Neurology Minute

In the second episode of this two-part series, Drs. Justin Abbatemarco, Valérie Biousse, and Nancy J. Newman discuss the risk of non-arteritic ischemic optic neuropathy and how to counsel patients around GLP-1 medications.  Show transcript:  Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco again with Valarie Biousse and Nancy Newman talking about non-arteritic ischemic optic neuropathy. I think the other major point that we had a discussion in the podcast was around the GLP-1 medications, which you mentioned have been truly life-changing for diabetes management and obesity. Can we talk about the risk of non-arteritic ischemic optic neuropathy and how you're counseling patients around this class of medications? Dr. Nancy J. Newman:  Absolutely. This is probably one of the most difficult things we are dealing with because it is something that is in process and progress right now. We don't have all the information yet, but it would appear that there is likely a small association of about slightly less than two times risk in patients who are taking these medications of having NAION with a resultant still very, very small overall risk. And it is not necessarily causal. This has prompted the European Medicines Agency to say that these patients should have their GLP-1 RAs stopped if they have NAION. Our own FDA and certainly the American Academy of Ophthalmology and the North American Neuro-Ophthalmology Society have not taken that step, but have suggested that this be shared decision-making, not only with the person who makes this diagnosis of an NAION in the patient, but with their primary care doctor or the provider who has felt that a GLP-1 receptor agonist is important for this patient's treatment and health. Dr. Justin Abbatemarco: More to come. We're going to have you back to have discussions as we learn more and better understand the disease and how we help our patients with both their diagnosis and treatment. Thank you so much for your time. 

In part one of this two-part series, Drs. Justin Abbatemarco, Valérie Biousse, and Nancy J. Newman discuss common myths around non-arteritic ischemic optic neuropathy (NAION). Show transcript:  Dr. Justin Abbatemarco: Hello and welcome. This is Justin Abbatemarco, and I just got done interviewing Valérie Biousse and Nancy Newman on all things around non-arteritic anterior ischemic optic neuropathy. I think one of my favorite takeaways from our interview were breaking some common myths around this disorder. Valérie and Nancy, could you maybe talk about one or two that you think are important that people should know are not true about this disease? Dr. Nancy J. Newman: So thing number one is that it's just another stroke of the eye. We know that it likely does have some vascular background to it, but the reality is it's not a stroke like neurologists know a stroke. You don't need to do an embolic workup. It has to do likely with the anatomy that a person is born with or that they acquire that crowds the front of their optic nerve. Secondly, thing number two, that it's a disease only of old people. I think that we know that you can be as young as age 11 and have this happen, mostly because you have a small, crowded optic nerve head. Thing number three, steroids really have not been proven to be helpful in this disorder and should likely not be used unless you are trying to decrease the optic nerve head edema, and the patient is insisting that they have some treatment. Dr. Justin Abbatemarco: So helpful. Please come back and check out the full podcast episodes where we dive into some of these elements in a little bit more detail.   

In part one of this two-part series, Drs. Justin Abbatemarco, Valérie Biousse, and Nancy J. Newman discuss common myths around non-arteritic ischemic optic neuropathy (NAION). Show transcript:  Dr. Justin Abbatemarco: Hello and welcome. This is Justin Abbatemarco, and I just got done interviewing Valérie Biousse and Nancy Newman on all things around non-arteritic anterior ischemic optic neuropathy. I think one of my favorite takeaways from our interview were breaking some common myths around this disorder. Valérie and Nancy, could you maybe talk about one or two that you think are important that people should know are not true about this disease? Dr. Nancy J. Newman: So thing number one is that it's just another stroke of the eye. We know that it likely does have some vascular background to it, but the reality is it's not a stroke like neurologists know a stroke. You don't need to do an embolic workup. It has to do likely with the anatomy that a person is born with or that they acquire that crowds the front of their optic nerve. Secondly, thing number two, that it's a disease only of old people. I think that we know that you can be as young as age 11 and have this happen, mostly because you have a small, crowded optic nerve head. Thing number three, steroids really have not been proven to be helpful in this disorder and should likely not be used unless you are trying to decrease the optic nerve head edema, and the patient is insisting that they have some treatment. Dr. Justin Abbatemarco: So helpful. Please come back and check out the full podcast episodes where we dive into some of these elements in a little bit more detail.   

Dr. Margarita Fedorova outlines how genetic, environmental, and pathological factors interact in Parkinson's disease and what this means for patient counseling.  Show citation:  Blauwendraat C, Morris HR, Van Keuren-Jensen K, Noyce AJ, Singleton AB. The temporal order of genetic, environmental, and pathological risk factors in Parkinson's disease: paving the way to prevention. Lancet Neurol. 2025;24(11):969-975. doi:10.1016/S1474-4422(25)00271-6  Show transcript:  Dr. Margarita Federova: Welcome to Neurology Minute. My name is Margarita Fedorova, and I'm a neurology resident at the Cleveland Clinic. Today we're exploring a framework for understanding how genetic, environmental, and pathological factors interact in Parkinson's disease and what this means for how we counsel our patients. A personal view paper by Blauwendraat and colleagues, published in The Lancet Neurology in September 2025, addresses a critical question. We've identified over 100 genetic loci for Parkinson's, but how do they act? The common saying is genetics loads the gun and environment pulls the trigger, but this paper suggests the relationship may be more complex. The key tool here is alpha-synuclein seeding amplification assays or SAAs. These detect misfolded alpha-synuclein protein in cerebrospinal fluid. Over 90% of Parkinson's patients test positive for misfolded alpha-synuclein using this assay. But here's what's notable. 2% to 16% of neurologically healthy older adults also test positive with prevalence increasing with age. This means there are more asymptomatic people with detectable alpha-synuclein pathology than people with actual Parkinson's disease. Most of these asymptomatic individuals will never develop symptoms. This raises an important question. What determines who converts to a disease and who doesn't? By integrating SAA results with genetic data, researchers can examine whether genetic factors drive initial protein misfolding or whether they modulate the response to pathology triggered by environmental or random events. Preliminary data suggests polygenic risk scores don't strongly associate with SAA positivity in healthy older adults. In other words, people with high genetic risk for Parkinson's aren't necessarily more likely to have misfolded alpha-synuclein if they're healthy. This suggests most Parkinson's genetic risk factors may not be causing initial misfolding. Instead, they may be determining what happens afterward, such as whether the pathology progresses to clinical disease. LRRK2 mutations support this model. About 33% of LRRK2 related Parkinson's patients are SAA-negative compared to only 7% in sporadic disease. This means many people with LRRK2 mutations develop Parkinson's without the typical alpha-synuclein pathology. LRRK2 mutations also show varied pathology. Sometimes alpha-synuclein, sometimes tau, sometimes neither. This suggests LRRK2 may modulate responses to different initiating events rather than directly causing protein misfolding. What does this mean for us as clinicians? Asymptomatic SAA-positive individuals could represent a window for intervention. If we can understand what protects them from converting to disease or what triggers that conversion, we could enable earlier identification of at risk individuals and potentially intervene before symptoms develop. The authors call for large scale studies using SAAs in older populations, combined with genetic analysis and longitudinal follow-up. By integrating pathological biomarkers with genetic and environmental data, we can better understand the temporal sequence of events in development of Parkinson's. This approach could fundamentally change how we think about disease prevention and early intervention, potentially allowing us to identify at risk individuals before symptoms appear and develop targeted prevention strategies. That's your neurology minute for today. Keep exploring, and we'll see you next time. If you want to read more, please find the paper by Cornelis Blauwendraat et al titled The Temporal Order of Genetic, Environmental and Pathological Risk Factors in Parkinson's Disease: Paving the Way to Prevention, published online in September 2025 in Lancet Neurology.

Dr. Tesha Monteith highlights the American Headache Society's position statement, which advocates for migraine screening in girls and women.  Show citation: Schwedt TJ, Starling AJ, Ailani J, et al. Routine migraine screening as a standard of care for Women's health: A position statement from the American Headache Society. Headache. Published online December 10, 2025. doi:10.1111/head.70023 Show transcript:  Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. Welcome back to our Women's Health and Headache Medicine series. Did you know the American Headache Society recently published a position statement to encourage screening for migraine in girls and women? The position statement was based on review of the literature to establish if migraine met standards for screening in subpopulations and to assess appropriate screening tools. The team achieved consensus, agreeing that migraine, due to its prevalence, morbidity, high cost, availability of screening methods and treatments, does meet criteria to justify screening for girls and women. The panel suggested that migraine should be screened annually as part of women's preventative care with tools like ID-Migraine. ID-Migraine is a self-administered three-question survey that has been validated in primary care settings. Patients answer yes or no to having the following with headache over the past three months. Patients are asked if headaches limited your ability to work, study, or do what they need to do on at least one day. You felt nauseated or sick to your stomach. Light bothered you a lot more than when you don't have headaches. Answering at least two of the three is positive for migraine. The panel acknowledged certain barriers, but they ultimately emphasize the overwhelming benefits of screening for migraine in women and children. Although the focus is for females, they recognize benefits in boys and men as well. Check out this position statement. It's a great read. This is Tesha Monteith. Thank you for listening to the Neurology Minute. 

