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Diagnosing and differentiating among the many possible localizations and causes of vision loss is an essential skill for neurologists. The approach to vision loss should include a history and examination geared toward localization, followed by a differential diagnosis based on the likely location of the pathophysiologic process. In this episode, Aaron Berkowitz, MD, PhD, FAAN speaks with Nancy J. Newman, MD, FAAN, author of the article “Approach to Vision Loss” in the Continuum® April 2025 Neuro-ophthalmology issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology at the University of California San Francisco in the Department of Neurology and a neurohospitalist, general neurologist, and clinician educator at the San Francisco VA Medical Center at the San Francisco General Hospital in San Francisco, California. Dr. Newman is a professor of ophthalmology and neurology at the Emory University School of Medicine in Atlanta, Georgia. Additional Resources Read the article: Approach to Vision Loss Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Nancy Newman about her article on the approach to visual loss, which she wrote with Dr Valerie Biousse. This article appears in the April 2025 Continuum issue on neuro-ophthalmology. Welcome to the podcast, Dr Newman. I know you need no introduction, but if you wouldn't mind introducing yourself to our listeners. Dr Newman: Sure. My name's Nancy Newman. I am a neurologist and neuro-ophthalmologist, professor of ophthalmology and neurology at the Emory University School of Medicine in Atlanta, Georgia. Dr Berkowitz: You and your colleague Dr Biousse have written a comprehensive and practical article on the approach to visual loss here. It's fantastic to have this article by two of the world's leading experts and best-known teachers in neuro-ophthalmology. And so, readers of this article will find extremely helpful flow charts, tables and very nuanced clinical discussion about how to make a bedside diagnosis of the cause of visual loss based on the history exam and ancillary testing. We'll talk today about that important topic, and excited to learn from you and for our listeners to learn from you. To begin, let's start broad. Let's say you have a patient presenting with visual loss. What's your framework for the approach to this common chief concern that has such a broad differential diagnosis of localizations and of causes? Where do you start when you hear of visual loss? How do you think about this chief concern? Dr Newman: Well, it's very fun because this is the heart of being a neurologist, isn't it? Nowhere in the nervous system is localization as important as the complaint of vision loss. And so, the key, as any neurologist knows, is to first of all figure out where the problem is. And then you can figure out what it is based on the where, because that will limit the number of possibilities. So, the visual system is quite beautiful in that regard because you really can exquisitely localize based on figuring out where things are. And that starts with the history and then goes to the exam, in particular the first localization. So, you can whittle it down to the more power-for-your-buck question is, is the vision lost in one eye or in two eyes? Because if the vision loss clearly, whether it's transient or persistent, is in only one eye, then you only have to think about the eyeball and the optic nerve on that side. So, think about that. Why would you ever get a brain MRI? I know I'm jumping ahead here, but this is the importance of localization. Because what you really want to know, once you know for sure it's in one eye, is, is it an eyeball problem---which could be anything from the cornea, the lens, the vitreous, the retina---or is it an optic nerve problem? The only caveat is that every once in a while, although we trust our patients, a patient may insist that a homonymous hemianopia, especially when it's transient, is only in the eye with the temporal defect. So that's the only caveat. But if it's in only one eye, it has to be in that side eyeball or optic nerve. And if it's in two eyes, it's either in both eyeballs or optic nerves, or it's chiasmal or retrochiasmal. So that's the initial approach and everything about the history should first be guided by that. Then you can move on to the more nuanced questions that help you with the whats. Once you have your where, you can then figure out what the whats are that fit that particular where. Dr Berkowitz: Fantastic. And your article with Dr Biousse has this very helpful framework, which you alluded to there, that first we figure out, is it monocular or binocular? And we figure out if it's a transient or fixed or permanent deficit. So, you have transient monocular, transient binocular, fixed monocular, fixed binocular. And I encourage our listeners to seek out this article where you have a table for each of those, a flow chart for each of those, that are definitely things people want to have printed out and at their desk or on their phone to use at the bedside. Very helpful. So, we won't be able to go through all of those different clinical presentations in this interview, but let's focus on monocular visual loss. As you just mentioned, this can be an eye problem or an optic nerve problem. So, this could be an ophthalmologic problem or a neurologic problem, right? And sometimes this can be hard to distinguish. So, you mentioned the importance of the history. When you hear a monocular visual loss- and with the caveat, I said you're convinced that this is a monocular visual problem and not a visual field defect that may appear. So, the patient has a monocular deficit, how do you approach the history at trying to get at whether this is an eye problem or an optic nerve problem and what the cause may be? Dr Newman: Absolutely. So, the history at that point tends not to be as helpful as the examination. My mentor used to say if you haven't figured out the answer to the problem after your history, you're in trouble, because that 90% of it is history and 10% is the exam. In the visual system, the exam actually may have even more importance than anywhere else in the neurologic examination. And we need as neurologists to not have too much hubris in this. Because there's a whole specialty on the eyeball. And the ophthalmologists, although a lot of their training is surgical training that that we don't need to have, they also have a lot of expertise in recognizing when it's not a neurologic problem, when it's not an optic neuropathy. And they have all sorts of toys and equipment that can very much help them with that. And as neurologists, we tend not to be as versed in what those toys are and how to use them. So, we have to do what we can do. Your directive thalmoscope, I wouldn't throw it in the garbage, because it's actually helpful to look at the eyeball itself, not just the back of the eye, the optic nerve and retina. And we'll come back to that, but we have in our armamentarium things we can do as neurologists without having an eye doctor's office. These include things like visual acuity and color vision, confrontation, visual fields. Although again, you have to be very humble. Sometimes you're lucky; 30% of the time it's going to show you a defect. It has to be pretty big to pick it up on confrontation fields. And then as we say, looking at the fundus. And you probably know that myself and Dr Biousse have been on somewhat of a crusade to allow the emperor's new clothes to be recognized, which is- most neurologists aren't very comfortable using the direct ophthalmoscope and aren't so comfortable, even if they can use it, seeing what they need to see. It's hard. It's really, really hard. And it's particularly hard without pupillary dilation. And technology has allowed us now with non-mydriatic cameras, cameras that are incredible, even through a small pupil can take magnificent pictures of the back of the eye. And who wouldn't rather have that? And as their cost and availability- the cost goes down and their availability goes up. These cameras should be part of every neurology office and every emergency department. And this isn't futuristic. This is happening already and will continue to happen. But over the next five years or so… well, we're transitioning into that. I think knowing what you can do with the direct ophthalmoscope is important. First of all, if you dial in plus lenses, you can't be an ophthalmologist, but you can see media opacities. If you can't see into the back of the eye, that may be the reason the patient can't see out. And then just seeing if someone has central vision loss in one eye, it's got to be localized either to the media in the axis of vision; or it's in the macula, the very center of the retina; or it's in the optic nerve. So, if you get good at looking at the optic nerve and then try to curb your excitement when you saw it and actually move a little temporally and take a look at the macula, you're looking at the two areas. Again, a lot of ophthalmologists these days don't do much looking with the naked eye. They actually do photography, and they do what's called OCT, optical coherence tomography, which especially for maculopathies, problems in the macula are showing us the pathology so beautifully, things that used to be considered subtle like central serous retinopathy and other macula. So, I think having a real healthy respect for what an eye care provider can do for you to help screen away the ophthalmic causes, it's very, very important to have a patient complaining of central vision loss, even if they have a diagnosis like multiple sclerosis, you expect that they might have an optic neuritis… they can have retinal detachments and other things also. And so, I think every one of these patients should be seen by an eye care provider as well. Dr Berkowitz: Thank you for that overview. And I feel certainly as guilty as charged here as one of many neurologists, I imagine, who wish we were much better and more comfortable with fundoscopy and being confident on what we see. But as you said, it's hard with the direct ophthalmoscope and a non-dilated exam. And it's great that, as you said, these fundus photography techniques and tools are becoming more widely available so that we can get a good look at the fundus. And then we're going to have to learn a lot more about how to interpret those images, right? If we haven't been so confident in our ability to see the fundus and analyze some of the subtle abnormalities that you and your colleagues and our ophthalmology colleagues are more familiar with. So, I appreciate you acknowledging that. And I'm glad to hear that coming down the pipeline, there are going to be some tools to help us there. So, you mentioned some of the things you do at the bedside to try to distinguish between eye and optic nerve. Could you go into those in a little bit more detail here? How do you check the visual fields? For example, some people count fingers, some people wiggle fingers, see when the patient can see. How should we be checking visual fields? And what are some of the other bedside tasks you use to decide this is probably going to end up being in the optic nerve or this seems more like an eye? Dr Newman: Of course. Again, central visual acuity is very important. If somebody is older than fifty, they clearly will need some form of reading glasses. So, keeping a set of plus three glasses from cheapo drugstore in your pocket is very helpful. Have them put on their glasses and have them read an ear card. It's one of the few things you can actually measure and examine. And so that's important. The strongest reflex in the body and I can have it duke it out with the peripheral neurologists if they want to, it's not the knee jerk, it's looking for a relative afferent pupillary defect. Extremely important for neurologists to feel comfortable with that. Remember, you cut an optic nerve, you're not going to have anisocoria. It's not going to cause a big pupil. The pupils are always equal because this is not an efferent problem, it's an afferent problem, an input problem. So basically, if the eye has been injured in the optic nerve and it can't get that information about light back into the brain, well, the endoresfol nuclei, both of them are going to reset at a bigger size. And then when you swing over and shine that light in the good optic nerve, the good eye, then the brain gets all this light and both endoresfol nuclei equally set those pupils back at a smaller size. So that's the test for the relative afferent pupillary defect. When you swing back and forth. Of course, when the light falls on the eye, that's not transmitting light as well to the brain, you're going to see the pupil dilate up. But it's not that that pupil is dilating alone. They both are getting bigger. It's an extremely powerful reflex for a unilateral or asymmetric bilateral optic neuropathy. But what you have to remember, extremely important, is, where does our optic nerve come from? Well, it comes from the retinal ganglion cells. It's the axons of the retinal ganglion cells, which is in the inner retina. And therefore inner retinal disorders such as central retinal artery occlusion, ophthalmic artery occlusion, branch retinal artery occlusion, they will also give a relative afferent pupillary defect because you're affecting the source. And this is extremely important. A retinal detachment will give a relative afferent pupillary defect. So, you can't just assume that it's optic nerve. Luckily for us, those things that also give a relative afferent pupillary defect from a retinal problem cause really bad-looking retinal disease. And you should be able to see it with your direct ophthalmoscope. And if you can't, you definitely will be able to see it with a picture, a photograph, or having an ophthalmologist or optometrist take a look for you. That's really the bedside. You mentioned confrontation visual fields. I still do them, but I am very, very aware that they are not very sensitive. And I have an extremely low threshold to- again, I have something in my office. But if I were a general neurologist, to partner with an eye care specialist who