Podcasts about parkinsonian

Play Episode Listen Later Oct 2, 2024 76:48

In the October 2024 replay features four episodes on approaches to clinical diagnosis of parkinsonism. The episode starts off with Dr. Colin Hoy discuss the concept of prodromal Parkinson disease and the ethical considerations surrounding its diagnosis. The episode leads into a conversation with Dr. Chris Gibbons discussing skin biopsies to detect phosphorylated α-synuclein. In the third episode Drs. Michiko K. Bruno and Lawrence Golbe about a practical diagnostic algorithm for atypical parkinsonian disorders Drs. Michiko K. Bruno and Lawrence Golbe discuss a practical diagnostic algorithm for atypical parkinsonian disorders. The episode concludes with Dr. Eduardo De Pablo-Fernández talking about the strengths of DAT imaging in diagnosing patients with Parkinsonian disorders. Previous Podcasts: The Ethical Landscape of Prodromal Parkinson Disease Skin Biopsy Detection of Phosphorylated α-Synuclein General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders Interpreting DAT Imaging Results in the Clinical Context Article Links: The Ethical Landscape of Prodromal Parkinson Disease Skin Biopsy Detection of Phosphorylated α-Synuclein in Patients With Synucleinopathies A General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders Neuropathologic Validation and Diagnostic Accuracy of Presynaptic Dopaminergic Imaging in the Diagnosis of Parkinsonism Disclosures can be found at Neurology.org.

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A General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders - Part 2

Play Episode Listen Later Sep 23, 2024 2:21

In part two of this two-part series, Drs. Jeff Ratliff, Michiko K. Bruno, and Lawrence Golbe discuss essential advice for general neurologists who suspect a patient might have an atypical disorder. Show reference: https://www.neurology.org/doi/full/10.1212/CPJ.0000000000200345

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A General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders - Part 1

Play Episode Listen Later Sep 20, 2024 3:23

In part one of this two-part series, Drs. Jeff Ratliff, Michiko K. Bruno, and Lawrence Golbe discuss practical tips for recognizing when a patient's response to levodopa may indicate the need for an alternate diagnosis. Show reference: https://www.neurology.org/doi/full/10.1212/CPJ.0000000000200345

journal practical disorders algorithms drs pd neurology diagnostic atypical neurologists cpj parkinsonian jeff ratliff

General Neurologist's Practical Diagnostic Algorithm for Atypical Parkinsonian Disorders

Inside Lyme Podcast with Dr. Daniel Cameron

Play Episode Listen Later Sep 19, 2024 20:29

Dr. Jeff Ratliff talks with Drs. Michiko K. Bruno and Lawrence Golbe about a practical diagnostic algorithm for atypical parkinsonian disorders, emphasizing the importance of recognizing these conditions in clinical practice. Read the related article in Neurology: Clinical Practice. Disclosures can be found at Neurology.org.

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Unexpected Lyme Disease Presentations

Play Episode Listen Later Sep 1, 2024 3:35

Welcome! Today, we're discussing the unexpected and unusual presentations of Lyme disease that I've encountered in my practice.Case Study: Unexplained Foot Pain One of my patients experienced severe foot pain, even while walking to the bathroom. A podiatrist diagnosed him with plantar fasciitis, and he tried various treatments including icing, NSAIDs, stretching, iontophoresis, shoe inserts, and cortisone injections. Despite these efforts, his foot pain persisted. In addition to foot pain, he suffered from exhaustion, poor sleep, impaired concentration, neck and back pain, mood disturbances, palpitations, lightheadedness, migratory pains, and sensitivity to light and sound. Remarkably, his foot pain and other symptoms resolved following treatment for Lyme disease. Expected Lyme Disease Presentations In my practice, the expected presentations of Lyme disease include:- Erythema migrans- Bell's palsy- Chronic Neurologic Lyme disease- Neuropsychiatric Lyme- Postural Orthostatic Tachycardia Syndrome (POTS)- Pediatric Acute-onset Neuropsychiatric Syndrome (PANS)- Lyme carditis- Lyme arthritis Unusual Lyme Disease Presentations However, I've also encountered several unusual presentations of Lyme disease that resolved with treatment. These include:- Thumb pain- Intermittent blue color of the hands and feet- Distorted vision and floaters- Uveitis- Atypical seizures- Temporomandibular joint (TMJ) disorder- Tinnitus- Movement disorders- ALS-like and MS-like presentations- Parkinsonian symptoms- Dementia- Gastroparesis- Mold sensitivity- Small intestinal bacterial overgrowth (SIBO)- Mast cell activation syndrome (MCAS)- Ehlers-Danlos syndrome (EDS)- Median arcuate ligament syndrome (MALS)- Fibromyalgia- Chronic fatigue syndrome- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)- Functional and somatic disorders- Anxiety, depression, OCD, and ADHD The Challenge of Diagnosis It can be challenging to determine whether Lyme disease is the cause of these unusual presentations, as patients may have multiple conditions. Proper diagnosis and treatment are crucial for resolving these complex symptoms. Conclusion Understanding the wide range of Lyme disease presentations helps us better identify and treat this complex illness. If you or someone you know has unexplained symptoms, consider consulting a Lyme-literate doctor. Thank you for watching, and stay tuned for more insights on Lyme disease.

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Autoimmune Movement Disorders With Dr. Bettina Balint

Continuum Audio

Play Episode Listen Later Aug 28, 2024 21:46

Autoimmune cerebellar ataxia and other autoimmune movement disorders encompass a broad spectrum of different clinical syndromes, antibodies, and immunopathophysiologic mechanisms. Given the overlap between phenotypes and antibodies, panel testing in serum and CSF is recommended. In this episode, Gordon Smith, MD, FAAN, speaks with Bettina Balint, MD, author of the article “Autoimmune Movement Disorders,” in the Continuum August 2024 Autoimmune Neurology issue. Dr. Smith is a Continuum® Audio interviewer and professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Balint is an assistant professor for clinical research on complex movement disorders and Parkinson's diseases, a consultant neurologist, the head of the Department of Movement Disorders, and co-lead for the Centre for Movement Disorders and Functional Neurosurgery in the Department of Neurology at the University Hospital Zurich in Zurich, Switzerland. Additional Resources Read the article: Autoimmune Movement Disorders 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: @gordonsmithMD Full episode transcript available here Dr Jones: This is Dr 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 Smith: This is Dr Gordon Smith. Today, I'm interviewing Dr Bettina Balint about her article on ataxia and other autoimmune movement disorders, which appears in the August 2024 Continuum issue on autoimmune neurology, which is a highly anticipated and exciting issue. Dr Balint, welcome to the podcast, and, perhaps, you can just introduce yourself to our audience and tell us a little bit about your practice and how you became interested in this topic. Dr Balint: Thank you, Gordon, for having me. I am an assistant professor for clinical research in complex movement disorders and Parkinson's disease at the University of Zurich and the Head of the Movement Disorders Department at the University Hospital in Zurich. So while I'm originally German (from Heidelberg), I have now been to Switzerland since end of 2021. Dr Smith: So, you know, how many movement disorder chiefs have a focus on autoimmune movement disorders? I found that really interesting. Most of the movement disorder folks I interact with, their primary interest is in neurodegeneration. Dr Balint: Very good question. Even so, I never asked myself that question, really, but I think I'm the only one with this designated focus as such. Many people come from the neurology angle - most of them. Even so, movement-disorder people really welcome this field and are interested, but I think somebody who has dedicated their interest and time to it? I think I can't actually think of many other people. Dr Smith: Yeah, I think it's really cool, and, of course, autoimmune neurology is the flavor of the day these days, right? I mean, I remember when I was at the University of Utah, we were recruiting Stacy Clardy (who I think many of our listeners will know). I remember thinking, you know, she's never going to be busy. How many of these autoimmune problems are there, really? And she was, like, deluged when she came. These are really common problems. I guess that was one question I had for you. You know, we think of these as rare disorders, and when we look at the article, you have these tables of these antibodies, and a lot of them are pretty uncommon – but, cumulatively, how common are autoimmune movement disorders? Dr Balint: It's a very difficult question, because we don't have good epidemiological data. And if you look at series, I mean, most papers addressing this issue come actually from the ataxia field. And then, depending on where you look at, you might find varying numbers, and they might be also influenced by the fact that they come from ataxia centers with own certain biases. Even so, it's very close to my heart, but, I also still think it's overall very rare. So, in my practice, I see all sorts of movement disorders, and overall, they're still quite rare, but the point is that they are treatable and have important management implications, so you want to be sure not to miss any of them. Dr Smith: Well, maybe we can go to that next. Part of the challenge here, of course, is there's just so many of these different syndromes and antibodies. Are there pearls that you can provide our listeners that would help them guide when they should be thinking about these disorders when they confront a patient with a particular phenotype? Like ataxia, for instance - you know, there are certain aspects of the clinical scenario that should trigger, “Wow, this might be an autoimmune problem”. Dr Balint: So, in general, I would say there are certain scenarios where you would want to think of an autoimmune etiology in your differential. One is a very characteristic phenotype. So, speaking broadly in terms of movement disorders, stiff-person spectrum disorders have a very characteristic phenotype which you need to recognize, and then you will be able to see it when a patient enters. Important phenotypes to know which are very characteristic are faciobrachial dystonic seizures, for example, with anti-GA1 antibodies, or pseudofinalistic movements in non-REM sleep is IgLON5 antibodies, leg myoclonus is CASPR2 antibodies. I don't want to necessarily enumerate all the scenarios. The point here is there are some characteristic phenotypes where you would think of autoimmune neurology. Another scenario where you would think of autoimmune, for example, the context of late-onset paroxysmal movement disorders. So, classically, when we think of paroxysmal dyskinesia, we think of a group of genetic disorders, but if somebody develops a paroxysmal movement disorder later in life in adulthood, then you would think of autoimmune neurology, and this applies also in the context of episodic ataxias. Another red flag might be a propensity to autoimmunity. For example, somebody with type one diabetes and vitiligo coming in for cerebellar ataxia, of course, you would think of anti-GAD ataxia. And, similarly, if somebody has recently been diagnosed with a cancer and develops a rapidly disabling syndrome, of course, then you would think of a paraneoplastic autoimmune disorder. And with autoimmune syndrome, there are some symptoms which are also like tell-tale signs. So, for example, somebody with a stiff-person spectrum disorder, an ataxia with long-lasting diarrhea over months, losing weight - investigations haven't found anything, then you would think of DPPX antibodies or celiac disease. Or, if you have, like, a neuropathic pain which is otherwise not explained, then you might think of CASPR2 antibodies in somebody with a cerebellar ataxia. So, there are some features of some antibodies. (Again, I will not now list all of them which might point you to a diagnosis.) Then, of course, another scenario which is important, I think, is if you have a hemisyndrome without a structural lesion on imaging. Classically, neurologists are trained to think of a hemisyndrome - we look for a lesion on the contralateral side. But if you have, like, for example, a hemichorea without a lesion or a hemiataxia without a lesion, one should also think of an autoimmune disorder with antibodies. And then, more generally, of course, if you have changes on brain MRI or information on CSF, of course, if the clinical cause is more rapidly progressive - and last, but not least, if somebody does not really fit into our categories of the degenerative symptoms or metabolic syndromes or functionality disorders, then, of course, one should just take a step back and think, could it be something autoimmune? Having said that, if I may, I just want to say that, I mentioned that rapid disease course, and on the other hand, it's important to stress that a slowly progressive disease cause does not exclude an autoimmune etiology. Dr Smith: So, that was a great summary. Thank you. I don't know if you're familiar with the term “Aunt Minnie” (something I learned in medical school and radiology). There are certain findings that are “Aunt Minnie”, you know what “Aunt Minnie” looks like, and if you see these particular findings, you should really think about a specific disease - and I think you gave a lot of pearls in that answer, so I appreciate that. This may seem like a bit of a random question, but it's interesting that there are some of these phenotypes that do replicate genetic phenotypes, and you used episodic ataxia, which, in a younger individual, we think of a spectrum of various genetic disorders. Is that random, or are there instances where the underlying mutation in a genetic disorder actually serves as a target for autoimmunity in a later-onset autoimmune problem? Not that the mutation causes autoimmunity, but are there shared targets - in one disease it's the mutation, and another, there's an antibody that binds to the protein, for instance? Dr Balint: That's an excellent topic, and even though it's not addressed in the Continuum article, I actually covered this in an article in Brain from 2018, where we also discuss parallels (immunogenetic parallels) with targets seen in genetic disease or in autoimmune disease, and there are actually some examples for cerebellar ataxia, and some of the targets are, indeed, the same for the antibodies and mutation. And some targets are a little bit more difficult, because for those, the antibodies would probably not be pathogenic, but it's more like an autoimmune overall target but it's T-cell mediated. But, for example, water-gated, um, calcium channels - we have antibodies and we have mutations. Or, another example would be glycine receptor antibodies give you acquired hyperekplexia, whereas the mutations give you hereditary hyperekplexia. So, there is, indeed, a bit of an overlap between autoimmune and genetic disorders, but often, also, like, the age at onset (because that might be the next question, the age at onset), and maybe family history and associated features, should help to distinguish the two. I think more from the pathophysiological point interesting, rather than clinically too confusing. Dr Smith: Wow, that's really cool. So, another question I have is regarding antibody panels, right? And so, I think, oftentimes (at least around here), folks confronting an unusual phenotype will send the Mayo panel - they'll send autoimmune encephalitis or a paraneoplastic panel – and, you know, I think one of the challenges I have thinking about the spectrum of phenotypes that you described, I mean, if you recognize “Aunt Minnie”, then you know where to go, but it seems to me that there's a lot of these that maybe folks don't recognize “Aunt Minnie”. What is the diagnostic utility and pearls and pitfalls of ordering these panels when you're not really certain? In other words, is there a risk of a false positive if the pretest probability is low? So, I guess that's a long question, but do you have guidance about when we should and maybe when we should not be ordering these panels? So, you know, undifferentiated ataxia that's chronically progressive - should we be sending a panel or not? Patients who are later-onset acute, maybe so. So, what's the guidance on when to order the panel? Dr Balint: It's a tricky topic also for many people in our practice, because, of course, as you said, we don't want to miss something, but, indeed, with any test which you order with a low pretest probability and which is not quite appropriate, you might have false positives, and that might cause much additional trouble in security, or maybe unnecessary and invasive immunotherapy with adverse effects – so, it's really important to think well about antibody testing. And, generally speaking, like always in medicine, we shouldn't order random tests, and antibody panels and neuronal antibodies are not designed as a screening test, so you need to have a phenotype and a reasonable suspicion - and clinical acumen is really key, and that's why also the article is so much focused on the phenotype. It's clearly not that any movement disorder patient who enters the outpatient clinic should get a blood test for antibodies that will likely cause harm, and it has been shown that these antibodies can be falsely positive, both in other diseases but also in healthy controls, and much depends also on which tests you use (but, let's not go into too much detail over here) - so, generally speaking, I would say if you have a suspicion of an autoimmune disease clinically (I mentioned some scenarios where you would think of an autoimmune disorder). And then, ataxias are, of course, a bit tricky, because often, we don't have too many other handles there, and there's still also a significant number of acquired late-onset ataxia where we don't know what the cause is. I think in the ataxia scenario, if I don't have a good answer or explanation, I would order antibody tests a bit more freely - I mean, if you do it properly, you do the serum and the CSF, and that also increases your sensitivity but also the specificities, so I wouldn't then just do the serum, but then go for serum and CSF. In other movement disorders, it depends also a little bit on the phenotype. So, somebody with a phenotype fitting well with Parkinson's disease, I wouldn't do any testing. Somebody with clear PSP phenotype without any red flags or not-fitting features, it is very unlikely to have an antibody finding, and this has been shown also in cohorts. But, if you have something which is not fitting in the phenotypes - for example, you have somebody where you think it might be a PSP phenotype with predominantly axial Parkinsonism falls, but you notice that the oculomotor disturbance is not a vertical gaze palsy, but a horizontal gaze palsy – so, it's not really fitting phenotype as you know it. That's a scenario where would probably think of antibody testing. Then, if you do the testing theorem - and CSF, in general, is gold standard - there are some antibodies where theorem is good enough (like, for example, with aquaporin-4 antibodies), but the reason why we do serum and CSF, as I mentioned, is the increased sensitivity and specificity. And nowadays, in the antibody world, we have something similar to the genetics - we have the variant of unknown significance and in the neurology world, we coin the term “antibody of unknown significance” to also give a name to the problem that, sometimes, we get a test result and it is difficult to interpret. Another handle over there would be to try to confirm the test result in another test method. So for example, if you have a cell-based assay with an antibody finding, you would like to confirm that on immunohistochemistry - the staining pattern is in keeping with that. Dr Smith: So, Bettina, that was a really great and comprehensive answer to the question with a lot of pearls packed into it, and I think the idea that, you know, oftentimes, it's helpful to do both serum and CSF testing is important - also looking for staining to further confirm the diagnosis. And, I think one of the things that I was struck by in your response was the example of a PSP patient who instead of vertical gaze palsy had horizontal gaze palsy as a red flag, and I think a lot of our listeners are probably familiar with the idea that maybe hyperkinetic movement disorders might be autoimmune, or certainly rapidly progressive ataxia, but at least I don't think of Parkinsonian syndromes as often. I know there are some that we need to consider. Maybe you can give us some pearls about when we should consider antibody testing in a patient who has a Parkinson syndrome? Dr Balint: So, I will not cover now the paraneoplastic Parkinsonian syndromes (because they typically develop as rapidly that you would anyway think about it, hopefully), but go more into those conditions which might mimic degenerative disease - and one of the most interesting antibodies in this regard is IgLON5, and you will be aware that it has been discovered in 2014 in patients who shared a characteristic sleep movement disorder (non-REM parasomnia). The spectrum has broadened a lot, and one possible manifestation is that it could come into the differential of Parkinsonian syndromes - so, for example, if you have axial Parkinsonism and a gaze palsy, you are in a PSP phenotype, but the red flag would be maybe if the eye movement disorders are not really fitting with the PSP phenotype. Also, in PSP patients, we don't expect parasomnias at night. If the bed partner is, for example, complaining that the patient is moving in his sleep and doing movements, then this would be a red flag, and in this context, you would think of IgLON5. IgLON5 could also give you Parkinsonism and cerebellar ataxia, and they might have dysautonomia, and, of course, with a sleep movement disorder, you are now in the ballpark of MSA phenotypes; however, if there are additional features (like, for example, fasciculations) which you don't expect in MSA, that would be, again, the red flag. So, typically, even in those differentials, there are some red flags on handles which would point you to the diagnosis - it is not that it completely mimics the phenotype of our default degenerative disease, but, sometimes, you need to hunt a little bit for those handles. Dr Smith: So, Bettina, that's really interesting. I wanted to ask you about IgLON5, and in particular, the sleep phenotype, but, you know, I wonder whether there's a risk of just confusing this with REM sleep behavior disorder and a chronic Parkinsonian syndrome - what's the time course of this, and any other wisdom in terms of how to differentiate it from, you know, a more common neurodegenerative problem? Dr Balint: So, the spectrum of sleep disorders in IgLON5 is actually a bit broad. The characteristic thing is the non-REM sleep parasomnia with the finalistic fine movements, but classic REM sleep behavior disorder has also been reported in these patients. And one of the tricky things is IgLON5 is a slowly progressive disease (some patients had symptoms for a decade prior to diagnosis), so it's really an important differential of autoimmune disease - but as mentioned, the features not fitting in, and they are typically also the cardinal features. So, gaze palsies are very frequent, ptosis, bulbar symptoms, vocal cord palsy, sleep movement disorders which might not fit to the original phenotype, and breathing problems (for example) so severe that they require a tracheostoma – so, these are some red flags which would alert you to this diagnosis of anti-IgLON5 disease. Dr Smith: I'm curious, Bettina, how do you keep up on all of this and keep it all straight? Right, there's a lot of information, and as I was reading your article, you've got these wonderful tables - and in fact, this whole issue for our listeners feels that way. I've read several of these articles now, and I'm just curious what your strategy is to stay up to date and stay organized. You have to be very organized to be an autoimmune neurologist, it seems to me. Dr Balint: And having a little bit of OCD helps clearly, as always, in neurology. I think it is just that I started to be interested in this area for a while and I have in my head the clinical phenotype to most important associated antibodies, and as the field continues, I just add up on that panel. But, I don't want people to be discouraged - you're right, many antibodies, but I think the point is not to know each and every antibody but to know in which scenario to think of an autoimmune syndrome and then to know where to look it up. Dr Smith: Well, I think that's a great way of ending our conversation, Bettina. I think your article does a great job of that, and one of the things I love about Continuum is these articles serve as point-of-care tools. I think our conversation will also serve as a useful framework, because I think you've talked a lot about how to organize your thinking, and, you know, pearls for when we should be thinking about these disorders which are uncommon, but you certainly don't want to miss one because the therapy can be very effective. So, Bettina, thank you so much for joining me. This has been a really great conversation. Dr Balint: Thank you so much, Gordon. Thank you very much for your good questions. Dr Smith: So, again, today, I've had the great pleasure of interviewing Dr Bettina Balint, whose article on ataxia and other autoimmune movement disorders appears in the most recent issue of Continuum, which is on autoimmune neurology. Be sure to check out Continuum Audio episodes from this and other issues. And thanks 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.

Interpreting DAT Imaging Results in the Clinical Context

Play Episode Listen Later Aug 16, 2024 1:37

Dr. Jeff Ratliff and Dr. Eduardo De Pablo-Fernández discuss the strengths of dopamine transporter imaging or DAT imaging in diagnosing patients with Parkinsonian disorders. Show references: https://doi.org/10.1212/WNL.0000000000209453

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Interpreting DAT Imaging Results in the Clinical Context

The Adam and Dr. Drew Show

Play Episode Listen Later Aug 15, 2024 18:03

Dr. Jeff Ratliff talks with Dr. Eduardo De Pablo-Fernández about the strengths of DAT imaging in diagnosing patients with Parkinsonian disorders. Read the related article in Neurology. Disclosures can be found at Neurology.org.

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#1886 Overlearned Material

Play Episode Listen Later Jul 3, 2024 35:33

Adam and Dr. Drew kick off the week discussing the recent, and first, presidential debate, Adam introduces Drew to the great Sugar Ray Leonard and Robert Duran, and Parkinsonian signs explained. Plus, cheap fakes and hands of stone! Leave us a voicemail: SpeakPipe.com/AdamandDrDrew OR Click the microphone at top of the homepage, AdamandDrDrew.com

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June 19th 2024 Queer Voices

Queer Voices

Play Episode Play 60 sec Highlight Listen Later Jun 20, 2024 57:59 Transcription Available

Send us a Text Message.What if you were suddenly faced with a life-altering diagnosis? This week on Queer Voices, we have an intimate and heartfelt conversation with David Taffet, senior staff writer for the Dallas Voice and co-host of Lambda Weekly. David opens up about his recent diagnosis with Parkinson's disease, sharing the challenges he encountered with everyday tasks like handwriting and walking. Through his story, we also hear from host Bryan Hlavinka, who reveals his own experience with Parkinsonian symptoms, shedding light on the personal and communal support systems that play a crucial role in navigating such a condition.Shifting gears, we move from personal battles to communal triumphs with an insightful interview with Robert Wallace. Robert talks about the upcoming Pride Brunch fundraiser in Houston, which aims to support the Montrose Center. He shares the backstory of this significant event, his personal motivations rooted in honoring his uncle who succumbed to the AIDS epidemic, and the incredible growth and impact the brunch has had over the years. Expect exciting details about the event's entertainment, featuring performances by drag queens Cinnamon LaRue and Lucy Paradisco, and a panel discussion with the Montrose Center's new CEO, Avery Belyeu.We round out this week's episode by celebrating queer creativity and inclusivity. Deborah Moncrief-Bell engages with John Marullo about his political fantasy novel, "All the Dwellers Upon the Earth," discovering the queer magic that inspired its diverse characters. We also explore the concept of "Family of Choice," a notion familiar to many in the LGBTQ+ community. Elizabeth McCall from Station Theater joins us to discuss the transformative power of improv, highlighting special Pride Month shows with an all-queer cast. This episode promises to be an enriching mix of stories, support, and celebration of the vibrant and diverse LGBTQ+ community.Queer Voices airs in Houston Texas on 90.1FM KPFT and is heard as a podcast here. Queer Voices hopes to entertain as well as illuminate LGBTQ issues in Houston and beyond. Check out our socials at:https://www.facebook.com/QueerVoicesKPFT/ andhttps://www.instagram.com/queervoices90.1kpft/