In the final installment of this series, Dr. Justin Abbatemarco and Dr. Divyanshu Dubey discuss the latest findings and some non-occupational exposures.  Show citation:  Hinson SR, Gupta P, Paramasivan NK, et al. Neural synaptic vesicle autoimmunity following aerosolized porcine neural tissue exposure: insights into autoimmune inflammatory polyradiculoneuropathy. EBioMedicine. 2025;122:106053. doi:10.1016/j.ebiom.2025.106053 Show transcript:  Dr. Justin Abbatemarco:  Hello, and welcome back. This is Justin Abbatemarco. I'm here with Divyanshu Dubey, discussing his article, Neural Synaptic Vesicle Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure: Insights Into Autoimmune Inflammatory Polyradiculoneuropathy. Div, maybe we could talk about non-occupational exposures? I think many of us don't see this cohort of patients commonly, but I really think this helps inform care, beyond just this specific occupational exposure. What did you guys find in your work? Dr. Divyanshu Dubey:  So, one of the inspirations for this study was driven by the phenotypic characterization of patients who were described in this 2010 paper, which is somewhat similar to some of the patients I currently see in my clinic who don't seem to meet GBS or CIDP criteria. But, based on their MRI findings, based on their CSF studies, the EMG nerve conduction studies, they seem to have this polyradiculoneuropathy presentation, often presenting with asymmetric disease onsets, starting on one leg and then sometimes transitioning to the other side. In some cases, even a non-length dependent pattern with sort of proximal cervical brachial nerve root plexus involvements, which don't really seem to have a blood test, or a biomarker right now. Currently, many of these cases are a diagnosis of exclusion. I was thinking if there's a biomarker that we can identify from this 2006 to 2008 unfortunate event, that might actually help us diagnose these patients. So, once we identified synaptophysin and GAP43 antibodies in the swine abattoir cohort, I went back to our storages of these patients with other inflammatory polyradiculoneuropathy, and found about 5% of these patients from a large cohort of close to 300 patients, did have these antibody biomarkers. Some of these patients had paraneoplastic trigger, where we had patients with neuroendocrine tumors, or hematological malignancies mounting a response to these antibodies. But a good chunk of these patients we did not truly understand, or know what the triggers were. That might be a potential for future studies, as we expand our cohort of these antibodies, as well as study further the phenotypic characterization of these cases. Dr. Justin Abbatemarco: Yeah, there's just so much there, really helping to inform future clinical care outside of this very specific occupational exposure. And then, as we talked about in the podcast, I think really helping to think through how neurological autoimmune diseases develop. So, just really exciting work. We really appreciate you coming on, sharing this. We're excited for how this evolves over the coming years. Dr. Divyanshu Dubey:  Thank you, Justin.  

In part one of this two-part series, Dr. Justin Abbatemarco and Dr. Divyanshu Dubey discuss the original patient cohort with occupational exposure, what motivated this line of research, and the key findings from the initial workup.  Show citation:  Hinson SR, Gupta P, Paramasivan NK, et al. Neural synaptic vesicle autoimmunity following aerosolized porcine neural tissue exposure: insights into autoimmune inflammatory polyradiculoneuropathy. EBioMedicine. 2025;122:106053. doi:10.1016/j.ebiom.2025.106053 Show transcript:  Dr. Justin Abbatemacro: Hello and welcome. This is Justin Abbatemacro. And I'm here with Divyanshu Dubey to discuss his article published in eBiomedicine, Neurosynaptic Vessel Autoimmunity Following Aerosolized Porcine Neural Tissue Exposure: Insight into Autoimmune Inflammatory Polyradicular Neuropathy. Dr. Justin Abbatemacro: Div is a professor of neurology at the Mayo Clinic, and we just finished our interview, which I would encourage everyone to check out. Div, maybe we could talk about the original cohort with this occupational exposure, what inspired you to do this work and then what did you find with that initial workup? Dr.  Divyanshu Dubey: As recounted in our paper, this story began in 2006 to 2008, when a group of swine abattoir workers developed a striking neurological syndrome. These people were previously healthy and suddenly developed severe neuropathic pain, tingling, and variable weakness. The localization stood out, these cases were initially identified by Dan Lachance, who characterized these patients having an autoimmune neuropathy, which was further phenotypically characterized by the work done by Dr. Dyck, calling these inflammatory polyradicular neuropathy based on their nerve root plexus and proximal nerve collisions. And interestingly, a lot of work done back then by Dr. Lennon showed these patients had a unique synaptic staining pattern suggesting there was an underlying antibody driving this disease process. So as I joined the neuroimmunology lab a few years ago, this was one of the areas I wanted to go back and study, not only to find this mystery biomarker which caused the disease in these patients, but also to try and understand how this can help. Dr. Justin Abbatemacro: Yeah. I think my takeaway is be curious, right? You hear the story, you see this pattern. Be curious and investigate, and it takes a team or a village to do it. Dr.  Divyanshu Dubey: 100%. So observation, communication between, as you said, a team or a village with like-minded, passionate individuals is one of the successes of many of our discoveries, not just this one in this biomarker space. Dr.  Divyanshu Dubey: So the technique we use for discovery of these biomarkers was called a phage display where we use the archive sera to test from these patients, the swine abattoir worker patients with autoimmune polyradicular neuropathy. And we ended up finding two dominant antigens, which was synaptophysin and GAP-43, which were present in majority of these cases. Dr. Justin Abbatemacro: Please come back and check out part two where we discuss the latest findings and maybe some non-occupational exposures. And check out the podcast. Thanks.  

In the second installment of this two-part series, Drs. Stacey Clardy, Ayush Gupta, and Kuntal Sen discuss the most practical testing approach to minimize both under‑ and over‑testing for these disorders. Show citation: Gupta A, Sahjwani D, Kahn I, Gombolay GY, Sen K. Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape. Neurol Genet. 2025;11(6):e200326. Published 2025 Nov 25. doi:10.1212/NXG.0000000000200326 Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. For a two-part podcast series this week, I've been speaking with Ayush Gupta, from the University of Nebraska Medical Center, and Kuntal Sen, from Children's National Hospital in Washington, DC about monogenic disorders that mimic neuroinflammatory disease. There are a lot of them, and they are no doubt sitting in our clinics waiting to be recognized. Ayush, for the minute, once a neurologist starts suspecting one of these disorders, what's the most practical testing strategy to avoid both under and over-testing for these disorders? Dr. Ayush Gupta: I think the most practical strategy is to write down all the phenotypic symptoms that you think could be related, put that exact information into a genetic testing panel that will be suitable. Or, if possible, try to do a broader genetic testing such as whole genome sequencing, and make yourself equipped to be able to analyze the results that you get from the testing. Dr. Stacey Clardy: I hear you saying, at least when you're thinking about this, be a bit of a lumper. As we covered in the podcast, if we are going to pursue that genetic testing, it is absolutely critical that we share that list with the interpreting geneticist because that determines how they score variants and how they rate them as related or not. Please take a listen to that two-part podcast series, where we get into all these details. I walked away with a great framework on how to do better in terms of picking these disorders out. Again, the paper that accompanies the two-part podcast series is in Neurology Genetics. It's a comprehensive review and called Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults in Evolving Landscape. Thank you, Ayush. Dr. Ayush Gupta: Thank you so much.

In the second installment of this two-part series, Drs. Stacey Clardy, Ayush Gupta, and Kuntal Sen discuss the most practical testing approach to minimize both under‑ and over‑testing for these disorders. Show citation: Gupta A, Sahjwani D, Kahn I, Gombolay GY, Sen K. Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape. Neurol Genet. 2025;11(6):e200326. Published 2025 Nov 25. doi:10.1212/NXG.0000000000200326 Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. For a two-part podcast series this week, I've been speaking with Ayush Gupta, from the University of Nebraska Medical Center, and Kuntal Sen, from Children's National Hospital in Washington, DC about monogenic disorders that mimic neuroinflammatory disease. There are a lot of them, and they are no doubt sitting in our clinics waiting to be recognized. Ayush, for the minute, once a neurologist starts suspecting one of these disorders, what's the most practical testing strategy to avoid both under and over-testing for these disorders? Dr. Ayush Gupta: I think the most practical strategy is to write down all the phenotypic symptoms that you think could be related, put that exact information into a genetic testing panel that will be suitable. Or, if possible, try to do a broader genetic testing such as whole genome sequencing, and make yourself equipped to be able to analyze the results that you get from the testing. Dr. Stacey Clardy: I hear you saying, at least when you're thinking about this, be a bit of a lumper. As we covered in the podcast, if we are going to pursue that genetic testing, it is absolutely critical that we share that list with the interpreting geneticist because that determines how they score variants and how they rate them as related or not. Please take a listen to that two-part podcast series, where we get into all these details. I walked away with a great framework on how to do better in terms of picking these disorders out. Again, the paper that accompanies the two-part podcast series is in Neurology Genetics. It's a comprehensive review and called Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults in Evolving Landscape. Thank you, Ayush. Dr. Ayush Gupta: Thank you so much.

