Podcasts about subarachnoid

Subarachnoid haemorrhage is a diagnosis that can't be missed, but it is not a simple process to detect it. The first paper for discussion this month questions if a CT scan within 6 hours is sufficient for exclusion in patients with acute headache. Then there is a large-scale analysis of over 400 million ED visits in the USA, focussing in on the significant issue of self-harm in the homeless population. Next is a paper on a decision tool for suspected acute aortic syndrome, and to finish, a discussion on the change in ED culture around safety since the COVID pandemic.   Read the issue highlights: December 2024 Primary Survey   Articles discussed in this episode: Subarachnoid haemorrhage in the emergency department (SHED): a prospective, observational, multicentre cohort study Suicide and self-injury-related emergency department visits and homelessness among adults 25–64 years old from 2016 to 2021 in the USA  Decision analytical modelling of strategies for investigating suspected acute aortic syndrome  Culture of safety in an adult and paediatric emergency department before and after the COVID-19 pandemic   The EMJ podcast is hosted by: Dr. Richard Body, EMJ Deputy Editor, University of Manchester, UK (@richardbody) Dr. Sarah Edwards, EMJ Social Media Editor, Leicester Royal Infirmary, UK (@drsarahedwards) You can subscribe to the EMJ podcast on all podcast platforms to get the latest podcast every month. If you enjoy our podcast, please consider leaving us a review or a comment on the EMJ Podcast iTunes (https://apple.co/4bfcMU0) or Spotify (https://spoti.fi/3ufutSL) page.

Send us a textSeason 2 - Episode 14This weeks episode is all about Stroke's a subject we have yet to cover.What is a stroke, In medicine, a loss of blood flow to part of the brain, which damages brain tissue. Strokes can be caused by blood clots and broken blood vessels in the brain but in todays case it was a Subarachnoid hemorrhage that was the cause.  Today's special guest Lesley Atherton tells us her story and her road to recovery in remarkable time purely to her grit and determination and with the support of her professional team family and friends not forgetting her dogs.A subarachnoid hemorrhage is bleeding in the space between your brain and the membrane that covers it. Most often, it occurs when a weak area in a blood vessel (aneurysm) on the surface of the brain bursts and leaks. The blood then builds up around the brain and inside the skull.We are so blessed with our guests and today is no exception, Lesley tells us her story from the moment she realised something was wrong right through her treatment, rehabilitation and to present days.She explains what drove her to her recovery, where she found inspiration and what she had to do to get back up on her feet and start living live again after a Stroke.How to identify a strokeThe FAST acronym (Face, Arms, Speech, Time) is a test to quickly identify if someone is having a stroke.Face weakness: Can the person smile? Has their mouth or eye drooped?Arm weakness: Can the person raise both arms?Speech problems: Can the person speak clearly and understand what you say?Time to call 999: if you see any of these signs.Thank you all once again for listening and we thank Lesley for joining us today and openly and honestly telling us her remarkable story# Stroke# Subarachnoid hemorrhage#Mediastinal Germ Cell Tumour#Prostate Cancer#Bronchiectasis#CharcotmarietoothDisease#Emphysema#The after life#Ghosts#Spirts#Ouija boards#Mediums#Psychics#Reincarnation#HeartTransplant#EbsteinsAnomaly#RareCondition#HealthJourney#LifeChangingDiagnosis#MentalHealth#Vulnerability#SelfCompassion#PostTraumaticGrowth#MedicalMiracle#BBCSports#Inspiration#Cardiology#Surgery#Podcast#Healthcare#HeartHealth#MedicalBreakthrough#EmotionalJourney#SupportSystem#HealthcareHeroes#PatientStories#CardiologyCare#MedicalJourney#LifeLessons#MentalWellness#HealthAwareness#InspirationalTalk#LivingWithIllness#RareDiseaseAwareness#SharingIsCaring#MedicalSupport#BBCRep#bbcupload#papyrusCheck out our new website at www.whostomanddick.comCheck out our website at www.whostomanddick.com

In this episode of the St Emlyn's podcast, Iain Beardsell is joined by Dan Horner, a consultant in Emergency Medicine and Neurocritical Care, and Tom Roberts, an Emergency Medicine Registrar and clinical lecturer, to discuss their recently published SHED study on subarachnoid haemorrhage in the Emergency Department (ED). This landmark study, published in the Emergency Medicine Journal, explores the safety of CT scans in diagnosing subarachnoid haemorrhage up to 24 hours after headache onset and evaluates the role of further investigations like a lumbar puncture. The study examines acute severe headache presentations in the ED and the diagnostic approach to ruling out subarachnoid haemorrhage, a critical and often feared diagnosis among emergency physicians. Conducted through the Trainee Emergency Research Network (TURN), the study included over 3,600 patients from 88 UK EDs with acute severe headaches reaching maximum intensity within one hour and no focal neurology. Data collection included CT scans, lumbar puncture results, and 28-day follow-up to identify missed cases of subarachnoid hemorrhage. Key findings from the study revealed a 6.5% prevalence of subarachnoid haemorrhage, with a significant number presenting within six hours of headache onset. The sensitivity of CT scans remained high beyond the traditional six-hour window, suggesting that CT alone could safely rule out subarachnoid haemorrhage up to 18 hours in many cases, potentially reducing the need for lumbar puncture. The risk of missing an aneurysmal subarachnoid haemorrhage after a negative CT was found to be extremely low, around 1 in 1,000. These findings challenge the routine use of lumbar puncture in patients presenting beyond six hours if the CT scan is negative, potentially changing ED practice and reducing unnecessary invasive procedures. The discussion also emphasized the importance of shared decision-making and recognizing that diagnostic testing is about managing probabilities, not certainties. For clinicians, the episode highlights the need to expedite CT scans for patients with acute severe headaches, especially those presenting within 10 minutes of onset, as they are more likely to have significant pathology. Emergency physicians are encouraged to own the decision-making process for ruling out serious causes of headaches and not defer solely to 'specialists'. The SHED study supports extending the diagnostic window for CT scans in ruling out subarachnoid hemorrhage up to 18 hours, reducing the need for lumbar puncture in many cases. This data empowers emergency clinicians to make informed decisions, manage patient expectations, and streamline ED processes.  For more information, listeners are encouraged to read the SHED Study in the Emergency Medicine Journal and explore the related blog post on the St Emlyn's website. Emergency clinicians are also invited to connect with TERN to get involved in future research opportunities.  This episode provides valuable insights for clinicians in managing acute severe headaches, emphasizing a more nuanced approach to subarachnoid hemorrhage diagnosis and the importance of clinical decision-making in the ED.

