 So I didn't finish my title actually, but so it's kind of like neuromuscular causes. It's like motor in plate and then just other kind of restrictive processes as well. So kind of one of the top ones that we think of is myosthenia gravis. So it's characterized clinically by muscle weakness, fatigue, common ocular complains for diplopia and ptosis. So this condition, you know, classically involves a skeletal and not visceral musculature. So pupil and ciliary muscles should be unaffected. Ikeloin involvement is common and it can be the initial complaint. So it's something we kind of have to pay attention to and always have on our radar. There's antibodies to the acetylcholine receptors in the motor in plate that reduce the number of receptors available for transmission of motor signal. And then they get cut off, but the ophthalmic kind of characteristic. So variability of muscle function within minutes, hours, days or weeks. And so I was seeing a patient in neuroclinic last year and I presented to Dr. Katz and then he went in and got totally different measurements and looked at me like I was an idiot. And then he goes, oh, what's the thing that makes residents look like idiots? Said myosthenia, that's what it was. So it can like vary from when you go in the room, somebody else goes in the room. It makes it really difficult when you're trying to present the patient. There's remissions and exacerbation. So it's not kind of a tonic process. It can vary in terms of body temperature, infection or other kind of insults. You can have onset at any age. There's ptosis, it can be unilateral or bilateral and it can shift from side to side. The extraocular movement involvement follows no set pattern. So it can be a gaze palsy, nice diagnosis in your nuclear ophthalmoplegia. And then in terms of OCAPs, it's not common, but kind of more common than you'd expect in association with dysthyroidism. So it goes the same way patients with dysthyroidism can also have myosthenia. So kind of the signs that we see typically lead fatigue with sustained up gaze, Kogan lead twitch if you have people look down for 10 to 15 seconds and then look up to primary position, you can have an overshoot of the eyelid. Enhanced ptosis, so this is one you look at in the plastics clinic with Dr. Karam all the time. So if the ptosis is asymmetric, they might convictivate their frontalis muscles to kind of help lift the lid. So that can produce an apparent lip retraction on one side. If you elevate the lower eyelid, that causes the retracted eyelid to fall. And so that's, you know, especially if you're doing like a unilateral external and libator resection, that's one thing you kind of check before you actually start cutting. And then myosthenia ptosis is often associated with orbicularis weakness too. So checking your orbicularis strength can be good. Thyroid eye disease is the next one. It's a restrictor myopathy. So most commonly kind of middle or older age patients, you get a lymphocytic and plasmocytic chronic infiltrate of the extracular muscles. So that gives you a demon and activation of fibroblasts. So there's production of acerbucal polysaccharide and fibrosis. And so like you'd expect, it can give you a variety of defects. So you can have what appears to be an elevator palsy. So it's a superduction deficit due to the fibrotic shortening of an inferior rectus. You can have AB dection weakness due to involvement of the medial rectus mimicking a cranial nerve 6 palsy. And you can have really anything else too as thyroid disease. And so it's always on your differential. The kind of classic way to memorize the frequency of the muscles involved is that I'm slow. So inferior is more common than medial is more common than superior is more common than lateral. Yeah. So some of the additional findings you can get proptosis, lid retraction, lid lag on down gaze, which is von Grafis sign is the eponym, kind of conjunctival injection or chemosis. Always make sure you're looking at the cornea, just they can get pretty bad corneal erosions or ulceration even. And then in the books, it's like 5% develop optic neuropathy due to compression of the orbital apex due to enlarged extracular muscles. So one another thing that comes up on Ocaps is kind of the order to proceed with with surgical repair. And so kind of the first thing is decompression and then strabismus and then eyelid surgery last. The eyelid surgery can also change the position of some of the extracular muscles that have been worked on during strabismus and that sort of thing and worsen any strabismus or anything like that. So that's why you did the lids last. This is for some reason specs didn't get capitalized here, but in terms of kind of grading classification, one of the or one of the mnemonics they've come up with is no specs. And just as a way to to grade the severity of thyroid eye disease. And so it starts off, you know, there's no size or symptoms. Then the next one is only signs of lid retraction, lid lag or a gaze stare. Then you can have soft tissue signs and symptoms, which this actually spells out relief. So resistance to retropulsion, a deem of the conjunctiva caruncle, lacrimoblain enlargement, injection of the rectus muscle insertions, a deem of the eyelids or fullness of the eyelids. Next is proptosis, extracular muscle enlargement and corneal involvement and kind of the most severe sight loss due to object nerve compression. So one other thing that comes up with surgical treatment of thyroid eye disease is the type of surgery you do in terms of the muscle surgery. So do you do a recession or a resection of muscles? Thyroid eye disease. What sort of recess? Correct. So any in general, not just thyroid disease, but any restrictive condition should be recessed and not resected because that can actually worsen your restriction. So just remember that if you have restriction in general, including things like intractively for your rectus, it should always be recessed and not resected. So the next one that I was going to talk about was this is a busier side, but chronic progressive external ophthalmoplegia. And so this is kind of a group of different conditions. So they're overall characterized as an insidiously progressive, symmetric immobility of the eyes. There's typically ptosis, orbicular sweetness, and then spearing of the pupils. The movements remain limited with doll's