 I'm Brandon. I'm one of the neurosurgery PGY ones. I was able to rotate over here for a month. A couple of months ago, I worked predominantly with Dr. Warner, Dr. C, Dr. Katz, and enjoyed my rotation and thankful for the opportunity to come and present. I have a patient, Dr. Warner, that would like to present a 49-year-old male, had a history of anxiety by the cataracts, diabetes on the foreman. He also likes to have a good time. He drinks 10 shots of liquor a week, which I think is probably an underestimation. He's a pack-per-day smoker. He was in New Orleans visiting in April of 2018. He got in a drunken bar fight. He sustained a spartan kick to the chest as part of that encounter. He had immediate onset of chest pain following. He went to the local ER in New Orleans, which was fortunately negative for any kind of traumatic injury. However, as an incidental finding on his chest x-ray, you can see on the right lung about in between the 6th and 7th River. So there's this small pulmonary nodule that he was told about and told that he needed further work up for, despite being otherwise okay from his trauma. So he underwent a CT of the chest, which showed right hyaluronic subcrinal lymph adenopathy. He underwent a bronchoscopy a couple of months after his initial presentation and had an acid fast culture performed as part of that bronch, which was positive for multi-drug resistant tuberculosis. This guy's just all around really healthy. He was started on lanaisalid SNIs and amontiloxin, given the multi-drug resistant scene on the bronchoscopy culture. So fast forward to February and early March of 2019. So approximately 10 months or so after he had been initially worked up and treated for the tuberculosis, he started noticing visual changes. These changes initially manifested as colors appearing brighter and more prominent. He said specifically that whites and yellows were more prominent. This started to progress to blurry vision that personally works to the point of within one week of initial onset that he was not even not able to see objects within even several yards distance from him. He notified the health department and said, I'm going blind. What's going on? They stopped his lanaisalid and isonized it right away. He had a full neurologic workup, was admitted to the neurology service inpatient in April 2019. He had an MRI done, this is a coronal view T1 post contrast. You can see on the left optic nerve, there's a little bit of hyperintensity there. The radiologist comment said, we don't know if this is just vascular syndrome, if this is true, optic nerve enhancement. So not really sure. He got IV steroids and was discharged. At this point he had been off antibiotics for some time. Vision didn't significantly change with the IV steroids, at least noticeably within the first several days after that. He underwent a lumbar puncture, had elevated protein, otherwise the lumbar puncture was pretty unremarkable. His CSF was negative for acid fast culture and VDRL. Sorry, this text is pretty small, but essentially his exam, the visual acuity on the right, he was 20 over 150 on the left, 10 over 200 when we saw him in the clinic. He had some subtle mild edema, bilaterally of the optic disc, in some typical exudates, but otherwise was fairly unremarkable with the exception of his poor visual acuity. This was, notably, significantly improved since the antibiotics had been stopped. As far as his visual field testing, you can see here that he has these superior nasal scutomas, they sound patchy distribution, partial vision loss, that was also improved from his initial onset. And I'll just kind of fast forward here, you can see he has some mild edema, bilaterally, you can see it there based on his OCTs. But I think what's important here is figuring out what the cause of his toxic optic neuropathy is. And he was on a couple of different agents that could explain this, and I think important, and I didn't include this in the slides, he had a full neurologic workup when he was admitted as an inpatient, including vitamin B testing. He was deficient in thiamine, which, you know, is not a huge surprise there. So I think given that these drugs affect, specifically as an eyes it affects the vitamin B levels and the metabolic pathways that require vitamin B, my opinion is that that's the most likely offending agent, but we'll kind of get more into that later. So the adverse events that are associated with eyes and eyes of use include peripheral neuropathy, hepatotoxicity, and optic neuritis. We give vitamin B6 to decrease the risk of these, although it doesn't entirely eliminate that, especially in someone like our gentleman who's probably just pan vitamin deficient. And his visual fields, classically you take on the appearance of bitemporal hymenopic scutomas, that's classic, that's not necessarily a hard and fast rule. With lanazolid use, adverse events include myelosuppression, peripheral neuropathy, and optic neuritis. So there's some overlap there between the two antibiotics. However, with lanazolid, the difference is this is a relatively new antibiotic. The mechanism is unclear as far as why it causes neuropathy, but it's thought to be due to some form of mitochondrial metabolism disruption. And since, as we all know, the optic nerve is highly modulated, has a high metabolic activity that if there's some element of mitochondrial metabolism disruption, that would preferentially affect those highly modulated nerves. And both eyes and eyes are induced, and lanazolid induced, toxic optic neuropathy improve with cessation of the drugs. And here's kind of a time course from a publication that I found regarding how the visual changes improve. You can see the visual acuity on the y-axis and time on the x-axis. It does take time. I think that's the critical thing. If you stop the drug, it's not going to be like the next day. They can suddenly see again. As you can see, based on these curves, you're looking at months to a year before you get your visual acuity back to baseline levels prior to drug initiation. And you can see that in this case, what I thought was interesting is that they used methylprenizolone, IV steroids after cessation of lanazolid therapy. So again, the steroids, if on the imaging as in our patient, there may or may not be evidence of optic nerve enhancement, or there's some concern of active optic nerve edema, IV steroids can be helpful. But really, the most important thing is stopping the affiliation on this. Just an interesting thing that you see, they marked that as logmar. Do you see that? And it actually has to be decimal. Because what's 1-0 logmar? 2,200. See, it says logmar. Basically, we've been pretty far. Good logmar is the first one. Good logmar is 0.00. And that's a decimal. So this is the first case report I could find. I believe this was in JAMA, where axonizid was first reported as a cause of optic neuritis and atrophy. So this is not a new concept. And in their initial report, they reported two cases by lateral optic nerve atrophy. And in both cases, discontinuous of the drug brought reversal of the process. So this has been known about for decades. This is not a new concept, not surprising that our patient might develop such deficits, especially in light of his medical comorbidities. What is not as well studied though is lanazolid. I was able to find a few case reports, really. There's not a whole lot of great information given that lanazolid is fairly new on the antibiotic circuit. Its mechanism, again, it inhibits the ribosomal subunits of the mycobacterium that inhibit bacterial translation. And so it's not really clear how that particular mechanism affects mitochondrial metabolism, especially since that subunit is specific to the bacteria. But it's a similar kind of presentation to the axonizid-induced optic neuropathy. And again, as I mentioned here at the bottom of the abstract, they experienced initial rapid partial improvement and subsequent gradual, almost complete recovery. So again, that's the key in these cases. So as I've kind of mentioned before, what's kind of interesting is that the axonizid specifically affects mycolic acid synthesis in the mycobacterium, which indirectly interferes with the NAD-NADH metabolic pathway, which can explain why these metabolic reactive nerve circuits would be preferentially affected. As I mentioned, it's not really clear how the lanazolid affects the mitochondrial metabolism. So that's all I had. So thanks for having me on service. I appreciate it.