 We're going to get started now, it's 8 a.m., so I'm going to be giving my last to zero topic presentation. It's going to be a short case. The title is a short but curious case of bitemporal hemianopsia. So, we have patient MF. It's a 17-year-old female. It's referred by an ophthalmologist to her in her ophthalmology clinic. She was complaining about a one-month history of scintillating lights in both eyes as well as a dense dark spot and her super temporal vision in the right eye. She denied any eye pain, headaches, floaters, photophobia, knowledge of vomiting, phonophobia, loss of central vision, or any motor or sensory abnormalities. Pass amenable history. She only had hypothyroidism as well as eczema. However, the rest of her amenable history was non-contributory. On examination, her visual acuity was 2015 in either eye. She exhibited no aphorine convoy defect. Her intraocular movements were full on both sides. Her intraocular pressures were within her limits on both sides. On her telexamination, she was 18 and 18 at 95. So, on visual field testing, she actually had a pattern that was consistent with the bitemporal hemianopsia, located superiorly. On fundus examination, it was completely unremarkable, including vitreous being very clear. No signs of inflammation anywhere. So, on RNFL and MACO CT, these were both unremarkable as well on both sides. On forcing an underground, the only finding we found was that very faint, mild leakage from the desk in the very late phases. But otherwise, it was normal. Now, the outside ophthalmologist, he performed his own visual fields and when he saw the bitemporal hemianopsia, he ordered an MRI because he was worried about an optic chiasmoleation. And the results came back as normal. He also ordered an MRA of the brain that was also normal. So, our team ordered a multi-global ERG. What they found was attenuated responses in the nasal magula near the peripathletic region. And this was seen on both sides. At this point, our Neurophthalmology team thought that this patient had a variety of the acute idiopathic blind spot enlargement syndrome, in short, it's called AXE. So, at this point in my talk, I'm just going to segue into discussing a little bit more about this disease because I was not familiar with AXE at all, during this point of my training. So, what exactly is AXE? It was first described by Fletcher and colleagues as an idiopathic disorder characterized by a acute onset of Phytopsias and a temposcatoma involving the blind spot occurring in young myopic women. By the classic definition, you're supposed to have an undemarkable one's examination and you had a cohort of seven patients. However, in the field, it's really, there's no consensus as to whether or not AXE is its own distinct clinical entity or is it really part of the spectrum of white dots syndrome? The reason why some people think this is because a lot of the white dots syndrome such as mutes, multifocal chorditis, punctated interchordology, acute macular and arachniditis, and azore can present within a large blind spot without any significant peripapillary findings. Pathophysiology-wise, the etiology has not been elucidated regarding AXE. However, it is thought that there's dysfunction of the coriorettin tissue of the peripapillary region. This is largely due to the concomitant abnormal multifocal ERGs, OCT findings, as well as a prolonged stress test, which I'll go over those in a minute. Some believe or speculate that hormonal and genetic factors are involved because of the dominance of the hundreds of females being affected. And lastly, there may be an environmentally triggered factor because it's thought to be non-progressive, as opposed to an autoimmune neurology, which is thought to have to be more of a progressive course. Clinical symptoms. So as described in our presentation, loss of vision and temporal fields affecting the blind spot. And then they also have ptoxia in the area of the loss of vision. Typically it presents unilaterally, but a number of bilateral cases have been reported. Fundus findings, classically, as Fletcher described, they were supposed to have a fund-emarkable fundus example. However, more recent large retrospective studies describe not only normal fundus, but also pigmentary changes in peripapillary regions. Great onset changes, if you follow them along, that are consistent with multifocal coriorettis, where you see these punched out coriorettin lesions in the mid periphery, as well as you can see changes that are consistent with the tube macular neurorettinitis, where you see this reddish-brown, wet-shaped lesion is macular. Other ocular findings include an atherin pubular defect, as well as the prolonged photo-stress recovery test. Visual field testing, which is obvious, you see in large blind spots of various sizes. Now, full field ERGs are normal. However, multifocal ERGs showed attenuated responses in the peripapillary region of the retina. This is coincident with areas that are affected on visual field testing. In the gym, the fluorescent angiogram is grossly normal. However, there are some reported cases of late and faint peripapillary leakage. And on OCT, typically, you see loss or disruption of the outer retinal layers. Two specific case studies, Shigahara et al. showed an absent virhoff snagering, virhoff snagering is that very outer segment tips of photoreceptors. And then period al showed a disruption of the external limiting membrane, as you can see between those two areas. Management, really, you have to rule out treatable causes of enlarged blind spot. But once the diagnosis is made, this observation is really recommended because it's a self-limited disease. Of course, the Phytopsias resolve with time. The visual field defects, they do improve, however, they don't completely go away. They don't resolve. And as I discussed before, it's non-progressive. It's not like it doesn't have a progressive force. So I went through the literature. I wanted to see if there's any reported cases where the presentation story was very similar to the one the patient that we saw in our clinic. So I should came across this paper. It was a 67-year-old female who came in with bitemporal hemianosia. She had a completely unremarkable fundus exam. Her OCT was normal as well as her multifocal ERG. However, four years later, she showed a dysfunction of the area of the retina on multifocal ERG that was coincident with the area of the blind spot, the enlarged blind spot. And then they also saw some coriorectal pigmentary changes in that area as well. So in summary, apse is a disease of predominantly young healthy women, scintillations in the temporal visual field associated with the large blind spot as how they present. Classically, there are no significant retinal or optic disc changes. However, more recent studies suggest otherwise. Visual fields may improve, however, it does not completely resolve. And lastly, there's still no consensus as to whether apse is its own clinical disease entity or it's part of the white dots syndrome spectrum disorders, largely because, as I stated earlier, the white dots syndrome is many of them present within a large blind spot. A lot of them that don't have any remarkable peripapillary changes, as well as more recent studies that show that there are some white dots syndrome type overlap changes that are seen apse if you follow them long enough. All right, no? No, my references. Thank you. That's my last neuro presentation, Dr. Warren. Any questions? Did y'all? Did y'all have a macro CT on her? Yeah, we did. Yeah, I showed it. It was normal. All right, thanks guys.