Podcasts about mmse

Dr Peter Connelly narrates his blog written for Dementia Researcher. In his first blog for Dementia Researcher, Dr Peter Connelly highlights the pivotal role memory clinics play in dementia clinical research. Despite often being perceived as distinct from everyday practice, he argues that the overlap between routine cognitive assessments and trial protocols offers an opportunity for better integration. From enhancing referrals through shared assessment tools like the MMSE to educating mainstream services, memory clinics can bridge gaps and increase trial participation. He calls for more seamless collaboration between clinical care and research, underlining the practical and strategic value of memory clinics in the clinical trial landscape. Find the original text, and narration here on our website. https://www.dementiaresearcher.nihr.ac.uk/blog-the-role-of-memory-clinics-in-clinical-research/ -- Dr Peter Connelly is a retired Old Age Psychiatrist who spent much of his career in Tayside, helping to establish clinical trials for dementia and neuroprogressive disorders in Scotland. Now working with the Scottish Neuroprogressive and Dementia Network, he combines professional insight with personal experience as a former carer. In retirement, he enjoys music, golf, and time with his grandchildren. -- Enjoy listening? We're always looking for new bloggers, drop us a line. http://www.dementiaresearcher.nihr.ac.uk This podcast is brought to you in association with Alzheimer's Association, Alzheimer's Research UK, Alzheimer's Society and Race Against Dementia, who we thank for their ongoing support. -- Follow us on Social Media: https://www.instagram.com/dementia_researcher/ https://www.facebook.com/Dementia.Researcher/ https://twitter.com/demrescommunity https://www.linkedin.com/company/dementia-researcher https://bsky.app/profile/dementiaresearcher.bsky.social

What's good for the heart is good for the brain. Guest Brittany Butts, PhD, RN, describes helping patients understand this connection and implement actions to decrease their risk for both cardiovascular and cognitive declines. MMSE: https://muhc.ca/sites/default/files/micro/m-PT-OT/OT/Mini-Mental-State-Exam-%28MMSE%29.pdfMOCA: https://mocacognition.com/paper (official site)https://geriatrictoolkit.missouri.edu/cog/MoCA-8.3-English-Test-2018-04.pdf (PDF only)PCNA CE Course: Preventing Stroke: Applying the Guidelines https://pcna.net/online-course/preventing-stroke-applying-the-guidelines/See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Neuroscientist Adrian Owen discusses his KevinMD article, "A wake-up call for dementia detection: the urgent need for precision tools across health care." Adrian highlights the alarming rate of dementia diagnoses worldwide and examines the shortcomings of outdated detection tools like MMSE, SLUMS, and MoCA. He emphasizes the need for innovative, digitally-enabled cognitive assessment tools to ensure early and accurate diagnoses. The conversation explores actionable strategies to integrate advanced neuroscience into primary care, aiming to reduce health care costs and improve patient outcomes. Our presenting sponsor is DAX Copilot by Microsoft. Do you spend more time on administrative tasks like clinical documentation than you do with patients? You're not alone. Clinicians report spending up to two hours on administrative tasks for each hour of patient care. Microsoft is committed to helping clinicians restore the balance with DAX Copilot, an AI-powered, voice-enabled solution that automates clinical documentation and workflows. 70 percent of physicians who use DAX Copilot say it improves their work-life balance while reducing feelings of burnout and fatigue. Patients love it too! 93 percent of patients say their physician is more personable and conversational, and 75 percent of physicians say it improves patient experiences. Help restore your work-life balance with DAX Copilot, your AI assistant for automated clinical documentation and workflows. VISIT SPONSOR → https://aka.ms/kevinmd SUBSCRIBE TO THE PODCAST → https://www.kevinmd.com/podcast RECOMMENDED BY KEVINMD → https://www.kevinmd.com/recommended GET CME FOR THIS EPISODE → https://www.kevinmd.com/cme I'm partnering with Learner+ to offer clinicians access to an AI-powered reflective portfolio that rewards CME/CE credits from meaningful reflections. Find out more: https://www.kevinmd.com/learnerplus

Welcome to PsychEd, the psychiatry podcast for medical learners, by medical learners. This primer covers the differential diagnosis of dementia. Hosts: Dr. Alastair Morrison (PGY-1) and Dr. Angad Singh (PGY-1) Audio editing by: Dr. Angad Singh (PGY-1) Resources: MoCA: https://dementia.talkbank.org/protocol/materials/MOCA.pdf MMSE: https://meded.temertymedicine.utoronto.ca/sites/default/files/assets/resource/document/mini-mental-state-examinationmmse.pdf Beers Criteria: American Geriatrics Society 2023 updated AGS Beers Criteria® for potentially inappropriate medication use in older adults PsychEd Episode 49: Dementia Assessment with Dr. Lesley Wiesenfeld References: American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596 Francis, J. & Young, B. (2022). Diagnosis of delirium and confusional states. UpToDate. Retrieved January 31, 2025, from https://www.uptodate.com/contents/delirium-and-acute-confusional-states-prevention-treatment-and-prognosis Larson, E. B. (2022). Evaluation of cognitive impairment and dementia. UpToDate. Retrieved January 31, 2025, from https://www.uptodate.com/contents/evaluation-of-cognitive-impairment-and-dementia PsychDB. (2022, Oct 3). Introduction to Dementia. Retrieved January 31, 2025, from https://www.psychdb.com/geri/dementia/home PsychDB. (2024, Feb 1). Delirium. Retrieved January 31, 2025, from https://www.psychdb.com/cl/1-delirium PsychDB. (2024, Feb 9). Alzheimer's Disease. Retrieved January 31, 2025, from https://www.psychdb.com/geri/dementia/alzheimers PsychDB. (2023, Oct 12). Vascular Dementia. Retrieved January 31, 2025, from https://www.psychdb.com/geri/dementia/vascular PsychDB. (2024, Jan 23). Frontotemporal Dementia. Retrieved January 31, 2025, from https://www.psychdb.com/geri/dementia/frontotemporal PsychDB. (2024, Feb 5). Dementia with Lewy Bodies. Retrieved January 31, 2025, from https://www.psychdb.com/geri/dementia/lewy-body For more PsychEd, follow us on Instagram (@psyched.podcast), Facebook (PsychEd Podcast), and X (@psychedpodcast). You can email us at psychedpodcast@gmail.com and visit our website at psychedpodcast.org.

Although Alzheimer disease (AD) is the most common neurodegenerative cause of dementia, other etiologies can mimic the typical amnestic-predominant syndrome and medial temporal brain involvement. Neurologists should recognize potential mimics of AD for clinical decision-making and patient counseling. In this episode, Kait Nevel, MD, speaks with Vijay K. Ramanan, MD, PhD, an author of the article “LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy,” in the Continuum December 2024 Dementia issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Ramanan is a consultant and assistant professor of neurology in the Division of Behavioral Neurology at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy 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 Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: IUneurodocmom Guest: @vijaykramanan Full episode transcript available here Dr Jones: This is Dr Lyle Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum 's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Nevel: This is Dr Kait Nevel. Today I'm interviewing Dr Vijay Ramanan about his article he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast. Vijay, can you please introduce yourself to the audience? Dr Ramanan: Thanks so much, Kait. I'm delighted to be here. So, I am a cognitive neurologist and neuroscientist at the Mayo Clinic in Rochester, Minnesota. I have roles in practice, education and research, but amongst those I see patients with cognitive disorders in the clinic. I help direct our Alzheimer's disease treatment clinic and also do research, including clinical trial involvement and some observational research on genetics and biomarkers related to Alzheimer's and similar disorders. Dr Nevel: Great, thanks for that. So, I'd like to start off by talking about why is LATE hippocampal sclerosis, why is this important for the neurologist practicing in clinic to know about these things? Dr Ramanan: That's a great question. So, if we take a step back, we know that degenerative diseases of the brain are really, really common, and they get more and more common as we get older. I think all neurologists, and in fact most clinicians and large swaths of the general public, are well aware of Alzheimer's disease, which is the most common degenerative cause of cognitive impairment in the population. But there are non-Alzheimer's degenerative diseases which can produce cognitive difficulties as well. And it's important to be aware of those disorders, of their specific presentations and their implications, in part because it's always a healthy thing when we can be as precise and confident about diagnosis and expectation with our patients as possible. I'll look to the analogy of a patient presenting with a myelopathy. As neurologists, we would all find it critical to clarify, is that myelopathy the result of a compressive spondylotic change? The result of an inflammatory disorder, of a neoplastic disorder, of an infectious disorder? It's critical to guide the patient and choose appropriate management options based on the cause of their syndrome. It would potentially harm the patient if you treated an infectious myelopathy with steroids or other immune-suppressant drugs. So, a similar principle holds in cognitive neurology. I accept with humility that we can never be 100% crystal clear certain about things in medicine, just because when you think you got it all figured out there's a curveball. But I want to get as close to that 100% as possible. And recognizing that disorders like LATE or PART can mimic the symptoms, sometimes even the imaging features of Alzheimer's disease. I think it's critical to have heightened awareness of those disorders, how they look, to be able to apply appropriate counseling and management options to patients. I think this becomes particularly critical as we move into an era of disease-specific, and sometimes disease-modifying, therapies, where applying a choice of a treatment option could have significant consequences to a patient if the thing you're treating isn't the thing that the drug is trying to accomplish. So, having awareness and spreading awareness about some of these non-AD causes of cognitive difficulty, I think, is a big mission in the field.  Dr Nevel: Yeah, that makes total sense. And kind of leaning into this, you know, trying to differentiate between these different causes of late-life amnestic cognitive impairment. You know, I'll point out to the listeners today to please read your article, but in addition to reading your article, I'd like to note that there's a really nice table in your article, Table 6-1, where you kind of go through the different causes of amnestic cognitive impairment and the different features that better fit with diagnosis X, Y, or Z, because I think it's a really nice table to reference and really easy to look at and reference back to. But on that note, what is your typical approach when you're seeing a patient in clinic, have a new referral for an older patient presenting with a predominantly progressive amnestic-type features? Dr Ramanan: Excellent question. And this is one that I think has relevance not just in a subspecialty memory clinic, but to all the clinicians who help to diagnose and manage cognitive disorders, including in primary care and general neurology and others. One principle that I think it's helpful to keep in our minds is that in cognitive neurology, no one data point takes precedence over all the others. We have a variety of information that we can gather from history, from exam, from imaging, from fluid biomarkers. And really the fun, the challenge, the reward is in piercing together that information. It's almost like being a lawyer and compiling the evidence, having possibilities on your list and raising and lowering those possibilities to get as close to the truth as you can. So, for patients with a cognitive syndrome, I think the first plank is in defining that syndrome. As you mentioned, if I'm seeing someone with a progressive amnestic-predominant syndrome, I first want to make sure, are we talking about the same thing, the patient, the care partner, and I?  Can often be helpful to ask them for some examples of what they see, because sometimes what patients may report as memory troubles may in fact reflect cognitive difficult in other parts of our mental functioning. For example, executive functioning or naming of objects. And so helpful to clarify that in the history to get a sense of the intensity and the pace of change over time, and then to pair that with a good general neurologic exam and some type of standardized assessment of their cognitive functioning. At the Mayo Clinic, where partial to the short test of mental status. There are other ways to accomplish that, such as with an MMSE or a MoCA. If I understand that the syndrome is a progressive amnestic disorder, Alzheimer's disease is the most common cause of that presentation in older adults, it deserves to be on my differential diagnosis. But there might be some other features in the story that could raise or lower those mimics on my list. So, in patients who are, say, older than the age of seventy five, disorders like LATE or PART start to rise higher on the likelihood for me, in particular if I know that their clinical course has been more slow brewing, gradually evolving. And again, most degenerative disorders we expect to evolve not over days or weeks, but over many months to many years. But in comparison with Alzheimer's disease, patients with LATE or with PART would be expected to have a little more slow change where maybe year over year they or their care partners really aren't noticing big declines. Their daily function is relatively spare. There might not be as much involvement into other non-memory cognitive domains. So, these are some of the pieces of the story that can help to perhaps isolate those other non-AD disorders on the list as being more likely and then integrating, as a next level, diagnostic testing, which helps you to rule in and rule out or support those different causes. So, for example, with LATE there can be often out of proportion to the clinical picture, out of proportion to what you see on the rest of their imaging or other profiles, very predominant hippocampal and medial temporal volume loss. And so that can be a clue in the right setting that you may not be dealing with Alzheimer's disease or pure Alzheimer's disease, but that this other entity is there. So, in the big picture, I would say being systematic, recognizing that multiple data points being put together helps you get to that confident cause or etiology of the syndrome. And in particular, taking a step back and thinking about big picture factors like age and course to help you order those elements of the differential, whether AD or otherwise. Dr Nevel: Great, thanks. In your article, you talk about different imaging modalities that can be used, as you mentioned, you know, just another piece of the puzzle, if you will, to try and put together what may be going on with the patient, and recognizing that some of these imaging techniques are imaging is special imaging, not available in a lot of places.  You know, and maybe other diagnostic type tests that could be helpful in differentiating between these different disorders may not be available, you know, for the general neurologist practicing in the community. So, what do you suggest to the general neurologist maybe practicing somewhere where they don't have access to some of these ancillary tests that could assist with a diagnosis?  Dr Ramanan: Critical question. And here I think there's not likely to be one single answer. As with most things, awareness and recognition is a good place to start. So, some of those clues that I mentioned earlier about the clinical course, about the age, the- we're talking about clinical setting there. So, comfort with and understanding that the clinical setting can help you to be more confident about, for example, LATE or PART being present in contrast to AD. That's important information. It deserves to be part of the discussion. It doesn't necessarily need other tests to have value on its own. A second piece is that tests help, in some cases, to rule in and rule out causes for cognitive difficulty. As part of a standard cognitive evaluation, we would all be interested in getting some blood tests to look for thyroid dysfunction or vitamin deficiencies. Some type of structural head imaging to rule out big strokes, tumors, bleeds. Head CT can accomplish some of that perspective. It's ideal if a brain MRI can be obtained, but again, keeping in mind, what's the primary goal of that assessment? It's to assess structure. Occasionally you can get even deeper clues into a syndrome from the MRI. For example, that very profound hippocampal or medial temporal atrophy. So, increasing awareness amongst clinicians throughout our communities to be able to recognize that change and put it in the context of what they see in other brain regions that can be affected by Alzheimer's or related disorders. For example, the parietal regions can be helpful. And recall that MRI can also be helpful in assessing for chronic cerebrovascular disease changes. This is another mimic that shows up in that table that you mentioned. And so multiple purposes can be satisfied by single tests. Now, you're absolutely right that there are additional test modalities that, perhaps in a subspecialty clinic at an academic medical center, we're very used to relying on and finding great value on; for example, glucose PET scans or sometimes fluid biomarkers from the blood or from the spinal fluid. And these are not always as widely available throughout our communities. Part of the challenge for all of us as a field is therefore to take the expertise that we have gathered in more subspecialty settings and tertiary care settings and translate and disseminate that out into our communities where we need to take care of patients. That's part of the challenge. The other challenge is in continued tool and technological development. There's a lot of optimism in our field that the availability of blood-based biomarkers relevant for Alzheimer's disease may play a part in helping to address some of the disparities in resource and access to care. You can imagine that doing a blood test to give you some high-quality information, there are going to be less barriers to doing that in many settings compared to thinking about a lumbar puncture or a PET scan, both in terms of cost to the patient as well as infrastructure to the clinicians and the care team. So I'm optimistic about a lot of those changes. In the meantime, I think there are, through both clinical evaluation and some basic testing including structural head imaging, there are clues that can help navigate these possibilities. Dr Nevel: So, let's say you have your patient in clinic, you've done your evaluation, maybe gotten some ancillary testing, and you highly suspect either LATE or PART. How do you counsel those patients and their families? How do you manage those patients moving forward who you really suspect don't have, you know, some sort of co-pathology? Dr Ramanan: So, it's- I think it's helpful to remember when patients are coming to see us, either they or the people around them have noticed an issue. And very likely it's an issue that's been brewing for a little while. I think it can be very valuable, very helpful for patients to have answers. What's the cause for the issue? Once you have answers, even if sometimes those answers are not the most welcome things or the things that you'd be looking forward to, answers give you an opportunity to grab hold of what's going on, to define a game plan. So, understanding there is a degenerative disease there, it sheds light on why that individual had had memory symptoms over the years. And it gives them a general expectation that over time on an individualized basis, but generally expecting gradually over many months to many years, there may be some worsening in some of those symptoms helps them to plan and helps them to make the adaptations that are a-ok and great to make to just help you to do the things you want to do. As much as I can, I try to put the focus here closer to how we would view things like high blood pressure or high cholesterol. Those are also chronic issues that tend to be more common as we get older, tend to get more troublesome as we get older. The goal is, know what you're dealing with and take the combination of lifestyle modifications, adaptations in your day-to-day and maybe medications to keep them as mild and as slow-changing as possible. With something like LATE, we don't have specific medication therapies to help support cognitive functioning at this time. There's a lot of hope that with additional research we will have those therapies. But even so, I think it's an important moment to emphasize some of those good healthy lifestyle habits. Staying mentally, socially and physically active, getting a good night's sleep, eating a healthy, balanced diet, keeping good control of vascular risk factors, all of that is critical to keeping the brain healthy, keeping the degenerative disease as mild and slow-brewing as possible. And understanding what some of the symptoms to expect could be. So, with LATE the syndrome tends to be very memory-predominant. There may be some trouble with maybe naming of objects or perhaps recall of emotionally salient historical knowledge, world events, but you're not expecting, at least over the short to medium term, huge intervening on other cognitive functioning. And so that can be helpful for patients to understand. So, the hope is once you know what what you're dealing with, you understand that the disease can look different from person to person. Having a general map of what to expect and what you can do to keep it in check, I think, is the goal. Dr Nevel: I agree with you 100% that it really can be helpful even if we can't, quote unquote, fix it, that for people, family, the patient have a name for what they have and kind of have some sort of idea of what to expect in the future. And they may come in thinking that they have Alzheimer's or something like that. And then, so, to get that information that this is going to be a little different, we expect this to go a little bit differently then it would if you had a diagnosis of Alzheimer's, I can see how that would be really helpful for people.  Dr Ramanan: I completely agree. And here's another challenge for us in the field when most patients have heard about Alzheimer's disease and many have perhaps even heard of dementia with Lewy bodies or frontotemporal dementia, but may not have heard of things like LATE. And they're not always easy to go online or find books that talk about these things. Having a name for it and being able to pair that with patient-friendly information is really critical. I see our appointments where we're sharing those diagnosis and making initial game plans as an initial foray into that process.  Dr Nevel: Yeah, absolutely. What is the greatest inequity or disparity that you see in taking care of patients with progressive amnestic cognitive impairment? Dr Ramanan: Yeah, great question. I think two big things come to mind. The first, you hinted at very well earlier that there are disparities in access to care, access to diagnostic testing, access to specialists and expertise throughout our communities. If we want diagnostics and therapeutics to be broadly applicable, they do need to be broadly available. And that's a big challenge for us as a field to work to address those disparities. There's not going to be one single cause or contributor to those iniquities, but as a field, I'm heartened to see thought and investment into trying to better address those. Another big weakness, and this is not just limited to cognitive neurology, it's a challenge throughout neurology, is that too many of our research studies are lacking in diversity. And that impacts our biological and pathophysiological understanding of these disorders. It also impacts our counseling and management. Again, if we want a new drug treatment to be broadly applicable throughout all of the patients that we take care of, we need to have data which guides how we apply those treatments. And so again, I'm heartened. This is a big challenge. It's a long standing challenge. It will take deep and long standing committed efforts to reverse. But I'm heartened that there are efforts in the field to broaden clinical trial enrollment, broaden observational research enrollment, and again, broaden access to tools and expertise. As a neurologist, I got into this field because I want to help people, use my expertise and my training to help people. These are steps that we can take to make sure that that help is broadly applicable throughout everybody in our communities. Dr Nevel: Yeah, absolutely. So, kind of segueing from you mentioning research and how we can better include patients in research. What do you think the next breakthrough is going to be? What do you think the next big thing is going to be in these disorders? What do we still need to learn? Dr Ramanan: There's a lot. I think for LATE and PART, the development of specific biomarkers would be top of the agenda. Now, biomarkers are by their nature imperfect. Even with Alzheimer's disease, where in comparison, we know quite a lot. We have a variety of imaging and fluid biomarkers that we can use to support or rule out a diagnosis. There are nuances in how you interpret those biomarkers. Patients can have signs of amyloid plaques in their brain and have completely normal cognition. They may be at risk for developing cognitive trouble due to Alzheimer's disease in the future, but it's one piece of the puzzle. Patients can have the changes of Alzheimer's disease amyloid plaques and tau tangles in the brain. We can confirm that through biomarkers. But at the end of the day, their cognitive syndrome might be driven by something else. Maybe it's Lewy body disease, maybe it's LATE, maybe it's a combination of factors. So, integrating and interpreting those biomarkers is challenging. But I do think, again, from the standpoint of giving patients answers with a diagnosis, having those biomarkers is really critical to just kind of closing the loop. It will also be critical to have those biomarkers as we're assessing for treatment response. So, for example, patients who may have coexistent Alzheimer's disease and LATE, I don't think we know the answer fully as to how likely they are to benefit from, say, newer antiamyloid monoclonal antibodies for Alzheimer's disease in the setting of that second pathology. So, wouldn't it be great if, similar to an oncologic setting where you engage in a treatment and then you're tracking two or three or four plasma measures and you're tracking tumor size with imaging, if we had this multimodal ability to track neurodegenerative pathology through biomarkers? I think that'll be a critical next step. And so, filling out that for non-Alzheimer's diseases, including LATE and PART, I think is item number one on the agenda. Dr Nevel: Wonderful, thank you so much. I really appreciate you taking the time to chat with me today about your article. I really enjoyed our conversation, certainly learned a lot. Dr Ramanan: Thank you so much, Kait. Love talking with you. And again, it was an honor to write this article. I hope it's helpful to many out in the field who take care of patients with cognitive issues.  Dr Nevel: Yeah, I think it will be. So again, today I'm interviewing Dr Vijay Ramanan about his article that he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the most recent issue of Continuum on dementia. Be sure to check out Continuum audio episodes from this and other issues. And thank you, Vijay, and thank you 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.