has an automated visual field perimeter in their office because it is much more likely to pick up a deficit. Confrontation fields. Just remember, one eye at a time. Never two eyes at the same time. They overlap with each other. You're going to miss something if you do two eyes open, so one eye at a time. You check their field against your field, so you better be sure your field in that eye is normal. You probably ought to have an automated perimetry test yourself at some point during your career if you're doing that. And remember that the central thirty degrees is subserved by 90% of our fibers neurologically, so really just testing in the four quadrants around fixation within the central 30% is sufficient. You can present fingers, you don't have to wiggle in the periphery unless you want to pick up a retinal detachment. Dr Berkowitz: You mentioned perimetry. You've also mentioned ocular coherence tomography, OCT, other tests. Sometimes we think about it in these cases, is MRI one of the orbits? When do you decide to pursue one or more of those tests based on your history and exam? Dr Newman: So again, it sort of depends on what's available to you, right? Most neurologists don't have a perimeter and don't have an OCT machine. I think if you're worried that you have an optic neuropathy, since we're just speaking about monocular vision loss at this point, again, these are tests that you should get at an office of an eye care specialist if you can. OCT is very helpful specifically in investigating for a macular cause of central vision loss as opposed to an optic nerve cause. It's very, very good at picking up macular problems that would be bad enough to cause a vision problem. In addition, it can give you a look at the thickness of the axons that are about to become the optic nerve. We call it the peripapillary retinal nerve fiber layer. And it actually can look at the thickness of the layer of the retinal ganglion cells without any axons on them in that central area because the axons, the nerve fiber layer, bends away from central vision. So, we can see the best we can see. And remember these are anatomical measurements. So, they will lag, for the ganglion cell layer, three to four weeks behind an injury, and for the retinal nerve fiber, layer usually about six weeks behind an entry. Whereas the functional measurements, such as visual acuity, color vision, visual fields, will be immediate on an injury. So, it's that combination of function and anatomy examination that makes you all-powerful. You're very much helped by the two together and understanding where one will be more helpful than the other. Dr Berkowitz: Let's say we've gotten to the optic nerve as our localization. Many people jump to the assumption it's the optic nerve, it's optic neuritis, because maybe that's the most common diagnosis we learn in medical school. And of course, we have to sometimes, when we're teaching our students or trainees, say, well, actually, not all optic nerve disease, optic neuritis, we have to remember there's a broader bucket of optic neuropathy. And I remember, probably I didn't hear that term until residency and thought, oh, that's right. I learned optic neuritis. Didn't really learn any of the other causes of optic nerve pathology in medical school. And so, you sort of assume that's the only one. And so you realize, no, optic neuropathy has a differential diagnosis beyond optic neuritis. Neuritis is a common cause. So how do you think about the “what” once you've localized to the optic nerve, how do you think about that? Figure out what the cause of the optic neuropathy is? Dr Newman: Absolutely. And we've been trying to convince neuro-radiologists when they see evidence of optic nerve T2 hyperintensity, that just means damage to the optic nerve from any cause. It's just old damage, and they should not put in their read consistent with optic neuritis. But that's a pet peeve. Anyway, yes, the piece of tissue called the optic nerve can be affected by any category of pathophysiology of disease. And I always suggest that you run your categories in your head so you don't leave one out. Some are going to be more common to be bilateral involvement like toxic or metabolic causes. Others will be more likely unilateral. And so, you just run those guys. So, in my mind, my categories always are compressive-slash-infiltrative, which can be neoplastic or non-neoplastic. For example, an ophthalmic artery aneurysm pressing on an optic nerve, or a thyroid, an enlarged thyroid eye muscle pressing on the optic nerve. So, I have compressive infiltrative, which could be neoplastic or not neoplastic. I have inflammatory, which can be infectious. Some of the ones that can involve the optic nerve are syphilis, cat scratch disease. Or noninfectious, and these are usually your autoimmune such as idiopathic optic neuritis associated with multiple sclerosis, or MOG, or NMO, or even sarcoidosis and inflammation. Next category for me would be vascular, and you can have arterial versus venous in the optic nerve, probably all arterial if we're talking about causes of optic neuropathy. Or you could have arteritic versus nonarteritic with the vascular, the arteritic usually being giant cell arteritis. And the way the optic nerve circulation is, you can have an anterior ischemic optic neuropathy or a posterior ischemic optic neuropathy defined by the presence of disc edema suggesting it's anterior, the front of the optic nerve, or not, suggesting that it's retrobulbar or posterior optic nerve. So what category am I- we mentioned toxic, metabolic nutritional. And there are many causes in those categories of optic neuropathy, usually bilateral. You can have degenerative or inherited. And there are causes of inherited optic neuropathies such as Leber hereditary optic neuropathy and dominant optic atrophy. And then there's a group I call the mechanical optic neuropathies. The obvious one is traumatic, and that can happen in any piece of tissue. And then the other two relate to the particular anatomy of the eyeball and the optic nerve, and the fact that the optic nerve is a card-carrying member of the central nervous system. So, it's not really a nerve by the way, it's a tract. Think about it. Anyway, white matter tract. It is covered by the same fluid and meninges that the rest of the brain. So, what mechanically can happen? Well, you could have an elevated intraocular pressure where that nerve inserts. That's called glaucoma, and that would affect the front of the optic nerve. Or you can have elevated intracranial pressure. And if that's transmitted along the optic nerve, it can make the front of the optic nerve swell. And we call that specifically papilledema, optic disk edema due specifically to raised intracranial pressure. We actually even can have low intraocular pressure cause something called hypotony, and that can actually even give an optic neuropathy the swelling of the optic nerve. So, these are the mechanical. And if you were to just take that list and use it for any piece of tissue anywhere, like the heart or the kidney, you can come up with your own mechanical categories for those, like pericarditis or something like that. And then all those other categories would fit. But of course, the specific causes within that pathophysiology are going to be different based on the piece of tissue that you have. In this case, the optic nerve. Dr Berkowitz: In our final moments here, we've talked a lot about the approach to monocular visual loss. I think most neurologists, once we find a visual field defect, we breathe a sigh of relief that we know we're in our home territory here, somewhere in the visual task base that we've studied very well. I'm not trying to distinguish ocular causes amongst themselves or ocular from optic nerve, which can be very challenging at the bedside. But one topic you cover in your article, which I realized I don't really have a great approach to, is transient binocular visual loss. Briefly here, since we're running out of time, what's your approach to transient binocular visual loss? Dr Newman: We assume with transient binocular vision loss that we are not dealing with a different experience in each eye, because if you have a different experience in each eye, then you're dealing with bilateral eyeball or optic nerve. But if you're having the same experience in the two eyes, it's equal in the two eyes, then you're located. You're located, usually, retro chiasmally, or even chiasm if you have pituitary apoplexy or something. So, all of these things require imaging, and I want to take one minute to talk about that. If you are sure that you have monocular vision loss, please don't get a brain MRI without contrast. It's really useless. Get a orbital MRI with contrast and fat suppression techniques if you really want to look at the optic nerve. Now, let's say you you're convinced that this is chiasmal or retrochiasmal. Well then, we all know we want to get a brain MRI---again, with and without contrast---to look specifically where we could see something. And so, if it's persistent and you have a homonymous hemianopia, it's easy, you know where to look. Be careful though, optic track can fool you. It's such a small little piece, you may miss it on the MRI, especially in someone with MS. So really look hard. There's very few things that are homonymous hemianopias MRI negative. It may just be that you didn't look carefully enough. And as far as the transient binocular vision loss, again, remember, even if it's persistent, it has to be equal vision in the two eyes. If there's inequality, then you have a superimposed anterior visual pathway problem, meaning in front of the chiasm on the side that's worse. The most common cause of transient binocular vision loss would be a form of migraine. The visual aura of migraine usually is a positive phenomenon, but sometimes you can have a homonymous hemianopic persistent defect that then ebbs and flows and goes away. Usually there's buildup, lasts maybe fifteen minutes and then it goes away, not always followed by a headache. Other things to think of would be transient ischemic attack in the vertebra Basler system, either a homonymous hemianopia or cerebral blindness, what we call cortical blindness. It can be any degree of vision loss, complete or any degree, as long as the two eyes are equal. That should last only minutes. It should be maximum at onset. There should be no buildup the way migraine has it. And it should be gone within less than ten minutes, typically. After fifteen, that's really pushing it. And then you could have seizures. Seizures can actually be the aura of a seizure, the actual ictal phenomenon of a seizure, or a postictal, almost like a todd's paralysis after a seizure. These events are typically bright colors and flashing, and they last usually seconds or just a couple of minutes at most. So, you can probably differentiate them. And then there are the more- less common but more interesting things like hyperglycemia, non-ketonic hyperglycemia can give you transient vision loss from cerebral origin, and other less common things like that. Dr Berkowitz: Fantastic. Although we've talked about many pearls of clinical wisdom here with you today, Dr Newman, this is only a fraction of what we can find in your article with Dr Biousse. We focused here on monocular visual loss and a little bit at the end here on binocular visual loss, transient binocular visual loss. But thank you very much for your article, and thank you very much for taking the time to speak with us today. Again, today I've been interviewing Dr Nancy Newman about her article with Dr Valerie Biousse on the approach to visual loss, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum audio episodes from this and other issues. Thank you so much to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
In this episode of Grounded, we dive into Josie's inspiring journey of resilience and adaptation. Living with vestibular neuritis and Persistent Postural-Perceptual Dizziness (PPPD), Josie has faced both physical and mental challenges, from managing symptoms to navigating daily life. She shares the ups and downs of her experience, the tools and strategies that have helped her along the way, and her journey toward thriving despite her diagnoses. Tune in to hear her empowering story and gain insights that may help others on similar paths. Links/Resources Mentioned: Vestibular Group Fit (code GROUNDED at checkout for 15% off!) Links/Resources Mentioned: The 4 Steps to Managing Vestibular Migraine The PPPD Management Masterclass What your Partner Should Know About Living with Dizziness The FREE Mini VGFit Workout The FREE POTS - safe Workouts Vestibular Group Fit (code GROUNDED at checkout!) Connect with Dr. Madison: @TheVertigoDoctor @TheOakMethod @VestibularGroupFit Connect with Dr. Jenna @dizzy.rehab.therapist Work with Dr. Madison 1:1, Vestibular Rehabilitation Therapy Vestibular Group Fit Why The Oak Method? Learn about it here! Love what you heard? Reviews really help us out! Please consider leaving one for us. This podcast is for informational purposes only and may not be the best fit for you and your personal situation. It shall not be construed as medical advice. The information and education provided here is not intended or implied to supplement or replace professional medical treatment, advice, and/or diagnosis. Always check with your own physician or medical professional before trying or implementing any information read here. Amazon Affiliate Disclaimer: As an Amazon Associate, I earn from qualifying purchases with no extra cost to you. Dr. Madison Oak, PT is a dedicated vestibular physical therapist committed to enhancing the quality of life for individuals grappling with chronic vestibular conditions. She is the proprietor of Oak Physical Therapy & Wellness, a reputable telehealth vestibular rehabilitation therapy practice catering to clients across six states. Additionally, Dr. Oak is the visionary behind Vestibular Group Fit, an esteemed international group program. With over 500 members, her program has successfully empowered individuals with vestibular disorders to reclaim control over their lives.