Aneurysmal subarachnoid hemorrhage (aSAH) is a rare but devastating condition, marked by high global rates of fatality and long-term disability. Key factors influencing patient outcomes include early brain injury, aneurysm rebleeding, and delayed cerebral ischemia. In this podcast, Dr. Chiara Robba and Dr. Laura Galarza explore the epidemiology, treatment strategies, and the identification and management of post-aSAH complications. This exclusive discussion provides valuable insights and practical clinical guidance specifically designed for intensivists.

Happy September! This month for the September 2024 episode of the RCEM Learning Podcast, we have a new in EM section looking at the use of NIV for preoxygenation in RSI. We then have Becky and Chris going over a new Guidelines for EM looking at the NICE Guidelines for meningitis. Rob puts on his TERN hat and speaks to the two former TERN Fellows and Dan Horner about the results of the Subarachnoid Haemorrhage in the ED Study before ending with New Online. If you'd like to email us, please feel free to do so here. After listening, complete a short quiz to have your time accredited for CPD at the RCEMLearning website! (02:30) New in EM - NIV for preoxygenation in RSI Noninvasive Ventilation for Preoxygenation during Emergency Intubation (Gibbs et al., 2024) (20:47) Guidelines for EM - NICE Guidance for Meningitis Meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management (NICE, 2024) (01:05:00) The TERN SHED Study - 36:30 Subarachnoid haemorrhage in the emergency department (SHED): a prospective, observational, multicentre cohort study (The Trainee Emergency Research Network, 2004) - link to the paper coming soon The TERN Website TERN on Twitter/X (01:41:35) New Online – new articles on RCEMLearning for your CPD Training for Research in Emergency Care (TREC) - The TREC Team Delivering Bad News - Charlotte Davies Ocular trauma - Deepa Elsa George, Sophie Seguin-Greenstein

In this episode, Dr James Shilston returns to talk us through the ins and outs of SAH. 

This episode covers subarachnoid haemorrhage.Written notes can be found at https://zerotofinals.com/medicine/neurology/subarachnoidhaemorrhage/ or in the neurology section of the 2nd edition of the Zero to Finals medicine book.The audio in the episode was expertly edited by Harry Watchman.

In this week's podcast, Neurology Today's editor-in-chief discusses the report on outcomes of IV thrombolysis for large vessel occlusions; the discovery of a new brain layer in the subarachnoid space; and the impact of mindfulness and exercise on cognition.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.25.525148v1?rss=1 Authors: Warming, H., Deinhardt, K., Garland, P., More, J., Bulters, D., Galea, I., Vargas-Caballero, M. Abstract: During subarachnoid haemorrhage, a blood clot forms in the subarachnoid space releasing extracellular haemoglobin (Hb), which causes oxidative damage and cell death in surrounding tissues. High rates of disability and cognitive decline in SAH survivors is attributed to loss of neurons and functional connections during secondary brain injury. Haptoglobin sequesters Hb for clearance, but this scavenging system is overwhelmed after a haemorrhage. Whilst exogenous haptoglobin application can attenuate cytotoxicity of Hb in vitro and in vivo, the functional effects of sub-lethal Hb concentrations on surviving neurons and whether cellular function can be protected with haptoglobin treatment remain unclear. Here we use cultured neurons to investigate neuronal health and function across a range of Hb concentrations to establish the thresholds for cellular damage and investigate synaptic function. Hb impairs ATP concentrations and cytoskeletal structure. At clinically relevant but sublethal Hb concentrations, synaptic AMPAR-driven currents are reduced, accompanied by a reduction in GluA1 subunit expression. Haptoglobin co-application can prevent these deficits by scavenging free Hb to reduce it to sub-threshold concentrations and does not need to be present at stoichiometric amounts to achieve efficacy. Haptoglobin itself does not impair measures of neuronal health and function at any concentration tested. Our data highlight a role for Hb in modifying synaptic function after SAH, which may link to impaired cognition or plasticity, and support the development of haptoglobin as a therapy for subarachnoid haemorrhage. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

On Episode 24 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the January 2023 issue of Stroke: “Covert Brain Infarction as a Risk Factor for Stroke Recurrence in Patients With Atrial Fibrillation” and “Subarachnoid Hemorrhage During Pregnancy and Puerperium.” She also interviews Dr. Georgios Tsivgoulis about his article “Clinical, Neuroimaging, and Genetic Markers in Cerebral Amyloid Angiopathy-Related Inflammation: A Systematic Review and Meta-Analysis.” Dr. Negar Asdaghi:         Let's start with some questions. 1) When during pregnancy is an intracranial aneurysm at the highest risk of rupture? 2) What does the presence of covert brain infarcts mean in the setting of atrial fibrillation? 3) And, finally, how is the inflammatory form of cerebral amyloid angiopathy different from the classic CAA form, and why is it important to differentiate between the two? We'll be answering these questions and much more in today's podcast. We're covering the latest in cerebrovascular disorders, and this is the best in Stroke. Stay with us. Welcome back to another issue of the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine and your host for the monthly Stroke Alert Podcast. Together with my co-editors, Drs. Nastajjia Krementz and Eric Goldstein, here's our article selection for the month of January. Symptomatic intracerebral hemorrhage is a feared complication of reperfusion therapies in acute stroke, so there's a lot of interest in looking for predictors of development of this complication, especially when you're making decisions for pursuing endovascular therapy. For many years now, we've known about some of these predictors, such as presence of a large infarct core and high blood glucose levels. But in the recent years, other radiographic markers of tissue viability, such as a poor collateral status and unfavorable venous outflow profile, have been shown to be predictors of post-reperfusion hemorrhagic transformation. In this issue of the journal, we learn about another imaging marker that can potentially predict parenchymal hemorrhage occurrence post-endovascular therapy, which is high hypoperfusion intensity ratio, or HIR, as measured by perfusion imaging. What is HIR? It's a long name for a simple ratio that can easily be measured by dividing the volume of tissue with Tmax delay of over 10 seconds to the volume of tissue with Tmax delays of over 6 seconds. Simply put, Tmax 10 