Podcasts about british neurologists

The latest guidelines on disease-modifying treatment in multiple sclerosis (MS) from the Association of British Neurologists is discussed in this intercontinental podcast with perspectives from the UK, the USA, and Australia.   Participants: Professor Alasdair Coles is Head of Department for Clinical Neuroscience and also Co-Director of the Cambridge Centre for Myelin Repair, UK. Dr. Tamara Kaplan is Assistant Professor of Neurology at Harvard Medical School, and is also affiliated with the Brigham and Women's Hospital, Boston, USA. Professor Michael Barnett is a consultant neurologist at Royal Prince Alfred Hospital Sydney, Central Clinical School, and Director of the RPAH MS Clinic and the MS Clinical Trials Unit at the Brain and Mind Centre, University of Sydney, Australia. Read the paper (https://pn.bmj.com/content/25/1/18) which is part of the February issue of the Practical Neurology journal.   Please subscribe to the Practical Neurology podcast on your favourite platform to get the latest podcast every month. If you enjoy our podcast, you can leave us a review or a comment on Apple Podcasts (https://apple.co/3vVPClm) or Spotify (https://spoti.fi/4baxjsQ). We'd love to hear your feedback on social media - @PracticalNeurol. Production and editing by Letícia Amorim. Thank you for listening.     

The first case for this issue's discussion is one of a young man with a history of involuntary jerks and photosensitivity (1:20). Several more seizures followed his initial presentation with a general tonic-clonic seizure. A number of examinations were done including an MR scan and EEG - (link) Case two involves a 69-yo woman who developed non-convulsive status epilepticus, having been examined as a gastroenterology inpatient for abdominal pain (22:20). A positive PCR for Whipple's disease in stools and saliva, but negative in the CSF, prompted further testing - (link) The case reports discussion is hosted by Prof. Martin Turner (1), who is joined by Dr. Ruth Wood (2) and Dr. Xin You Tai (3) for a group examination of the features of each presentation, followed by a step-by-step walkthrough of how the diagnosis was made. These case reports and many others can be found in the February 2024 issue of the journal. Further reading: Panegyres PK. Diagnosis and management of Whipple's disease of the brain. Practical Neurology 2008;8:311-317.   Association of British Neurologists. Rare Diseases Ascertainment and Recruitment (RaDAR).   (1) Professor of Clinical Neurology and Neuroscience at the Nuffield Department of Clinical Neurosciences, University of Oxford, and Consultant Neurologist at John Radcliffe Hospital. (2) Neurology Registrar, University Hospitals Sussex. (3) Clinical Academic Fellow, Nuffield Department of Clinical Neurosciences, Oxford University, and Neurology Specialty registrar, Oxford University Hospital.  Please subscribe to the Practical Neurology podcast on your favourite platform to get the latest podcast every month. If you enjoy our podcast, you can leave us a review or a comment on Apple Podcasts (https://apple.co/3vVPClm) or Spotify (https://spoti.fi/4baxjsQ). We'd love to hear your feedback on social media - @PracticalNeurol. The PN podcast is produced by Letícia Amorim and edited by Brian O'Toole. Thank you for listening. 

Recorded LIVE on Twitter Spaces on Wednesday 28th September 2022. Primarily aimed at Clinicians and Healthcare Professionals, through this discussion we hope to share some insights as to the different ways to become involved in clinical research, why you might want to do that, and what that might look like. Adam Smith, Dementia Researcher Programme Director hosts this informal discussion with five people working within the NHS and in research to share their experience. Guests are Dr Ross Paterson and Dr Alex Tsui all from University College London Hospitals NHS Foundation Trust, Dr Brady McFarlane from Southern Health NHS Foundation Trust, Dr Antoinette O'Connor from Tallaght University Hospital, Ireland, and Dr Emma Broome from Nottingham Biomedical Research Centre. -- Below are links to some of the resources mentioned during the chat: Careers Webinar - https://bit.ly/3CsOCq4 Trials information - https://bit.ly/3UNIbVs Dr Anna Volkmer Blogs - https://bit.ly/3Eb80ZU NIHR Clinical Careers Funding - https://bit.ly/3y8hpxr Alz Forum Grants - https://bit.ly/3RuQBy7 Dementia Research Careers Festival – https://bit.ly/3LWDIMl Dementia Researcher Meet the Researchers - https://bit.ly/3LWDIMl Association of British Neurologists - https://www.theabn.org/# Royal College of Nursing Research Careers - https://bit.ly/3E6KvRC -- Guest mini bios Dr Emma Broom Bio - https://bit.ly/3SREL2q Dr Alex Tsui Bio - https://bit.ly/3CsTpYx Dr Brady McFarlane Bio - https://bit.ly/3CaOhbe Dr Ross Patterson Bio - https://bit.ly/3CaOhbe Dr Antoinette O'Connor Bio - https://bit.ly/3LYxjQx -- Like what you hear? Please review, like, and share our podcast - and don't forget to subscribe to ensure you never miss an episode. This podcast is brought to you in association with Alzheimer's Research UK and Alzheimer's Society, who we thank for their ongoing support. -- A full transcript of the podcast can be found on our website at https://www.dementiaresearcher.nihr.ac.uk/podcast or find a video version on our YouTube Channel with closed captions at https://www.youtube.com/dementiaresearcher