A pragmatic and organized approach is needed to recognize patients with symptomatic Alzheimer Disease in clinical practice, stage the level of impairment, confirm the clinical diagnosis, and apply this information to advance therapeutic decision making. In this episode, Aaron Berkowitz, MD, PhD, FAAN, speaks with Gregory S. Day, MD, MSc, MSCI, FAAN, author of the article “Diagnosing Alzheimer Disease,” in the Continuum December 2024 Dementia issue. Dr. Berkowitz is a Continuum® Audio interviewer associate chief medical information officer at the Cleveland Clinic in Cleveland, Ohio. Dr. Day is an associate professor in the Department of Neurology at Mayo Clinic Florida in Jacksonville, Florida. Additional Resources Read the article: Diagnosing Alzheimer Disease 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 Guest: @GDay_Neuro Full episode transcript available here Dr Jones: This is Doctor Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors, who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I have the pleasure of interviewing Dr Gregory Day about his article on Alzheimer disease, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast, Dr Day. Would you mind introducing yourself to our audience?  Dr Day: Thanks very much, Aaron. I'm Gregg Day. I'm a behavioral neurologist at Mayo Clinic in Jacksonville, Florida, which means that my primary clinical focus is in the assessment of patients presenting typically with memory concerns and dementia in particular. Dr Berkowitz: Fantastic. Well, as we were talking about before the interview, I've heard your voice many times over the Neurology podcast and Continuum podcast. I've always learned a lot from you in this rapidly changing field over the past couple of years, and very excited to have the opportunity to talk to you today and pick your brain a little bit on this very common issue of evaluating patients presenting with memory loss who may have concerns that they have dementia and specifically Alzheimer disease. So, in your article, you provide a comprehensive and practical approach to a patient presenting for evaluation for possible dementia and the question of whether they have Alzheimer disease. The article is really packed with clinical pearls, practical advice. I encourage all of our listeners to read it. In our interview today, I'd like to talk through a theoretical clinical encounter and evaluation so that I and our listeners can learn from your approach to a patient like this. Let's say we have a theoretical patient in their seventies who comes in for evaluation of memory loss and they and/or their family are concerned that this could be Alzheimer disease. How do you approach the history in a patient like that? Dr Day: It's a great way to approach this problem. And if you're reading the article, know that I wrote it really with this question in mind. What would I be doing, what do we typically do, when we're seeing patients coming with new complaints that concern the patient and typically also concern those that know the best? So be that a family member, close friend, adult child. And in your scenario here, this seventy year old individual, we're going to use all the information that we have on hand. First off, really key, if we can, we want to start that visit with someone else in the room. I often say when talking to individuals who come alone that there's a little bit of irony in somebody coming to a memory assessment alone to tell me all the things they forgot. Some patients get the joke, others not so much, but bringing someone with them really enhances the quality of the interview. Very important for us to get reliable information and a collateral source is going to provide that in most scenarios. The other thing that I'm going to start with, I'm going to make sure that I have appropriate time to address this question. We've all had that experience. We're wrapping up a clinical interview, maybe one that's already ran a little bit late and there's that one more thing that's mentioned on the way out the door: I'm really concerned about my memory or I'm concerned about mom 's memory. That's not the opportunity to begin a memory assessment. That's the opportunity to schedule a dedicated visit. So, assuming that we've got someone else in the room with us, we've got our patient of interest, I'm going to approach the history really at the beginning. Seems like an easy thing to say, but so often patients in the room and their caregivers, they've been waiting for this appointment for weeks or months. They want to get it out all out on the table. They're worried we're going to rush them through and not take time to piece it together. And so, they're going to tell you what's going on right now. But the secret to a memory assessment, and particularly getting and arriving at an accurate diagnosis that reflects on and thinks about cause of memory problems, is actually knowing how symptoms began. And so, the usual opening statement for me is going to be: Tell me why you're here, and tell me about the first time or the first symptoms that indicated there was an ongoing problem. And so, going back to the beginning can be very helpful. This article is focused on Alzheimer disease and our clinical approach to the diagnosis of Alzheimer disease. And so, what I'm going to expect in a patient who has a typical presentation of Alzheimer disease is that there may be some disagreement between the patient and the spouse or other partners sitting in the room with me about when symptoms began. If you've got two partners sitting in the room, maybe an adult child and a spouse, there may be disagreement between them. What that tells me is at the onset, those first symptoms, they're hard to pin down. Symptoms typically emerge gradually in patients with symptomatic Alzheimer disease. They may be missed early on, or attributed or contributed to other things going on in the patient's time of life, phase of life. It's okay to let them sort of duke it out a little bit to determine, but really what I'm figuring out here is, are we talking about something that's happened across weeks, months or more likely years? And then I'm going to want to listen to, how did symptoms evolve? What's been the change over time? With Alzheimer disease and most neurodegenerative diseases, we expect gradual onset and gradual progression, things becoming more apparent. And at some point, everyone in the room is going to agree that, well, as of this state, there clearly was a problem. And then we can get into talking about specific symptoms and really begin to pick that apart the way that we traditionally do in any standard neurological assessment. Dr Berkowitz: Fantastic. And so, what are some of the things you're listening for in that history that would clue you in to thinking this patient may indeed be someone who could have Alzheimer's disease and going to require a workup for that diagnosis? Dr Day: It's pretty common when I have new trainees that come to clinic, they just head into the exam room and they sort of try to approach it the way that we would any patient in the emergency department or any other clinical scenario. The challenge with that is that, you know, we're taught to let the patient speak and we're going to let the patient speak - open-ended questions are great - but there's only so many questions you need to sort out if someone has a memory problem. And memory is really only one part, one component, of a thorough cognitive evaluation. And so, I'm going to help by asking specific questions about memory. I'm going to make sure that there is memory challenges there. And whenever possible, I'm going to solicit some examples to back that up, add credibility and sort of structure to the deficits. I'm also going to choose examples that help me to understand how does this concern, or this complaint, how does that actually affect the patient in their day-to-day life? Is it simply something that they're aware of but yet hasn't manifested in a way that their partner knows about? Is it to a level where their partner's actually had to take over their responsibility? It's causing some difficulties, disability even, associated with that. That's going to be important for me as I try to understand that. So, I'll ask questions when it comes to memory, not just, you know, do you forget things, but do you manage your own medications? You remember to take those in the morning? Do you need reminders from your partner? What about appointments; health appointments, social appointments? Are you managing that on your own? Sometimes we need a little bit of imagination here. Partnerships, and particularly those who have been together for a long time, it's natural that different people are going to assume different responsibilities. And so, might have to say, Imagine that you went away for the weekend. Would you worry about your partner remembering to take their medications over that time frame? That can help to really solidify how much of an impact are these challenges having on a day-to-day basis. I may ask questions about events, something that they maybe did a couple of weeks ago. Is the patient likely to remember that event? Are they going to forget details? Maybe the most important of all, with each of these, when there's a yes or an affirmation of a problem, we want to be clear that this represents a change from before. We all have forgetfulness. Happens on a day-to-day basis, and we all pay attention to different details, but what we're concerned about and typically the reasons patients want to come and see us as neurologists is because they've noticed a change. And so, I'm going to focus in on the things that represent a change from before. After I've discussed memory, I think it's really important to talk about the other domains. So, how is judgment affected? Decision-making?  In a practical way, we often see that borne out in financial management, paying the bills. Not just paying them on time and consistently, but making wise choices when it comes to decisions that need to be made. You're out at a restaurant. Can you pay the bill? Can you calculate a tip? Can you do that as quickly and as efficiently as before? Are we starting to see a breakdown in decision-making abilities there? We can sometimes lump in changes in behavior along with judgment as well. The patient that you know, maybe isn't making wise choices, they've picked up the phone and given their social security number out to someone that was calling, seeming to be well-meaning. Or maybe they've made donations to a few more institutions than they would have otherwise? Again, out of- out of order. Again, something that could be atypical for any individual. Looking for behavioral changes along with that as well. And then I'm going to talk about orientation. What's their ability to recognize days of the week, date of the month? Do they get lost? Is there concerns about wayfinding? Thinking about that, which is really a complex integration of some memory, visuospatial processing, judgment, problem solving, as we look to navigate our complex world and find our way from point A to B. And then I like to know, you know, what are they doing outside of the home? What are they doing in the community? How are they maintaining their engagement? Do they go to the store? Do they drive? An important topic that we may need to think about later on in this patient 's assessment. And inside the home? What responsibilities do they maintain there? Are the changes in decision making, memory problems, are they manifesting in any lost abilities inside the home? Cooking being a potentially high-risk activity, but also using typical appliances and interacting with technology, in a way that we are all increasingly, increasingly doing and increasingly reliant on. And last but not least, you know, maybe the one that everyone wants to think about, well, I can still manage all of my own personal care. Well, good news that many of our patients who have early symptoms can manage their own personal care. Their activities of daily living are not the big problem. But we do want to ask about that specifically. And it's not just about getting in the shower, getting clean, getting out, getting your teeth brushed. Do you need reminders to do that? Do you hop in the shower twice because you forgot that you'd already been in there once during the day? And so, asking some more of those probing questions there can give us a little bit more depth to the interview and really does sort of round out the overall comprehensive history taking in a patient with a memory or cognitive concern. Dr Berkowitz: Fantastic. That was a comprehensive master class on how to both sort of ask the general questions, have you noticed problems in fill in the blank memory, judgment, behavior, orientation, navigation and to sort of drill down on what might be specific examples if they're not offered by the patient or partner to try to say, well, in this domain, tell me how this is going or have you noticed any changes because the everyone's starting from a different level cognitively based on many factors. Right? So, to get a sense of really what the change is in any of these functions and how those have impacted the patient's daily life. So, let's say based on the history, the comprehensive history you've just discussed with us, you do find a number of concerning features in the history that do raise concern for dementia, specifically Alzheimer's disease. How do you approach the examination? We have the MoCA, the mini-mental. We have all of these tools that we use. How do you decide the best way to evaluate based on your history to try to get some objective measure to go along with the more subjective aspects of the history that you've ascertained? Dr Day: And you're honing in on a really good point here, that the history is one part of the interview or the assessment. We really want to build a story and potentially and hopefully a consistent story. If there are memory complaints, cognitive complaints from history, from reliable- that are supported by reliable collateral sources, we're going to expect to see deficits on tests that measure those same things. And so, I think that question about what neuropsychological measures or particular bedside tests can we integrate in our assessment is a good one. But I'll say that it's not the end-all-be-all. And so, if you've got a spouse, someone that lives with an individual for twenty or thirty years, and they're telling you that they notice a change in daily activity and it's impairing their day to day function, or where there's been some change or some concern at work, that's going to worry me more than a low score on a cognitive test with a spouse saying they haven't noticed any day-to-day impact. And so, we're going to take everything sort of in concert and take it all together. And it's part of our job as clinicians to try to process that information. But often we're going to see corroborating history that comes from a bedside test. He named a few that our listeners are probably pretty familiar with. I think they're the most common ones that are used. The Mini-Mental State Exam, been in practice for a long time. All the points add up to thirty and seems to give a pretty good sample of various different cognitive functions. The Montreal Cognitive Assessment, another favorite; a little bit more challenging of a test, I think, if we're if we're looking at how people tend to perform on it. And like the MMSE, points add up to thirty and gives a pretty good sample. There are others that are out there as well, some that are available without copyright and easy for use in clinical practice. The Saint Louis Mental Status Exam comes to mind. All these tests that we're willing to consider kind of share that same attribute. They can be done relatively quickly. They should sample various different aspects of function. There should be some component for language reading, spoken, spoken word, naming items, something that's going to involve some kind of executive function or decision making, problem solving. Usually a memory task where you're going to remember a set of words and be asked to recall that again later. So, learn it, encode it, and recall it later on. And then a few other features, I mean, some of them, these tests, most of these tests use some sort of drawing tasks so that we can see visuospatial perception and orientation questions about date, time, location, sort of the standard format. Any of these tests can be used aptly in your practice. You're going to use the one that you're most comfortable with, that you can administer in a reasonable amount of time and that seems to fit with your patient population. And that's the nuance behind these tests. There are many factors that we have to take into account when we're picking one and when we're interpreting the test results. These tests all generally assume that patients have some level of traditional sociocultural education that is westernized for the most part. And so, not great tests for people that aren't well into integrated into the community, maybe newcomers to the United States, those that have English as a second, third, or fourth language, as many of our patients do. Statements like no ifs, ands, or buts may not be familiar to them and may not be as easy to repeat, recall and remember. And so, we want to weigh these considerations. We may need to make some adjustments to the score, but ideally, we're going to use these tests and they're going to show us what we expect and we're going to try to interpret that together with the history that we've already ascertained. When I obtain that history and I'm thinking about memory loss, I'm going to look at the specific domain scores. And so, if I'm using the mini mental state examination thirty point test, but three questions that relate to relate to recall. Apple, penny, table. And so, depending on how our patients do on that test, they could have an overall pretty good score. Twenty seven. Oh, that looks good. You're in the normal range according to many different status. But if I look at that and there's zero out of three on recall, they could not remember those three items, that may support the emergence of a memory problem. That may corroborate that same thing on the MoCA, which uses five-item recall, and other tests in those same parameters. I mentioned some other caveat cities testing. Are patients who are presenting with prominent language deficits important part of cognition. They can't get the words out. They can't frame their sentences. They may really struggle with these tests because a lot of them do require you to both understand verbal instructions and convey verbal instructions. People with prominent visual problems, either visual problems that come because of their neurodegenerative disease and so part of cognition, visual perceptual problems, or people who simply have low vision. Are there difficulties for that? These tests require many people to read and execute motor commands, to draw things, to follow lines and connect dots, all very difficult in that setting. And so, we have to be cautious about how we're interpreting test results in patients who may have some atypical features or may arrive with sort of preexisting conditions that limit our ability to interpret and apply the test to clinical practice.  Dr Berkowitz: Really fantastic overview of these tests, how to use them, how to interpret them. It's not all about the number. As you said, it depends if all the points are lost in one particular domain, that can be salient and then considering, as you said, the patient 's background, their level of education, where English falls in their first language, second, third or fourth, as you said, and then some of the aspects of the MoCA, right, are not always as culturally sensitive since it's a test designed in a particular context. So, let's say your history and exam are now concerning to you, that the patient does indeed have dementia. Tell us a little bit about the next steps in the laboratory neuroimaging evaluation of such a patient?  Dr Day: I've got a history of memory and thinking problems. I've got some corroborating evidence from bedside cognitive testing, a normal neurological exam. This is where we think about, well, what other tests do we need to send our patients for? Blood testing really can be pretty cursory for most patients with a typical presentation who have typical risk factors, and that can include a thyroid study and vitamin B12. So, measuring those in the blood to make sure that there's no other contributions from potential metabolic factors that can worsen, exacerbate cognitive function. And pretty easy to do for the most part, if patients have other things in their history, maybe they come from a high-risk community, maybe they engage in high risk behaviors, I may think about adding on other tests that associate with cognitive decline. We'll think about the role of syphilis, HIV, other infections. But generally, that's when it's driven by history, not a rule of thumb for me in my typical practice. But beyond the blood tests, neuroimaging, some form of structural brain imaging is important. A CT scan will get you by. So, if you have a patient that can't get in the scanner for one reason or another or won't get in the scanner, or you don't have easy access to an MRI, a CT scan can help us in ruling out the biggest things that we're looking for. That's strokes, hemorrhages, and brain masses. So other things that obviously would take us down a very different path, very different diagnosis and very different treatment approach. An MRI, though, is going to be preferred, not only because it gives us a much higher-resolution view, but also because it helps us to see sort of regional areas of atrophy. It's a sensitive scan to look for small vessel disease, tiny strokes, tiny bleeds, microhemorrhages that again might point towards meteorology for us. Of course, it's better at finding those small masses, whether they be metastasis or primary masses, that could give us something else to consider in our diagnostic evaluation. I get an odd question often from patients, well, can you see Alzheimer's disease on an MRI? And the true answer to that is no, you can't. Can we see the signs of Alzheimer's disease? Sure, in some patients, but really what we see on an MRI is a reflection of neurodegeneration. And so, we see evidence of tissue loss and typically in areas that are most often involved early on in Alzheimer's disease. The hippocampus, the entorhinal areas around the hippocampus, we may see atrophy there. We may see biparietal atrophy, and of course, as the disease progresses, we're going to see atrophy distributed throughout other areas of the brain. But if you're looking for atrophy, you've got to have a pretty good idea what's normal for age and what you expect in that patient population. So, I do encourage clinicians who are assessing patients routinely, look at your own images, look at the images for patients with and without cognitive impairment. So we develop a pretty good sense for what can be normal for age, and of course work with our colleagues in radiology who do this for a living and generally do an excellent job at it as well.  Dr Berkowitz: Perfect. So, you're going to look for the so-called reversible causes of dementia with serum labs, structural imaging to either rule out or evaluate for potential structural causes that are not related to a neurodegenerative condition or patterns of regional atrophy suggestive of a neurodegenerative condition, and maybe that will point us in an initial direction. But the field is rapidly expanding with access to FDG-PET, amyloid PET, CSF biomarkers, genetic testing for APOE 4, probably soon to be serum biomarkers. So, patients may ask about this or a general neurologist referring to your clinic may ask, who should get these tests? When should we think about these tests? How do you think about when to send patients for advanced imaging, CSF biomarkers, genetic testing for APOE 4? Dr Day: It's not that patients may ask about this. Patients will ask about this. And you've probably experienced that in your own world as well. They're going to ask about any of these different biomarkers. Certainly, whatever they've recently read or has been covered on television is going to be common fodder for consideration in the clinic environment. It's important to know what tests you can get, what reliable tests that you can get, and to know the differences between some of these tests when making a recommendation or weighing the pros and cons of doing additional testing. I think common practice principles apply here. Let's order tests that are going to change our next steps in some way. And so, if we have a patient, particularly a patient like the one that we've been talking about: seventy something year old, presenting with memory complaints, they're concerned, the family is concerned. We've got that history, physical exam, and now we may need to really hone in on the etiology. Well, I say may need because for that patient it may be enough to know, yeah, I agree, there's a problem here. And I can say it's an amnestic, predominant, gradual-onset progressive cognitive decline. This is probably Alzheimer disease based on your age. And maybe that's all they want to hear. Maybe they're not ready to pursue additional testing or don't see the value or need for additional testing because it's not going to change their perspective on treatment. In that case, it's okay to apply an often underrated test, which is the test of time. Recognizing this is a patient I can follow. I can see them in six months or twelve months, depending on what your clinic schedule allows. If this is Alzheimer disease, I'm going to expect further gradual progression that may affirm the diagnosis. We can think about symptomatic therapies for a patient like that, perhaps Donepezil as an early, early medication that may help with symptoms somewhat and we can leave it at that for the time being. But there's many scenarios where that patient or the family member says, look, I really need to know. We really want this answer. And as you pointed out, there are good tests and increasingly good tests that we have access to.  Dr Berkowitz: Well, that's a very helpful overview of the landscape of more precise diagnostic testing for Alzheimer disease specifically and how you think about which tests to order and when based on your pretest probability and the patient 's candidacy for some of these new potential therapies. To close here, as you said, treatment is discussed in another podcast. There's another article in this issue. So, we won't get into that today. But let's say you have gotten to the end of the diagnostic journey here. You are now convinced the patient does have Alzheimer's disease. How do you present that diagnosis to the patient and their family? Dr Day: I think here we're going to recognize that different styles align with different patients and families, and certainly different clinicians are going to have different approaches. I do tend to take a pretty direct approach. By the time that patients are coming to see me, they've probably already seen another neurologist or at least another physician who's maybe started some of the testing, maybe even built the foundation towards this diagnosis and shared some indications. Certainly, when they look up my profile before they come to see me, they know what I specialize in and so, they may even have done their own research, which has ups and downs in terms of the questions that I'll be faced with at that point in time. The way I like to start is first acknowledging the symptoms. And the symptoms that the patients have shared with me, recognizing if those symptoms are impacting daily life, how they impacted daily life, and usually using that information to synthesize or qualify the diagnosis. Is there cognitive impairment, yes or no? And at what level is that cognitive impairment? Is this mild cognitive impairment? Is this mild dementia? Is it maybe more moderate or severe dementia? So, using those terms directly with patients and explaining the meaning of them. But I then transition in relatively quickly to the important point of not leaving it at the syndrome, but actually thinking about the cause. Because it is cause that patients come to talk about. And if they don't say that directly, they say it in their next question, which is what are we going to do about it and how are we going to treat this? And so, I will use the information I have available at that time to suggest that based on your age, based on the history, the normal physical examination, the performance and the bedside testing that we've done. And hey, that's pretty normal structural imaging or imaging that only shows a little bit of atrophy in a few areas. I think that this condition is most consistent with symptomatic Alzheimer's disease, mild cognitive impairment due to Alzheimer's disease, or mild dementia due to Alzheimer's disease. And then I'll discuss the next options in terms of testing and try to get a feel of what our patients are thinking about when it comes to treatment. Do they want to be on the cutting edge with brand-new therapies that offer potential benefits but counterbalance by pretty substantial risks that warrant individualized discussions? Are they interested in symptomatic therapies? Would that be appropriate for them? And I can usually round out the discussion with advice that works for everyone. And that's where we talk about the importance of brain health. What are the other things that I should be doing, you should be doing, and our patients and their partners should be doing as well to maintain our brain in its best possible state as we hope that we all continue to age and look towards the future where we maintain our cognition as best as possible? And that is still the goal. Even when we're talking to patients who have neurodegenerative diseases that are working against our efforts, we still want to do what we can to treat other problems, to evaluate for other problems that may be contributing to decline and may be amenable to our management as well.  Dr Berkowitz: Well, thank you so much for taking the time to speak with us today. I've learned a lot from your very nuanced and thoughtful approach to taking the history, performing the examination, making sense of cognitive tests and how they fit into the larger picture of the history and examination, and thinking about which patients might be candidates for more advanced imaging as we try to make a precise diagnosis in patients who may be candidates and interested in some of the potential novel therapies, which we both alluded to a few times, but are deferring to another podcast that we'll delve more deeply into that topic in this series. So, thank you so much again, Dr Day. Again, I've been interviewing Dr Gregory Day from the Mayo Clinic, whose article on Alzheimer's disease appears in the most recent issue of Continuum on Dementia. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining 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.