Dr. Habib Rizk, MD is a Neurotologist and Associate Professor at the Medical University of South Carolina (MUSC). He joins Dr. Abbie Ross, PT, NCS, and Dr. Danielle Tolman, PT to discuss his experience not only as an expert clinician in the field of treating vestibular dysfunction, but also as a person who has experienced vestibular dysfunction first hand following an episode of Vestibular Neuritis! Where to find Dr. Rizk: MUSC Health: https://providers.muschealth.org/sc/mount-pleasant/habib-rizk-md-msc Email: rizkh@musc.edu The Vestibular Disorders Association: https://vestibular.org/ VeDA's Provider Directory: https://vestibular.org/healthcare-directory/ Hosted by Dr. Abbie Ross, PT, NCS, and Dr. Danielle Tolman, PT For Episode Recommendations or Requests, email us info@balancingactrehab.com Where to find us: https://link.me/balancingactrehabwww.BalancingActRehab.com Facebook: @BalancingActRehab Instagram: @BalancingActRehab Twitter: @DizzyDoctors TikTok: @BalancingActRehab Check out our self guided self help courses! How to Live with Dizziness How to Treat Positional Dizziness https://balancing-act-rehab-s-school.teachable.com/courses/
Dr. Drew Carey interviews Dr. John J. Chen on the trends and use patterns of plasma exchange therapy for optic neuritis, from his Ophthalmology article, “Trends in Plasma Exchange Use in Optic Neuritis Hospitalizations in the United States.” Trends in Plasma Exchange Use in Optic Neuritis Hospitalizations in the United States. Akosman, Sinan et al. Ophthalmology, Volume 131, Issue 10, 1207 – 1214.
What are blepharitis, conjunctivitis, meibomitis, iritis, uveitis, keratitis, retinitis, neuritis, and meningitis? Dr. Cremers reviews eye anatomy and diseases related to the different parts of the eye
In this episode, I open up about my recent health struggles and the profound emotional toll they've taken on me. Living with an incurable disease has been incredibly challenging, especially coming to terms with situations that can't be fixed or where answers are elusive. I share my personal journey with optic neuritis, the constant fear of relapse, and the irreversible damage revealed by my MRI results. Through candid reflections on anger, resentment, and grief, I navigate the invisible losses that accompany chronic illness. Join me as I emphasize the importance of self-compassion and discovering meaningful ways to live fully despite the pain.Follow me on Instagram @martis_mslifeVideo Pod: https://youtu.be/-Pl4AV5LUm4?si=nXznLhHzm7F9a8sMSend me a question and I will share it on the pod!: marti@marthines.com www.martihines.comProduced by Natalie Byrdsong
If you're a runner with heel pain you may think you have plantar fasciitis. But if it is not getting better, your heel pain may be caused by "neuritis." I was just giving a lecture to a group of physicians getting their continuing medical education credits at the International foot Medical Foundation medical conference in Lake Tahoe. I was giving a lecture called “When Heel Pain is NOT Plantar Fasciitis in Runners.” One of the conditions I was talking about was "medial calcaneal neuritis." One of the doctors in the audience asked a really great question... He said, “I see a lot of people that have Baxter's neuritis, and it's down on the bottom of the heel it's plantar , it's not on the side of the heel, it's not medial neuritis, it's different. What would you do to tell the difference between these two conditions in a runner, given the circumstances you just explained in the talk?” Today on the Doc On The Run Podcast we're talking about medial calcaneal neuritis versus Baxter's neuritis in a runner.
In this episode we do a deep dive into Vestibular Neuritis, hypofunction, when it may have turned into persistent postural perceptual dizziness (PPPD) and more! Join us on this 30 minute, quick adventure to learn what to do if you're new to vestibular neuritis and hypofunction, or if you've had it for a while now and feel stuck! Remember, there are always always answers when it comes to neuritis, you just need the right tools in your toolbox! Links/Resources Mentioned: Vestibular Group Fit (code GROUNDED at checkout!) Links/Resources Mentioned: The 4 Steps to Managing Dizziness for Good The PPPD Management Masterclass What your Partner Should Know About Living with Dizziness The FREE Mini VGFit Workout The FREE POTS - safe Workouts Vestibular Group Fit (code GROUNDED at checkout!) Connect with Dr. Madison: @TheVertigoDoctor @TheOakMethod @VestibularGroupFit Connect with Dr. Jenna @dizzy.rehab.therapist Work with Dr. Madison 1:1, Vestibular Rehabilitation Therapy Vestibular Group Fit Small Group Coaching (offered throughout the year, sign up for our email list to learn when!) Why The Oak Method? Learn about it here! Love what you heard? Reviews really help us out! Please consider leaving one for us. This podcast is for informational purposes only and may not be the best fit for you and your personal situation. It shall not be construed as medical advice. The information and education provided here is not intended or implied to supplement or replace professional medical treatment, advice, and/or diagnosis. Always check with your own physician or medical professional before trying or implementing any information read here.
MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: June 14, 2018 As a pupil of neurology and medicine, I feel like it is my responsibility to cover this topic at least once on the podcast. This topic came to me in a vision. But not one of phosphenes or impaired stereopsis--both of which we'll cover today. This week, we're discussing inflammation of the optic nerve, from the historical aspects to current concepts. And while you're listening, there's no need to lash out at my puns. You can stop rolling your eyes now. Produced by James E Siegler. Music by Lee Rosevere, Kevin McLeod, Steve Combs, and Unheard Music Concepts. Voiceover by Erika Mejia. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. REFERENCES Balcer LJ. Clinical practice. Optic neuritis. N Engl J Med 2006;354(12):1273-80. PMID 16554529Beck RW, Cleary PA, Anderson MM Jr, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med 1992;326(9):581-8. PMID 1734247Hickman SJ, Dalton CM, Miller DH, Plant GT. Management of acute optic neuritis. Lancet 2002;360(9349):1953-62. PMID 12493277Liu GT, Volpe NJ, Galetta SL. Neuro-Ophthalmology: Diagnosis and Management. 2nd Ed. Elsevier, 2010.O'Doherty M, Flitcroft DI. An unusual presentation of optic neuritis and the Pulfrich phenomenon. J Neurol Neurosurg Psychiatry 2007;78(8):906-7. PMID 17635984Toosy AT, Mason DF, Miller DH. Optic neuritis. Lancet Neurol 2014;13(1):83-99. PMID 24331795Volpe NJ. Optic neuritis: historical aspects. J Neuroophthalmol 2001;21(4):302-9. PMID 11756864 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.
Do you have post-COVID or post-vax dizziness and vestibular hypofunction? In this episode we talk about Kristi's journey working for herself, returning to work, returning to exercise, and more! Dizziness, no matter where is comes from, is common and is also manageable so dizziness doesn't have to control your life! Topics we cover: Vestibular Neuritis COVID related hypofunction and dizziness Vaccine Related Dizziness Vestibular Hypofunction Returning to work, taking a break, and scaling back to work with a vestibular disorder Connect with Kristi: Encircled's Instagram Encircled.ca Kristi's Instagram Links/Resources Mentioned: The 4 Steps to Managing Dizziness for Good The PPPD Management Masterclass What your Partner Should Know About Living with Dizziness The FREE Mini VGFit Workout The FREE POTS - safe Workouts Vestibular Group Fit (code GROUNDED at checkout!) Outlive by Peter Attia Connect with Dr. Madison: @TheVertigoDoctor @TheOakMethod @VestibularGroupFit Work with Dr. Madison 1:1, Vestibular Rehabilitation Therapy Vestibular Group Fit Small Group Coaching (offered throughout the year, sign up for our email list to learn when!) Why The Oak Method? Learn about it here! Love what you heard? Reviews really help us out! Please consider leaving one for us. This podcast is for informational purposes only and may not be the best fit for you and your personal situation. It shall not be construed as medical advice. The information and education provided here is not intended or implied to supplement or replace professional medical treatment, advice, and/or diagnosis. Always check with your own physician or medical professional before trying or implementing any information read here.
