 Questions for today, the first is from one of our great neurology residents rotating in neuro ophthalmology, Fais Ramani. Fais grew up in Kenya, attended medical school in Pakistan and actually did internal medicine residency in Kenya before coming here to do a neurology residency. He'll be talking to us today about Famanimus hemianopia. So I'll start by presenting a case of a 42 year old right handed woman who was seen in our clinic. Has a long standing history of multiple sclerosis diagnosed in 2007. She was banned positive at that time. She met McDonald's criteria on MRI. Pretty stable on Avonex. She also has a history of seizures and migraines. In January of this year, she started having this flashing and flickering light in her left half of her visual fields, which was initially concerning for a complex migraine, although she never had headaches at that time. And then this turned gradually over a few days to left homo monomous hemianopsia. During this time, she was also having these episodes of altered mental status. And so she saw her neurologist who imaged her and treated her with IV solumedral, thinking that perhaps this was a flare up of her multiple sclerosis. And this did resolve her altered mental status, but she continued to have this persistent left homo monomous hemianopsia. Of course, she was tapped at that time on the puncture and her CSF was pretty bland, not suggestive for an infection. And so when she came to our clinic, her exam, her visual accuracy was pretty intact. 2020 on the right, 2025 on the left. She didn't have a small relative afferent pupillary defect on the left. And her visual fields were consistent with left homo monomous hemianopia, which we knew. Otherwise, her fundus exam was pretty unremarkable, and she had had an OCT done by an ophthalmologist in an outside hospital that looked pretty normal. Her neurologic exam was pretty unremarkable. And so we had a Humphrey visual field, which, as you can see, is pretty convincing for a left homo monomous hemianopia. And so we looked at her imaging, and this is her initial MRI that was done at the onset of her symptoms, especially when she started getting the altered mental status. And as you can see in the top left figure here, this is a diffusion weighted imaging. And I've tried to contrast it so that I can illustrate this area of hyperintensity in the right occipital lobe. Kind of involves the cortex there. But if you look at the ADC, there is no corresponding darkness there, which would be consistent with a true diffusion restriction. If anything, you can see there's some hyperintense ADC there as well. Now what you see there is her old lesion, which was always present in her previous MRIs. So not a true diffusion restriction, but definitely hyperintense on DWI. And then if you look at her T2 flare right here, you can actually see a corresponding area here that looks, again, hyperintense on the T2 flare. But no gadolinium enhancement. This is a post-GAD sequence. And so when we initially saw this MRI, you know, when you think about sudden onset, homonymous, haemianopsis, the first thing that comes to the mind is stroke. And she does have hyperintense there, but it's not a true diffusion restriction. So if this MRI was done during her onset of symptoms, then it should have shown some diffusion restriction or true diffusion restriction, unless this MRI was done maybe a few weeks, more than two weeks later, where you have pseudonormalization of the ADC and kind of like a T2 shine through, as we call it. And then because of her history of MS, we also wondered whether this was, you know, a flare-up of her multiple sclerosis. And you can see diffusion restriction. You can also see similar pictures we can see on this MRI where you have a hyperintense DWI, but no corresponding ADC. And the mechanism is basically from vasogenic edema, which looks different from cytotoxic edema that you see in strokes, for example. But then she doesn't have any contrast enhancement on her post-GAD, which is what we would expect with active lesions in MS. And then she has this weird cortical involvement, which again is very unusual for demyelinating lesions because they tend to involve the, you know, the white matter rather than the cortex, per se. And this was her MRI six months later. And as you can see, the lesion that we saw in the occipital area has more or less resolved. She still has the old flare abnormalities from her old MS. Again, there's no contrast enhancement there. And this basically effectively rules out tumors that you would think about because you still have the lesion there. And so I thought it was important to look at the differential diagnosis of homonymous hemianopsias in general and kind of looking at our case. Of course, as I mentioned earlier, vascular lesions including ischemic strokes, hemorrhagic strokes, and press. And I should mention press, posterior reversible encephalopathy syndrome, which can present with occipital lesions that look very similar to ours, but they tend to be symmetric and they tend to be bilateral. So again, this was very atypical for press. And she's not on any immunosuppressant that is associated with press or she's not hypertensive either. So we