Episode 161: Depression FundamentalsFuture doctors Madeline Tena and Jane Park define depression and explain different methods to diagnose it. Non-pharmacologic and pharmacologic treatment is mentioned briefly at the end.  Written by Madeline Tena, MSIII, and Jane Park, MSIII. Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. Editing by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Definition. Per the language of Mental Health, depression can be defined as a mood, a symptom, a syndrome of associated disorders, or a specific mental disorder. As a state of mood, depression is associated with feelings of sadness, despair, emptiness, discouragement, and hopelessness. The sense of having no feelings or appearing tearful can also be a form of depressed mood. A depressed mood also can be a part of a collection of symptoms that explain a syndrome. Depression as a mental disorder can encompass depressive syndromes. Per the American Psychiatric Association DSM-5-TR, depressive disorders commonly include sad, empty, irritable mood, accompanied by changes in one's functional capacity. They can be classified by severity and recurrence, and associated with hypomania, mania, or psychosis. Depressive disorders include major depressive disorder (including major depressive episodes), persistent depressive disorder, premenstrual dysphoric disorder, substance-induced depressive disorder, depressive disorder due to medical condition, other specified depressive disorder, and unspecified depressive disorder.Today, we will cover unipolar depressive disorder, also known as major depressive disorder. MDD.Major depressive disorder is a mood disorder primarily characterized by at least one major depressive episode without manic or hypomanic episodes. Depressive episode is a period of at least 2 weeks of depressed mood or anhedonia in nearly all activities for most of the day nearly every day, with four or more associated symptoms in the same 2 weeks. We will discuss specific symptoms for diagnosis further on. Epidemiology of depression.Nationally or regionally representative surveys in 21 countries estimate that the 12-month prevalence of major depressive disorder across all countries is 5 percent. Furthermore, the prevalence of major depressive disorder plus persistent depressive disorder in developed countries (United States and Europe) is approximately 18 percent. Multiple studies consistently indicate that in the general population of the United States, the average age of onset for unipolar major depression and for persistent depressive disorder (dysthymia) is approximately 30 years old. During 2020, approximately ⅕ US adults have reported receiving a diagnosis by a healthcare provider, with the highest prevalence found among young adults age (18-24 year age… generation Z). Within the US there was considerable geographic variation in the prevalence of depression, with the highest state and county estimates of depression observed along the Appalachian and southern Mississippi Valley regions. Why do we care about depression?Because depression is associated with impaired life quality. It can impair a patient's social, physical, and psychological functioning. Also, depression is associated with mortality. A study done by UPenn Family Practice and Community Medicine in 2005 showed that among older, primary-care patients over a 2-year follow-up interval, depression contributed as much to mortality as did myocardial infarction or diabetes. A prospective study from 2005-2017 that followed 186 patients for up to 38 years further showed that patients with major depressive disorder had 27 times higher incidence rate of suicide than the general population. (1, 2). Also, patients dying by suicide visit primary care physicians more than twice as often as mental health clinicians. It is estimated that 45% of patients who died by suicide saw their primary care physician in the month before their death. Only 20% saw a mental health professional a month before their death. (3)Suicidality in depression.It seems that primary care physicians often do not ask about suicidal symptoms in depressive patients. A 2007 study by Mitchell Feldman at the University of California San Francisco showed that 152 family physicians and internists who participated in a standardized patient with antidepressants, suicide was explored in only 36% of the encounters. (4)Physicians, including primary care physicians, should ask patients with depression about suicidality with questions such as: Do you wish you were dead? In the past few weeks, have you been thinking about killing yourself? Do you have a plan to kill yourself? Have you ever tried to kill yourself? (5) Screening for depression.The USPSTF recommends screening for depression in all adults: 18 years old and over regardless of risk factors. Some factors increase the risk of positive screening, such as temperament (negative affectivity/neuroticism), general medical illness, and family history. First-degree family members of people with MDD have a 2-4 times higher risk of MDD than the general population. Furthermore, social history can increase risk as well: sexual abuse, racism, and other forms of discrimination.It is important to highlight the risk in women because they may also be at risk related to specific reproductive life stages (premenstrual period, postpartum, perimenopause). The USPSTF includes pregnant individuals and patients in the postpartum period to be screened for depression. Screening tools. The US Preventive Services Task Force recommends depression screening for major depressive disorder (MDD) in adolescents aged 12 to 18 years (grade B). Similarly, the Guidelines for Adolescent Depression in Primary Care (GLAD-PC) has also recommended annual screening for depression in children aged 12 and older. (6) Some tools used for screening in this age group are the Patient Health Questionnaire for Adolescents (PHQ-A) and the primary care version of the Beck Depression Inventory (BDI). For the general adult population, it is recommended that all patients not currently receiving treatment for depression be screened using the Patient Health Questionnaire-2 (PHQ-2) (7)PHQ 2 is a survey scored 0-6. The survey asks two questions: Over the last 2 weeks, how often have you been bothered by any of the following problems?Little interest or pleasure in doing things.Feeling down, depressed, or hopeless.Answers should be given in a numerical rating. 0=Not at all; 1=Several days; 2=More than half the days; 3=Nearly every day. A score ≥ 3 is considered positive, and a follow-up full clinical assessment is recommended. The PHQ-2 has a sensitivity of 91% and a specificity of 67% when compared to a semi-structured interview. Keep in mind that the PHQ-2 may be slightly less sensitive to older individuals. Individuals who screen positive with PHQ-2 should have additional screening with the PHQ-9, which is a nine-item, self or clinician-administered, brief questionnaire that is specific to depression. (8) Its content maps directly to the DSM-5 criteria for major depression. (9)The PHQ-9 is a set of 9 questions. The answers are scored similarly to PHQ-2, with a numerical scoring between 0 and 3. (0=Not at all; 1=Several days; 2=More than half the days; 3=Nearly every day). Dr. Arreaza, you will be my patient today, are you ready? It's important that you think about the last 2 weeks.Over the last 2 weeks, how often have you been bothered by any of the following problems?Little interest or pleasure in doing things. [Dr. Arreaza answers, “sometimes”. Jane asks, “is it several days or nearly every day?”. Dr. Arreaza answers, “nearly every day” 3]Feeling down, depressed or hopeless [Dr. Arreaza: every day 3]Trouble falling or staying asleep, or sleeping too much [Dr. Arreaza: not at all 0]Feeling tired or having little energy [Dr. Arreaza: not at all 0]Poor appetite or overeating [Dr. Arreaza: every day 3]Feeling bad about yourself- or that you are a failure or have let yourself or your family down [Dr. Arreaza: several days 1]Trouble concentrating on things, such as reading the newspaper or watching television [Dr. Arreaza: Several days 2]Moving or speaking so slowly that other people could have noticed. Or the opposite, being so fidgety or restless that you have been moving around a lot more than usual. [Dr. Arreaza: Not at all 0]Thoughts that you would be better off dead, or of hurting yourself [Not at all 0]Jane: Your score is 12.Maddy: Regarding severity, a total score of 1-4 suggests minimal depression. 5-9 suggests mild, 10-14 moderate, 15-19 moderately severe, and 20-27 severe depression. PHQ-9 with patients' scores over 10 had a specificity of 88% and sensitivity of 88% for MDD. (10)But if there are at least 4 non-zero items, including question #1 or #2, consider a depressive disorder and add up the scores. If there are at least 5 non-zero items including questions #1 or #2, consider major depressive disorder specifically. The questionnaire is the starting point for a conversation about depression.A couple of things to note: 1. Physicians should make sure to verify patient responses given the questionnaire can be self-administered. Diagnosis also requires impairment in the patient's job, social, or other important areas of functioning. 2. Diagnosis requires a ruling-out of normal bereavement, histories of manic episodes, depressive episodes better explained by schizoaffective disorder, any superimposed schizophrenia, a physical disorder, medication, or other biological cause of depressive symptoms.Once a patient is newly diagnosed and/or started on treatment, a regular interval administration (e.g. 2 weeks or at every appointment) of PHQ-9 is recommended. The PHQ-9 has good reliability, validity, and high adaptability for MDD patients in psychiatric hospitals for screening and evaluation of depression severity. (12) Other than PHQ-9, there is also Geriatric Depression Scale-15 for older patients with mini mental status exam (MMSE) that scored over 10. (13)For postpartum depression, the preferred screening tool is the Edinburgh postnatal depression scale[Click here (stanford.edu)].Non-pharmacologic and pharmacologic treatment.Now that we have diagnosed the patient, we have to start management. Patients can consider non-pharmacologic treatment such as lifestyle modifications. This can include sleep hygiene, reduction in drug use, increased social support, regular aerobic exercise, finding time for relaxation, and improved nutrition. Furthermore, based on severity, patients can start psychotherapy alone or psychotherapy + pharmacotherapy. Admission is required for pts with complex/severe depression or suicidality. There should be an assessment of efficacy at 6 weeks.There is a warning about patients aged 18-24 who are at increased risk of suicide when taking SSRI within the first couple weeks of treatment. Mediations: SSRI, SNRI, tricyclic antidepressants, MAOIs, and Atypical antidepressants: including trazodone, mirtazapine (Remeron), bupropion (Wellbutrin SR). More research is being done on psychedelic drugs such as ketamine and psilocybin as possible treatments. There are therapies such as ECT available too.Potential Harm of Tx: Potential harms of pharmacotherapy: -SNRI:  initial increases in anxiety, insomnia, and restlessness, and possible sexual dysfunction and headaches as well. Compared with the SSRI class, the SNRI class tends to induce more nausea, insomnia, dry mouth, and in rare cases hypertension.-Tricyclic: Cause of numerous side effects, very infrequently prescribed unless the patient is not responding to other forms of treatment. Side effects that are included are: dry mouth. slight blurring of vision, constipation, problems passing urine, drowsiness, dizziness,  weight gain, excessive sweating (especially at night). Avoid TCAs in elderly patients.-MAOIS: MAO-IS can cause side effects too, including dizziness or lightheadedness, dry mouth, nausea, diarrhea or constipation, drowsiness, and insomnia. Furthermore, other less common side effects can include involuntary muscle jerks, hypotension, reduced sexual desire/ ability to orgasm, weight gain, difficulty starting urine flow, muscle cramps, and paresthesia.Remember to screen your patients. In case you establish a diagnosis, discuss treatments, including non-pharmacologic and pharmacologic options. Warn your patients about side effects and the timing to see the benefits of the medication, usually after 6 weeks. __________________Conclusion: Now we conclude episode number 161, “Depression Fundamentals.” Future doctors Park and Tena discussed depression and its risk factors, screening, and treatment. They went through the PHQ2 and PHQ9 as screening tools, as well as commonly used treatments and their side effects, such as SSRIs. Dr. Arreaza also highlighted the importance of asking about suicidality in your depressed patients, there is a lot of room for improvement in that aspect. This week we thank Hector Arreaza, Madeline Tena, and Jane Park. Audio editing by Adrianne Silva.Talk_OutroEven without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Angst F, Stassen HH, Clayton PJ, Angst J. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord. 2002;68(2-3):167-181. doi:10.1016/s0165-0327(01)00377-9. https://pubmed.ncbi.nlm.nih.gov/12063145/Miron O, Yu KH, Wilf-Miron R, Kohane IS. Suicide Rates Among Adolescents and Young Adults in the United States, 2000-2017. JAMA. 2019;321(23):2362-2364. doi:10.1001/jama.2019.5054. https://pubmed.ncbi.nlm.nih.gov/31211337/ Feldman MD, Franks P, Duberstein PR, Vannoy S, Epstein R, Kravitz RL. Let's not talk about it: suicide inquiry in primary care. Ann Fam Med. 2007;5(5):412-418. doi:10.1370/afm.719. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2000302/.Brief Suicide Safety Assessment,National Institute of Mental Health (NIMH), July 11, 2020. https://www.nimh.nih.gov/sites/default/files/documents/research/research-conducted-at-nimh/asq-toolkit-materials/adult-outpatient/bssa_outpatient_adult_asq_nimh_toolkit.pdfBeck A, LeBlanc JC, Morissette K, et al. Screening for depression in children and adolescents: a protocol for a systematic review update. Syst Rev. 2021;10(1):24. Published 2021 Jan 12. doi:10.1186/s13643-020-01568-3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7802305/Williams, John; Nieuwsma, Jason. Screening for depression in adults, UpToDate, updated on November 30, 2023. https://www.uptodate.com/contents/screening-for-depression-in-adults.Instrument: Patient Health Questionnaire-9 (PHQ-9), National Institute on Drug Abuse, https://cde.nida.nih.gov/instrument/f226b1a0-897c-de2a-e040-bb89ad4338b9.Lowe B, et al. Monitoring depression-treatment outcomes with the Patient Health Questionnaire-9 (PHQ-9). Med Care, 42, 1194-1201, 2004.Sun, Y., Fu, Z., Bo, Q. et al.The reliability and validity of PHQ-9 in patients with major depressive disorder in psychiatric hospital. BMC Psychiatry20, 474 (2020). https://doi.org/10.1186/s12888-020-02885-6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701937/Conradsson M, Rosendahl E, Littbrand H, Gustafson Y, Olofsson B, Lövheim H. Usefulness of the Geriatric Depression Scale 15-item version among very old people with and without cognitive impairment. Aging Ment Health. 2013;17(5):638-645. doi:10.1080/13607863.2012.758231. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701937/.Royalty-free music used for this episode: Old Mexican Sunset by Videvo, downloaded on Nov 06, 2023 from https://www.videvo.net

Tijdens de zomer bespreken we om de week een film die gaat over één van de thema's die we in onze podcast behandelen. Vandaag bespreken we de film Still Alice (2014) waarin de hoofdpersoon, Alice, kort na haar 50e verjaardag de diagnose #Alzheimer krijgt. De film gaat over de uitdagingen waar zij en haar familie mee te maken krijgen tijdens het verloop van de ziekte. Hoewel deze thematiek natuurlijk over het #geheugen gaat, is er ook een sterke link met #identiteit. Hoe lang blijft Alice still Alice? Heb je de film (nog) niet gezien, dan kun je hier lezen hoe je deze kunt bekijken. Je vindt hier ook een samenvatting van de film.Benieuwd in welke afleveringen we het al over het geheugen en identiteit hebben gehad? Bekijk dan hier het overzicht met alle thema's uit de podcast en de bijbehorende afleveringen. BronnenOverzicht van de huidige stand van zaken rondom Alzheimer, National Institute on Aging:https://www.nia.nih.gov/health/alzheimers-disease-fact-sheetOverzicht vragen Mini-Mental State Examination (MMSE): https://meetinstrumentenzorg.nl/wp-content/uploads/instrumenten/MMSE-meetinstr-gestand.pdfOnderzoek: Dr. Anita Eerland, prof.dr. Rolf ZwaanPresentatie: Rolf Zwaan & Anita EerlandMuziek geschreven en gespeeld door Rolf Zwaan Hosted on Acast. See acast.com/privacy for more information.