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Terran Biosciences is Developing New Regimens for Schizophrenia Therapies

cc: Life Science Podcast

Play Episode Listen Later Jun 19, 2024 18:38

At BIO2024, I spoke Sam Clark, CEO and founder of Terran Biosciences, about their development of new long-duration dosage forms for the treatment of schizophrenia . We discussed the development of prodrugs, the potential of psychedelics, and the journey of founding a biotech company. The Genesis of Terran BiosciencesSam's journey into biotech was personal. Growing up around friends and family members with severe mental illnesses like bipolar disorder and Alzheimer's disease, he saw the limitations of existing treatments. Through his studies at MIT and Columbia, he recognized the slow pace of development and the significant side effects of available medications. Existing treatments for mental illnesses have many unpleasant side effects from cause weight gain to Parkinsonian symptoms and hormonal disruptions. All of that led to his decision to found Terran Biosciences hoping to transform the standard of care.Terran's PipelineTerran's lead asset, TerXT, is a novel combination of prodrugs of xanomeline and trospium, compounds that have been around for a long time, but with less than ideal pharmacokinetics. They also have Idazoxan XR, an adjunctive treatment for schizophrenia, and several new forms of psychedelics like psilocybin and MDMA with differentiated pharmacokinetics aimed at making these treatments more accessible and affordable.Sam explained the significance of prodrugs in their approach. Unlike simple reformulations, prodrugs are entirely new compounds created by attaching a side chain to the original molecule. This attachment improves pharmacokinetics, allowing for more effective absorption and longer-lasting effects. For example, the older compounds xanomeline and trospium, which need to be taken twice daily, have been modified into prodrugs that can be administered once daily or as long-acting injectables with multi-month durations. This innovation not only simplifies the regimen for patients but also leverages the FDA's accelerated 505(b)(2) pathway, potentially bringing these new treatments to market faster.Overcoming Development ChallengesCreating effective prodrugs is no small task. Sam described the extensive process, involving a team of world experts and over 200 FTE chemists working tirelessly. They designed over 10,000 prodrugs, synthesized 700, and conducted 500 preclinical studies to refine their approach. This massive undertaking, though challenging, has led to promising results.Are you subscribed yet? If not, let's fix that.The Potential of PsychedelicsI also wanted to explore psychedelics, a field that has generated significant interest in recent years. Terran is developing new forms of MDMA, psilocybin, and 5-MeO-DMT, aiming to improve their pharmacokinetics and make these treatments more accessible. Sam highlighted MDMA's potential, currently under FDA review for treating PTSD, with a decision expected soon. (Right after we spoke, the FDA advisory panel recommended rejecting approval for MDMA. The decision has not been made yet.) By creating new forms and leveraging the 505(b)(2) pathway, Terran aims to overcome patent barriers and ensure these treatments are affordable.Insights into Brain FunctionI am particularly curious about anything we can learn about neurobiology from studies around these therapeutic compounds and psychedelics. Here is the challenge: Psychedelics, for example, act on multiple receptors. Teasing out different pathways in the brain is complicated. Functional MRI studies of people undergoing psychedelic trips show reproducible changes in brain pathways, suggesting potential mechanisms but the circuitry is complicated. There are no simple answers yet.The Journey of a First-Time FounderI asked Sam about his experience as a first-time founder. Terran's success is in large part due to its corporate structure, modeled after fast-moving Silicon Valley companies. By avoiding traditional hierarchical structures and instead utilizing a flat organization with world experts leading sub-teams, Terran has managed to solve complex problems efficiently.Team building has been essential to Terran's achievements. Sam's approach involves creating specialized teams for different facets of a problem, ensuring a comprehensive and collaborative effort. “Workflows” for the WinI have seen a pattern in several interviews recently. Changing a process can have as big of an effect on solving a problem (and creating success for a company) as developing a new product. In this case, it's a bit of both. The problem being solved by TerXT is the patient regimen. Prodrugs with longer-duration pharmacokinetics make adherence easier for the patient. At the same time, I appreciate the enormous amount of development effort that went into creating those prodrugs. A different approach to assembling teams and managing them is also a significant change in the workflow that will have an impact.Your deepest insights are your best branding. I'd love to help you share them. Chat with me about custom content for your life science brand. Or visit my website.If you appreciate this content, you likely know someone else who will appreciate it too. Please share it with them. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit cclifescience.substack.com

Understanding Genetics, Pathology, and Progression in Parkinson's Disease and Atypical Parkinsonian Syndromes with Huw Morris

The Michael J. Fox Foundation Parkinson's Podcast

Play Episode Listen Later Mar 5, 2024 43:54

Atypical Parkinsonian Syndromes, such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA), corticobasal degeneration (CBD), and dementia with Lewy bodies are often initially diagnosed as Parkinson's disease. Incorrect, incomplete, or delayed diagnoses are barriers to beginning the most appropriate treatment early in the disease course. More research is needed to facilitate early diagnoses, understanding of disease pathogenesis, and monitoring of disease progression. However, largescale, collaborative initiatives are making meaningful progress in understanding genetic contributors to disease pathology and progression in Parkinson's disease. Our guest in this episode, Dr. Huw Morris, has spent more than twenty five years researching Parkinson's disease and parkinsonian syndromes, and he shares highlights from recent work, including studies on the genetics and pathogenesis of Parkinson's disease and other parkinsonian syndromes. Huw is Professor of Clinical Neuroscience at University College London Institute of Neurology, as well as an Honorary Consultant Neurologist at the Royal Free Hospital and the National Hospital for Neurology and Neurosurgery Queen Square. This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

professor disease cbd syndrome morris parkinson genetics progression pd neurology pathologies psp atypical incorrect msa lewy huw national hospital clinical neurosciences royal free hospital parkinsonian university college london institute honorary consultant neurologist

10: Understanding Genetics, Pathology, and Progression in Parkinson's Disease and Atypical Parkinsonian Syndromes with Huw Morris

The Parkinsonâ€™s Research Podcast: New Discoveries in Neuroscience

Play Episode Listen Later Mar 5, 2024 43:54

Cognitive Decline

Movers and Shakers: a podcast about life with Parkinson's

Play Episode Listen Later Mar 2, 2024 27:51

The Movers and Shakers are back in the pub and this week they're staring fear square in the eyes, and talking about a major fear: cognitive decline. What is the difference between Parkinsonian dementia and Alzheimer's? How does Parkinson's impact your chances of getting dementia? And when does forgetting your keys, of the neighbour's son's wife's surname, stop simply being a function of getting older? To answer all these questions, and provide practical tips for keeping the brain fit and healthy, the gang are joined by expert neurologist, Professor Rimona Weil.Presented by Rory Cellan-Jones, Gillian Lacey-Solymar, Mark Mardell, Paul Mayhew-Archer, Sir Nicholas Mostyn and Jeremy Paxman.Produced and edited by Nick Hilton for Podot.Additional production by Ewan Cameron.Music by Alex Stobbs.Artwork by Till Lukat.PR by Sally Jones.Movers and Shakers is generously sponsored by the Judge's old chambers, and by the contributions of private donors. Hosted on Acast. See acast.com/privacy for more information.

music pr judge alzheimer's disease acast parkinson artwork movers shakers cognitive decline jeremy paxman rory cellan jones podot nick hilton parkinsonian sally jones mark mardell paul mayhew archer

Blepharoclonus in Parkinsonism - Part 2

Play Episode Listen Later Feb 8, 2024 2:02

In part two of this two-part series, Dr. Jeff Ratliff and Dr. Jason Margolesky discuss what his team found when they looked for the presence or absence of blepharoclonus in patients with Parkinson disease or other Parkinsonian disorders. Show reference: https://www.neurology.org/doi/abs/10.1212/CPJ.0000000000200240

journal parkinson pd neurology parkinsonism cpj parkinsonian jeff ratliff

Blepharoclonus in Parkinsonism

Substantial Matters: Life & Science of Parkinson’s

Play Episode Listen Later Feb 5, 2024 13:42

Dr. Jeff Ratliff talks with Dr. Jason Margolesky about the frequency of blepharoclonus in Parkinson disease and atypical Parkinsonian disorders to explore whether this clinical phenomenology may be useful in the evaluation and diagnosis of patients with Parkinsonism. Read the related article in Neurology: Clinical Practice. Disclosures can be found at Neurology.org.

journal parkinson pd neurology disclosures parkinsonism parkinsonian neurology clinical practice jeff ratliff

Episode 49 - "Gremlins" w/Dr. Sulman Mirza (@thekicksshrink)

Analyze Scripts

Play Episode Listen Later Dec 11, 2023 54:33

Welcome back to Analyze Scripts, where a psychiatrist and a therapist analyze what Hollywood gets right and wrong about mental health. Today, we are joined by our friend Dr. Sulman Mirza (@thekicksshrink) to discuss his favorite holiday movie "Gremlins." This campy 1984 thriller comedy horror follows the Peltzer family as they unwittingly adopt (?steal) the mogwai Gizmo at Christmastime. As a father and child & adolescent psychiatrist, Dr. Mirza shares his interpretation of this movie as an allegory for parenthood. We also explore themes of trauma, gender roles, and consumerism. We hope you enjoy! WATCH THIS EPISODE NOW ON YOUTUBE! https://www.instagram.com/analyzescriptspodcast/ TikTok Website [00:10] Unknown Speaker: Hi, I'm Dr. Katrina Fieri, a psychiatrist. And I'm Portia Pendleton, a licensed clinical social worker. And this is Analyze Scripts, a podcast where two shrinks analyze the depiction of mental health in movies and TV shows. Our hope is that you learn some legit info about mental health while feeling like you're chatting with your girlfriends. There is so much misinformation out there, and it drives us nuts. And if someday we pay off our student loans or land a sponsorship, like with a lay flat airline or a major beauty brand, even better. So sit back, relax, grab some popcorn and your DSM five, and enjoy. Welcome back to another episode of Analyze Scripts. We are really excited to be joined again by one of our favorite guests. Don't tell the others. Maybe Solman Mirza, who is a triple board certified physician in Adult psychiatry and child and adolescent psychiatry and addiction medicine. Just in case you didn't catch our last episode that he was on, I'll share a little bit about him. He works with the largest healthcare system in North Virginia as the staff psychiatrist for an adolescent partial hospitalization program. He sees children and adolescents as outpatients there as well. He also has his own private practice, Luku Psych, where he sees adult outpatient patients with a focus on ADHD, autism, substance abuse issues, as well as being Blue Duns County's first Loudon, I was like, we're in the Northeast here. The first certified provider of bravado, the FDA approved intranasal eschetamine product for treatment resistant major depressive disorder. Dr. Mirza is also a certified provider in the National Basketball Players Association Mental Health and Wellness Program for the Washington Wizards. Begrudgingly realizing that the only way he was going to make it into the NBA was by being a doctor, which is super cool. That's a tough realization. Way to spin, know, way to find positive reframe. Yeah. And then, in addition to his clinical work, Dr. Mirza has a growing social media presence, which is how we found hiM. You can find him at the Kicks shrink with a following over 85,000 across TikTok, Instagram, Twitter, and YouTube, with an accompanying podcast as well, where he creates educational, entertaining videos and content with the goal of breaking down mental health stigma, combating mental health misinformation, which we also agree is really important, and rehabilitating the often negative image of psychiatry and psychiatrist. Often in movies, which we see really frequently. Yes. So he interviews leaders in the field, all while hoping to make viewers laugh and learn something, but also really like sneakers. Yeah. I'm curious, are you hoping for a special sneaker gift this holiday season. Well, it was my birthday recently, and I know. Birthday. Thank you. It's been like a month. Plus now it kind of flew under the radar because I was, like, bugging my wife. I was like, where's my gift? Where's my gift? And she's been like, along the way. She's like, sending me Instagram posts of this Pakistani artist who does custom artwork on Air Force ones. So she's like, oh, if you were to get a shoe like this, what kind of artwork would you like on there? Theoretically. Theoretically. And I was like, I'm still wondering because I haven't gotten it yet. And now it's like six weeks, seven weeks later, I'm like, what's happening here? So it's going to be like some Pakistani truck art on these Air Force Ones. I'm kind of excited for that. Yeah, that's really cool. Yeah, I love that. Do you have a big sneaker collection? Oh, Porsche. Do I have a sneaker closet? I have a sneaker wall in my basement. It's like over 100 pairs of sneakers. So people come down to the basement and they're like, whoa. And I have to tell them. I was like, I have some more hidden away in another closet, so don't worry. Do you actually wear them or are they for display only? No, I try to rotate through them. I try to spice up and wear a different pair every day or so. Cool. But I have my go to. I go to on a regular. And I bet you have a way of keeping them really clean. Yeah. So I've got the cases for them. So they come in the clearish display cases. Like a Beanie baby. Yeah. Container store has these boxes, essentially. So they sell them by the six pack, essentially, of them. So you end up spending just as much on the storage as you do on sometimes the shoes. I love the container store. Yeah. It's trouble. They have containers for everything, every shape, every size. Every now and then I go through these fantasies of just organizing my whole house. Right. Like a place for everything. And I have this fantasy, like, the rest of my family members will just do it and they won't. Of course, they won't make a good point about the Beanie babies, but I think we also used to store, like, furbies in those glass containers as well, which leads us to our movie today. Yes. So we're talking about the 1984 movie Gremlins, which was a smash hit at the time. It still is. It's like one of those classic movies, but totally. Every time I watch this. I think about furbies, which came after Gremlins, but I always wonder, how did that fly? Because they look identical. And I think they actually even came out with a gizmo. Furby at one point. That's, like, super hard to get now. Yeah, they were creepy. Esop. Furby's were creepy. Yeah. One of my friend's fathers, when we were eight years old, got really annoyed at her furbies for not being turned off, and he threw them all over the balcony. Down. Obviously, that was probably. He maybe had something else going on issue. But I remember she was devastated. So what I think about when I think of Furby's hope she therapy today, but I don't know. Talk about a core memory. Yeah, I'll say there's some issues going on there. I think that explains plenty of stuff there, but. So, Sullivan, give us your hot take on this movie. Why do you like it so much? What made you want to revisit it? Yeah, so Gremlins is one of my know, I remember way back when we had. When I was growing up, me and my sister in upstate New York and Summertime, our parents weren't big on doing stuff, so they're like, you guys just stay in the. Just, like, do nothing. They're like, here's some math books and some books to read and stuff. And then we'd be like, me and my sister hanging out. Be like, let's just watch some movies. And so we'd go through the whole VHS tapes that we had at home, and my dad would always tape stuff off the TV, so we'd have to fast forward through the commercials and blah, blah, blah. For the people who remember VHS tapes. Do you remember the rewinding machine? Did you have one of those, or did you do it by. We just rewounded in the VCR itself. So after a movie, you have to be like, all right, guys, let's wait around for another five or ten minutes to rewind this movie. But Gremlins Two was always in the rotation. Gremlins Two, which is, like, the worst of the movies. It's very cheesy and crappy, but I always kind of liked it for whatever reason, that was our rotation. Mighty Ducks Two was in our rotation, and Star wars was in our rotation. Sequel, not the original. It was very bizarre. But for whatever reason, that was the one that was there. And then I remember watching Gremlins one. I loved Gremlins Two, but I remember watching Gremlins one later and being like, oh, my God, this is so much better. And fantastic. And it's amazing. And then I watched it again a few years ago, and I was like, oh, I have a different appreciation for it now. And then I watched it again over the weekend. I was like, oh, another different appreciation and interpretation viewing on it. The other thing, too with it is when people always ask me, like, oh, what's your favorite Christmas movie? It's always, like, the time of year. We're getting there. Right? I don't celebrate Christmas. I'm a Muslim. We don't celebrate it. Kind of growing up. So for me, it was always like, my favorite Christmas movies are Gremlins, Die Hard, and Home Alone. Right? Yeah, Home Alone is universal. We all like that one. But that was, like, my thing. So I always appreciate it as, like, a non Christmas Christmas mOvie, I guess. Yeah. And there's a lot of controversy about diehard, whether it's a Christmas movie or not. I hear this in the ether. It's a Christmas movie. Yeah. I think we can agree. So what do you love about this movie? I liked it because one of the things I always like about movies is the practical effects. So this is, like I said, 1984, and I was two years old at the time, so I don't remember when it came out, obviously. But I love the class, the practical effects of it. I love that you created these creatures who are iconic. Right. What is it, 30 years, 40 years later? 40 years later. Oh, my God. 40 years later that we're still talking about them, that people are still clamoring for, like, a Gremlins three. I think there was just, like, a cartoon series on Max that just came out in the last year. Gizmo was super cute. Oh, my God. The cutest picture that's out there. I guess there's probably a lot of Shih tzus out there named Gizmo. Yeah, my cousin had one, and now I get it. Yeah. So that was, like, the appeal of it, and it was a great kind of send up of a lot of these classic kind of Christmas stories, too. Like a very obvious kind of send up of, like, it's a wonderful life. And just like, that dark kind of humor that's in there that was always appealing to me. And then more recently, I think we're talking before the idea of, oh, this is kind of like a metaphor for parenting and getting into adulthood and all that stuff. So say more about that. Yeah. When I watched it again over the weekend, and I watched it with my eldest son, my only son, but I have four kids. Right. So this was like, let me just watch it again. I always kind of originally thought of it as just a basic kind of horror movie, but like a comedy horror movie. Not a comedy horror, but a horror comedy, right? Yeah. And then nothing more. I thought it was a very superficial, pop, kind of culturish movie. And there it is. When I watched it again with the kid, right. I was like, oh, this is hitting different because it's a story of parenting. IT's a story of the ideas of what we're supposed to do, the rules that are there. And then what happens when you break the rules of parenting? You have the old grandfather in the beginning, and it's very kind of straightforward as a grandfather who's very wise. And these are the rules of here's your new baby, right? Here's Gizmo being the baby and a child. And he's like, this is what you're supposed to do. Again, the three rules are like, don't feed them after midnight. Don't get them wet and keep them out of sunlight or else they'll die, right? And we see this when you become a new parent, right, and have gone through it the four times, it's like everyone kind of telling you this is what you're supposed to do. And your own parents, right? The grandparents of the child telling you, these are the rules. These are the things you're supposed to do. Funny enough, sorry to interrupt, but our rules are the direct opposite. Feed them whenever they want, get them outside, except your parents maybe, who say, stay inside all summer and make sure you bathe them. Yeah. So it was interesting from that point of view. I hadn't thought about that before. And then as kind of this journey through, like, we're going to be cute and cuddly. Gizmo is fantastic. And we love him. And he sings these songs. He's like cooing and it's, know, he's so super nice. He's like, better than the dog, right? We think he's going to replace the dog, right? So it's like a new baby, a new child in the household. And then we get into adolescence, right? We get into adolescence, or even the terrible twos or whatever you want to say, where it's like, now we've broken the rules and now they are these gremlins, these terrible monsters who are just destroying everything. So that was what really struck me upon this more recent viewing. It was like, oh, this is what it's kind of like an allegory for. Wow, I never thought of that, but I can totally see that now. And I'm just thinking now about this scene where the mom, Lynn, I think was her name, is trapped in the house with the Gremlins who are trying to hurt her, and she kills them one by one in these very graphic, violent ways. And as she keeps doing it, you see this pleasure in her face that she's doing that. And I thought that was a really interesting depiction of her finding this sadistic joy in killing these creatures, given her role as the stay at home mom who doesn't really have a say and has all this husband who's off all the time with these wild inventions that don't really work. Terrible invention. And she's just like, yeah. She's just, like, stuck at home alone. I don't know. I thought that was interesting. Yeah. And it's interesting, too, because Billy, the main character, he's portrayed as, like, the perfect all American boy. He's, like, living at home, being there, works at a bank, has a dog, and he's hanging out with Mom. They're getting ready for the holidays together, super supportive, while dad is again, out being a terrible inventor on these road trips and absent all the time. And then again, all this stuff happens to him and the world. Kingston Falls gets burned to the ground. That felt like a little neglectful, just like with his even dismissing of the instructions when he kind of, I guess, stole his totally, and then laughing about it, like, oh, well, I think you got to do these three things. I was like, wow, you remembered them. I was impressed that he could then tell his son how to kind of do it. But then if you think about it in kind of, like, not the context of a movie, it's like you've got this bizarre creature that is not a dog or a kitten or a bird or a toy or a toy, and you're like, leaving it with your son, giving these random instructions that seem ridiculous, and then you're going off again, and it's like, well, right. Any danger? Oh, I probably shouldn't do this. Oh, this is a bad idea. It's like, there's none of that. I don't know. I think we see that, though, and I think stereotypically we see that with the busy working dad, who's not really physically or emotionally present, but will shower the children with gifts as sort of like a token of their affection, but then isn't even around to appreciate the children with the gift. And I think even beyond that, I would imagine a lot of parents feel that this time of year, at the holidays, there's just so much pressure and chaos and busyness. And it's like, does anyone sit in front of the tree and just be together? Right? It was always the competition of who's going to get the biggest gift, the best, and, like. And then even then, when he gives the gift or he gives Gizmo to his son, to Billy, he's like, I need to find a way that I can make more of these. And this is going to replace the dog. This is going to be like the pet of America. And he uses his last name, right? The Pendleton or something, like pet. And it's just like, he's so. I don't know. It's just like, that's really only where his brain goes. It's like if we think about just priorities, it's like his priority is to almost a little bit of self importance versus, like, financial gain. Like, he wants to be celebrated. He wants to be known. He wants to be important. Famous. Famous. I was just going to say. And even within the home, right? So all the stuff is in the home, and the orange juice maker doesn't work, the coffee machine doesn't work, and the phone thing doesn't work. And it's funny in a way, it was kind of mean and self granditizing. Like you're saying, it's like, even when the mom picks up the phone and talks on the regular phone and he's asking, he's like, well, you're using the device, right? You're using the thing, right? You can tell that he's always still just like, even if this terrible thing, nothing works. He's like, we're still going to use it. And she goes along with it. She totally plays into it. And I think that scene you're talking about in particular, we don't even hear him say that dialogue. We just hear her response where she's making an excuse like, oh, no. I was out on the porch. I couldn't get to it or something. But we saw her try to use it, and it failed three times. And that is so interesting to me that everyone has this almost, like, shared delusion. It's too strong of a word. But we're all, like, boosting his ego up and his image up, even though none of his stuff works. And I can't imagine it's lucrative. I kept wondering, how do they afford their travel? It's upstate New York, so upstate New York is, like, extremely cheap. So there you go. Yeah. So then we meet. We saw the little boy who's, like, Billy's friend, who's in my favorite movie ever, Goonies or the Goonies, which I was just like a pleasant surprise of. So did more movie question, did the same director directed both of those, right? Or there's the same something that brought him over. I know, like Spielberg, Steven Spielberg produced both of them. At least I think I know he was a producer for Gremlins. I can't remember if he did Goonies. I think I want to say he did Goonies, but he was a producer at least for it probably. Yeah. Because he really liked. And then Goonies is where he kind of like blew up on. Yeah. So you had shared a little fun fact also before we got rolling, which I think the viewers would love to hear about the rating of the. Oh, yeah. So, so Gremlins was rated PG and I was kind of like doing a little reading on it and I saw that there was so many families that were going into the movie expecting cute Little Gizmo. I think the advertisement was around Gizmo and how this was going to be like a Christmas movie and a family movie. And finally it came out in the middle of summer. I think it was like that. And Ghostbusters came out on the same weekend and it held its own. This was like one of the top three or four grossing movies of the year with Ghostbusters and Indiana Jones and the Temple of Doom, which we'll get to in a like. So this came out and then everyone was like, oh, this is going to be a fun little movie, family movie, right? Oh, my. This devolves into this terrible mess of horror and gore and violence. And families were like walking out because they're like, oh, my, can'T. My children can't see this movie. So that was happening. Indiana Jones and Temple of Doom came out that year, I think, as well. It was rated PG as well. And of course, we all remember Indiana Jones's Temple of Doom with Galima and the guy ripping everyone's heart out and eating monkey brains and all that fun stuff. And we're like, oh, my God, what is going on? So those movies, it led to the formation of the PG 13 rating because people were like, we need to find something that's in between PG and R to kind of have this there. So I think it was important historically from that point of view as well, too. Oh, yeah. I mean, it's definitely not like a PG film. And I think that I saw online that they toned it down a lot, actually. Mom was supposed to die and there was supposed to be a shot of her head rolling down the stairs and all of this other stuff. And they were like, no, it needs to be more marketable for a wider audience. And so thinking of it even then, in that context, it's like it was a horror movie that they kind of made more globally. It will just be seen. But that's really interesting. The things you learn on. She kind of, for me, came out of nowhere with just, like, this really tragic story that I was not expecting at all. Yeah, Phoebe Cates again, who, for a lot of guys in the 80s, turned them from boys into men. But, yeah, she has these two scenes, right? Like, these two major scenes in the movie, the one where they're walking and then the other part where they're randomly just spills her beans about her father and how had this tragic thing happen to him and why she hates Christmas, which I thought was really interesting from a point of view from us in the mental health field, right? Like, when we're with patients, clients, and when we're around this time of year and we're like, well, Merry Christmas, or have a good Thanksgiving, or have happy holidays, and we say it very cheerfully and we assume that everybody loves the holidays and this really great for them. It's like the best time of the year. And it's like, not always. It can be really painful time of year for enough people, right? They're very difficult times of year. Sometimes there's a lot of family trauma that's there, and then they're forced to be around other family members or they're potential abusers or again, there's other memories associated with the holidays. And so when we thrust upon our idea of, like, it's the holidays and you should be happy and just get the Christmas spirit, we can't do that. So it was something that I've changed over the course of my years has been like, well, when I asked people, I was like, well, how are the holidays for you? How is this time of year for you? So you have an idea of how to approach it or how to kind of sign off or even just talk and process about it with them. That's a really helpful point. Even just like, if you're not in the mental health field, like, asking, what are your plans? And I think even in that way, you can get a little bit of an, oh, well, my plans are you're like, okay, you seem a little bit more happy. You're like, oh, I'm not really sure even in the little kind of subtext can give you a clue. But, man, I mean, there's a lot of substance use this time of year. It's really hard, I think, especially with all the family gatherings. I think we all assume holidays are a time for family gatherings, but a lot of people don't have big families or any family to go to, so there's a lot of loneliness or they might be housebound. And there is a lot of substance use this time of year. Yeah, we see so much drinking just because it's, like, normalized or encouraged a lot of times, too. So we have a lot of issues with that. I was working with a patient recently who we've been working with her on their alcohol use and getting it down, and they've kind of reintroduced drinking a bit, right. And I was like, okay, cool, we'll keep an eye on it. And it becomes the whole thing of like, well, it becomes special occasions, right. On special occasions, we'll have a drink or two, and then it's like, we're getting to holidays time, right, where it's a lot of special occasions. And then does every little thing, every family gathering become, like a special occasion? And then I was going to start that. I tell them, I was like, let's keep an eye on how often those special occasions are occurring. And if it's like, is Friday becoming a special occasion? Is coming home from work a special occasion? Now, let's just keep an eye on that as a whole. And I think the same could translate to food as well, either. Overeating, undereating people's relationships with their bodies, with other people's bodies, especially if you grow up in a family with sort of that toxic food culture. Same thing. I think we see a lot of this stuff around the holidays. Eating disorders, too. Right? So whenever I have patients, clients with eating disorders, again, it's like Thanksgiving is seen as like, oh, my God. It's like this culture of celebrating food in Turkey and all that fun stuff. Overeating. Yeah. It's like gluttony is very much like, this is what the plan is. We're going to eat too much and we're going to pass out and go to sleep. And the comments of, like, the normalization of the comments of like, oh, well, I'm going to skip all of the meals except Thanksgiving dinner. And it's like, okay, well, then of course you're going to overeat. And it's encouraging people to eat as you normally would throughout the day. And it's a way to help you keep a little bit more regulated. But it's so hard. It's a hard time of year. But that scene with Billy and Kate walking home in the snow, where she know. Starting to talk about her negative feelings about the Christmas time of year. And she mentions, like, well, it's the know. It's the time of year where there's the most suicides. I thought it was important to point out that that's actually not true. I think that's a common misconception and it makes sense. Right. For all the reasons we're talking about, all the stress and everything. But the CDC actually consistently reports that the time of year with the highest suicide rate is between April and June, which a lot of people wouldn't think. I think we often think it's like between Thanksgiving and Valentine's Day. But there's some thought that perhaps there is something to that. Increased light exposure, people getting outside. I think there's some thought that there might be a correlation with the increase in manic episodes that happen during the springtime. Again, more impulsive, taking more risks and things like that. But the suicide rate is actually the lowest in the winter. So I wanted to hear both of your thoughts about that and your thoughts about this movie sort of portraying it incorrectly. Portia, you can go. I mean, I can see why it's common. I think we think of the winter, we think of seasonal depression, and especially in certain parts of the country, like the Northeast, where there's more seasons, it's like dark. We have less of that vitamin D. We can be more isolated, which I think, again, is why we might think that there'd be more death by suicide. But I think what's interesting, too, is there's also, and I don't know if this is related at all, but I'm just thinking of the crime rates, how they kind of spike in the summer, too, and it's just like the heat or you're out more, you're exposed more to things, maybe to more like. I don't know if that has anything to do with it. But that's just what that made me think of. I was a little bit surprised when you were saying that, that it's higher in April, June versus the winter. I think I was kind of like before I was kind of working under that assumption that it was also higher during the winter, not necessarily just based on gremlins. Maybe it's a left, maybe a lefty mark, who knows? But yeah, there's that aspect. I think it is just interesting that when we do kind of, like, research and stuff and see what are the statistics, what are the kind of evidence of when these things happen. When I work with kiddos, I reference a lot of the work of Dr. Tyler Black a lot, who's done so much kind of research into suicides and suicide rates with children adolescents. The highest suicide rates are always Monday through Friday and then highest during the school months. And they always take a dip during the school years. And I think the takeaway is that school drives a lot of suicides for children and adolescents. So it's that aspect, that other part of it that I always kind of bring up and say, so it was interesting. I think I hear that from a lot of. Yeah, and I hear that from a lot of my friends who are child and adolescent psychiatrists, that the summers tend to be a little slower, and then it's, like, quiet. As soon as you get to that first parent teacher conference, it's know everyone wants to come. And like, Portia, you were saying in the, like, I do PHP partial hospitalization work in the summer, it's, like, barren, right? I'm always like, everyone's like, they're encouraging you take your vacations during the summer. You want to take extra week off, take an extra week off. It's really quiet. And then end of September, October starts, and it's like, PHP is full. It is full until June. Yeah, that's really interesting. And gosh, what a commentary on how stressed kids are by, like, that sucks. Yeah. So when people discuss, it's funny because you get into the debates about people who will be like, oh, it's social media, and it's like, Instagram's fault and TikTok's fault that kids are suicidal. We didn't have this when we were growing up. I was like, yes, of course you did. But nobody talked about it. But I was like, you can access TikTok and Instagram during the summer, right? You have plenty of that stuff during the summertime. Might even access it. You can have it on the weekends, right? You can get it on Saturdays and Sundays, right? But data is dramatic. It is like, significant differences that occur between school days and school months. That's really interesting. It's sad. That makes me sad. I think it's hard for scheduling. This is just like a me problem, not a patient problem, but it's like, we'll meal you if you're in a group dynamic drops so drastically in the summer. And same with, I have all of these openings, but I'll see someone monthly. And then all of a sudden, September hits, and it's like, we need every week, and it also needs to be after soccer, and it also needs to be before we have tutoring. And it's just like. But then if you think about it, it's like, okay, now the kids are in school all day, and then they have an after school activity, and then they have sat prep, and then they have this, and it's like, well, maybe that's why they're stressed. They're kind of being pulled in a million directions and maybe feeling like a failure, and it's just poor case. One of the greatest interventions I do is tell people to do less. I was like, is there one thing that you can drop? And they're like, oh, my God. It made a huge difference. Oh, 100%. And it is like, I think I try to keep that in mind as a parent myself, not to over schedule, but it's hard because there's so many activities going on, and you don't want your kid to feel left out or you want them to participate. But then it's kind of just like the holiday season, too. It just gets to be too much. We all just need to take a deep breath and sit down. You need to chill. Yeah, yeah. As Taylor Swift says, you need to calm down. So talk about trauma with finding her dad deceased for days with a smell, and he was dressed as Santa. I mean, what a obvious reason to not like Christmas anymore. Yeah. So that was like this terrible story that, again, comes out of nowhere. That was one of the kind of the criticisms of the movie as well. I could imagine all the families going to see the movie and then being like, oh, my God, dad is trying to be Santa Claus and come down the chimney. And he gets stuck and he dies. And then they start being like, oh, what is this weird smell? And then doom. There's dad in the chimney, and that is a smell. I don't know if you ever rotated through forensic pathology. Solman I did, because I'm just a morbidly curious person, I guess. THat's a distinct smell. All the true crime shows say that. And it is true. There is the smell of death that's there. That is not fun for anybody. But also, why wasn't anyone looking for him for days? I can't remember. I think they were, but everyone was like, they just, oh, they were. I mean, nobody could find them, right? Because they're like the work, I think they called like work, and they're like, he's not here or something. Okay, that makes sense, actually. No one would think to look in the chimney. No one thinks to look in the chimney. Hot take. If you can't find someone, check your chimney. I think maybe this is why chimneys are much narrower now. But no, this is a very obvious trauma. And for some reason, I don't know why, but I knew that there was a twist of something that happened with dad. And for some reason I was thinking that it was like an assault or abuse that occurred to her. And then it was like, oh, yeah, it was the dad gets stuck in the chimney. So I remember there was like a trauma that occurred. The thing that we're talking about before is that there is these moments that occur, right? These associations that occur again, we see so many times with sexual abuse, incest kind of situations that occur, like it's the creepy uncle or the aunt or somebody like that. And again, what are you supposed to do in family kind of gatherings when they get invited and whether parents may know or not know, they still. Or they kind of decide to not do anything about it or let's not talk about it. I think a really good kind of reference for this was that Indian movie that came out many years ago. I can't remember the name of it. It was like some wedding. Monsoon wedding. I think it was right. And I don't remember. I don't know if you guys watch or not, but that was kind of the premise is like, the uncle had assaulted one of the girls as a child and everyone was like, we're not going to talk about it. Let's just leave it alone. And then she couldn't take it anymore and then had a big fit at him. And the family members are like, why are you yelling at him? Why are you still talking about this? It happened like, 2030 years ago. Why are you bringing this up right now? But this happens all the time. All the time, all the time. So many times, right? And then people are just supposed to just pretend like nothing happened, right? Keep the peace, just go along with it. And it's like, gosh, not only was this person traumatized and violated in such a major way, now we're all perpetuating it by telling them, don't talk about it, just suppress. We're retraumatizing them. It's so awful. So then when bringing it back to Phoebe, Kate's character, we see every year, like, oh, Christmas stories and families and Christmas cards and dad being sit on Santa's lap. And it's this. All the stuff that goes along with Christmas time. And how else can you. Well, like, where you're supposed to be with your family and Santa's this wonderful character and he's popping down chimneys and dropping off presents with kids and it's like oh my God. Can you also like Santa? If you really think about it, it's kind of creepy. Like this old man, stranger, you don't know, like you sit on his lap and ask for things and then he just comes in your house. Are you good? Are you noding your. When you're. Sees you when you're sleeping? It's like kind of creepy. Very creepy. Kind of creepy. I think too, in my work as a reproductive psychiatrist, I see a lot of grief around the holidays, at least in our American culture. From a know religious standpoint, with all the focus on the baby, baby Jesus and family and growing your family and gatherings, there's a lot of grief for women who've lost children or want one so badly. And I think that applies to whatever your family system or structure is. If there's been tragic loss or even untragic loss, like, loss is hard no matter what, but especially this time of year, the first holiday after someone died, or now we're doing things differently. It's just hard. And I don't think we leave enough space in all of our busy schedules to just allow ourselves to feel that or to even kind of accept that other people have different experiences. Right. Still get into the Christmas spirit and still have your pumpkin spice lattes and continue on. Yeah, like, go sing a carol. It'll make everything better. Yeah. You see Billy do that a little bit until she shares her story. But she's really kind of like pushing her to be like, well, what do you mean? And it's the best time of the year. And why that's weird. And then she kind of like, whether she wanted to or not, I would imagine, felt inclined to be like, well, this is why. And I think a lot of people also, it's like when they are being pushed or encouraged kind of forcefully to get into the spirit, it does really feel kind of like non consensual. And oftentimes you're kind of forced to share something that maybe you don't want to or you're not ready to. Or some people like, again, I do sadly see the same example you mentioned about there being some sort of abuse or violation in the past and having to see that extended family member. And often it might be this type of situation coming up that finally leads to someone disclosing it for the first time to, like, parents and how unfortunately, some parents might be upset. Like, why'd you have to tell me now you've ruined Christmas. Ruining the holiday. Christmas. Yeah, exactly. It's like, holy moly, come on. Yeah, I do think, though it is possible, even when the holidays are hard, it is possible that maybe they won't always be hard. And I like to encourage my patients when they're at that point to. Also, something I use is thinking about, like grief and love can be like two sides of the same coin. And sometimes when you've experienced a lot of loss or grief around a certain time of year, a certain anniversary, whether it's holidays or otherwise, when you can make room to sit with it and accept it and let yourself just process it, how you process it, you can also open yourself up to feeling that love for that person or for other people, or you can appreciate life in a different way sometimes if you can just allow yourself to hold on to all of those complicated, big emotions. Yeah. Also with trauma. Talking about that a little bit, too. There is also the community trauma that occurs, right. Which we don't get much of in the first movie, but it gets referenced to a little bit in the second. Gremlins or Gremlins, too. So you have this small, idyllic postcard town that gets totally destroyed and ravaged by the Gremlins. Right. Theater gets blown up, everything else, people get killed and all these things occur. And you see what happens to a little bit in the second movie. Not too much, right. They moved to New York City. Right? That's where the main setting is. And they're like, we had to get away from there. We had to get out of that place. Right. We had to run away from there. And it is that aspect. We have to remember that communities, places we live are like people as well. They can have a trauma occur to them that doesn't go away. I think we see it with things like New York City and 911. Right. That's, again, we never forget kind of thing. Right. That's never going to be forgotten. So when tragedies occur to areas, that's a thing that we have to kind of remember. And collectively, society wise, community wise, have to remember, too. It makes me think of towns who experience school shootings. I was just thinking like, sandy hook holiday time or like. And it's like there's so many families with a huge loss and what do the holidays look like? And that almost like too, just like survivors guilt, like, your kid is alive and it's very complicated. And I think you're right. That community aspect is totally not to be forgotten either. So I was thinking that either of you two could kind of talk a little bit about delusions or hallucinations with just like we see that scene where Billy's at the police station and telling them that this is going to happen, all these terrible things. And he shows them Gizmo like, he's super cute and they don't believe him because it Sounds. Right. Like, not true. Unbelievable. Yeah. So what is a delusion? If a patient told you this, what might you ask them? What are some other questions or assessment tools that you could use? Yeah. So delusion is a fixed false belief. Right. That's kind of the boilerplate definition of it. So fixed in regards to no matter what you do, no matter what you say, there's no way that you can change that person's mind. And then false is that it's obviously false. It's not true. And these are, I do mostly child adolescent work, but I have some adults and I have, I would say, like, one patient, I would say that has delusional disorder. And there are some of, like, I want to say, the hardest but most challenging kind of patients to work with. I would agree. Again, it's fixed. Right. That belief is not going to go away. And there's a recent kind of discussion on Twitter that was coming up about how do you approach a delusional patient? And there was this old school of thought, I want to say maybe where you kind of challenge it. And then I think that really has fallen away to be like, you kind of go along with it. You say, like, okay. And then we try not to put too much stock in it into that fixed false belief. Right. Like, you don't want to go along with it too much. Okay, well, this is a thought. Let's kind of see what else is going on or how else we can help out and try not to challenge it or fight it either, or kind of convince the other person that, no, this is wrong. So that's like, what's it called, the aspect or definition of what a delusion would be, bringing it to the movie. And it's important to keep it in the cultural context. We saw this with the movie side effects, that there was a man who identified as Haitian who was in the ER, who I guess this was more of a hallucination, but thought he saw a deceased relative and they were like, oh, he's got to be hospitalized. And then it's like, oh, no, actually in that culture, that's accepted. So it's important to have that framework, and that's hard because I don't understand every single culture in the world. Right. So if I'm in the New York City er, it's a lot. So it's kind of that something that's going to be totally bizarre ish. And then there's that, like your family, that people doesn't believe. People around them are less like, no, this is new and this is different, and this is not okay. This is not normalish. So that's what a delusion is from the movie point of view, kind of bringing it back to the parenting. There's again, like this delusion where people around when you have this baby, right? They're like, this is going to be a perfect child and nothing could ever go wrong with them. What are you talking about? That they're going to grow up and become terrible teens or terrible adolescents or adults, right? They're going to be perfect little kids just like you, little gizmo, forever. And then we know that that doesn't happen because there are terrible people out there. People do terrible things. So people make mistakes. People make mistakes even if they're not terrible at their core. But some people are having antisocial personality disorder. Yeah. And I think we saw this, too with our recent episode on American Horror Story. Delicate. That if it hadn't actually been happening, these people would be delusional. And yet it is happening because we're in this fantastical story. But you even see how people react to it, like how the police officers in this movie reacted. And it's not really in a supportive way and how you just have to be so careful. Because I think if we're talking about people with clinical delusions or a delusional disorder, I think, at least in my experience, it's very hard to get people with these disorders into psychiatric treatment. Usually it's other providers. I'm thinking of delusional parasitosis, which is where you think you have an infection or a parasite or a skin. A lot of times it's skin rashes, bedbugs, things like that. So these people show up to the dermatologist over and over, the pathologist over and over. And, I mean, it can get pretty severe in terms of. I've seen people who've taken their own samples, like cut off some of their skin to bring or traps the bugs in a container, and there's nothing in it. But to try to get someone like that into psychiatric treatment is incredibly hard. And we don't have great medications for it. Maybe an antipsychotic, but it's tricky. Another thing is like MRIs, right? Because they'll be like, I'm convinced I have a tumor in my brain, or they have the whole body scans, right? So they get a lot of imaging, they're convinced something is there. And every time it's coming up, like it's normal. Nothing is there. Or even right. There's pseudosyesis, which is a delusional belief that you're pregnant when you're not. I saw a case of that in my training, which was fascinating. And it's just fascinating to me that our brains can do this. Yeah, we see this. I was going to say we see this in Parkinson's. Right. One of the more common delusions in Parkinson's is, like, the spouse is cheating on. And again, there's no evidence to this that's there, but it's like a unique kind of, like, Parkinsonian delusion. Yeah. And then, of course, we think about erotomanic delusions, which we've talked about a lot on our podcast, specifically with the show you, which we love. But, Portia, like, you'll appreciate this. I remember one time I had a patient, an elderly man, who had a neurotomanic disillusion about Taylor Swift and would listen to the radio all day long in his hospital room, waiting for her song to come on. And it would come on a lot, and he would be like, that's my girl. She's sending me a message. That's my girl. For real. And he was in the hospital for a totally non psychiatric reason. But when the team picked this up, they asked us to consult. I was on the consult team at the time, and we were like, well, he's not hurting anyone. He's not stalking her. We can't really change it. Yeah, there's an aspect of, like, we have to go along with it. We have to kind of keep an eye on it until it becomes problematic. Right. Until it crosses over into be like, oh, it's a problem. Right. And again, one thing we all want to keep emphasizing is that people with psychiatric conditions are much more likely to be victims of violence than perpetrators of violence. But at some point, I think, especially with more erotomanic or violent delusions targeted toward a specific person, that's when your red flags go up, and you have to be really careful in your assessment. I know. So poor Billy, seeking some help, and just really, his dad's not there. The cops aren't helping him save the day, the vet or the school teacher. God, that was so graphic. Yeah, it was a good movie. I have not seen it before, ever. So I enjoyed, thought. I didn't know what to expect. I think I thought it was going to be weirder. It was pretty weird, but I thought it was like, funny. It is funny. Yeah, it is pretty funny. And now, like Katrita says, which I thought was a good word, it's like, know. I wasn't scared watching it. It was great. Like the scene, they spent a lot of time when the gremlins are at the bar and they're just, like, doing all this stupid ****, right? They're, like, drinking, they're smoking. One of them has, like, a gun, like, just randomly shooting the other grandma's. And it's like, oh, this is all not, like, ideal teenage behavior, but not, ideally, not shooting each other. But this is what teenagers sometimes, right? Unfortunately, this is the idea. This is what teens do. They do stupid ****, right? They just get together and they act stupid around each other. They drink, and they make poor decisions, and things happen. And that was the thing, again, on this recent reviewing, I was like, oh, my goodness, I didn't see this before. I know. It's so interesting to me when you can rewatch movies as you grow up and take different things from them based on your own personal experience. And I always wonder, the people who made Gremlins, was that their goal, or is it just like an interesting coincidence? No, I don't think we'll know. I don't know. Well, someone, thank you so much for joining us today and for recommending holiday favorite holiday classic. Can you let us know where we can find you and follow you and join your TikTok Instagram? Follow Kick Shrink on, like, what's it called? Instagram and TikTok and YouTube. I'm trying to put a lot more effort into the YouTubing nowadays because that's where the money is trying to retire from know, but it's fun, too. And then Twitter is my old high school nickname, Sol Money, S-U-L money that I've had like that. I like that. Well, again, thank you so much for joining us, and we can't wait to see those cool sneakers whenever you get them. Thank you guys for having me. And you can find us, as always, at analyze Scripts podcast on TikTok Instagram, and now on YouTube as well. And we will see you next week for a new episode. Take care. All right, bye. This podcast and its contents are a copyright of analyzed scripts, all rights reserved. Any redistribution or reproduction of part or all of the contents in any form is prohibited unless you want to share it with your friends and rate, review, and subscribe. That's fine. All stories and characters discussed are fictional in nature. No identification with actual persons, living or deceased places, buildings, or products is intended or should be inferred this podcast is for entertainment purposes only. The podcast and its contents do not constitute professional mental health or medical advice. Listeners might consider consulting a mental health provider if they need assistance with any mental health problems or concerns. As always, please call 911 or go directly to your nearest emergency room for any psychiatric emergencies. Thanks for listening and see you next time.