thought press probably on the differential, but not likely in this case. And then of course, any sort of hematomas in the occipital area, aneurysms, which our patient had an MRA of the head and neck, which was negative for any atherosclerotic lesions, significant lesions or any aneurysms for that matter. And of course, autoimmune diseases have been known to cause homonymous hemianopsias if they involve the right area. So SLE, they're pretty significant case reports of SLE of systemic lupus erythomatosis, causing a homonymous hemianopsis, newer sarcoidosis, PML. And then of course, our demyelinating disease. So both multiple sclerosis and ADM have been noted to cause a homonymous hemianopsis depending on where the lesion is. NMO, definitely a differential. Our patient had negative antibodies to NMO. And then tumors, as I mentioned earlier, there's nothing suggestive in our patient. Traumatic brain injury in real life happens to be a pretty common cause of homonymous hemianopsias probably after vascular causes. And then any sort of surgery or manipulation of the brain involving those areas that would lead to a homonymous hemianopsia. And then interestingly, seizures can also cause a homonymous hemianopsia, but seizures tend to cause more of a transient homonymous hemianopsia. In our patients, hemianopia was more or less permanent. And then complicated migraines, of course. And this patient did have some visual phenomena initially that suggested that this was perhaps a migraine, but then the defects or the deficits have persisted, which again makes migraines pretty unlikely. Then we have our psychogenic causes of hemianopia as well. So I thought it was helpful to look at the general principles of homonymous hemianopias. In general, they're caused by retrocazmal lesions, so any lesions basically behind the plasma. And this is because of the cross nasal and uncross temporal fibers basically. These visual defects tend to respect midline, so they don't cross over to the other side, as opposed to, for example, glaucoma, where you can have deficits on the other side of the midline. And then in general, depending on where the lesions are, the more posterior you get, the more congruent it gets. So more anterior, more incongruous, in other words, asymmetric, and more posterior, more congruent. And so we'll start by looking at the optic tract lesions, which tend to cause incongruous, homonymous deficits, contralateral to the effective optic tract. And often you have a contralateral relative afferent peopler defect, which is what we initially suspected in our patient, because our patient has a relative afferent peopler defect on the other side. Vision equity and color vision are pretty much preserved, unless there's bilateral involvement, or anterior extension to involve optic nerve or chasm. Of course, the disc on the contralateral side shows typically this bow tie atrophy, which I tried to illustrate here. You can see pal there and pal there. It almost looks like a bow tie. And then in ipsilateral disc, you may see temporal atrophy. And this is basically pretty typical. Again, causes can be mass lesions like tumors, aneurysms, demyelination, ischemic lesions are usually uncommon. And then we have the lateral geniculate body lesions, which are very interesting because they produce distinct sort of hemianopias. And these tend to be almost always bascular. So if you have involvement of the posterior choroidal artery, which is a branch of the PCA, then you have a very highly congruous horizontal sectoronopia, which is what I've illustrated right there. So you can see this. Really interesting. And if the anterior choroidal artery is affected, which is a branch of the MCA, then you have what we call a quadruple sectoronopia, where you have loss of the upper and the lower visual fields, but then you have sparing sort of a wedge right there. And then of course we have temporal lesions, temporal lobe lesions, which tend to affect the optic radiations inferiorly. And so you have the pine sky appearance, where you have contralateral superior incongruous homonymous quadrant tonopia. So not really truly a hemianopia, but you can have involvement of the inferior visual fields, but it's almost always more dense in the superior aspect. Of course the Myers loop is what is involved there. And then the parietal lesions tend to cause the pie on the floor appearance, which basically means contralateral inferior homonymous quadrant tonopia. Again, you can have superior involvement, but it's more dense inferiorly. Interestingly, with parietal lesions, if you check an optokinetic nystagmus, you'll note that it's abnormal, just because the pathways for the optokinetic nystagmus tend to come into the parietal area and process there. And so the causes, again, tumor, surgery, strokes, and demyelinating disease in both the temporal lobe and parietal lobe lesions. And then occipital lobe lesions, as in our case, have a pretty congruous, homonymous hemianopia. In cases of stroke causing this hemianopia, you have macular sparing, and that's because there's a dual blood supply to the tip of the occipital lobe from the MCA and PCA, and that area tends to get spared if one arteries, for example, are