Welcome to the Aphasia Access Conversations Podcast. I'm Jerry Hoepner. I'm a professor at the University of Wisconsin – Eau Claire and co-facilitator of the Chippewa Valley Aphasia Camp, Blugold Brain Injury Group, Mayo Brain Injury Group, and Thursday Night Poets.  I'm also a member of the Aphasia Access Podcast Working Group. Aphasia Access strives to provide members with information, inspiration, and ideas that support their aphasia care through a variety of educational materials and resources. I'm today's host for an episode that will feature Dr. Alyssa Lanzi. In this episode, we'll be discussing Dr. Lanzi's research on mild cognitive impairment and the role of the LPAA approach in serving individuals with mild cognitive impairment and dementia. Biosketch: Alyssa M. Lanzi, Ph.D., CCC-SLP, is a speech-language pathologist and Research Assistant Professor in the Department of Communication Sciences and Disorders at the University of Delaware. She is an executive committee member of the Delaware Center for Cognitive Aging Research at the University of Delaware. Dr. Lanzi is the PI of a K23 award from the National Institute on Aging to investigate the effects of an intervention designed to improve the independence of older adults with mild cognitive impairment from probable Alzheimer's disease. She is also MPI of awards that develop, test and disseminate a large-scale online database to study the language and cognitive skills of older adults to help develop cost-effective biomarkers to identify adults at risk for dementia from Alzheimer's disease. Dr. Lanzi's research broadly focuses on investigating person-centered assessment and treatment approaches for individuals with mild cognitive impairment and dementia and prioritizes the implementation and dissemination of evidence-based practice to practicing health professionals.  Take aways: The LPAA fits interventions for mild cognitive impairment too. We need to focus on training the next generation to understand the applications of LPAA to other disorders and contexts. You don't always need a standardized test, you can use goal attainment scales to measure anything. We need to be prepared to counsel individuals with mild cognitive impairment, as we are often the discipline having those conversations. When we intervene with individuals with mild cognitive impairment early, we can involve them as collaborators. There is a continuum of counseling needs that changes over time. See Alyssa's counseling plus paper in SIG 2 Perspectives.   Interview Transcript: Jerry Hoepner: Hi Alyssa. Good to see you. Alyssa Lanzi: Hi, good to see you. I'm happy to have a conversation with you today. Jerry Hoepner: Likewise, I'm looking forward to this conversation. It's kind of tradition that at the beginning of podcast we talk a little bit about your journey in your path to the life participation approach. So, I'm hoping that you can share a little bit about why an LPAA approach is so crucial to your research and clinical interactions. Alyssa Lanzi: Yeah, Absolutely. Well, thanks for having me, and I'm excited to kind of give a glimpse into how we can start to think about the LPAA approach outside of aphasia, because I think I'm a little bit unique in that way. And I am clinically trained as a speech language pathologist, and I was fortunate that most of my master's training was in a really strong university-based life participation approach model for aphasia. So, I had a large amount of experience working with Dr. Sarah Wallace and Katerina Staltari, and really thinking about group-based approaches for aphasia care. And I really fell in love with the functional nature of that model and with my master's thesis really tried to think about, well, how can we do this with individuals at risk for dementia with thinking about group-based approaches and functional care. And then I went on to get my PhD at the University of South Florida with Michelle Bourgeois. With a really strong research focus on functional approaches for mild cognitive impairment and dementia but also had the opportunity to work clinically the entire time during my PhD at voices of hope for aphasia under Jackie Hinckley, really learning about the life participation approach for aphasia. So, I feel super fortunate in that I have a lot of clinical work and exposure with the life participation approach that really has driven my research. Although I don't clinically practice with the life participation approach anymore, it really is a key foundation and a key kind of framework to how I have conducted all of my research and run the lab at the University of Delaware, which I'm currently a research assistant professor at right now. Jerry Hoepner: Excellent. Yeah. And thanks for sharing that, I really believe there is not a lot of transferability and generalizability of the LPAA in the approach being someone who has one world or one foot in the traumatic brain injury world, and another foot in the aphasia world. There's definitely some strong carryover across those contexts, and I think members of aphasia access are really interested in thinking about how that extends into those contexts. So, I really appreciate that. And like I said before, you have quite the pedigree in terms of experiences with very life participation approach minded academics, and having some of those clinical experiences, is really just so crucial for those, you know, when you step into the research world that you're doing something that really applies. So, I know you already talked about Sarah Wallace and Dr. Satari and Dr. Bourgeois and Jackie Hinckley. But are there other people along that journey that have kind of shaped the way that you think about LPAA applications to aphasia but beyond obviously? Alyssa Lanzi: yeah, I think you know, really the names that you mentioned were kind of the key mentors in the process. However, individuals like Roberta Elman, and really her approach to kind of book and learning and reintegration was structured. But flexible activities are really kind of key to my thinking, and also, as you know, an early career researcher as well. Folks like yourself and Tom and Katie really show how we can also train students in this approach as well, which is kind of being key to figuring out how I really run this lab that's based in life participation. That's not only my line of research, but also supporting the next generation. I feel fortunate in that I have mentors that really have integrated a life participation approach in many different settings from big R1 universities to smaller, R2, and R3 universities to clinical practice settings to nonprofits. And I think I've taken pieces of all of those to really support my research and teaching pedagogy, and really life participation in that way, and without aphasia access, I wouldn't have had access to those leaders and mentors in the field like yourself, and it really has given me an opportunity to have conversations with these folks, and every single conversation has really impacted and influenced my work thus far. Jerry Hoepner: I think that tends to be a really common reflection on aphasia access that everyone is so accessible. So, the name really says it, and willing to have those conversations. And certainly, that supports us in all of those avenues, research, clinic, well and academic in terms of teaching as well so completely agree with that. Alyssa Lanzi: I think that's what's a beautiful thing about aphasia access and the life participation approach is that it's not just research, either. Right? It's research, it's clinical, it's teaching, it's mentoring, it's service. And I think we will probably talk about in a little bit. But in all of my work that's really what I try to think about, I don't just try to think about, you know, research, I try to think about well, how can I study this so it can actually be implemented in clinical practice? And then how can I also teach the next generation using this approach in that way? And I think that framework, although we often think of life participation as like a clinical approach. In some ways it's really this entire framework to all those kind of core components that are necessary in terms of teaching, research, clinical care and service. Jerry Hoepner: I really love the way that you describe that, because I don't know that that's been done really clearly before. But there is a thread running through all of those pieces, and it kind of speaks to your experience with Jackie Hinckley in terms of thinking about that implementation piece, and how we make sure what we're doing matters, and is the right stuff in the first place. And obviously teaching is near and dear to my heart, and being able to frame that in a way that students understand, but also feel like it's not something that's high in the sky that you know only a few people do, but that's accessible and usable by everyone, and even for my students. I mean, I know that a lot of my students will end up in a school setting, and I know that these foundational principles of LPAA still have relevance to them. So, I say, you know, regardless of where you're going. This content matters, and it should shape the way that you think conduct LPAA work. Alyssa Lanzi: Yeah, you don't have to be at a center to conduct LPAA work, you don't have to be with people with aphasia to conduct LPAA work, and that's the cool part of it. And having these conversations is an opportunity to kind of brainstorm with one another of, well how do we take you know, from the traditional mold, how do we kind of break that and really think of it as threads that can be kind of interwoven into all these elements that are core components of our discipline in a lot of ways. Jerry Hoepner: Agreed. Maybe that's a new task for aphasia access worker to kind of map all of those pieces, because I do think not. Maybe individuals have those pieces, but it hasn't been all put together. So, I appreciate that overview. Alyssa Lanzi: And yeah, hopefully. Jerry Hoepner: well. I've been having fun re-reading and refreshing myself on your work on. I used a lot of it within my teaching so. But it's always fun to see when you read something again that you pick up something that you just didn't even like process before or you don't remember you process it, maybe. But clearly, I mean, there's this thread going through all of it about person-centered strength-based care right at the heart of all of that. It really one of the things that stood out to me the last couple of days as I've been meeting is that emphasis on fostering choice and collaboration along the way in every single step with the with the individual, with mild cognitive impairment or dementia, with their family members. And I think that's really crucial. I mean whether you're kind of choosing an external memory aid, or script, or whatever is best right. Can you talk about how you facilitate those choices? Maybe a little bit about the kinds of tools that you use on one end, but also a little bit about how you just foster a mindset of that collaborative decision making, because, you know, sometimes people can just want to defer to you and say you tell me so. I'm interested in your thoughts on both of those pieces. Alyssa Lanzi: Yeah, Absolutely. Well, thanks for the flattering words, and I'm happy. You picked out the core elements there, because I think those are really kind of the key words of a lot of the work that I try to do, and starting really with person or family centered, in that way, and it's tricky. I think a lot of people say that their work is person centered, and we can always argue. What do you mean by that? And how do you ensure that, same with functional right? But something I try to teach people, and my students are just because it's related to something practical doesn't necessarily mean it's a functional approach, either, you know, so really kind of parsing out by what we mean by that. But in particular, with working with folks with mild cognitive impairment and dementia, the goal is to really support their independence for as long as possible, and then to support their quality of life right? And a lot of times when thinking about people with chronic aphasia, it's very similar in that way, right? And that, you know, kind of gotten to a point. Not that improvements can no longer been made, but the shift is really about like, well how can you live the best life as possible? Right? How can we get you participating in as many things as possible, and that's the same mindset when we're working with people with mild cognitive impairment in particular. So, when I'm trying to design the treatment approaches that I'm testing with my clinical trials. Really, the whole framework is, how can we make something structured and standardized but flexible to that individual's needs. So, I think it starts from a treatment level, figuring out what are the active ingredients? What are the things that can't be changed, what are the core elements that can't be changed. And then, once we figure that out, then the meat of the sandwich, you know the meat of the treatment can be customizable to that individual right. And a lot of this work really comes from McKay Solberg, and views of cognitive rehab as well. But I think, when we think about person centered, we need to think about what are the core elements of this evidence-based approach? What are the active ingredients? And then what are the things that can change in between right? And when we're talking about external memory aids, it's not enough just to give somebody a calendar right. We're not seeing that individuals actually continue to use this calendar later on. And I would argue that's because of 2 reasons, one because we didn't systematically train them, and the use of it and 2 is because we didn't include them in the process from the start to the finish. And you are asking about what kind of tools and what things can be helpful. And in terms of thinking about goal development tools, a lot of times we can lean on our colleagues and occupational therapy and use a lot of the models that they have for goal development. So, they have the COPM which I'm probably going to butcher the name, but it's the Canadian Occupational Performance Measure, I believe it is, and that can be a really great tool to have a structured approach to goal setting. Same with goal attainment scaling, and incorporating some motivational interviewing techniques on top of it. But the key is that you have some type of structure, some type of evidence-based approach, on top of the conversation that you're having right, just asking somebody their interests is important, but we need to think about what's the best thing for our buck, since we have such limited time with them. So those 2 tools, in terms of goal setting have been really helpful for me, paired with using patient reported outcome measures and kind of figuring out how to use that as an initial conversation, and then paired with some further probing of tell me more about these items. Tell me more about the issues that you're facing. And then what I think is tricky, and where I relate most to my life participation colleagues are, what are the outcome tools, or what are the treatment planning tools that we can use to design these participation approaches. And it's hard because most of the outcome tools that we have are developed for looking at impairment-based improvements, right? So very decontextualized type tasks and that's really tricky. If the treatments that we're doing are all meant to be functional and person centered and improved participation. But we're not looking at necessarily improvements in worthless learning, or serial sevens or things like that. So, I couldn't figure out any tools. So, part of my dissertation work was designing a measure that was really aimed to help drive treatment planning. And then look at if there's gains an actual participation, so that tools called the functional external memory aid tool, and my lab in the last year or so have tried to do a lot of work, and coming up with free resources to train students, clinicians, and researchers, and how to use this tool to drive treatment planning because it's a little bit of a different way than we think of how to use assessment tools. Traditionally we think of assessment tools to tell us is that that person has an impairment or not and this is not designed in that way. It's really designed to tell you how to design your treatment, and a functional meaningful in person-centered way. I don't have great answers of what the tools are, but I think collaborating with clinicians and collaborating with evidence-based researchers really helps us to try to fill that gap in some ways. Jerry Hoepner: Yeah, and I think you got at part of it when you talked about goal attainment scales that you could make that a measure of any goal that the person identifies themselves. You don't necessarily have to try to fit a tool around that you can just measure what they hope to change right, or what they hope to sustain in terms of function. So, I think that's really good and really helpful. Just want to kind of circle back to a couple of things you talked about active ingredients, and how to really recognize what those active ingredients are, what the cores are, and what is content that you can do without, so to speak, made me think of some of the recent work in RTSS from the standpoint of really mapping that out. But I think that principle of my own is really important. Just to be able to say what is at the core? What do I always need to do? And what is kind of supportive of that, and can be individualized? So that's really helpful. Alyssa Lanzi: That shouldn't be on the clinician either right? If you're a clinician listening to this like that shouldn't be on you. This is on the researchers to consider from the beginning, and this should be really clearly outlined in this plan. And it is somewhat hard to figure out what some of these analyses like what are the active ingredients? But that's really, if you go to a talk, if you're a clinician on this call like that's what you should be asking, when you go to these talks like, what are the active ingredients? What do you think is really evident of what's making the change? It's not on you to decide. It's really on researchers to be thinking about this from the beginning, and not for you to try to figure out by any means. Jerry Hoepner: Yeah, I think that's a really some really sound advice, because finding out what those active ingredients are that's really crucial, and I think there's times, and I won't say who, but I reached out to a researcher once to do some work related to their work, and I said, “So do you have some place where you have more specific information about what exactly you did?” And they said “it's all in the paper” and I was kinda like no, it's not all in the paper, and I think we're getting better at that, providing that information, at least to the best of our knowledge, what those active ingredients are. And you know this is on the researcher to provide that, and then to allow that clinician to be able to work within that framework. So, I'm really glad that you said that. I also wanted to highlight the fact that you talked about your measure, and I think the acronym is FEAT right? Alyssa Lanzi: FEMAT, yep, close. Jerry Hoepner: Sorry. Missed it. I missed one letter, but we'll make sure that that is in the list of resources at the end as well, so that people know how they can access that information, and you mentioned that you're trying to make as much freely available as possible. So I think that's really helpful for our listeners to know where to find that information. Alyssa Lanzi: Yeah, the tool can be downloaded completely for free. And there's educational and training resources for free on there as well as we just publish an open access manuscript, describing with case examples of how to use it as well, because if we as researchers want clinicians to use our work. Constantly, we're hearing the biggest barriers pay walls and everything else so really trying to make this as accessible as possible, so that individuals can actually use it in their practice. Jerry Hoepner: Well, that's really excellent. I really appreciate it, so I'll double check with you at the end, and we'll make sure we have all of that information there for the for the listeners to follow up on that. So, getting into the connection and the differences between someone with aphasia and someone with a mild cognitive impairment. There's a lot of overlap and most communication supports. And as I was reading your work, I was like overlap, overlap, overlap. But there's also some ground that isn't overlapping individuals with aphasia, particularly when you get to the cognitive kinds of constructs, and so forth. So, in terms of supporting someone with MCI or dementia. What are the key distinctions that you have in your mind about how to approach that. So, distinguishing them from maybe what you would use for a language assessment, or language support excuse me, for someone with aphasia Alyssa Lanzi: I think the good thing is, there's many more similarities than differences. Right? We have this strength-based approach, this idea of participation, reintegration, isolation, depression. These are all major psychosocial factors that we know are associated with both populations and also acute. You know older adults are highest at risk. Right? We're seeing similar populations in some ways as well, so that strength-based participation-based reintegration, type approaches are all very similar. You know the key distinction or the key differences, I should say, is unlike people with a stroke, there wasn't an event that caused the impairments right, and that instead, we need measures that are really sensitive to early declines right? So, it's not like these individuals had a stroke or a brain injury, and immediately referred to speech, language, pathology. That's a very different pipeline to referral in that way. So, speech, language, pathologists need to do a much better job of advocating for our role early on where I don't think we have to do as much of that advocacy with people with aphasia now. Yes, all the aphasia folks don't come at me either because I know there's plenty of advocacy work that we need to do as well, but it it's a little bit different right, and that once aphasia is diagnosed, it's pretty clear that SLPs are the one to go to for the most part. For individuals with mild, cognitive impairment it's a bit different. So, we need to do a lot of advocacy work, and many of our tools, unfortunately, are not sensitive enough to these early declines. What's exciting is that language is actually showing as a pretty promising tool, a pretty sensitive metric. So, hopefully in the next, you know, 5 to 10 years we're starting to actually definitely be involved because we're noticing language changes or sensitive to these early declines, but so one is the early process, and the referral process is quite different. The other key difference in my mind is the preparation for the future and that individuals of mild cognitive impairment are at a very high risk for developing dementia due to Alzheimer's disease and in my work I am talking about mostly these clinical syndrome due to Alzheimer's disease is usually the bulk of my work. But for individuals with mild cognitive impairment. We really want to set them up with these tools, so that we can develop really strong habits and routines now and really rely on the strength of procedural memory, so that if they decline, they have these really good systems in place, and that's a very different mindset than people with aphasia. So, the mindset in that way is very different in our role in preparing for the future. So, I think the referrals is probably the big pipeline. How they get to you. The coping and the depression is all there. But viewed a bit differently. It's not, Oh, my God! My life has drastically changed instead it's, Oh, my God! What's gonna happen, you know, in 2 3 5 years. So, it's all those same constructs are there, but the rationale and the underpinnings are a bit different. Jerry Hoepner: I want to just go back to a couple of the points that you said again. When I'm thinking about that that early intervention or early work with someone with MCI, I'm always telling my students part of what you said that idea that we want to establish those routines and habits. But the other thing I always think about going back to our previous discussion is that's the opportunity for them to make as many decisions about their future as they possibly can, and do that planning for the future. I find that to be a really effective way from a counseling standpoint to get them involved in kind of planning their future, and also building that acceptance right like this is coming. What can I do now to kind of take ownership and to take control of that versus if I wait, then it's going to be someone else's decision. Alyssa Lanzi: Exactly. Exactly. We describe it. A lot of you want to be in the driver's seat and not the passenger seat. Jerry Hoepner: Yeah, great metaphor. And I just wanted to mention one other thing when you were talking about that the fact that language is a really sensitive measure. You believe for individuals with MCI and predictors of for their dementia. You know some great work with the dementia bank in terms of talking about collecting samples and interpreting those samples. So, I know I'm kind of putting you on the spot for this. But any thoughts about that might lead us in the future in terms of knowledge. Alyssa Lanzi: Yes, stay tuned. We more than likely have a pretty big grant coming our way, which is going to be exciting. But the current biomarker tools for detection, are costly and invasive. We're having MRI and imaging techniques which are costing, You know, so much money. Blood is becoming, you know, blood based biomarkers are at least a bit more cost effective. However, there's still quite still, quite invasive, and there's only a certain person who wants to come into a lab, you know, and do those types of things. So what we're hoping is that we can use language, and that people can provide us with language samples in the comfort of their own home, right and really reflective of these functional tools and paired with these other. You know data, this, this other data that we're collected, we can make this really kind of informed decision or inform diagnosis. So, hopefully, you know, we can get to the point where that is the case that people can kind of just answer some questions from the comfort of their own home and their smart home and their computer. And you know, on the back end we can analyze their language, and then, provide them with some information about what we're thinking in terms of diagnosis and things like that. The most exciting thing to me in my mind about language is that hopefully, we can get a sample of individuals to participate who are actually representative of those who have the disease and that with many of these imaging techniques, and with many of the blood-based biomarkers and these invasive techniques, there's only a certain type of person you know who wants to come to campus and do these things, and most of our large databases are really white, high SES folks who are just, not those who are at greatest risk for the disease. So, what I'm really hoping for with as really the area of language grows, thanks to a lot of the work that we're doing, and Carnegie Mellon are doing with Brian and Davida, and also Kim Mueller and her group at Wisconsin. Is that not only can we use it as a sensitive measure, but we can get people to participate because, hopefully, it reduces the common barriers to participation in research studies. So that's really kind of a focus of where we're going. And then, hopefully, with that information, we can better support those who are at greatest risk living with this disease. Jerry Hoepner: Right and it seems like there's kind of a secondary effect to once you have those answers. There's a lot more SLP's than there are, you know, other mechanisms for measuring those bio measures. So, if you know that contact, maybe we can contribute to that earlier detection as well, so that's fantastic. Alyssa Lanzi: Yeah, which is why we need more SLPs going in this space, and I love aphasia work. I'm an aphasia clinician at heart. But I hope we see after today and through many of my other colleagues that the world overlap so much. But we really need a lot of researchers in this space, because speech language pathologists have a lot that they can contribute, and could very soon be at the forefront of the of the diagnosis as well. So, any students on the call or clinicians wanting to go back. My labs and others are really recruiting, and we need more individuals who are interested in researching in this space. Jerry Hoepner: Yeah, that's great to share. And hopefully there are some students and professionals out there that are thinking about that so definitely need that. Well, I'm going to change gears just a little bit. You've talked a little bit about depression and other mental health issues a little bit, isolation that occurs not only with aphasia, but with mci and dementia. I think we're all starting to get a better idea of our roles as speech, language, pathologists, in terms of counseling individuals with aphasia, MCI, dementia, traumatic brain injuries, etc. In re-reading your 2021 paper about counseling, plus I was really struck by how you and your co-authors mapped out this continuum of counseling needs kind of makes me want to do the same for everything so in activities from the first symptoms and diagnosis to the end of life, and I'll refer our listeners to figure one because it's a really eloquent framework for, and timeline for those changes. Will you share a little bit about the development and kind of the purpose of that timeline figure. Alyssa Lanzi: Yeah, thank you for the kind words that was probably one of the hardest things I've ever done was writing that paper, but we knew it needed to be done for many different reasons, but really to paint the picture that SLPs have a key role from the start all the way to the finish with these folks, and that's really what that figure is trying to highlight is that we can provide both primary and supportive roles to our colleagues from prevention and education all the way through end of life. And fortunately, that figure has really resonated with a lot of people which has been really helpful and I've actually gotten a lot of feedback from clinicians who've been able to use it to advocate for their role in this working with this population and doing support groups and things like that. So that's really great, because that's the whole point of it. But what's unique about this paper is that I work on a very interdisciplinary team of neuropsychologists and geriatric psychiatrists. And it was really interesting to come at it with all 3 of our mindsets for kind of developing this, because everybody has a very different education in terms of these important psychosocial constructs. So a really big shout out to my colleagues, Matt Cohen and Jim Allison, who really also helped me push my mindset of thinking about counseling as much more than just a conversation, and really thinking about counseling, plus as we call it, in terms of everything else right, and that a conversation is only the start of it, and that education and management and advising and referrals, that's all, that's all the big piece of it. So, I think that's why we were able to really round out this figure is because we were coming at it from 3 different disciplines as well, and then being able to go back to okay Well, what's within the scope of practice, of speech, language, pathology. The other thing about this figure is you'll see that the x-axis, the way that we looked at over time was by residential status, not by necessarily MMSE score or MoCA score right, and that framework was very much from my background in life participation approach in thinking about okay, let's think about them on a continuum of like residential needs versus what is their cognitive status on like an impairment type measure. I encourage people to think that way when we think about working with older adults in particular with neurodegenerative conditions, and that not thinking about them as a numerical value in a stage on one type of those measures because I think it opens up our roles, and also shows how hopefully within that figure that you can see that the roles overlap. Right, there's some roles that we start from our first conversation that we're going to continue all the way through the end of life. The other really important thing to consider with the figure, is in our field we have a really strong understanding of like language milestones in pediatrics, right? But what we don't have a really good strong foundation is, is understanding what is typical aging right, and our role in supporting healthy aging as well. Just as we support language development in pediatrics. So that's a big piece of this figure and a big piece of the counseling article is that we have a major role like we do in language development in healthy aging development as well, and that we can do a lot to support healthy aging and prevention just like we do in language development of kids, and also like we do like with the FAST acronym for stroke or with concussion protocols and management, we just haven't, yet kind of adapted that approach to aging, and that's what hopefully this figure gets us to start to think and talk about as well. Jerry Hoepner: I think it definitely does. And I really like that analogy or metaphor comparison between the developmental milestones, because I was thinking that as I was looking at the figure, this is really similar. It kind of reminds me of, like the norms we looked at when we were in child phono or child language development laid out in the same kind of framework. So, I think that's something that is really comprehendible by the average SLP, and I think that's helpful, and I and I love how you describe x-axis in terms of those descriptions rather than numbers, just so crucial to see the person from that lens rather than as simply those numbers. So. Alyssa Lanzi: Yeah, in addition to my LPAA colleagues, my early intervention birth to 3 colleagues, or who were the closest with in a lot of ways, I definitely the treatment approaches the in-home approaches. They're in the next group, I would say. That is pretty close to LPAA as well in some ways is early intervention. Birth of 3. Jerry Hoepner: Agreed. Yeah, that's it. Another really great point. The other thing I really liked about the terms and you mentioned this: I think part of this comes out of the interprofessional kind of nature of development. But when you look at them, sure some of them are, you know, you think. Oh, yeah, that's counseling still, but many of them you don't necessarily wait to. Oh, yeah, that's in my counseling tool belt, and I think it's important for people to recognize those things are a part of that counseling process, and that can make it a little bit more accessible. I mean, we know that from an education standpoint that people are intimidated by counseling, and they feel unprepared and inadequate to carry out those steps. So, I mean just being able to see that on paper and say, I can do these things, I know these things, I think, are a really valuable part of that framework as well. So. Alyssa Lanzi: And to make sure that when we are describing counseling to our students, we're describing that as well, right, because its such a daunting thing for our students and if we help them in the beginning set up education, it really breaks down some of the common barriers to providing counseling of its daunting and scary. But a support group is one really small element of counseling that's within our scope of practice and our scope of practice does define it really well. I just think that how we describe it in articles is way too specific, and we need to think about it much more broadly and through, like the journal that you're responsible for with teaching and language. And you know we're starting to develop these models which is really helpful as well. But I agree, I think we just need to step outside of our really kind of specific way of thinking about counseling, because once again, then, by having a more broad continuum viewpoint. It really shines through our role. And why we are such key players of the team. Jerry Hoepner: Yeah, agreed. I mean, we are always going to be the ones who are put in that moment, that counseling moment we have to be prepared and stepped into it so obviously. That's my bias. But I think we always are. Well, this has been a fantastic conversation, and I could go all afternoon, but want to keep this reasonable for our listeners too. So, I want to end on kind of a broad question, just in terms of what's your advice for SLPs and other disciplines, for that matter, in terms of working with individuals, with mild cognitive impairment and dementia, specific to the use of the external strategies and supports, but kind of weaving, counseling into those interactions? Alyssa Lanzi: Make sure we're really listening to our patients and our families and take that extra second to pause and really make sure they feel valued and heard because especially for these individuals, they're scared. They may not yet see consequences in their everyday life. So, we need to really have a lot of buy in, and good rapport with them from the beginning, because they can make key changes in their life that may actually delay the onset of dementia. But they need to have buy in from you, and they we need to really promote behavior change and to do that they need to feel, listened to and heard. So, take the extra second and make sure you're doing that. Then I think, make sure that we are providing evidence-based approaches around these strategies that we are teaching and the 3-step approach by Solberg and Mateer and the pie framework. All of these, you know, meta-cognitive strategy frameworks. It starts with education, and we need to make sure that our clients have a really big education of what even is the strategy? What are all the components of the different strategy? Why is it they are even using the strategy right? Don't, jump into training the strategy yet, really start with the education and use the teach back approach, and make sure that they can help you in that way and then make sure you also don't view your approach as linear, things are going to change right, and you're going to have to go back a step and go to education. But you know I think functional is key and important, but it doesn't mean that we take away the evidence based, either right. And it's really thinking about how to integrate both of those things, and being honest with yourself and your client if things aren't working, and you need to readjust as well. But if your patient feels valued and heard, then that's the first step, and we need to make sure that we're continuing that step all the way through to the end of the sessions. Jerry Hoepner: Absolutely agree. Well, again, it's been a fantastic conversation. So really, thank you so much on behalf of Aphasia Access for your time and your insights and hope to see you again soon. Alyssa Lanzi: Yes, thank you. Please feel free to reach out. And if you ever see myself or my Doc students, Anna or Faith, or my colleague, Mike Cohen, at a conference. Please say hi to us as well. We love talking about our work and brainstorming with others, especially in the LPAA world. Jerry Hoepner: Sounds terrific. Thank you, Alyssa. Alyssa Lanzi: Thank you. Jerry Hoepner: On behalf of Aphasia Access, thank you for listening to this episode of the Aphasia Access Conversations Podcast. For more information on Aphasia Access and to access our growing library of materials go to www.aphasiaaccess.org. If you have an idea for a future podcast series or topic, email us at info@aphasiaaccess.org. Thanks again for your ongoing support of Aphasia Access. Articles & Resources: Cohen, M. L., Harnish, S. M., Lanzi, A. M., Brello, J., Victorson, D., Kisala, P. A., ... & Tulsky, D. S. (2021). Adapting a Patient–Reported Outcome Bookmarking Task to be Accessible to Adults With Cognitive and Language Disorders. Journal of Speech, Language, and Hearing Research, 64(11), 4403-4412. Lanzi, A., Burshnic, V., & Bourgeois, M. S. (2017). Person-centered memory and communication strategies for adults with dementia. Topics in Language Disorders, 37(4), 361-374. Lanzi, A., Wallace, S. E., & Bourgeois, M. S. (2018, July). External memory aid preferences of individuals with mild memory impairments. In Seminars in Speech and Language (Vol. 39, No. 03, pp. 211-222). Thieme Medical Publishers. Lanzi, A. M., Saylor, A. K., Fromm, D., Liu, H., MacWhinney, B., & Cohen, M. L. (2023). DementiaBank: Theoretical Rationale, Protocol, and Illustrative Analyses. American Journal of Speech-Language Pathology, 32(2), 426-438. Lanzi, A. M., Ellison, J. M., & Cohen, M. L. (2021). The “counseling+” roles of the speech-language pathologist serving older adults with mild cognitive impairment and dementia from Alzheimer's disease. Perspectives of the ASHA special interest groups, 6(5), 987-1002. Links:  FEMAT Website  FEMAT Open Access Manuscript  Delaware Center for Cognitive Aging Research- Free Memory Screenings  Counseling+ Open Access Manuscript  DementiaBank Open Access Manuscript  DementiaBank- Free Discourse Protocol 

Welcome to PsychEd, the psychiatry podcast for medical learners, by medical learners. In this episode, we'll explore a topic that we're sure many listeners are eager to learn about: The Assessment of Major Neurocognitive Disorder, also known as dementia with Dr. Lesley Wiesenfeld who is a Geriatric Psychiatrist and Psychiatrist-in-Chief at Mount Sinai Hospital in Toronto, where she leads the Geriatric Consult Liaison Psychiatry Service. She is also an Associate Professor in the Department of Psychiatry at the University of Toronto.   The learning objectives for this episode are as follows:   Define Major Neurocognitive Disorder (aka Dementia) as per DSM-5 diagnostic criteria Identify differential diagnoses for cognitive decline and list differentiating clinical features  Outline an approach to the assessment of a patient presenting with cognitive decline, including the role of a comprehensive history, psychometric tools and other investigations [ Relevant PMH/risk factors, ADLs/IADLs to cover on history, psychometric tools such as MMSE, MoCA and tie this back into major cognitive domains when to consider imaging, bloodwork including specialized testing such as ApoE genetic tests]  Classify the major subtypes of Neurocognitive Disorders, their epidemiology, and clinical presentations [ Vascular dementia, Alzheimer's, Frontotemporal, Lewy Body, Parkinson's,    Mixed dementia - Early onset dementia]   Guest: Dr. Lesley Wiesenfeld ( Lesley.Wiesenfeld@sinaihealthsystem.ca )   Hosts: Dr. Luke Fraccaro (PGY-3), Dr. Mark Fraccaro (PGY-4), Sena Gok (international medical graduate)   Audio editing by: Sena Gok   Show notes by: Sena Gok   Interview Content: Introduction: 0:13 Learning Objectives: 02:35 Diagnostic criteria of Major Neurocognitive Disorder: 03:20 Difference between Major and Mild Neurocognitive Disorder: 05:20 Red Flags of Cognitive Declines: 06:50 Normal Aging vs Major Neurocognitive Disorder: 10:00 Clinical Vignette – introduction: 11:35 Patient Assessment: 16:50 Past medical/family / Psychosocial history: 21:55 Clinical Vignette - Assessment: 37:45 Physical examination: 43:50 Investigations: 45:53 Role of genetic testing: 53:24 Clinical Vignette – Diagnosis: 57:50   References:   American Psychiatric Association. (2022). Neurocognitive Disorders. In Diagnostic and statistical manual of mental disorders (5th ed., text rev.).   Sadock, B. J., Sadock, V. A., Ruiz, P., & Kaplan, H. I. (2015). Neurocognitive Disorders. Kaplan and Sadock's Synopsis of Psychiatry (11th ed.). Wolters Kluwer   DSM-5-TR Fact Sheets (https://psychiatry.org/psychiatrists/practice/dsm/educational-resources/dsm-5-tr-fact-sheets )   Gauthier S, Patterson C, Chertkow H, Gordon M, Herrmann N, Rockwood K, Rosa-Neto P, Soucy JP. Recommendations of the 4th Canadian Consensus Conference on the Diagnosis and Treatment of Dementia (CCCDTD4). Can Geriatr J. 2012 Dec;15(4):120-6. doi: 10.5770/cgj.15.49. Epub 2012 Dec 4. PMID: 23259025; PMCID: PMC3516356.   Gauthier S, Chertkow H, Theriault J, Chayer C, Ménard MC, Lacombe G, Rosa-Neto P, Ismail Z. CCCDTD5: research diagnostic criteria for Alzheimer's Disease. Alzheimers Dement (N Y). 2020 Aug 25;6(1):e12036. doi: 10.1002/trc2.12036. Erratum in: Alzheimers Dement (N Y). 2022 Feb 03;6(1):e12088. PMID: 32864413; PMCID: PMC7446944. CPA Note: The views expressed in this podcast do not necessarily reflect those of the Canadian Psychiatric Association.   For more PsychEd, follow us on Twitter (@psychedpodcast), Facebook (PsychEd Podcast), and Instagram (@psyched.podcast). You can provide feedback by email at psychedpodcast@gmail.com. For more information, visit our website at psychedpodcast.org.

A new research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 17, entitled, “Extracellular microRNA and cognitive function in a prospective cohort of older men: The Veterans Affairs Normative Aging Study.” Aging-related cognitive decline is an early symptom of Alzheimer's disease and other dementias, and on its own can have substantial consequences on an individual's ability to perform important everyday functions. Despite increasing interest in the potential roles of extracellular microRNAs (miRNAs) in central nervous system (CNS) pathologies, there has been little research on extracellular miRNAs in early stages of cognitive decline. In a new study, researchers Nicole Comfort, Haotian Wu, Peter De Hoff, Aishwarya Vuppala, Pantel S. Vokonas, Avron Spiro, Marc Weisskopf, Brent A. Coull, Louise C. Laurent, Andrea A. Baccarelli, and Joel Schwartz from Columbia University Mailman School of Public Health, University of California San Diego, VA Boston Healthcare System, Boston University School of Medicine, and Harvard TH Chan School of Public Health leveraged the longitudinal Normative Aging Study (NAS) cohort to investigate associations between plasma miRNAs and cognitive function among cognitively normal men. “In a cohort of older men from Massachusetts, we investigated associations between plasma miRNAs and global cognition and rate of global cognitive decline measured by the MMSE.” Full press release - https://aging-us.net/2022/09/15/aging-extracellular-microrna-and-cognitive-function-in-a-prospective-cohort-of-older-men-the-veterans-affairs-normative-aging-study/ DOI: https://doi.org/10.18632/aging.204268 Corresponding Author: Nicole Comfort – nicole.comfort@columbia.edu Keywords: plasma, extracellular RNA, RNA-seq, microRNA, cognitive decline, cognitive impairment Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204268 About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, contact media@impactjournals.com.