christmas america god tv jesus christ american new york tiktok thanksgiving new york city hollywood starting talk nba merry christmas er mom funny theater santa eating indian taylor swift turkey temple adhd muslims adult doom terrible air force cdc indiana jones fda santa claus ghostbusters sequels parkinson steven spielberg die hard sees vhs pg increased northeast home alone summertime porsche gremlins unbelievable spielberg haitian ruining kicks christmastime goonies pakistani container american horror story scripts washington wizards dsm php overeating delicate vcr monsoons gizmo mris pendleton furby beanie theoretically mirza wellness programs esop youtubing loudon shih phoebe cates begrudgingly galima kingston falls parkinsonian north virginia

Atypical Parkinsonism Series: Unique Care Needs of PSP, CBD and MSA and Helpful Resources

Play Episode Listen Later Oct 17, 2023 32:16

Considered “atypical Parkinsonian syndromes,” over half of people with progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA) are initially misdiagnosed with Parkinson's disease (PD) due to similarities in early symptoms as well as lack of awareness of these rare, neurodegenerative diseases among many healthcare professionals and the general public. This is the third of three podcast episodes within our atypical parkinsonism podcast series, organized in partnership with CurePSP and designed to address the unique care needs across the disease stages of PSP, CBD and MSA. Jessica Shurer, Director of Clinical Affairs and Advocacy at CurePSP, and Nancy Montgomery, who cared for her husband who was diagnosed with progressive supranuclear palsy, cover common challenges experienced by people living with PSP, CBD or MSA and describe helpful resources and roles played by healthcare teams that support the quality of life of patients and family care partners. Jessica Shurer, Nancy Montgomery, and podcast host, Dan Keller, have disclosed that they have no relevant financial disclosures.

director care unique cbd advocacy parkinson helpful pd psp atypical parkinsons msa clinical affairs parkinsonism parkinsonian dan keller

Atypical Parkinsonism Series: Treatment and Interdisciplinary Approach to Care

Substantial Matters: Life & Science of Parkinson’s

Play Episode Listen Later Oct 3, 2023 29:53

Considered “atypical Parkinsonian syndromes,” over half of people with progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA) are initially misdiagnosed with Parkinson's disease (PD) due to similarities in early symptoms as well as lack of awareness of these rare, neurodegenerative diseases among many healthcare professionals and the general public. This is the second of three podcast episodes within our atypical parkinsonism podcast series, organized in partnership with CurePSP and designed to address the treatment interdisciplinary approach of PSP, CBD and MSA. In this second episode of the series, Heather Cianci, Outpatient Neurological Team Leader and founding therapist of the Dan Aaron Parkinson's Rehabilitation Center, Penn Therapy & Fitness at Pennsylvania Hospital in Philadelphia, Pennsylvania and Julia Wood, Director of Professional and Community Education at the Lewy Body Dementia Association, cover the treatment and interdisciplinary approach to care for atypical parkinsonism. Julia Wood, Heather Cianci, and podcast host, Dan Keller, have disclosed that they have no relevant financial disclosures.

Effects of Cerebrovascular and Lewy Body Pathology on Parkinsonian Signs in Community-Dwelling Older Adults

Play Episode Listen Later Sep 14, 2023 1:31

body signs effects dwellings pathologies lewy bodies cerebrovascular parkinsonian community dwelling older adults

Effects of Cerebrovascular and Lewy Pathology on Parkinsonian Signs

signs journal effects drs pd neurology pathologies lewy cerebrovascular parkinsonian

Play Episode Listen Later Sep 11, 2023 19:28

Dr. Matt Barrett talks with Drs. Julie A. Schneider and Sonal Agrawal about whether Lewy body and cerebrovascular pathologies act synergistically to increase the severity of parkinsonism beyond their separate effects. Read the related article in Neurology. Visit NPUb.org/Podcast for associated article links.

Episode 158: Atypical Parkinsonism Series: Overview, Diagnosis and Prevalence

Substantial Matters: Life & Science of Parkinson’s

Play Episode Listen Later Sep 5, 2023 32:46

Considered “atypical Parkinsonian syndromes,” over half of people with progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA) are initially misdiagnosed with Parkinson's disease (PD) due to similarities in early symptoms as well as lack of awareness of these rare, neurodegenerative diseases among many healthcare professionals and the general public. This is the first of three podcast episodes within our atypical parkinsonism podcast series, organized in partnership with CurePSP and designed to address the overview, treatment and care of PSP, CBD and MSA. In this first episode of the series, Dr. Alex Pantelyat, Associate Professor of Neurology at Johns Hopkins University School of Medicine shares an overview of atypical parkinsonism, overlaps and differences with Parkinson's disease, the red flags and how PSP, CBD and MSA are diagnosed. Dr. Pantelyat has disclosed that he is a Scientific Advisory Board Consultant for MedRhythms, Inc. and a consultant for both Ferrer Internacional, S.A. and SciNeuro Pharmaceuticals. Podcast host, Dan Keller, has disclosed that he has no relevant financial disclosures.

medicine associate professor cbd diagnosis parkinson johns hopkins university pd neurology psp prevalence atypical parkinsons msa parkinsonism parkinsonian dan keller

[IMJ On-Air] A tiger in the mallee: Victoria's JEV cluster

Pomegranate Health

Play Episode Listen Later Jul 16, 2023 43:46

On the 28th of January 2022 a 75-year-old man was admitted to the regional Albury Wodonga Health Service with a high fever and Parkinsonian symptoms. The patient spent over a week in intensive care, but brain scans did not reveal an obvious aetiology and assays for a range of pathogens came up negative.When serology eventually revealed the presence of antibodies against Japanese encephalitis virus this became only the second ever locally-acquired case on Australia's mainland. Even more startling was the fact that the previous one had been way back in 1998 in Cape York, far north Queensland. The Victorian patient was the first what would become an outbreak of 43 symptomatic human cases that resulted in six deaths. The JE virus would be detected in all mainland states and retrospectively linked to another fatality in March 2021 from the Tiwi islands of the Northern Territory. In this podcast we hear about the confluence of factors that brought a classically tropical disease to the southern states. The story is told from the perspective of the treating clinicians, microbiology specialist and public health physician who started putting the puzzle together from four sentinel cases. Key ReferenceSamuel Thorburn, Deborah Friedman, John Burston, Paul M Kinsella, Genevieve E Martin, Deborah Williamson, Justin Jackson. Sentinel cluster of locally acquired Japanese encephalitis in southern Australia. Internal Medicine Journal. 2023;53(5):835-840Member access to Internal Medicine Journal, Journal of Paediatrics and Child Health and Occupational Medicine JournalGuestsAdjunct Associate Professor Ian Woolley FRACP (Monash Infectious Diseases; Monash University) Dr Justin Jackson FRACP (Albury Wodonga Health)Dr Sam Thorburn (Austin Health)Dr Paul Kinsella (Victorian Infectious Diseases Reference Laboratory, Peter Doherty Institute for Infection and Immunity)Associate Professor Deborah Friedman FRACP (Victorian Department of Health; Deakin University)ProductionProduced by Mic Cavazzini DPhil. Music licenced from Epidemic Sound includes ‘Dusty Delta Day' and ‘Hard Shoulder' by Lennon Hutton. Image from Smith Collection/ Gado licenced from Getty Images. Editorial feedback kindly provided by Dr Aidan Tan. Please visit the Pomegranate Health web page for a transcript and supporting references. Login to MyCPD to record listening and reading as a prefilled learning activity. Subscribe to new episode email alerts or search for ‘Pomegranate Health' in Apple Podcasts, Spotify,Castbox, or any podcasting app.

