 But there is a lot of discussion about whether NMO is a spectrum of disorders. And so what we've noticed on NMO is that there are a lot of very different clinical outcomes and radiologic signs that occur with NMO in different than MS. So we have patients come in with difficulty seeing in one eye and maybe some neurologic signs, numbness or tingling on their arms. And so we get a MRI and people, the radiologists, discuss that we have a cancer in an optic nerve. What we've been seeing and what neurologists across the country have been noticing and writing about for the past 10 years is that there is an association with how long the enhancement is in an optic nerve. So for optic neuritis you can have a short amount of enhancement in an optic nerve, but usually the enhancement is more posterior in an optic nerve closer to the chiasm in NMO and it is more loss, longer. Longitudinally extensive could be a word that you use, but longitudinally extensive also discusses some of the findings of enhancement within the spinal cord. And people associate NMO with transverse myelitis. And so we call it this longitudinally extensive transverse myelitis. Opiporn IV, IgG, is very well correlated with this disease. Calcium is a water channel and so this antibody is controlling the water channels within the nerves and it's very highly associated. Am I projecting well? Yes. Okay. There's certainly more urgent need for treatment than an MS. An optic neuritis, you know the patients normally go through a period where they have abnormalities with their vision and they do recover vision very well. In NMO they don't recover their vision. They have a very long course of visual loss and even if we try to treat them as steroids initially, assuming maybe that they have MS, they don't get better. And even if you treat them with IV IgG and plasmapheresis, they don't have as much of an improvement as we have seen in MS and optic neuritis in the past. So it's this very different entity from multiple sclerosis. There was this visual outcome study from Brazil where all but one of the patients with NMO were treated with IV methylprednisolone and the suspicion of NMO is raised if patients have a severe visual field defect. It was lowered if they had complete visual field recovery. So we assume and we've known from the optic neuritis treatment trial that if you treat with IV steroids that they about 95% of patients almost recovered to 2025-2020 in their vision and their peripheral visual field deficits resolve. But in NMO it doesn't and so this is a very scary disorder for people until they realize that it was different from MS. For an evaluation of optic neuritis we suggest an MRI brain. And MRI orbits absolutely if you can add that onto your MRI brain that's great but recently insurance has been denying both of them instead of just one or the other. So this study in Neurologic Neuro-Science showed a longer segment of that optic nerve enhancement in NMO over 17 millimeters and certainly more posterior as what I was describing before and then looking at that MRI brain identifying whether it shows some of the classic findings of where T2 lesions are in MS versus lesions that can be primarily in the brainstem that is a common finding in NMO and these spectrum of diseases that are now starting to be clumped into NMOSD or Neuromilatis Optica Spectrum Disorder. If the brain is normal we need to start checking for inflammatory and infectious causes certainly inflammatory such as ANCA and ANA as Dr. Katz was mentioning. So this article from Japan also showed that 30 to 50 percent of NMO patients had brain lesions that looked like MS. But I think that there's this radiologic overlap that a lot of radiologists can hear optic neuritis and a lot of people can still think of MS and some of these they see T2 hyperintensity enhancing lesions then our thought is for MS and so we need to start to distinguish and radiologically identify exactly what looks like MS lesions and what looks like NMO. And of course the brain is never going to be able to have classic lesions of NMO and classic lesions of MS. There is still some crossover so we'll have to do more work and identify what are and where the lesions are. But NMO isn't, we can't fully distinguish if we're looking at a brain MRI between NMO and MS. So why should we look for ANCA? Usually about 30 to 40 percent of patients with NMO have these associated disorders, chogrens, SLE, thyroid, isthenia. There was this article that Kathleen DeGree actually found and not going to pronounce the name of the author but published in 2014 and they looked at 269 patients with presumed NMO spectrum disorder and 595 controls, the controls were found to be patients that had ischemic stroke, Guillain-Barre and Myosthenia Gravis. Now MS was included with NMO, recurrent optic neuritis and recurrent longitudinally extensive transverse myelitis in the cases. ANCA positivity rates were low in all patients. 9.5 had P-ANCA positivity and 2.3 had C-ANCA positivity. So 82 patients were positive for ANCA, P-ANCA and 19 were positive for C-ANCA out of 864 patients. That's a lot for me because when I was looking up how, what the prevalence of vasculitis is, I only found this article about incidents of vasculitis which is new cases are about 10 to 20 cases per million per year. So the overall rate of ANCA positivity and ANCA associated vasculitis is very low. To have such an abnormally high rate of ANCA positivity, 9% is extremely high. So there were 72 patients with NMO 21 with recurrent longitudinally extensive transverse myelitis. And so they broke down all the patients that had a demyelinating eopathic disorder. These were the percentages of C-ANCA positivity and P-ANCA positivity in the number of patients that they had. With monophasic transverse myelitis, longitudinal extensive transverse myelitis, you had rates of 22%, 14% very odd from the natural prevalence that you might assume in population. They also found a higher occurrence of ANCA in patients with the NMO SD rather than patients with MS. And there was a very high positive association between spinal cord lesions and ANCA. So what they did then was they checked everyone who had the antibody that is presumed to be associated with NMO. Now it's not a very sensitive antibody. You can still have NMO even though you don't have the antibody. And what they found was ANCA positive patients who did have this antibody and also were diagnosed as NMO patients. They were older. They had higher disability status when they started. They had more other antibodies that are inflammatory antibodies, ANA, ACE, lysozyme, other inflammatory antibodies. They had longer spinal cord lesions and fewer brain abnormalities than ANCA negative patients. So they were discussing these possible pathogenic roles for ANCA and how vasculitis can affect neurons and affect endothelial cells. And that the endothelial cells, ANCA activity attacking the endothelial cells might cause more vasculitic damage. So NMO is, think of it more as a vasculitis and a neuronal demyelinating disorder in combination than MS as a demyelinating disorder. Thank you.