Do you want to brush up on your knowledge of MoCA, ADAS-Cog, the MMSE and other cognitive tests? Join Sarah to hear about the 7 papers published in August 2021 where we're evaluating existing tests for their specificity and sensitivity in detecting Alzheimer's disease and mild cognitive impairment.  -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1w5W2UPrmR7vRgFtjsWj4KBMXh3qhFHoN/view?usp=sharingTo access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works together to bring you every episode of AMiNDR. In particular, this episode was scripted, hosted and edited by Sarah Louadi, and reviewed by Kira Tosefsky and Ellen Koch. The bibliography and wordcloud were created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for sorting all the papers published in August 2021 into themes for our episodes: Jacques Ferreira, Ellen Koch, Nicole Corso, Kate Van Pelt, Christy Yu, Dana Clausen and Elyn Rowe. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Jacques Ferreira, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!"  

As we continue our series on Biohacking for Amazon Sellers. Today I bring in David Toman from NootropicExperts.com to discuss how you can turn your brain back on. We talk about the stigma around nootropics and then difference between them and smart drugs. We discuss building stacks... David built two for me, one AM (to optimise my productivity) and one PM (for sleep, or lack of). We also chat about some quick wins for you guys sitting in front of the computer day in and day out in order to squeeze out some more productivity and get time back for your family and downtime. About David Toman I was diagnosed with Adult ADD several years ago. Up to then I had no idea why I had a problem with focus all my adult life. Ritalin turned the lights back on for me. A couple of years after the ADD diagnosis I ended up in the ER. And was told I was hypothyroid. A full-page, two-column list of symptoms including brain fog. Not only was I struggling to focus, my memory was failing too. Episodes of not remembering dates and appointments, a failing business, and a crumbling marriage. I saw psychologists, doctors, endocrinologists, neuroscience specialists and therapists. Two unrelated doctors tested me for dementia, and early-onset Alzheimer’s disease. One of the tests is the “Mini-Mental State Exam”. A “health professional” asks a series of questions designed to test a range of everyday mental skills. The maximum MMSE score is 30 points. A score of 20 to 24 suggests mild dementia, 13 to 20 suggests moderate dementia, and less than 12 indicates severe dementia. I got 30 points on every test. Nootropics Saved My Life I’m a Virgo. And this means I’m very methodical in my approach to life. There had to be another answer to my cognitive problems. And thus began years of research and experimenting. I had to find out if there was a way to deal with brain fog and ADHD naturally. Ritalin was able to help me focus. But was not helping in the memory and thinking department. Years of searching websites, reading stacks of books, and combing through the forums. And I was able little by little to get my brain working again. Better than ever before. With the right combination of supplements and lifestyle changes, I’ve been able to reduce my use of prescription stimulants. My business turned around, my relationship is better than the day we got married, and my brain is firing on all cylinders. And I continue to tweak and refine every area of my brain and cognition. Check out his website to find out more... https://nootropicsexpert.com/

Jaime Perales, PhD, presents statistics, screening tools and useful resources for primary care providers for Alzheimer’s disease. The KIDs list is presented. Question of the month: Fever and Cough.Introduction: KIDs List and Cognitive Impairment in the ElderlyBy Hector Arreaza, MDToday is May 3, 2021.  In family medicine, we believe in caring for patients “from the cradle to the grave.” During this introduction, we want to inform first of the KIDs list[1] and then some updates on cognitive impairment screening in older adults[2].First, KIDs stand for Key Potentially Inappropriate Drugs in Pediatrics. It is a list of medications that are potentially inappropriate in children. It contains 67 drugs with their risks, recommendations, strength of recommendation and quality of evidence. Common meds include anti-infectives, antipsychotics, dopamine antagonists and GI agents. 85% of these meds require a prescription, and are taken by mouth, or used by parenteral route or even for external use. For example: Mineral oil, oral, carries the risk of lipid pneumonitis, recommended to avoid in patients younger than 1 year old, this recommendation is strong with low quality of evidence. For all the “abuelas” (Spanish for grandmothers) out there, listen to this: Camphor carries a risk of seizures, the recommendation is “use with caution in children.” However, the recommendation is weak and quality of evidence is low, but the concern is enough to include it on the list, in other words, use “vi-vah-pore-oo” with caution in children. I recommend you look up the KIDs list and use your clinical judgment to incorporate it into your practice. From childhood, now we go to the elderly. On February 25, 2020, the USPSTF posted their final recommendation statement regarding screening for cognitive impairment in older adults. This is a Grade I recommendation (Insufficient Evidence). It means that more research is needed to recommend for or against it. This is the same recommendation given in 2014. An article published in JAMA on the same date, Feb 25, 2020, reports that screening instruments can adequately detect cognitive impairment, however there is no evidence that this screening improves patient or caregiver outcomes or causes harm. It is still uncertain if early detection of cognitive impairment is important to provide interventions for patients or caregivers with significant clinical benefits.Jaime Perales, PhD, will present some statistics on Alzheimer’s disease, he will explain some useful tools to screen for cognitive impairment and address the issue of Alzheimer’s disease at the primary care level. This is Rio Bravo qWeek, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it’s sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home.  Question of the Month: Fever and CoughWritten by Hector Arreaza, MD, read by Claudia Carranza, MD, and Valerie Civelli, MDThis is a 69-yo male patient, who has history of controlled hypertension. He comes to an urgent care clinic for acute onset of fever (102 F), cough, and shortness of breath which has progressively worsened over the last 3 days. He does NOT smoke tobacco, but uses recreational marijuana once a month, and drinks 1-2 beers a week. He goes to the doctor once a year for check-ups. He takes benazepril 10 mg daily for his hypertension. He does not believe in vaccines and his last shot was a tetanus shot 5 years ago. He has no surgical history. He retired as an accountant 5 years ago. Vital signs are normal except for tachycardia of 110 (his baseline is 85) and temperature of 101.5 F (38.6 C). He has bibasilar crackles on auscultation. You perform labs in clinic and he has a white count of 13.5, and a chest x-ray shows a right lower lobe consolidation. He has a negative rapid COVID-19 test. What are your top 3 differential diagnoses and what is the acute management of this patient’s condition? Let’s repeat the question: What are your top 3 differential diagnoses and what is the acute management of a 69-year-old male, non-smoker, who has fever, cough, shortness of breath, tachycardia, bibasilar crackles, elevated WBCs, a right lower lobe consolidation, and a negative rapid COVID-19 test?Send us your answer before May 7, 2021, to rbresidency@clinicasierravista.org and the best answer will win a prize!____________________________Screening for Alzheimer’s. With Jaime Perales Puchalt, PhD, and Hector Arreaza, MD Jaime Perales Puchalt is an Assistant Professor in the Department of Neurology. His main areas of interest include dementia among minorities and populations of Latin American origin in the Americas. He currently spearheads the Latino Alzheimer's education efforts at the University of Kansas Alzheimer’s Disease Center (KU ADC) and the Latino Cohort in which he recruits and conducts clinical dementia assessments of English and Spanish speaking Latinos. He has also led the integration of the Spanish National Alzheimer's Coordinating Center Unified Data Set 3.0 into REDCap. Together with Dr. Vidoni, Dr. Perales developed Envejecimiento Digno, a curriculum to increase Alzheimer's disease awareness among individual Latino community with different literacy levels.  Dr. Perales completed his MS in Psychology at the University of València, and his MPH in Public Health and PhD in Biomedicine at the University Pompeu Fabra, Barcelona. He started his research career at the University of València, where he collaborated in several stress-related projects among breast cancer patients, Latin American immigrants and caregivers of schizophrenia patients. Dr. Perales co-managed a four-year European Commission-funded multi-country study on healthy aging (COURAGE in Europe) at the Parc Sanitari Sant Joan de Déu. He also spent one year as a visiting researcher at the Institute of Public Health, University of Cambridge conducting dementia-related epidemiological research and collaborating in successful aging literature reviews. At Juntos: Center for Advancing Latino Health (KU), he contributed to the cultural and linguistic adaptation of several smoking cessation interventions for Latinos[3].Questions discussed during this episode:  Incidence and prevalence of dementia in the US: under-diagnosis, death risk, caregiver, Recommendations on screening for dementia by national organizations: American Academy of Neurology, examining models of dementia care (page 22), USPSTF, grade I, no evidence, screening early improves outcomes; ARDADBest evidence-based tools for screening for dementia: MMSE, MoCA (better for MCI), AD8, MiniCog. Useful resources for primary care providers: Alzheimer’s Association: Unidos Podemos (soap opera), NIH Caring for a person with Alzheimer’s Disease, Course: USDHHS,  Any other information you would like to provide us: The course, Jul 23, 2021, and Sep 3, 2021. Conclusion.Now we conclude our episode number 50 “Screening for Alzheimer’s Disease”. You heard from our experts the importance of assessing and treating your patients with Alzheimer’s Disease. We hope you can find all the resources mentioned during our interview with Jaime Perales, make sure you check our episode notes to find the links or just Google them, they are readily available online. Do not forget to send us your answer to the question of the month: What are your top 3 differential diagnosis and acute management of a 69-year-old male with new onset of fever, cough, shortness of breath, and right lower lobe consolidation. Even without trying, every night you go to bed being a little wiser.Thanks for listening to Rio Bravo qWeek. If you have any feedback about this podcast, contact us by email RBresidency@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created with educational purposes only. Visit your primary care physician for additional medical advice. This week we thank Hector Arreaza, Ariana Lundquist, Jaime Perales, Claudia Carranza, and Valerie Civelli. Audio edition: Suraj Amrutia. See you next week! References and resources mentioned during this episode:Meyers RS, Hellinga RC, Hoff DS. The KIDs List: Medications That Are Potentially Inappropriate in Children. Am Fam Physician. 2021 Mar 15;103(6):330. PMID: 33719376. https://www.aafp.org/afp/2021/0315/p330.html Cognitive Impairment in Older Adults: Screening, February 25, 2020. U.S. Preventive Services Task Force.  https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/cognitive-impairment-in-older-adults-screening Patnode CD, Perdue LA, Rossom RC, et al. Screening for Cognitive Impairment in Older Adults: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2020;323(8):764–785. doi:10.1001/jama.2019.22258.  https://jamanetwork.com/journals/jama/article-abstract/2761650 KU Medical Center, The Univeristy of Kansas, Core Faculty, https://www.kumc.edu/ku-adc/core-faculty/jaime-perales-puchalt-phd.html 2021 Alzheimer’s Disease Facts and Figures, Special Report on Race, Ethnicity and Alzheimer's in America, published by the Alzheimer’s Association, Chicago, Illinois, USA.  https://www.alz.org/media/documents/alzheimers-facts-and-figures.pdf Examining Models of Dementia Care: Final Report, U.S. Department of Health & Human Services, September 1, 2016, https://aspe.hhs.gov/pdf-report/examining-models-dementia-care-final-report ¡Unidos Podemos! (Fotonovela, Spanish), Alzheimer’s Association, http://www.alz.org/espanol/downloads/Novella_spanish_081213.pdf Together We Can! (Picture Novel, English), Alzheimer’s Association, http://www.alz.org/espanol/downloads/Novella_english_081213.pdf Alzheimer’s Disease, Caring for a Person with Alzheimer's Disease: Your Easy-to-Use Guide, U.S. Department of Health & Human Services, National Institute on Aging, https://order.nia.nih.gov/sites/default/files/2019-03/Caring_for_a_person_with_AD_508_0.pdf 

The Saint Louis University Mental Status Examination (SLUMS) is a method of screening for Alzheimer's disease and other kinds of dementia. It was designed as an alternative screening test to the widely used Mini-Mental State Examination (MMSE). The idea was that the MMSE is not as effective at identifying people with very early Alzheimer's symptoms.1 Sometimes referred to as mild cognitive impairment (MCI) or mild neurocognitive disorder (MNCD), these symptoms occur as people progress from normal aging to early Alzheimer's disease.

In this episode of MMSE I tell two stories based on the theme "THE OTHER SIDE".   The first story is titled "Sweat Shop” and the second story is called "This Old Fool".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast #storyslam #podcasting #podcaster, #podcastersofinstagram #podcastlife, #podcastshow, #newpod, #podcastoninstagram, #speaker, #talltales, #moth, #mothstories, #toastmasters --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Unexpected Gifts".   The first story is titled “Alchemist " and the second story is called " New Perspective ".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast #storyslam #podcasting #podcaster, #podcastersofinstagram #podcastlife, #podcastshow, #newpod, #podcastoninstagram, #speaker, #talltales, #moth, #mothstories, #toastmasters --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

n this episode of MMSE I tell two stories based on the theme "D.C. Stories".   The first story is titled "White House Belly" and the second story is called " Catholic Football ".  Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast #storyslam #podcasting #podcaster, #podcastersofinstagram #podcastlife, #podcastshow, #newpod, #podcastoninstagram, #speaker, #talltales, #moth, #mothstories, #toastmasters --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Christmas GIFTS".   The first story is titled "Ten Speed terror” and the second story is called "A twenty from heaven".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast #storyslam #podcasting #podcaster, #podcastersofinstagram #podcastlife, #podcastshow, #newpod, #podcastoninstagram, #speaker, #talltales, #moth, #mothstories, #toastmasters --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "DRIVING ".   The first story is titled “The Slow and the Serious" and the second story is called "Lottery Run".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast #storyslam #podcasting #podcaster, #podcastersofinstagram #podcastlife, #podcastshow, #newpod, #podcastoninstagram, #speaker, #talltales, #moth, #mothstories, #toastmasters --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Uber Stories".   The first story is titled "Uber Senses" and the second story is called " No Dash Cam No Problem".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam #podcasting #podcaster #podcastersofinstagram #podcastlife #podcastshow #newpod #storyslam #podcastoninstagram #speaker #talltales #moth #mothstories #toastmasters --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Black Friday ".   The first story is titled "Peacoat Pressure" and the second story is called "Hoodies In Walmart ".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam #podcasting #podcaster #podcastersofinstagram #podcastlife #podcastshow #newpod #storyslam #podcastoninstagram #speaker #talltales --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

周末八卦：老年痴呆新药真的能起死回生吗？老年痴呆（AD）的新药研发可谓竞争激烈，但至今没有一个能活过三期临床研究。就在5天前，这个领域出了件大事。也就是2020年11月2日，Nature Medicine发了一个新闻《阿杜单抗aducanumab临床研究的事后分析真的能使这个药起死回生吗？》总部位于美国麻省剑桥市的BIOGEN是一个主攻神经系统疾病,自身免疫性疾病的生物制药公司。 BIOGEN公司研发的阿杜单抗（aducanumab）的3期临床研究，ENGAGE研究和EMERGE研究，2015年开始启动，2019年因为中期分析没有达到预期终点，研究被终止，而且一度被公司从官网上删除了。但是，今年7月，BIOGEN公司又宣称先前的分析错了，虽然ENGAGE研究没有达到预期的终点，但是EMERGE研究中，高剂量组的患者认知功能障碍的减退速度延缓了。而且已经向FDA提出了新药上市的申请，这是大家都始料未及的。FDA咨询委员会会议公告 (1)11月4日，周三，FDA发布了对于阿杜单抗（aducanumab）新药申请的综述。 综述里FDA对一个有效的三期临床试验和一个小型的安全实验给予了肯定。 FDA总结：“ BIOGEN 提供了非常有说服力的证据来证明药物的有效性。 ” 同时，FDA认为对于药物安全性的担忧是可以通过药品说明书标签的文字来解决。综述同时弱化了对此类药物的负面看法， 认为BIOGEN的药和其他竞争对手不同的，其他的药物的实验失败可能是实验设计不好造成的。但让人最无法理解的是，虽然综述官方的语气对阿杜单抗非常的认可，但是综述的统计分析部分的结论却和综述的官方语气有很大的不同。 在统计分析里，FDA的专家认为BIOGEN停止了两项三期实验导致实验无法按照计划正常结束。 援引统计专家的结论： “整体的数据看上去不能支持最大剂量的有效性。最好的情况下，也只能说有一个研究得倒了阳性结果，然而另一个研究的结果直接与之有冲突。”同一篇综述里，前后两段居然意见相差这么，十分令人惊讶。FDA在批准前，不仅需要采纳统计专家的意见，还需要进行第三方专家讨论和投票；在听取各方意见之后，FDA拥有最终审批权。 这篇综述发表的当天，BIOGEN的股票涨了160亿美元（44%）。 投资者的兴奋是可以理解的。原因在于如果被批准，此药即将是第一个早期AD的药物。更可观的是，仅仅在美国，到2025年的适应症患者就会有100万人，而此药可能成为有史以来全球销售额最高的药物。2025年的销售额预计可以达到75亿美元。 如果不能被批准，公司现在只有一个已经销售多年的多发性硬化的药物，销售额在年年递减。可以说，这一个药物一旦批准，不但让公司起死回生，还能一步登天。四种针对淀粉样蛋白的新药 (2)大量证据表明-淀粉样蛋白在AD的发病机制中起着起始作用。然而，只有少数抗淀粉样蛋白制剂在临床试验中显示出有意义的疗效。四种近期有可能获得批准的药物包括：三种可注射的单克隆抗体（阿杜单抗aducanumab、甘特单抗gantenerumab和BAN2401），以及一种小分子口服药物ALZ-801。这四种药物的药理学作用、对β淀粉样蛋白的选择性、血浆半衰期、血脑屏障渗透性和达到脑内峰值所需的时间均决定了他们的最终临床效果。但总的来说，这四种药物的共同特征是：可以不同程度的、和可溶性的β样淀粉蛋白低聚物结合。其中阿杜单抗（aducanumab）和甘特单抗（gantenerumab）靶向β淀粉样蛋白低聚体、主要清除不溶性淀粉样斑块；BAN2401优先靶向可溶性原纤维（较大的低聚物），而不是斑块；ALZ-801可以在不结合斑块的情况下，阻止聚合物的形成。在临床研究中，药物对低聚物的选择性程度、和脑组织的暴露程度驱动了临床疗效，而斑块的清除被认为与血管源性脑水肿有关。目前只有最高剂量的阿杜单抗（aducanumab）和BAN2401显示出适度的疗效，更高的剂量受到血管源性脑水肿风险增加的限制，特别是在ApoE4基因携带者中。AD患者约有15%是ApoE4/4基因纯合子，约有2/3是ApoE4基因的携带者。但是ALZ-801，作为一种选择性抑制β淀粉样蛋白低聚物生成的小分子物质，因为不通过清除淀粉样斑块起效，则不存在这个问题。在目前的临床研究中，脑脊液、血浆和影像学生物标志物的监测可以加深我们对于可溶性β淀粉样蛋白低聚物在AD发病机制中的作用及其对疾病进展的影响。阿杜单抗（Aducanumab）(3)2012年，多中心的2期临床研究PRIME研究启动，筛选前驱期、或轻型的AD患者166人。2015年，PRIME研究的中期分析发表在AD/PD会议上，阿杜单抗以剂量依赖的方式降低脑内淀粉样蛋白的沉积、改善MMSE（简易精神状态量表）评分、改善CDR-SB（临床痴呆量表）评分。但是血管源性脑水肿随着剂量的增加也逐步增加，最大剂量组中有1/3的患者出现症状性血管源性脑水肿，症状包括头痛和思维混乱。2017年的发表的2年开放标签延伸部分研究的结果显示，阿杜单抗aducanumab可以最多减少淀粉样蛋白在脑内的沉积达70 centiloid，并延缓认知功能的恶化。此处centiloid是一个PET诊断AD的测量单位，0代表没有AD，100代表确诊AD。2015年，两个完全相同的3期临床研究启动（ENGAGE研究和EMERGE研究），ENGAGE研究在北美、欧洲、澳洲和亚洲进行，EMERGE研究在北美和欧洲进行。针对的人群是AD伴有轻度认知功能障碍的患者，两个研究均计划招募1350人。2019年3月，中期分析没有达到预期的终点，因此研究被停止。有趣的是，探索性分析中发现，虽然ENGAGE研究没有达到预期的终点，但是EMERGE研究中用药剂量≥10mg/kg组的患者，认知功能障碍的减退速度被延缓了。2020年1月，一项开放标签的3b期临床研究，招募了之前研究的参与者，计划给予10mg/kg剂量每月一次，持续2年。预计研究将延续至2023年。2020年7月，阿杜单抗（Aducanumab）已向FDA递交上市申请。FDA最晚将于2021年3月给出答复。2020年11月，Nature Medicine发表了《阿杜单抗研究的事后分析》。甘特单抗（Gantenerumab） (4)在4项1期临床研究中，甘特单抗（gantenerumab）被认为是安全且耐受性良好的。2012年发表的一篇1期临床研究中，发现最高剂量组的6名患者中，有2名患者的淀粉样蛋白减少得最多，他们的脑部MRI中，发现了局部炎症或血管源性水肿。另一项研究中的16位患者在6个月的最高剂量治疗后，淀粉样蛋白的变化达11%。2010-2012年，2/3期临床研究（SCarlet RoAD）纳入患有早期AD的799例患者，但2014年因为没有达到主要和次要终点停止了该研究。事后分析中认为高剂量可能有效，故研究以开放标签的形式继续进行，将持续到2020年7月。2014年，3期临床研究（Marguerite RoAD）计划纳入了轻度AD的患者共1000人，但2016年的中期分析也没有达到预期的终点，因此停止招募参与者，并改为开放标签继续随访。2018年的AAIC会议上，公布了SCarlet RoAD研究和Marguerite RoAD研究的扩展部分研究结果，结果提示最大剂量的甘特单抗gantenerumab可以减少淀粉样蛋白在脑内的沉积达59 centiloid，1/3的患者出现无症状性的局部炎症和血管源性脑水肿。2012年，另一个2/3期临床研究（DIAN-TU研究）在常染色体显性遗传突变的AD患者中开展。2020年2月报导研究没有达到预期的终点。研究结果在AAT-AD/PD2020会议上进行了汇报，其中有39名患者完成了研究，甘特单抗（gantenerumab）可以大量的减少脑内淀粉样斑块、使脑脊液中β淀粉样蛋白42水平正常化、降低脑脊液中总tau蛋白和p-tau181蛋白的浓度、并且延缓脑脊液中神经丝轻链的升高。研究中认知功能受损的参与者认知功能继续恶化，基线时没有认知功能受损的参与者病情稳定。该研究将进入开放标签阶段，持续3年。2018年，另两项大型3期临床研究启动（GRADUATE 1研究、GRADUATE 2研究），针对前驱期或轻型的AD患者开展，预计研究会延续至2023年。BAN2401 (5)2012年，为期18个月的、2期临床研究启动，纳入了856名轻症、早期或可能患有AD的患者，18个月结束后，进入开放标签阶段，为期5年。2017年，18个月的双盲对照研究提示，高剂量的BAN2401可以延缓认知功能恶化、减少脑内淀粉样蛋白的沉积。AAIC2018会议上公布了2b期研究的结果，最高剂量组中，可以减少脑内淀粉样蛋白的沉积达93%，延缓认知功能恶化达30%-47%。患者脑脊液β淀粉样蛋白42的浓度剂量依赖性的出现升高，约10%的患者出现了血管源性脑水肿，但大多数没有症状。2019年3月，3期临床研究（Clarity AD研究）启动，针对早期症状性AD患者，计划纳入1566人，共18个月。2020年2月，另一项3期临床研究（AHEAD 3-45研究）启动，针对认知功能正常、但脑内淀粉样蛋白升高的人群，计划招募1400人。ALZ-801 (6)1期临床研究中，ALZ-801被认为安全且耐受性良好。2017年10月，3期临床研究启动，计划纳入携带ApoE4/4基因纯合子的、轻中度AD患者，为期18个月。2020年8月，该研究得到美国国家衰老研究所（U.S. National Institute on Aging）的资助。预计将于2021年开始招募参与者。“Alzheimer drug is very expensive to develop, unlikely to be effective, and also very hard to kill.”老年痴呆的新药研发都很昂贵，似乎有效性都很可疑，但都像打不死的小强、总能起死回生。参考文献1.FDA. Peripheral Central Nervous System (PCNS) Drugs Advisory Committee Meeting. https://wwwfdagov/media/143502/download. 2020.2.Tolar M, Abushakra S, Hey JA, Porsteinsson A, Sabbagh M. Aducanumab, gantenerumab, BAN2401, and ALZ-801-the first wave of amyloid-targeting drugs for Alzheimer's disease with potential for near term approval. Alzheimers Res Ther. 2020;12(1):95.3.aducanumab. https://wwwalzforumorg/therapeutics/aducanumab. 2020.4.Gantenerumab. https://wwwalzforumorg/therapeutics/gantenerumab. 2020.5.BAN2401. https://wwwalzforumorg/therapeutics/ban2401. 2020.6.ALZ-801. https://wwwalzforumorg/therapeutics/alz-801. 2020.