Rit2 loss in dopaminergic neurons drives a progressive Parkinsonian phenotype

Play Episode Listen Later Apr 28, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.26.538430v1?rss=1 Authors: Kearney, P. J., Zhang, Y., Tan, Y., Kahuno, E., Conklin, T., Fagan, R. R., Yue, Z., Melikian, H. E., Shaffer, S. A., Pavchinskiy, R. G. Abstract: Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Modeling synaptic integration of bursty and beta oscillatory inputs in ventromedial motor thalamic neurons in normal and parkinsonian states

Play Episode Listen Later Apr 15, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.14.536959v1?rss=1 Authors: Cavarretta, F., Jaeger, D. Abstract: The Ventromedial Motor Thalamus (VM) is implicated in multiple motor functions and occupies a central position in the cortico-basal ganglia-thalamocortical loop. It integrates glutamatergic inputs from motor cortex (MC) and motor-related subcortical areas, and it is a major recipient of inhibition from basal ganglia. Previous experiments in vitro showed that dopamine depletion enhances the excitability of thalamocortical cells (TC) in VM due to reduced M-type potassium currents. To understand how these excitability changes impact synaptic integration in vivo, we constructed biophysically detailed VM TC models fit to normal and dopamine-depleted conditions, using the NEURON simulator. These models allowed us to assess the influence of excitability changes with dopamine depletion on the integration of synaptic inputs expected in vivo. We found that VM TCs in the dopamine-depleted state showed increased firing rates with the same synaptic inputs. Synchronous bursting in inhibitory input from the substantia nigra pars reticulata (SNR), as observed in parkinsonian conditions, evoked a post-inhibitory firing rate increase with a longer duration in dopamine-depleted than control conditions, due to different M-type potassium channel densities. With beta oscillations in the inhibitory inputs from SNR and the excitatory inputs from drivers and modulators, we observed spike-phase locking in the activity of the models in normal and dopamine-depleted states, which relayed and amplified the oscillations of the inputs, suggesting that the increased beta oscillations observed in VM of parkinsonian animals are predominantly a consequence of changes in the presynaptic activity rather than changes in intrinsic properties. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Structural Plasticity of GABAergic Pallidothalamic Terminals in MPTP-treated Parkinsonian Monkeys: A 3D Electron Microscopic Analysis

Play Episode Listen Later Apr 6, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.05.535706v1?rss=1 Authors: Masilamoni, G. J., Kelly, H., Swain, A., Pare, J.-F., Villalba, R., Smith, Y. Abstract: The globus pallidus pars interna (GPi) is a major source of GABAergic inhibition upon the motor thalamus. GPi neurons are endowed with properties that allow them to fire at a high rate and maintain a tonic inhibitory influence upon thalamocortical neurons. In parkinsonism, the firing rate of GPi neurons is further increased and their firing pattern switches from a tonic to a bursty mode, two pathophysiological changes associated with increased GABAergic pallidothalamic activity. At the thalamic level, GPi terminals display ultrastructural features (large diameter, multiple synapses, large number of mitochondria) that allow them to maintain tonic synaptic inhibition at high firing rate upon thalamocortical neurons in the parvocellular ventral anterior nucleus (VApc) and the centromedian nucleus (CM), the two main GPi-recipient motor thalamic nuclei in nonhuman primates. To determine if changes of GPi neurons activity are associated with neuroplastic reorganization of GPi terminals and their synapses, we used a Single Block Facing/Scanning Electron Microscopy (SBF/SEM), high resolution 3D electron microscopic approach to compare the morphometry of GPi terminals between 2 control and 2 MPTP-treated parkinsonian monkeys. Our findings demonstrate that pallidothalamic terminals in VApc and CM undergo major ultrastructural changes in parkinsonian monkeys: (1) increased terminal volume in both nuclei, (2) increased surface area of synapses in both nuclei, (3) increased number of synapses/GPi terminals in the CM, but not VApc, (4) increased total volume of mitochondria/terminals in both nuclei but not in the number of mitochondria. In contrast, the ultrastructure of putative GABAergic terminals from the reticular thalamic nucleus was not affected in both the VApc and CM of parkinsonian monkeys. Our findings also show striking morphological differences in terminal volume, number/area of synapses and volume/number of mitochondria between GPi terminals in VApc and CM of control monkeys. In conclusion, results of this study demonstrate that GABAergic pallidothalamic terminals are endowed with a high level of structural plasticity that may contribute to the development and maintenance of the abnormal increase in pallidal GABAergic outflow to the thalamus in the parkinsonian state. Furthermore, the evidence for ultrastructural differences between GPi terminals in VApc and CM suggests that morphologically distinct pallidothalamic terminals underlie specific physiological properties of pallidal inputs to VApc and CM in normal and diseased states. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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The autophagy protein Atg9 functions in glia and contributes to parkinsonian symptoms in a Drosophila model of Parkinson's disease

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Play Episode Listen Later Apr 3, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.03.535355v1?rss=1 Authors: Yi, S., Wang, L., Ho, M. S., Zhang, S. Abstract: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the motor deficits, selective loss of dopaminergic (DA) neurons, and the brain accumulation of [alpha]-synuclein ([alpha]-syn)-composed protein aggregates called Lewy bodies (LBs). Whereas dysfunction in the protein degradation pathway, like autophagy in neurons, has been demonstrated as a critical mechanism for eliminating protein aggregates in PD, how protein aggregates are eliminated in the other brain cell type, glia, is less well characterized. In the present study, we show that Atg9, the only transmembrane protein in the core autophagy pathway, is highly expressed in Drosophila adult brain glia. Results from immunostaining and live-cell imaging analysis reveal that a significant portion of Atg9 localizes to the trans-Golgi network (TGN), autophagosomes, and lysosomes in glia; Atg9 is persistently in contact with these organelles. Lacking glial atg9 reduces the number of omegasome and autophagosome and impairs autophagic substrate degradation, suggesting that glial Atg9 participates in the early steps of autophagy, hence the control of autophagic degradation. Importantly, loss of glial atg9 induces parkinsonian symptoms in Drosophila including progressive DA neuron loss and locomotion deficits. Our findings identify a functional role of Atg9 in glial autophagy and establish a potential link between glial autophagy and PD. These results provide new insights on the underlying mechanism of PD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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THG Episode: 113 | The Hippocratic Truth: Healing, Politics, and Modern Medicine

The Hidden Gateway

Play Episode Listen Later Mar 23, 2023 62:29

Join us for Episode 113 on the Hidden Gateway Podcast, where we welcome Dr. David Marquis! Dr. David Marquis is skilled in the functional medicine approach to evaluation and care of complex and chronic health concerns. He has a focused interest in neurodegenerative and neurodevelopmental conditions including autism spectrum, TBI, Parkinsonian tremors, dementia, Alzheimer's, and CTE, and also has 25+ years of experience supporting patients with common metabolic conditions including endocrine-related disorders of thyroid, diabetes, and sex hormone imbalances. Dr. Marquis continuously advances his knowledge in Functional Medicine and Functional Neurology with over 100 hours annually of post-doctorate education. He is an accomplished public speaker and writer as well as a recurring guest lecturer. In this episode, we discuss the truths behind the pandemic, vaccines, proper care for C19 patients, and how the chaos and confusion are linked to spiritual warfare. This is an important conversation that you need to hear! Don't miss this BANGER!!! Connect with Dr. Marquis Website: https://pathwaystohealth.net/ Twitter: https://twitter.com/DrDavidMarquis1 Facebook: https://www.facebook.com/DrDavidMarquis/ YouTube: https://www.youtube.com/channel/UCfvrkTOtnRzz2vuEpRItqwQ . . . . . . #soulawakening #consiousness #innerwisdom #quantumfield #higherdimensions #lightbody #raiseyourfrequency #conciousness #thirdeyeawakening #metaphysics #quantumhealing #ascendedmasters #consciousawakening #awakenyoursoul #thirdeyethirst #manifestingdreams #powerofpositivtiy #spiritualawakenings #higherconscious #spiritualthoughts #lightworkersunited #highestself #positiveaffirmation #loaquotes #spiritualinspiration #highvibrations #spiritualhealers #intuitivehealer #powerofthought #spiritualityreignssupreme --- Support this podcast: https://podcasters.spotify.com/pod/show/thehiddengateway/support

Cerebellar Activity in Hemi-Parkinsonian Rats during Volitional Gait and Freezing

Play Episode Listen Later Mar 1, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.28.530475v1?rss=1 Authors: DeAngelo, V., Gehan, A., Paliwal, S., Ho, K., Hilliard, J. D., Chiang, C.-H., Viventi, J., McConnell, G. C. Abstract: Parkinson's disease is a neurodegenerative disease characterized by gait dysfunction in the advanced stages of the disease. The unilateral 6-OHDA toxin-induced model is the most studied animal model of Parkinson's disease, which reproduces gait dysfunction after greater than 68% dopamine (DA) loss in the substantia nigra pars compacta (SNc). The extent to which the neural activity in hemi-parkinsonian rats correlates to gait dysfunction and DAergic cell loss is not clear. In this paper we report the effects of unilateral DA depletion on cerebellar vermis activity using micro-electrocorticography (ECoG) during walking and freezing on a runway. Gait and neural activity were measured in 6-OHDA lesioned and sham lesioned rats at 14d, 21d, and 28d after infusion of 6-OHDA or control vehicle into the medial forebrain bundle (MFB) (n=20). Gait deficits in 6-OHDA rats were different from sham rats at 14d (p less than 0.05). Gait deficits in 6-OHDA rats improved at 21d and 28d except for run speed, which decreased at 28d (p=0.018). No differences in gait deficits were observed in sham lesioned rats at any time points. Hemi-parkinsonian rats showed hyperactivity in the cerebellar vermis at 21d (p less than 0.05), but not at 14d and 28d, and the activity was reduced during freezing epochs in lobules VIa, VIb, and VIc (p less than 0.05). These results suggest that DAergic cell loss causes pathological cerebellar activity at 21d post-lesion and suggests that compensatory mechanisms from the intact hemisphere contribute to normalized cerebellar activity at 28d. The decrease in cerebellar oscillatory activity during freezing may be indicative of neurological changes during freezing of gait in Parkinson's disease patients making this region a potential location for biomarker detection. Although the unilateral 6-OHDA model presents gait deficits that parallel clinical presentations of Parkinson's disease, further studies in animal models of bilateral DA loss are needed to understand the role of the cerebellar vermis in Parkinson's disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Parkinsonian rest tremor can be distinguished from voluntary hand movements based on subthalamic and cortical activity using machine learning

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Play Episode Listen Later Feb 8, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.07.527275v1?rss=1 Authors: Todorov, D., Schnitzler, A., Hisrchmann, J. Abstract: Tremor is one of the cardinal symptoms of Parkinson's disease. The neurophysiology of tremor is not completely understood, and so far it has not been possible to distinguish tremor from voluntary hand movements based on local brain signals. Here, we re-analyzed magnetoencephalography and local field potential recordings from the subthalamic nucleus of six patients with Parkinson's disease. Data were obtained after withdrawal from dopaminergic medication (Med Off) and after administration of levodopa (Med On). Using gradient-boosted tree learning, we classified epochs as tremor, self-paced fist-clenching, static forearm extension or tremor-free rest. While decoding performance was low when using subthalamic activity as the only feature (balanced accuracy mean: 38%, std: 7%), we could distinguish the four different motor states when considering cortical and subthalamic features (balanced accuracy mean: 75%, std: 17%). Adding a single cortical area improved classification by 17% on average, as compared to classification based on subthalamic activity alone. In most patients, the most informative cortical areas were sensorimotor cortical regions. Decoding performance was similar in Med On and Med Off. Our results demonstrate the advantage of monitoring cortical signals in addition to subthalamic activity for movement classification. By combining cortical recordings, subcortical recordings and machine learning, future adaptive systems might be able to detect tremor specifically and distinguish between several motor states. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

BrainWaves #68 Teaching through clinical cases: A man with falls

MedLink Neurology Podcast

Play Episode Listen Later Feb 2, 2023 21:44

MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: July 18, 2017 People fall for a lot of reasons when they get older, but that doesn't mean they should see a neurologist. A person can fall because of weakness, back or leg pain, instability, clumsiness, vision impairment, a sensory disturbance, and a myriad of other causes. Some of these are neurological, and these require special attention. In this week's Teaching through Clinical Cases episode, Dr. Sneha Mantri discusses a patient who presented to her clinic with falls due to rigidity and ocular dysmotility. Produced by James E Siegler. Music by Josh Woodward and Julie Maxwell. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. REFERENCES Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 6th ed. Lippincott Williams and Wilkins, 2011.Hess CW, Okun MS. Diagnosing Parkinson disease. Continuum (Minneap Minn) 2016;22(4 Movement Disorders):1047-63. PMID 27495197Garbutt S, Riley DE, Kumar AN, Han Y, Harwood MR, Leigh RJ. Abnormalities of optokinetic nystagmus in progressive supranuclear palsy. J Neurol Neurosurg Psychiatry 2004;75(10):1386-94. PMID 15377682McFarland NR. Diagnostic approach to atypical Parkinsonian syndromes. Continuum (Minneap Minn) 2016;22(4 Movement Disorders):1117-42. PMID 27495201 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.

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Intragastric administration of low-dose rotenone post-colitis exacerbates damage to the nigrostriatal dopaminergic system in Parkinson's disease: The pace accelerates even more

Play Episode Listen Later Dec 22, 2022

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.22.521569v1?rss=1 Authors: Sharma, N., Sharma, M., Thakkar, D., Kumar, H., Smetanova, S., Buresova, L., Andrla, P., Khairnar, A. Abstract: Background: The contribution of gastrointestinal (GI) inflammation and local exposure to neurotoxins in the gut offers the most in-depth explanation of Parkinson's disease (PD) etiopathogenesis through abnormal accumulation and spreading of alpha-synuclein (-syn) aggregates from the gut to the brain. Objectives: This study was designed to investigate whether dextran sodium sulfate (DSS)-mediated colitis may have lasting effects on dopaminergic pathways in the brain and whether or not colitis exacerbated susceptibility to later exposure to the neurotoxin rotenone. Methods: To induce chronic colitis, 10 months old C57BL/6 mice were pre-exposed to 3 cycles of 7 days of 1% (w/v) DSS administration in drinking water followed by 14 days of regular drinking water. After colitis-induction, animals received a low dose of intragastric rotenone for the next 8 weeks, followed by testing for Parkinsonian behavior and GI phenotypes of inflammation. At the end of the 8th week after colitis, colon, brain stem, and midbrain tissue were isolated and analyzed for -syn, inflammatory markers, and dopaminergic neuronal loss. Gut microbial composition was assessed by 16S rRNA sequencing analysis. Results: We found that local rotenone exposure for 8 weeks did not affect colitis severity and colonic tight junction (TJ) protein expression (ZO-1, Occludin, and Claudin-1). On the other hand, we found that while eight weeks of chronic rotenone administration led to an increase in inflammatory markers, the presence of pre-existing colitis resulted in a considerable change in gut microbiota composition and a decrease in TJ's protein expression. In addition, the administration of rotenone in mice post-colitis caused gastrointestinal function impairment and poor behavioral performances. Itworsened rotenone-induced -syn pathology in the colon, which extended upward and resulted in severe dopaminergic neuron loss and significant astroglia activation in the dorsal motor nucleus of the vagus (DMV), locus coeruleus, substantia nigra as well as in striatum. Interestingly, in the case of rotenone alone, we found that -syn induced ChAT+ neuronal death is restricted to the DMV. These findings indicate that long-term rotenone exposure in conjunction with early inflammatory intestinal milieu exacerbates the progression of -syn pathology and aggravates neurodegeneration in the intragastric mouse PD model. Conclusions: This work provides detailed insight into the involvement of GI inflammation triggered after a neurotoxic insult in the colon and explores their potential to impact central dopaminergic degeneration in PD. This way, we can identify potential therapeutic targets that stop the enteric inflammatory processes involved in progressing PD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Drug repurposing of dopaminergic drugs to inhibit Ataxin-3 aggregation

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Play Episode Listen Later Dec 2, 2022

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.01.518659v1?rss=1 Authors: Figueiredo, F., Sarkany, Z., Silva, A., Martins, P. M., Macedo-Ribeiro, S. Abstract: The accumulation of mutant ataxin-3 (Atx3) in neuronal nuclear inclusions is a pathological hallmark of Machado-Joseph disease (MJD), also known as Spinocerebellar Ataxia Type 3. Decreasing the protein aggregation burden is a possible disease-modifying strategy to tackle MJD and other neurodegenerative disorders for which only symptomatic treatments are currently available. We performed a drug repurposing screening to identify inhibitors of Atx3 aggregation with known toxicological and pharmacokinetic profiles. Interestingly, dopamine hydrochloride and other catecholamines are among the most potent inhibitors of Atx3 aggregation in vitro. Our results indicate that low micromolar concentrations of dopamine markedly delay the formation of mature amyloid fibrils of mutant Atx3 through the inhibition of the earlier oligomerization steps. Although dopamine itself does not pass the blood-brain barrier, dopamine levels in the brain can be increased by low doses of dopamine precursors and dopamine agonists commonly used to treat Parkinsonian symptoms. These findings disclose a possible application of dopaminergic drugs to halt or reduce Atx3 accumulation in the brains of MJD patients. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Music Mends Minds, Part 1

Answers For Elders Radio Network

Play Episode Listen Later Nov 5, 2022 13:25

Carol Rosenstein, the founder of Music Mends Minds, joins Suzanne to talk about how music transforms people's lives, particularly those suffering from Parkinson's disease, dementia, or Alzheimer's. Carol was deeply affected by this story: “In 1992, Dr. Concerto Tomano was a newly graduated music therapist. She was summoned to a local facility of end-stage dementia patients. The facility said, come and entertain our people. They are "the water and feeding group" because their brains are gone. She showed up in a communal area flanked by dementia patients that were in wheelchairs, some with mittens and their hands secured so that they couldn't get out of the wheelchair, others that were standing around in catatonic states, and she started to play the piano. Within seconds, these people started singing, mouthing, and moving to the music. “I was so transfixed by her story. My precious Owen, who is now gone almost two years, had Parkinson's and dementia. Ten years into the journey, he had medication issues. As a Parkinsonian patient, he was taking synthetic dopamine several times a day. His brain was on overload. He was hallucinating, he was agitated. Our neurologist read these clinical findings, and said, it's the dopamine, Carol, bring down the dose. You know that your beloved becomes a wet noodle – the hallucinations were gone, the agitation was gone, but my guy was spent. He played the piano socially, sitting at the piano, as a wet noodle. I would see him become a dry one. Within five, ten minutes he had re-entered the environment as if I had given him a dose of med. And seeing this repeatedly, and with my clinical eye, I told the doctor, and he said that we're watching the power of music changing brain chemistry. “I said, can I get a few like-minded souls and let's jam and make music together and have all of them respond? He says yes. And that's when everything started to change in my household, and in many many other households. Because I called for a launch. Thirty strangers arrived at a local private school in their music studio. They had the Steinway piano and the drum kit and a wall full of instruments for any kid to choose whatever they want for the session. And here thirty people gathered. One of them went to the Steinway piano, another to the drum kit as a drummer. My husband took a saxophone off the wall, and Sam opened up his jacket pocket and pulled out a harmonica out of his jacket pocket, and before you knew it, 15 minutes later, these total strangers, all with our diagnoses, were joined at the hip making music together. That was the start of the Fifth Dementia band. “It just is so important to understand music is medicine for the mind, regardless of what ails you. We have a partnership with Rotary International that takes us global. ''Rotary'' magazine featured us in the May 2022 edition with a seven page story and me on the cover. So we reach out to share with people how they can start a musical group through their organizations to reach the seniors who need the music. Because music is medicine, and changed their lives.” Learn more at https://www.musicmendsminds.org/. You can also text or call (818) 326- 0500.

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Music Mends Minds, Part 2

Answers For Elders Radio Network

Play Episode Listen Later Nov 5, 2022 13:34

Carol Rosenstein, the founder of Music Mends Minds, joins Suzanne to talk more about how music transforms those suffering from Parkinson's disease, dementia, or Alzheimer's. Carol wants to bring our attention to two important takeaways. First, there are cells in our brains that have to do with music memory storage. Those cells are generated when a fetus in utero is six months old. They're already hearing a lullaby of "Twinkle Twinkle Little Star" being played in mommy's bedroom. Research shows that those lullabies are recognized after they're born. The second thing is that we have a personal pharmacy within our own brains. Music is a catalyst that can release a neurotransmitter chemical. A Parkinson patient, they have dopamine deficiency. Music triggers a release of dopamine so that a Parkinsonian walks better, thinks better, talks better, feels better. Somebody sitting clapping to a melody, or tapping to a melody, doesn't have exactly the same trigger in the brain as somebody playing piano. There's music, there's notes, there's pedals, there's harmonics, and so the intensity of the music making has the most important effect on how much of that chemical is going to be released into the system. Carol says, “We don't only administer to the patients. How about the caregiver? Ehree seconds, somebody's being diagnosed with dementia, every 65 seconds somebody with Alzheimer's, every five minutes somebody with Parkinson's. We're on a pandemic parallel pathway that COVID took us on, and we can show that music helps to stabilize us all.” For more information, email Carol at info@musicmendsminds.org/, call her at (818) 326-0500, and you can donate to keep them growing at https://www.musicmendsminds.org/.

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Apoptotic factors and mitochondrial complexes assist determination of strain-specific susceptibility of mice to Parkinsonian neurotoxin MPTP

Play Episode Listen Later Oct 7, 2022

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.05.511004v1?rss=1 Authors: Haorei, Y., Vidyadhara, D., Nambisan, A. K., Raju, T. R., Sagar, B. K. C., Alladi, P. A. Abstract: Identification of genetic mutations in Parkinson's disease (PD) promulgates the genetic nature of disease susceptibility. Resilience-associated genes being unknown till date, the normal genetic makeup of an individual may be determinative too. Our earlier studies comparing the substantia nigra (SN) and striatum of C57BL/6J, CD-1 mice and their F1- crossbreds demonstrated neuroprotective role of admixing, against the neurotoxin MPTP. Further, the differences in levels of mitochondrial fission/fusion proteins in the SN of parent strains, imply effect on mitochondrial biogenesis. Our present investigations suggest that the baseline levels of apoptotic factors Bcl-2, Bax and AIF differ across the three strains and, are differentially altered in SN following MPTP-administration. The reduction in complex-I levels exclusively in MPTP-injected C57BL/6J, reiterate mitochondrial involvement in PD pathogenesis. The MPTP induced increase in complex-IV, in the nigra of both parent strains may be compensatory in nature. Ultrastructural evaluation showed fairly preserved mitochondria in the dopaminergic neurons of CD-1 and F1-crossbreds. However, in CD-1, the endoplasmic reticulum demonstrated distinct luminal enlargement, bordering onto ballooning, suggesting proteinopathy as a possible initial trigger. The increase in -synuclein in the pars reticulata of crossbreds suggests a supportive role for this output nucleus in compensating for the lost function of pars compacta. Alternatively, since -synuclein over-expression occurs in different brain regions in PD, the -synuclein increase here may suggest similar pathogenic outcome. Further understanding is required to resolve this biological contraption. Nevertheless, admixing reduces the risk to MPTP by favouring anti-apoptotic consequences. Similar neuroprotection may be envisaged in the admixed populace of Anglo-Indians. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Improving fMRI in Parkinson's Disease by Accounting for Brain Region-Specific Activity Patterns

university children minnesota illinois ptsd adult alzheimer's disease engage cbd autism adults parkinson medications genetics condition physical body aging adults parkinsonian

Play Episode Listen Later Sep 1, 2022

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.08.30.505786v1?rss=1 Authors: Torrecuso, R., Mueller, K., Sieger, T., Vymazal, J., Ruzicka, F., Roth, J., Ruzicka, E., Schroeter, M. L., Jech, R., Möller, H. E. Abstract: In functional magnetic imaging (fMRI) in Parkinson's disease (PD), a paradigm consisting of blocks of finger tapping and rest along with a corresponding general linear model (GLM) is often used to assess motor activity. However, this method has three limitations: (i) Due to the Strong magnetic field and the confined environment of the cylindrical bore, it is troublesome to accurately monitor motor output and, therefore, variability in the performed movement is typically ignored. (ii) Given the loss of dopaminergic neurons and ongoing compensatory brain mechanisms, motor control is abnormal in PD. Therefore, modeling of patients' tapping with a constant amplitude (using a boxcar function) and the expected Parkinsonian motor output are prone to mismatch. (iii). The motor loop involves structures with distinct hemodynamic responses, for which only one type of modeling (e.g., modeling the whole block of finger tapping) may not suffice to capture these structure's temporal activation. The first two limitations call for considering results from online recordings of the real motor output that may lead to significant sensitivity improvements. This was shown in previous work using a non-magnetic glove to capture details of the patients' finger movements in a so-called kinematic approach. For the third limitation, modeling motion initiation instead of the whole tapping block has been suggested to account for different temporal activation signatures of the motor loop's structures. In the present study we propose improvements to the GLM as a tool to study motor disorders. For this, we test the robustness of the kinematic approach in an expanded cohort (n=31), apply more conservative statistics than in previous work, and evaluate the benefits of an event-related model function. Our findings suggest that the integration of the kinematic approach offers a general improvement in detecting activations in subcortical structures, such as the basal ganglia. Additionally, modeling motion initiation using an event-related design yielded superior performance in capturing medication-related effects in the putamen. Our results may guide adaptations in analysis strategies for functional motor studies related to PD and also in more general applications. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

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Q and A Episode: Autism and the Physical Body

