 All right, so I hope we have Dom and Portal. You were with the Miami students, yeah? Yeah. So he's a neurology resident. Did his medical in Miami, so he's going to talk about syphilovethyl. Let me just pull this up. So Dr. DeGree called last night and had me make this more appropriate for this audience. Hopefully I don't put you guys to sleep. She says, too much neurology in it. So I'm going to talk today about distinguishing visual symptoms from a syphilovol epilepsy from visual symptoms we see in migraine. And to illustrate this, a case report on a patient who I saw in the neurology ward who was seen in the Neuroophthalmology Clinic. So it was a 51-year-old right-handed lady. She had a history of obesity, hypertension, and asaphalgic migraine with visual aura. She presented to the emergency room with five months of progressively worsening proxysmal episodes that included her visual hallucinations but were now followed by nausea, vomiting, headache, and in-balance gait, and some complaints of her vision moving, sort of bouncy vision. She decided to come in that day because she'd had a couple of these episodes in a row and thought they were becoming increasingly frequent and severe. That precipitated her presentation that day. And she described, she wasn't quite sure, but at least 20 years of having these visual symptoms that, at onset, were not associated with any sort of headache or any other neurologic symptoms. But she described them as brief, round lights that would appear, but seem like in both fields of vision, at least in both eyes, it will last seconds to minutes. Her past medical and ophthalmologic history was pretty unremarkable. She had a history of endometrial adenocarcinoma that was resected. Otherwise in that, no eye disease in herself or her family. She was sort of a normal functioning person. She was a cook at a restaurant, had normal developmental history, and not really any other relevant medical or surgical history. So her basic exam, she had normal visual acuity. Her pupils were normal, no afferent defect. Her extraocular movements were full. Color testing was normal. She did have quite a few misses on terms of depth perception of the circle test. Her slitlet exam was largely normal. She did have some temporal pallor when you looked at her optic nerves bilaterally, but she had a normal effusion flicker test. Her nerve exam was largely unremarkable. She had maybe some prolonged trigger while it's extinguished in gaze and stagmus, maybe eight beats, a little bit more than what you expect physiologically. But all the other provoking maneuvers to elicit any kind of peripheral nerve or vestibular problem were unremarkable. She had no other cranial nerve or focal neurologic findings. And I have to say, these were sort of intraectal exams. So this was not when she was having her symptoms. So she underwent an MRI, and to everyone's surprise had this relatively striking abnormality. She had never had neuroimaging before. And so this is called colposephaly, and it's describing the asymmetric dilatation of her posterior monogrelateral ventricles. And it's actually defined, radiographically, that this posterior axial link should be two to three times as large as her anterior horn. This is normally found in pediatric patients, usually in the workup of other developmental abnormalities. So it's very rare. I think there's only two or three case reports of this actually found in otherwise normal humans. In the literature, I think the cases, often the two that I could find present with sort of migraness or epilepsy-like symptoms. But usually, in kids, there can be other abnormalities, particularly the menline structures, the corpus callosum, along the spectrum are sort of set to optic dysplasia. So I thought that this is not a, this is actually a congenital abnormality. This patient had this for years. It's more people think it has to do more with problems with the morphogenesis in those regions, not necessarily destruction of tissue or injury. And it's associated with a lot of genetic and chromosome abnormalities. Again, it's something she's had since she was a child. So the question was, given her symptoms and her newly found abnormal neuroanatomy, were these visual symptoms more consistent with a migraine or with a simple procedure? So this has been discussed really in the late 90s by a great neurologist, Pania Tropoulos. Probably saying that incredibly wrong. But he wrote a series of papers, and he was focused on the differentiating migraine with visual aura and basilar migraine from occipital lobe seizures and mostly the adolescent population. There's a benign occipital lobe epilepsy that is really responsive to carbamazepine. But often, these kids would get misdiagnosed and not be treated for years. So his argument is that the visual symptoms in occipital lobe epilepsy are distinguishable based on the patient's description. The complicating factor is that in these occipital lobe seizures, you can often have headache post-acidally as well as nausea and vomiting. So in order to tease these two apart can be quite difficult clinically. But his description of the elementary visual hallucinations seen in occipital lobe epilepsy, he thought were fairly characteristic. These are, I think, six patient renderings of their visual symptoms during a seizure. They're predominantly colored and rounded, involve at least circular shapes. They're very typical in this immunology so that the visual symptoms will be the same pretty much every time they have them. Obviously, the progression to non-visual symptoms, which would represent migration of the seizure or generalization of the seizure, were highly suggestive of occipital lobe epilepsy. And the other thing he found was that these typically are much shorter, simply in the realm of seconds, maybe a minute, and the extreme three minutes long, which is contrasted to what we see in migraine. I think we all know that the typical features of migraine are the scallion and scatoma shown in these corner or these top two windows. These usually are associated with the scatoma. They can progress and sort of move to the periphery. They can present with fortification spectra or progress to that, which is shown by those sort of bright zigzag lines. They can leave residual scatomas after they're gone. And phosphines are also reported, which are just bright flashes of light, which can move across the visual field and are quite short as well. But typically, the onset and the progression of these last many minutes, at least one to at least half an hour, that can be helpful in distinguishing these from these sipital lobe visual hallucinations. So in terms of this treatment, she was admitted, she had a lumbar puncture, because everyone was, in the emergency room was at least convinced she had an acute hydrocephalus. Her opening pressure was obviously normal. We hooked her up to continuous EEG and indeed found medium to large, intermittent shark waves on the right, a sipital temporal area, which is actually where her copacephala was worse. It was a bit asymmetric, which was very suggestive of vocal seizure. She was started on capra, which did improve her visual symptoms. She still had some residual headaches, so eventually as an outpatient switched her to topomax for sort of due coverage. And not only did her visual symptoms improve, so did her intermittent unsteadyness as well the EEG changes, abnormalities disappeared. So in conclusion, I think based on her description, these obviously fit a sipital lobe seizures and that's supported by the evidence seeing with a structural abnormality on MRI imaging and on EEG, which reverse with treatment. So these were probably a longstanding incorrectly attributed to asaphalosid migraine in the visual aura. While some suggest you can actually tease these apart based on clinical history, based on their symptom, the description of ending around colored hallucinations that are relatively short duration, sometimes this can be difficult to distinguish largely just on how the patient can describe them. So obviously an EEG can be helpful when there's a question. And certainly in her case, if an EEG had been performed 20 years ago, I think the finding of a focal epilepsy would have led to an MRI, perhaps different treatment for her. And that's all I have if there's any questions. You think the optic nerve powder was just retrograde at half a feet from the type of cell? Yeah, I kind of left out. There were some other model findings on her MRI as well. I don't think we saw anything in terms of optic nerve size on the MRI, but I guess I was seeing what that is. Actually, I thought I had a, because it got deleted, I had a picture of her visual fields and she had a very mild shallow left. I'm not almost 10 years, yeah. Almost un-preciable, but maybe there. Are there five of their analysis? You know, we didn't, yeah, we didn't. What do you do to make it interesting to have? Any other questions? Well, thanks for looking to talk.