In this episode of MMSE I tell two stories based on the theme "THANKSGIVING".    The first story is titled "Jive Turkey" and the second story is called " Pass The Yak".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam #podcasting #podcaster #podcastersofinstagram #podcastlife #podcastshow #newpod #storyslam #podcastoninstagram #speaker #talltales --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Changed Future". The first story is titled "Beowulf to Polygamy" and the second story is called "Hot Stitch". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Inappropriate". The first story is titled "SAT with CTE" and the second story is called " Preaching "Ghostface Killah". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "FEAR". The first story is titled "Grandpa Cures" and the second story is called "Jail Time". Please follow on Instagram @manleymythicalstory Twitter: @Manleystorypod Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Halloween". The first story is titled "All Pimps No Hoes" and the second story is called " Crank That Solider Boy In that Church". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "When Worlds Collide". The first story is titled "Can We Play Army" and the second story is called " Where Do We Pee". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "DISGUISES". The first story is titled "Bamboozled Bankers" and the second story is called " Water to Wine". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #talltales #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Out on a Limb". The first story is titled "Putting Post In Holes" and the second story is called " Trusting The In-Laws". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic #talltales --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Snowed In". The first story is titled "Platinum Skies" and the second story is called " Proud Son in The Snow". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "First Kiss". The first story is titled "Juicy Pockets" and the second story is called " Kisses From Warrenton!". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and DM or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "Transplanted". The first story is titled "Back to The Boro" and the second story is called " To The Mountain Top". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "When It Rains it Pours". The first story is titled "Wedding Day Cookout" and the second story is called " Warehouse Work". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast, #stories, #storytelling, #storyteller, #MMSE, #newpodcast, #storyslam, #podcasting, #podcaster, #podcastersofinstagram, #podcastlife, #podcastshow, #podcastyoutube, #comedy, #funnystories, #truestories, #truestory, #openmic --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "The Road Less Traveled". The first story is titled "Quaker Or Aggie" and the second story is called "Black Panthers in Khakis". Please follow on Instagram @manleymythicalstory Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com YouTube- https://www.youtube.com/channel/UCUpwDXtbrjhvf1fWQ-d-skg/featured #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam #podcasting #podcaster #podcastersofinstagram #podcastlife #podcastshow --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode of MMSE I tell two stories based on the theme "OOPS!".   The first story is titled "Doug who?" and the second story is called " which hotel did we get?".   Please follow on Instagram @manleymythicalstory   Please download podcast on all platforms and dm or email story request Manleystory@Gmail.com #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam #podcasting #podcaster #podcastersofinstagram #podcastlife #podcastshow --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.18.256321v1?rss=1 Authors: Zamani, J., Sadr, A., Javadi, A.-H. Abstract: Alzheimer's disease (AD) is a neurodegenerative disease that leads to anatomical atrophy, as evidenced by magnetic resonance imaging (MRI). Automated segmentation methods are developed to help with the segmentation of different brain areas. However, their reliability has yet to be fully investigated. To have a more comprehensive understanding of the distribution of changes in AD, as well as investigating the reliability of different segmentation methods, in this study we compared volumes of cortical and subcortical brain segments, using automated segmentation methods in more than 60 areas between AD and healthy controls (HC). A total of 44 MRI images (22 AD and 22 HC, 50% females) were taken from the minimal interval resonance imaging in Alzheimer's disease (MIRIAD) dataset. HIPS, volBrain, CAT and BrainSuite segmentation methods were used for the subfields of hippocampus, and the rest of the brain. While HIPS, volBrain and CAT showed strong conformity with the past literature, BrainSuite misclassified several brain areas. Additionally, the volume of the brain areas that successfully discriminated between AD and HC showed a correlation with mini mental state examination (MMSE) scores. The two methods of volBrain and CAT showed a very strong correlation. These two methods, however, did not correlate with BrainSuite. Our results showed that automated segmentation methods HIPS, volBrain and CAT can be used in the classification of AD and HC. This is an indication that such methods can be used to inform researchers and clinicians of underlying mechanisms and progression of AD. Copy rights belong to original authors. Visit the link for more info

The Gary Null Show is here to inform you on the best news in health, healing, the environment.  If you would like to sign up for the new PRN Newsletter provide your email to Prnstudio@gmail.com   Cancel Culture doxxed me (as an ex-Google tech lead) Millennials, Generation Zs trying to foster a workplace 'culture of victimhood'   Turmeric could have antiviral properties Wuhan Institute of Bioengineering, August 5, 2020 Curcumin, a natural compound found in the spice turmeric, could help eliminate certain viruses, research has found.  A study published in the Journal of General Virology showed that curcumin can prevent Transmissible gastroenteritis virus (TGEV) - an alpha-group coronavirus that infects pigs - from infecting cells. At higher doses, the compound was also found to kill virus particles.  Infection with TGEV causes a disease called transmissible gastroenteritis in piglets, which is characterised by diarrhoea, severe dehydration and death. TGEV is highly infectious and is invariably fatal in piglets younger than two weeks, thus posing a major threat to the global swine industry. There are currently no approved treatments for alpha-coronaviruses and although there is a vaccine for TGEV, it is not effective in preventing the spread of the virus.  To determine the potential antiviral properties of curcumin, the research team treated experimental cells with various concentrations of the compound, before attempting to infect them with TGEV. They found that higher concentrations of curcumin reduced the number of virus particles in the cell culture. The research suggests that curcumin affects TGEV in a number of ways: by directly killing the virus before it is able to infect the cell, by integrating with the viral envelope to 'inactivate' the virus, and by altering the metabolism of cells to prevent viral entry. "Curcumin has a significant inhibitory effect on TGEV adsorption step and a certain direct inactivation effect, suggesting that curcumin has great potential in the prevention of TGEV infection," said Dr Lilan Xie, lead author of the study and researcher at the Wuhan Institute of Bioengineering. Curcumin has been shown to inhibit the replication of some types of virus, including dengue virus, hepatitis B and Zika virus. The compound has also been found to have a number of significant biological effects, including antitumor, anti-inflammatory and antibacterial activities. Curcumin was chosen for this research due to having low side effects according to Dr Xie. They said: "There are great difficulties in the prevention and control of viral diseases, especially when there are no effective vaccines. Traditional Chinese medicine and its active ingredients, are ideal screening libraries for antiviral drugs because of their advantages, such as convenient acquisition and low side effects." The researchers now hope to continue their research in vivo, using an animal model to assess whether the inhibiting properties of curcumin would be seen in a more complex system. "Further studies will be required, to evaluate the inhibitory effect in vivo and explore the potential mechanisms of curcumin against TGEV, which will lay a foundation for the comprehensive understanding of the antiviral mechanisms and application of curcumin" said Dr Xie.   A quarter of arthritis cases linked to excess weight Weight loss from young adulthood to midlife was associated with substantially reduced risk of developing arthritis Boston University, August 4, 2020   A new Boston University School of Public Health (BUSPH) study shows that weight loss between early adulthood and midlife lowers arthritis risk, and found no evidence of any persistent risk of arthritis for people who were heavier earlier in life and then lost weight. The study, published in the journal Arthritis Care & Research, also estimates that nearly a quarter of arthritis cases in the U.S., corresponding to 2.7 million people, are attributable to excess weight. "Policies that address the social and structural factors that promote weight gain are urgently needed. Our findings suggest that such measures could have a significant impact on reducing the incidence of arthritis, a leading cause of disability and chronic pain in the US," says study corresponding author Dr. Andrew Stokes, assistant professor of global health at BUSPH. "Although weight loss could represent a viable way to reduce arthritis risk at the individual level, we found that the best solution at the population level would be to prevent weight gain," says study lead author and BUSPH alumna Kaitlyn Berry, who was a research fellow at BUSPH while working on the study and is now at the University of Minnesota School of Public Health.  The researchers used data from the National Health and Nutrition Examination Survey (NHANES) on adults 40-69 years old, to categorize individuals based on the changes in their body mass indices (BMI) from early adulthood to mid-life, and analyzed the association between these BMI trajectories and the risk of developing an arthritis condition within 10 years. Of the 13,669 people in the study, 3,603 developed an arthritis condition. Compared with those who had a BMI in the "normal" range in both early adulthood and middle age, those who went from the "normal" range to the "overweight" or "obese" ranges, those who went from the "overweight" range to the "obese" range, and those whose BMIs were in the "obese" range at both points were all significantly more likely to develop arthritis conditions.  On the other hand, those whose BMIs went from the "obese" down to the "overweight" range had a significantly lower risk of developing arthritis compared to those whose BMI remained in the "obese" range. Additionally, those who lost weight had the same likelihood of developing arthritis as those whose BMIs stayed in the "overweight" range.  "These findings highlight the need for lifelong public health measures to prevent obesity at younger ages as an important step to curb later life musculoskeletal and joint health problems such as osteoarthritis. This is particularly important as musculoskeletal pain is a leading cause of disability globally," says study co-author Dr. Tuhina Neogi, professor of epidemiology at BUSPH, professor of medicine at the Boston University School of Medicine, and chief of rheumatology at Boston Medical Center.   Consumption of a blueberry enriched diet by women for six weeks alters determinants of human muscle progenitor cell function Cornell University, August 5, 2020  A new research study, published in the Journal of Nutrition, investigated how serum from subjects consuming a diet enriched with blueberries would affect the cells responsible for muscle growth and repair. The emerging study, "Consumption of a blueberry enriched diet by women for six weeks alters determinants of human muscle progenitor cell function," was conducted at Cornell University. The study was conducted over six weeks with 22 women, 12 aged 25-40 and 10 aged 60-75. For the blueberry-enriched diet, participants consumed the equivalent of 1.75 cups of fresh blueberries/day, given as freeze-dried blueberries (19 g in the morning and 19 g in the evening), along with their regular diet. Participants were also asked to avoid other foods rich in polyphenols and anthocyanins. Serum was obtained from the participants 1.5 hours after consuming the morning dose of blueberries. The researchers then investigated how the serum would affect muscle progenitor cell function through proliferation or cell number, capacity to manage oxidative stress and oxygen consumption rate or metabolism. The results showed the six-week blueberry-enriched serum obtained from the women aged 25-40 increased human muscle progenitor cell numbers in culture. There was also a trend toward a lower percentage of dead human muscle progenitor cells, suggesting a resistance to oxidative stress, as well as increased oxygen consumption of the cells. There were no beneficial effects seen in the muscle progenitor cells treated with serum from participants aged 60-75 who consumed the blueberry enriched diet. "The consequences associated with the deterioration of skeletal muscle are a loss of mobility, decreased quality of life, and ultimately, loss of independence. Currently, research on dietary interventions to support skeletal muscle regeneration in humans is limited. This preliminary study of muscle progenitor cell function paves the way for future studies to develop clinical interventions," said Anna Thalacker-Mercer, Ph.D., the study's lead investigator. "While the results cannot be generalized to all populations, this study is an important step in translating findings from cell culture and rodent studies to a potential dietary therapy for improving muscle regeneration after injury and during the aging process." According to the Centers for Disease Control and Prevention (CDC), muscles lose strength, flexibility, and endurance over time. Muscle mass decreases three to five percent every decade after 30 years of age, and that rate increases over age 60. Therefore, strategies to improve muscle progenitor cell proliferation and lower oxidative stress may also benefit muscle regeneration during the aging process. Research on the role that blueberries may play in promoting good health is ongoing across multiple areas, including cardiovascular health, diabetes management, brain health, exercise and the gut microbiome.     From mitochondria to healthy aging: role of branched-chain amino acid treatment University of Turin (Italy), August 3, 2020   According to news originating from Turin, Italy, research stated, “Malnutrition often affects elderly patients and significantly contributes to the reduction in healthy life expectancy, causing high morbidity and mortality. In particular, protein malnutrition is one of the determinants of frailty and sarcopenia in elderly people.” Our news journalists obtained a quote from the research from the University of Turin, “To investigate the role of amino acid supplementation in senior patients we performed an open-label randomized trial and administered a particular branched-chain amino acid enriched mixture (BCAAem) or provided diet advice in 155 elderly malnourished patients. They were followed for 2 months, assessing cognitive performance by Mini Mental State Examination (MMSE), muscle mass measured by anthropometry, strength measure by hand grip and performance measured by the Timed Up and Go (TUG) test, the 30 s Chair Sit to Stand (30-s CST) test and the 4 m gait speed test. Moreover we measured oxidative stress in plasma and mitochondrial production of ATP and electron flux in peripheral blood mononuclear cells. Both groups improved in nutritional status, general health and muscle mass, strength and performance; treatment with BCAAem supplementation was more effective than simple diet advice in increasing MMSE (1.2 increase versus 0.2, p = 0.0171), ATP production (0.43 increase versus -0.1, p = 0.0001), electron flux (0.50 increase versus 0.01, p< 0.0001) and in maintaining low oxidative stress. The amelioration of clinical parameters as MMSE, balance, four meter walking test were associated to increased mitochondrial function.” According to the news editors, the research concluded: “Overall, our findings show that sustaining nutritional support might be clinically relevant in increasing physical performance in elderly malnourished patients and that the use of specific BCAAem might ameliorate also cognitive performance thanks to an amelioration of mitochondria bioenergetics.”     20-year sedentary lifestyle linked to twice the risk of premature death: Being physically active is key to a longer life Norweign University of Science and Technology, August 4, 202 It's easy to fall into the habit of skipping exercise because you're busy with work or chores. Yet according to a study, having a sedentary lifestyle for at least 20 years is linked to twice the risk of premature death, especially compared to those who exercise regularly. Results from the Trøndelag Health Study (the HUNT study) was presented at ESC Congress 2019 and the World Congress of Cardiology. The HUNT study was conducted to determine how changes in physical activity within two decades were linked to “subsequent death from all causes and from cardiovascular disease.” Other studies on the association between physical activity and longevity only ask volunteers about their level of physical activity once and followed them for several years. However, physical activity is a behavior that constantly changes, highlighting the importance of looking into how these changes over time are linked to the risk of death later in life. Physical activity levels linked to premature death risk Researchers asked residents of Norway aged 20 and older to participate during three points: 1984 to 1986, 1995 to 1997 and 2006 to 2008. For all three time points, the volunteers reported their frequency and duration of leisure time physical activity. The researchers then examined data from the first and third surveys. Data for the analysis was obtained from 23,146 male and female volunteers. Physical activity was classified as: Inactive Moderate (Less than two hours a week.) High (Two or more hours per week.) The volunteers were divided into groups based on their activity levels for each survey. The physical activity data were linked to information on deaths until the end of 2013 via the Norwegian Cause of Death Registry. The risk of death in the two physical activity groups was compared to the reference group, which included participants who reported a high level of exercise during both surveys. Analyses were also adjusted for factors that influence prognosis: Age Blood pressure Body mass index (BMI) Education level Sex Smoking Unlike volunteers in the reference group, participants who were inactive in both 1984-1986 and 2006-2008 had twice the risk of premature death and a 2.7-fold greater risk of dying from cardiovascular disease. Compared to the reference group, participants with moderate activity at both time points had a 60 percent and 90 percent greater risk of all-cause and cardiovascular deaths, respectively. Exercising consistently is key Dr. Trine Moholdt, a study author from the Norwegian University of Science and Technology at Trondheim, Norway, explained that to reap the maximum health benefits of physical activity and prevent premature all-cause and cardiovascular death, people must be physically active consistently. Moholdt noted that even if you had a sedentary lifestyle, you can still reduce your risk by exercising later in life. Adults should have at least 150 minutes of moderate-intensity exercise a week or 75 minutes of vigorous-intensity aerobic physical activity a week to effectively boost their overall well-being. But these numbers aren't set in stone, said Moholdt. She added that even exercise below the recommended levels will offer some benefits. Instead of focusing on how much you're exercising, Moholdt suggests setting goals to be more physically fit. Consult a trusted physician for activities that suit your health condition. Even smaller amounts of activity can help you be more physically fit, as long as your workout “makes you breathe heavily.” (Related: If you have an 8-hour desk job, exercise for 30 minutes daily to significantly improve your health.) Set aside some time to go to the gym, or sneak in mini-workouts throughout a regular day. Moholdt recommends any exercise that you might enjoy, such as: Using the stairs at work instead of the elevator. Walking instead of driving to your destination. Getting off the bus one stop early and walking the rest of the way. Exercise during work breaks. Break out a sweat in the office break room by doing jumping jacks or squats. Going for a long walk with your dog. Enjoying a walk around the neighborhood with your family. Following online workout videos if you can't leave the house. Some participants changed categories between surveys and those who went from inactive to highly active had a mortality risk “between those who were continually active or continually sedentary.” On the other hand, volunteers who went from highly active to inactive had a similar risk of dying like those who were inactive at both surveys. Moholdt said that it's never too late to start exercising even if you've been sedentary for most of your life. Starting exercise sooner ensures that you also see positive results sooner. Moholdt concluded that you should start and maintain good exercise habits as early as you can. Being physically active doesn't just help prevent premature death, it also helps improve your mental and physical health. Exercising regularly is key to having a longer and healthier life.   Researchers say where you live could add years to your life People who live in blue states are living longer, and the gap is widening Syracuse University, August 4 2020   Could where you live dictate how long you live? New research at Syracuse University's Maxwell School, published today in the Milbank Quarterly, shows Americans who live in so called blue states tend to live longer than those in red states, primarily due to state policies. Among the findings: U.S. state policies since the 1980s have cut short American lives, particularly for women. U.S. life expectancy gains since 2010 would be 25% greater for women and 13% greater for men if states policies had not changed in the way they did, with many becoming more conservative. Enacting more liberal state policies could raise U.S. life expectancy by over 2 years, whereas enacting more conservative state policies could reduce it by 2 years. In the greatest gap between states, residents in Connecticut outlive their counterparts in Oklahoma by as many as seven years. The study examined how state policy environments contributed to U.S. life expectancy trends from 1970 to 2014. It used information on 18 policy domains such as abortion and guns, each measured on a liberal-to-conservative scale, for every state and calendar year. The analysis then predicted U.S. life expectancy trends from all policy domains, controlling for characteristics of states and their residents. "Americans die younger than people in other high-income countries," said Jennifer Karas Montez, sociology professor at Syracuse University's Maxwell School and lead author of the study. "This gap in life expectancy between the U.S. and other countries emerged in the 1980s and has grown ever since. Since that time, gaps in life expectancy between U.S. states also expanded. The difference between the highest and lowest life expectancy states has grown to 7.0 years--the largest ever recorded. These two trends are related: the dismal life expectancy trends of some states have been an anchor on overall U.S. life expectancy."'  For instance, between 1980 and 2017, life expectancy rose by just 2.2 years in Oklahoma (73.6 to 75.8 years) but 5.8 years in Connecticut (74.9 to 80.7 years). Life expectancy in Oklahoma now falls between that of Serbia and Brazil, while Connecticut falls between Denmark and Costa Rica.  The study found that Oklahoma and Connecticut differ in other ways. While these two states were diverging in life expectancy, they were also diverging in their policy orientation. Oklahoma made one of the largest transitions toward a conservative state policy environment among all 50 states. Conversely, Connecticut made one of the largest transitions toward a liberal state policy environment. This polarization in state policy environments has occurred across the U.S. and helps to explain the growing gap in life expectancy between states and the troubling trends in U.S. life expectancy since the 1980s.  Among the 18 policy domains studied, 10 strongly predict life expectancy. More liberal versions of those policies generally predict longer lives and more conservative versions generally predict shorter lives. This is especially the case for policies on tobacco, immigration, civil rights, labor (e.g., Right to Work laws, minimum wage), and the environment. For instance, by changing its labor laws from the most conservative to the most liberal orientation, a state could experience a large 1-year increase in life expectancy. State policies have particularly important consequences for women's life expectancy. This finding reflects the reality that state policies such as minimum wage, EITC, abortion laws, and Medicaid are more relevant for women's than men's lives. According to Montez, "During the 1980s and after 2010, overall changes in state policies had a negative impact on U.S. life expectancy. After 2010, the small gains in U.S. life expectancy would have been 13% steeper among men and 25% steeper among women if state policies had not changed in the way that they did, with many becoming more conservative." If all 50 states enacted either liberal or conservative policies, what would happen to U.S. life expectancy? "If all states enacted liberal policies across the 18 domains, our study estimated that U.S. life expectancy would increase by 2.8 years for women and 2.1 years for men," said Montez. "However, if all states enacted conservative policies, U.S. life expectancy would decline by 2.0 years for women and 1.9 years for men. If all states followed current national policy trends, there would continue to be little improvement in life expectancy. This is partly due to countervailing forces: gains in U.S. life expectancy associated with some national policy trends (e.g., toward liberal policies on the environment and civil rights) would be offset by losses associated with other trends (e.g., toward conservative policies on abortion and guns)." Montez said that trends in state policies since the 1980s have cut short many lives. "Improving U.S. health and longevity requires changing many of those policies," said Montez. "In particular, it is essential to enact policies that protect the environment, regulate tobacco and firearms, and ensure labor, reproductive, and civil rights." But Montez believes e nacting these changes in state policies will not be easy. "On the contrary: policymakers in many states have put the interests of corporations and their lobbyists--particularly the American Legislative Exchange Council (ALEC)--and wealthy donors over the interests and health of their constituents." To drive home her point, Montez points out Oklahoma, for example, is one of the most active states in terms of enacting the corporate-friendly and politically-conservative policies promoted by ALEC, while Connecticut is among the least active states. "Policymakers and the public must recognize," she said, "that putting profits over people cuts lives short."   Gut microbes shape our antibodies before we are infected by pathogens University of Bern (Germany), August 5, 2020   B cells are white blood cells that develop to produce antibodies. These antibodies, or immunoglobulins, can bind to harmful foreign particles (such as viruses or disease-causing bacteria) to stop them invading and infecting the body's cells. Each B cell carries an individual B cell receptor (BCR) which determines which particles it can bind, rather like each lock accepts a different key. There are many millions of B cells with different receptors in the body. This immense diversity comes from rearranging the genes that code these receptors, so the receptor is slightly different in every B cell resulting in billions of possibilities of different harmful molecules that could be recognized. Intestinal microbes trigger expansion of these B cell populations and antibody production, but until now it was unknown whether this was a random process, or whether the molecules of the intestinal microbes themselves influence the outcome.  In a research article published in the journal Nature, Dr. Hai Li, Dr. Julien Limenitakis, Prof. Stephanie Ganal-Vonarburg and Prof. Andrew Macpherson of the Department for BioMedical Research, University of Bern, and Inselspital, University Hospital Bern, have analyzed the billions of genes that code the antibodies in a system that allows the responses to individual benign intestinal microbes to be understood.  The range of available antibodies depends on where beneficial microbes are in the body The number of benign microbes living in our intestines is about the same as the number of cells in our body. Mostly these bacteria stay within the intestinal tube rather than penetrate the body tissues. Unfortunately, some penetration is unavoidable, because the intestine only has a single layer of cells that separate the inside of the tube from blood vessels that we need to absorb our food.  Dr. Limenitakis used specially designed computer programs to process millions of genetic sequences that compare the antibody repertoire from B cells, depending on whether the microbes stay in the intestine, or whether they reach the bloodstream. In both cases the antibody repertoire is altered, but in rather different ways depending on how the exposure occurs.  "Interestingly, this is rather predictable depending on the microbe concerned and where it is in the body, indicating that the intestinal microbes direct the development of our antibodies before we get a serious infection and this process is certainly not random", explains Ganal-Vonarburg. There are different sorts of antibodies in the lining of the intestine (IgA) compared with the bloodstream (IgM and IgG). Using the powerful genetic analysis, the researchers showed that the range of different antibodies produced in the intestine was far less that those produced in central body tissues. This means that once microbes get into the body, the immune system has many more possibilities to neutralize and eliminate them, whereas antibodies in the intestine mainly just bind the bacterial molecules that they can see at any one time. How the antibodies change when the body is exposed to different microbes Over their life-span mammals face a huge variety of different microbial challenges. It was therefore important to know how once the antibody repertoire could change once had been shaped by a particular microbe when something else came along. The research team answered this question by testing what happened with the same microbe at different sites or with two different microbes on after another.  Although intestinal microbes do not directly produce an especially wide range of different antibodies, they sensitize the central immune tissues to produce antibodies if the microbe gets into the bloodstream. When a second microbes comes along, the rather limited intestinal antibody response changes to accommodate this microbe (rather like changing the lock in one's door). This is different from what happens when microbes get into the blood stream to reach the central body tissues when a second set of antibodies is made without compromising the first response to the original microbes (like installing another lock, so the door can be opened with different keys). This shows that central body tissues have the capacity to remember a range of different microbial species and to avoid the dangers of sepsis. It also shows that different B cell immune strategies in different body compartments are important for maintenance of our peaceful existence with our microbial passengers.  Dr. Li comments that "Our data show for the first time that not only the composition of our intestinal microbiota, but also the timing and sequence of exposure to certain members of the commensal microbiota, happening predominantly during the first waves of colonisations during early life, have an outcome on the resulting B cell receptor repertoire and subsequent immunity to pathogens."   Meta-analysis finds higher circulating vitamin D levels associated with lower risk of gestational diabetes Ahvaz Jundishapur University (Iran), August 5, 2020   According to news reporting out of Ahvaz, Iran, by NewsRx editors, research stated, “Several meta-analyses of observational studies revealed a modest increase in the risk of gestational diabetes (GDM) among pregnant women with low levels of serum vitamin D. However, no study examined a dose-response meta-analysis as well as a high versus low analysis in this regard.” Financial support for this research came from Ahvaz Jundishapur University of Medical Sciences. Our news journalists obtained a quote from the research from the Ahvaz Jundishapur University of Medical Sciences, “We systematically searched PubMed, Embase, ISI Web of Science, and Scopus up to August 2019 to find prospective observational studies investigating the association of serum 25(OH)D with the risk of developing GDM. Using a random-effects model, the reported risk estimates were pooled. Nine cohort studies and six nested case-control studies were included in the final analysis (40,788 participants and 1848 cases). Considering linear analysis, each 10 nmol/L increase in circulating 25(OH)D was associated with a 2% lower risk of GDM (effect size (ES): 0.98; 95% CI: 0.98, 0.99; I=85.0%, p