Martin's clinical research interests are in the degenerative dementias, particularly familial disease, and more recently in general cognitive impairment in systemic disease and multimorbidity. He established the Queen Square Dementia Research Centre and has served as the editor of the Journal of Neurology, Neurosurgery and Psychiatry, President of the Association of British Neurologists, Director of the NIHR Clinical Research Network for Dementia and Neurodegenerative diseases (DeNDRoN), and Director of the NIHR Queen Square Dementia Biomedical Research Unit. As part of the activities of DeNDRoN he established Join Dementia Research (JDR), a national system for linking patients and public to research studies. He has served on numerous advisory boards and is currently an associate member of the World Dementia Council, member of the 2020 Dementia Programme Board, and Chairman of the Senate for the German Centre for Neurodegenerative Diseases (DZNE).

Tune in to today’s episode of A Better Self Daily show with fascinating scientist and great entrepreneur Dr. Jason McKeown MD to learn why you should care about things like neuroscience, vestibular nerve and your hypothalamus, if you want to turn your body and mind into your weight loss allies, not enemies. Jason is a Bachelor of Medicine, Bachelor of Surgery and Bachelor of Obstetrics from Queen's University, Belfast. He is a member of the Association of British Neurologists and the Royal College of Emergency Medicine and is a Visiting Scholar at the UCSD Center for Brain & Cognition. In 2015, Jason was invited onto the Propel Programme by InvestNI – a business accelerator aimed at "high caliber entrepreneurs who have the passion and energy to succeed on the international stage." Upon his completion of the program, Neurovalens (Modius Wearable) was awarded Company of the Year 2015. Jason enjoys electronics and technology and is very proactive in the health & fitness community. Modius is a groundbreaking Careable TechnologyTM product from Californian health tech company Neurovalens. It can help you get lean and stay lean. It is a non-invasive, drug-free device that activates the vestibular system and helps you achieve a leaner body when used in conjunction with a healthy diet and appropriate levels of exercise. https://www.modiushealth.com With Dr. Jason McKeown we will talk about: Why our body and brain resists your weight loss plans and efforts Why it’s so hard for us to lose weight and maintain weight Why dieting doesn’t work for so many of us long-term and why we tend to get back to our “normal” weight What we can do to lose weight and maintain weight easier, using a bit of help from technology and neuroscience What is the best proven strategy to lose weight permanently What might be the best exercise for weight loss, according to neuroscience and micro-gravity research from Nasa And so much more! TUNE IN for this fascinating conversation to turn your body and mind into your weight loss allies, not enemies. And till next time – live as A Better Self Daily. Created by Angela Shurina and http://www.createyourself.today/ Support the show (https://www.patreon.com/FoodSchool)

Nodding syndrome affects children from 5 to 15 years old in some parts of the African continent. In this podcast, David Nicholl, Department of Neurology, City Hospital, Birmingham, UK, is joined by Mark Ellul, ABN fellow, University of Liverpool, UK, to discuss the latest research in this epileptic disorder. They talked at the Association of British Neurologists annual meeting, Liverpool, May 2017. http://pn.bmj.com/