Autism in the Adult

Play Episode Listen Later Jul 5, 2022 40:28 Transcription Available

Join Dr. Regan for an episode in which she answers listener questions related to autism and the physical body. Topics include genetics, brain pathways and neurology, nature versus nurture, medications, and nutrition/diet. Genetics and Autism article Neurogenetics: Smith-Magenis Syndrome Autism and Medication review Dr. Regan's Resources New Course for Clinicians - Interventions in Autism: Helping Clients Stay Centered, Connect with Others, and Engage in Life New Course for Clinicians: ASD Differential Diagnoses and Associated Characteristics Book: Understanding Autism in Adults and Aging Adults, 2nd ed Audiobook Book: Understanding Autistic Behaviors Autism in the Adult website homepage Website Resources for Clinicians Read the Transcript: 00:00:11,040 --> 00:00:14,410 Hello and thanks for joining me. 3 00:00:14,420 --> 00:00:18,220 This is Dr Theresa Regan welcoming you to the podcast, 4 00:00:18,230 --> 00:00:19,960 autism in the adult. 5 00:00:19,970 --> 00:00:22,170 I am a neuropsychologist, 6 00:00:22,180 --> 00:00:24,880 a certified autism specialist. 7 00:00:24,890 --> 00:00:30,150 The director of an autism diagnostic clinic for adolescents, 8 00:00:30,340 --> 00:00:32,100 adults and aging. 9 00:00:32,100 --> 00:00:36,760 Adults in Illinois and the parent of a teen on the spectrum. 10 00:00:39,040 --> 00:00:47,950 Last episode I invited listeners to write in questions they would like me to field in a question and answer podcast. 11 00:00:48,640 --> 00:01:01,940 So what I've done is that I have gone through and tried to group some of the questions into related categories and I won't get to all of the questions in this episode. 12 00:01:01,940 --> 00:01:09,560 But I am going to focus on several questions today that have to do with autism and the physical body. 13 00:01:10,240 --> 00:01:14,150 So we're going to review things like genetics, 14 00:01:14,460 --> 00:01:18,850 neuro anatomy and the physical brain in autism. 15 00:01:19,240 --> 00:01:26,060 We're also going to talk about things like nutrition and diet and other physical aspects, 16 00:01:26,440 --> 00:01:30,160 things that may impact the individual on the spectrum. 17 00:01:30,540 --> 00:01:33,450 Let's take the topic of genetics First. 18 00:01:35,840 --> 00:01:57,660 A recent article about the genetics of autism found that at least 80 percent of the likelihood that someone will have autism neurology is driven by the genetic code and it's the code that impacts the development of the neurology within that individual. 19 00:01:58,040 --> 00:01:58,390 So, 20 00:01:58,390 --> 00:02:04,960 the neurology includes of course the brain and its nuclei and its pathways, 21 00:02:05,440 --> 00:02:07,850 genetics includes code, 22 00:02:07,860 --> 00:02:11,650 parts that are inherited that is, 23 00:02:11,650 --> 00:02:20,340 there are some families with autism characteristics across multiple family members. 24 00:02:20,430 --> 00:02:24,460 Some members may not have any characteristics, 25 00:02:24,520 --> 00:02:28,960 some may have a clustering of autistic characteristics, 26 00:02:28,970 --> 00:02:31,420 but not a formal diagnosis. 27 00:02:31,420 --> 00:02:37,650 They don't meet full threshold for the diagnosis and others will meet full threshold. 28 00:02:38,140 --> 00:02:42,230 So for some people who are diagnosed with autism, 29 00:02:42,230 --> 00:02:44,760 they can see characteristics, 30 00:02:44,760 --> 00:02:49,450 qualities of this neurology and various family members, 31 00:02:49,840 --> 00:02:57,230 genetics also includes possible alterations in the code during development. 32 00:02:57,230 --> 00:03:02,210 So it can also mean that the genetics were not inherited, 33 00:03:02,220 --> 00:03:10,950 but that there were some unexpected alterations of the code as the brain and the nervous system were developing. 34 00:03:11,540 --> 00:03:22,250 That brings forth this autistic neurology and it is not as simple as saying that someone has the gene and someone does not. 35 00:03:22,260 --> 00:03:34,660 This is a hugely complex Condition that is a reflection of at least 200 likely many more genetic contributions. 36 00:03:35,140 --> 00:03:46,850 So that can be part of why we see autism on a spectrum that a certain clustering of genetics may produce certain characteristics, 37 00:03:46,850 --> 00:03:49,800 while another clustering may produce others, 38 00:03:49,800 --> 00:03:51,010 we just don't know, 39 00:03:51,020 --> 00:03:54,410 we're not at the point where we have all of that nailed down, 40 00:03:54,410 --> 00:04:06,960 but what we do know is that genetics plays a role in the development of the nervous system and specifically in the development of the neurology associated with autism. 41 00:04:10,240 --> 00:04:10,670 Also, 42 00:04:10,670 --> 00:04:18,460 autism may co occur with other physical conditions that are related to genetics. 43 00:04:19,140 --> 00:04:21,750 They're related to development. 44 00:04:22,140 --> 00:04:22,680 Um, 45 00:04:22,690 --> 00:04:24,980 as guided by the genetic code. 46 00:04:24,990 --> 00:04:25,670 So, 47 00:04:25,670 --> 00:04:26,550 for example, 48 00:04:26,550 --> 00:04:33,740 some individuals have a difference in the way their heart was formed or the kidneys or their palate, 49 00:04:33,740 --> 00:04:35,250 like a cleft palate. 50 00:04:36,240 --> 00:04:41,850 Also in some Children who have childhood cancers, 51 00:04:41,850 --> 00:04:45,950 there's some association with a genetic difference, 52 00:04:45,950 --> 00:04:52,560 that something in the code has been different and is related to the triggering of this cancer. 53 00:04:56,340 --> 00:05:02,280 What that can mean is that for people with a heart difference, 54 00:05:02,280 --> 00:05:03,200 for example, 55 00:05:03,200 --> 00:05:04,610 that is congenital, 56 00:05:04,610 --> 00:05:07,990 this is something that happened during development. 57 00:05:08,000 --> 00:05:10,150 It has been there since birth. 58 00:05:10,740 --> 00:05:31,460 There can be an increased presence of also a typical neurology that these things that have developed around the same time or secondary to similar parts of the genetic code can co occur. 59 00:05:32,140 --> 00:05:32,700 So, 60 00:05:32,710 --> 00:05:33,760 research shows, 61 00:05:33,760 --> 00:05:34,650 for example, 62 00:05:34,650 --> 00:05:42,620 that about 30% of individuals with some developmental heart conditions are also on the autism spectrum, 63 00:05:42,630 --> 00:05:47,960 because various organ systems can be impacted by the code during development. 64 00:05:51,040 --> 00:06:00,250 The other 20% of the variants that was not assigned to genetics in the research study. 65 00:06:00,840 --> 00:06:00,990 So, 66 00:06:00,990 --> 00:06:04,910 if we're saying 80% is driven by genetics, 67 00:06:04,910 --> 00:06:11,090 the other 20% my understanding is that it includes all of the measurement error. 68 00:06:11,100 --> 00:06:13,650 So that is kind of um, 69 00:06:13,650 --> 00:06:15,760 statistical artifact. 70 00:06:15,770 --> 00:06:28,290 It's just variants that doesn't actually um relate to a causative factor and it can also include things in the environment, 71 00:06:28,300 --> 00:06:31,920 which can include physical things as well. 72 00:06:31,930 --> 00:06:32,760 So, 73 00:06:33,240 --> 00:06:36,890 there have been theories that perhaps for some people, 74 00:06:36,900 --> 00:06:37,250 um, 75 00:06:37,260 --> 00:06:42,830 a virus might interact with the genetics or for some people, 76 00:06:42,840 --> 00:06:43,220 um, 77 00:06:43,220 --> 00:06:52,810 some type of substance in the environment may trigger uh differences in the way that the neurology has developed. 78 00:06:52,970 --> 00:07:00,260 So The 20% is not well defined in in very specific ways. 79 00:07:00,270 --> 00:07:18,050 But the statistics do help us understand the prominence of a genetic factor here and that's one of the reasons that a correct diagnosis of autism can be so important because we see what the foundation of a behavioral pattern might be. 80 00:07:18,440 --> 00:07:31,310 And at its very base we're trying to distinguish and to figure out whether a behavioral pattern is neurologic or whether it falls into what we more traditionally call a mental health diagnosis. 81 00:07:31,310 --> 00:07:33,260 And I know that there, 82 00:07:33,640 --> 00:07:33,980 you know, 83 00:07:33,980 --> 00:07:40,010 as imprecision and how we might separate neurology from mental health. 84 00:07:40,010 --> 00:07:46,210 But let's consider an example of mental health as PTSD, 85 00:07:46,210 --> 00:08:03,600 that we could put that we could put depression into a more traditional mental health category in order to demonstrate why it makes a difference to know if a behavioral pattern is neurologic versus traditionally mental health, 86 00:08:03,610 --> 00:08:05,760 let's consider a different example, 87 00:08:06,140 --> 00:08:12,850 let's say that two separate clients go to a psychology appointment for the same concern. 88 00:08:12,860 --> 00:08:15,050 They both have memory concerns. 89 00:08:15,840 --> 00:08:27,800 Let's suppose that one client has an evaluation of memory and the psychologist concludes that the profile is very classic for an alzheimer's dementia, 90 00:08:27,810 --> 00:08:32,860 a very clear neurologic factor that's impacting memory. 91 00:08:34,440 --> 00:08:47,360 The second client who has the same concern undergoes an evaluation and this person is found to have memory loss due to disassociative episodes secondary to trauma. 92 00:08:47,740 --> 00:09:01,960 So this is a person who has experienced such significant life trauma that their brain kind of goes offline for periods of time in order to protect the person from re experiencing the trauma. 93 00:09:02,540 --> 00:09:06,620 But this is not a physically based memory issue. 94 00:09:06,620 --> 00:09:09,950 This is based in the psychology of trauma. 95 00:09:10,940 --> 00:09:15,830 So even though they're presenting for the same experience and concern, 96 00:09:15,840 --> 00:09:21,350 one is clearly in the neurologic domain and one is clearly in the mental health domain. 97 00:09:21,940 --> 00:09:24,460 Now the implications of that are really important. 98 00:09:24,940 --> 00:09:42,090 So one is that doing talk therapy with a patient with Alzheimer's or telling them that remembering things is very important and they should do so talking through past histories of relationships or trauma or doing E. 99 00:09:42,090 --> 00:09:42,260 M. 100 00:09:42,260 --> 00:09:42,440 D. 101 00:09:42,440 --> 00:09:42,720 R. 102 00:09:42,720 --> 00:09:43,750 For trauma, 103 00:09:43,760 --> 00:09:46,260 reminding them that it's safe to remember. 104 00:09:47,340 --> 00:10:03,430 These aren't going to be effective as far as improving that person's memory but these approaches as part of psychotherapy for the a person who does have disassociative episodes secondary to trauma, 105 00:10:03,430 --> 00:10:06,490 these might really be effective. 106 00:10:06,500 --> 00:10:23,550 So it helps us understand what's likely to be effective and choose um something that's likely to be helpful rather than something that's really not going to change the symptoms because we're not going to change that neurologic base. 107 00:10:24,540 --> 00:10:24,820 Now, 108 00:10:24,820 --> 00:10:40,340 one individual asked me to highlight in a bit more detail what parts of the brain are involved in autism and first I'll state that there's really nobody that can outline everything about the neurology of autism at this point. 109 00:10:40,370 --> 00:10:43,960 There are just so many things to understand from genetics, 110 00:10:44,340 --> 00:10:45,580 cellular mechanics, 111 00:10:45,580 --> 00:10:46,560 biochemistry, 112 00:10:46,560 --> 00:10:48,260 physiological issues. 113 00:10:48,270 --> 00:10:51,360 There's lots of nuclei and pathways in the brain. 114 00:10:52,640 --> 00:10:54,590 And even in the area of genetics. 115 00:10:54,590 --> 00:10:55,210 As I said, 116 00:10:55,210 --> 00:11:00,430 there are hundreds of possible genes involved and the genetics in one individual, 117 00:11:00,430 --> 00:11:02,960 the neurology of one individual. 118 00:11:02,960 --> 00:11:09,910 The biochemistry of one individual is likely to be somewhat different than that and another individual. 119 00:11:09,920 --> 00:11:10,610 However, 120 00:11:10,610 --> 00:11:12,160 in broad strokes, 121 00:11:12,640 --> 00:11:19,150 a lot of the characteristics have to do with the nuclei and the pathways in the center of the brain. 122 00:11:19,740 --> 00:11:23,960 And this area is called the sub cortical area of the brain, 123 00:11:24,440 --> 00:11:29,060 sub meaning under and cortex meaning the outer layer. 124 00:11:29,940 --> 00:11:32,160 In addition to the center of the brain, 125 00:11:32,540 --> 00:11:45,050 the frontal lobes are also densely connected to the sub cortical pathways and these areas are also uh involved with things that are seen on the autism spectrum. 126 00:11:46,240 --> 00:11:48,570 Now this is extremely simplistic, 127 00:11:48,580 --> 00:11:58,560 but it is a place to start in understanding that the sub cortical nuclei in pathways uh and the dense connections to the front of the brain. 128 00:11:59,840 --> 00:12:05,750 The functions that are impacted by these areas include things like executive function, 129 00:12:06,140 --> 00:12:15,730 which everyone on the spectrum will have some difficulty with the ability to start, maintain, and complete behaviors. 130 00:12:15,810 --> 00:12:19,660 Whether that's talking tours tasks, 131 00:12:20,040 --> 00:12:25,300 the ability to switch gears to handle interruptions to deal with, 132 00:12:25,300 --> 00:12:26,060 change, 133 00:12:26,540 --> 00:12:43,430 the ability to show flexibility to think abstractly as opposed to categorically or literally the whole issue of repetition is very key in this part of the brain repetition of speech movements, 134 00:12:43,440 --> 00:12:45,750 rituals behavior patterns. 135 00:12:45,930 --> 00:12:50,750 These sub cortical areas are really involved in that kind of repetition, 136 00:12:51,640 --> 00:12:54,300 motor coordination sequencing. 137 00:12:54,310 --> 00:13:03,340 There's a lot that goes on in the support sub cortical nuclei with that attention to detail versus seeing the big picture, 138 00:13:03,350 --> 00:13:05,780 knowing what is most and least important, 139 00:13:05,790 --> 00:13:06,400 etcetera. 140 00:13:06,400 --> 00:13:19,660 So there are a lot of the behavioral features seen in the autism neurology that are features having to do with those pathways and those nuclei. 141 00:13:20,940 --> 00:13:21,300 Now, 142 00:13:21,300 --> 00:13:27,470 other characteristics of the autism spectrum likely have to do with inter plays between the cortex, 143 00:13:27,470 --> 00:13:31,070 the outside of the brain and the sub cortical areas, 144 00:13:31,070 --> 00:13:34,550 the inside things like social communication, 145 00:13:34,550 --> 00:13:35,470 relationships, 146 00:13:35,470 --> 00:13:36,860 sensory processing. 147 00:13:37,440 --> 00:13:43,930 So really when we're talking about the neurology of autism in broad strokes, 148 00:13:43,940 --> 00:13:55,450 it has a lot to do with the dense connections in the middle of the brain and the front of the brain as well as interplay between more complex areas of the cortex. 149 00:13:56,440 --> 00:14:01,680 Now that genetics and neurology are being understood at a much deeper level. 150 00:14:01,700 --> 00:14:18,730 There is a field called behavioral genetics and it's really interesting and I was able to take genetics in my undergrad and then I took behavioral genetics through an online course at University of Minnesota. 151 00:14:18,730 --> 00:14:20,760 That was also very interesting. 152 00:14:21,840 --> 00:14:32,660 This was a free online course and really gave me a nice flavor of the types of research that is evolving in this area. 153 00:14:34,040 --> 00:14:52,460 I've also gotten to read multiple articles and I've seen patients with various genetic differences and one thing that we're seeing is that patients who had a genetic profile done 10 years ago and they didn't find anything different or unexpected. 154 00:14:52,740 --> 00:14:52,990 You know, 155 00:14:52,990 --> 00:15:01,160 those same patients are going back to have the genetic code redone and they're seeing these, 156 00:15:01,540 --> 00:15:02,130 um, 157 00:15:02,140 --> 00:15:03,140 uh, 158 00:15:03,150 --> 00:15:07,060 these smaller kinds of micro deletions, 159 00:15:07,540 --> 00:15:09,100 micro additions, 160 00:15:09,110 --> 00:15:13,740 so much at a much smaller scale and more detailed scale. 161 00:15:13,750 --> 00:15:17,170 We're able to see some differences in the genetic code. 162 00:15:17,180 --> 00:15:17,620 Now, 163 00:15:17,620 --> 00:15:19,290 the genotype, 164 00:15:19,300 --> 00:15:27,530 if you hear that term is the code itself in the phenotype is the expression of the code. 165 00:15:27,540 --> 00:15:28,210 Uh, 166 00:15:28,220 --> 00:15:33,860 so the phenotype could be eye color or height or hair color. 167 00:15:34,440 --> 00:15:39,750 And sometimes we talk about phenotype as relates to autism. 168 00:15:40,140 --> 00:15:41,300 So, 169 00:15:41,350 --> 00:15:49,860 there are behavioral phenotypes of various genetic conditions or states or combinations of code. 170 00:15:50,740 --> 00:15:51,250 So, 171 00:15:51,260 --> 00:16:10,890 the that's basically a complex way of saying that this code does impact this expression of behavior in an individual sometimes for someone who does not meet full criteria for autism, 172 00:16:10,900 --> 00:16:13,120 but they have characteristics. 173 00:16:13,130 --> 00:16:18,150 Someone might refer to that as the broader autistic phenotype. 174 00:16:18,640 --> 00:16:26,210 That just means that there are these expressions there of neurology that are important to understand, 175 00:16:26,210 --> 00:16:30,830 but the person doesn't meet full criteria for a diagnosis. 176 00:16:30,830 --> 00:16:33,850 So that's the broader autistic phenotype. 177 00:16:35,140 --> 00:16:54,370 one of the interesting lines of research is starting to connect repetitive stereotyped behaviors with genetic codes and repetitive stereotyped behaviors is one of the criteria that may be met within autism, 178 00:16:54,370 --> 00:16:55,960 although it's not required, 179 00:16:56,440 --> 00:16:59,050 but it is a common um, 180 00:16:59,060 --> 00:17:00,530 neurologic expression, 181 00:17:00,530 --> 00:17:02,000 a com common phenotype. 182 00:17:02,000 --> 00:17:17,170 Ipic expression of the neurology and some people are concerned about the word stereotyped because they feel that it might be a disparaging comment about the autistic individual. 183 00:17:18,040 --> 00:17:19,350 Um actually, 184 00:17:19,360 --> 00:17:30,140 stereotyped behaviors are seen all across neurologic states and conditions and they're seen in some conditions, 185 00:17:30,140 --> 00:17:31,160 but not others. 186 00:17:31,540 --> 00:17:37,450 So someone with a traumatic brain injury or a stroke is not likely to show stereotyped behaviors, 187 00:17:37,840 --> 00:17:46,560 but individuals with dementia can start to show these individuals with different genetic or developmental conditions. 188 00:17:46,570 --> 00:17:58,080 I've seen these um expressions of neurology and people who have had infectious disease or autoimmune kinds of responses to an infection. 189 00:17:58,090 --> 00:18:03,060 And so it is just a standard neurologic term. 190 00:18:03,440 --> 00:18:06,150 A stereotyped behavior um, 191 00:18:06,160 --> 00:18:09,670 is expressed in a similar way every time, 192 00:18:10,040 --> 00:18:18,010 even though the environment or the context of the behavior changes. 193 00:18:18,020 --> 00:18:22,520 And so the behavior is not specific to the context, 194 00:18:22,530 --> 00:18:24,860 It's not required by the context. 195 00:18:25,240 --> 00:18:27,870 It may be soothing to the individual. 196 00:18:27,880 --> 00:18:30,670 It may be something the person doesn't even notice, 197 00:18:31,040 --> 00:18:33,420 but it is the same each time. 198 00:18:33,420 --> 00:18:35,860 It's the stereotyped replica. 199 00:18:36,340 --> 00:18:47,550 We could call it a repetitive, replica behavior and you might see that within autism in regards to movement what people say. 200 00:18:47,560 --> 00:18:47,840 So, 201 00:18:47,840 --> 00:18:53,350 verbalization is whether that's echoing or repeating words or phrases. 202 00:18:53,360 --> 00:18:56,940 And you can also see stereotyped use of objects. 203 00:18:56,950 --> 00:19:11,450 That's where you'll uh kind of see when a youngster might line up their toys or an adult may keep a coin in their pocket that they flip back and forth between two of their fingers. 204 00:19:11,940 --> 00:19:14,860 This kind of stereotyped repetition. 205 00:19:14,860 --> 00:19:18,530 This replica um of the behavior, 206 00:19:18,540 --> 00:19:21,190 it may be soothing to the person, 207 00:19:21,200 --> 00:19:23,260 or again they may not notice it. 208 00:19:23,270 --> 00:19:31,680 I've had patients recently who have tongue movements or tongue kind of um curling behaviors that they don't even notice. 209 00:19:31,680 --> 00:19:33,840 And so it could occur either way, 210 00:19:33,850 --> 00:19:35,770 but it's neurologically driven. 211 00:19:36,040 --> 00:19:38,260 If you ask the person to stop it, 212 00:19:38,260 --> 00:19:45,410 they can stop it in the moment but it will just recur and that is common in neurology. 213 00:19:45,410 --> 00:19:49,250 So if we think about um you know, 214 00:19:49,250 --> 00:19:51,450 if I ask you to stop breathing, 215 00:19:51,840 --> 00:19:54,840 you can stop breathing but it's going to then kick in, 216 00:19:54,840 --> 00:20:00,950 it's going to recur ... an example in neurology is in Parkinson's disease. 217 00:20:01,640 --> 00:20:05,940 Part of what you see is changes in the step pattern, 218 00:20:06,000 --> 00:20:08,450 the gait pattern of walking. 219 00:20:08,940 --> 00:20:14,170 And you'll start to see neurologically very small shuffling steps. 220 00:20:14,210 --> 00:20:24,450 That's really classic for a Parkinsonian gait and if you tell the person to lift their feet they can do that. 221 00:20:24,840 --> 00:20:30,270 Um And you know that's what a physical therapist will say now remember to lift your feet. 222 00:20:30,640 --> 00:20:33,830 Um But when the therapist isn't there, 223 00:20:33,840 --> 00:20:37,100 they just and they don't have that verbal cue, 224 00:20:37,110 --> 00:20:39,460 their brain goes back to their default, 225 00:20:39,840 --> 00:20:44,910 which is this um just shuffling gait pattern that's neurologic. 226 00:20:44,910 --> 00:20:47,760 So like other neurologic things. 227 00:20:48,440 --> 00:20:52,200 These are behaviors that repeat. 228 00:20:52,210 --> 00:20:55,670 Um but can be suppressed in the moment. 229 00:20:57,140 --> 00:21:11,300 One of the super interesting things that amazes even me is that genetic studies are starting to link stereotyped behaviors to certain genetic differences. 230 00:21:11,840 --> 00:21:20,410 And this is not a 1-1 correlation where someone with this genetic difference always does this stereotyped behavior. 231 00:21:20,420 --> 00:21:30,760 But sometimes it really is astonishing how connected the code in this particular chromosome is to a behavioral pattern. 232 00:21:32,040 --> 00:21:39,090 I'm going to link in the show notes um a website from the U. 233 00:21:39,090 --> 00:21:39,590 K. 234 00:21:39,590 --> 00:21:47,430 That talks about neuro genetic conditions and they're talking about smith magnus syndrome, 235 00:21:47,440 --> 00:21:53,170 which is a genetic difference that causes the neurology to develop differently. 236 00:21:53,540 --> 00:22:06,270 And one of the things that's interesting about this condition is that there are a few stereotyped behaviors that could easily go unnoticed at first at least. 237 00:22:06,740 --> 00:22:13,180 But that um really are very common in people with this genetic pattern. 238 00:22:13,470 --> 00:22:15,950 And one of these is self hugging. 239 00:22:16,340 --> 00:22:30,460 So the individual will hug themselves many times in response to being happy about something in the same way that someone could have hand flapping in response to being excited or happy. 240 00:22:31,140 --> 00:22:36,560 And at first the self hugging is just delightful in these kids. 241 00:22:36,940 --> 00:22:37,590 But you know, 242 00:22:37,590 --> 00:22:44,080 as they grow older and as this behavior is repeated without specific context, 243 00:22:44,080 --> 00:22:47,610 like it starts to look really unusual. 244 00:22:47,680 --> 00:22:54,950 And indeed it is a repetitive stereotyped behavior that is related to the genetic code. 245 00:22:56,340 --> 00:23:03,710 The other stereotype that's very common within this genetic pattern is called lick and flip. 246 00:23:03,720 --> 00:23:14,960 And this happens when the individual licks their hand or their fingers and then uses it to rapidly turn pages in a book, 247 00:23:15,540 --> 00:23:17,550 lick and flip stereotype. 248 00:23:18,040 --> 00:23:18,800 And again, 249 00:23:18,800 --> 00:23:22,930 it looks delightful in a little kid and they'll say, 250 00:23:22,940 --> 00:23:25,510 oh this person loves reading, 251 00:23:26,440 --> 00:23:28,680 but actually they're not reading. 252 00:23:28,700 --> 00:23:31,880 And turning the pages isn't functional, 253 00:23:31,890 --> 00:23:35,710 but it's a repetitive stereotyped behavior, 254 00:23:35,720 --> 00:23:39,360 it's neurologic and it's related to the genetic code. 255 00:23:41,340 --> 00:23:46,670 So what do I want you to walk away from this information with? 256 00:23:47,140 --> 00:23:52,590 I don't want you to worry about the terminology, 257 00:23:52,600 --> 00:23:53,960 the statistics. 258 00:23:54,640 --> 00:24:16,860 What I would like you to take away is this understanding that there is a physical base for our neurology and that is what is the base of the autistic behavioral pattern and that this physical base is related to the genetic code in some way. 259 00:24:18,540 --> 00:24:22,850 This does not mean that everyone is an automaton. 260 00:24:23,540 --> 00:24:36,680 Um but I think the value of thinking about the physical aspects of behavior is that it balances out our understanding of a very complex interplay between nature, 261 00:24:36,690 --> 00:24:39,750 the physical form of the brain and nurture, 262 00:24:39,750 --> 00:24:42,170 which is our experience in the world, 263 00:24:42,940 --> 00:24:48,360 and the truth lies in the complexity of the interplay of both. 264 00:24:48,840 --> 00:24:56,700 But what we tend to do as humans is think in these categorical ways and in our culture, 265 00:24:56,710 --> 00:25:00,450 we lean very heavily on the nurture point of view, 266 00:25:00,450 --> 00:25:03,720 at least in this time, 267 00:25:03,730 --> 00:25:05,150 this generation, 268 00:25:05,160 --> 00:25:07,290 where um you know, 269 00:25:07,290 --> 00:25:21,930 it really strikes home to me sometimes when um I was recently traveling and I got to walk through high school and there's all these posters up and you know what I'm talking about, 270 00:25:21,930 --> 00:25:26,360 they say things like the sky is the limit, reach for the stars. 271 00:25:26,840 --> 00:25:30,770 The only limit you have is how you limit yourself. 272 00:25:31,940 --> 00:25:33,700 And if you can dream it, 273 00:25:33,700 --> 00:25:34,850 you can achieve it. 274 00:25:35,840 --> 00:25:39,820 So we love that individualistic, 275 00:25:39,830 --> 00:25:42,460 empowered framework. 276 00:25:43,940 --> 00:25:51,460 It appeals to this um part of ourselves that does want to be able to make our way, 277 00:25:52,040 --> 00:25:54,310 I don't want to have limitation, 278 00:25:54,320 --> 00:25:59,770 I really want to be able to achieve anything if I apply myself hard enough. 279 00:26:02,140 --> 00:26:03,060 However, 280 00:26:03,540 --> 00:26:05,920 it's actually not one or the other, 281 00:26:05,930 --> 00:26:12,270 it's not all effort and it's not all fatalistic that everything is determined, 282 00:26:12,940 --> 00:26:14,770 it's not that simplistic, 283 00:26:15,640 --> 00:26:15,960 you know, 284 00:26:15,960 --> 00:26:20,860 it's not as simplistic as thinking that all we need to do is try hard enough, 285 00:26:21,440 --> 00:26:29,270 nor is it as simplistic as thinking that there's nothing we can do because our neurology dictates everything. 286 00:26:30,140 --> 00:26:35,190 It's very hard to hold the complexity of the truth in our minds and as humans, 287 00:26:35,190 --> 00:26:43,460 we love to be able to take aside or categorize opinions and even when we try to stay centered in the complexity, 288 00:26:43,460 --> 00:26:48,770 we often slide from one side to the other no matter what the topic, 289 00:26:49,540 --> 00:26:58,660 but to be able to hold complexity in our minds about something most often is what we need in order to be in the most truth. 290 00:26:59,740 --> 00:27:05,590 We should feel empowered to work hard because we can influence the outcome of our lives, 291 00:27:05,600 --> 00:27:12,260 but we should also feel grounded in the fact that there are going to be things that we just can't change. 292 00:27:12,840 --> 00:27:17,840 And someone pointing out that we have limitations. 293 00:27:17,850 --> 00:27:19,950 That's not a criticism. 294 00:27:20,640 --> 00:27:21,560 You know, 295 00:27:21,570 --> 00:27:30,860 we all have set limitations as a function of being human and my limitations are not the same as yours and vice versa, 296 00:27:31,740 --> 00:27:36,060 But we can't be 10 ft tall if we try hard enough. 297 00:27:37,040 --> 00:27:41,100 And the person who is blind cannot see if they try hard enough. 298 00:27:41,110 --> 00:27:51,550 And the person who wants to live to be 400 isn't going to be able to achieve that with just good attitude and high effort or commitment. 299 00:27:54,240 --> 00:27:59,390 So this brings me to another topic mentioned in the Q and A emails, 300 00:27:59,390 --> 00:28:02,960 which is the topic of whether autism is all good. 301 00:28:03,640 --> 00:28:14,530 That is ... is autism a wonderful reflection of diversity that should always be celebrated or is autism all bad? 302 00:28:14,540 --> 00:28:23,550 The diagnosis is stigmatizing and limiting and it's something to hide or be ashamed of and it represents something that must be fixed. 303 00:28:25,240 --> 00:28:31,310 I think it's really easy to find people on each side of this topic. 304 00:28:31,320 --> 00:28:31,990 But again, 305 00:28:31,990 --> 00:28:40,550 the truth is in the complexity and I want to invite you to dive back into complexity and be able to live there. 306 00:28:42,240 --> 00:28:57,970 Every individual whether they're on the spectrum or not has great deep inherent value as a person being on the spectrum or you're neurotypical does not change any of that. 307 00:28:58,030 --> 00:28:59,860 Every person, 308 00:29:00,440 --> 00:29:06,350 whether on the spectrum or not has gifts and strengths and can bless people around them. 309 00:29:06,740 --> 00:29:08,160 Every individual, 310 00:29:08,170 --> 00:29:11,360 whether on the spectrum or not has limitations, 311 00:29:11,840 --> 00:29:35,860 challenges and struggles and we need to allow there to be gift and challenge in every autistic individual rather than needing it to be all good or trying to convince people that it's all bad. 312 00:29:37,040 --> 00:29:40,150 One of the blessings of knowing that there's autism, 313 00:29:40,150 --> 00:29:59,360 neurology is just understanding the context for this person's strengths and challenges and being able to tap into our understanding of that and also a direction that might be most helpful when things are a challenge. 314 00:30:00,140 --> 00:30:11,560 I'm going to switch gears just a moment to a few other physical questions I received about the spectrum and then we're going to close up and we'll talk about next episode. 315 00:30:13,140 --> 00:30:17,270 So one of the questions I was asked is about medication. 316 00:30:18,040 --> 00:30:27,170 Um and I'll just give a general general kind of summary of medication in autism. 317 00:30:28,940 --> 00:30:35,960 One of the things to know is that there are often four categories if someone is taking a medication. 318 00:30:36,540 --> 00:30:40,890 Um it's often within these four categories Of difficulty. 319 00:30:40,890 --> 00:30:42,760 So one would be attention. 320 00:30:43,640 --> 00:30:50,360 Another category of difficulty that someone may take a medication or supplement for is sleep, 321 00:30:50,940 --> 00:30:56,960 that sleep onset is often very difficult or just getting enough sleep. 322 00:30:59,040 --> 00:31:02,570 Another category is anxiety, 323 00:31:02,580 --> 00:31:09,450 which is often very prevalent on the spectrum and also depression that goes along with. 324 00:31:09,460 --> 00:31:09,790 Um, 325 00:31:09,790 --> 00:31:15,610 some of life experiences and the fourth category has to do with agitation, 326 00:31:15,610 --> 00:31:18,060 irritability or explosiveness. 327 00:31:19,440 --> 00:31:23,460 Not everyone on the spectrum benefits from medication, 328 00:31:23,840 --> 00:31:26,730 but it often can be for some people, 329 00:31:26,740 --> 00:31:31,640 a nice layer of support in one or more of these areas. 330 00:31:31,650 --> 00:31:32,670 However, 331 00:31:33,440 --> 00:31:45,720 medication on the spectrum does not uh show itself as effective um for these challenges as for people who are, 332 00:31:45,720 --> 00:31:57,460 you're a typical and taking the medication and the reason for that is that it doesn't change the neurologic connectivity that has developed in the nervous system, 333 00:31:58,340 --> 00:32:03,860 but it can offer a layer of support that the person didn't have before. 334 00:32:04,640 --> 00:32:15,400 But let's say someone has anxiety related to the autism neurology and another person has anxiety related to something else. 335 00:32:15,410 --> 00:32:21,770 They don't have autism neurology medications likely to work better for that second person. 336 00:32:23,540 --> 00:32:26,990 The reason that's important to know is just that sometimes people are, 337 00:32:27,000 --> 00:32:43,460 are determined to go on a quest to find um this really effective combination of medications that will make things a lot easier and that's not the typical outcome that you'll have. 338 00:32:44,240 --> 00:32:44,660 Now, 339 00:32:44,660 --> 00:32:54,260 the medications that are used for autism a lot of times that's not going to change just because you have a diagnosis and the reason for that is that, 340 00:32:54,740 --> 00:32:55,390 um, 341 00:32:55,400 --> 00:32:55,830 you know, 342 00:32:55,830 --> 00:32:57,410 it's symptom based, 343 00:32:57,430 --> 00:33:02,660 so the medications would be prescribed based on your symptoms, 344 00:33:02,660 --> 00:33:04,730 not based on your diagnosis, 345 00:33:04,780 --> 00:33:08,410 but the expected outcome is different if, 346 00:33:08,410 --> 00:33:08,810 you know, 347 00:33:08,810 --> 00:33:17,950 that you have autistic neurology and there are sometimes um side effects that can be more common on the spectrum. 348 00:33:18,540 --> 00:33:21,360 So if you're taking attention medication, 349 00:33:21,370 --> 00:33:32,260 you may have increased anxiety or some repetitive movements or ticks at a higher rate than someone else. 350 00:33:35,540 --> 00:33:44,260 Another question was about whether marijuana improved social function or other aspects of functioning for the autistic individual. 351 00:33:45,440 --> 00:33:46,130 Um, 352 00:33:46,140 --> 00:34:02,550 my experience and my understanding from the literature and what I've seen with patients and clients is that whether someone's taking CBD oil or smoking marijuana, 353 00:34:02,940 --> 00:34:03,160 um, 354 00:34:03,160 --> 00:34:07,130 I just find people responding differently. 355 00:34:07,140 --> 00:34:17,130 So I have clients that tell me it's extremely helpful and I have clients that tell me it's actually very upsetting and they don't care for it at all. 356 00:34:17,140 --> 00:34:21,960 And I have clients feel like it really just doesn't doesn't do anything for them. 357 00:34:22,340 --> 00:34:47,610 So that ends up being kind of an individualized thing that you would discuss with your medical team and your physicians there are studies looking at compounds um from other substances just to see if they can be used um to help even out the anxiety or to help with social interaction. 358 00:34:47,620 --> 00:34:51,280 Those are really just in a very experimental stages, 359 00:34:51,280 --> 00:34:52,980 sometimes not even with humans. 360 00:34:52,980 --> 00:34:55,760 And so I don't know what the outcome will be, 361 00:34:55,770 --> 00:34:58,060 but everyone's hoping that over time, 362 00:34:58,060 --> 00:35:00,160 as we understand the neurology better, 363 00:35:00,440 --> 00:35:14,470 uh we can have some more things to help people who are struggling with some of those characteristics or seasons of life in the final physical question that I was asked has to do with autism and diet. 364 00:35:15,340 --> 00:35:16,750 And um, 365 00:35:16,760 --> 00:35:19,670 there is a particular diet out there. 366 00:35:19,670 --> 00:35:24,250 The gluten free and casein free... casein is a milk protein. 367 00:35:24,840 --> 00:35:25,240 Um, 368 00:35:25,250 --> 00:35:26,700 if you've heard of lactose, 369 00:35:26,700 --> 00:35:28,470 that's actually a milk sugar. 370 00:35:29,140 --> 00:35:34,660 But typically people find that gluten which is also a protein and casein, 371 00:35:35,040 --> 00:35:41,670 These are the things that some people will target in their diet by removing them. 372 00:35:42,540 --> 00:35:43,120 Um, 373 00:35:43,130 --> 00:35:48,460 and there's not a lot of research support for that. 374 00:35:49,440 --> 00:35:50,360 However, 375 00:35:50,840 --> 00:35:53,520 I will say that in our home, 376 00:35:53,530 --> 00:35:58,360 my son had really extreme difficulties with sleep and colic, 377 00:35:58,840 --> 00:35:59,260 um, 378 00:35:59,260 --> 00:36:02,650 which is just a lot of crying and discomfort. 379 00:36:03,430 --> 00:36:05,430 I was very overwhelmed. 380 00:36:05,430 --> 00:36:07,990 I had tried lots of things. 381 00:36:08,080 --> 00:36:10,340 Somebody said I should try this diet. 382 00:36:10,350 --> 00:36:17,050 I was overwhelmed with the prospect of having to learn a whole new diet and eliminate a bunch of things. 383 00:36:17,430 --> 00:36:18,050 Um, 384 00:36:18,430 --> 00:36:19,350 at 18 months, 385 00:36:19,350 --> 00:36:23,480 I just felt like I had no other choice. 386 00:36:23,480 --> 00:36:24,250 I really, 387 00:36:24,730 --> 00:36:25,350 uh, 388 00:36:26,030 --> 00:36:28,930 I had nothing left to try and I said, 389 00:36:28,930 --> 00:36:37,660 I'm just going to try this for one month and then I'm not even going to think beyond that because the thought of doing it forever. 390 00:36:37,660 --> 00:36:39,920 Just felt overwhelming. 391 00:36:39,920 --> 00:36:40,690 So, 392 00:36:40,700 --> 00:36:41,120 um, 393 00:36:41,130 --> 00:36:43,420 I did do that. 394 00:36:43,430 --> 00:36:47,460 And within 2.5 weeks he was, 395 00:36:47,930 --> 00:36:48,370 um, 396 00:36:48,380 --> 00:36:50,490 well ever since infancy, 397 00:36:50,490 --> 00:36:54,010 he took a 20 minute nap twice a day and that's it. 398 00:36:54,020 --> 00:36:57,050 And he would wake up like five times a night. 399 00:36:57,530 --> 00:36:58,250 Um, 400 00:36:58,630 --> 00:37:02,190 2 1/2 weeks after the diet began, 401 00:37:02,200 --> 00:37:06,000 he started taking an hour and a half nap, 402 00:37:06,010 --> 00:37:07,960 sometimes up to three hours. 403 00:37:08,430 --> 00:37:09,660 Uh and believe me, 404 00:37:09,660 --> 00:37:15,050 we had tried everything before and did nothing different except the diet change. 405 00:37:16,630 --> 00:37:31,510 Um He stayed gluten free and casein free um until really just recently in his high school years and now he seems to do okay with without that elimination. 406 00:37:31,660 --> 00:37:58,550 So he is eating gluten and casein now having said that um it is something that you need to um do in conjunction with your medical team being aware so that your child and get enough nutrients and won't be missing out on calcium or other things that dairy might provide or gluten gluten products. 407 00:37:59,630 --> 00:38:00,620 Also, 408 00:38:00,630 --> 00:38:07,030 what really seems to be true is that many people do not respond to this at all. 409 00:38:07,040 --> 00:38:09,340 They don't get any benefit from it. 410 00:38:09,820 --> 00:38:12,640 And um I don't know why, 411 00:38:13,720 --> 00:38:17,050 I just think it's a very individual kind of response. 412 00:38:17,060 --> 00:38:20,920 So um you know, 413 00:38:20,920 --> 00:38:29,600 if you feel and you've talked to your doctors and medical team that a trial isn't going to harm anyone's health, 414 00:38:29,610 --> 00:38:31,040 you can try that. 415 00:38:31,420 --> 00:38:34,490 Um On the other hand, 416 00:38:34,500 --> 00:38:39,630 I have not seen adults try it to be honest. 417 00:38:39,640 --> 00:38:47,950 I really don't know if adults who try it for the first time as an adult would feel benefit. 418 00:38:48,420 --> 00:38:52,340 Um but that has been my experience with that particular diet. 419 00:38:52,720 --> 00:38:54,170 Other kinds of diets. 420 00:38:54,170 --> 00:38:57,320 You can find lots um Bill, 421 00:38:57,330 --> 00:39:01,270 a lot of them are kind of focusing on being healthy. 422 00:39:01,270 --> 00:39:07,430 So people will take out things like artificial colors or flavors. 423 00:39:07,440 --> 00:39:09,530 There are other kinds of diets. 424 00:39:09,540 --> 00:39:18,800 There's just too many to list off other approaches really talk about decreasing sugar. 425 00:39:18,810 --> 00:39:19,390 Um, 426 00:39:19,390 --> 00:39:21,240 getting good protein. 427 00:39:21,250 --> 00:39:21,650 Um, 428 00:39:21,650 --> 00:39:25,450 so that's a whole um, 429 00:39:25,820 --> 00:39:31,430 a whole broad journey that you can take if you desire. 430 00:39:31,440 --> 00:39:37,610 And I know some people who have really benefited from that and I know other people who have tried really, 431 00:39:37,610 --> 00:39:40,840 really hard and just haven't found uh, 432 00:39:40,850 --> 00:39:43,750 what might help help them feel a little bit better. 433 00:39:45,620 --> 00:39:55,940 So I want to say thank you for the question and answer emails you sent to adult and geriatric autism at gmail dot com. 434 00:39:56,720 --> 00:40:05,900 And thank you for giving me these ideas for a session here about autism and the physical body, 435 00:40:05,900 --> 00:40:07,250 the physical condition. 436 00:40:08,020 --> 00:40:10,160 Next episode, 437 00:40:10,160 --> 00:40:15,480 I'll be formulating some other themes about emails I received. 438 00:40:15,490 --> 00:40:16,300 For example, 439 00:40:16,300 --> 00:40:18,450 I received some questions about parenting, 440 00:40:18,450 --> 00:40:22,120 some questions about autism in the workplace and more. 441 00:40:22,130 --> 00:40:22,950 I'll see you then.