head and caloric stimulation. So some of the ones that they talk about is oculofaryngeal muscular dystrophy. On OCAPS, kind of the association is like French Canadian families. And then there's this polyadenylate binding protein, nuclear one gene that's been characterized in this condition. There's dysphagia, so the oculofaryngeal portion, and then the family history of ophthalmoplegia. Current seer is the one that we're probably most familiar with. So it's a triad of CPEO. There's cardiac conduction deficits, which the OCAP likes, because that's one thing that can kill people and they want to make sure you're getting that on boards and everything. And then pigmentary retinopathy. And then there's also the CPEO, ophthalmoplegia plus conditions, which is CPEO with some other additional findings. So it can be pretty variable. So elevated CSF protein, you can have spongiform degeneration of the brain or brain stem. It's a slowed EEG and then hearing loss. And then on muscle biopsy, so either ocular or limb, you should see the ragged red fibers. So mitochondrial accumulation between the myofibrils are beneath the plasma in the brain. Myotonic dystrophy is one that don't, I didn't ever really think of as much in terms of double vision, but it can. So it's autosomal dominant muscular dystrophy, in which myotonia is accompanied by dystrophic changes in other tissues. So trinucleutide repeats on chromosome 19 or chromosome three. Kind of the classic things that we think of in terms of the ophthalmology would be the early cataracts, the Christmas tree or polychromatic cataracts. But you can also get my bilateral ptosis. They can have a progressive external ophthalmoplegia. They can have myotonia of lead collusion, gaze holding, orbicularis weakness, myotic pupils, and then retinal pigmentary degeneration. I put this in here and we'll get, this is more kind of in the headache category, but one thing was kind of ophthalmoplegic migraines. So migraines can also give you double vision, binocular double vision, and it can mimic a third nerve palsy. I guess classic you to expect this to resolve, but this function could be permanent. And it usually kind of starts, the cranial nerve finding usually starts to come on after the headache abates, or as the headache starts to abate. This was, there were some other things, because this was kind of the garbage can one for double vision. So I didn't talk about, or I'm not going to talk about, you know, entrapment from orbit fractures, but common things being common, we're in Utah and nobody wears helmets when they drive their ATVs off cliff. So always think about that. You can have like a silent sinus syndrome. There's that sort of thing. Orbital inflammatory syndrome can also give you double vision. But, you know, and all the ones that I've seen, that's never been the presenting complaint is my eyes are doubled, so their eye is killing them and that's super red and bolting out of their head. But those are other things that can give you double vision. This was, you know, one that I've actually only seen like twice myself. So Brown syndrome or superior oblique sheath syndrome, it's limitation of elevation of the eye and adduction due to restriction of the superior oblique tendon and the trochlea. Elevation and adduction is usually normal or near normal. So the affected eye is usually hypotropic and then the patient adopts a chin up and then face turned away from the affected eye. And really to make this diagnosis for the restriction within the trochlea, you need to do four stuctions. So the two that I've seen have been traumatic. Like one was a kid that got stepped on pretty bad and had a bunch of bad facial fractures and the other one was actually kind of at the beginning of this year. One we got, or it was technically last year, when we got nailed in the face with the fin sludge and she had a pretty big hematoma on top of the glow. But the eye was hypotropic and so she ended up seeing patellin. She disinserted her levator and I think he was going to fix that. But then she was kind of persistently hypotropic as well and saw Hoffman. Oh you did? How'd it go? Awesome. So was it, was adduction positive? Awesome. So yeah, it was one, you see a lot more test questions on this, I guess, than you actually see it, but it does happen, it turns out. So I thought that was kind of cool to see it. Just to mention something about Brown, to me at least, Brown syndrome isn't really a traumatic syndrome. So when I think of Brown syndrome, it's usually restriction without trauma. And so the one thing to allow in children to come in with the findings of Brown syndrome, and usually, you know, you do have occasional adults, but it's generally children, is sinusitis. So I guess for me with Brown syndrome or trauma, well, it's not true restriction and it's not true trochial abnormality per se, because there's trauma to explain that. So often the cases that you will get presented with Brown syndrome are actually just kind of spontaneous to both of you and children, and then you have to differentiate between a Brown syndrome and fear of weak palsy and one thing to remember and like, you know, if this than that, I think if you see Brown syndrome, think about CT, sinus is true, sinusitis is true. And then this is the last one I had in here was superior of bleak myocymia. And so you get the paroxysmal, rapid, vertical, and torsional movements of the eye. They're usually super small and then can often require this slowly to visualize. And you can kind of precipitate this bias in the patient's to the direction of the suit, the effect of superior of bleak and the treatment with these departments would be that sort of stuff. Anything else that I should have included? The only other thing is neuro-myotonia. Oh, yeah. And neuro-myotonia is usually, it can be third nerve, neuro-myotonia, but the muscle will go into kind of spasm and often what happens is it can kind of like get stuck for a period of time, they get better. The typical scenario is the person has had radiation for a pituitary tumor and that's one of the things that you can see it after. But I've seen it just spontaneously occur as well. It's like a spasm of one of the muscles, like usually the urectus, it could either be urectus, it can no make light of six nerve closing for an intermittent six and you can also treat that with neuro-myotonia as well.