involved. You can have more atypical lesions or visual field defects, including a monocular defect of the temporal crescent only. Again, strokes on the top of the list, press, tumors, traumatic brain injuries, and demyelination, appear to be etiologies. And so how do we treat this homonymous hemianopias? Of course, we can use optical aids. We can use our simple standard frontal prisms, which tend to displace them just to the apex. So you can have them as press-on lenses that you can apply to the hemium-nopic half of each lens. The only problem is that central vision is affected, so most patients will complain of central scotomas, and not everybody would like these prisms. And so people have come up with these monocular sectorial prisms, which tend to work better, and these are prisms that are restricted to the peripheral fields on each side of the hemianopia above and below the pupil, and the prism expands the peripheral field of course causes peripheral dyplopia, which is what happens in normal people as well. But you have improved walking, improved obstacle avoidance, and so improved overall care. And then we have various visual training techniques. Some are commercially available. They have different names, but the principles appear to be basically three. We have what we call blind-sight retraining, and this is based on the assumption that although you may have a complete hemianopia or a harmonious hemianopia, and you don't have visual perception on the side of the hemianopia, you can still tell whether they're moving objects or obstacles for some reason. And there are various theories that have been put forward, and basically you can train or retrain people to detect targets in those hemianopic hemipheals and potentially improve their walking and their obstacle avoidance. And then there's the visual exploration training, which basically trains patients to practice their saccades, their large saccades into the blind fields and therefore detect any objects or obstacles. And then of course we have the more easier rehabilitation, the reading rehabilitation, because a lot of these patients have trouble reading just because they can't follow those words and the lines. And so you can have them use rulers, for example, to know where exactly what line they're reading. You can also train them to read up and up down rather than side to side, and that can actually help them as well. So in conclusion, it's important to recognize that there are different etiologies of harmonious hemianopias, it's not just strokes. And it's important to recognize that demyelinating disease is a cause or an important cause of harmonious hemianopia. And lastly that there are various rehabilitative strategies that are available for treatment. And so we should refer these patients for visual rehab as they can benefit from this. Thank you. I think they have to go for a driving test again. If they can prove that they're safe, you know, they can pass the driving test, then it should be okay. But you can't just allow them to drive with their hemianopias until they've done their driving test again. Dr. Bordner. Yes, sir? So it's not clear cut. We're leaning more towards MS, but it's not 100% just because of the etiopal features that I mentioned. I think in the event of, for example, if this was stroke and it does kind of follow a vasculitis distribution, we've already worked the patient up with vessel imaging, didn't see anything there. And the fact that the lesion appears to have completely disappeared kind of goes against stroke because if you had a significant stroke and see some gliosis or some sequelae of the stroke, you know, a few months later, isn't the case. But it's definitely not 100%. We're not 100% sure about what the etiologist is, but it appears to be leaning more towards multiple sclerosis. And these patients' medications were adjusted and she appears to be stable at this point. Yes, sir? Yeah, I mean, a little controversial because some of the studies for these commercial programs have been pretty nice and promising, whereas others have not been that nice and promising. It just depends on what technique is used. There are a few techniques that are considered not very clear-cut, especially like the blinds-type training, for example, that I mentioned. And the visual exploration training is pretty well documented. So, of course, the reading rehabilitation is also very well documented. I think it's worthwhile sending these patients to visual rehab and seeing if they can improve. I think you do have to report... Is that driving form that you have to place, that they have to undergo a driving rehab? I don't think we have to report as far as I understand. I mean, it's the case with, for example, seizures. There's no reporting. It's like seizures. We don't allow them to drive for three months, but we don't call the DMB and say this patient has had seizures and can't drive. It's based on the patient himself or herself. Not drive. Yes. Yeah, it's typically patients, and I've seen these patients with seizures, they're like, oh, I'm fine with driving, and you have to tell them, well, you're fine, but what about the other pedestrians and drivers? They have to be safe, too. Thank you.