Dr. Aaron Zelikovich discusses the utility of neurofilament light chain as a serum biomarker in peripheral neuropathy.  Show citation: Karam C. Clinical Utility of Serum Neurofilament Light Chain in Peripheral Neuropathy. Muscle Nerve. 2026;73(1):86-92. doi:10.1002/mus.70073 Show transcript: Dr. Aaron Zelikovich: Welcome to today's neurology minute. My name is Aaron Zelikovich, a neuromuscular specialist at Lenox Hill Hospital in New York City. Today, we will discuss a recent article on the utility of neurofilament light chain as a serum biomarker in peripheral neuropathy. It has been studied in other neurological diseases like ALS and multiple sclerosis, as in the 2024 study by Robert Fox et al, which highlighted the limitations of serum neurofilament light chain in patients with multiple sclerosis, since the elevation was inconsistent and tended to occur weeks after MRI changes, and was really only found to be helpful in certain clinical situations. The study we highlight today is a single-center retrospective study that highlights the opportunities and limitations of using serum neurofilament light chain as a biomarker to monitor treatment response and peripheral neuropathy. Serum neurofilament light chain has been shown as an indicator of neuronal injury in both central and peripheral nervous system disease that has been associated with axonal injury or degeneration. It is now commercially available. The authors in this study provide a real-world single-center retrospective study that looked at various forms of peripheral neuropathy over 12 months. Patients had to be evaluated and meet criteria for peripheral neuropathy with either genetic testing, nerve conduction studies, and/or clinical exams. Neuropathies included TTR amyloid, vasculitis, CMT, CIDP, GBS, and anti-MAG neuropathy. Patients with TTR amyloid who were treatment naive and had elevated serum neurofilament light chain showed a reduction in neurofilament light chain levels with treatment. Additionally, patients with CIDP who were treatment naive with elevated serum neurofilament light chain also showed a reduction in neurofilament light chain levels with treatment. All patients with idiopathic peripheral neuropathy had normal serum neurofilament light chain levels. However, serum neurofilament light chain can vary in patients based on age, if they have diabetes, renal dysfunction, and body weight. And this makes it really challenging to interpret it in an isolated setting. Serum neurofilament light chain is a new biomarker for peripheral neuropathies. It can be a supplemental tool in the appropriate clinical context. Future studies are needed to identify its potential to be used as a treatment response biomarker in neuropathies like CADP, GBS, and TTR amyloid. Thank you so much, and have a wonderful day. 

Dr. Tesha Monteith discusses the different forms of menstrual migraines.  Show transcript:  Dr. Tesha Monteith: Hi, this is Tesha Monteith with the Neurology Minute. Welcome to our series on headache medicine and women's health. I want to start off this series with a discussion on menstrual migraine. Menstrual migraine is considered more frequent, more severe, and is associated with most migraine-associated symptoms with the exception of aura. The pathophysiology is linked to the effects of estrogen withdrawal and the impacts on the trigeminal vascular system. Do check out a recent paper by Pan and colleagues published just in neurology in November showing a robust hypothalamic activation prior to the headache phase in patients with menstrual migraine compared to controls. Now, there are two forms of menstrual migraine recognized in the International Classification of Headache Disorders III. First is menstrually related migraine which consists of attacks that occurred during the perimenstrual window. That's day one of menses plus or minus two days and at least two of three menstrual cycles and during additional times outside of the window. Perimenstrual migraine attacks occur exclusively during the perimenstrual window and is much less common than menstrually related migraine. A key point is that there's a predictable timing with each cycle, yet the condition is still very much underdiagnosed. Advise your patients to use an e-diary to improve the diagnosis and hopefully reduce disability. This is Tesha Monteith. Thank you for listening to the Neurology Minute.  

In the second part of this series, Dr. Neishay Ayub discusses levetiracetam and one of its most common side effects, irritability.  Show citations:  Abou-Khalil B. Levetiracetam in the treatment of epilepsy. Neuropsychiatr Dis Treat. 2008;4(3):507-523. doi:10.2147/ndt.s2937  Löscher W, Gillard M, Sands ZA, Kaminski RM, Klitgaard H. Synaptic Vesicle Glycoprotein 2A Ligands in the Treatment of Epilepsy and Beyond. CNS Drugs. 2016;30(11):1055-1077. doi:10.1007/s40263-016-0384-x Rogawski MA. Brivaracetam: a rational drug discovery success story. Br J Pharmacol. 2008;154(8):1555-1557. doi:10.1038/bjp.2008.221 Ulloa CM, Towfigh A, Safdieh J. Review of levetiracetam, with a focus on the extended release formulation, as adjuvant therapy in controlling partial-onset seizures. Neuropsychiatr Dis Treat. 2009;5:467-476. doi:10.2147/ndt.s4844 Wu PP, Cao BR, Tian FY, Gao ZB. Development of SV2A Ligands for Epilepsy Treatment: A Review of Levetiracetam, Brivaracetam, and Padsevonil. Neurosci Bull. 2024;40(5):594-608. doi:10.1007/s12264-023-01138-2 Mahmoud A, Tabassum S, Al Enazi S, et al. Amelioration of Levetiracetam-Induced Behavioral Side Effects by Pyridoxine. A Randomized Double Blind Controlled Study. Pediatr Neurol. 2021;119:15-21. doi:10.1016/j.pediatrneurol.2021.02.010 Major P, Greenberg E, Khan A, Thiele EA. Pyridoxine supplementation for the treatment of levetiracetam-induced behavior side effects in children: preliminary results. Epilepsy Behav. 2008;13(3):557-559. doi:10.1016/j.yebeh.2008.07.004 Romoli M, Perucca E, Sen A. Pyridoxine supplementation for levetiracetam-related neuropsychiatric adverse events: A systematic review. Epilepsy Behav. 2020;103(Pt A):106861. doi:10.1016/j.yebeh.2019.106861 Show transcript:  Dr. Neishay Ayub: Hello, my name is Neishay Ayub, and today we will be discussing levetiracetam and one of its most common side effects, irritability. While levetiracetam can be remarkably helpful for patients, behavioral adverse effects were noted in post-marketing analysis and open-label studies in adult and pediatric patients. For this, physicians started using vitamin B6 supplementation, particularly in the pediatric populations. Why would physicians use B6? Well, low vitamin B6 has been associated with neuropsychiatric disorders, which could be related to the fact that vitamin B6 is an essential co-factor for several neurotransmitters that affect mood and behavior, such as serotonin, dopamine, and GABA. There is an epilepsy syndrome associated with vitamin B6 deficiency. And vitamin B6 deficiency is seen with enzyme-inducing anti-seizure medications, although levetiracetam is not an enzyme-inducing seizure medication. These are some of the possibilities as to why vitamin B6 supplementation was initially explored. Some initial anecdotal evidence and case reports were suggested that it was helpful in reducing behavioral side effects and the need to discontinue levetiracetam. There was a meta-analysis reviewing pyridoxine use, which included 11 case reports and retrospective studies, as well as one prospective study, case-control study, which was not placebo controlled. While evidence was suggestive of a benefit, the quality of the evidence was poor due to selection, reporting, and assessment biases. Overall, the authors recommended a larger randomized, controlled, double-blind trial with adequate statistical power, well-defined eligibility criteria and standardized assessment tools to evaluate B6 efficacy in treating levetiracetam-induced irritability. Since then, there was one small randomized, controlled, double-blind study involving 105 children for whom neuropsychiatric adverse effects were noted after levetiracetam was introduced. Children were randomized to receive a therapeutic dose of pyridoxine, which was 10 to 15 milligrams per kilogram per day, up to 200 milligrams, or a homeopathic dose of 0.5 milligrams per kilogram per day. They were scored on a behavioral checklist and monitored for up to six months. While there was a reduction in behavioral symptoms reported in the therapeutic pyridoxine group, there was no validated assessment tools used, and there was an absence of a true placebo group. Lastly, there are a few studies reporting on adverse effects of B6 toxicity, which is possible, but it's typically seen at higher daily doses, although something to keep in mind if considering B6 supplementation. In summary, while there has been a clinical practice of prescribing pyridoxine at 50 to 100 milligrams as a low-cost, well-tolerated adjunctive supplement, there may be a modest benefit for some patients, but the overall efficacy for the treatment of neuropsychiatric side effects for levetiracetam remain unclear, and more evidence is needed. 

In part one of this two-part series, Dr. Stacey Clardy and Drs. Ayush Gupta and Kuntal Sen discuss the key clinical features that should shift suspicion from autoimmune encephalitis or demyelinating disease to monogenic mimics.  Show citation: Gupta A, Sahjwani D, Kahn I, Gombolay GY, Sen K. Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape. Neurol Genet. 2025;11(6):e200326. Published 2025 Nov 25. doi:10.1212/NXG.0000000000200326 Show transcript:  Dr. Stacey Clardy: Hi, this is Stacey Clardy from the Salt Lake City VA in the University of Utah. For a two-part podcast series, I've been speaking with Ayush Gupta from the University of Nebraska Medical Center and Kuntal Sen from Children's National Hospital in Washington DC about the monogenic disorders that mimic neuroinflammatory disease that are lurking in all of our clinics just waiting to be diagnosed. Ayush, for the minute, when you're seeing a patient with a presumed autoimmune encephalitis or demyelinating disease, what single cluster of features should instead most strongly push us to think of monogenic mimics at the top of our differential? Dr. Ayush Gupta: So when you are seeing a patient with presumed autoimmune encephalitis or a demyelinating disorder, cluster of features such as earlier onset in terms of age, developmental delays, CSF or imaging finding that's non-concordant with the diagnosis such as a non-inflammatory CSF, a symmetric white matter or deep gray matter involvement and relentless progression despite immunotherapy, these are the red flags where you should stop, seriously consider the possibility of a monogenic disorder and reach out to help from colleagues. Dr. Stacey Clardy: That's a great list, and we get into far more detail in the two-part podcast series. So please listen to both of those and take a read of the neurology genetics review titled Monogenic Mimics of Neuroinflammatory Phenotypes in Children and Young Adults: An Evolving Landscape.