Myelin oligodendrocyte glycoprotein-related optic neuritis is typically associated with good visual outcome in most patients, but poor outcomes are reported in 15% to 36.8% of patients. Dr. Drew Carey sits down with Dr. Edward Margolin to discuss the possible factors associated with poor outcomes, from his Ophthalmology article, “Predictors of Poor Visual Outcome in MOG-related Optic Neuritis.” Predictors of Poor Visual Outcome in Myelin Oligodendrocyte Glycoprotein-Related Optic Neuritis. Handzic, Armin et al. Ophthalmology, Volume 130, Issue 9, 993 - 995
This week Dr. Daniel Correa sits down with mixed media artist Laura Bundesen to discuss her journey of being diagnosed with vestibular neuronitis. Laura shares the symptoms she experienced and the therapies she has utilized to improve her condition, as well as how the brain inspires her colorful fiber art. Next Dr. Correa speaks with Dr. Olwen Cait Murphy, a neurologist and assistant professor at Johns Hopkins University in Baltimore, Maryland. Dr. Murphy explains the vestibular system and how it relates to vestibular neuronitis, how this condition affects people's lives, and the various therapies available to manage symptoms. Additional Resources View Laura Bundesen's Neuro Art Gallery Vestibular Disorders Association (VEDA) Brain & Life: Exercises to Improve Balance Can Reduce Falls and Boost Confidence American Stroke Association: Learn more about F.A.S.T We want to hear from you! Have a question or want to hear a topic featured on the Brain & Life Podcast? Record a voicemail at 612-928-6206 Email us at BLpodcast@brainandlife.org Social Media: Guest: Laura Bundesen @LauraBundesen (Twitter & Instagram); Johns Hopkins University @HopkinsMedicine (Twitter) Hosts: Dr. Daniel Correa @neurodrcorrea
Die Ursachen für Schwindel können vielfältig sein. Bei einer speziellen Form - der "Neuritis vestibularis" - sind die Schwindelanfälle besonders heftig. Die gute Nachricht: die Erkrankung lässt sich gut behandeln. Von Beate Bossdorf und Ursula Stamm
When a patient presents to you and you're concerned about the diagnosis of optic neuritis, it can sometimes feel a bit tricky. On the one hand, the patient's vision can be quite poor and the systemic implications of such a diagnosis can be quite significant; on the other hand, the teaching for some time has not been so definitive on what, if anything, we should do in the short-term. So what does the current evidence show? What is role for steroids? How urgent is an MRI? How essential is an accurate diagnosis? Neuro-ophthalmologist Dr. Andrew Lee joins the podcast. Dr. Andrew Lee's YouTube Channelhttps://www.youtube.com/channel/UC5HcfsELV0W9AqtvJvpQQSg
Dr. John Chen, renown Neuro-ophthalmologist takes us through the history of optic neuritis, starting with the optic Neuritis Treatment Trial. Lots has changed since that time, and Dr. Chen teaches us about new, atypical causes of optic neuritis like MOGAD and NMO. Subscribe to the podcast: https://MayoClinicOphthalmology.podbean.com Follow and reach out to us on Twitter: @mayocliniceye
Episode 550 Wellness Wednesday episode in which we talk about Multiple Sclerosis stuff: MS Facts, MS Symptoms, Optic Neuritis, Intellectual Compatibility, White Rice, Oxidative Stress. #MS, #MultipleSclerosis, #healthtalk, #MonSter, #brain Send comments, questions and tips to kevintheduckpool@gmail.com please help us out by rating and reviewing us and telling a friend. Also check out audio and video versions of Crimson Cowl Comic Club & Under the Cowl podcasts. A fun variety of great people talk comic books, entertainment or whatever and you can see or hear me on many episodes of those podcasts as well with many more great episodes to come out in the future. --- Send in a voice message: https://podcasters.spotify.com/pod/show/kevin-kleinhans/message Support this podcast: https://podcasters.spotify.com/pod/show/kevin-kleinhans/support
An interesting runner called me for a second opinion. He had a couple of things going on that created a pretty confusing picture. He had a plantar plate sprains (at least he was told he had plantar plate injuries) because his MRI showed evidence of injuries to the plantar plate ligaments of toes two, three, and four. He also had some nerve type symptoms. But on the bottom of the foot, he also had this very interesting ridge of callus. So what was REALLY causing all of his trouble when he ran? Today, on the Doc On The Run Podcast, we're talking about a runner with a plantar plate injury and deep perineal neuritis.
HOST: Dr. Jimmy Stewart, Professor of Internal Medicine and Pediatrics at the University of Mississippi Medical Center.TOPICS DISCUSSED: Dry mouth (Xerostomia), eye twitching, neuropathy (Neuritis), eczema (skin inflammation), burning mouth syndrome (Glossodynia), tennis elbow (Lateral Epicondylitis), Magnesium, B-12, B-3 and Vitamin D. EMAIL: remedy@mpbonline.orgIf you enjoyed listening to this podcast, please consider making a contribution to MPB: https://donate.mpbfoundation.org/mspb/podcast. Hosted on Acast. See acast.com/privacy for more information.
Axel Petzold (National Hospital for Neurology and Neurosurgery and Moorfields Eye Hospital, London, UK, and Amsterdam University Medical Center, Amsterdam, Netherlands) discusses a Position Paper, published in the December issue of The Lancet Neurology, which sets out new criteria for the diagnosis and classification of optic neuritis.Read the Position Paper:Diagnosis and classification of optic neuritis
The majority of those diagnosed with MS at some point will have one of the two eye disorders occur. They are both very different in symptoms but rather common in length of time to recover. Take a listen if it could help you or a loved one. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app
In this episode, we review the high-yield topic of Optic Neuritis from the Opthalmology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets
Jimmy Pedro from Communards tells Lexman about his experience with neuritis and how music can help ease the symptoms. Lexman and Pedro discuss the relationship between music and health and what benefits music has for people with various diagnoses.
Six years ago Em went through a health crisis after the birth of her second child. Her symptoms of dizziness, brain fog, derealization, eyes that didn't want to focus, anxiety, vestibular migraines (and more) were a chaotic storm that hit her system. Her symptoms were 24/7 for close to two years. Eighteen months into her journey she was diagnosed with vestibular neuritis and vestibular migraines (but also had other labels thrown at her). She dedicated herself to learning about holistic nutrition, embarked on a journey of healing the root cause, embraced a non-toxic lifestyle, neuroplasticity and furthered her knowledge of fueling health every step of the way (and continues to). These days she coaches other Vestibular Warriors to move through their vestibular something aS well as being a holistic nutritionist helping people utilize lifestyle medicine to fuel health. She shares her story extensively over on Vestibular Warrior YouTube channel and in her two books "Uncovering Bliss: A Journey With A Vestibular Condition and Beyond" as well as "Creating Bliss In Your Life With A Vestibular Condition and Beyond". She is also the founder of bliss-out.co, the happy wellness space for Vestibular Warriors. Her passion is to inspire and empower others to find freedom from their vestibular something, create vibrant health and follow their dreams along the way. If you would like more information on vestibular disorder's please visit VeDA (Vestibular Disorders Association). Here you will find more information on balance disorders, diagnosis, treatment, medical professionals, support groups, even a new patient tool kit and so much more. It has been an amazing resource. If you would like to get a free copy of Ems newly released book Creating Bliss In Your Life With A Vestibular Condition and Beyond. – reach out to and mention the Meniere's Muse podcast. Find Em on her YouTube at Vestibular Warriors Talks , Instagram, her podcast or her website. If you would like to connect with myself Heather Davies, please feel free to reach out to me via email Menieresmuse@gmail.com or find me on Instagram. If you or someone you know has an inspiring vestibular journey, I would love to speak with them, please direct message me and let's connect! Thank you so much for being here. I would like to take a moment and say thank you for being a part of the Meniere's Muses Community. I love to share stories of people making a positive impact in the vestibular community. Your feedback means the world to me. If you haven't already left a review please do so and let me know what you would like to hear more of on the show. Please be sure to subscribe to Meniere's Muse for updates. Thank you for listening! I'll see you next week warriors!
This week I am talking with Lara, about her vestibular journey with Labyrinthitis, Vestibular Neuritis and Vestibular Migraine that began after delivering her twin daughters, over twelve years ago. Her symptoms began to increase, and she was experiencing hyperacusis, light sensitivity and small vertigo episodes that got progressively worse over 2 years. Which lead to scary debilitating vertigo, disequilibrium, panic attacks, agoraphobia and like many vestibular warriors' bouts of depression and some suicidal thoughts. Having strong support from family and wanting to be an active parent in her daughter's lives helped her find the inner strength to push on. She began her blog, rightfully called Mummy Seeing Double, to share her healing journey and so others would feel less alone. Lara lives in Surrey, England with her beautiful family and continues to be an inspiration to many. If you would like more information on vestibular disorder's please visit VeDA (Vestibular Disorders Association). Here you will find more information on balance disorders, diagnosis, treatment, medical professionals, support groups, even a new patient tool kit and so much more. It has been an amazing resource. If you would like to connect with Lara at Mummy Seeing Double | Facebook or find her on Instagram. If you would like to connect with myself Heather Davies, please feel free to reach out to me via email Menieresmuse@gmail.com or find me on Instagram. If you or someone you know has an inspiring vestibular journey, I would love to speak with them, please direct message me and let's connect! Thank you so much for being here.
Finding her passion by sharing her story. This week I am talking with Tammy about her vestibular journey with drop attacks, vestibular migraine, neuritis and Meniere's disease after a labyrinthectomy. She also shares how finding the right support in a Facebook group helped her feel less alone and changed her life. Finding the support of a vestibular family helped her find her passion for helping others with chronic illness, she connects with others as a Creator on the platform Clapper. As a vlogger on Clapper, she connects with other chronic illness warriors and currently has over 106k followers. She shares about her day-to-day challenges while giving other warriors support while they face new obstacles in their lives. Thank you for being here warriors! If you would like more information on vestibular disorder's please visit VeDA (Vestibular Disorders Association). Here you will find so much information on balance disorders, from diagnosis, treatment, medical professional, support groups, even a new patient tool kit and so much more. It's been an invaluable tool. If you would like to connect with Tammy, please find her on Clapper – or Instagram (Click here to go directly to her IG account). If you would like to connect with me, Heather Davies, please feel free to reach out via email at Menieresmuse@gmail.com or find me on Instagram. Have an amazing week warriors!
When Vikki Farrell of Pennsylvania woke up one morning in October of 2014, she had trouble seeing out of her left eye. After being diagnosed with optic neuritis, a form of MS, she was put on medication that caused her to lose weight. Her husband Mike, a former cop, started her on cannabis oil thereby arresting further degradation of her eyesight. In this delightful story, they also have some harsh words for some in the medical profession.
Dr. Christos Ganos discusses the article, "A neural network for tics: insights from causal brain lesions and deep brain stimulation". Show references: https://academic.oup.com/brain/advance-article-abstract/doi/10.1093/brain/awac009/6506575 To hear the full podcast: https://www.neurology.org/podcast
Unvermittelt auftretender Schwindel kann Übelkeit und Angst auslösen. Neuritis vestibularis wird dieses Phänomen genannt. Dahinter verbirgt sich eine besondere Form des Drehschwindels. Durch eine Entzündung im Ohr gelangen die normalen Informationen des Gleichgewichtsorgans nicht mehr zum Gehirn. Von Laura Will
In some cases, MS can try to steal your identity. Karen Dwyer shares how she leaned into her core values to "heal" her MS and live her best life. She now helps others to do the same. Karen's TEDx talk, What's Your Shoe Size Got to do With Chronic Illness? released last month already has thousands of views. Karen is thriving! Instagram: @iamkarendwyer Facebook: https://www.facebook.com/iamkarendwyer Website: https://www.karendwyer.com/ Instagram: @thrivingoversurivingpodcast Website: httpss://thrivingoversurvivingpodcast.com
In some cases, MS can try to steal your identity. Karen Dwyer shares how she leaned into her core values to "heal" her MS and live her best life. She now helps others to do the same. Karen's TEDx talk, What's Your Shoe Size Got to do With Chronic Illness? released last month already has thousands of views. Karen is thriving! Instagram: @iamkarendwyer Facebook: https://www.facebook.com/iamkarendwyer Website: https://www.karendwyer.com/ Instagram: @thrivingoversurivingpodcast Website: httpss://thrivingoversurvivingpodcast.com
If you're a runner with running pain on the top of the foot, it could be lots of different things. The actual diagnosis depends on what happened, what you did, and what it feels like now. There are a couple of really common things causing pain in the top of the foot in runners. Let's talk about two common causes. It may be either a tendon or a nerve on the top of your foot. Today on the Doc On The Run Podcast, we're talking about how a runner can tell tenosynovitis from neuritis in the top of the foot.
