 Okay, so I guess I'll introduce myself, everybody else, the people I work with are at the NANAS conference. So I'm flying solo. Anyway, my name is Victor Wong and I'm a DUI4 Uralge resident and I'm here to briefly tell you about a case of really bad optic rights. So this was a case that was seen by Dr. Warner in 2008, or starting in 2008, is a 23-year-old patient that presented with payments patient loss in her left eye over two months prior to her first presentation. On exam, her visual acuity was 2100 in her left eye and 2030 in her right eye. She had no APD, her optic nerve was normal, and she had a normal OCT. So as I visited her visual fields in her left eye, she had a superior left quadrant effect in her right eye. Her retinal nerve fiber layer was normal, and then over the course of a month, her right eye felt worse and blurriness, so she was diagnosed with bilateral sequential optic arthritis. They did an MRI that showed bilateral optic nerve enhancement on T2 with no evidence of myelitis. So they started treatment with IMU for this long per O&T protocol, and she got a little better. One month later, further histories, her mother came in and said that her grandmother would have an OCT. So that's where some genetic analysis and they found in 11778 mutations was one of the labor's mutations. But she was started on coenzyme to be 10 at that point. Overall, she improved on IV and PO steroids. We lapsed at one year and then responded again to steroid treatment. At her follow-up at one year, they got a no-ray MRI, showed no further enhancement of her optic nerves, but showed new periventricular legions concerning formal sclerosis. This meant the endowment criteria for diagnosis, so she was started on MS treatment, and then also continued on IV-pulse steroids, depending on her fluctuating region changes. She responded pretty well at the time. This is the MRI from that visit. So on the axiocut on the left side, you can see a couple new regions, periventricular and then on the right side, a little even on the axiocut. So that made this question whether there's a link between labor's or LHON and MS. It's far too described and mostly in case studies appears to be higher than chance the coexistence of these two. But it's hard to study since LHON is relatively rare. But opal sclerosis is pretty common. It's the most common demyelinating disease in the CNS, caraparite by multiple areas of demyelination with loss of all of the dendrocyte and master wheel scarring. There's some clinical features for MS. It's not specific. But MS is using a relapsing or bidding pattern. Age of onset is 15 to 50. Other symptoms include apicneuritis, ILO, herniasine, the utopsis, and so on. As far as the diagnosis of MS, the most, well, relatively most recent is the McDonald criteria that I kind of mentioned earlier. This came out in 2010. And that's probably very much the dissemination in space and time. The dissemination of space is basically defined as one or more key to readings on two of the MS typical regions. These are the peregrine tricular infantorial spinal cord and juxtaportable regions. And dissemination of time means simultaneous enhancing lesions and non-enhancing lesions or a new vision on a follow-up MRI or a development of a second clinical attack. Just recently, the Magnum's group, which is a magnetic resonance imaging MS a couple of months ago, came out with stricter criteria for the diagnosis in the dissemination of space, which is because we get, as MRI imaging improves, we can try to pull in on diagnosis better. And so, again, there's a 2010 McDonald criteria, which I just mentioned. But in 2016, they added a couple things. And there's two of the following. There's three or more peregrine tricular lesions. Again, the infantorial lesion, spinal cord lesion. And then they added an optic nerve lesion as part of criteria as well. And then, of course, the juxtaportable regions. There's just an example of a more typical MRI. And I've also experienced patients on the left again actually cut with several lesions. And then on the right is the cellular cut with... So, these... These come off the ventricle, probably the term, the dozen's fingers. And so that's typical MS. As far as labors, or LHON, there are 300 DNA mutations at positions 11, 7, 7, 8, 14, 44, and 34, 60. These are mis-sense mutations in these sub-UNGs for electron transport chain. They can cause profound impairment in the complex one dependent on ATP synthesis. And clinically, LHON is an eternally inherited form of blindness. They're derived by loss of retinal gait in themselves, an optic nerve generation. Prognosis is poor. The onset's usually between 10 and 30 degrees. It's usually pretty severe bilateral vision loss. And the visual defect usually starts with the central or super-central scutoma. It's a predominantly male and rare one, and it's usually 50,000. So why would we care? So there's a lot of similarities between the two LHON MS, including the AIDS onset, vision involvement, central vision loss with the neuronal fundage. But there are a lot of differences in that LHON is more common in men, whereas MS is more women affected by MS. LHON patients usually have only two visual events that are, and both eyes separated within six months, to use a painless improvement in MS where they have several visual events. It affects the optic nerves, and sometimes painful. And then finally, it's complicated to use. There's the combination element LHON MS, which has recently been described. Harding was the first one to describe it. So it's a men's heart disease. This is the concurrent LHON and MS. One study looked at all the LHON diagnoses in the UK and found five cases of concurrent diagnoses. So in that paper, considering that normal MS prevalence in the UK is one in a thousand, they conclude that the co-occurrence is 50 times greater than chance. Just FYI, the Utah MS rate is a lot higher, and it has to be about one year. So for patients with the combination LHON and MS, it's usually women. Some of them have one to two visual events, and usually there's a long interval between both eyes being affected from one and a half years to 17 years. So that raises a lot of questions in the literature. Several of them. Does MS inflammatory stress provoke women to show symptoms of LHON? Is this a coincidence? Is there an interaction between mitochondrial dysfunction and immunologic mechanism? And finally, is LHON and MS a different entity from LHON and more MS by themselves? So as far as treatment, you probably will know that LHON doesn't really have established treatment, but there is a period of benefit of any absence. In DevDome or CoQ10, it's been prescribed. There is a new intrabutrile injection study done by Massimo Colman. So that's all there is for LHON. For MS, there's several treatments now for attacks. We usually use steroids and platelet braces, and there's a lot of disease-modified therapies, including beta-intolerance and the tumor. And then finally, for the combination, there's still this question of whether it exists or not, and there's only one case report with a description on treatment, specifically for this, where they found that in this patient who had optic neuropathy, she didn't respond to IVL for this long, but she did have spastic paraphernesis, which is more of an opus sclerosis symptom, which improved in DevDome, worsened without, and improved again when restarted. So again, the question is, maybe is this an MS-like syndrome, improved by a mitochondrial default? So for follow-up of that patient that I talked about, she was diagnosed with both MS and LHON. She's tried a variety of MS drugs in addition to steroids, stabilized versus stabilized version. In 2010, she had a new lead, and so at that point, we started to tie the IV with IV steroids in combination with MS treatment. And she kind of continued this course, stabilized, and was seen last month, now on Gelena, which is a P.O. MS drug. At that visit, her visual acuity was 2,300 in her right eye and 2,100 left eye, and she's still on P.O.Q. 10. Her visual fields are stable, a little worse, but in the same pattern, and written on fiber layer, which shows things in both eyes. So that's it. So I need therapy in here. It's G therapy. That's what I was going to comment. Most of the therapies that are in current clinical trials are all T therapy, but I don't remember which treatment I looked at. ND4. Okay, thanks.