In this episode I tell two stories based on the theme " Sixth Sense". The First Story is "Down Town Lunch" and secound story is "Whats Wrong With My Boy". Please download podcast on all platforms and dm or email story request or ideas Manleystory@Gmail.com #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

In this episode I tell two stories titled "Nearly Missed My Bride"  and "Nearly Missed the Point".  In "Nearly Missed My Bride" I tell how I almost missed out on my wife but not going to a summer camp.  In the second story "Nearly Missed The Point"  I tell the story of how I always miss the point at Sunday school, I told this story in more like a speech based on suggestion of my Toastmaster friends. Please download podcast on all platforms and dm or email story request or ideas Manleystory@Gmail.com #podcast #stories #storytelling #storyteller #MMSE #newpodcast #storyslam --- Support this podcast: https://podcasters.spotify.com/pod/show/mmse/support

Dialogzentrum Leben im Alter (DZLA)www.dzla.de Die Episode auf dem Blog des DZLA: https://www.dzla.de/wissenstransfair-eps-003/ Diskutieren Sie mit uns! In der Episode 003 des Podcasts des Dialogzentrum Leben im Alter (DZLA) geht es um folgende Themen:1. Aktuelles DZL-Akteur: Spenden an das DZLAVerlegung der DialogKonferenz auf den 4. November 2020 (Thema: Team)2. „Nur ein Gedanke“ – Wer bringt den Professor*innen das Lehren bei?3. Serie „Lichtblicke“: Christian Müller-Hergl zu einer Studie aus dem Jahr 2017 zur Anwendung von Ketamin und Elektrokrampftherapie (ECT) bei depressiven Personen mit DemenzElektrokrampftherapie (ECT) gilt als eine Behandlungsmöglichkeit, wenn alle anderen Therapieansätze versagen. Auch Anwendungen bei Menschen mit Demenz sind beschrieben worden, die zu deutlichen kognitiven Verbesserungen geführt haben. Vorgestellt wird die Anwendung von ECT zusammen mit dem Narkosemittel Ketamin, das über die Blockade der Glutamat-Rezeptoren seine Wirkung entfaltet und Bewusstsein, nicht aber Atmung unterbricht. Dieses Narkosemittel zeigt positive Wirkungen auf den Hippocampus und den präfrontalen Kortex und bietet einen gewissen Schutz vor den möglicherweise die Kognition schädigenden Effekten der ECT. Beschrieben wird die Anwendung bei einer Patientin, die unter einer schweren, behandlungsresistenten Depression mit katatonischer Ausprägung zusammen mit gemischter Demenz leidet. Im Verlauf der Anwendung von insgesamt 16 ECT verbesserte sich der Zustand unter Ketamin kontinuierlich und deutlich. Die katatonischen Symptome verschwanden vollständig, sie wurde freundlich, kooperativ, konnte Speisen selbstständig einnehmen und ihre Ausscheidungen wieder kontrollieren. Die Kognition verbesserte sich deutlich von MMSE 13/30 auf MMSE 21/30. Offen bleibt, ob die Verbesserung eher auf ECT oder Ketamin zurückzuführen ist. Die Autoren vermuten, dass die Verbesserungen der Kognition mit dem Rückgang depressiver Symptome zusammenhängt.Studie: Litvan, Z., Bauer, M., Kasper, S., Frey, R. (2017). Electroconvulsive therapy with S-ketamine anestesia for catatonia in coexisting depression and dementia. International Psychogeriatrics 29(7), 1223-12254. Serie „Haustheater“: Christian Müller-Hergl und Detlef Rüsing diskutieren das das Thema „Sexualität“ in der gerontopsychiatrischen Versorgung INFOS UND LINKS ZUM HAUSTHEATER „SEXUALITÄT“Theo Kienzle (2016): Vortrag: Gibt es ein Recht auf Sexualität? https://youtu.be/fypsHK2jio4Christian Müller-Hergl (2016): Vortrag: Sexualität und Alter: https://youtu.be/zryiG5e6I1kStephanie Klee (2016): Vortrag: Sexualassistenz in der Praxis. https://youtu.be/zx2Vq4wj4-8Stephanie Klee (2016): Interview: Sexualassistenz in der Praxis. https://youtu.be/BNra26Yz7mgMGEPA (2015): Abschlussbericht Runder Tisch Prostitution. https://www.aids-nrw.de/front_content.php?idcat=2504&idart=6331Royal College of Nursing (2018): Older People in Care Homes: Sex, Sexuality and Intimate Relationships An RCN discussion and guidance document for the nursing workforce. https://www.rcn.org.uk/professional-development/publications/pub-007126 Folge direkt herunterladen

I first became aware of Sarah when she shared a video clip on twitter of her waiting for an appointment sitting in her wheelchair. Her voice was strained and she was a bit difficult to understand, but as soon as Sarah was in a horizontal position her voice was clear as a bell. I immediately reached out to Sarah to learn more about her incredible health care journey.  Doctors diagnosed Sarah with Schizoid Affective Disorder and gave her antipsychotic medications. When those didn’t work, they gave Sarah over 116 rounds of electric shock therapy  - they put electrodes on Sarah’s temples and zapped her with electricity so her brain had a seizure. Doctors also had Sarah on 5 classes of psychiatric medications amounting to 37 different combinations. In spite of this, for 12 years Sarah lived with voices in her head 24/7 telling her how and why to kill herself - all while working toward her Masters Degree. As Sarah would eventually discover with a proper diagnosis, her psychiatric symptoms were not from schizo affective disorder, they were from hepatic encephalopathy and her brain was marinating in toxins. Once Sarah received proper treatment the voices disappeared. But that’s not the end of Sarah’s story - all those electric shock treatments have damaged Sarah’s brain affecting her speech, memory, and ability to walk.  We had to end Sarah’s interview prematurely as you’ll hear, when she was overcome with dizziness, her speech quickly deteriorated, and she had to lie down on the floor to remove the pressure on her brainstem. Listen to how Sarah’s voice changes during this - Sarah’s final words are in the voice she had before electrical brain injury. SHOW NOTES First Psychosis 0:06:30 Sarah grew up in sunny San Diego, a 3rd generation San Diegan - wonderful parents, but struggles like all families - Sarah is the oldest child and only daughter - when frustrated her Dad would say 'Well Sarah, I've not had a daughter before' - she has 2 younger brothers - her parents did their best to provide a loving and supportive environment 0:08:30 Sarah's Mom is a wonderful lady, but they did butt heads - they have reconciled and Sarah considers her Mom to be one of her best friends now - after high school Sarah moved to Rexburg, Idaho where she learned about living in snow and -30 Fahrenheit 0:09:30 Sarah went to a college made famous by (the film) Napolean Dynamite, called Rex College, but now known as Brigham Young University Idaho - graduated and transferred to BYU (Brigham Young University) in Provo, Utah - after 1 semester studying English, Sarah served a mission for Church of Jesus Christ of the Latter Day Saints and learned to speak Spanish and serve the people of Texas - after 18 months Sarah was invited to join the American Sign Language program and worked for 2 months with deaf people - and then returned home to BYU 0:10:30 Sarah had bad chronic and seasonal allergies causing asthma, sinus infections and bronchitis - growing up Sarah had been given a lot of antibiotics, like 4 - 8 times a year throughout childhood through her Mission - she got pneumonia when she got back and was put on another antibiotic and within a few doses had her first psychotic break 0:11:30 Sarah was on campus trying to find her way and she could see people dressed in pioneer era clothing - she was hauled off campus and put in the psych unit and put in a straight jacket for more then 36 hours 0:12:30 That was scary because she didn't know why they were putting her in a straight jacket - it was a very vulnerable place to be - that brought up childhood traumas she had with a babysitter - being in a straight jacket was very traumatic 0:13:30 Initially they told Sarah she was Bipolar with Psychosis - then was labeled with Schizoid Affective Disorder with Bipolar type, meaning she had symptoms of schizophrenia and bipolar - then the medication they gave Sarah could not be metabolized by her body and she became catatonic - they didn't realize ammonia was marinating in her brain - it took about 4 years of those meds before she became completely catatonic 0:14:30 In those 4 years, Sarah was able to take 1 class at a time - she was determined and worked hard to get her degree in 8 years - Schizo Affective Disorder has symptoms of schizophrenia 0:15:30 'Positive' symptoms are 'added' to the patients experience: they see, hear, taste things others don't - 'negative' symptoms 'take away' from the person: motivation, ability to speak, organize thoughts and environment - those are the 'schizoid' part - 'affective' refers to mood0:16:30Lots of mental illnesses have affective disorders: mania with high energy, difficulty following thoughts, rash decisions, depression, difficulty processing info and energy or connect emotionally with people Voices in her head 0:17:30Sarah's problem was mixed mania, so all the energy of mania, and all the symptoms of depression - plus symptoms of schizophrenia, so for 12 years Sarah lived with voices 24/7 telling her how and why to kill herself - her brain was marinating in toxins - every time she started to believe the voices, she became very proactive in seeking out help - that was interpreted as attention-seeking, not trying to prevent her own demise 0:18:30S arah would check herself into the hospital asking for help, and then be ridiculed for asking for help - she was called a 'frequent flyer' and a lot of things by staff, probably because they were frustrated they couldn't 'get the medications right' or thought Sarah wasn't being compliant - but Sarah always took her meds as prescribed, always filled her prescriptions on time because she had been trained to believe she needed those medications in order to survive, and she was not doing a very good job surviving 0:19:30 To Sarah, not taking the medications was not an option because she was told over and over that meds were the only way she'd be able to function - they kept trying different meds for psychosis, mood, depression, anxiety, and sleep - 5 classes of medications and Sarah cycled through 37 combinations and they played with the chemicals in her brain in order to find the 'right' combo that would stabilize her 0:20:30 It was difficult - they would try to make the hospital less welcoming so Sarah wouldn't want to come back because they thought she was attention-seeking - Sarah says 'dude, if I wanted to get attention I would do something good like write a book, or travel the world and set a record or something - nobody wants negative attention' 0:21:30 Sarah would endure strip searches every time she was hospitalized, which was every 3 - 5 weeks, but her father says it was more frequent because sometimes she'd be re-admitted within 72 hours - Sarah was marinating and they couldn't recognize that because there are not really any tests - they don't do cerebrospinal taps for these symptoms - they don't recognize encephalopathy very often unless its associated with seizures 0:22:30 Most doctors will just refer a patient to psychiatry instead of someone who understands encephalopathy - even a lot of encephalopathy not hepatic encephalopathy, her 1st diagnosis - and that wasn't diagnosed properly until 2.5 years ago - Sarah had learned a lot of adapting skills over the 12 years of hell 0:23:30 During that period because none of the meds worked, and Sarah became catatonic in 2002, they didn't do any blood work or brain scans to find out why she was catatonic, they just assumed they'd probably diagnosed her with schizophrenia - since she's not responding to the medications we'll give her a higher dose - when that didn't help, they said it was time to do shock treatment Shock treatment, aka ECT 0:24:30 They gave Sarah bilateral electroconvulsive therapy (ECT), where they put the electrodes on either side of her forehead and used 460 volts of electricity to briefly stimulate the brain into a gran mal seizure - they feel a therapeutic seizure should be at least 25 seconds - so if the patient doesn't seize for 25 seconds they will immediately give them more so they have another seizure - they gave Sarah ECT 3 times a week - but there was one time where she was ECTed twice in one day - every time a person seizes, the brain tries to protect itself and prevent itself from having a seizure 0:25:30 So they have to increase the voltage higher and higher - when there at 100% charge, it is 0.9MC which is below 1.0mc of immediate death - at 100% and the patient still isn't seizing, they put in an IV with caffeine so that it pushes the brain and body to the brink so you'll seize 0:26:30 They have to push through the anaesthesia and mood stabilizers that prevents seizures - the first several were not at 100% of the machines strength, but Sarah had more then a 100 at 100%, and 60% were also with IV caffeine 0:27:30 ECT was invented in Italy in 1938 - Italy has since banned it - it was brought to America - they never did safety studies - they never did any kind of scientific decision making about appropriate dosage or methods to use - there more then are 7 variables involved - it is not standardized - it is not regulated - it has never been safety tested - some people feel ECT has saved their lives - others feel ECT has destroyed their lives 0:28:30 And families will tell how ECT killed their loved one - Sarah had 116 ECT treatments over 18 months - from 2002 to 2004 - then over 14 months from 2006 to 2007 - Sarah quit against medical advice in 2007 - she was required to sign 'informed consent' before each ECT procedure, but they don't provide all the info - it says the most pressing concern would be headaches 0:30:30 Sarah had to tell them her biggest worry when filling out the forms, so she always put headache, as that was all she was told about potential side effects - but they don't understand the risks because they've never done longitudinal studies to see the long term effects or neurological factors or even addressing patient satisfaction because the the surveys get a very low response rate, like 28% - and then say of the 28% who returned the survey, 80% were happy 0:31:30 But some of those people who could not put the stamp on the letter, or needed help filling it out, or were so angry at what had been done to them that it would go immediately in the garbage - Sarah says it is interesting when you start to look at the research and ask critically 'what are they not telling us?' What are the holes in the methodology? They will use the MMSE (mini mental state examination) a simple 18 question test for brain injury and dementia 0:32:30 What they don't say is that the MMSE can be passed by people who've had lobotomies - so it is immaterial, it can't be used at school or work for accommodations - so not a good measure of the damage actually caused, but it is the most used assessment for people having ECT....if they're given an assessment, but most people are not Memory loss 0:33:30 Sarah can't remember the first few ECT treatments because she can't remember the first 36 years of her life - she's lost 85-90% of her memories - she was 34 years old when she stopped ECT, but it took another 2 years for her brain to start to make new memories - Sarah has 38 journals and she reads them frequently so she knows what has happened in her life - so unless she's read it read recently, she wouldn't be able to tell many specifics 0:34:30 When Sarah 12 years old a Sunday School teacher told her about Wilford Woodruff who wrote in a journal every day by the time he was 90 he had many volumes - at the time Sarah wanted to be a writer and decided she would journal daily - she's very grateful, without them she wouldn't know about family vacations or formative experiences - she doesn't remember her grandparents and holidays - all our life decisions are based on our previous experience and memories - our relationships are based on shared memories 0:35:30 It can be very challenging living without formative memories - Sarah had a massive identity crisis because she didn't know the symptoms of memory loss 0:36:30 When Sarah looks at pictures with her family, its like playing 'Where's Waldo' because if she can find herself in a picture, she knows she'd been there, but it doesn't trigger any memories - it has been a grieving process about her loss, but she's learned its not helpful to focus on her loss, she needs to be moving forward because she has a life that still needs to be lived 0:37:30 In 2015, Sarah was on her 37th combo of meds - she'd been on meds for 17 years and her meds just stopped working - they generally only work for 5 years, part of that the brain has become dependent and the dose has been raised as high as they can 0:38:30 Sarah had just been married, had just finished her Masters and just started working full time when her meds stopped working and she was scared spit less and she didn't want to freak out her husband who had never seen her when she was very symptomatic, and she didn't want to lose her job or all her colleagues have know because Sarah worked so hard to establish herself as a professional - she also worried about her family because she was finally starting to re-build bridges that had been burnt when she was very symptomatic 0:39:30 Sarah was trying to minimize her symptoms, but was very scared - a friend had been trying to get Sarah interested in micro-nutrition, but Sarah had put her off for 18 months - Sarah is a scientist at heart and the friend gave her the research to review - randomized control trials, solid methodology, so Sarah took the info to her psychiatrist and they decided to taper Sarah off the meds - but psychiatry is not prepared to taper people off meds 0:40:30 Sarah started taking the micronutrients and after a few weeks started to feel cognitively weird so talked to the manufacturer - they said you've been over-medicated and should taper off the meds, your brain now doesn't need the medications as much An accurate diagnosis: Hepatic Encephalopathy 0:41:30 The psychiatrist says that Sarah is 50mg over the upper limit of the antidepressant, so they cut that 50mg first - Sarah never understood withdrawal until she worked with someone who didn't understand tapering - it was a very scary process, caused a lot of problems 0:42:30 They learned to support Sarah's body by supporting it enzymatically , a lot of amino acids, specifically protein isolate to support her blood sugar - she drank shakes every 90 minutes and she would function very well, but if she missed the protein isolate shake she would deteriorate very fast 0:43:30 Sarah had a friend who was getting amino acid IV, so Sarah started looking and found Dr John Humiston and he recognized the symptoms of withdrawal - by this time Sarah had been off the meds for 18 months - he said they first needed to get her gut healthy before amino acid IVs 0:44:30 Sarah was like 'dude, food has never affected me, hurt or harmed me, don't worry about it' - but he had Sarah track her diet and then cut out fermented foods, sprouted food, nuts, dairy, a whole swath of food - he recognized all those antibiotics Sarah had as a child caused an overgrowth of candida and that caused hepatic encephalopathy - Sarah went home and cleared the kitchen of foods that did not meet the new diet 0:45:30 Within 3 days, the psychosis Sarah had been experiencing left and she hasn't had it since - except once when she took an antibiotic for a kidney infection - by the 2nd dose she was being followed by someone she knew was dead 0:46:30 And being talked to by a dead ancestor - by the 3rd dose she was paranoid, pacing, pulling her hair out, non-verbal, shaking, sweating - her family took her to the ER but she didn't want to go back and being given meds, she'd just gotten off them - Sarah knew she needed to occupy her mind with something systematic, so she began folding paper, tearing it, just doing something very basic 0:47:30 When the psychiatrist saw the very tiny pieces of paper he asked Sarah what was going on - she said she thought he had cameras watching her, but she realizes her brain is on fire and she needs to reign it in - he looks at Sarah and said 'I've never had anyone say that before - tell me more' - Sarah told him she was faculty as San Diego State University and teach in the clinical classes about psychiatric rehabilitation and recovery and this is one of the strategies I teach people who are dealing with false voices that are distressing and they need something simple as distraction - he says 'you're doing a good job, you can go home' - that was the 1st time Sarah had gone to an ER and walked out 0:48:30 Sarah says we have yeast producing bacteria in our stomach to process food, and when they ferment our food they produce over 20 different alcohols as by-products, in small amounts is no big deal - but if you have fungal over growth they produce a lot of by-products Dystonia 0:49:30 That goes for bacterial by-products too - we need to have a healthy balance of bacteria, yeast and fungus in our guts, if we don't these by-products start producing too much of these alcohols like acetone, acetate and start marinating the brain and can cause problems with behaviour, emotion, sleep, autoimmune - because brain and body trying to maintain healthy balance - Sarah found a doctor who put her on anti-fungal medication and within 3 days all of her psychiatric symptoms were gone 0:50:30 Sarah tries not to dwell on the fact that a strict diet and anti-fungals may have prevents 17 years of suffering - missed out getting married earlier, missed out on having kids, missed out working and earning a retirement, missed out on family events 0:51:30 It caused a lot of strife and hardship on Sarah's family - if she dwells on it she gets pulled into the 'poor me' gravitational pit, so Sarah works hard on re-focusing on gratitude and here and now, and focusing on what she can do to prevent this from happening to other people - Sarah has to make meaning of her experience, its the only thing she can do 0:52:30 Sarah takes that sense of oppression, injustice, being misunderstood, misjudged, judged harshly - Sarah needs to make sense of her experience so that she can feel like what she went through was not in vain - Sarah has been on the strict diet for 2.5 years and must adhere to it 0:53:30 She was on anti-fungal meds for a looooong time: 18 months - since she'd been infected for a looooong time - she still takes supplements to support her gut - but about 7.5 years after the last shock treatment, Sarah experienced a worsening of neurological symptoms, worse then she'd ever had before - problems with muscle twitches (fasciculations) and fatigue easier, problems with her voice 0:54:30 Sarah started to have dystonia, especially the muscles in her neck, and started have dizziness when exposed to a lot of visual or auditory hallucination - so in the car this past April, she was driving for about 45 minutes and by the time she got to University to teach, she had difficulty standing to get out of her car 0:55:30 Sarah started to have muscle contractions on one side of her body, she didn't realize she'd been over-stimulated driving - she then drove to her doctors appointment, a 50 minute drive, and then started to have muscle contractions on the left side of her body and pull her it into a contorted position 0:56:30 Sarah then started to feel a current of electricity down her sternum with diaphragmic paralysis - then she'd be able to breathe again - then the right side of her body would have contraction and contort her body into weird positions - in went back and forth for the next 4 hours - it was intense at first, then less so with more time between - her doctor started to refer her to a neurologist and she saw lots of them Iatrogenic hot potato 0:57:30 When they see Sarah has a history of shock treatment, then the orders for their testing don't get placed, for brain scans, EMGs, etc - instead Sarah is referred to another neurologist, and so and so on - Sarah is now on her 7th neurologist - Sarah has become an iatrogenic hot potato - she thinks the neurologist recognize that she was harmed by treatment, so they keep passing her along 0:58:30 Finally Sarah found a functional neurologist, he was first a chiropractor then did 2 years of neurology - he did VNG (Videonystagmography) - they put goggles on Sarah to track her eye movements and move dots in her vision - supposed to be 45 minute test in a bunch of different ways 0:59:30 The interesting thing was they were able to create a concussion response - with that stimulation, one of Sarah's pupil's was huge - they stopped the testing and said they needed to let her brain rest, and then continue the testing later 1:00:30 A decade previous, Sarah found a brain injury specialist, and she asked why Sarah why she was wearing sunglasses indoors, Sarah said 'when I take them off I get a bad headache' - the specialist said 'oh, you have a brain injury' and Sarah said 'no, I had shock treatment' - the specialist said shock treatment is brain injury - but Sarah protested that her doctor told her the symptom would go away - since then, Sarah has learned through research that one doctor, a neurologist at Berkeley, outspoken against ECT spoke at the New York State Assembly 1:01:30 He told them the ECT put out 100 joules of electricity, that is the equivalent force of dropping 73 pounds (30 kg) onto a brain from a foot (33 cm) above it - for Sarah that was 116 times, so essentially Sarah has a repetitive brain injury and developed the bulgar symptoms seen in people with motor neuron disease 1:02:30 Motor neuron disease have 4 risk factors: people with ALS get it due genetics; people with toxic exposures; people with a history of electric injury; people with history of repetitive injury - Sarah doesn't have the genetic component, but does have the other 1:03:30 Sarah neurologist says she probably has a conversion disorder since she's not happy with her ECT experience - Sarah says that doesn't explain the saliva problems, speaking problems, breathing problems, thinking, walking, heart, etc - Sarah found a good GP who would order the tests the neurologist wouldn't order so she can take the results to the neurologist 1:04:30 The ECT research is constructed so that they don't talk about electrical injury - they never track patients more than 9 months - delayed electrical injury happens 2.5 to 10 years after treatment - Sarah's onset was about 7.5 years after her last ECT - and Sarah has worsened since then 1:05:30 Research on delayed low voltage electrical injury have studied quite a few people - low voltage is less then 1,000 volts - electrical injury has 2 components: the immediate effect - for Sarah this was memory loss, balance issues, proprioception issues Delayed electrical injury 1:06:30 Aphagia, word finding problems, executive function - but they've realized that a lot of people with electrical injury have 'delayed electrical injury' - that research shows a lot of motor neuron problems - it fascinating they've been able to separate these 2 things (electrical injury vs ECT) 1:07:30 But natural law doesn't respond to benevolent intent - good intentions is not going to change how the human cell responds to electricity - it is so apparent that delayed electrical injury and ECT survivors share the same speech, swallowing, dystonia 1:08:30 Fatigue and dropping things because no longer have ability to hold them - we're on a spectrum - Sarah knows 4 people who've had ECT and are on that symptom spectrum - it needs to be studied - Sarah has annotated bibliography connecting the research on low voltage injury, delayed voltage injury, and ECT and she needs it to be published 1:09:30 Doctors are siloed in their research and not connecting dots among themselves - they assume the organ they specialize in is not connected to the rest of the body - we can't have siloed research, they are excluding important data - Sarah would never have thought that her neurological symptoms had anything to do with the ECT if not for another person who had ECT and has similar symptoms to Sarah, and this person was forced to retire from being a trauma nurse 1:10:30 When the nurse heard Sarah's story, she told Sarah she had to look into electrical injury research - Sarah was like 'dude, I was never told any of this when I was given my 'informed consent'' - recently, one of the manufacturers of ECT devices had a lawsuit against them and they settled out of court 1:11:30 Shortly after that, the manufacturer updated their user guide, and buried on page 4 is '7 risks associated with permanent brain damage and permanent memory loss' - all the informed consents need to be update, internationally - patients need to know about the risk of permanent brain damage, permanent memory loss - a lot of doctors don't take these risks very seriously so don't inform their patients about them, and minimize the risks - because it is not standardized or regulated, every doctor does it differently 1:12:30 Doctors are never followed ECT patients longitudinally - an inpatient doctor will not be following up with that patient 5 or 10 years later, so they're not going to be seeing the effect that survivors are seeing among themselves - that is why Sarah started an international petition to update informed consent, update core competencies for doctors trained and certified to give ECT, pre-assessments and post-assessments to track longitudinally 1:13:30 When people starting having cognitive problems, they are not even assessed for brain injury and given rehab for a better quality of life - Sarah had to navigate living with ECT brain by herself, with her family saying 'the doctors said your memory would return, so get over it' and her doctor saying 'you'll get your memory back, so get over it' - it is a constant battle - going forward, if we had something safety tested......"Sorry, I'm getting dizzy" Sarah's speech deteriorates during interview 1:14:30 Scott: Sarah's speaking deteriorates - she says we should end the interview - I am concerned about her immediate well being - I ask if I should stay on the line with her to make sure she's safe 1:15:30 Sarah says she should lie down because "her brain stem does better when its not under pressure" and carries her laptop with her and lays down on the floor - Sarah takes a few breathes and says "Its like immediately" and voice is perfectly clear, unlike the entire interview when she was sitting up - I ask Sarah if she needs to call any one? - She says she'll just hang out on the floor for a while 1:16:30 Sarah says "Its weird to find your new normal. Who would've thought when you were a kid 'by new normal will be laying on the floor so I can think and speak clearly" - we laugh at the absurdity of it all - Sarah continues: when she did the research into the neuropathology of the animals they tested, and the autopsies they did in the '50s, all the animals had compressed brainstems from ECT - so Sarah's symptoms are very consistent with the animal studies - and consistent to what you would expect to see in a human 1:17:30 I ask Sarah if she's heard of 'cranio cervical instability (CCI)'? Sarah says she recently heard of someone with mold exposure who has CCI - I reply "Jen Brea" and Sarah confirms and says she has a history of mold exposure - the building she did her research has history of flooding and a bad roof - one time when she came home from vacation, she had left her air conditioning on in her small apartment, the water drain had plugged and that caused a water bulge in the paint - it took the building manager 3 weeks to replace the wall and carpe 1:18:30 You can't isolate any of things Sarah has experienced, as humans, our body keeps the score, it is influenced by what it is exposed to, and throughout our life, it becomes a cumulative effect - I tell Sarah that I will send her Jeff Wood's website link, Jeff is 'patient zero' for CCI and it was his experience that prompted Jen Brea to look into CCI 1:19:30 Jeff was bedridden for 3 years - they both had neck surgery and are almost completely symptom-free - Sarah says the idea of surgery scares her to death - she's been exposed to so many of the gaba drugs that she's developed acute respiratory responses when given anaesthesia - even lidocaine or novocaine will trigger phrenetic nerve paralysis - it will look like Sarah is having convulsions, but it is the frenetic nerve malfunctioning1:20:30Sarah says "My poor body, I'm doing the best I can, I'm only 44 years old and I'm having a lot of problems" CONNECT WITH SARAH PRICE HANCOCK: Twitter: @PsychRehab Facebook: Psych Recovery and Rehab Linkedin Website:http://www.psychrecoveryandrehab.com/ Podcast:https://www.psychrecoveryandrehab.com/esrpodcast/ Youtube:https://www.youtube.com/channel/UCMRPmYh9SrE3RcdmFObhyYw?view_as=subscriber Sarah's petition for ECT regulation and standardization: http://chng.it/rBGJNSKB5m  __________________________________________________________ Be a podcast patron Support Medical Error Interviews on Patreon by becoming a Patron for $2 / month for audio versions.  Premium Patrons get access to video versions of podcasts for $5 / month. Be my Guest I am always looking for guests to share their medical error experiences so we help bring awareness and make patients safer. If you are a survivor, a victim’s surviving family member, a health care worker, advocate, researcher or policy maker and you would like to share your experiences, please send me an email with a brief description:  RemediesPodcast@gmail.com  Need a Counsellor? Like me, many of my clients at Remedies Counseling have experienced the often devastating effects of medical error. If you need a counsellor for your experience with medical error, or living with a chronic illness(es), I offer online video counseling appointments. **For my health and life balance, I limit my number of counseling clients.**  Email me to learn more or book an appointment:  RemediesOnlineCounseling@gmail.com Scott Simpson:  Counsellor + Patient Advocate + (former) Triathlete I am a counsellor, patient advocate, and - before I became sick and disabled - a passionate triathlete. Work hard. Train hard. Rest hard. I have been living with HIV since 1998. I was the first person living with HIV to compete at the triathlon world championships. Thanks to research and access to medications, HIV is not a problem in my life. I have been living with ME (myalgic encephalomyelitis) since 2012, and thanks in part to medical error, it is a big problem in my life. Counseling / Research I first became aware of the ubiquitousness of medical error during a decade of community based research working with the HIV Prevention Lab at Ryerson University, where I co-authored two research papers on a counseling intervention for people living with HIV, here and here.  Patient participants would often report varying degrees of medical neglect, error and harms as part of their counseling sessions. Patient Advocacy I am co-founder of the ME patient advocacy non-profit Millions Missing Canada, and on the Executive Committee of the Interdisciplinary Canadian Collaborative Myalgic Encephalomyelitis Research Network. I am also a patient advisor for Health Quality Ontario’s Patient and Family Advisory Council, and member of Patients for Patient Safety Canada. Medical Error Interviews podcast and vidcast emerged to give voice to victims, witnesses and participants in this hidden epidemic so we can create change toward a safer health care system. My golden retriever Gladys is a constant source of love and joy. I hope to be well enough again one day to race triathlons again. Or even shovel the snow off the sidewalk. Remedies Counseling - Making Life Better Have you had traumatic experiences with the health care system? Are you living / struggling with a chronic illness?  Do you need a counsellor with proven expertise and experience to make life better? Book an appointment with Scott online at RemediesCounseling.com RemediesOnlineCounseling@gmail.com

