anisocoria we're looking for, or the dilation of the miotic pupil, that confirms that this a Horner's syndrome using apraclonidine. So now you should know that we can use cocaine and apraclonidine to confirm the presence of Horner's syndrome and differentiate it from physiologic anisocoria and we can use the hydroxy amphetamine once we have confirmed its Horner's to differentiate whether we are dealing with a preganglionic primary or second order neuron from a tertiary third-order neuron post ganglionic lesion. and if you can't remember all these drops in the clinic and in the emergency room setting, we're just going to image the entire axis from the hypothalamus all the way down the thoracic t2 in the Chest. In the ER, that's a CT CTA of head and neck to make sure it's not a carotid dissection or in the outpatient setting MRI and MRA hypothalamus to T2 of the chest including of course the apex of the lung. So you should now know about Horner's syndrome and pharmacologic testing. |
| Date |
2019-03 |
| Language |
eng |
| Format |
video/mp4 |
| Type |
Image/MovingImage |
| Collection |
Neuro-Ophthalmology Virtual Education Library: Andrew G. Lee Collection: https://novel.utah.edu/Lee/ |
| Publisher |
North American Neuro-Ophthalmology Society |
| Holding Institution |
Spencer S. Eccles Health Sciences Library, University of Utah |
| Rights Management |
Copyright 2019. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright |
| ARK |
ark:/87278/s6fz1pfp |
| Setname |
ehsl_novel_lee |
| ID |
1403732 |
| Reference URL |
https://collections.lib.utah.edu/ark:/87278/s6fz1pfp |