Dr. Elizabeth Coon and Prof. Franziska Hopfner discuss the frequency and disease trajectory of MSA patients who do not experience dysautonomia, in comparison to those with autonomic involvement. Show citation:  Wilkens I, Bebermeier S, Heine J, et al. Multiple System Atrophy Without Dysautonomia: An Autopsy-Confirmed Study. Neurology. 2025;105(11):e214316. doi:10.1212/WNL.0000000000214316 Show transcript:  Dr. Elizabeth Coon: Welcome to the Neurology Minute. I'm Elizabeth Coon, and I'm delighted to welcome Professor Hopfner, who will give us a summary of her recently published paper in Neurology, "Multiple System Atrophy Without Dysautonomia and Autopsy Confirmed Study." Welcome, Professor Hopfner. Please tell us about this study and the key findings. Prof. Franziska Hopfner: So this work reframes how we think about MSA. So, autonomic failure is common but not universal and its absence does not rule out the diagnosis of MSA. So recognizing motor only in multiple system atrophy expands our diagnostic accuracy, improves patients consulting and broadens inclusions in future therapeutic trials. Dr. Elizabeth Coon: Excellent. Thank you. And thank you for listening to this Neurology Minute.

In part one of this two-part series, Dr. Neishay Ayub discusses the history of a novel anti-epileptic drug, levetiracetam.  Show citations:  Abou-Khalil B. Levetiracetam in the treatment of epilepsy. Neuropsychiatr Dis Treat. 2008;4(3):507-523. doi:10.2147/ndt.s2937  Löscher W, Gillard M, Sands ZA, Kaminski RM, Klitgaard H. Synaptic Vesicle Glycoprotein 2A Ligands in the Treatment of Epilepsy and Beyond. CNS Drugs. 2016;30(11):1055-1077. doi:10.1007/s40263-016-0384-x Rogawski MA. Brivaracetam: a rational drug discovery success story. Br J Pharmacol. 2008;154(8):1555-1557. doi:10.1038/bjp.2008.221 Ulloa CM, Towfigh A, Safdieh J. Review of levetiracetam, with a focus on the extended release formulation, as adjuvant therapy in controlling partial-onset seizures. Neuropsychiatr Dis Treat. 2009;5:467-476. doi:10.2147/ndt.s4844 Wu PP, Cao BR, Tian FY, Gao ZB. Development of SV2A Ligands for Epilepsy Treatment: A Review of Levetiracetam, Brivaracetam, and Padsevonil. Neurosci Bull. 2024;40(5):594-608. doi:10.1007/s12264-023-01138-2 Mahmoud A, Tabassum S, Al Enazi S, et al. Amelioration of Levetiracetam-Induced Behavioral Side Effects by Pyridoxine. A Randomized Double Blind Controlled Study. Pediatr Neurol. 2021;119:15-21. doi:10.1016/j.pediatrneurol.2021.02.010 Major P, Greenberg E, Khan A, Thiele EA. Pyridoxine supplementation for the treatment of levetiracetam-induced behavior side effects in children: preliminary results. Epilepsy Behav. 2008;13(3):557-559. doi:10.1016/j.yebeh.2008.07.004 Romoli M, Perucca E, Sen A. Pyridoxine supplementation for levetiracetam-related neuropsychiatric adverse events: A systematic review. Epilepsy Behav. 2020;103(Pt A):106861. doi:10.1016/j.yebeh.2019.106861 Show transcript:  Dr. Neishay Ayub: Hello, my name is Neishay Ayub, and today we are discussing the history of a novel anti-epileptic drug, levetiracetam. It's a story of a scientific dead end, a radical new testing method, and a mystery that took years to unravel. To set the scene, let's go back to 1974. The pharmaceutical company, UCB Pharma, was working on compounds to boost cognitive function. They were looking for a successor to their drug piracetam. During this research, levetiracetam was first synthesized, but the compound didn't show any significant brain-boosting effects. With no discernible purpose, it was filed away and largely forgotten. For nearly two decades, this medicine sat on a shelf an anonymous entry in a long list of failed drug candidates. The story could have ended there, but in the early 1990s, researchers took a different approach to drug discovery. Researchers screened their entire library of forgotten compounds against audiogenic seizure-susceptible mice. These are mice prone to seizures triggered by sound. Levetiracetam was incredibly ineffective in chronic epileptic mice. Interestingly, levetiracetam had previously failed traditional screening tests which was to prevent acute seizures in normal animals subjected to maximal electroshock or pentylenetetrazole. Levetiracetam was pushed forward to human clinical trials and was found to be efficacious in three placebo-controlled, randomized, blinded clinical trials for adults with refractory focal epilepsy. Two of the clinical trials reviewed levetiracetam three grams per day compared to placebo. They found the responder rate, i.e., 50% reduction in seizure frequency, was 39% to 42% for patients on three grams per day versus placebo at 10% to 16% when used as adjunctive therapy. One of these trials also used levetiracetam as monotherapy, noting a median percent reduction in focal seizure frequency of 73%, a responder rate of 59%, and 18% of patients achieving seizure freedom. In November 1999, the FDA gave its approval for adjunctive treatment of partial onset seizures. While levetiracetam was effective, how it worked was still unclear. It didn't affect the ion channels and neurotransmitter receptors that older, more traditional anti-epileptic drugs targeted. Eventually in 2004, scientists made another breakthrough. They identified the drug's primary molecular target, a protein called SV2A. This protein is involved in regulating the release of neurotransmitters. Instead of suppressing all neurologic activity, levetiracetam appears to bind to SV2A and selectively modulate neurotransmitter release in overactive seizing neurons. This precise mechanism is why it has such a favorable side effect profile. With the mystery solved and a novel mechanism understood, levetiracetam continues to be a popular anti-seizure medication to this day, and its use has been expanded. Further clinical trials led to FDA approvals for use in adult and pediatric patients with myoclonic epilepsy for myoclonic seizures as well as adult and pediatric patients with idiopathic generalized epilepsy for primary generalized tonic-clonic seizures. There is an off-label use for status epilepticus and seizure prophylaxis in TBI, in traumatic brain injury, subarachnoid hemorrhage, and neurosurgical cases. Formulations have also expanded to include tablets and liquid formulations for immediate release, extended-release tablets, and intravenous formulations. Today, with the original patent expired, generic versions are available, making this treatment accessible to millions. The journey of levetiracetam from an abandoned compound to a frontline treatment is a powerful reminder that in science, a failure might just be a success waiting to be tested in a different way.

Dr. Tesha Monteith discusses menstrual migraine and treatment options. 

In the January episode of the President's Spotlight, Dr. Jason Crowell and Dr. Natalia Rost discuss AAN's plans for 2026, including a general neurology boot camp, Autoimmune Conference, and new resources for members.    Stay informed by watching the President's Spotlight video.     

Dr. Derek Stitt and Drs. Joseph Safdieh and Matthew S. Robbins discuss subspecialization's impact on patient care, why preserving a core neurologist identity matters, and how training can reinforce it. Show citation: Safdieh JE, Robbins MS. Opinion & Special Articles: The Core Identity of the Neurologist. Neurology. 2025;105(9):e214265. doi:10.1212/WNL.0000000000214265 

Dr. Shuvro Roy and Dr. Rosa Cortese discuss new ways to improve MS and MOGAD diagnosis, including how AI and imaging could enhance accuracy and influence future care. Show citations: Cortese R, Sforazzini F, Gentile G, et al. Deep Learning Modeling to Differentiate Multiple Sclerosis From MOG Antibody-Associated Disease. Neurology. 2025;105(6):e214075. doi:10.1212/WNL.0000000000214075 

Dr. Bradley Ong discusses evidence for candesartan in migraine prevention. Show citation: Øie LR, Wergeland T, Salvesen Ø, et al. Candesartan versus placebo for migraine prevention in patients with episodic migraine: a randomised, triple-blind, placebo-controlled, phase 2 trial. Lancet Neurol. 2025;24(10):817-827. doi:10.1016/S1474-4422(25)00269-8

In the second part of this two-part series, Dr. Shuvro Roy examines the study's findings and their implications for clinical practice moving forward. Show citation: Kim M, Park YH, Song YS, et al. Gait Improvement Following CSF Tap Test in NPH Patients With and Without Striatal Dopaminergic Deficit: A Preliminary Study. Neurol Clin Pract. 2025;15(6):e200549. doi:10.1212/CPJ.0000000000200549

In part one of this two-part series, Dr. Shuvro Roy explains idiopathic normal pressure hydrocephalus (iNPH), its diagnostic challenges, and a study on whether dopamine transporter (DAT) scan results affect gait improvement after a CSF tap test. Show citation: Kim M, Park YH, Song YS, et al. Gait Improvement Following CSF Tap Test in NPH Patients With and Without Striatal Dopaminergic Deficit: A Preliminary Study. Neurol Clin Pract. 2025;15(6):e200549. doi:10.1212/CPJ.0000000000200549

Drs. Mahinda Yogarajah, Benjamin Tolchin, and Jon Stone discuss recommendations for clinicians, patients, and other stakeholders on the management of functional seizures.  Show citation: Tolchin B, Goldstein LH, Reuber M, et al. Management of Functional Seizures Practice Guideline Executive Summary: Report of the AAN Guidelines Subcommittee. Neurology. 2026;106(1):e214466. doi:10.1212/WNL.0000000000214466  Show transcript:  Dr. Mahinda Yogarajah: Welcome to this edition of Neurology Minute. I'm your host for this. My name's Mahinda Yogarajah. I've just finished interviewing Dr. Ben Tolchin and Jon Stone for this week's Neurology® Podcast. For today's Neurology Minute, I'm hoping Ben can tell us the main points of the podcast and the paper discussed in that podcast. Dr. Ben Tolchin: We discussed the AAN guideline on the Management of Functional Seizures. This is the first American Academy of Neurology evidence-based guideline on functional neurologic disorder. It includes a systematic review of the randomized controlled trials relating to the treatment of this disorder, which found that psychological interventions are possibly effective in improving the chance of achieving freedom from functional seizures, in reducing the frequency of functional seizures, in improving quality of life, and in improving anxiety. In addition to the systematic review, there are clinical recommendations based on the systematic review and on related evidence. The recommendations deal with all stages of the diagnosis, management, and treatment of functional seizures and are particularly relevant to neurologists caring for patients with functional seizures. In addition, there are recommendations for future research relating to the diagnosis and management of functional seizures. Dr. Mahinda Yogarajah: Thank you, Ben. For more information, I'd recommend go to the main podcast or go and have a read of the article that's been published in Neurology® on the Management of Functional Seizures Practice Guidelines.