This episode actually comes from a question I got during the live question and answer period at the end of a talk I was giving at the International Foot and Ankle Foundation meeting in Hawaii. The question was about one of the conditions that can often be misdiagnosed as plantar fasciitis, and that's a condition called medial calcaneal neuritis. With this condition a nerve on the inside of the heel becomes inflamed and painful. In short, the patient had alcohol injection under ultrasound guidance by another doctor, but the condition dod not get any better. The question from the doctor in the audience was basically asking me what my opinion about that procedure using ultrasound. Today on the Doc On The Run Podcast, we're talking about heel neuritis in a situation where a doctor did an alcohol injection with ultrasound and another doctor wanted to know if that was a scam.
Dr. Rani Banik is an integrative neuro-ophthalmologist. She focuses on both western and holistic medicine. She joins me for the first of three episodes focusing on brain and eye health. In this episode, Dr. Banik shares her insights about Optic Neuritis; causes, triggers, and how to prevent future occurrences. More about Dr. Banik: Her practice promotes an integrative approach to vision and brain health that incorporates nutrition botanicals supplements and lifestyle modification, along with traditional western medical therapies. Instagram: @dr.ranibanik Facebook Groups: Eye on Migrain & EnVision Health Sign up for my weekly newsletter beginning in October www.thrivingoversurvivingpodcast.com Instagram: @thrivingoversurvivingpodcast
Dr. Rani Banik is an integrative neuro-ophthalmologist. She focuses on both western and holistic medicine. She joins me for the first of three episodes focusing on brain and eye health. In this episode, Dr. Banik shares her insights about Optic Neuritis; causes, triggers, and how to prevent future occurrences. More about Dr. Banik: Her practice promotes an integrative approach to vision and brain health that incorporates nutrition botanicals supplements and lifestyle modification, along with traditional western medical therapies. Instagram: @dr.ranibanik Facebook Groups: Eye on Migrain & EnVision Health Sign up for my weekly newsletter beginning in October www.thrivingoversurvivingpodcast.com Instagram: @thrivingoversurvivingpodcast
In this episode we'll discuss everything we need to know about MS and visual impairment. We'll dive into the research, diagnosis processes, and typical treatment protocols for a variety of visual disturbances common for people with MS, including Optic Neuritis and Photophobia. We'll also cover helpful strategies and tools that exist for us to use to help us better manage our visual impairment, as well as ways to limit future damage.
In this podcast, Dr Auerbach discusses the causes of vision loss that occur in optic neuritis, the subtypes and possible treatments.
Multiple Sclerosis News Today's columnist, Jenn Powell, discusses two biomarkers found to predict MS onset in people with optic neuritis. Multiple Sclerosis News Today's columnist, Jessie Ace, talks about a show she watched and how disability was perceived by strangers. ===================================== Treatment for Relapsing MS Progression | MAYZENT® (siponimod) Read about MAYZENT, a once daily pill that can significantly slow down disability progression in people with relapsing MS. See full prescribing & safety info. https://www.mayzent.com/?utm_source=changeinrms&utm_medium=vanityurl&utm_campaign=novartis_mayzent_2020&utm_content=soundcloud ===================================== Are you interested in learning more about multiple sclerosis? If so, please visit: https://multiplesclerosisnewstoday.com/ ===================================== To join in on conversations regarding multiple sclerosis, please visit: https://multiplesclerosisnewstoday.com/forums/
Vidcast: https://youtu.be/lEjT1k3ouG4 CoVid can trigger autoimmune disease like rheumatoid arthritis, autoimmune, muscle inflammation, and so-called CoVid toes. For the first time, radiologists at Northwestern University release images of these CoVid-induced maladies. Using multi-modality imaging including conventional radiography, CT, MR, and ultrasound, the investigators assembled pictoral proof of CoVid attacks on muscle, nerves, joints, bone, and soft tissues including skin. As radiologists begin to image more patients with CoVid, their abilities to detect viral-induced tissue and organ damage increases. If you or yours have a CoVid infection with symptoms that are dragging on besides the usual respiratory ones, suggest imaging to search for CoVid-triggered rheumatic and autoimmune type damage. https://link.springer.com/article/10.1007/s00256-021-03734-7 #CoVid #autoimmune #rheumatic #arthritis #neuritis #myositis
If you over-stretch any nerve it can become inflamed and painful. If you roll your ankle on a trail you can get a condition called traction neuritis. Most of the time when I am on a telemedicine or second opinion call with a runner with traction neuritis, they have been misdiagnosed with some other condition. If you understand how to tell the difference, you can understand how to get back to running sooner. Today on the Doc On The Run Podcast we're talking about traction neuritis in a runner and what it really means.
From Q&A - 304 - Eczema, Moringa Oleifera, Optic Neuritiswww.drmorsesherbalhealthclub.comHave a question? Send it to: questios@dmhhc.com
In this episode, I explore Optic Neuritis and how it could possibly present in an OSCE scenario. Some of the questions I answer are; what is Optic Neuritis? What are its types? How to distinguish between them? What are the most important signs and symptoms? And how to manage such a condition? Join the UKME PLAB 2 buzz on telegram: https://t.me/joinchat/MlKz3kycXEI5EOBORA1ZTg #Team_UKME #hundreds_of_doctors_cannot_be_wrong Order the UK Made Easy Mock Service at: www.ukmadeeasy.net/book-online The UK Made Easy podcast is now available on YouTube: https://www.youtube.com/channel/UCJErxo95pM3iP5hE3jmiUqA Disclaimer The information in this episode and other ones is the fruit of our own studying and practice with hundreds of doctors. Even though we rely heavily on patient.info for researching our content but it should only be used for entertainment purposes and never to replace your own preparation. It's also important to declare that we are not related to the PLAB 2 OSCE examination in any formal shape, way, or form. The fees you pay for our services are solely for locking the free time of our doctors for your assistance based on common OSCE scenarios.
How can a Specific Chiropractor help a patient who is suffering from low back and sciatica without every adjusting the lumbar spine? Could the causative subluxation be found in the upper cervical area?
Interview with Stacy L. Pineles, MD, author of Assessment of Pediatric Optic Neuritis Visual Acuity Outcomes at 6 Months
Interview with Stacy L. Pineles, MD, author of Assessment of Pediatric Optic Neuritis Visual Acuity Outcomes at 6 Months
Interview with Tasanee Braithwaite, author of Trends in Optic Neuritis Incidence and Prevalence in the UK and Association With Systemic and Neurologic Disease
Interview with Tasanee Braithwaite, author of Trends in Optic Neuritis Incidence and Prevalence in the UK and Association With Systemic and Neurologic Disease
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.09.141432v1?rss=1 Authors: Song, K., Li, J., Zhu, Y., Ren, F., Cao, L., Shao, Y., Huang, Z. Abstract: Purpose: This study investigated changes in small-world topology and brain functional connectivity in patients with optic neuritis (ON) by resting-state functional magnetic resonance imaging (rs-fMRI) and based on graph theory. Methods: A total of 21 patients with ON (8 males and 13 females) and 21 matched healthy control subjects (8 males and 13 females) were enrolled at the First Affiliated Hospital of Nanchang University and underwent rs-fMRI. Data were preprocessed and the brain was divided into 116 regions of interest. Small-world network parameters and area under the integral curve (AUC) were calculated from pairwise brain interval correlation coefficients. Differences in brain network parameter AUCs between the 2 groups were evaluated with the independent sample t-test, and changes in brain connection strength between ON patients and control subjects were assessed by network-based statistical analysis. Results: In the sparsity range from 0.08 to 0.48, both groups exhibited small-world attributes. Compared to the control group, global network efficiency, normalized clustering coefficient, and small-world value were higher whereas the clustering coefficient value was lower in ON patients. There were no differences in characteristic path length, local network efficiency, and normalized characteristic path length between groups. In addition, ON patients had lower brain functional connectivity strength among the rolandic operculum, medial superior frontal gyrus, insula, median cingulate and paracingulate gyri, amygdala, superior parietal gyrus, inferior parietal gyrus, supramarginal gyrus, angular gyrus, lenticular nucleus, pallidum, superior temporal gyrus, cerebellum_Crus1_L, and left cerebellum_Crus6_L compared to the control group (P < 0.05). Conclusion: The brain network in ON has a small-world attributes but shows reduced and abnormal connectivity compared to normal subjects. These findings provide a further insight into the neural pathogenesis of ON and reveal specific fMRI findings that can serve as diagnostic and prognostic indices. Keywords: Optic neuritis; Small-world network; Brain network connectivity; Network-based statistical analysis Copy rights belong to original authors. Visit the link for more info
In our first episode, we discuss an early symptom of MS called optic neuritis. My guest is Kristina who lost her vision when she was 25-years-old. She explains how this condition led to a life changing diagnosis of MS. Her story is full of hope and encouragement for young women diagnosed with the disease. Due to the COVID-19 pandemic, this year will be a Virtual MS Bike Details at http://www.msbike.ca Guest: Follow kristina__rose on Instagram Contact: Host Andrea Dunn @TeamDunner For more information on the MS Society of Canada @MSSocietyCanada or online at https://mssociety.ca/ See omnystudio.com/listener for privacy information.
Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I’m looking forward to sharing with you some of our community’s questions that have come in over the past few weeks… Let’s get started! Ryan: Thoughts on the Kangen water machine please? :) Jamie: Hi Dr. Cabral! I was wondering what your thoughts on Whole Body Vibration machines are. I have one that oscillates in a triangle pattern (up and down on each side - one side up while the other side is down and vice versa). I know you don't have much time on the housecalls but would you consider doing a podcast on these machines and how they can possibly fit in the DESTRESS protocol? Thanks as always! Anonymous: Hi Dr. Cabral, my friend was diagnosed with stage 4 breast cancer that is hormone positive. She did chemo & hormone therapy and has since eliminated all estrogen production in her body. She is 39 years old and just had a hysterectomy and will have her estrogen eliminated for the rest of her life. As an IHP in training I know that all hormones are there for a reason and I'm wondering as her friend how can I help guide her to be healthy for the rest of her life without estrogen? Any tips? Any books you can recommend on this? Thanks! Anonymous:Hi Dr. Cabral, I know you mentioned that eventually you will be developing a pet line of products. My dog is having some digestive issues & skin issues that I think could be leaky gut and/or gut dysbiosis. My question to you is if you have any recommendations on companies to buy from or books to read or mentors to follow to learn about how to holistically restore my dog's health? Thanks as always for all you do! You truly are a great human being!! Paula: Hi Dr. Cabral, thank you so much for helping us in our health journey! My stool test results were ok but leaky gut was not tested and I also have high igA. I have horrible eczema, acne and major food sensitivities so I am in the process of healing leaky gut through diet and supplementation as I’m pretty sure I have it. I have eliminated all common allergies from my diet but I continue to have eczema and acne. I cannot afford an IgG test so my question is: Can I heal my gut by just eliminating gluten, dairy, eggs, soy, nuts and grains? Or do I have to do an IgG test to eliminate those foods that I may also be sensitive to? Ryan: I always took my urine being somewhat clear to mean I'm well hydrated, but I've heard you say it could mean losing electrolytes? Does gulping water make it go straight through you? How/why? Christy: I am a 42 female and was diagnosed with MS in 2006. I recently went to the eye doctor and said I had Optic neuritis which I had a year ago, but now it’s worse. Not sure what to do. Thanks Paula: Hi Dr Cabral. Should meals be divided equally in protein/carbs/fat and do I need to eat protein at every meal to build muscle? Thank you so much for what you do, you truly are amazing! Laura: I've heard that it is better to eat carbs (including fruits) later in the day and having a protein based breakfast to avoid blood sugar spikes. Why do you recommend eating fruits/oats for breakfast? Laura: Hi Dr Cabral! I’m in the process of healing leaky gut and I was wondering what your thoughts are on grains/legumes right now? I’m also sensitive to hemp hearts now so any protein substitutes for meals? Thank you for tuning into this weekend’s Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! - - - Show Notes & Resources: http://StephenCabral.com/1514 - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - - Dr. Cabral’s Most Popular Supplements: > “The Dr. Cabral Daily Protocol” (This is what Dr. Cabral does every day!) - - - > Dr. Cabral Detox (The fastest way to get well, lose weight, and feel great!) - - - > Daily Nutritional Support Shake (#1 “All-in-One recommendation in my practice) - - - > Daily Fruit & Vegetables Blend (22 organic fruit & vegetables “greens powder”) - - - > CBD Oil (Full-spectrum, 3rd part-tested & organically grown) - - - > Candida/Bacterial Overgrowth, Leaky Gut, Parasite & Speciality Supplement Packages - - - > See All Supplements: https://equilibriumnutrition.com/collections/supplements - - - Dr. Cabral’s Most Popular At-Home Lab Tests: > Hair Tissue Mineral Analysis (Test for mineral imbalances & heavy metal toxicity) - - - > Organic Acids Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Thyroid + Adrenal + Hormone Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Adrenal + Hormone Test (Run your adrenal & hormone levels) - - - > Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Omega-3 Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - > Stool Test (Use this test to uncover any bacterial, h. Pylori, or parasite overgrowth) - - - > Genetic Test (Use the #1 lab test to unlocking your DNA and what it means in terms of wellness, weight loss & anti-aging) - - - > Dr. Cabral’s “Big 5” Lab Tests (This package includes the 5 labs Dr. Cabral recommends all people run in his private practice) - - -
In this episode, we review the high-yield topic of Brachial Neuritis (Parsonage-Turner Syndrome) from the Shoulder & Elbow section. --- Send in a voice message: https://anchor.fm/orthobullets/message
SRNA is joined by Dr. Amanda Henderson and Dr. Elias Sotirchos for a podcast on "Optic Neuritis: When is just ON and when does it mean more?" The medical experts begin by explaining what optic neuritis is, the symptoms, and how it is diagnosed. Treatments, both acute and ongoing, are discussed, as well as circumstances surrounding relapses. The medical experts then discuss ON in the context of other diagnoses such as neuromyelitis optica spectrum disorder, MOG antibody-associated disease, and multiple sclerosis. Finally, rehabilitation and current research on ON is discussed.
Talk to a Dr. Berg Keto Consultant today and get the help you need on your journey (free consultation). Call 1-540-299-1557 with your questions about Keto, Intermittent Fasting, or the use of Dr. Berg products. Consultants are available Monday through Friday from 8:30 am to 9 pm EST. Saturday & Sunday 9 am to 5 pm EST. USA Only. Take Dr. Berg's Free Keto Mini-Course! Dr. Berg talks about the chili pepper extract in relation to its biological effect on pain relief. The active ingredient that creates the effect is called Capsaicin. This compound has the potential to block sensory nerve signals for pain and inflammation. Capsaicin Benefits: • Good for pain from rheumatoid arthritis • Good for pain from osteoarthritis • Neuritis (inflammation of the nerve) • Neuropathy which is nerve damage • Diabetic in the feet and the hands • Neurological pain from shingles • Trigeminal neuralgia (nerve pain on the face) • Sinus mucus • Sinus headaches • Improving circulation • Allergies Dr. Eric Berg DC Bio: Dr. Berg, 51 years of age is a chiropractor who specializes in weight loss through nutritional & natural methods. His private practice is located in Alexandria, Virginia. His clients include senior officials in the U.S. government & the Justice Department, ambassadors, medical doctors, high-level executives of prominent corporations, scientists, engineers, professors, and other clients from all walks of life. He is the author of The 7 Principles of Fat Burning. ABOUT DR. BERG: https://bit.ly/2FwSQQT DR. BERG'S STORY: https://bit.ly/2RwY5GP DR. BERG'S SHOP: https://bit.ly/2RN11yv DR. BERG'S VIDEO BLOG: https://bit.ly/2AZYyHt DR. BERG'S HEALTH COACHING TRAINING: https://bit.ly/2SZlH3o Follow us on FACEBOOK: https://www.messenger.com/t/drericberg TWITTER: https://twitter.com/DrBergDC YOUTUBE: https://www.youtube.com/user/drericberg123 Send a Message to Dr. Berg and his team: https://www.messenger.com/t/drericberg
Dr. David Lapides discusses the importance of early antibody evaluation in the setting of a new case of optic neuritis.
This week, Amanda and Ben review Atypical Optic Neuritis. Also, we are doing a survey to assess the impact of the podcast. If you'd like to support us, take this 4 minute survey: bit.ly/2VpPRND
This week Andrew couldn't make it, so we have Amanda back to talk about Optic Neuritis! Also, we are doing a survey to assess the impact of the podcast. If you'd like to support us, take this 4 minute survey: bit.ly/2VpPRND You also can enter to win a $100 Amazon gift card!
As a pupil of neurology and medicine, I feel like it is my responsibility to cover this topic at least once on the podcast. This topic came to me in a vision. But not one of phosphenes or impaired stereopsis--both of which we'll cover today. This week, we're discussing inflammation of the optic nerve, from the historical aspects to current concepts. And while you're listening, there's no need to lash out at my puns. You can stop rolling your eyes now. Produced by James E. Siegler. Music by Lee Rosevere, Kevin McLeod, Steve Combs, and Unheard Music Concepts. Voiceover by Erika Mejia. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision making. REFERENCES Balcer LJ. Clinical practice. Optic neuritis. The New England journal of medicine. 2006;354:1273-80. Volpe NJ. Optic neuritis: historical aspects. J Neuroophthalmol. 2001;21:302-9. Hickman SJ, Dalton CM, Miller DH and Plant GT. Management of acute optic neuritis. Lancet. 2002;360:1953-62. O'Doherty M and Flitcroft DI. An unusual presentation of optic neuritis and the Pulfrich phenomenon. Journal of neurology, neurosurgery, and psychiatry. 2007;78:906-7. Liu GT, Volpe NJ and Galetta SL. Neuro-Ophthalmology: Diagnosis and Management, 2nd Ed.: Elsevier; 2010. Beck RW, Cleary PA, Anderson MM, Jr., Keltner JL, Shults WT, Kaufman DI, Buckley EG, Corbett JJ, Kupersmith MJ, Miller NR and et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. The New England journal of medicine. 1992;326:581-8. Toosy AT, Mason DF and Miller DH. Optic neuritis. The Lancet Neurology. 2014;13:83-99.
When she's not creating beautiful, real, outspoken pieces on her blog www.fuckms.ca. This talented writer, Angela Gagliardi, is also a youth worker for high schoolers and an MS CHAMPION. Our conversation today covers everything from her battle with Neuritis, the cost of medical treatments and the stigma around the appearance of 'not looking sick'. Hope you'll join us!