divided by Tmax 6. These volumes, as you know, are typically provided to us by almost all post-processing perfusion softwares, and so this ratio can be easily calculated in the acute setting. So, in this paper led by Dr. Tobias Faizy from University Medical Center in Hamburg and colleagues, we learned that higher hypoperfusion intensity ratios are strongly associated with parenchymal hemorrhage occurrence after endovascular therapy. So, in summary, HIR, that is a quantitative ratio, can be used as a marker to risk stratify patients that are undergoing endovascular therapy in terms of helping us predicting the risk of development of intracerebral hemorrhage after reperfusion therapies. In a separate study in this issue of the journal, we read a very interesting paper titled "Anti-Epileptic Drug Target Perturbation and Intracranial Aneurysm Risk." How are intracranial aneurysms even related to anti-epileptic drugs? Well, first of all, it's been known for a long time based on genome-wide association studies that there are multiple common genes that are associated with increased risk of intracranial aneurysm development. Now, some of the largest genetic studies to date have shown pleiotropy between genetic causes of development of intracranial aneurysms and genes encoding targets for anti-epileptic drugs. Now that's a fascinating finding because finding commonalities between these genes may help find new treatment targets for intracranial aneurysms. So, in this paper in this issue of the journal, the investigators from the University Medical Center in Utrecht found an association in the expression of anti-epileptic drug target gene CNNM2 and intracranial aneurysm risk. They found that certain anti-epileptic drugs, such as phenytoin, valproic acid, and carbamazepine, that are expected to lower CNNM2 levels in the blood may subsequently lead to a lower risk of development of intracranial aneurysms. And, of course, a reasonable follow-up study to this would be to investigate whether persons exposed to these anti-epileptic drugs have indeed a lower risk of unruptured intracranial aneurysms and subarachnoid hemorrhage, and how variation in CNNM2 expression can lead to development of aneurysms. Bottom line, CNNM2 may be a relevant drug target for treatment of cerebral aneurysms. As always, I encourage you to review these papers in detail in addition to listening to our podcast today. My guest on the podcast today is the Chairman of Neurology at the University of Athens, Dr. Georgios Tsivgoulis. He joins me all the way from Greece to talk about cerebral amyloid angiopathy-related inflammation, or CAA-ri. He's a remarkable researcher, and I can say with absolute confidence that we cannot find a better summary of this very tough topic elsewhere. He ends the interview with an intriguing account of the early description of dementia in Greek mythology. But first, with these two articles. What are covert brain infarcts, or CBIs? Are these the John Wick or the James Bond of the stroke world? After all, they operate undercover. They're ominous and attack without warning. That's probably why they're also called silent infarcts. Now, whatever we call them, we need to know how prevalent they are and what does their presence actually mean. Let's dive into this topic. For at least two centuries, if not longer, we've known about covert brain infarcts. Early description of these lesions is credited to Amédée Dechambre, a medical intern at Salpêtrière Hospital in Paris who noted that there are strokes that can cause symptoms like hemiplegia, but also strokes that are asymptomatic, or so he thought at the time. In the modern times, while we agree with our pathology forefathers that CBIs are different from symptomatic strokes, we also know that they are not entirely asymptomatic. The symptoms can be subtle and tend to sneak up on the patient, but what is clear is that amassing of covert brain infarcts results in an overall decline in cerebrovascular reserve of the brain. With the advent of neuroimaging, we now know that CBIs are age-dependent and prevalent, seen in almost 10 to 30% of even healthy adults, but much more prevalent in those with vascular risk factors, and they can be caused by nearly the entire spectrum of neurovascular disease, including large vessel, small vessel disorders, cardioembolism, and others. Now, how do these covert infarcts catch up in those with atrial fibrillation? Neuroimaging studies have shown that patients with A-fib, especially those untreated, have a higher percentage of embolic-appearing CBIs, and conversely, those with embolic formed pattern of CBIs are more likely to have undiagnosed A-fib. So the question is, what's the significance of CBI in those with confirmed A-fib? In this issue of the journal, Dr. Do Yeon Kim from Seoul National University and colleagues help us answer this question using the EAST-AF, which stands for East Asian Ischemic Stroke Patients With Atrial Fibrillation Study. So, the paper included over 1300 patients with A-fib and first-ever stroke without a prior history of TIA or stroke. And then they categorized these patients into those who had evidence of CBI on neuroimaging and those who didn't. So, what did they find? Forty-two percent of patients with A-fib and first-ever stroke had evidence of covert brain infarcts on neuroimaging. Let's think about it for a moment. These patients presented with what was thought to be their first-ever stroke, not knowing they already had some in their brain. Now, what makes things really worse is that over a quarter of these subjects had more than just one covert infarct. Not surprisingly, those with CBI tended to be older, had higher blood pressure, and had worse white matter hyperintensity burden. This is kind of expected and also not expected was the fact that most of these covert infarcts were actually embolic in pattern. Over 60% of them were embolic. Another 14% of cases had combined embolic and non-embolic-appearing CBIs. Now, overall, the one-year incidence of ischemic stroke and all-cause mortality was higher in those that had CBIs at baseline. When they started looking at the specific patterns of CBIs, those embolic-appearing CBIs had a threefold higher risk of recurrent ischemic stroke, whereas those with non-embolic-appearing covert infarcts had oddly a higher all-cause mortality rate but not recurrent ischemic stroke. And finally, just briefly, the authors noted that the addition of CBIs to the classic CHA2DS2-VASc score didn't meaningfully otherwise statistically improve the scoring metrics, so they left it at that. So, the take-home message is that 42% of A-fib patients presenting with first-ever stroke actually had prior strokes without even knowing based on this study. And most of these strokes were embolic-appearing, and these covert brain infarcts can be used as predictors of future clinical