Drs. Greg Cooper, Natalia Rost, and Behnam Sabayan discuss preventive neurology and the need for neurologists to move beyond diagnosis and treatment toward proactive strategies for brain health.  Show citation: Sabayan B, Boden-Albala B, Rost NS. An Ounce of Prevention: The Growing Need for Preventive Neurologists. Neurology. 2025;105(1):e213785. doi:10.1212/WNL.0000000000213785 Show transcript:  Dr. Greg Cooper: Hi, this is Greg Cooper. I just finished interviewing Behnam Sabayan and Natalia Rost for this week's Neurology® Podcast. For today's Neurology Minute, I'm hoping you can tell us the main points of your paper, An Ounce of Prevention, the Growing Need for Preventative Neurologist. Dr. Behnam Sabayan: We are living in a very exciting time for the field of neurology where we are not just getting very good at diagnosis and treatment of neurological condition, but also we are stepping one step back, and that means that we will find the root causes of neurological conditions. We would act as preventive specialists and we would decrease the burden of neurological conditions, not just at the individual level, but also at the population level. And this paper calls for thinking about playing roles at different levels and stages from our offices and our rounds all the way to the community to be brain health advocates and helping other fields and disciplines to reduce the burden of neurological conditions. Dr. Greg Cooper: Well, thank you for that summary and for all of your work on this topic. Please check out this week's podcast to hear the full interview or read the full article published in Neurology®, An Ounce of Prevention: The Growing Need for Preventative Neurologists. Thank you.

In the final episode of this seven-part series, Dr. Jon Stone and Dr. Gabriela Gilmour wrap up the conversation discussing future directions.  Show citations: Functional Neurological Disorder Society Finkelstein SA, Carson A, Edwards MJ, et al. Setting up Functional Neurological Disorder Treatment Services: Questions and Answers. Neurol Clin. 2023;41(4):729-743. doi:10.1016/j.ncl.2023.04.002  Show transcript:  Dr. Gabriela Gilmour: This is Gabriela Gilmour with the Neurology Minute. Jon Stone and I are back for our final episode of our seven-part series on functional neurological disorder. Today, we will discuss future directions for the field of FND. So Jon, where do you see the field of FND going in terms of diagnosis and treatment? Dr. Jon Stone: So we've seen a tremendous increase in interest in FND, particularly in the last five years since we started the FND Society. I think there's much more awareness of making rule-in diagnoses compared to before. There's much more positivity about treatment and I think people who experience their own patients doing very well with treatment makes them want to see that again. But we've got a long way to go. I think the diagnostic ruling features that we talked about in an earlier episode are still largely clinical. I think we could really benefit from seeing those becoming more laboratory supported, particularly for research, particularly for looking at FND comorbidity and other neurological conditions like MS and Parkinson's. So I think we might see more of that, AI helping us with that maybe, but things like quantifying some of the physical signs that we use. In terms of treatment, I think it's great all the different ideas about treatment that we've had and we know that the rehabilitation therapy for FND benefits from a more FND focused approach. But we have to be honest as well and say that the treatments, there's still large numbers of patients who are not improving. And so we do need to think about other ways to help people. People are interested in treatments, modalities such as using virtual reality, people looking at medications such as psychedelics or things like that. We've got to be careful with that obviously in peoples where their brains don't work properly. But I think we can do better than we are and people are exploring those options interestingly. Dr. Gabriela Gilmour: Yeah. And I think on the note of treatment, as we've sort of spoken through this podcast series, we've talked about places or environments where there's already services set up for patients. And so I think another major goal for the future for the FND Society is to build more services and have more expertise and knowledge across the world. What would you tell neurologists to do or how would you support them if they don't have other health professionals to help in their local environment? Dr. Jon Stone: Well, I'm aware that that's probably what most neurologists feel like. That they can recognize FND, but they don't have people to refer to or therapists who know about FND. So I certainly share that frustration. What I would say has happened locally here in Edinburgh, and also I see this in other centers as well. If you just start referring patients, helping to send patients to your colleagues who want to have therapy, educating your colleagues, then the people around you can develop that expertise that's needed. You don't necessarily need a whole new team. If you're an enthusiastic neurologist interested in FND, be careful about doing it just on your own because I think there's a lot of good you can do, but it'd be quite easy to burn out there without some help. So I think it's a slow process of gathering together interested health professionals. Ideally, of course, you want to have a psychologist to do therapy, a psychiatrist for more detailed assessments of complex patients, physio, OT, speech and language therapy. Once you get that, what I find is that then locally, they will start to teach each other because this is work that most people in rehabilitation actually enjoy when they know how to do it. They like seeing people with FND. They like the fact that this is a disorder that will often be static for many years or a long time anyway, and where therapy can actually change that trajectory. So just sort of hang in there. There are articles you can read about more details about how to set up services and think about that as well. Dr. Gabriela Gilmour: Well, thank you so much, Jon, for joining me for this series. This is our final episode of the Neurology Minute series on Functional Neurological Disorder. And thank you to all of our listeners. Dr. Jon Stone: Thank you very much, Gabriela.  

In part six of this seven-part series on FND, Dr. Jon Stone and Dr. Gabriela Gilmour discuss the prognosis of functional neurologic disorders.  Show citation:  Gelauff J, Stone J. Prognosis of functional neurologic disorders. Handb Clin Neurol. 2016;139:523-541. doi:10.1016/B978-0-12-801772-2.00043-6  Show transcript:  Dr. Jon Stone: This is Jon Stone with the Neurology Minute. Gabriela Gilmour and I are back to continue with part six of our seven-part series on FND. Today we're going to talk about prognosis. What's the outlook for people with FND? It's obviously a question that patients and relatives desperate to know the answer. Gabriela, what do you say to your patients with FND when they say, "What's going to happen to me? Dr. Gabriela Gilmour: That's a difficult question because the prognosis is variable and I'll talk in a moment about what we know about prognosis from the literature. But I think when patients ask me what's going to happen, I try to instill hope because we do know that this is a condition that can improve and it can improve, especially when patients have access to rehabilitation programs or psychotherapy or other treatment plans. So I try to emphasize that piece and emphasize hope when I'm talking about that with my patients. But if we sort of take a step back and we look at what is the overall prognosis from what we know in the literature with FND, fundamentally, FND for many is a chronic and often relapsing condition. As I mentioned, it can certainly improve with rehabilitation. A challenge is that most of our published studies on the prognosis of FND really come from a time when we knew a lot less about the condition and we had fewer treatment options. So these studies are somewhat difficult to apply today, but in these studies, we see that at least without treatment, most patients are the same or worse at follow-up. However, now we're starting to develop more rehabilitation programs and we have more evidence that shows that people certainly improve with rehabilitation and with therapy. There are some factors that I try to emphasize to patients as being good prognostic factors when I'm talking with them. These may be things like younger age, a shorter duration between symptom onset and diagnosis and patient agreement with the diagnosis or the perception of having control over their illness. When these types of things are present, I try to highlight them to, again, help build that hope for recovery. The one thing that I would also add maybe a bit of a different question, but I think is important to mention is that we as neurologists still have a lot to provide to our patients, even those who may not see much recovery in their symptoms and live with chronic illness. It's really important to consider that regular check-ins. In these check-ins, we can monitor for changing perpetuating factors. We can facilitate social services, mobility aids that help overall quality of life. We can still offer a lot to our patients. The other piece that I would mention too is that our patients are at risk of iatrogenic harm. So there is definitely a role for the neurologist to look at, are there medications that might not be indicated that are causing harm? Are there other things that we can communicate clearly with other care providers to make sure that we reduce that risk for our patients? Dr. Jon Stone: So it's about balancing some realism, but also making sure the patient doesn't lose hope. A good outcome isn't always necessarily that symptoms gone away. It might be similar to other chronic neurological conditions that we look after where we're okay with an outcome where the patient still has symptoms if they understand their condition and can learn to live with it better. We'll be back for our final Neurology Minute episode on FND with myself and Gabriela Gilmour talking about future directions in FND. Thanks for listening.