[intro music]   Host – Dan Keller Hello, and welcome to Episode Forty-Seven of Multiple Sclerosis Discovery, the podcast of the MS Discovery Forum. I’m your host, Dan Keller.   This week’s podcast features the second part of a two-part interview with Dr. Hans Lassmann, who discusses oxidative stress as a mechanism of tissue injury in progressive MS. But first, here are some of the new items in the MS Discovery Forum.   According to our curated list of the latest scientific articles related to MS, 56 such articles were published last week. To see the list, go to msdiscovery.org and click on Papers. We selected two of those papers as Editors’ Picks. One of them includes revised guidelines from the Association of British Neurologists on prescribing disease-modifying treatments for MS. The other describes an international consensus on diagnostic criteria for neuromyelitis optica and related disorders.   Our Drug-Development Pipeline includes continually updated information on 44 investigational agents for MS. During the month of June, we added 10 new trials, we updated information on 6 other trials, and we’ve added 67 other pieces of information. The drugs with important additions and changes are alemtuzumab, cladribine, cyclophosphamide, daclizumab, dalfampridine, dimethyl fumarate, fingolimod, glatiramer acetate, idebenone, interferon beta-1a, interferon beta-1b, laquinimod, rituximab, natalizumab, and ocrelizumab. To find information on all 44 compounds, visit msdiscovery.org and click first on Research Resources and then on Drug-Development Pipeline.   [transition music]   Now to our interview with Dr. Hans Lassmann of the Medical University of Vienna in Austria. Last week we spoke about biomarkers, and this week we’ll discuss oxidative stress as a mechanism of tissue injury in progressive MS.   Interviewer – Dan Keller What's interesting there at this point?   Interviewee – Hans Lassmann The big problem in multiple sclerosis is that we have very good therapies for the early stage of multiple sclerosis, and they all interfere with the inflammation and the immune system. But when the patients have reached a progressive stage of the disease, then all these therapies are currently noneffective. So the key points were to define what are actually the mechanisms of inflammation and tissue injury in the progressive stage of multiple sclerosis, and there are still a lot of open questions. It is clear that even in the progressive stage there is an inflammatory process, and this inflammatory process is associated with active tissue damage. From that certainly we cannot definitely conclude that the inflammatory process drives the tissue damage; however, it's clearly associated.   Now, we were then very interested to see what are the mechanisms of tissue injury. And this involves, first of all, studies on the nature of the inflammatory process. And here what we found is that in the progressive stage of multiple sclerosis the inflammatory reaction is predominantly hidden within the central nervous system behind a repaired blood-brain barrier. So that means this inflammatory process is no longer really under control of the peripheral immune system. And also, the therapies which we have currently mainly interfere with immune functions in the periphery, and they have actually very little access to an inflammatory process which is taking place within the central nervous system.   So that means that new drugs have to be developed and tested which actually exert an antiinflammatory or some neuroprotective action directly within the central nervous system. And there are now a number of the large companies fully engaged in this process, and there are new candidates coming up, which will have to be tested in proper clinical trials in patients with progressive MS.   The second question, which we have mainly addressed during the last year, was the mechanisms how the tissue damage is induced. And in this regard, we concentrated on cortical lesions in multiple sclerosis, which are very, very specific for the disease. And we compared in gene expression studies these cortical lesions not only with normal controls but also with inflammatory controls. And we used here a disease which has very similar inflammatory infiltrates, as you see in multiple sclerosis brain, but doesn't lead to the MS typical demyelination, and this is tuberculous meningitis. And then we also used as a control for neurodegeneration Alzheimer's disease just to see what is a reaction in gene expression due to degeneration of neurons.   And when we did that, actually it was interesting to see that there were relatively few genes which were specifically changed in their expression in multiple sclerosis patients in comparison to these other disease controls. And these genes were, in part, associated with inflammatory processes. A large part of the genes were associated with a more or less single pathway of tissue injury, which includes oxidative injury leading to mitochondrial injury and its secondary consequences. And then, there were also some genes involved which were MS specifically related to tissue regenerative processes.   We have then looked in further detail, and it now turns out that this cascade of oxidative injury leading to mitochondrial dysfunction and with that to a state of energy deficiency is actually one of the major driving forces of neurodegeneration in the progressive stage of multiple sclerosis. So this oxidative injury is, in part, driven by the inflammatory process. But it is also augmented by factors which are related to age of the patients and to the accumulation of lesion burden due to the chronic disease.   