Dr. Prem Subramanian
KFP | Ophthalmology | Optic Neuritis by Dr Thomas Perkins
Karl C. Golnik, MD, MEd
In this podcast, Professor Elliot Frohman discusses the treatment of acute optic neuritis and its connection with multiple sclerosis. Elliot Frohman is Professor of Neurology and Neurotherapeutics and Ophthalmology and Director of the Multiple Sclerosis and Neuroimmunology Program, at the University of Texas. Read the full paper here: http://jnnp.bmj.com/content/early/2014/10/29/jnnp-2014-308185.full
Rare Genomics / RareShare Podcast Series: Ask the Expert & Patient Navigation
Rare Genomics Institute RareShare Ask the Expert:Podcast Series, Disease Specific Q&A Sessions, For feedbacks contact, Scientific Director, Rare Genomics Institute: Deepa Kushwaha, deepa.kushwaha@raregenomics.org (Music credit: www.bensound.com)
Do you or a loved one suffer with vertigo? Today we will be discussing two of the most common causes of vertigo, Vestibular Neuritis and Meniere’s disease. New information from scientific journals is associating both of these conditions of the inner ear to be caused by the immune system. We […]
Each week Martin Pytela begin_of_the_skype_highlighting end_of_the_skype_highlighting and Scott Paton discuss Holistic principles for healthy living. Life Enthusiast Co-op is built on over 25 years in study, health consultations and market research in the field of holistic and alternative medicine. We deliver solid time tested expertise. We are in this business not for the money, but for the passion, we have for sharing with others what we had to learn the hard way, through experience. We focus on high quality, innovative holistic solutions. Length: 25:27 Go to iTunes and review our podcast: iTunes Life Enthusiast Reviews and 5 star ratings If You Enjoyed This, Please Go To "FANS OF THIS SHOW" On The RIGHT And Then Click On "BECOME A FAN". In Addition, PLEASE CLICK On The “SEND TO A FRIEND” At The Bottom Of This Podcast…. COPY THE DATA And SEND THIS, and “My Pod Home Page URL”, To EVERYONE In Your ADDRESS BOOK…. FRIENDS Or ENEMIES! WANT TO BE NOTIFIED OF NEW EPISODES? ~~~~~~~~~~~~~~~~~~~~ Go To “Join my mailing list ” On The RIGHT………. When It Comes Up You Will See On This Page “Add me to Life Enthusiast''s mailing list:” ………. And Then type in your name and email address ………. Now Just Click “Save”. Assimilation and elimination are the two key stones that make us tick. Edgar Cayce said that if we could control these aspects of the human form, we could extend life to whatever we chose, that's how important these two principles are. Assimilation Assimilation is defined as the measure of the ability of any body to utilize foods we eat. Some people think that having massive doses of food will give them all they need. They could not be more wrong: it is all right shoving nutrition in but it is quite another thing if the body can absorb it and use it in that form. Typical assimilation rates might vary from 20% to 80% and nutrition supplied in some forms will not be absorbed at all. That means out of every 454 grams of food you might only absorb 20-80% of that. What happens to the food after you swallow it depends to a large degree on the other three principles of your body, namely circulation, relaxation and elimination. Circulation is crucial if assimilation is to be maintained at high levels. Circulation is helped greatly by some important factors; exercise, especially cardiovascular. Apparently something like 50 or so times as many blood vessels open up when exercising than just sitting. We have about 60,000 miles of vessels, mostly capillary type, so you can imagine the effect of increased blood flow. Massage, hydrotherapy treatments and osteopathic adjustments help because the blood stream carries the rebuilding forces to the body in these channels. They need to be clear and stimulated so that the blood will flow to feed the cells and tissues. Elimination Every activity your body does produces waste. We get rid of that waste through the skin, the lungs, the kidneys and the intestines. Major problems start to occur when any of these important channels are stopped from doing their job. We start to accumulate waste, bacteria start growing at alarming rates which leads to all sorts of problems as we become toxic. Imagine not cleaning up the kitchen very often -leaving waste- what would happen, your kitchen would become literally alive with all sorts of creepy bacteria. The same with your body. The fact that poor elimination is the most cited cause of disease within the Edgar Cayce research papers totaling over 14,000 gives you some idea just how important this aspect really is. It gives you an idea of the importance of getting rid of toxins, rid of waste from our bodies. Some of the diseases which elimination problems either cause or play a big and major part include: Arthritis, Acne, Anemia, Apoplexy-stroke, Appendicitis, Asthenia, Asthma, Atrophy, Balding-poor circulation, Bladder stricture, Blepharitis, Some cases of blindness, Boils, Brain tumors -poor circulation, Bronchitis, Bursitis, Cancers and tumors, Skin cancer, Canker sores and herpes simplex, Cataracts, Cirrhosis, Colds, Colic-poor assimilation, Colitis, Colon impaction, Complexion problems, Cystitis, Cysts, Some cases of deafness, Dermatitis, Eczema, Edema, Enteritis, Feet swelling, Gall bladder -gall stones, Halitosis-bad breath, Headaches general, Hemorrhoids, Hepatitis, Hernia, Herpes zoster, Unwanted hair, Indigestion, Insomnia, Iritis, Kidney problems, Laryngitis, Leukemia, Lumbago, Lupus, Lymphangitis, Malaria, Measles, Menopause problems, Migraine, Some cases of myopia, Polyps, Nephritis, Neuritis, Oophoritis, Phlebitis, Pneumonia problems, Poison ivy, Prostatitis, Pruritus, Psoriasis, Purpura, Pyorrhea, Rheumatic fever, Sarcoma, Sciatica, Rheumatism, Scolliosis -eliminations were a cause and an effect, Seborrhea, Skin ulcers, Female/ male sterility, Streptococcus infection, Tic douloureux, Tonsillitis, Torticollis, Ulcers, Vaginitis, Varicose veins, Vertigo-some cases, Xeroderma So if you are suffering from any of these complaints it is highly likely that you could be helped by increasing your body's ability to rid itself of toxins and wastes. It is as simple as that. Phenomenal results have been obtained from increasing your eliminations. Peoples lives have literally been turned around. Read more about Assimilation and Elimination Technorati Tags: weight loss, Diet, Obesity, Dieting, Healthy Living,Food, Exercise, Fitness, Nutrition, Supplements, Lose Weight, Martin Pytela, Scott Paton.
Acute unilateral peripheral and central vestibular lesions can cause similar signs and symptoms, but they require different diagnostics and management. We therefore correlated clinical signs to differentiate vestibular neuritis (40 patients) from central ‘‘vestibular pseudoneuritis’’ (43 patients) in the acute situation with the final diagnosis assessed by neuroimaging. Skew deviation was the only specific but non-sensitive (40%) sign for pseudoneuritis. None of the other isolated signs (head thrust test, saccadic pursuit, gaze evoked nystagmus, subjective visual vertical) were reliable; however, multivariate logistic regression increased their sensitivity and specificity to 92%.
Tierärztliche Fakultät - Digitale Hochschulschriften der LMU - Teil 03/07
In dieser Arbeit wurden einhundert Vögel mit der Verdachtsdiagnose Neuropathische Magendilatation untersucht. Es handelt sich um Papageienvögel, die entweder klinisch, vorberichtlich oder pathologisch-anatomisch Anzeichen einer NPMD zeigten. Bei insgesamt 73 % der Vögel wurde die Erkrankung in Form einer Neuritis nonpurulenta im Bereich des Magen-Darm-Trakts, des Herzens, der adrenalen Ganglien oder des Gehirns histologisch bestätigt. Klinisch zeigten 56,2 % der an NPMD erkrankten Tiere NPMD typische Symptome. In der Mehrzahl handelte es sich bei den erkrankten Vögeln um Bestandstiere (64,4 %). Dabei waren, bis auf Nestlinge alle Altersgruppen vertreten, mit einem deutlichen Anteil von Jungtieren bis zu einem Jahr (15,1 %). Die Auswertung der Daten hinsichtlich der erkrankten Vogelgattungen ergab, dass in der untersuchten Klientel besonders Graupapageien (41,1 %) und Aras (30,1 %) vertreten waren. Amazonen, welche ebenfalls sehr häufig als Heimtiere gehalten werden, wurden dagegen deutlich seltener (4,1 %) untersucht. Eine saisonale Häufung von Erkrankungen zeichnete sich nicht ab. Bei der pathologisch-anatomischen Untersuchung zeigten nahezu alle Tiere (87,7 %) einen starken Grad der Auszehrung. In 75,3 % der Fälle war eine Drüsenmagendilatation vorhanden und in 37 % eine Atrophie der Magenwand des Muskelmagens. Die wichtigsten histologischen Ergebnisse bei diesen Tieren waren Veränderungen im Sinne einer Neuritis nonpurulenta. Im Bereich des Magen-Darm-Trakts trat diese in 83,6 % aller an NPMD erkrankten Papageien auf. Besonders häufig wies der Muskelmagen (68,6 %) eine Neuritis auf, während im Vergleich dazu der Drüsenmagen (59,6 %) seltener betroffen war. Noch seltener wurden derartige Veränderungen in Kropf (28,0 %) und Dünndarm (12,5 %) gefunden. Darüber hinaus traten Veränderungen im Sinne einer Neuritis auf, die das Gehirn (41,1 %) und das Herz (43,1 %) betrafen. Beeindruckend war, dass jedes Gehirn histologische Veränderungen zeigte, wobei es sich in der Hauptsache um degenerative Veränderungen (96,4 %) handelte. Degenerative Veränderungen (Plexus-brachialis-Bereich 66,7 %, Thorakalbereich 83,3 %, Synsakralbereich 73,3 %) wurden ebenfalls häufig im ZUSAMMENFASSUNG 98 Rückenmark gefunden, jedoch keine Entzündungszellen. Eine Neuritis zeigten dagegen in 36,4 % der Fälle die adrenalen Ganglien. Darüber hinaus ergab die Untersuchung der Nebennieren selbst eine Degeneration der Markzellen (52,3 %), sowie Infiltration mit nichteitrigen Entzündungszellen (81,8 %). Weitere degenerative Veränderungen fanden sich in den Parenchymen von Leber (73,3 %), Herz (43,1 %) und Nieren, die sich dort in Form einer Tubulonephrose (85,7 %) und Glomerulopathie (49,2 %) äußerten. Bei 27 % der Patienten, die klinisch bzw. pathologisch-anatomisch Merkmale der NPMD aufwiesen, konnte histologisch keine Polyneuritis als Zeichen einer NPMD diagnostiziert werden. Tiere dieser Gruppe wiesen allerdings Organveränderungen auf, die mit denen der NPMD-Vögel zum Teil vergleichbar waren. In den Organen des Magen-Darm-Trakts konnten sehr häufig Neurodegenerationen (Kropf 66,7 %, Muskelmagen 72 %) gefunden werden, sowie seltener nichteitrige Entzündungszellen (Drüsenmagen 31,3 %, Muskelmagen 28 %), die außerhalb neuronalen Gewebes gelegen waren. Wie auch bei den bestätigten NPMD-Fällen, waren im Vergleich zu den Drüsenmägen (50 %) besonders die Muskelmägen (72 %) histologisch in Mitleidenschaft gezogen worden. Sämtliche Nebennieren wiesen histologische Veränderungen auf, davon mehr als drei Viertel (76,9 %) Markzelldegeneration. Zu 100 % verändert waren die Gehirne, welche durchweg degenerative Veränderungen zeigten und hier zudem sehr häufig Gliazellproliferation und Neuronophagie (85 %) nachgewiesen werden konnte. Diese mit den NPMD-Vögeln vergleichbaren degenerativen Veränderungen lassen vermuten, dass es auch bei diesen Vögeln infolge von Neurodegeneration zur Drüsenmagenerweiterung kam. Somit kann es sich auch bei diesen unbestätigten Fällen um an NPMD erkrankte Tiere handeln, welche jedoch auf Grund des variablen Krankheitsbildes und des begrenzten Probenmaterials unentdeckt blieben. Insgesamt verdeutlichen die Ergebnisse der Arbeit, dass für eine Diagnosefindung nicht nur der Magen-Darm-Trakt histologisch untersucht werden sollte, sondern dass auch Herz, Nebennieren und Gehirn mit ihren neuronalen Anteilen wichtige Hinweise auf das Vorliegen einer NPMD bieten. Mittels einer Kropfbiopsie kann im Falle eines positiven Ergebnisses eine Diagnose gestellt werden. Jedoch scheint diese auf Grund der zu erwartenden zwei Drittel negativen Ergebnisse nur im Einzelfall empfehlenswert. ZUSAMMENFASSUNG 99 Zudem belegen diese Untersuchungen an dem bisher größten untersuchten Kollektiv, dass neben dem Vorliegen der charakteristischen Polyneuritis, generalisierte degenerative und entzündliche Veränderungen der großen Parenchyme auftreten. Dies betrifft insbesondere die Nieren, Leber und Herz, aber auch die Nebennieren. Diese Befunde deuten darauf, dass in Folge der Anschoppung Folgeschäden entstehen und eine nachfolgende Entgleisung des Stoffwechsels zu einem Multiorganversagen führt. Eine klinische Behandlung von Patienten mit der klinischen Verdachtsdiagnose NPMD sollte daher auf eine symptomatische Stützung des Patienten ausgerichtet sein. Sie ist als lebensverlängernd anzusehen. Eine Heilung der Erkrankung ist damit nicht zu erzielen, so dass die Prognose einer NPMD als infaust zu stellen ist.