strokes in this population. Strokes should be the last thing to worry about when we think of pregnancy. In the United States, around 30 in 100,000 women, unfortunately, experienced a stroke during pregnancy, and between 6 to 8 in 100,000 deliveries are complicated by subarachnoid hemorrhage. What's the most common cause of pregnancy-associated subarachnoid hemorrhage? In the general population, close to 80% of subarachnoid hemorrhage cases are aneurysmal. Is this true for the pregnant population as well? And importantly, what's the contemporary incidence trend, risk factors, and outcomes of pregnancy-related subarachnoid hemorrhage? In this issue of the journal, Dr. Korhonen and Petra [Ijäs] and their colleagues from the Departments of Neurology and Obstetrics and Gynecology at Helsinki University Hospital will give us the answers to some of these questions through a nationwide population-based study in Finland. So, they looked at over one and a half million pregnant women who gave birth during a 30-year time period between 1987 to 2016. Subarachnoid hemorrhage was identified through appropriate ICD codes and then further adjudicated based on confirmatory information, including neuroimaging and data from lumbar puncture. A total of 57 cases of pregnancy-related subarachnoid hemorrhage was identified in this paper. The mean age of women was 33, ranging from 23 to 45, and the clinical presentation was typical for subarachnoid hemorrhage, including thunderclap headache and mild neurological symptoms. So, what did they find? So, first off, in terms of general observations, the overall incidence rate of pregnancy-related subarachnoid hemorrhage in this study was 3 over 100,000 deliveries. This is almost half the incidence rate reported from the nationwide registries in the United States. Seventy-seven percent of pregnancy-related subarachnoid hemorrhage cases were aneurysmal, so very similar to the general population. The other 23% were non-aneurysmal cases, but it's important to note that 40% of those non-aneurysmal cases also had vascular etiologies, so etiologies such as moyamoya syndrome, postpartum angiopathy, AVM, to name a few. Like non-pregnant patients with subarachnoid hemorrhage, the aneurysmal cases were sicker patients in general. They had a lower GCS at presentation, higher Hunt and Hess scores, and required more ICU admissions. The next finding is very important because it actually shows that development of subarachnoid hemorrhage during pregnancy significantly impacted obstetrical care. A total of 66% of women with subarachnoid hemorrhage during pregnancy ended up having a C-section and a high percentage of these cesarean sections were actually elective. This is in contrast with subarachnoid hemorrhages in the postpartum period where 67% of women had spontaneous vaginal deliveries. The other important finding of the paper was really highlighting the differences between pregnancy-related aneurysmal versus non-aneurysmal subarachnoid hemorrhages. We already talked about how, in general, aneurysmal cases had more severe neurological presentations, so, not surprisingly, they also had worse outcomes with a mortality rate of 16% for the aneurysmal subarachnoid hemorrhage cases, and only 68% of women with pregnancy-related aneurysmal subarachnoid hemorrhage reached a favorable outcome, which was defined in this study as modified Rankin Scale of 0 to 2. Other important differences included the fact that the incidence of aneurysmal subarachnoid hemorrhage increased towards the end of pregnancy and was highest in the third trimester. This ties in with the findings from prior studies all indicating that rupture of an aneurysm is most common in the third trimester. By contrast, the incidence of non-aneurysmal subarachnoid hemorrhage peaked in the second trimester in this study. And finally, in terms of risk factors, first let's talk about age. The incidence rate of pregnancy-associated subarachnoid hemorrhage increased with age of the mother. So, in this study, there were no cases noted amongst women aged below 20 years of age to an incident rate of 12 per 100,000 deliveries among women aged 40 years or over. So that's a fourfold increase from the overall incidence rate of pregnancy-related subarachnoid hemorrhage, and very important point that we learned from this paper. Apart from age, smoking beyond 12 weeks of gestation and hypertension were also independent factors associated with pregnancy-related subarachnoid hemorrhage. So, overall, hypertension, smoking are bad and are significant risk factors for pregnancy-related subarachnoid hemorrhage. And if we have to remember just one thing from this paper, let it be this one: The rupture of an aneurysm is most common in the third trimester of pregnancy. Cerebral amyloid angiopathy, or CAA, is an important cause of intracranial hemorrhage and refers to deposition of β-amyloid fibrils in the wall of the small- and medium-sized cerebral blood vessels, mostly involving cortical and leptomeningeal arteries. It is believed that the deposition of β-amyloid results in architectural disruption of the blood vessels, which then leads to perivascular leakage. That's the pathophysiological mechanism behind the development of cerebral microbleeds. And this process, of course, can cause frank vascular rupture resulting in cortical intracerebral hemorrhage or development of high-convexity subarachnoid hemorrhages. It is important to note that varying amounts of perivascular inflammation, that is inflammation surrounding β-amyloid-laden blood vessels, may be present in some CAA cases, rendering them the designation of inflammation-related CAA. However, frank vasculitic destruction of the vessel wall, such as what is found in amyloid-β-related angiitis, or ABRA, and primary angiitis of the central nervous system, is usually absent in most CAA-related inflammation cases. How these entities are best defined, diagnosed, and treated is subject of intense research. In this issue of the journal, in the study titled "Clinical, Neuroimaging, and Genetic Markers in CAA-Related Inflammation," Dr. Georgios Tsivgoulis and colleagues take us through a systematic review and meta-analysis of published studies of patients with CAA-related inflammation. I am joined today by Dr. Tsivgoulis himself to discuss this paper. He's a Professor of Neurology and Chairman of the Second Department of Neurology at the University of Athens School of Medicine. Dr. Tsivgoulis is the residency program director and the director of cerebrovascular fellowship program with extensive research and expertise in the field of stroke. Good morning, Georgios, and welcome to our podcast. Dr. Georgios Tsivgoulis: Good morning, Negar. I'm delighted to be here and delighted to present our findings, on behalf of all our co-authors. Dr. Negar Asdaghi:         Thank you very much for being