So here the central portion is the activation of microglial cells which can, on the one hand, be activated in the inflammatory process, but they also get activated when tissue is damaged due to completely different causes. And they also get activated just simply in an aging process. And in this respect, then they get activated in a pro-oxidative form. And then, the tissue injury can further be propagated through additional age-related changes, including, for instance, the accumulation of iron in the central nervous system and also obviously the chronic microglia activation due to retrograded and anterograde degeneration when lesions already present within the central nervous system.   MSDF Are the microglia just overdoing what they normally would be expected to do? I mean macrophages use oxidative systems to get rid of pathogens.   Dr. Lassmann Yeah, this is absolutely true. That is a key element of microphage and microglia function. And this is exaggerated in both the aging process, as well as in the chronic inflammatory state like multiple sclerosis. The question only remains what is really driving this massive microglia activation in MS, which is even more and more pronounced than even in very severe other inflammatory diseases of the central nervous system.   MSDF Can you identify or has anyone identified factors that disappear with aging or are increased with aging that may lead to this state?   Dr. Lassmann That is also not really very clear now. I think one interesting aspect is that this massive microglia activation in the direction of oxidative stress you don't really see in rodents and even not in primate experimental models; you see it in humans. And the reason for that is not completely clear, but it may very well be that environmental factors actually play a major role. I think one of the major differences between humans and these experimental animals is that the experimental animals are genetically very homogenous; they are generally inbred strains. And the second is that they are kept under a very constant pathogen-free environment. And this is very different in a human situation, and these animals also have a very … standardized diet. Now this is completely different in human situations, and there are certainly many factors, including peripheral infections but also including diet changes, and many other factors can actually have an influence on microglia in the central nervous system.   MSDF And experimental animals also have optimized diets; people have figured out the nutrients they need I suppose. They're getting a good diet compared to people who knows how everybody is eating these days.   Dr. Lassmann Yes, that's absolutely the case. They have a standardized diet, and they certainly are not exposed to very much of the fats, for instance, which we take into when we eat fat pork meat.   MSDF Do any of the antiinflammatory agents modify the course? Things like lipoxygenase inhibitors and things like that? Not necessarily NSAIDs but now that you bring up fats?   Dr. Lassmann I think there is certainly an aspect behind that is that lifestyle control certainly has a beneficial effect. One can just see that in a way that environmental lifestyle factors, which actually also increase the risk for vascular injury or other things, will be certainly deleterious in a patient with progressive multiple sclerosis where the brain is already damaged due to the original disease process and where the functional reserve capacity of the brain is already partially exhausted. So in that case, even minor changes – which are related to lifestyle or aging – will have a more dramatic effect in such a brain than in a normal aging brain.   MSDF Finally, circling back to something you said at the beginning, in progressive MS I think you said that the immune system the cells have now entered the brain, but the blood-brain barrier has – once again – become a real barrier. So do you really have an immune response running autonomously in the brain no longer subject to any sort of peripheral control?   Dr. Lassmann Yeah, this is certainly a very important open question. We know that the inflammatory cells are present within the central nervous system in the progressive stage and that they are associated with the degenerative processes and the demyelination. We know currently very little about the exact phenotype and functional activation of the inflammatory cells within the central nervous system. This is actually a large research project, which is running currently in my lab, to try to define exactly the functional polarization of the cells within the MS lesions and to determine their activation state, their proliferation rate, and so on.   What we can say from our preliminary data on that is that they are present, they are in part activated. They also express certain transcription factors, which would be associated with a proinflammatory state in the central nervous system. However, overall all these changes are relatively small in comparison to an acute, for instance, virus-induced inflammatory process in the brain. So it seems to be that there is a slow and low-grade activation state which, however, could be completely sufficient to drive the degenerative process in the patients. But that is not the final answer yet.   [transition music]   MSDF Thank you for listening to Episode Forty-seven of Multiple Sclerosis Discovery. This podcast was produced by the MS Discovery Forum, MSDF, the premier source of independent news and information on MS research. MSDF’s executive editor is Robert Finn. Msdiscovery.org is part of the non-profit Accelerated Cure Project for Multiple Sclerosis. Robert McBurney is our President and CEO, and Hollie Schmidt is vice president of scientific operations.   Msdiscovery.org aims to focus attention on what is known and not yet known about the causes of MS and related conditions, their pathological mechanisms, and potential ways to intervene. By communicating this information in a way that builds bridges among different disciplines, we hope to open new routes toward significant clinical advances.   We’re interested in your opinions. Please join the discussion on one of our online forums or send comments, criticisms, and suggestions to editor@msdiscovery.org.   [outro music]      