ALLFTD Research Mini-Series: All About MRIs with Dr. Howie Rosen of UCSF

Remember Me

Play Episode Listen Later Jun 16, 2022 25:35

As a follow up to our recap of Day 2, we interviewed Dr. Howie Rosen to learn more about MRIs and how they're used in the ALLFTD Study and in diagnosing FTD. Dr. Howie Rosen, is a behavioral neurologist and holds the Dorothy Kirsten French Foundation Endowed Professorship for Parkinsonian and Other Neurodegenerative Disorders. He is an investigator on multiple federal and state-funded research grants and serves as director of the California State Alzheimer's Disease Center at UCSF, associate director of UCSF's federally funded Alzheimer's Disease Research Center, director of UCSF's Behavioral Neurology Training Program, and director of Curriculum for the Global Brain Health Institute. And, he is one of the three ALLFTD Principal Investigators. We loved Dr. Rosen! Enjoy the science side of our experience, you guys! Special thank you to the ALLFTD Study for their support in the creation of this series. You can support Remember Me by visiting our website www.remembermeftd.com where you can shop our merch, join re-members only or donate. You can follow us on instagram @remembermepodcast. ---- Today's sponsor is The Bluefield Project: The Bluefield Project to Cure FTD, is on a mission to support research to improve our understanding of a genetic form of Frontotemporal dementia, and to help find a cure for this devastating disease. So how can you help? If FTD runs in your family, participating in a Natural History Study, or in a therapeutic clinical trial, makes an enormous contribution. To learn more, please go to ftdregistry.org ---- Remember Me is a podcast created by two moms who became fast friends on Instagram while caregiving for their parents. It features stories of Frontotemporal Dementia (FTD) with a focus on remembering individuals for who they were before the disease. The stories shared are raw, real, and so full of love. We hope it inspires you to "accept the good." --- Support this podcast: https://anchor.fm/rememberme/support

research alzheimer's disease curriculum miniseries rosen howie ucsf mris ftd disease research center frontotemporal disease center global brain health institute parkinsonian frontotemporal dementia ftd

DD SIG: CSM 2022 Poster Award: Differences in Spatiotemporal Gait Characteristics between Freezing of Gait Subtypes in Parkinson's Disease – with Jason Longhurst

4D: Deep Dive into Degenerative Diseases - ANPT

Play Episode Listen Later Jun 2, 2022 23:35

In this episode, we highlight one of the winners of our poster awards at CSM 2022. Jason Longhurst talks to Katy McGraw about his research on gait characteristics in people with PD. His research looks at data from people without freezing, people with freezing on initiation, and people with non-initiation-type freezing. He discusses the role of gait variability in clinical presentation and expands on how this research might inform PT intervention and make interventions more specific to patients with different presentations in the future. The Degenerative Disease Special Interest Group is part of the Academy of Neurologic Physical Therapy – www.neuropt.org Guest information: Jason Longhurst Ph.D., PT, DPT, NCS Assistant Professor St. Louis University Related Articles Ziegler K, Schroeteler F, Ceballos-Baumann AO, Fietzek UM. A new rating instrument to assess festination and freezing gait in Parkinsonian patients. Mov Disord. 2010 Jun 15;25(8):1012-8. doi: 10.1002/mds.22993. PMID: 20310009.

academy disease differences parkinson characteristics pd freezing poster dpt pmid csm gait subtypes longhurst parkinsonian spatiotemporal mov disord

Deep Brain Stimulation Care at RUSH with Neepa Patel, MD

Rounding at Rush

Play Episode Listen Later Feb 2, 2022 21:18

The movement disorders neurology group at RUSH University Medical Center is one of the largest and most experienced groups in the world, with clinicians who specialize in managing the symptoms of Parkinson's disease and other movement disorders. One of the treatment modalities they use to treat these patients is deep brain stimulation (DBS). DBS helps patients with movement disorders control their symptoms of tremor, rigidity, stiffness, slowed or abnormal movements and walking problems. RUSH treats the largest number of DBS patients in the Midwest. Dr. Neepa Patel is a neurologist in the RUSH University System for Health and the director for the Movement Disorder Interventional Program in the Department of Neurological Sciences. Her interests include improving the quality and delivery of care for patients receiving deep brain stimulation (DBS) and education to improve the utilization of new therapies in movement disorders. She is also part of the RUSH team caring for essential and Parkinsonian tremor patients with MR-guided focused ultrasound, an incisionless treatment designed to reduce hand tremor. “We work in a very comprehensive, multidisciplinary, team-based approach at RUSH to treat patients with movement disorders using DBS. We share our ideas and experiences because everyone comes from different training backgrounds, different expertise and years of experience in managing patients. This helps us take care of patients who are nontraditional, but who still could benefit from this therapy.” CME credit link: https://cmetracker.net/RUSH/Publisher?page=pubOpenSub#/event/484707/

health care midwest rush parkinson patel cme dbs rush university medical center deep brain stimulation neurological sciences parkinsonian rush university system

Living and Making Memories with Alzheimer's Disease with Jim McAleer

OC Talk Radio

Play Episode Listen Later Oct 13, 2021 47:54

Dementia is recorded as the seventh leading cause of death and one of the major causes of disability and dependency among older adults globally. Just like heart disease and cancer, dementia is an umbrella term for a set of syndromes that leads to deterioration in cognitive function. It is caused by the damage of brain cells that results in the inability to communicate, think, feel, or behave appropriately. Alzheimer's disease is the most common type of dementia that worsens over time. It kills the brain cells and leads to memory loss and cognitive decline. This disease is incurable and affects mainly people ages 65 years and older. Memories are beautiful and priceless. It strengthens our sense of self-identity and purpose, as well as our bonds with others. When these memories slowly fade, everything will change and that's why we need to have a support system to help guide us in living with someone who has this condition. Dr. Dung Trinh is joined by Jim McAleer to share his organization, “Alzheimer's Orange County”, which provides hands-on care and support for patients with Alzheimer's.A person with dementia is most likely to be socially isolated, less likely to exercise, forget medications, and less connected to society. And having a good support system can benefit the psychological aspect of that person suffering from this neuro-degenerative health condition. Don't miss Episode 3 of Health Talks with Dr. Trinh to know what dementia is all about. Listen now!Memorable Quotes:Patients with Alzheimer's are still with us. It's just the memories that are lost. - Jim McAleerSeniors with dementia are the most vulnerable in society. - Dr. Dung TrinhOther Resources Mentioned:Our GangAlzheimer's Orange County Important Points:Learn a new game because your brain is very adaptable and you can keep your brain active. A person with dementia is most likely to be socially isolated, less likely to exercise, forget medications, and less connected to society.“Dementia” is an overlying term for a neurologically impairing condition that impacts the ability to function.There are a couple of different conditions of dementia: Parkinsonian dementia, frontotemporal dementia, Lewy body dementia, alcohol-related dementia, and others.About the Guests:Jim McAleer is the president and CEO of Alzheimer's Orange County. AlzOC runs two adult day centers, Acacia Adult Day Center and South County Adult Day Center. He also mentors and leads an Executive Team composed of 5 highly-qualified and industry-experienced individuals in developing and implementing the agency's strategic plan.About the Host:Dung Trinh, MD is the Chief Medical Officer of Irvine Clinical Research, medical missionary with TongueOut Medical Missions, and holds leadership positions with multiple health care organizations in Orange County. He is a keynote speaker, best-selling author, and Host of “Health Talks with Dr Trinh” which can be heard weekly on OC Talk Radio.Connect with Dr. TrinhHealthTalks OC WebsiteTongue OutFacebookLinkedIn

ceo md alzheimer's disease dementia orange county chief medical officers health talk making memories executive team lewy trinh mcaleer parkinsonian