here and congrats again on the paper. So, Georgios, let's start with this interest that's going on with using clinical and radiographic features to make the diagnosis of CAA-related inflammation in contrast to moving ahead and performing brain biopsy. Can you please start us off with a brief review of the newly proposed clinico-radiographic criteria for this condition, please? Dr. Georgios Tsivgoulis: Yes. As you mentioned, Negar, CAA-ri is a distinct, however, rare subset of cerebral amyloid angiopathy. Firstly, Greenberg and the Boston group published in Neurology in 2007 a paper highlighting that a diagnosis of a probable CAA-ri patient could be made on the basis of characteristic clinical and neuroimaging findings without requiring a biopsy. Following this observation, Chung and colleagues in 2010, in a seminal paper in JNNP, proposed the first diagnostic criteria for probable and definite CAA-ri. For the definite diagnosis, besides the typical clinical presentation with headache, encephalopathy, focal neurological signs and seizures, and the characteristic neuroimaging findings with T2 or FLAIR hyperintense asymmetric white matter lesions complicated with microbleeds and leptomeningeal or parenchymal gadolinium enhancement, and histopathological confirmation with amyloid deposition within cortical leptomeningeal vessels associated with perivascular, transmural or intramural inflammation was also required. The latest criteria developed in 2015 by Auriel and colleagues that were published in JAMA Neurology using a validation study modified the current criteria for the diagnosis of CAA-ri. In this paper, the author supported the use of empirical immunosuppressive therapy, avoiding brain biopsy, for patients meeting the criteria proposed for probable CAA-ri. They suggested that a brain biopsy should be considered in empirically treated patients who failed to respond to corticosteroid therapy within three weeks. The criteria by Auriel and colleagues are widely applicable in everyday clinical practice, and we also use this criteria for the inclusion of studies in our current meta-analysis. I would like to highlight for our audience that the latest criteria for CAA-ri were published in 2015 by Auriel and colleagues. However, these are different for the criteria for cerebral amyloid angiopathy than the latest criteria were published in 2022 in Lancet Neurology, OK? Dr. Negar Asdaghi:         Georgios, that was a great start for this interview. You had mentioned a lot of information here. I just want to highlight what you just said. So, we are using for this meta-analysis, the latest criteria in CAA-related inflammation published in JAMA by Auriel and colleagues. That's slightly different than, we're not referring to the 2022 criteria of cerebral amyloid angiopathy. It's an important distinction. We're going to talk about this a little more as we go through the interview, but I want to come back to your current paper and start from there. Can you please tell us about the importance of this paper, why doing a meta-analysis was important in your view, and tell us a little bit about the studies that were included in your paper? Dr. Georgios Tsivgoulis: Yes, thank you for that question. CAA-ri is an increasingly recognized entity since the recent diagnostic criteria by Auriel and colleagues published in 2015. In collaboration with the greater availability of the high-resolution MR, we can have now a reliable non-invasive diagnosis of possible or probable CAA-ri, avoiding the risk of brain biopsy. However, I need to highlight that the early diagnosis remains a great challenge for the clinicians and neurologists. Searching the literature, we observe that there is scarce data regarding the prevalence of the distinct clinical, neuroimaging, and genetic markers among patients diagnosed with CAA-ri. We believe that pooling all this information in the current meta-analysis would be very helpful for every clinician, increasing a comprehensive understanding of this rare cerebrovascular disorder. Consequently, we conducted this meta-analysis including 21 studies that recruited a total of 378 patients with CAA-ri. Our study involved only 4 prospective and 17 retrospective hospital-based cohorts of patients diagnosed with CAA-ri based on autopsy or biopsy or on the recent Auriel diagnostic criteria that do not require autopsy or biopsy. Due to limited data in the literature regarding this entity, we had to include only small cohort studies with at least five patients in our meta-analysis. We excluded case reports and case series with less than five patients. This is, by far, the largest available sample of CAA-ri patients in the literature. Dr. Negar Asdaghi:         OK, great. So, let me just recap this, more so for myself. So, we have 21 studies, and you excluded studies that included less than 5 patients. So, practically speaking, case reports. Dr. Georgios Tsivgoulis: Yes, and single-case reports. Dr. Negar Asdaghi:         Yes. And practically speaking, of the total number of patients that are included in this meta-analysis, you have 378 cases, and basically the diagnosis of CAA-related inflammation was either based on the newly proposed criteria or based on biopsy-confirmed or autopsy cases. Dr. Georgios Tsivgoulis: Which is the standard criteria. Dr. Negar Asdaghi:         So, now, I'm dying to ask you about these clinical and radiographic characteristics of patients with CAA-related inflammation in this meta-analysis. Dr. Georgios Tsivgoulis: The mean age of patients in the included studies was approximately 72 years old, and there was no obvious gender predominance. Fifty-two percent of the patients were of female sex. In our study, 70% of the included patients presented with cognitive decline, which was the most common neurological manifestation, while 50% of the total sample had focal neurological signs and 54% encephalopathy presentation. Symptoms such as headache and seizures were less common, 37 and 31% respectively. With regard to the radiological findings, hyperintense T2 FLAIR white matter lesions were very, very common in 98% of our patients, and they were also complicated with lobar cerebral microbleeds, with a prevalence of 96%, and these two were, by far, the most prevalent neuroimaging findings, that white matter hyperintensities coupled with a cerebral microbleed. The pooled prevalence rates of gadolinium-enhanced lesions was 54%, and also the prevalence of cortical superficial siderosis was 51%, which is also very high in this cohort of patients with CAA-ri. Dr. Negar Asdaghi:         OK. So many of the features Georgios said, you mentioned, from presence of white matter hyperintense lesions on T2 FLAIR to presence of cortical microbleeds or superficial siderosis, these features are also seen in patients with cerebral amyloid angiopathy. What are some of the important