February's JNNP is a neuropsychiatry special issue, with papers on a broad range of disorders which lie between neurology and psychiatry. Associate editor Alan Carson discusses the contents, and the thinking behind the edition.To accompany the issue, JNNP and the Association of British Neurologists convened a roundtable of experts to discuss, and advise on, diagnosing and treating functional symptoms. Dr Carson takes part in this, along with:Kailash Bhatia, professor of neurology, Institute of NeurologyMark Edwards, neurologist at the National Hospital for Neurology and NeurosurgeryJon Stone, neurologist, University of Edinburgh, Western General HospitalThis podcast is one of a series produced in collaboration with the Association of British Neurologists. You can find all the podcasts in the series here: soundcloud.com/tags/abn%202013

Callum Duncan, neurologist at Aberdeen Royal Infirmary, convenes a round table of experts to discuss advances in headache, particularly the pathophysiological understanding of cluster headache, managing cluster headache and migraine, and new onset chronic daily headache.Taking part are:Phillip Holland, postdoctoral researcher, Centre for Cognitive and Neural Systems, University of EdinburghManjit Matharu, clinical lead of the Headache Group at The National Hospital for Neurology and Neurosurgery, LondonAlok Tyagi, neurologist, Southern General Hospital, GlasgowThis podcast is one of a series produced in collaboration with the Association of British Neurologists, of which there will be more to come over the next few months. You can find all the podcasts in the series here: soundcloud.com/tags/abn%202013

This month, we get an update on the latest in clinically diagnosing the dementias, with a roundtable of experts convened by the Association of British Neurologists. Taking part are John Greene, Southern General Hospital, Glasgow, Chris Butler, Department of Clinical Neurology, University of Oxford, Nick Fox, Dementia Research Centre, UCL Institute of Neurology, and Huw Morris, Cardiff University School of Medicine.And using theory of mind deficits as an early marker of frontotemproal dementia. Matteo Pardini, Department of Neurosciences, University of Genoa, talks us through his research.See also:Isolated theory of mind deficits and risk for frontotemporal dementia: a longitudinal pilot study http://bit.ly/19figvN

Ralph Gregory, secretary for the Association of British Neurologists and consultant neurologist in Dorset, gets an update on multiple sclerosis research and implications for practice from Neil Robertson, professor of neurology, Cardiff University.They discuss new therapeutics BG-12 and alemtuzumab, the understanding of treatment risks, prognosis, prevalence and incidence, and MS and pregnancy.This podcast is one of a series produced in collaboration with the Association of British Neurologists, of which there will be more to come over the next few months. You can find all the podcasts in the series here soundcloud.com/tags/abn%202013.

Ralph Gregory, secretary for the Association of British Neurologists and consultant neurologist in Dorset, gets an update on peripheral nerve disease research and practice from James Overell, consultant neurologist, Institute of Neurological Sciences, Glasgow.They discuss treatment for CIDP, differences in neuropathy prevention and management in type 1 and type 2 diabetes, chronic inflammatory neuropathies, and hereditary motor sensory neuropathies.This podcast is one of a series produced in collaboration with the Association of British Neurologists, of which there will be more to come over the next few months. You can find all the podcasts in the series here https://soundcloud.com/tags/abn%202013.

Where are we with stem cell treatments for stroke and Parkinson’s disease? At the Association of British Neurologists’ recent annual meeting in Glasgow, Neil Scolding, director of the Bristol Institute of Clinical Neurosciences, spoke to Keith Muir, Institute of Neuroscience and Psychology, Univeristy of Glasgow, and Roger Barker, John van Geest Centre for Brain Repair, University of Cambridge, about current research, and the expensive, unproven treatments already on the market.And using enlarged perivascular spaces to identify arteriopathy in intracerabral haemorrhage. Nick Ward, JNNP associate editor, asks David Werring, reader in neurology, UCL Institute of Neurology, what his MRI study reveals.See also:Enlarged perivascular spaces as a marker of underlying arteriopathy in intracerebral haemorrhage: a multicentre MRI cohort study http://bit.ly/12iZWieStriatal cell transplants for Huntington’s disease: where are we now? http://bit.ly/18InWwa