The Gary Null Show - 06.22.21

The Gary Null Show

Play Episode Listen Later Jun 22, 2021 54:16

Clinical Significance of Micronutrient Supplementation in Critically Ill COVID-19 Patients with Severe ARDS University Hospital Wuerzburg (Germany), June 12, 2021 Abstract The interplay between inflammation and oxidative stress is a vicious circle, potentially resulting in organ damage. Essential micronutrients such as selenium (Se) and zinc (Zn) support anti-oxidative defense systems and are commonly depleted in severe disease. This single-center retrospective study investigated micronutrient levels under Se and Zn supplementation in critically ill patients with COVID-19 induced acute respiratory distress syndrome (ARDS) and explored potential relationships with immunological and clinical parameters. According to intensive care unit (ICU) standard operating procedures, patients received 1.0 mg of intravenous Se daily on top of artificial nutrition, which contained various amounts of Se and Zn. Micronutrients, inflammatory cytokines, lymphocyte subsets and clinical data were extracted from the patient data management system on admission and after 10 to 14 days of treatment. Forty-six patients were screened for eligibility and 22 patients were included in the study. Twenty-one patients (95%) suffered from severe ARDS and 14 patients (64%) survived to ICU discharge. On admission, the majority of patients had low Se status biomarkers and Zn levels, along with elevated inflammatory parameters. Se supplementation significantly elevated Se (p = 0.027) and selenoprotein P levels (SELENOP; p = 0.016) to normal range. Accordingly, glutathione peroxidase 3 (GPx3) activity increased over time (p = 0.021). Se biomarkers, most notably SELENOP, were inversely correlated with CRP (rs = −0.495), PCT (rs = −0.413), IL-6 (rs = −0.429), IL-1β (rs = −0.440) and IL-10 (rs = −0.461). Positive associations were found for CD8+ T cells (rs = 0.636), NK cells (rs = 0.772), total IgG (rs = 0.493) and PaO2/FiO2ratios (rs = 0.504). In addition, survivors tended to have higher Se levels after 10 to 14 days compared to non-survivors (p = 0.075). Sufficient Se and Zn levels may potentially be of clinical significance for an adequate immune response in critically ill patients with severe COVID-19 ARDS. Pilot Study of the Tart Cherry Juice for the Treatment of Insomnia and Investigation of Mechanisms Louisiana State University, June 20, 2021 Insomnia is common in the elderly and is associated with chronic disease, but use of hypnotics increases the incidence of falls. Montmorency tart cherry juice has improved insomnia by self-report questionnaire. Study Question: Is insomnia confirmed by polysomnography and is tryptophan availability a potential mechanism for treating insomnia? Study Design: A placebo-controlled balanced crossover study with subjects older than 50 years and insomnia were randomized to placebo (2 weeks) or cherry juice (2 weeks) (240 mL 2 times/d) separated by a 2-week washout. Measures and Outcomes: Sleep was evaluated by polysomnography and 5 validated questionnaires. Serum indoleamine 2,3-dioxygenase (IDO), the kynurenine-to-tryptophan ratio, and prostaglandin E2 were measured. In vitro, Caco-2 cells were stimulated with interferon-gamma, and the ability of cherry juice procyanidin to inhibit IDO which degrades tryptophan and stimulates inflammation was measured. The content of procyanidin B-2 and other major anthocyanins in cherry juice were determined. Results: Eleven subjects were randomized; 3 with sleep apnea were excluded and referred. The 8 completers with insomnia increased sleep time by 84 minutes on polysomnography (P = 0.0182) and sleep efficiency increased on the Pittsburgh Sleep Quality Index (P = 0.03). Other questionnaires showed no significant differences. The serum kynurenine-to-tryptophan ratio decreased, as did the level of prostaglandin E2 (both P < 0.05). In vitro, cherry juice procyanidin B-2 dose-dependently inhibited IDO. Conclusions: Cherry juice increased sleep time and sleep efficiency. Cherry juice procyanidin B-2 inhibited IDO, increased tryptophan availability, reduced inflammation, and may be partially responsible for improvement in insomnia. Many with migraines have vitamin deficiencies, says study Cincinnati Children's Hospital, June 10, 2021 A high percentage of children, teens and young adults with migraines appear to have mild deficiencies in vitamin D, riboflavin and coenzyme Q10—a vitamin-like substance found in every cell of the body that is used to produce energy for cell growth and maintenance. These deficiencies may be involved in patients who experience migraines, but that is unclear based on existing studies. "Further studies are needed to elucidate whether vitamin supplementation is effective in migraine patients in general, and whether patients with mild deficiency are more likely to benefit from supplementation," says Suzanne Hagler, MD, a Headache Medicine fellow in the division of Neurology at Cincinnati Children's Hospital Medical Center and lead author of the study. Dr. Hagler and colleagues at Cincinnati Children's conducted the study among patients at the Cincinnati Children's Headache Center. She will present her findings at 9:55 am Pacific time Friday, June 10, 2016 at the 58th Annual Scientific Meeting of the American Headache Society in San Diego. Dr. Hagler's study drew from a database that included patients with migraines who, according to Headache Center practice, had baseline blood levels checked for vitamin D, riboflavin, coenzyme Q10 and folate, all of which were implicated in migraines, to some degree, by previous and sometimes conflicting studies. Many were put on preventive migraine medications and received vitamin supplementation, if levels were low. Because few received vitamins alone, the researchers were unable to determine vitamin effectiveness in preventing migraines. She found that girls and young woman were more likely than boys and young men to have coenzyme Q10 deficiencies at baseline. Boys and young men were more likely to have vitamin D deficiency. It was unclear whether there were folate deficiencies. Patients with chronic migraines were more likely to have coenzyme Q10 and riboflavin deficiencies than those with episodic migraines. Previous studies have indicated that certain vitamins and vitamin deficiencies may be important in the migraine process. Studies using vitamins to prevent migraines, however, have had conflicting success. Research suggests mask-wearing can increase struggles with social anxiety University of Waterloo (Canada), June 21, 2021 People who struggle with social anxiety might experience increased distress related to mask-wearing during and even after the COVID-19 pandemic. A paper authored by researchers from the University of Waterloo's Department of Psychology and Centre for Mental Health Research and Treatment also has implications for those who haven't necessarily suffered from social anxiety in the past. "The adverse effects of the COVID-19 pandemic on mental health outcomes, including anxiety and depression, have been well-documented," said David Moscovitch, professor of clinical psychology and co-author of the paper. "However, little is known about effects of increased mask-wearing on social interactions, social anxiety, or overall mental health. "It is also possible that many people who didn't struggle with social anxiety before the pandemic may find themselves feeling more anxious than usual as we emerge out of the pandemic and into a more uncertain future -- especially within social situations where our social skills are rusty and the new rules for social engagement are yet to be written." Social anxiety is characterized by negative self-perception and fear that one's appearance or behaviour will fail to conform with social expectations and norms. Social anxiety disorder is an extreme manifestation that affects up to 13 per cent of the population. The researchers reviewed existing literature addressing three factors that they hypothesized might contribute to social anxiety associated with mask-wearing: hypersensitivity to social norms, bias in the detection of social and emotional facial cues, and propensity for self-concealment as a form of safety behaviour. "We found that mask-wearing by people with social anxiety is likely to be influenced by their perception of social norms and expectations, which may or may not be consistent with public-health guidelines and can vary widely by region and context," said Sidney Saint, an undergraduate psychology student at Waterloo and lead author of the paper. The paper also highlights that people with social anxiety have difficulty detecting ambiguous social cues and are likely to interpret them negatively. These individuals also tend to worry about sounding incomprehensible or awkward. "We believe that both issues are likely to be magnified during interactions with masks," Saint said. Another highlighted impact is that masks can function as a type of self-concealment strategy that enables people with social anxiety to hide their self-perceived flaws. Therefore, the desire for self-concealment may motivate their use of masks over and above their desire to protect themselves from contagion. "Due to their self-concealing function, masks may be difficult for some people to discard even when mask-wearing is no longer required by public health mandates," Saint said. In addition to contributing insights to guide clinicians toward effective assessment and treatment, the paper shows that people with social anxiety may be particularly vulnerable to periods of norm transitions where expectations for mask-wearing are in flux or become a matter of personal choice. Going with your gut can result in better decision-making than using detailed data methods, study shows City University London, June 21, 2021 Managers who use their gut instinct together with simple decision-making strategies may make equally good, but faster, decisions as those who use data to reach an outcome, a new study has found. The report, co-authored by academics at the Business School (formerly Cass), King's Business School, and the University of Malta, finds that the reliance on data analysis in decision-making might be counterproductive as this reduces decision-making speed without ensuring more accuracy. The research, based on information from 122 advertising, digital, publishing, and software companies, finds that using data to inform decision making under high uncertainty is often not optimal. This may explain why 12 different publishers initially rejected the opportunity to publish "Harry Potter and the Philosopher's Stone' – because it had no data to inform its potential. A recent survey revealed that 92 percent of Fortune 1000 companies were reporting increased investment in data initiatives, although it appears this may not always be necessary. The authors asked managers how they made decisions on their most recent innovation project, including the extent to which they used data, instinct, and other simple heuristics (mental strategies). The findings outlined that among those decision-making methods were: Majority—choosing what the most people wanted Tallying—picking the choice with the greatest quantity of positive points Experience—selecting the option that the most experienced individual on the team wanted. Managers were asked whether they think they made the right decision and how fast they were in reaching that decision. Results showed that managers relied on their own instinct as much as data, using 'tallying' more than any other metric. Dr. Oguz A. Acar, Reader in Marketing at the Business School and co-author of the report, said: "This research shows that data-driven decision-making is not the panacea in all situations and may not result in increased accuracy when facing uncertainty. "Under extreme uncertainty, managers, particularly those with more experience, should trust the expertise and instincts that have propelled them to such a position. The nous developed over years as a leader can be a more effective than an analytical tool which, in situations of extreme uncertainty, could act as a hindrance rather than a driver of success." "Choosing among alternative new product development projects: The role of heuristics" is published in Psychology and Marketing. Pretreatment by rosemary extract or cell transplantation improves memory deficits of Parkinson disease Damghan University (Iran) June 21 2021 According to news originating from Damghan, Iran, research stated, “The therapeutic effect of adipose tissue-derived stem cells (ADSCs) or RE on hippocampal neurogenesis and memory in Parkinsonian rats were investigated. Male rats were lesioned by bilateral intra-nigral injections of 6-OHDA and divided into six groups: 1. Lesion 2 and 3: RE and water groups were lesioned rats pretreated with RE or water, from 2weeks before neurotoxin injection and treated once a day for 8weeks post lesion. 4&5: Cell and alpha-MEM (alpha-minimal essential medium) received intravenous injection of BrdU-labeled ADSCs or medium, respectively from 10days post lesion until 8weeks later. 6: Sham was injected by saline instead of neurotoxin.” Our news journalists obtained a quote from the research from Damghan University, “Memory was assessed using Morris water Maze (MWM), one week before and at 1, 4 and 8weeks post 6-OHDA lesion. After the last probe, the animals were sacrificed and brain tissue obtained. Paraffin sections were stained using cresyl violet, anti-BrdU (Bromodeoxyuridine / 5-bromo-2'-deoxyuridine), anti-GFAP (Glial fibrillary acidic protein) and anti-TH antibodies. There was a significant difference of time spent in the target quadrant between groups during probe trial at 4 and 8 weeks' post-lesion. Cell and RE groups spent a significantly longer period in the target quadrant and had lower latency as compared with lesion. Treated groups have a significantly higher neuronal density in hippocampus compared to water, alpha-MEM and lesion groups. BrdU positive cells were presented in lesioned sites. The GFAP (Glial fibrillary acidic protein) positive cells were reduced in treated and sham groups compared to the water, alpha-MEM and lesion groups.” According to the news editors, the research concluded: “Oral administration of RE (Rosemary extract) or ADSCs injection could improve memory deficit in the Parkinsonian rat by neuroprotection.” Inadequate vitamin D levels associated with interstitial lung disease Johns Hopkins University, June 20 2021. An article appearing in the Journal of Nutrition documents a link between decreased vitamin D levels and a greater risk of early signs of interstitial lung disease (ILD), a group of disorders characterized by inflammation and scarring that can lead to lung damage. Although ILD can be caused by environmental and other factors, some cases have unknown causes. The investigation included 6,302 participants in the Multi-Ethnic Study of Atherosclerosis who had information available concerning their initial serum 25-hydroxyvitamin D concentrations and computed tomography (CT) imaging that included partial views of the lungs. Ten years after enrollment, 2,668 participants had full lung CT scans that were evaluated for presence of scar tissue and other abnormalities. Subjects who had deficient vitamin D levels of less than 20 ng/mL had more spots on their lungs that were suggestive of damage in comparison with subjects whose vitamin D was adequate. Among those who had full lung CT scans, deficient or intermediate (between 20-30 ng/mL) vitamin D levels were associated with a 50-60% greater risk of abnormalities suggestive of ILD. "We knew that the activated vitamin D hormone has anti-inflammatory properties and helps regulate the immune system, which goes awry in ILD," commented senior author Erin Michos, MD, MHS. “There was also evidence in the literature that vitamin D plays a role in obstructive lung diseases such as asthma and COPD, and we now found that the association exists with this scarring form of lung disease too." "Our study suggests that adequate levels of vitamin D may be important for lung health,” she concluded. “We might now consider adding vitamin D deficiency to the list of factors involved in disease processes, along with the known ILD risk factors such as environmental toxins and smoking.”

covid-19 university social marketing research boys psychology positive san diego fortune nutrition hospitals harry potter journal patients iran md stone essential memory treatments male studies pacific twenty results investigation morris previous managers reader forty icu malta insomnia philosophers oral measures majority waterloo ml neurology subjects treated business school sham mem copd inadequate nk serum zn micronutrients pct crp mhs igg ards cincinnati children atherosclerosis hagler lesion caco hospital medical center ild acar mental health research pilot study montmorency paraffin cd8 t brdu parkinsonian annual scientific meeting gary null pretreatment american headache society tart cherry juice waterloo canada multi ethnic study headache center

What is PSP? Understanding this Parkinsonian-like syndrome

Power Over Parkinson's

Play Episode Listen Later Apr 14, 2021 33:44

CurePSP President, David Kemp, discusses how his organization aids those with PSP, the similarities to Parkinson's Disease, and updates on the latest in neurological disease research. To learn how POP is supporting the Parkinson's community, visit us at poweroverpd.org.

mental health pop disease syndrome parkinson psp parkinsons parkinson's disease parkinson's disease parkinsonian parkinson's david kemp

Alterity Therapeutics' (ASX: ATH) phase 2 clinical trial nears, commercialisation plans continue for MSA drug (w/ David Stamler)

Small Caps

Play Episode Listen Later Mar 11, 2021 20:09

Alterity Therapeutics (ASX: ATH) chief executive officer Dr David Stamler joins Small Caps to discuss the company’s lead drug candidate ATH434, which has been developed to combat the side effects of Parkinsonian disorders. The disorder includes multiple system atrophy (MSA), which Alterity is focused on treating with ATH434 in clinical trials. Dr Stamler points out there is a substantial unmet need for MSA treatments with forecast potential annual sales of ATH434 in the US of $550-725 million.

investing drug stocks pharma biotech clinical trials phase2 therapeutics asx msa small caps commercialisation parkinsonian alterity

Parkinsonian syndromes and Parkinson's subtypes: Will a single neuroimaging modality ever be enough?

MDS Podcast

Play Episode Listen Later Feb 1, 2021

Dr. Sara Schaefer speaks with Dr. Nicola Pavese about the imaging modalities currently in use and emerging to differentiate parkinsonian syndromes and Parkinson's subtypes, and how imaging helps us to understand, study, and treat these conditions. Read the article

single syndrome parkinson modality neuroimaging subtypes sara schaefer parkinsonian

Pain in Parkinson’s Disease – A Podcast With Ray Chaudhuri and Yazead Buhidma

IASP Pain Research Forum Podcasts

Play Episode Listen Later Dec 14, 2020 36:53

This podcast features K. Ray Chaudhuri, MD, DSc, Professor of Movement Disorders and Neurology at King’s College Hospital and King’s College London, UK, and Medical Director of the Parkinson Foundation International Centre of Excellence at King’s College, and Yazead Buhidma, a PhD student at the Wolfson Centre of Age-related Diseases at King’s College London. Chaudhuri studies Parkinson’s disease (PD) and is a world leader in defining non-motor symptoms and non-motor phenotypes of PD. Meanwhile, Buhidma is working to elucidate the underlying mechanisms of PD pain and test potential treatments, by linking findings from Parkinsonian animal models with functional neurological changes, pharmacological tests, and post-mortem analysis of Parkinson patient tissue. Chaudhuri and Buhidma speak with PRF Correspondent Jayden O'Brien, a PhD candidate at the University of Sydney, Australia, to discuss the problem of pain in Parkinson’s disease (PD), how researchers are studying PD pain in animals and what they are learning about its mechanisms, and more.

Fibrillar α-synuclein induces neurotoxic astrocyte activation via RIP kinase signaling and NF-κB

Play Episode Listen Later Nov 17, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.17.387175v1?rss=1 Authors: Chou, T.-W., Chang, N. P., Krishnagiri, M., Patel, A. P., Atkins, C., Daniels, B. P. Abstract: Parkinson's disease (PD) is a neurodegenerative disorder characterized by death of midbrain dopamine neurons. The pathogenesis of PD is poorly understood, though misfolded and/or aggregated forms of the protein -synuclein have been implicated in several neurodegenerative disease processes, including neuroinflammation and astrocyte activation. Astrocytes in the midbrain play complex roles during PD, initiating both harmful and protective processes that vary over the course of disease. However, despite their significant regulatory roles during neurodegeneration, the cellular and molecular mechanisms that promote pathogenic astrocyte activity remain mysterious. Here, we show that -synuclein preformed fibrils (PFFs) induce pathogenic activation of human midbrain astrocytes, marked by inflammatory transcriptional responses, downregulation of phagocytic function, and conferral of neurotoxic activity. These effects required the necroptotic kinases RIPK1 and RIPK3, but were independent of MLKL and necroptosis. Instead, both transcriptional and functional markers of astrocyte activation occurred via RIPK-dependent activation of NF-{kappa}B signaling. Our study identifies a previously unknown function for -synuclein in promoting neurotoxic astrocyte activation, as well as new cell death-independent roles for RIP kinase signaling in the regulation of glial cell biology and neuroinflammation. Together, these findings highlight previously unappreciated molecular mechanisms of pathologic astrocyte activation and neuronal cell death with implications for Parkinsonian neurodegeneration. Copy rights belong to original authors. Visit the link for more info

rip daniels copy patel chang pd activation atkins signaling nf kinase biorxiv astrocytes parkinsonian pffs astrocyte neurotoxic

Cell-Type-Specific Decrease of the Intrinsic Excitability of Motor Cortical Pyramidal Neurons in Parkinsonian Mice

Play Episode Listen Later Oct 21, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.20.347732v1?rss=1 Authors: Chen, L., Kim, Y., Chu, H.-y. Abstract: The hypokinetic motor symptoms of Parkinsons disease (PD) are closely linked with a decreased motor cortical output as a consequence of elevated basal ganglia inhibition. However, whether and how the loss of dopamine alters the cellular properties of motor cortical neurons in PD remains undefined. We induced experimental parkinsonism in adult C57BL6 mice of both sexes by injecting neurotoxin, 6-hydroxydopamine, into the medial forebrain bundle. By using ex vivo patch-clamp recording and retrograde tracing approach, we found that the intrinsic excitability of pyramidal tract neurons (PTNs) in the motor cortical layer 5b was greatly decreased following the degeneration of midbrain dopaminergic neurons; but the intratelencephalic neurons (ITNs) were not affected. The cell-type-specific intrinsic adaptations were associated with a significant broadening of the action potentials in PTNs but not in ITNs. Moreover, the loss of midbrain dopaminergic neurons impaired the capability of M1 PTNs to sustain high-frequency firing, which could underlie their abnormal pattern of activity in the parkinsonian state. We also showed that the decreased excitability and broadened action potentials were largely caused by a disrupted function of the large conductance, Ca2+-activated K+ channels. The restoration of dopaminergic neuromodulation failed to rescue the impaired intrinsic excitability of M1 PTNs in parkinsonian mice. Altogether, our data show cell-type-specific decreases of the excitability of M1 pyramidal neurons following the loss of midbrain dopaminergic neurons. Thus, intrinsic adaptations in the motor cortex, together with pathological basal ganglia inhibition, underlie the decreased motor cortical output in parkinsonian state and exacerbate parkinsonian motor deficits Copy rights belong to original authors. Visit the link for more info

motor mice pd decrease m1 chu intrinsic parkinsons neurons cortical biorxiv ca2 pyramidal parkinsonian

Assessing and treating older adults with dementia symptoms during the COVID-19 pandemic: A Masterclass with Dr. Sanjay Gupta

MDedge Psychcast

Play Episode Listen Later Oct 14, 2020 20:48

Sanjay Gupta, MD, conducts a Masterclass on treating geriatric patients with symptoms of dementia, particularly amid the restrictions tied to COVID-19. Dr. Gupta is chief medical officer at BryLin Hospital in Buffalo, N.Y. He is also is a clinical professor in the department of psychiatry at the State University of New York, Syracuse, and is affiliated with SUNY at Buffalo. Dr. Gupta attends at 8-10 nursing homes. He disclosed serving on the speakers’ bureaus of AbbVie, Acadia, Alkermes, Intra-Cellular Therapies, Janssen, and Otsuka. Take-home points Common neuropsychiatric symptoms in patients with dementia include agitation, aggression, delusions, insomnia, anxiety, and depression. One-third of community-dwelling elders and between 60%-80% of nursing facility patients have these neuropsychiatric symptoms. The most common medication class Dr. Gupta uses is antipsychotics. The use of these medications in individuals with dementia is off label. The Food and Drug Administration maintains a black-box warning on the use of antipsychotics for geriatric patients because of the increased risk of sudden death. Risperidone is supported by the most data, then olanzapine, then aripiprazole, and finally quetiapine. Quetiapine has very limited data to support its efficacy. Most antipsychotics have modest efficacy data for their use in this population. The riskiest adverse effects are cardiovascular adverse events, which are higher in risperidone. Dr. Gupta starts risperidone at a low dose of 0.25 mg taken by mouth b.i.d. and titrates to a maximum dose of 2 mg/24 hours. The starting dose for olanzapine is 2.5 mg up to a maximum dose of 10 mg. The starting dose of aripiprazole is 1 mg, and maximum dose 5 mg or less. Selective serotonin reuptake inhibitors (most commonly sertraline or citalopram), the atypical antidepressant mirtazapine, and anticonvulsants (valproic acid) are also used for agitation in dementia but there is limited evidence for their efficacy. Melatonin and trazodone have a positive effect on sleep that can have downstream improvement on aggressive behaviors. Summary To choose an effective treatment, it’s essential to obtain a detailed history of the symptoms from patients and collateral, such as relatives and staff members from the facility. Staff members can be educated about what information is most important to the clinician, or they may provide vague information, such as “the patient is confused.” Specific symptoms that can be used guide treatment include the presence of disorganized thoughts, delusions and paranoia, or visual and/or auditory hallucinations; the timing of the behavior (day vs. night); and patterns of aggressive behaviors. Dr. Gupta emphasizes that it’s important to rule out delirium as the cause of agitation by evaluating underlying medical issues with laboratory evaluations, and when possible, a physical exam. Antipsychotics work best in the context of aggression driven by paranoia and/or delusions of persecution. Antipsychotics seem to work less well for general agitation that may be driven by triggers that need to be uncovered through investigation of the history and environment. Reasons for agitation and aggression might include sensory or activity deprivation, difficulty emptying bladder or bowels, or depression and loneliness, both of which are prevalent during the pandemic. Adverse effects of antipsychotics will be greater in older adults, and include sedation, gait problems that increase the risk of falls, and extrapyramidal or Parkinsonian symptoms. In a geriatric patient, tardive dyskinesia can occur with as little as 1 month of exposure to an antipsychotic, compared with 3 months in younger adults. Before starting an antipsychotic, the clinician must obtain informed consent from the health-care proxy and inform them that using antipsychotics in a patient with dementia is a non–FDA-approved treatment with a black-box warning. Gradual dose reduction, a Medicare policy about the use of psychotropic medications within nursing homes, is defined as “stepwise tapering of a dose to determine if symptoms, conditions, or risks can be managed by a lower dose or if the dose or medication can be discontinued.” Dr. Gupta addresses this policy by assessing which medications are essential and often stopping some medications once the patient is started on antipsychotics. References Steinberg M, Lyketsos CG. Am J Psychiatry. 2012 Sep;169(9):900-6. Maher AR et al. JAMA. 2011 Sep 28;306(12):1359-69. Schneider LS et al. JAMA. 2005 Oct 19;294(15):1934-43. Seitz DP et al. Cochrane Database Sys Rev. 2001 Feb 16;(12):CD0089. Ballard C et al. Cochrane Database Sys Rev. 2006 Jan 25. doi: 10.1002/14651858. Ballard C, Waite J. Cochrane Database Sys Rev. 2006 Jan 25;(1):CD003476. Department of Health & Human Services. State Operations Manual Surveyor Guidance Revisions Related to Psychosocial Harm in Nursing Homes. CMS.gov. 2016 Mar 25. * * * Show notes by Jacqueline Posada, MD, associate producer of the Psychcast; assistant clinical professor in the department of psychiatry and behavioral sciences at George Washington University, Washington; and staff physician at George Washington Medical Faculty Associates, also in Washington. Dr. Posada has no conflicts of interest. * * * For more MDedge Podcasts, go to mdedge.com/podcasts Email the show: podcasts@mdedge.com

Changes in excitability properties of ventromedial motor thalamic neurons in 6-OHDA lesioned mice

Play Episode Listen Later Oct 5, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.05.327379v1?rss=1 Authors: Bichler, E. K., Cavarretta, F., Jaeger, D. Abstract: The activity of basal ganglia input receiving motor thalamus (BGMT) makes a critical impact on motor cortical processing, but modification in BGMT processing with Parkinsonian conditions have not be investigated at the cellular level. Such changes may well be expected due to homeostatic regulation of neural excitability in the presence of altered synaptic drive with dopamine depletion. We addressed this question by comparing BGMT properties in brain slice recordings between control and unilaterally 6-OHDA treated adult mice. At a minimum of 1 month post 6-OHDA treatment, BGMT neurons showed a highly significant increase in intrinsic excitability, which was primarily due to a decrease in M-type potassium current. BGMT neurons after 6-OHDA treatment also showed an increase in T-type calcium rebound spikes following hyperpolarizing current steps. Biophysical computer modeling of a thalamic neuron demonstrated that an increase in rebound spiking can also be accounted for by a decrease in the M-type potassium current. Modeling also showed that an increase in sag with hyperpolarizing steps found after 6-OHDA treatment could in part but not fully be accounted for by the decrease in M-type current. These findings support the hypothesis that homeostatic changes in BGMT neural properties following 6-OHDA treatment likely influence the signal processing taking place in basal ganglia thalamocortical processing in Parkinson's disease. Copy rights belong to original authors. Visit the link for more info

parkinson copy modeling motor properties mice jaeger neurons biorxiv biophysical parkinsonian bgmt

Co-editing PINK1 and DJ-1 genes via AAV-delivered CRISPRCas9 system in adult monkey brains elicits classic Parkinsonian phenotypes

Play Episode Listen Later Sep 20, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.19.305003v1?rss=1 Authors: Li, H., Wu, S., Ma, X., Li, X., Cheng, T., Chen, Z., Wu, J., Lv, L., Li, L., Xu, L., Wang, W., Hu, Y., Jiang, H., Yin, Y., Qiu, Z., Hu, X. Abstract: Whether direct manipulation of Parkinson's disease (PD) risk genes in monkey brain can elicit Parkinsonian phenotypes remains an unsolved issue. Here, we employed an adeno-associated virus (AAV)-delivered CRISPR/Cas9 system to directly co-edit PINK1 and DJ-1 genes in the substantia nigra (SN) region of four adult monkey brains. After the operation, two of the monkeys exhibited all classic PD symptoms, including bradykinesia, tremor, and postural instability, accompanied by severe nigral dopaminergic neuron loss (over 60%) and -synuclein pathology. The aged monkeys were more vulnerable to gene editing by showing faster PD progression, higher final total PD scores, and severer pathologic changes compared with their younger counterparts, suggesting both the genetic and aging factors played important roles in PD development. This gene editing system can be used to develop a large quantity of genetically edited PD monkeys over a short period, thus providing a practical transgenic monkey model for future PD studies. Copy rights belong to original authors. Visit the link for more info

dj system adult parkinson copy editing li delivered chen genes wang pd yin wu hu sn cheng lv xu jiang crispr cas9 aav phenotypes biorxiv qiu monkey brains parkinsonian