In part five of this seven-part series on FND, Dr. Jon Stone and Dr. Gabriela Gilmour discuss treatment options.  Show citation:  Gilmour, G.S., Nielsen, G., Teodoro, T. et al. Management of functional neurological disorder. J Neurol 267, 2164–2172 (2020). https://doi.org/10.1007/s00415-020-09772-w  Gilmour GS, Langer LK, Bhatt H, MacGillivray L, Lidstone SC. Factors Influencing Triage to Rehabilitation in Functional Movement Disorder. Mov Disord Clin Pract. 2024;11(5):515-525. doi:10.1002/mdc3.14007  Stone J, Carson A. Multidisciplinary Treatment for Functional Movement Disorder. Continuum (Minneap Minn). 2025;31(4):1182-1196. doi:10.1212/cont.0000000000001606 Tolchin B, Goldstein LH, Reuber M, et al. Management of Functional Seizures Practice Guideline Executive Summary: Report of the AAN Guidelines Subcommittee. Neurology. 2026;106(1):e214466. doi:10.1212/WNL.0000000000214466  Show transcript:  Dr. Jon Stone: Hello, this is Jon Stone with the Neurology Minute. Gabriela Gilmour and I are back to continue with part five of our seven-part series on FND. Today we'll be discussing treatment. Gabriela, talk us through what the rehabilitation or therapy approaches exist for FND now. Dr. Gabriela Gilmour: I would start actually even before jumping into rehabilitation and therapy to again emphasize something that we talked about in the last episode, which is that rehabilitation very much starts at our first visits with our patients when we examine for positive signs and show these to our patients and explain what they mean. So education about FND is really a fundamental treatment step, and I think we as neurologists have so much to offer to our patients in these visits. Next, when we're thinking about rehabilitation for FND, this often includes some combination of physical rehabilitation and psychological therapy and really should be individualized to each patient. So multidisciplinary or integrated therapy approaches are the gold standard and treatment strategies with these are really guided by our evolving understanding of the mechanisms of FND. So for example, this means using strategies like distraction, motor visualization, relaxation and mindfulness to target that underlying mechanism of FND. And then we use psychological therapies to also address perpetuating factors. So as we have discussed in this series, patients often experience many symptoms. So we also want to think about those other symptoms in our treatment plan, whether that be chronic pain or sleep disturbance or treating comorbid psychiatric or neurological illness. When we think about the subtypes of FND, there is some research into specific strategies for each. So psychotherapy, in particular, cognitive behavioral therapy is the focus for functional dissociative seizures with strategies aimed at attack prevention. Whereas for functional movement disorder, motor retraining physiotherapy has the most evidence. One big thing that I want to emphasize though is that rehabilitation for FND really relies on patient self-management and patient engagement. So I often explain to my patients that I can't retrain their brain, but I can help support them in this process and doing this for themselves. Dr. Jon Stone: So when you meet a patient with FND, how do you decide whether therapy is going to be helpful for them? I think people often have a tendency to say, "Oh, it's FND right off you go to psychotherapy or physiotherapy," but is that always the right option? How should we try and help our patients to decide if it's the right time for them to do these treatments? Dr. Gabriela Gilmour: Yeah, I think that that's something that's really maybe not unique, but something that's really important to FND and to treatment planning and FND. When we're supporting our patients as they embark on a treatment pathway, we really want to set them up for success. And so this really does rely on a robust triage process. So unlike other neurological conditions where you have X disease, therefore, why is the treatment? For FND, we've got a host of different types of treatments, and we want to individualize that and we want to time it right. Fundamentally, we really want to select the right treatment for our patients, and that relies on us understanding what symptoms are most bothersome to our patients, and we want to then provide that treatment at the right time. And I think right time is really what I would emphasize as being so, so important. So this means that patients are ready for active participation and rehabilitation, they're enthusiastically opted in. They think that treatment's going to help, and there aren't major barriers that are going to impact their ability to participate fully, so things like severe pain that could get in the way. And this is a conversation that I have really openly with my patients, and I really try to let them guide the timing. They will let me know, "Hey, I'm a teacher, and I'm in school right now. Now is not the right time for me to embark on this, but what about in June or July?" And then we revisit and regroup at that time. So really I do let my patients guide this process, but I would say that there are a subset of patients that don't need these more advanced rehabilitation type programs. Maybe are spontaneously improved or are able to implement some of their own self-management strategies on their own and have a significant improvement in symptoms already. Dr. Jon Stone: We need to make it easy for our patients to tell us when it's not the right time, but also, there's no one-size-fits-all, basically. Dr. Gabriela Gilmour: Absolutely. Dr. Jon Stone: So we'll be back for more Neurology Minute to continue our discussion on FND. We'll be talking about prognosis. Thanks for listening.

Dr. Zohaib Siddiqi talks with Dr. Catarina Bernardes about a case involving a 35-year-old woman presenting with personality changes and gait impairment.  Show citation:  Bernardes C, Lemos JM, Santo GC. Clinical Reasoning: A 35-Year-Old Woman With Personality Change and Gait Impairment. Neurology. 2025;104(2):e210252. doi:10.1212/WNL.0000000000210252  Show transcript:  Dr. Zohaib Siddiqi: Hi, everyone. My name is Zohaib Siddiqi and I'm a fifth-year neurology resident and a part of the Neurology® Resident and Fellow Section Editorial Board. I just finished interviewing Catarina Bernardes about her article, Clinical Reasoning: A 35-year-old Woman with Personality Change and Gait Impairment. Catarina, can you tell us the main points of the article? Dr. Catarina Bernardes: So in this article, we discussed the case of a 35-year-old woman who presented with a three-year history of walking difficulties. On examination, she had signs of a frontal temporal dysfunction, a dorsal lateral myelopathy, optic atrophy, and pes cavus. Her brain and spinal cord MRI was completely normal, but her son's brain MRI was being studied for spastic paraparesis showed signs of hypomyelination involving the subcortical U fibers. Given the suggestive inheritance pattern, we considered an X-linked leukoencephalopathy and central nervous system hypomyelination points to Pelizaeus-Merzbacher disease. Important learning points. When differentiating leukoencephalopathies, remember that hypomyelinating disorders often have less pronounced hypointensity on T2 and hypointensity on T1, and in demyelinating disorders, there is very prominent hyperintensity on T2 and hypointensity on T1. Also, Pelizaeus-Merzbacher is a hypomyelinating disorder affecting the subcortical U fibers, while X-linked adrenoleukodystrophy presents a demyelinating pattern sparing the subcortical U fibers and involving mainly the parietooccipital regions. Dr. Zohaib Siddiqi: Thanks so much for that summary, Catarina. A lot of learning points there. For those of you who want to learn more about the case, you can listen to the full-length podcast available now on all streaming platforms and find the article titled, Clinical Reasoning: A 35-year-old Woman with Personality Change and Gait Impairment on the Neurology® Resident Fellow Website. Thanks so much for joining today, and see you next time. 

In part four of this seven-part series on FND, Dr. Jon Stone and Dr. Gabriela Gilmour discuss the diagnostic explanation.  Show citation:  Stone J. Functional neurological disorders: the neurological assessment as treatment. Pract Neurol. 2016;16(1):7-17. doi:10.1136/practneurol-2015-001241  Gilmour GS, Lidstone SC. Moving Beyond Movement: Diagnosing Functional Movement Disorder. Semin Neurol. 2023;43(1):106-122. doi:10.1055/s-0043-1763505  Podcast transcript:  Dr. Gabriela Gilmour: This is Gabriela Gilmour with the Neurology Minute. Jon Stone and I are back to continue with part four, of seven, of our series on functional neurological disorder. Today we will focus on the diagnostic explanation. So many patients have never heard of FND before receiving this diagnosis. Can you share how you explain the diagnosis to your patients? Dr. Jon Stone: So I'm aware that many neurologists do find this difficult. And I have to say, having thought about it for 20 years or so now, I think the answer is, don't be weird. Do what you normally do with any condition, when you explain it to patients. I think what goes wrong is that people see FND as something weird and other, and they start to do weird things like telling people that their scans are normal, or telling them what they don't have before they've started to tell them what they do. If you go with the normal rules of explanation, first of all, starting by giving it a name that you prefer, so you've got FND, or try and be specific if you can. You've got functional seizures, functional movement disorder. Give it a name to start with. Don't sort of spend a long time beating around the bush before you do that. Talk a bit about why you've made the diagnosis, because that's what you normally do. So if someone's got a weak leg, show them their Hoover's sign. I think actually showing people their physical signs is probably one of the most powerful things you can do, brings the diagnosis away from the scanner and into the clinic room. And also, they can see in front of them the potential for improvement. So it feeds forward into treatment. Yes, you might need to explain why they don't have some other conditions that they're worried about, but you can leave discussions about why it's happened for later. I think what tends to go wrong is people jump into that too early. So the bottom line, just do what you normally do and things generally go a lot more smoothly. Dr. Gabriela Gilmour: And when you're providing the diagnostic explanation, it can be really helpful to link the patient's experience and their symptoms to the diagnosis. And so, I wonder how you integrate that piece into your diagnostic explanation, or how you tailor your explanation to an individual patient. Dr. Jon Stone: Yeah, I think tailoring is really important here. And this is where obviously if you've done your assessment, so helpful to ask the patient is, "Well, what do you think's wrong? What things were you worried about? " Some people say, "Look, I'm really worried I've got MS." Or some people say, "I haven't got FND. I've read about that. " Or sometimes people are wondering if they've got FND. So, you've got to try and tailor it to what the person is expecting and particularly previous experiences. If they're telling you how angry they were about doctors A, B, and C, then obviously you want to use that and try not to end up with the same outcome. Why would there be a problem with this diagnosis? It's because they haven't heard about it, because they've got misconceptions about it. Do they feel that this diagnosis would be saying it's all in their mind or something like that? You might need to be explicit about that. But I think this links into how, it's not just about the diagnostic label, it's about a formulation, which is something we don't think about much in neurology. So there's a label for what's wrong, but in FND, a formulation, why have you got FND, in your particular case, is what we're sort of moving on to there based on the story that you've heard. Dr. Gabriela Gilmour: Yeah. And I think in my experience and in working with trainees, really just practicing, saying it, is so important and saying it in a way that feels honest and correct to you as a clinician. Dr. Jon Stone: Yeah, absolutely. Dr. Gabriela Gilmour: So we will be back for more Neurology Minute episodes to continue our discussion on FND. Next, we're going to be talking about treatment. Thanks for listening.