differentiating features between the two conditions? Dr. Georgios Tsivgoulis: Yes, this is an excellent clinical question. First of all, the lower age threshold for CAA-ri is 40 years old, whereas in cerebral amyloid angiopathy, the lower age threshold is 50 years. So, patients who are younger than 50 years can be diagnosed with CAA-ri, but they cannot be diagnosed with CAA. Another issue is that comparing the result of this meta-analysis with another recent meta-analysis focusing on CAA, on cerebral amyloid angiopathy, that our international multi-collaborative group published in Stroke in 2002, we also evaluated the presence of clinical phenotypes and radiological markers among patients with cerebral amyloid angiopathy. We have documented that transient focal neurological episodes are much more common in patients with cerebral amyloid angiopathy in contrast to patients with CAA-ri. These episodes, which are called TFNEs, transient focal neurological episodes, are attributed to cortical subarachnoid hemorrhage or cortical superficial siderosis. So, I think this is another important clinical distinction. The most important, however, differentiating features between the two entities are neuroimaging markers, in specific, in particular, T2 FLAIR hyperintense unifocal or multifocal lesions with mass effect. These are the most prevalent neuroimaging features among patients with CAA-ri, but they're very seldomly described in patients with cerebral amyloid angiopathy, in patients with CAA. Another characteristic neuroimaging finding very indicative of the inflammation is the leptomeningeal or parenchymal gadolinium enhancement. This finding has been very rarely described in patients with non-inflammatory cerebral amyloid angiopathy. So, the clinical distinction is not so solid. However, the neuroimaging distinction would provide us with very strong information that can help us differentiate these two conditions. Dr. Negar Asdaghi:         Excellent points, I have to say, golden points, not just excellent points. I'm going to try to recap this and see if I understood it correctly. So, for our listeners, we have two conditions that potentially have many common points. One is the cerebral amyloid angiopathy, and the second one, which is obviously the subject of this interview, is cerebral amyloid angiopathy-related inflammation. The most important differentiating factors between the two are actually the neuroimaging features, as Georgios mentioned. So, the first feature that was mentioned is presence of T2 FLAIR hyperintense lesions. Some of them are large and have actually mass effects. This feature is rarely seen in patients with CAA, and it's an important radiographic factor that is seen in patients with CAA-related inflammation. The second distinguishing feature was leptomeningeal enhancement, again, rarely seen in non-inflammatory CAA, but was seen in a significant proportion of patients with CAA-related inflammation. These were the neuroimaging features. You also mentioned two other factors. The median age of CAA-related inflammation was lower than CAA. That can be helpful. And also the entity of transient focal neurological episodes, or TFNE, is rarely seen in inflammatory cases of CAA, whereas it is described in cases with cerebral amyloid angiopathy and mostly related to development of either cortical subarachnoid hemorrhage or cortical superficial siderosis. I think I got this all, correct? Dr. Georgios Tsivgoulis: Excellent. Dr. Negar Asdaghi:         All right, so let's come now to the genetics of CAA. The apolipoprotein E gene is associated with the presence of amyloid angiopathy and development of lobar intracerebral hemorrhage, and we've learned about this in cases with cerebral amyloid angiopathy. Is there an association with ApoE, and did you find anything in this meta-analysis? Dr. Georgios Tsivgoulis: Another very exciting question. In 2007, there was a first report that the apolipoprotein ε4 homozygosity may be considered a risk factor for CAA-ri, and there was a strong correlation reporting a high prevalence of 77% of this apolipoprotein ε4 alleles among patients with CAA-ri. To justify this correlation, the hypothesis was that an underlying pathogenic mechanism, which increases the amyloid-β deposition and has a pro-inflammatory effect, may be suspected as the cause of this disorder. The largest, however, prospective cohort of CAA-ri patients conducted by Antolini and colleagues and was published in 2021 in Neurology, reported a much lower prevalence of apolipoprotein ε4 carriers accounting for 37%, 23% heterozygotes and 14% homozygotes. So, we also documented a pool prevalence of apolipoprotein ε4 homozygosity of 34%. So, we did not confirm the initial finding of 77%. However, in our meta-analysis, the homozygosity was 34%, and we need to have a cautious interpretation of these results because data is limited, and we need larger future population-based studies and in larger cohorts to evaluate the prevalence rate of these specific genetic markers. So, we can confirm an association between apolipoprotein ε4 homozygosity, however not as strong as originally reported in 2007. Dr. Negar Asdaghi:         OK. So, Georgios, thank you. And again, very important factor to keep in mind for our clinicians listening in. Unfortunately, based on what you mentioned, we don't have yet a genetic marker to, for sure, tell us if we're dealing with CAA-related inflammation, yes or no, as you mentioned. Just to recap, earlier on, there was studies to suggest a very strong association between apolipoprotein ε4 homozygosity and CAA-related inflammation. But later on, this was not confirmed by subsequent studies, and in your meta-analysis, you found 34% ApoE ε4 homozygosity amongst patients with CAA-related inflammation and could not confirm that original high association. OK, so with all of that, it's a lot of information. I have to go to the next question regarding controversies involving the levels of Aβ40, Aβ42, and P-tau proteins in CSF in the setting of CAA-related inflammation. Can you please tell us more about these biomarkers? Dr. Georgios Tsivgoulis: Yes. The overlap of Alzheimer's disease and CAA can be attributed to the coexistence of some degree of cerebrovascular amyloid deposition and amyloid plaque pathology, which is very common. And, of course, the evaluation of amyloid and tau proteins in CSF is of high significance for the prognosis and the evolution of CAA patients. In our previous review, we have summarized the literature and noticed that CSF concentrations of Aβ40 and, secondarily, Aβ42 were much lower in patients with cerebral amyloid angiopathy compared with Alzheimer's disease. Total tau and phospho-tau CSF levels were comparable to healthy controls in CAA and lower than patients with Alzheimer's disease. Moving now to CAA-ri, there were scarce data about these