Experimental Allergic Neuritis by Raymond Adams, MD
An Interview with Raymond Adams, MD, author of Waksman BH, Adams RD. J Exp Med. 1955;102:213-235 and Waksman BH, Adams RD. J Neuropath Exp Neurol. 1956;15:29-314. Interviewed by Ted Burns, MD and Robert, Pascuzzi, MD
An Interview with Raymond Adams, MD, author of Waksman BH, Adams RD. J Exp Med. 1955;102:213-235 and Waksman BH, Adams RD. J Neuropath Exp Neurol. 1956;15:29-314. Interviewed by Ted Burns, MD and Robert, Pascuzzi, MD
Tierärztliche Fakultät - Digitale Hochschulschriften der LMU - Teil 01/07
Ziel der vorliegenden Arbeit war es das Vorkommen und die morphologischen Charakteristika endokriner und metabolischer Neuropathien beim Haustier zu untersuchen. Dazu wurden Nervenproben von 37 Hunden, 36 Katzen und zwei Pferden mit endokrinen und metabolischen Grunderkrankungen mittels Histologie, Nervenfaserzupfpraeparation und zum Teil auch Elektronenmikroskopie ausgewertet. Insgesamt zeigten 78,4% der Hunde, 58,3% der Katzen und beide untersuchten Pferde Anzeichen einer Neuropathie. Auf die einzelnen Grunderkrankungen gerechnet waren beide diabetischen Hunde, sechs von sieben diabetischen Katzen, sechs von acht uraemischen Hunden, acht von 16 uraemischen Katzen, vier von sechs Hunden und sieben von 16 Katzen mit Hepatopathie sowie 19 von 21 Hunden mit bestaetigtem oder vermutetem Hyperadrenokortizismus betroffen. Mit Ausnahme der caninen Cushing-Neuropathie und einer CIDP-aehnlichen, entzuendlichen Erkrankung bei uraemischen Katzen, aeusserten sich die metabolischen/endokrinen Neuropathien Tierarten-uebergreifend vorwiegend in einem axonalen Schaedigungsmuster. Dabei praesentierte sich das pathologische Bild bei den Hunden innerhalb der Gruppen sehr einheitlich, wohingegen die veraenderten Katzennerven eine beachtenswerte Heterogenitaet aufwiesen. Bei diabetischen Hunden und Katzen konnte, im Gegensatz zu einigen anderen Studien, fast ausschliesslich eine axonale Neuropathie mit sekundaeren Myelinscheidenveraenderungen festgestellt werden. Letztere umfassten bei Hunden lediglich Myelinscheidenanpassungen an eine axonale Atrophie, bei Katzen jedoch auch De- und Remyelinisierungen. Bei zwei Drittel der Katzen traten ausserdem interlamellaere Myelinscheidenoedeme auf. Sowohl bei uraemischen Hunden als auch bei uraemischen Katzen dominierte eine axonale Neuropathie mit sekundaeren De-/Remyelinisierungen und Myelinscheidenanpassungen das pathologische Bild. Waehrend diese bei Hunden die einzige Neuropathieform war, kam es bei einigen Katzen auch zu einer entzuendlichen, zellvermittelten Demyelinisierung. Auch bei Hunden und Katzen mit Hepatopathie kam eine zumeist axonale Neuropathie vor. Die Haeufigkeit ihres Auftretens legt zwar die Vermutung nahe, dass die hepatische Neuropathie bei Hund und Katze als eigenstaendige Entitaet existiert, doch konnte ein kausalgenetischer Zusammenhang mit dem Leberschaden aufgrund einer hohen Frequenz von PNS-relevanten Begleiterkrankungen bei beiden Tierarten nicht zweifelsfrei hergestellt werden. Abweichend vom axonopathischen Bild bei Hund und Katze zeigte ein Pferd mit perivaskulaerer Hepatitis eine geringgradige interstitielle Neuritis. Die Untersuchung von Hunden mit erwiesenem oder vermutetem Hyperadrenokortizismus bestaetigte nicht nur die Existenz der bisher nur vereinzelt beschriebenen caninen Cushing-Neuropathie, sondern sie konnte auch eine unerwartet hohe Praevalenz und ein auffaelliges pathologisches Bild dieser Komplikation aufzeigen. Es konnte darueber hinaus erstmals nachgewiesen werden dass diese Neuropathie unabhaengig vom Bestehen einer Hyperglykaemie auftritt. Sie ist pathologisch durch Demyelinisierungen und Anzeichen einer Myelinscheideninstabilitaet in Form von fokalen Myelinscheidenverdickungen und Tomakula charakterisiert. In weniger als der Haelfte der Faelle tritt eine, dann vorwiegend milde, axonale Begleitpathologie auf. Auch das Pferd mit equinem Cushing-Syndrom zeigte krankhafte Nervenveraenderungen, doch lag diesen keine Demyelinisierung sondern eine axonale Pathologie zugrunde. Ausserdem konnte hier, im Gegensatz zur Situation beim Hund, das Zugrundeliegen einer diabetischen Situation nicht ausgeschlossen werden. Insgesamt konnte im Laufe der vorliegenden Untersuchung gezeigt werden, dass endokrine und metabolische Neuropathien bei Hunden und Katzen haeufiger vorkommen, als sie klinisch festgestellt werden, und dass es sich dabei, mit Ausnahme der caninen Cushing-Neuropathie und der CIDP-aehnlichen Neuropathieform bei uraemischen Katzen, um vorwiegend axonale Neuropathien handelt. Pathogenetisch scheinen die meisten endokrinen und metabolischen Erkrankungen also primaer einen schaedigenden Einfluss auf den neuronalen Zellkoerper oder sein Axon auszuueben, waehrend ein Hyperadrenokortizismus vorwiegend auf den Schwannzellstoffwechsel und die Myelinscheide einwirkt. Darueber hinaus legen die Ergebnisse dieser Untersuchung die Vermutung nahe, dass Katzen mit metabolischen Grunderkrankungen im Vergleich zu Hunden anfaelliger fuer entzuendliche demyelinisierende Neuropathieformen sind.
Tierärztliche Fakultät - Digitale Hochschulschriften der LMU - Teil 02/07
Ein Tauben APMV-1 Impfstoff (ParamyxovacÒ, Fa. Intervet), der auf einem schwach virulenten homologen Tauben APMV-1 Stamm basiert, wurde auf seine Schutzwirkung nach drei, sechs, neun und zwölf Monaten getestet. Anhand ungeimpfter Kontrolltiere wurde die Manifestation der experimentellen APMV-1 Infektion bei Tauben untersucht, unter besonderer Berücksichtigung der feingeweblichen Veränderungen. Bei den ungeimpften Kontrolltauben wurden durch die Infektion (10 5,5 EID50, i.m.) klassische neurologische APMV-1 Krankheitsanzeichen in Form von motorischen Ausfallserscheinungen der Flügel induziert. Histologisch war mit dem siebten Tag im Rückenmark im Bereich des Plexus lumbosacralis eine nicht-eitrige Panmyelopathie sowie eine nicht-eitrige Neuritis bzw. Ganglionitis nachweisbar. In den geschädigten Gebieten des Rückenmarks wurde immunhistochemisch APMV-1 Antigen nachgewiesen. Auch die histopathologischen Befunde der inneren Organe wiesen auf eine generalisierte Infektion hin. Neben einer nicht-eitrigen Pankreatitis, die bei 22 von 39 der Tauben auftrat, wurden bei 16 von 39 Tieren Nekrosen des Pankreasparenchyms und bei 3 von 29 Nekrosen des Nebennierenparenchyms beobachtet. Gegenüber uninfizierten Negativ-Kontrolltauben, bei denen in der Niere eine geringgradige Infiltration mit mononukleären Entzündungszellen zu beobachten war, trat bei den experimentell infizierten Tauben eine mittel- bis hochgradige nicht-eitrige, interstitielle Nephritis auf. Für den quantitativen Vergleich zwischen den unterschiedlichen Gruppen wurde ein Histologischer Pathogenitätsindex (HPI) herangezogen. Neu im Zusammenhang mit der APMV-1 Infektion der Taube ist der Befund einer nicht-eitrigen Polyserositis, der bei 23 von 39 der APMV-1 infizierten Kontrolltauben erhoben wurde. Bei den geimpften Tauben wurde nach Belastungsinfektion, die drei, sechs und neun Monate nach der Impfung erfolgte, keine klinischen Symptomatik beobachtet. In der Gruppe D, die zwölf Monate nach der Impfung infiziert wurde, zeigte eine von 15 Tauben reduzierte Flugfähigkeit bis Flugunfähigkeit, so dass der prozentuale Anteil der kummulativ erkrankten Tauben in dieser Gruppe bei 7,7 % lag. Histologisch konnte aufgezeigt werden, dass die Impfung eine Reduktion der APMV-1 induzierten Veränderungen an den inneren Organen vermittelt. So trat zwar bei 14 von 52 APMV-1 geimpften Tieren eine nicht-eitrige Serositis auf, der HPI weist jedoch in Bezug auf Häufigkeit und Ausprägungsgrad eine statistisch signifikant geringere Ausprägung (p = 0,001) gegenüber den ungeimpften Tauben nach. Durch Betrachtung des HPI konnte ebenfalls gezeigt werden, dass die geimpften gegenüber den ungeimpften Tauben vor spezifischen Veränderungen am Pankreas (Pankreasnekrosen, mononukleäre Infiltrate) sowie an der Niere geschützt waren. Durch die Impfung wurde ebenfalls eine deutliche Reduktion der Virusausscheidung erreicht.
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 01/19
Background: The multifocal pattern electroretinogram (mfPERG) allows analysis of local ganglion cell dysfunction by multifocal stimulation. Aim of this study was to investigate if this method is an useful tool for diagnosing and following glaucoma patients. Methods: Measurements on 52 age-matched normal eyes were compared to those on 23 eyes with different stages of glaucoma. A RETIScan system was used to generate a stimulus pattern of 19 hexagons, each consisting of 6 triangles. The triangles pattern-reversed black to white at 75 Hz. Those 19 hexagons form 3 stimulus regions: a central field, a middle and a peripheral ring. The complete array subtended 48° at the eye. The hexagons alternated black-white following a corrected binary m-sequence (length 512, 10 cycles with 39 second each). Corneal loop electrodes were used with reference electrode on temple. Results: The mfPERGs were analyzed for significant changes in amplitude and latency of the positive and negative responses. For patients with glaucoma the positive P-50 and negative N-95 components were significantly reduced for the central area and both rings compared to normal volunteers (p