In part three of this seven-part series on FND, Dr. Jon Stone and Dr. Gabriela Gilmour discuss causes of functional neurologic disorder.  Show citation:  Hallett M, Aybek S, Dworetzky BA, McWhirter L, Staab JP, Stone J. Functional neurological disorder: new subtypes and shared mechanisms. Lancet Neurol. 2022;21(6):537-550. doi:10.1016/S1474-4422(21)00422-1 Show transcript:  Dr. Gabriela Gilmour: This is Gabriela Gilmour with the Neurology Minute. Jon Stone and I are back to continue with part three of our seven-part series on functional neurological disorder. Today, we will focus on the causes of FND. So Jon, there have been many advances in our understanding of the mechanism of FND in the last 10, 15 years. And so what do we know about this now? Dr. Jon Stone: I think the key message I want to get across here is that whereas previously we had a very psychiatric, purely psychiatric view of FND, it used to be called conversion disorder, what we've got now is a multi-perspective view of the mechanisms, which mean that we can understand FND at a kind of neural level or brain circuit level, but we can also still retain the importance of psychological factors, traumatic events. And I think it's also important to separate out, as you've done here with a question, what's the mechanism? How is the symptom happening versus why is it happening? Which often people don't do. So for this question, how is it happening? How is it that somebody, for example, gets a weak leg? Well, at a very simple level, their brain is disconnecting from their leg and that's what dissociation is. And you can explain that to patients at sort of brain circuit level. We've learned that there are disruptions probably in the circuits in our brain that relate to that sense of agency, the parts of our brain that tell us that our bodies belong to us. And people are particularly interested in an area called the temporary parietal junction. And at a higher broader level, people are particularly interested in the idea that FND is a disorder that you would expect to happen based on our understanding of the brain as a predictive organ. So if the brain spends its time predicting things, maybe in FND what's gone wrong is this is very strong prediction that the leg is weak or that there's a tremor or that a seizure's about to happen that overrides sensory input telling our brain otherwise. Dr. Gabriela Gilmour: And I guess to follow into that, you mentioned what is going on. So now can you talk a little bit about why somebody might develop FND or the etiology of FND? Dr. Jon Stone:  I think this helps clinically as well as neurologists, because we can talk about mechanism as we would, for example, with MS as inflammation, but why is there inflammation? So okay, the brain's gone wrong, but why has it gone wrong? And there we need a much more complex view of multiple range of risk factors, predisposing, precipitating, and perpetuating that we know are associated with FND, but vary a lot from person to person. So no one person's the same. If you've had traumatic experiences in the past, that will make you more prone to dissociation. If you've had other functional disorders, if you have almost certainly some forms of genetics make people predisposed. And then as we said in the last episode, having another neurological condition, so having migraine aura, a physical injury, an infective illness, these are powerful reasons to trigger neurological symptoms. And it's not so much why they happen. It's more why do they get there and get stuck? We all probably have transient functional symptoms actually, but why they get stuck in people with FND for various reasons to do with the way their brains work or their past experiences, or sometimes what happens to them in medical systems. So developing a very open idea about why someone might have FND really helps you, I think, explain that back to patients and produce individual sort of formulations of the problem. Dr. Gabriela Gilmour: Yeah. And I often say to my patients, "I don't know exactly why you, why today have this." And that's true in medicine in general. We actually often don't know why anybody develops any medical condition with a few exceptions, but we know about risk factors really. Dr. Jon Stone: Absolutely. It's one of the reasons I hate the term medically unexplained. Actually, I think FND is perhaps more explained in some ways than some of the other conditions like multiple sclerosis and ALS that we actually deal with where we really don't know why they happen. Dr. Gabriela Gilmour: Well, we will be back for more Neurology Minute episodes to continue our discussion on FND. Thanks for listening. 

In part two of this two-part series on this year's World Stroke Congress, Dr. Andy Southerland and Dr. Seemant Chaturvedi discuss the ATLAS meta-analysis.  Learn more on the World Stroke Congress website. 

In part two of this series, Dr. Jeff Ratliff and Dr. Dara Albert discuss what advice they have for people who care for patients with FND.  Show citation:  Miller R, Lidstone S, Perez DL, Albert DVF. Education Research: Targeting Self-Described Knowledge Gaps to Improve Functional Neurologic Disorder Education Among Clinicians. Neurol Educ. 2025;4(3):e200239. Published 2025 Sep 5. doi:10.1212/NE9.0000000000200239 

Drs. Dan Ackerman, Valérie Biousse, and Nancy J. Newman discuss the clinical presentations, diagnostic challenges, and the importance of accurate diagnosis in managing CRAO and BRAO.  Show citation: Bénard-Séguin É, Nahab F, Pendley AM, et al. Eye stroke protocol in in the emergency department. J Stroke Cerebrovasc Dis. 2024;33(9):107895. doi:10.1016/j.jstrokecerebrovasdis.2024.107895 

In part one of this two-part series on this year's World Stroke Congress, Dr. Andy Southerland and Dr. Seemant Chaturvedi discuss the TRIDENT trial.  Learn more on the World Stroke Congress website. 

In part two of this seven-part series on FND, Dr. Jon Stone and Dr. Gabriela Gilmour discuss pitfalls in the diagnostic process.  Show citation:  Finkelstein SA, Popkirov S. Functional Neurological Disorder: Diagnostic Pitfalls and Differential Diagnostic Considerations. Neurol Clin. 2023;41(4):665-679. doi:10.1016/j.ncl.2023.04.001   

In part one of this seven-part series on FND, Dr. Jon Stone and Dr. Gabriela Gilmour discuss the process of diagnosing FND.  Show citation:  Aybek S, Perez DL. Diagnosis and management of functional neurological disorder. BMJ. 2022;376:o64. Published 2022 Jan 24. doi:10.1136/bmj.o64 

In the final episode of our five-part series on primary progressive aphasia (PPA), Dr. Rogan Magee discusses bedside testing for PPA.  Show citations:  Show citations:  Grossman M, Seeley WW, Boxer AL, et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers. 2023;9(1):40. Published 2023 Aug 10. doi:10.1038/s41572-023-00447-0  Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014. doi:10.1212/WNL.0b013e31821103e6 Santos-Santos MA, Rabinovici GD, Iaccarino L, et al. Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol. 2018;75(3):342-352. doi:10.1001/jamaneurol.2017.4309 Mandelli ML, Lorca-Puls DL, Lukic S, et al. Network anatomy in logopenic variant of primary progressive aphasia. Hum Brain Mapp. 2023;44(11):4390-4406. doi:10.1002/hbm.26388  Putcha D, Erkkinen M, Daffner KR. Functional Neurocircuitry of Cognition and Cognitive Syndromes. In: Silbersweig DA, Safar LT, Daffner KR. eds. Neuropsychiatry and behavioral neurology: principles and practice. McGraw Hill; 2021. Accessed November 6, 2025. https://neurology.mhmedical.com/content.aspx?bookid=3007§ionid=253215676  Montembeault M, Brambati SM, Gorno-Tempini ML, Migliaccio R. Clinical, Anatomical, and Pathological Features in the Three Variants of Primary Progressive Aphasia: A Review. Front Neurol. 2018;9:692. Published 2018 Aug 21. doi:10.3389/fneur.2018.00692 Clark DG. Frontotemporal Dementia. Continuum (Minneap Minn). 2024;30(6):1642-1672. doi:10.1212/CON.0000000000001506 

Dr. Alex Menze and Dr. Kristen Dams-O'Connor discuss traumatic encephalopathy syndrome and its relationship with traumatic brain injury.  Show Citation:  Dams-O'Connor K, Selmanovic E, Pruyser A, et al. Traumatic Encephalopathy Syndrome in the Late Effects of Traumatic Brain Injury (LETBI) Study Cohort. Neurology. 2025;1(2):e000015.  doi:10.1212/WN9.0000000000000015

In part one of this series, Dr. Jeff Ratliff and Dr. Dara Albert discuss the themes or buckets that self-identified FND knowledge gaps fall into.  Show citation:  Miller R, Lidstone S, Perez DL, Albert DVF. Education Research: Targeting Self-Described Knowledge Gaps to Improve Functional Neurologic Disorder Education Among Clinicians. Neurol Educ. 2025;4(3):e200239. Published 2025 Sep 5. doi:10.1212/NE9.0000000000200239 

In the final episode of our five-part series on primary progressive aphasia (PPA), Dr. Rogan Magee discusses bedside testing for PPA.  Show citations:  Grossman M, Seeley WW, Boxer AL, et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers. 2023;9(1):40. Published 2023 Aug 10. doi:10.1038/s41572-023-00447-0  Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014. doi:10.1212/WNL.0b013e31821103e6 Santos-Santos MA, Rabinovici GD, Iaccarino L, et al. Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol. 2018;75(3):342-352. doi:10.1001/jamaneurol.2017.4309 Mandelli ML, Lorca-Puls DL, Lukic S, et al. Network anatomy in logopenic variant of primary progressive aphasia. Hum Brain Mapp. 2023;44(11):4390-4406. doi:10.1002/hbm.26388  Putcha D, Erkkinen M, Daffner KR. Functional Neurocircuitry of Cognition and Cognitive Syndromes. In: Silbersweig DA, Safar LT, Daffner KR. eds. Neuropsychiatry and behavioral neurology: principles and practice. McGraw Hill; 2021. Accessed November 6, 2025. https://neurology.mhmedical.com/content.aspx?bookid=3007§ionid=253215676  Montembeault M, Brambati SM, Gorno-Tempini ML, Migliaccio R. Clinical, Anatomical, and Pathological Features in the Three Variants of Primary Progressive Aphasia: A Review. Front Neurol. 2018;9:692. Published 2018 Aug 21. doi:10.3389/fneur.2018.00692 Clark DG. Frontotemporal Dementia. Continuum (Minneap Minn). 2024;30(6):1642-1672. doi:10.1212/CON.0000000000001506 