biomarkers amongst CAA-ri patients. The majority of the relevant studies have found relatively low levels of Aβ42 and Aβ40 in the CSF and high levels of P-tau. In the present meta-analysis, the pooled means of biomarker levels were based on the findings of only two studies with heterogeneity, and these limit substantially the validity of our observations. However, they confirm the previous reports indicating, as I said before, but I would like to repeat, low levels of Aβ42 and Aβ40 in the CSF and high levels of P-tau. Dr. Negar Asdaghi:         Perfect. So, thank you, Georgios. I'm going to recap what you said. So, we're talking about CSF biomarkers, and first what you mentioned is going back to the original studies concentrated on using these biomarkers as ways of differentiating between cerebral amyloid angiopathy and Alzheimer's disease. And very briefly, to recap what you said, in general, the levels of Aβ40 and, secondarily, Aβ42 was found to be much lower than the Alzheimer's levels in patients with CAA. Now coming to the inflammatory form of CAA, what you mentioned and what you found in this meta-analysis, practically speaking, confirmed that the levels of Aβ40 and Aβ42 in CSF are low and the levels of P-tau are high in this condition as well. So, one thing I want to ask as a secondary question to that is, that it sounds like these biomarkers are more or less similar in CAA and CAA -related inflammation, not that different. Is that correct? Dr. Georgios Tsivgoulis: It's absolutely correct. And I would also like to highlight a major limitation of the meta-analysis that we had available data from only two studies to pool the mean of these CSF biomarker levels. So, these results need to be acknowledged with caution, and we would love to repeat our meta-analysis after the publication of more studies and prospective cohorts measuring the CSF biomarkers in patients with CAA-ri. Dr. Negar Asdaghi:         OK. So, again, important to note, as you mentioned, that there's heterogeneity in data because of just paucity of information on this, but as we stand today, the biomarkers won't really help us in terms of differentiating between the two conditions that are CAA or CAA-related inflammation. And so, I think I've learned a lot from this interview myself, but I think we have to just talk briefly about the available therapies for CAA-related inflammation. Dr. Georgios Tsivgoulis: Yes. In our meta-analysis, we sought to summarize the available information regarding different therapeutic strategies and outcomes among CAA-ri patients. Our results supported our clinical experience indicating that corticosteroids represent the first-line treatment in these patients' outlook. Steroids have been associated with clinical and radiological improvement of the primary disease episode and decreased risk of subsequent relapses in patients with CAA-ri. Additional immunosuppressive therapies, including cyclophosphamide, mycophenolate mofetil, azathioprine, IVIG, or rituximab, have been also reported as adjunct therapies in selected cases with a more severe course of the disease. However, this is another limitation that needs to be acknowledged. That data regarding the treatment and the outcomes are limited and heterogeneous, which prevented us from drawing robust conclusions using a meta-analytical approach. And we believe that we need future cohort studies with prospective data validation in order to generate a proposal for a therapeutic algorithm management in these cases. Dr. Negar Asdaghi:         Thank you, Georgios. So, we have a condition that is now being more and more recognized. We now have criteria based on clinical and radiographic presentation features of patients that might help us with this diagnosis to differentiate it from cerebral amyloid angiopathy. And in terms of therapies, the idea is that the most studied drug is really just first-line therapy, that's corticosteroids. And then there's positive data regarding use of all other forms of immunosuppression, including, as you mentioned, cyclophosphamide, rituximab, and oral agents such as mycophenolate mofetil or azathioprine. We have limited information about those, but I want to highlight something you actually mentioned earlier on in the interview, which is the field is moving towards making these diagnoses based on clinical features and radiographic features that you had highlighted and actually giving patients immunosuppression early on and only move on to a biopsy if the patient had failed these therapies for a period of time, which you mentioned three weeks. So, I think it's important for us as clinicians to keep this evolving criterion and recommendations in mind. And before we end, I want to ask you a hypothetical question, Georgios. In your opinion, what's an ideal randomized trial for CAA-related inflammation in the future? Dr. Georgios Tsivgoulis: I think before going to the randomized, the ideal randomized trial for CAA-ri, and designing this trial, we need much more information regarding the underlying pathophysiological mechanisms. There are many unanswered questions. What is the diagnostic value of CSF biomarkers such as amyloid, we discussed earlier, and tau protein? And, of course, what is the value of CSF and the amyloid-β autoantibodies, if there is any? What is the value of genetic markers such as apolipoprotein E genotype and a correlation with the co-existing inflammation in CAA-ri? However, I don't want to defer this question. So, a typical answer would be that with regard to the ideal patients, we would want a young patient without comorbidities after the first manifestation of CAA-ri who has shown a good clinical and radiological response to corticosteroids in order to define the best second-line therapy. However, before answering all these questions in a clinical trial, if we can, I think that we need to understand the CSF and genetic biomarkers in order to uncover mechanisms regarding pathophysiology that can help us to design more targeted clinical trials studying novel disease-modifying treatments. Dr. Negar Asdaghi:         Thank you. Dr. Georgios, it's been a pleasure having you on the podcast, and I can say we've learned a lot. We look forward to having you back here and talk about that hypothetical randomized trial, and I'm sure one day hopefully will happen in our lifetime. Thank you for being here. Dr. Georgios Tsivgoulis: Thank you. Thank you for having me. It was a pleasure. Dr. Negar Asdaghi:         Thank you. Homer, the legendary Greek poet, described a case of dementia in his seminal work, The Odyssey, in the late eighth century before Christ. He described the cognitive decline of Odysseus's father, King Laertes. The detailed account of the king's mental decline, loss of short-term memory with retention of long-term memory combined with his depression and despair over the loss of his