Nootropic Treatments Address Specific PTSD SymptomsI was diagnosed with Adult ADD several years ago. Up to then I had no idea why I had a problem with focus all my adult life. Medication helped at first, but then didn't work as well, and I wondered what I could do. ~ David TomenPTSD Nootropics Address Treatment Failure"I had to find out if there was a way to deal with brain fog and ADHD naturally. Ritalin was able to help me focus. But was not helping in the memory and thinking department. Years of searching websites, reading stacks of books, and combing through the forums. And I was able little by little to get my brain working again. Better than ever before. With the right combination of supplements and lifestyle changes, I've been able to reduce my use of prescription stimulants. My business turned around, my relationship is better than the day we got married, and my brain is firing on all cylinders. And I continue to tweak and refine every area of my brain, cognition, and my own PTSD." My Thinking Problem Wasn't Dementia"A couple of years after the ADD diagnosis I ended up in the ER. And was told I was hypothyroid. A full-page, two-column list of symptoms including brain fog. Not only was I struggling to focus, but my memory was also failing. Episodes of not remembering dates and appointments, a failing business, and a crumbling marriage. I saw psychologists, doctors, endocrinologists, neuroscience specialists, and therapists. Two unrelated doctors tested me for dementia and early-onset Alzheimer's disease. One of the tests is the “Mini-Mental State Exam”. A “health professional” asks a series of questions designed to test a range of everyday mental skills. The maximum MMSE score is 30 points. A score of 20 to 24 suggests mild dementia, 13 to 20 suggests moderate dementia, and less than 12 indicates severe dementia. I got 30 points on every test. I didn't have dementia but suffered from cognitive disarray." Photo: alexander-andrews-421601-unsplash

For PT's working in residential facilities, two things are often true - most patients will have decreased ADL function, and there are not many studies addressing the effects of high intensity functional exercise on these populations.  Alyssa looks at an article that addresses theses concerns, along with the feasibility of including pts with decreased cognitive function (MMSE 10 or higher). linked article https://academic.oup.com/ptj/article/86/4/489/2805059 ------------ This episode is sponsored by the Academy of Geriatric Physical Therapy. Check out their FREE resources they've given you, listeners of SRP -http://GeriatricsPT.org/SRP Don't Forget! Early Registration for CSM ends soon.  The AGPT is offering 3 Pre-Conference Courses in DC before CSM kicks off. * Fundamentals of Tai Chi * How to apply a comprehensive approach to Successful Aging * How to effectively manage Kyphosis                              ------------ SRP is brought to you by the generous support of the SRP Game Changers. If you want to Join SRP, Crush Mediocrity, Join the Monthly Meetups, & Get some free swag!...go to http://SeniorRehabProject.com/Join

The American Academy of Neurology recently published the first updated practice guideline on mild cognitive impairment since 2001. Listen to this week's episode for an overview of the updated practice guideline, which includes a systematic review of prevalence, prognosis, screening, and treatment research with clear recommendations for practicing clinicians. Guest: Robert A. Baldor, MD, FAAFP

Anterograde - Unable to remember new thingsRetrograde - Unable to remember things of the pastPossible causes of amnesia:infection of the brain (meningitis)tumour in the braininflammation of the brainseisureIntervention due to mental health treatmentChronic alcohol users (confabulations)Accute stress distorder (psycholoigcal)Potential diagnosis methods:MOCAmini-mental state examination  (MMSE)electro encathelogramCT Brain scanIn Malaysia, traumatic brain injury is main cause of amnesia due to number of accidents.  Please wear safety gear, particularly helmet.No specific medication.Shoutout to PM LIVE! ###See me on MyDoctors on ASTRO Ria tonight - 19th Feb 2018 at 11pm, and every Monday after that.We are on Raku!  Thank you for hosting our podcast. www.raku.myFind me on twitter @DrAmerSiddiqPsy or #medtweetmy @medtweetmyhq or on FaceBook at DrAmerSiddiqPsych.  Looking forward to reading your comments and tweets!Also MyMentalHealth on Youtube - focusing more on Malay content

Measuring magnesium. MMSE test for diagnosing and predicting dementia. The cost of healthcare. Preventative vs. curative care. “Effortless power.” Benefits of fasting. Vegetable vs. fruit fasts. Traditional Chinese Medicine (TCM), Western Perspective, Integrative and Functional Medicine. Live streaming. The Balancing Point health radio talk show about Traditional Chinese Medicine, supplements, nutrition, and more.  Host Dr. [...]Read More »

Background: The National Institutes of Health Stroke Scale (NIHSS) is widely used to measure neurological deficits, evaluate the effectiveness of treatment and predict outcome in acute ischemic stroke. It has also been used to measure the residual neurological deficit at the chronic stage after ischemic events. However, the value of NIHSS in ischemic cerebral small vessel disease has not been specifically evaluated. The purpose of this study was to investigate the link between the NIHSS score and clinical severity in a large population of subjects with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), a unique model to investigate the pathophysiology and natural history of ischemic small vessel disease. Methods: Demographic and clinical data of 220 patients with one or more lacunar infarcts confirmed by MRI examination and enrolled from a prospective cohort study were analyzed. Detailed neurological examinations, including evaluation of the NIHSS and modified Rankin Scale score (mRS) for evaluating the clinical severity, were performed in all subjects. The sensitivity, specificity, positive and negative predictive values of various NIHSS thresholds to capture the absence of significant disability (mRS < 3) were calculated. General linear models, controlling for age, educational level and different clinical manifestations frequently observed in CADASIL, were used to evaluate the relationships between NIHSS and clinical severity. Results: In the whole cohort, 45 (20.5%) subjects presented with mRS >= 3, but only 16 (7.3%) had NIHSS >5. All but 1 subject with NIHSS >5 showed mRS >= 3. NIHSS

Background/Aims: The diagnostic accuracy of the German version of the revised Addenbrooke's Cognitive Examination (ACE-R) in identifying mild cognitive impairment (MCI), mild dementia in Alzheimer's disease (AD) and mild dementia in frontotemporal lobar degeneration (FTLD) in comparison with the conventional Mini Mental State Examination (MMSE) was assessed. Methods: The study encompasses 76 cognitively healthy elderly individuals, 75 patients with MCI, 56 with AD and 22 with FTLD. ACE-R and MMSE were validated against an expert diagnosis based on a comprehensive diagnostic procedure. Statistical analysis was performed using the receiver operating characteristic method and regression analyses. Results: The optimal cut-off score for the ACE-R for detecting MCI, AD, and FTLD was 86/87, 82/83 and 83/84, respectively. ACE-R was superior to MMSE only in the detection of patients with FTLD {[}area under the curve (AUC): 0.97 vs. 0.92], whilst the accuracy of the two instruments did not differ in identifying MCI and AD. The ratio of the scores of the memory ACE-R subtest to verbal fluency subtest contributed significantly to the discrimination between AD and FTLD (optimal cut-off score: 2.30/2.31, AUC: 0.77), whereas the MMSE and ACE-R total scores did not. Conclusion: The German ACE-R is superior to the most commonly employed MMSE in detecting mild dementia in FTLD and in the differential diagnosis between AD and FTLD. Thus it might serve as a valuable instrument as part of a comprehensive diagnostic workup in specialist centres/clinics contributing to the diagnosis and differential diagnosis of the cause of dementia. Copyright (C) 2010 S. Karger AG, Basel

Background: This article describes the methods of a door-to-door screening survey exploring the distribution of disability and its major determinants in northeastern Spain. This study will set the basis for the development of disability-related services for the rural elderly in northeastern Spain. Methods: The probabilistic sample was composed of 1,354 de facto residents from a population of 12,784 Social Security card holders (age: 6 50 years). Cognitive and disability screenings were conducted (period: June 2008-June 2009). Screening instruments were the MMSE and the World Health Organization Disability Assessment Schedule. Participants screened positive for disability underwent an assessment protocol focusing on primary care diagnoses, disability, lifestyle, and social and health service usage. Participants screened positive for cognitive functioning went through in-depth neurological evaluation. Results: The study sample is described. Usable data were available for 1,216 participants. A total of 625 individuals (51.4%) scored within the positive range in the disability screening, while 135 (11.1%) scored within the positive range of the cognitive screening. The proportion of positively screened individuals was higher for women and increased with age. Conclusions: Screening surveys represent a feasible design for examining the distribution of disability and its determinants among the elderly. Data quality may benefit from methodological developments tailored to rural populations with a low education level. Copyright (C) 2010 S. Karger AG, Basel

This Podcast for the Neurology Journal begins and closes with Dr. Robert Gross, Editor-in-Chief, briefly discussing highlighted articles from the print issue of Neurology. In the second segment Dr. Heather Harle interview Dr. Rod Adam about his paper on coccidioidal meningitis and brain abscesses. In the next segment, Dr. Ryan Overman is reading our e-Pearl of the week about isolated medial rectus palsy in midbrain infarction. The next part of the podcast is Dr. Alberto Espay interviews Dr. Daniel Weintraub for our Lesson of the week toolbox about MoCA vs MMSE. In concluding, there is a brief statement where to find other up-to date patient information and current Patient Page. The participants had nothing to disclosure except Drs. Espay and Weintraub. Dr. Espay has received personal compensation as a consultant for Boehringer Ingelheim; grant support from Codman; Medtronic, Inc; Allergan, Inc.; and CleveMed, and honoraria from UCB-SCHWARZ PHARMA AG; Medtronic, Inc. and Novartis.Dr. Weintraub has served on a scientific advisory board for Boehringer Ingelheim ; serves on the editorial board of Movement Disorders; has received honoraria from Boehringer Ingelheim, ACADIA Pharmaceuticals Inc., Novartis, Osmotica Pharmaceutical Corp., BrainCells Inc., Merck Serono, Sanofi-aventis, and Pfizer Inc; and receives research support from Boehringer Ingelheim and the NIH [#K23 MH067894 (Principal Investigator)].

Background: Neuronal and synaptic function in Alzheimer's disease (AD) is measured in vivo by glucose metabolism using positron emission tomography (PET). Objective: We hypothesized that neuronal activation as measured by PET is a more sensitive index of neuronal dysfunction than activity during rest. We investigated if the correlations between dementia severity as measured with the Mini Mental State Examination (MMSE) and glucose metabolism are an artifact of brain atrophy. Method: Glucose metabolism was measured using {[}F-18]fluorodeoxyglucose PET during rest and activation due to audiovisual stimulation in 13 mild to moderate AD patients (MMSE score >= 17). PET data were corrected for brain atrophy. Results: In the rest condition, glucose metabolism was correlated with the MMSE score primarily within the posterior cingulate and parietal lobes. For the activation condition, additional correlations were within the primary and association audiovisual areas. Most local maxima remained significant after correcting for brain atrophy. Conclusion: PET activity measured during audiovisual stimulation was more sensitive to functional alterations in glucose metabolism in AD patients compared to the resting PET. The association between glucose metabolism and MMSE score was not dependent on brain atrophy. Copyright (C) 2005 S. Karger AG, Basel.

The objective of the study was to identify clinical features that distinguish patients with dementia with Lewy bodies (DLB), who were classified as Alzheimer's disease ( AD) patients, from patients with AD. We examined a group of 27 patients from our memory clinic, originally diagnosed with AD, of whom 6 were postmortem found to have DLB. For the present study, we compared cognitive, noncognitive and neurological symptoms between the two groups. We found that there were no differences on ratings of dementia and scales for activities of daily living. Patients with DLB performed better on the MMSE and the memory subtest of the CAMCOG, but there was no difference in any other cognitive domain. Furthermore, genetic risk factors, including family history of dementia or allele frequency of the apolipoprotein epsilon 4, did not discriminate between the two groups, and there were no differences on CCT scans. Taken together, our findings suggest that Lewy body pathology may be present in patients who do not show the typical clinical features which distinguish DLB from AD. Copyright (C) 2005 S. Karger AG, Basel.

Background: White matter hyperintensities (WMH) on MRI scans indicate lesions of the subcortical fiber system. The regional distribution of WMH may be related to their pathophysiology and clinical effect in vascular dementia (VaD), Alzheimer's disease (AD) and healthy aging. Methods: Regional WMH volumes were measured in MRI scans of 20 VaD patients, 25 AD patients and 22 healthy elderly subjects using FLAIR sequences and surface reconstructions from a three-dimensional MRI sequence. Results: The intraclass correlation coefficient for interrater reliability of WMH volume measurements ranged between 0.99 in the frontal and 0.72 in the occipital lobe. For each cerebral lobe, the WMH index, i.e. WMH volume divided by lobar volume, was highest in VaD and lowest in healthy controls. Within each group, the WMH index was higher in frontal and parietal lobes than in occipital and temporal lobes. Total WMH index and WMH indices in the frontal lobe correlated significantly with the MMSE score in VaD. Category fluency correlated with the frontal lobe WMH index in AD, while drawing performance correlated with parietal and temporal lobe WMH indices in VaD. Conclusions: A similar regional distribution of WMH between the three groups suggests a common (vascular) pathogenic factor leading to WMH in patients and controls. Our findings underscore the potential of regional WMH volumetry to determine correlations between subcortical pathology and cognitive impairment. Copyright (C) 2004 S. Karger AG, Basel.