In the December episode of the President's Spotlight, Dr. Jason Crowell speaks with Dr. Natalia Rost to provide an overview of the Academy's journey through 2025.  Show reference:  https://www.aan.com/about-the-aan/presidents-spotlight  

In the fourth installment of our series on primary progressive aphasia (PPA), Dr. Rogan Magee discusses semantic variant PPA.  Show citations:  Grossman M, Seeley WW, Boxer AL, et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers. 2023;9(1):40. Published 2023 Aug 10. doi:10.1038/s41572-023-00447-0  Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014. doi:10.1212/WNL.0b013e31821103e6 Santos-Santos MA, Rabinovici GD, Iaccarino L, et al. Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol. 2018;75(3):342-352. doi:10.1001/jamaneurol.2017.4309 Mandelli ML, Lorca-Puls DL, Lukic S, et al. Network anatomy in logopenic variant of primary progressive aphasia. Hum Brain Mapp. 2023;44(11):4390-4406. doi:10.1002/hbm.26388  Putcha D, Erkkinen M, Daffner KR. Functional Neurocircuitry of Cognition and Cognitive Syndromes. In: Silbersweig DA, Safar LT, Daffner KR. eds. Neuropsychiatry and behavioral neurology: principles and practice. McGraw Hill; 2021. Accessed November 6, 2025. https://neurology.mhmedical.com/content.aspx?bookid=3007§ionid=253215676  Montembeault M, Brambati SM, Gorno-Tempini ML, Migliaccio R. Clinical, Anatomical, and Pathological Features in the Three Variants of Primary Progressive Aphasia: A Review. Front Neurol. 2018;9:692. Published 2018 Aug 21. doi:10.3389/fneur.2018.00692 Clark DG. Frontotemporal Dementia. Continuum (Minneap Minn). 2024;30(6):1642-1672. doi:10.1212/CON.0000000000001506 

In the third installment of our series on primary progressive aphasia (PPA), Dr. Rogan Magee discusses nonfluent/agrammatic PPA.  Show citations:  Grossman M, Seeley WW, Boxer AL, et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers. 2023;9(1):40. Published 2023 Aug 10. doi:10.1038/s41572-023-00447-0  Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014. doi:10.1212/WNL.0b013e31821103e6 Santos-Santos MA, Rabinovici GD, Iaccarino L, et al. Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol. 2018;75(3):342-352. doi:10.1001/jamaneurol.2017.4309 Mandelli ML, Lorca-Puls DL, Lukic S, et al. Network anatomy in logopenic variant of primary progressive aphasia. Hum Brain Mapp. 2023;44(11):4390-4406. doi:10.1002/hbm.26388  Putcha D, Erkkinen M, Daffner KR. Functional Neurocircuitry of Cognition and Cognitive Syndromes. In: Silbersweig DA, Safar LT, Daffner KR. eds. Neuropsychiatry and behavioral neurology: principles and practice. McGraw Hill; 2021. Accessed November 6, 2025. https://neurology.mhmedical.com/content.aspx?bookid=3007§ionid=253215676  Montembeault M, Brambati SM, Gorno-Tempini ML, Migliaccio R. Clinical, Anatomical, and Pathological Features in the Three Variants of Primary Progressive Aphasia: A Review. Front Neurol. 2018;9:692. Published 2018 Aug 21. doi:10.3389/fneur.2018.00692 Clark DG. Frontotemporal Dementia. Continuum (Minneap Minn). 2024;30(6):1642-1672. doi:10.1212/CON.0000000000001506 

Dr. Alex Menze and Professor Hakan Cetin discuss the need to reevaluate the approach to diagnosing and treating seronegative myasthenia gravis.  Show citations:  Krenn M, Wagner M, Schuller H, et al. Screening for Congenital Myasthenic Syndromes in Adults With Seronegative Myasthenia Gravis Using Next-Generation Sequencing. Neurology. 2025;105(8):e214177. doi:10.1212/WNL.0000000000214177 

Dr. Gregg Day and Professor Jonathan Rohrer discuss the significance of studying individuals at risk of developing genetic frontotemporal dementia, focusing on how early cognitive changes before symptoms appear can inform research and future therapeutic trials.  Show citation: Russell LL, Bouzigues A, Convery RS, et al. Executive Function Deficits in Genetic Frontotemporal Dementia: Results From the GENFI Study. Neurol Genet. 2025;11(4):e200248. Published 2025 Jul 21. doi:10.1212/NXG.0000000000200248 

In the second installment of our series on primary progressive aphasia (PPA), Dr. Rogan Magee discusses logopenic PPA.  Show citations:  Grossman M, Seeley WW, Boxer AL, et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers. 2023;9(1):40. Published 2023 Aug 10. doi:10.1038/s41572-023-00447-0  Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014. doi:10.1212/WNL.0b013e31821103e6 Santos-Santos MA, Rabinovici GD, Iaccarino L, et al. Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol. 2018;75(3):342-352. doi:10.1001/jamaneurol.2017.4309 Mandelli ML, Lorca-Puls DL, Lukic S, et al. Network anatomy in logopenic variant of primary progressive aphasia. Hum Brain Mapp. 2023;44(11):4390-4406. doi:10.1002/hbm.26388  Putcha D, Erkkinen M, Daffner KR. Functional Neurocircuitry of Cognition and Cognitive Syndromes. In: Silbersweig DA, Safar LT, Daffner KR. eds. Neuropsychiatry and behavioral neurology: principles and practice. McGraw Hill; 2021. Accessed November 6, 2025. https://neurology.mhmedical.com/content.aspx?bookid=3007§ionid=253215676  Montembeault M, Brambati SM, Gorno-Tempini ML, Migliaccio R. Clinical, Anatomical, and Pathological Features in the Three Variants of Primary Progressive Aphasia: A Review. Front Neurol. 2018;9:692. Published 2018 Aug 21. doi:10.3389/fneur.2018.00692 Clark DG. Frontotemporal Dementia. Continuum (Minneap Minn). 2024;30(6):1642-1672. doi:10.1212/CON.0000000000001506 

In the first part of this series, Dr. Rogan Magee provides an introduction to primary progressive aphasia (PPA) and explains its three subtypes.  Show citations:  Grossman M, Seeley WW, Boxer AL, et al. Frontotemporal lobar degeneration. Nat Rev Dis Primers. 2023;9(1):40. Published 2023 Aug 10. doi:10.1038/s41572-023-00447-0  Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification of primary progressive aphasia and its variants. Neurology. 2011;76(11):1006-1014. doi:10.1212/WNL.0b013e31821103e6 Santos-Santos MA, Rabinovici GD, Iaccarino L, et al. Rates of Amyloid Imaging Positivity in Patients With Primary Progressive Aphasia. JAMA Neurol. 2018;75(3):342-352. doi:10.1001/jamaneurol.2017.4309 Mandelli ML, Lorca-Puls DL, Lukic S, et al. Network anatomy in logopenic variant of primary progressive aphasia. Hum Brain Mapp. 2023;44(11):4390-4406. doi:10.1002/hbm.26388  Putcha D, Erkkinen M, Daffner KR. Functional Neurocircuitry of Cognition and Cognitive Syndromes. In: Silbersweig DA, Safar LT, Daffner KR. eds. Neuropsychiatry and behavioral neurology: principles and practice. McGraw Hill; 2021. Accessed November 6, 2025. https://neurology.mhmedical.com/content.aspx?bookid=3007§ionid=253215676  Montembeault M, Brambati SM, Gorno-Tempini ML, Migliaccio R. Clinical, Anatomical, and Pathological Features in the Three Variants of Primary Progressive Aphasia: A Review. Front Neurol. 2018;9:692. Published 2018 Aug 21. doi:10.3389/fneur.2018.00692 Clark DG. Frontotemporal Dementia. Continuum (Minneap Minn). 2024;30(6):1642-1672. doi:10.1212/CON.0000000000001506 

In this episode of the Neurology Minute, Dr. Nara Miriam Michaelson delves into another women's history minute to discuss Sylvia Lawry. 

Dr. Jason Crowell and Dr. YuHong Fu discuss the importance of differentiating between dementia with Lewy bodies and Parkinson disease dementia.  Show citatiion:  Fu Y, Halliday GM. Dementia with Lewy bodies and Parkinson disease dementia - the same or different and is it important?. Nat Rev Neurol. 2025;21(7):394-403. doi:10.1038/s41582-025-01090-x 

Dr. Dan Ackerman and Dr. Isabel Hostettler discuss the diagnosis, risk factors, and prognosis of RCVS, highlighting the need to recognize symptoms and distinguish it from other causes of subarachnoid hemorrhage.  Show reference:  Hostettler IC, Ponciano A, Wilson D, et al. Outcomes After Reversible Cerebral Vasoconstriction Syndrome With Convexity Subarachnoid Hemorrhage: Individual Patient Data Analysis. Neurology. 2025;105(5):e213984. doi:10.1212/WNL.0000000000213984 

In the November episode of the President's Spotlight, Dr. Jason Crowell talks with Dr. Natalia Rost about the Centers for Medicare & Medicaid Services final rule for how physicians are reimbursed in 2026.  Show reference:  https://www.aan.com/about-the-aan/presidents-spotlight