 I'll talk about anisechoria and I'll give a terrorist presentation as well because she's not here right now. So when we think about anisechoria and pathology we think about anisechoria first, whether the anisechoria is greater in bright light or anisechoria greater in dim light. So and I'll go over all of these but in bright light the pathologic pupil is usually is the dilated one and some of our differential includes an ADs, a third nerve, a palsy, pharmacologic medriasis and direct damage to the iris sphincter. In these situations in dim light the anisechoria decreases so they look more equal. In anisechoria that increases in dim light some of the differential includes Horner's syndrome and pharmacologic myosis. At least in this review they also say physiologic anisechoria. This is a very important chart from the BCSC which I'll go over little by little but again for anisechoria that is same in dim and bright light it's usually physiologic anisechoria. I'll talk first about this pathway anisechoria greater in bright light before I talk about the last part. So a couple of points for physiologic anisechoria. The difference in the pupil area size is usually anywhere from 0.4 to 1 millimeter. Greater than 1 millimeter we have to think about probably not physiological anisechoria. In this first pathway that we see anisechoria greater in bright light we first ask whether there is iris damage. And if there is an iris damage we can probably see it anatomically. So the first question is iris anatomy normal. If it's not then you know there's iris damage. One thing that we can get tested on as well is that it does not respond to pylocarpine and mimics pharmacologic medriosis as well but that's why we always look first. The other couple of things other signs of its sphincter damage by notches in the pupillary margin or transillumination defects near the sphincter muscle. Next is pharmacologic medriosis. There's no response to light and near stimulation. 1% or 2% will not constrict pupils that are pharmacologically dilated. For example we can have even segmental iris policy there's a good movie and novel about this and it is not super sensitive to either the 0.1 pylocarpine or the 1% or even the 2% and that's how we would diagnose pharmacologic medriosis. Some of the sympathomimetics include cocaine epinephrine and phenylpherin. Some of the parasympatholytics are the atropine tropicomide and scopolamine and we have to think about adrenergic medriosis as well but in here what we can get tested on is that accommodation is not impaired in these. The next in line is adrenergic medriosis. For adetonic pupils we really don't understand what's the path of physiology but people think about the damage of the ciliary ganglion and we've studies have shown that there's reduced ganglion cells. Let me tell you a little bit about the natural history of adetonic pupil and the acute face it is both pupils are poorly reactive to light and accommodation. For the next few months there is still light dissociation but constriction could be a little better but the redilation phase is still slow. This can be caused by several things including surgery, trauma, infection, inflammation or ischemia. This is associated with several systemic diseases including diabetes, chronic alcoholism, neurosophilus, amyloidosis, sarcoid, miller fissure, and charco maritouth. After we rule out all of these things the adiopathic tonic pupil is adi's pupil. The epidemiology is usually 70% of people are women and in their mid-age 20 to 50 years old. It's usually unilateral in 80% but there could be bilateral cases. The Holmes ad syndrome is basically an adi tonic with diminished deep tendon reflexes as well as orthostatic hypertension. And then finally you know to diagnose this 80% have cholinergic denervation super sensitivity to low pilocarpine and so the bigger pupil which is the 80s pupil will become the smaller pupil but we have to wait 45 to 60 minutes. The last thing I'm going to talk about is the third nerve palsy. Third nerve palsy as most of you probably already know is almost always accompanied by ptosis and limited ocular motility. We have to think about an aneurysm at the junction of the internal carotid and posterior communicating arteries. So I think those are the highlights. The next part is anisecoria greater in dim light. So for mechanical anisecoria as well again we can have previous trauma or inflammation that would lead to posterior synechia preventing dilation. We can have pharmacologic meiosis. One of the things is one of the meiotic agents is pilocarpine. So we always have to think about that. The next is Horner syndrome. So the symptoms of Horner syndrome include ipsilateral meiosis, facial anhydrosis and ptosis. The ptosis is because there's denervation of both tarsal muscles which result in a basically a narrow paupupril fissure. Anhydrosis we really don't test clinically but physiologically we get anhydrosis of the ipsilateral face from first or second order lesions. In third order lesions it usually spares the lower face and has anhydrosis in the ipsilateral forehead. And then finally the meiosis part it's slow to re-dilate when lights are turned off. This is just a picture. So for Horner syndrome just always remember that the lesion is always ipsilateral. So the first order neuron is thought to be coming from somewhere in the hypothalamus. It goes down anywhere from C7 to T2 here in the cilia spinal center of budge wallar. The second order neuron goes up kind of comes around and then synapses in the superior cervical ganglion and the third order neurons goes up. Testing for Horner syndrome is very important to know. The first test is a cocaine. This blocks re-uptake of norepinephrine release at the synaptic nerve terminals. It would cause usually pupillary dilation, eyelid retraction, and conjunctival blanching of the unaffected eye. But in the affected eye there is no effect. And so post-cocaine anisocorea of greater than one millimeter is still diagnostic of the Horner's. Just remember for cocaine after you give it there's no change in anisocorea. The other test for Horner's is aproclonidine. This is an alpha one adrenergic agonist which dilates the pupil sympathetically, especially in denervated eyes like a Horner syndrome. In the unaffected eye it has no effect. But in the affected eye there's dilation. So compared to cocaine just remember that anisocorea reverses with aproclonidine testing. The last test for Horner's that we usually don't do in clinic is hydroxyamphetamine. And this basically tries to localize where the lesion is either the first second neurons or presynaptic neurons or the third order neurons. So again this enhances the release of the presynaptic norepinephrine from an intact third order. So in the unaffected eye it causes the eye to dilate because it has normal third order neuron. In the affected eye if the first or second order neurons are affected it'll cause it to dilate. But if it's a third order neuron problem there is no change. Some of the causes of Horner's syndrome anatomically first order could be vascular problems, tumors, demyelination. I can also show other brain symptoms including ataxia, nystagmus and hemisensory defect. For second order neurons problems we can have pancoast tumors, mediastinal lesions, thyroid mass, thoracic aortic aneurysms and brachal plexus trauma. We can have associated symptoms of arm pain, you know for shoulder stuff, cough, hemoptysis, swelling of neck. And then finally for third order neurons it's a carotid artery dissection. This is what we need to think about cluster headache, cavernous sinus lesions, and associated symptoms include numbness and cranial nerve 5 and double vision. With the apoconidine the other thing to look for is the ptosis resolution as well, so not just the anisocorrhea being affected by that so that's a helpful binding. And then the important point to make just in your last slide that you've mentioned is the localization of Horner's syndrome plus S6 balls. That is your like classic classic cavernous sinus so you need to kind of put it away in your mind when you see a six and a Horner's you have to look there. And the last thing that Tara wanted to mention is the Horner's imaging so for central processes and MRI of the brain and upper cervical cord for the pre-ganglionic we have to look at CT chest and MRI of the neck and for postganglionic again MRI of the brain and MRI of the head. And then just the last thing is a think of an internal carotid artery dissection with the painful Horner's syndrome. That's it.