 I give kind of a case presentation from a patient that I saw in the Neurothymology Clinic. This was an 18-year-old young man. So his chief complaint was a two-month history of a black spot in his superior temporal visual field of his left eye. The spot had become gradually smaller over the last few weeks. It was not associated with any other visual changes or any eye pain. Although he did have, when he first noticed the spot, some brief headaches lasting 15 minutes for about the first two days, but those had since resolved. Around the time that he noted the onset of these visual changes, he noticed some tingling in his feet, and that worsened for a little while and then kind of stabilized. So other history, he had a long-standing history of pectus excavatum and he'd recently undergone this placement of what's called a NUSPAR, which sounds like a brutal procedure, it's like a metal bar to try to change the shape of the chest wall. And he unfortunately developed a postoperative staphylococcal infection that was pretty significant, required long-term antibiotic treatment. There was no significant family history. He was a student, didn't have any other remarkable social history. He, at the time that we saw him was on intravenous naphthalone and he previously had long-term IV vancomycin and lanazolet. So on exam his vital signs were normal. His visual acuity was actually normal, 2020 in H.I. He did have a small left aphor and pupillary defect. The intraocular pressures were normal, motility was normal. His stereo was decreased a little bit. Color vision was normal, but he endorsed his mild subjective red dissaturation also in the left eye. The rest of his exam was unremarkable except for his neurologic exam which showed some diminished vibratory sensation in his extremities. So this was kind of his depiction of a, like, AMSLA grid in both eyes, what kind of, what he would see. He did close in one eye versus the other and the visual field defect was in his left eye. So here's some funness photos. You can see a little blurring of the disc margin actually in both eyes. So he had some mild optic nerve edema at this time and it's hard to see in this photograph but he had a couple of spots in his left eye where he had some resolving peripapillary hemorrhage. So the left eye seemed to be a little more effective than the right. He had a visually evoked potential that showed a P100 that was 113, given his young age, this was felt to be a little, a little delayed. Okay, written on there fiber layer OCT scans which showed, actually you can, you can see the mild edema here. As you can see the tracing up above normal in the left eye and you can see the asymmetry between the two eyes. So this is again consistent with the left eye being a little more effective than the right and some mild optic nerve edema. So just kind of thinking about differential diagnosis. You can think about genetic things. This is possible but less, much less likely you could think about a toxic or nutritional optic neuropathy. Of course, there's, you know, infectious or inflammatory possibilities, maybe a demyelinating process. Now, in this case, he had this interesting history of being on these antibiotics for a long time. And so just kind of a little additional history that I didn't want to give like right up front just to kind of give the whole thing away. He was, he was instructed by his infectious disease doctor to stop his lanazolid immediately upon any visual changes. So that happened actually two months before he came to see us. So at the point that we saw him, he, at the point that he experienced the initial visual changes, he'd been on lanazolid for six months. And in the intervening two months, since the time he stopped lanazolid and the time that we saw him in clinic, his visual field defect had improved as we mentioned but it hadn't completely resolved. So actually when he initially had his visual field changes, he went in to see another provider and got a baseline visual field which showed a slight enlargement of the blind spot and at the time we saw him, when he was two months off of lanazolid, again, he had mild symptoms but his visual field had normalized. Okay, so we saw him again three months later. This was five months off of lanazolid. At that point his visual acuity was 2015 in both eyes. There was no evidence of an RAPD, no evidence of residual optic nerve edema and he had complete resolution of his symptoms. Just a quick discussion about what we feel like was the etiology of the symptoms for this patient. So we feel like this picture is consistent with lanazolid-induced optic neuropathy. So lanazolid is a broad spectrum antibiotic first introduced back in 2000. You know, the recommended course for lanazolid is less than 28 days. That's the manufacturer's recommendation. It can be taken orally as well as IV and it's a valuable antibiotic because it has activity against MRSA and penicillin-resistant strep and VRE. So this is kind of one of the big gun antibiotics that the infectious disease folks kind of hold in reserve. And this patient had a very serious infection. You know, he had a staphylococcal infection that had been going on for months. The first two cases of lanazolid-related optic neuropathy were reported in 2003, a 71-year-old female and 45-year-old male. Each of these patients had developed visual changes after a long-term use of lanazolid and upon discontinuing the medication, each patient had a significant visual recovery that neither of them recovered completely. And this visual recovery, the follow-up was like out at five or six months. So again, it took quite a while for things to improve for those patients. Now several subsequent case reports have been published. Almost all of those seem to be linked to extended duration of lanazolid use in months for most patients, although there is one reported case of visual changes consistent with lanazolid-induced optic neuropathy after only 16 days of lanazolid use. Features that are seen with this optic neuropathy are secocentral scatoma, color vision loss, loss of visual acuity, APD, and optic nerve edema, and ultimately atrophy can be seen. But most patients do experience significant visual recovery with the potential of complete visual recovery as occurred in our case after discontinuation of the medication. So the potential mechanism for this optic neuropathy, lanazolid is a protein synthesis inhibitor. It acts by binding the 23S ribosomal RNA portion of the 50S bacterial subunit and inhibits formation of the 70S ribosomal initiation complex. Similar to lanazolid chloramphenicol also causes peripheral and optic neuropathies. And we mentioned this patient had this decreased vibratory sensation in his extremities and he did have a peripheral optic neuropathy which was thought to be related to lanazolid as well. So it also inhibits protein synthesis that mines to a different portion of this same molecule, 50S ribosomal subunit. Both of these agents also have some off-target effects and block mitochondrial protein synthesis to some degree. Now the optic nerve is highly dependent upon mitochondrial function and is susceptible even to relatively low levels of inhibiting a mitochondrial protein synthesis and mitochondrial function. So it's thought to be a mitochondrial based mechanism from off-target effects of protein synthesis within the mitochondria. Now other medications thought to cause similar optic neuropathies. We talked about chloramphenicol, also a thambutol, antibiotics erythromycin, streptomycin and then also nucleoside analog anti-retroviral medications such as AZT. It's a very nice recent review in the Journal of Neuroophthalmology about these mitochondria related optic neuropathies and most of these are felt like lanazolid to improve after discontinuation of the medication. So in summary lanazolid is a new broad spectrum antibiotic. It is becoming more frequently prescribed. We're gonna be seeing more and more patients on this medication for serious infections. Now particularly in the setting of extended duration usage lanazolid carries a risk of both peripheral neuropathy and optic neuropathy. The optic neuropathy seems to be reversible in many cases. The peripheral neuropathy unfortunately is usually not reversible. Patients and providers should be aware of this risk and of course consider discontinuing the medication immediately if they experience any visual changes but this should of course be in consultation with an infectious disease specialist because patients should not be on lanazolid unless they have a very serious infection. And here are my some of the references and I'd be happy to answer any questions. So in prolonged use is there any sense of what the incidence of this is? Is this a consider a rare event or is this a question that we just don't know? Yeah I think they just don't know yet what the incidence is. But I think there'll be a better idea that as you get a little more experience with the medication and it can happen in all ages. This patient was 18. Of course I found a reference for kids that specifically discussed lanazolid neuropathy in children. The youngest patient who's been shown to have optic neuropathy related to lanazolid use was six years old. Okay thanks.