Stimulation of zona incerta selectively modulates pain in humans

PaperPlayer biorxiv animal behavior and cognition

Play Episode Listen Later Sep 3, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.02.277921v1?rss=1 Authors: Lu, C. W., Harper, D. E., Askari, A., Willsey, M. S., Vu, P. P., Schrepf, A. D., Harte, S. E., Patil, P. G. Abstract: Stimulation of zona incerta in rodent models has been shown to modulate behavioral reactions to noxious stimuli. Sensory changes observed in Parkinsonian patients with subthalamic deep brain stimulation suggest that this effect is translatable to humans. Here, we utilized the serendipitous placement of subthalamic deep brain stimulation leads to directly investigate the effects of zona incerta stimulation on human pain perception. We found that stimulation at 20 Hz, the physiological firing frequency of zona incerta, reduces experimental heat pain by a modest but significant amount, achieving a 30% reduction in one fifth of implants. Stimulation at higher frequencies did not modulate heat pain. Modulation was selective for heat pain and was not observed for warmth perception or pressure pain. These findings provide a mechanistic explanation of sensory changes seen in subthalamic deep brain stimulation patients and identify zona incerta as a potential target for neuromodulation of pain. Copy rights belong to original authors. Visit the link for more info

pain humans copy zona sensory vu stimulation hz harte modulation patil selectively askari biorxiv parkinsonian

Practical Design and Implementation of Animal Movements Tracking System for Neuroscience Trials

Play Episode Listen Later Jul 26, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.26.221754v1?rss=1 Authors: Memarian Sorkhabi, M. Abstract: Background: The nervous system functions of an animal are predominantly reflected in the behaviour and the movement, therefore the movement-related data and measuring behavior quantitatively are crucial for behavioural analyses. The animal movement is traditionally recorded, and human observers follow the animal behaviours; if they recognize a certain behaviour pattern, they will note it manually, which may suffer from observer fatigue or drift. Objective: Automating behavioural observations with computer-vision algorithms are becoming essential equipment to the brain function characterization in neuroscience trials. In this study, the proposed tracking module is eligible to measure the locomotor behaviour (such as speed, distance, turning) over longer time periods that the operator is unable to precisely evaluate. For this aim, a novel animal cage is designed and implemented to track the animal movement. The frames received from the camera are analyzed by the 2D bior 3.7 Wavelet transform and SURF feature points. Results: Implemented video tracking device can report the location, duration, speed, frequency and latency of each behavior of an animal. Validation tests were conducted on the auditory stimulation trial and the magnetic stimulation treatment of hemi-Parkinsonian rats. Conclusion/ Significance: The proposed toolkit can provide qualitative and quantitative data on animal behaviour in an automated fashion, and precisely summarize an animal's movement at an arbitrary time and allows operators to analyse movement patterns without requiring to check full records for every experiment. Copy rights belong to original authors. Visit the link for more info

design system practical trials animal tracking neuroscience copy validation surf implementation movements 2d biorxiv parkinsonian wavelet

Theoretical analysis predicts an optimal therapeutic strategy in distinct parkinsonian landscapes of the striatum

PaperPlayer biorxiv biophysics

Play Episode Listen Later Jul 19, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.19.210690v1?rss=1 Authors: Heltberg, M. L., Awada, H. N., Lucchetti, A., Jensen, M. H., Dreyer, J. K., Rasmussen, R. Abstract: Parkinsons disease (PD) results from a loss of dopaminergic neurons. The age of disease onset, its progression and symptoms vary significantly between patients, pointing to a complex relationship between neuron loss and PD etiology. Yet, our understanding of the clinical variability remains incomplete. Here, we use biophysical modelling to investigate the dopaminergic landscape in the healthy and denervated striatum. Based on currently proposed mechanisms causing PD, we model three distinct denervation patterns, and show notable differences in the dopaminergic network as denervation progresses. We find local and global differences in the activity of two types of striatal neurons as a function of the denervation pattern. Finally, we identify the optimal cellular strategy for maintaining normal dopamine signaling when neurons degenerate within our model. Our results derive a conceptual framework in which the clinical variability of PD is rooted in distinct denervation patterns and forms testable predictions for future PD research. Copy rights belong to original authors. Visit the link for more info

strategy copy optimal pd therapeutic predicts rasmussen landscapes distinct theoretical dreyer biorxiv parkinsonian striatum

Human embryonic stem cells-derived dopaminergic neurons transplanted in parkinsonian monkeys recover dopamine levels and motor behavior

behavior monkeys levels parkinson recover copy motor dopamine pd post mortem imaging hallway neurons derived transplanted biorxiv carlos aguilar embryonic stem cells parkinsonian

Play Episode Listen Later Jul 11, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.08.192591v1?rss=1 Authors: Adolfo Lopez-Ornelas, Itzel Escobedo-Avila, Gabriel Ramirez-Garcia, Rolando Lara-Rodarte, Cesar Melendez-Ramirez, Beetsi Urrieta-Chavez, Tonatiuh Barrios-Garcia, Veronica Caceres-Chavez, Xochitl Flores-Ponce, Francia Carmona, Carlos A Reynoso, Carlos Aguilar, Nora E Kerik, Luisa Rocha, Leticia Verdugo-Diaz, Victor Trevino, Jose Bargas, Veronica Ramos-Mejia, Juan Fernandez-Ruiz, Aurelio Campos-Romo, Ivan Velasco Abstract: Human embryonic stem cells (hESCs) differentiate into specialized cells, including midbrain dopaminergic neurons (DAN). Non-human primates (NHPs) injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine develop some alterations observed in Parkinson disease (PD) patients. We obtained DAN from hESCs and confirmed that they express dopaminergic markers, generate action potentials, and release dopamine (DA) in vitro. DAN were transplanted bilaterally in the putamen of parkinsonian NHPs. After grafting, animals improved motor behavior, evaluated by the HALLWAY task, and in agreement with this recovery, DA release was detected by microdialysis. Imaging techniques revealed changes in fractional anisotropy and mean diffusivity in magnetic resonance imaging and higher 11C-DTBZ binding in positron-emission tomography scans, associated with grafts. Postmortem analysis showed that transplanted DAN survived over ten months in the putamen, without developing tumors, in the immunosuppressed NHPs. These results indicate that cell replacement therapy with hESCs-derived DAN causes long-term biochemical, anatomical, and physiological improvements in this model of PD.Competing Interest StatementThe authors have declared no competing interest. Copy rights belong to original authors. Visit the link for more info

Disrupted basal ganglia output during movement preparation in hemi-parkinsonian mice accounts for behavioral deficits

Play Episode Listen Later Jun 20, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.19.160457v1?rss=1 Authors: Tekriwal, A., Lintz, M., Thompson, J. A., Felsen, G. Abstract: Parkinsonian motor deficits are associated with elevated inhibitory output from the basal ganglia (BG). However, several features of Parkinson's disease (PD) have not been accounted for by this supra-inhibition framework, including the potentially therapeutically-relevant observation that movements guided by external stimuli are less impaired than otherwise-identical movements generated based on internal goals. Is this difference due to divergent processing within the BG itself, or to the recruitment of extra-BG pathways by sensory processing? In addition, surprisingly little is known about precisely when, in the sequence from selecting to executing movements, BG output is altered by PD. Here, we address these questions by recording activity in the SNr, a key BG output nucleus, in hemiparkinsonian (hemi-PD) mice performing a well-controlled behavioral task requiring stimulus-guided and internally-specified directional movements. We found that hemi-PD mice (n = 5, male) exhibited a bias ipsilateral to the side of dopaminergic cell loss, consistent with supra-inhibition of contralateral movements by BG output, and that this bias was stronger when movements were internally specified rather than stimulus guided, consistent with clinical observations in parkinsonian patients. We further found that changes in SNr activity during movement preparation could account for the ipsilateral behavioral bias, as well as its greater magnitude for internally-specified movements. These results suggest that parkinsonian changes in BG output underlying movement preparation contribute to the greater deficit in internally-specified in comparison to stimulus-guided movements. Copy rights belong to original authors. Visit the link for more info

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Impaired hand dexterity function in a non-human primate model with chronic Parkinson's disease

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Play Episode Listen Later May 1, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.01.072058v1?rss=1 Authors: Seo, J., Won, J., Kim, K., Park, J., Yeo, H.-G., Kim, Y. G., Baek, S. H., Lee, H., Jeon, C.-Y., Choi, W. S., Lee, S., Kim, K. J., Park, S.-H., Son, Y., Jeong, K. J., Lim, K. S., Kang, P., Lee, H.-Y., Son, H.-C., Huh, J.-W., Kim, Y.-H., Jin, Y. B., Lee, D.-S., Lee, S.-R., Choi, J.-W., Lee, Y. Abstract: Symptoms of Parkinson's disease (PD) caused by loss of dopaminergic neurons are accompanied by movement disorders, including tremors, rigidity, bradykinesia, and akinesia. Non-human primate (NHP) models with PD play an essential role in the analysis of PD pathophysiology and behavior symptoms. As impairments of hand dexterity function can affect activities of daily living in patients with PD, research on hand dexterity function in NHP models with chronic PD is essential. Traditional rating scales previously used in the evaluation of animal spontaneous behavior were insufficient due to factors related to subjectivity and passivity. Thus, experimentally designed applications for an appropriate apparatus are necessary. In this study, we aimed to longitudinally assess hand dexterity function using hand dexterity task (HDT) in NHP-PD models. To validate this assessment, we analyzed an alteration in Parkinsonian tremor symptoms, loss of dopaminergic neuron, and positron emission tomography (PET) imaging of dopamine transporters (DAT) in these models. HDT latency significantly increased in NHP-PD models. In addition, a significant inverse correlation between HDT and DAT was identified, but no local bias was found. The correlation with intention tremor symptoms was lower than the resting tremor. In conclusion, the evaluation of HDT may reflect behavioral symptoms of NHP-PD models. Furthermore, HDT was effectively used to experimentally distinguish intention tremors from other tremors. Copy rights belong to original authors. Visit the link for more info

Stochastic Resonance Therapy and Parkinson's

Parkinsons Recovery

Play Episode Listen Later Apr 2, 2020 31:00

Stochastic Resonance Therapy (SRT) was born in the German city of Frankfurt when Dietmar Schmidtbleicher developed a new training device for Olympic athletes. Since then, the whole-body vibration device he developed has been studied and shown to be effective in the treatment of Parkinson's motor symptoms. While you may have already heard of the benefits of vibration therapy and Parkinson's, chances are you haven't heard of SRT until now. SRT is different from other types of vibration devices. It delivers randomized and non-uniform oscillations and perturbations to the body, whereas all other devices on the market deliver uniform, sinusoidal vibrations. The random nature of SRTvibrations elicits the automatic stretch reflex in the muscles, which leads to postural adjustments being made in the spinal cord and the cerebellum (the part of the brain that automatically adjusts movement patterns). These adjustments keep the head still and the body upright while on the device. Hundreds to thousands of stimuli are delivered to the spinal cord and cerebellum in a matter of minutes. In the literature, SRT has been shown to decrease tremor and rigidity, improve postural control and balance, and lead to better gait patterns in Parkinsonian patients. For further information contact: Kyle Harris, MS, CSCS, SRT Zeptoring Cell: 605.454.1418 Email: kyledharris2017@gmail.com Brady Volmering Cell: 989.551.9503

Episode 8 - ABC's of PD - Festination

The Parkinson's Road Podcast

Play Episode Listen Later Jan 27, 2020 11:51

Installment 2 of the ABC's of PD. Did you know that Parkinson's has a distinctive walk? It is called the Parkinsonian gait, and one of the potential characteristics of this is festination. This episode explains what festination or festinating gait means. Here is a great video demonstrating what festination looks like: https://www.youtube.com/watch?v=B5hrxKe2nP8** disclaimer ** I have no affiliation with any Parkinson's specific exercise program I only mention PD Warrior as a point of reference. ** I say posterior chain in the podcast but know that working your posterior chain will also strengthen the anterior muscles including your quadriceps, hip flexors, and abdominals.**Support the show (https://www.facebook.com/parkinsonsrdpod/)

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Misdiagnosis

When Life Gives You Parkinson's

Play Episode Listen Later Jan 7, 2020 54:11

I will introduce you to Jeanette and Barry Pynn. They are friends of Rebecca and mine that just went through a gut-wrenching couple of years dealing with a misdiagnosis. Jeanette was a runner for her whole life. After decades of raising kids, a great marriage, and dreams of traveling and enjoying the final decades of life together, Jeanette’s gait changed. “I couldn’t flatten my foot out during a run,” she says. Doctors treated her foot issues for years through orthotics and creams. Three years later, the whole left side of her body shutdown after jumping into the Adriatic Sea. Something was definitely wrong. After months of tests, Jeanette received a diagnosis in the Parkinsonian family that she was not expecting: Multiple System Atrophy, also known as MSA. It carries similar symptoms to Parkinson’s but is more aggressive, has a quicker progression and is deadly. The Mayo Clinic reports people with MSA typically live seven to ten years after symptom onset. This is an important fact that Jeanette and Barry did not know and a vital detail that her neurologist failed to mention. Barry remembers leaving the appointment somewhat encouraged, “When we heard that it might be a relative of Parkinson's, it was actually it was a relief.” That relief quickly gave way to fear, when Jeanette was waiting for her new prescriptions at Costco surfing the internet, “I was reading up on the disease and I looked over at Barry and I said, I don't think this is very good. And he said, In what way? And I said, I think you better read this because I can't I can't really explain it to you.” After two years of wrestling with the diagnosis, the disease, and her own impending death, Jeanette and Barry reached out for help. They were in search of support, community, information, context and understanding. Rebecca and I met Barry in the Spring of 2019 at the annual meeting for the Parkinson Society of British Columbia. They were listeners to the podcast and had traveled from Bowen Island, because they read we would be at the event and they wanted to connect. We chatted, they shared their story, and soon we discovered we got along. We became fast friends. And in the back of our heads, we understood we were entering into a friendship with Jeanette, at least, was a proposition that wouldn’t likely survive the next decade. Rebecca’s cell phone rang on a Saturday morning in September last year. It was Jeanette. She had seen a new neurologist, a movement disorder specialist, at the UBC Brain Centre. “She said that it's most likely certain that I have Parkinson's disease and not MSA.” Jeanette continued through tears, “Whoever thought they'd be so happy to have Parkinson’s?” The misdiagnosis of MSA is certainly not rare. A 2015 study featured on Neurology.org examined 134 autopsied brains of people who were clinically diagnosed MSA while living and only 63% had the correct diagnosis at death. As it relates to Parkinson’s disease, a new Parkinson’s UK study shows 25% of people with Parkinson’s are misdiagnosed. A third of those were given medication for an illness they didn’t have and a 10% underwent a needless operation or procedure. Misdiagnosis is likely to continue until researchers discover reliable biomarkers to aid in the diagnosis of Parkinson’s and related disease. Feel free to comment by leaving us a voice message here: https://www.speakpipe.com/WhenLifeGivesYouParkinsons Follow me, Larry Gifford Twitter: @ParkinsonsPod Facebook: Facebook.com/ParkinsonsPod Instagram: @parkinsonspod Follow Co-host and Producer Niki Reitmeyer Twitter: @Niki_Reitmayer Thank you to our special guests: Jeanette Fisher Pynn Barry Pynn Wendy Edey, Facilitor of Hope at “Hope Studies Central” https://sites.google.com/a/ualberta.ca/hope-studies/home Dr. Jonathon Squires at Djavad Mowafaghian Centre for Brain Health Dr. Stuart Factor, Director of Movement Disorders Program at Emory University School of Medicine. Rebeca Gifford Our presenting partner is Parkinson Canada http://www.parkinson.ca/ The toll free hotline 1-800-565-3000 Follow them on Twitter @ParkinsonCanada Find the new Parkinson Clinical Guideline www.parkinsonclinicalguideline.ca Thanks also to our content and promotional partners Parkinson’s IQ + You– A free, series of Parkinson’s events from the Michael J. Fox Foundation Spotlight YOPD – The only Parkinson’s organization dedicated to raising awareness for Young Onset Parkinson’s disease and funds for the Cure Parkinson’s Trust.

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Mark Colo, findcures.org

Global Business Talk Radio

Play Episode Listen Later Nov 7, 2019 21:44

Mark Colo Secretary Co-founder Director Mark is one of the four Founders of FINDcures. As a Parkinson's patient, he is passionate about the FINDcures mission. Mark also has a history of volunteerism. In January 1977, while still a teenager, he volunteered to leave his home in sunny Southern California to serve for two years as a full-time missionary in the significantly colder climate of Scotland and Northern Ireland, during a period of that country's intense civil unrest. Of serving others while as a missionary Mark says, “The greatest lesson I learned about serving my fellowman is the more I help others, the happier I am, and the greater sense of identity I come to recognize within myself. Giving of myself to others had the effect of lifting me above my moments of doubt, worry, and potholes of despair, to a higher plane of thought. Simply put, by losing myself in serving others, I found my true self.” While serving the wonderful people of Scotland and Northern Ireland, Mark began to form what became his top four credos of life. First, “The only constant is change. Embrace it.” Second,“If you think things can't get worse, you're wrong. Endure it.” Third, “Control is an illusion. Let go of it.” And fourth, “Life isn't always fair. Accept it.” As fate would have it, these four concepts along with his undying faith in a loving God, have been a source of strength for him as he has dealt with the challenges of Parkinson's disease. Mark provides a unique perspective to the FINDcures Leadership Team. He is intimately aware of the challenges an individual and family face when dealing with a neurological disease diagnosis. Professionally, Mark has had a very successful career in the van line industry since January, 1980. During his over 3 decades of experience in the relocation industry, he leveraged his passion for learning to become a Certified Relocation Professional (C.R.P.), of which there are less than 200 in the U.S. He is also a licensed California Real Estate Broker (R.E.B.). In addition, his dedication to client satisfaction resulted in him becoming a 5-time member of the United Masters Club, a distinction that put him in the top 5% of his peers nationwide. Over the course of his career, it has been estimated that Mark has relocated more than 15,000 families from and to all points in the United State and overseas. In his personal life, Mark enjoys spending time with his family, cycling, overseas travel, reading and furthering public awareness of Neurological Diseases. Why FINDcures? Mark's back-story. Shortly following his 48th birthday, Mark noticed an unusual physical change. His right hand pinky finger had developed an almost unnoticeable resting tremor. He observed that it became more pronounced when he conducted a meeting or gave a talk in church. “Speaking in front of groups with a few hundred members might seem like enough to make anyone's hands shake, but only my right hand was affected.” He told himself that this must be due to a pinched nerve or spinal irregularity. This unique event prompted him to make an appontment post haste to see his general MD. His recommendation was that he meet with a neurologist. The neurologist performed a series of tests that included electro-analysis and observing him walking down a hallway. His diagnosis on that day was he felt his sysmptoms were pre-Parkinsonian. Mark left the neurologist's office in a daze of disbelief. When he left the doctor's office he felt as though the weight of the world had just been placed upon his shoulders. He felt profound sadness and also bitterness for this added burden that had been handed to him. His mind began spinning to the past in search for answers, and into the future imagining what his life would be like. Loneliness, fear and doubt, began to creep into his thoughts. This was without exception the greatest blow to his peace of mind and sense of self-worth, that he had ever experienced.

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Ask about constipation, calling patients in the middle of the night

Blood & Cancer

Play Episode Listen Later Jun 6, 2019 35:14

James C. Reynolds, MD, of the University of Pennsylvania, Philadelphia, joins Blood & Cancer host David H. Henry, MD, also of the University of Pennsylvania, to discuss the ins and outs of constipation among cancer patients: how to recognize it, how to treat it, and why you need to ask about it. Plus, in Clinical Correlation, Ilana Yurkiewicz, MD, of Stanford (Calif.) University talks about those tough phone calls. You can interact with the show on Twitter: @DavidHenryMd @IlanaYurkiewicz @MDedgeHemOnc Show notes By Emily Bryer, DO, resident in the department of internal medicine, University of Pennsylvania, Philadelphia Stool dysmotility is defined by a both objective imaging and the Bristol stool scale. Narcotics, mechanical issues (anastomoses), nausea, lack of exercise, and low-liquid or low-fiber diet contribute to constipation. There is a placebo effect of up to 40% for drugs given for constipation. Reglan (metoclopramide) in low doses, used sporadically, is relatively safe. However, it has been associated with Parkinsonian-type movement disorders and depression. Gastric emptying tests (and stomach function) are influenced by stress, mood, nausea, side effects, and hormones. They are not efficacious to evaluate gastric motility in the inpatient setting. Anal pain and fecal incontinence can occur during acute therapy (including radiation proctitis). It is important for clinicians to ask patients about constipation as it may be paradoxical and manifest as diarrhea. Fecal incontinence and sphincter dysfunction following therapy is multifactorial. Flat plate, proctosigmoidoscopy, and anal manometry can give a detailed description of anal function and compliance. It is important for clinicians to ask patients about constipation and fecal incontinence. Further reading: Managing constipation in adults with cancer (J Adv Pract Oncol. 2017 Mar;8[2]:149-61). Bristol Stool Chart For more MDedge Podcasts, go to mdedge.com/podcasts Email the show: podcasts@mdedge.com Interact with us on Twitter: @MDedgehemonc

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Blogcast 3: how to die well (part 1)

Mind Manifest Podcast

Play Episode Listen Later May 4, 2019 13:03

We are all shuffling towards death. Could psychedelics help it to be a bit less Parkinsonian and be a bit more of a Charleston?

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The Brain's Way of Healing: Remarkable Discoveries and Recoveries from the Frontiers of Neuroplasticity - By: Norman Doidge (Book Club Review) - LOF Podcast Episode 129

Life of a Fighter Podcast

Play Episode Listen Later Aug 25, 2018 15:16

This week is our Book Club of the Month Breakdown, and we are reviewing " "The Brain's Way of Healing: Remarkable Discoveries and Recoveries from the Frontiers of Neuroplasticity" By: Norman Doidge ... Exciting information, I hope you enjoy. Table of Contents: Physician hurt, then heal thyself : Michael Moskowitz discovers that chronic pain can be unlearned A man walks off his Parkinsonian symptoms : how exercise helps fend off degenerative disorders and can defer dementia The stages of neuroplastic healing : how and why it works Rewiring a brain with light : using light to reawaken dormant neural circuits Moshe Feldenkrais, physicist, black belt, and healer : healing serious brain problems through mental awareness of movement A blind man learns to see : using Feldenkrais, Buddhist, and other neuroplastic methods A device that resets the brain : stimulating neuromodulation to reverse symptoms. A cane against the wall ; Three resets: Parkinson's, stroke, multiple sclerosis ; The cracked potters ; How the brain balances itself with a little help A bridge of sound : the special connection between music and the brain. A dyslexic boy reverses his misfortune ; A mother's voice ; Rebuilding the brain from the bottom up: autism, attention deficits, and sensory processing disorder ; Solving the mystery at the abbey : how music: raises our spirits and energy. Click Here to Access Kuai Fit Plan - Kickboxing Intervals Week 1 Click Here to Access Kuai Fit Plan - Kickboxing Intervals Week 1 Spreadsheet @EggWeights Instagram Click Here to see more about ProLon Click Here to Get Zion Medicinals Hemp Oil Click Here to Get o2 Trainer Click Here to Buy Detach Coconut Water This episode and every episode is brought to you by our LOF Shop where you can find products and services for reaching your fitness goals on any budget go to www.lifeofafighter.com/shop This episode you by Audible 30 Day Free Trial This episode you by Amazon Are you a Fitness and Nutrition Vault Member Click Here to access the Full Fighters Guide Section Social Media Accounts: @LifeofaFighter Twitter @MikeCaulo Twitter @TheLifeofaFighter Instagram @MikeCaulo Instagram Life of a Fighter Facebook Michael Caulo Facebook

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Research Updates on Parkinsonian Disorders - Research on Aging

Parkinson's Disease (Video)

Play Episode Listen Later Aug 11, 2016 85:11

Irene Litvan, MD, FAAN, FANA, Director of UC San Diego’s Movement Disorder Program, discusses the latest advances in detection and treatment of Parkinsonian Disorders including examples of her fascinating work in PSP and Parkinson’s disease. She will also provide practical advice for reducing the risk of developing these disorders. Series: "Stein Institute for Research on Aging" [Health and Medicine] [Show ID: 30569]

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eCareDiary will interview Trish Caruana, Vice President of Programs and Education at CurePSP, an international non-profit organization that funds research and provides education and support for people suffering from atypical Parkinson's disorders.

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Imaging: What Can it Tell Us About Parkinsonian Gait?

vol imaging mds gait abstracts movement disorders parkinsonian

Play Episode Listen Later Oct 30, 2013 2:09

MDS presents the latest research and findings from the field of Movement Disorders. Abstracts of articles from the Society Journal, Movement Disorders, are taken from the September 15, 2013 (Vol. 28, Issue 11) issue.

Clinical Syndromes: Parkinsonian Gait

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Play Episode Listen Later Oct 30, 2013 0:50

Levodopa infusion does not decrease the onset of abnormal involuntary movements in Parkinsonian rats

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Play Episode Listen Later Aug 9, 2013 2:13

MDS presents the latest research and findings from the field of Movement Disorders. Abstracts of articles from the Society Journal, Movement Disorders, are taken from the July 2013 (Vol. 28, Issue 8) issue.

Protective stepping response in Parkinsonian patients and the effect of vibrotactile feedback

patients stepping vol protective mds abstracts movement disorders parkinsonian

Play Episode Listen Later May 20, 2013 1:57

MDS presents the latest research and findings from the field of Movement Disorders. Abstracts of articles from the Society Journal, Movement Disorders, are taken from the April 2013 (Vol. 28, Issue 4) issue.

Validation of parkinsonian disease-related metabolic brain patterns

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Play Episode Listen Later May 20, 2013 1:35

An electromyographic study of parkinsonian swallowing and its response to levodopa