son, is dramatically accurate for a nearly 3,000-year-old description of dementia. Before I ended the interview, I had to use this opportunity to ask Georgios about lessons learned from ancient Greeks and this seemingly timeless disease. Dr. Georgios Tsivgoulis: Thank you for this question. King Laertes was indeed Odysseus's father, and it's a great paradigm describing dementia. However, the ancient history of dementia may be separated according to the Greek philosopher Posidonius in two periods. The first period is called dementia appearing due to old age, which is called in Greek, eros. And the second one is dementia appearing in other ages and mainly due to other reasons, called morosis. Posidonius of Rhodes was a Greek stoic philosopher of the second first century BC who strongly believed and suggested that morosis, which is that dementia appearing in younger ages due to other disorders, should be treated immediately after its onset. So, if I would like to end this podcast, I would just suggest that CAA-ri could be classified as morosis according to Posidonius. And what we could learn is that the early diagnosis is essential since the prompt initiation of corticosteroids should not be unreasonably delayed. Dr. Negar Asdaghi:         And this concludes our podcast for the January 2023 issue of Stroke. Please be sure to check this month's table of contents for the full list of publications, including a series of Focused Updates on post-stroke neurological recovery, from management of post-stroke attention deficit, neglect and apraxia to post-stroke memory decline. And with this, we end the start of our 2023 podcast series. Like all new things, a new beginning can come with new directions, and sometimes a new direction is all that we need. After all, as the legend has it, it was a direction of that falling apple back in the year 1666 that gave Isaac Newton the idea of the universal law of gravitation. Now, Isaac Newton has, without a doubt, given science some of its biggest discoveries in mathematics, physics, and astronomy. But most may not know that Newton had a pretty rough start in life. A January-born premature baby, he was thought not to survive the first few days of life. Newton had a difficult childhood, and at the age of 16, he was pulled out of school by his family and forced to become a farmer, a job he didn't like and he was miserably bad at. So, as we start a new year, let's remember that even the smartest people are not good at everything, and it does take time to find one's passion in life. Now, while things may not always be clear, what is clear is that a great way to find that center of gravity is, as always, staying alert with Stroke Alert. This podcast is produced by Wolters Kluwer and supported by the editorial team of Stroke. Our Stroke Alert podcast and production staff includes Danielle Cross, Eric Goldstein, Nastajjia Krementz, Ishara Ratnayaka, Erinn Cain, Rebecca Seastrong, and Negar Asdaghi. This program is copyright of the American Heart Association, 2023. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

Roughly 1 in 20 subarachnoid hemorrhages are missed during initial presentation in the emergency department – substantially increasing the risk of complications and mortality. That's scary. But is it a reason to do a lumbar puncture every time a patient's head hurts? EMRA*Cast host Will Smith (@WTSmithMD IG/Twitter) shares some expert insight from Lt. Col. Roderick Fontenette (@RodFontenette1).

Nazih Assaad provides his expertise on the treatment of subarachoid haemorrhage. Treatment for aneurysmal subarachnoid haemorrhage (SAH) is an area that has had extensive research but not a great deal of success. Promising animal studies have not turned out as hoped in clinical trials and many questions remain unanswered. Nazih guides the listener through his approach on how to address the complicated presentation of SAH. Firstly, subarachnoid haemorrhages can be graded clinically and radiologically. Clinical grades provide useful prognostic information, with poorer grades less likely to do as well as more favourable grades, despite best medical and intervention management. Nazih mentions the Fisher Scale which is useful for predicting vasospasm and how he integrates both into practise. Nazih will guide you through the four elements in the management of established SAH. Moreover, these are the four areas he believes every clinician working in this space should consider with every patient presenting with a SAH. The first is the effect of the haemorrhage itself on the patient. The sudden rise of intracranial pressure secondary to aneurysm rupture leads to dramatic clinical signs. These includes loss of consciousness and seizure like activity. There are no known agents to reverse the effects of the initial insult. Secondly, managing the degree of hydrocephalus that most, if not all, patients will have if critical. Clinical hydrocephalus is treated with CSF drainage. Thirdly, the prevention of re-haemorrhage is important. In bygone eras, patients with aneurysmal SAH did not have immediate management of the bleed. This has changed. Finally, delayed cerebral ischaemia (usually relating to vasospasm) should be addressed. Gold standard of diagnosis is digital subtraction angiography, and following this, Nazih describes his aggressive management approach.  Nazih takes the listener through what he considers the most critical aspects of managing a patient with an aneurysmal SAH. This talk explores diagnostic techniques, patient examination, surgical options, and other management considerations. He touches on the most recent guidelines and protocols around Australia and the world.  Please note this episode was recorded in November 2018 as part of Brain, a CICM Neuro Special Interest Group meeting click here for more info. For more like this, head to our podcast page #CodaPodcast

Want to experience the greatest in board studying? Check out our interactive question bank podcast- the FIRST of its kind here: emrapidbombs.supercast.com. We promote this awesome ACEP PeerCert question about the Ottawa SAH Rule. We love our friends up on the other side of our Northern Border, and really enjoy digging into the high yield aspects of how to not miss SAH!

Welcome to the Wellbeing and Career World Podcast, I am delighted to be chatting with a gentleman who currently co-hosts the show Happy Hour with Heather and Guest. He writes crime fiction novellas, short stories, and volunteers. In 2018 he survived a ruptured brain aneurysm and Subarachnoid hemorrhage. He's going to start a Clinical Mental Health Counseling program in January '22 Today we will be chatting about Brain Aneurysm Awareness A very warm Welcome to the podcast Andrew Davie.   Andrew answers some of the questions asked during the podcast or answers as part of the conversation: Andrew chats about his background, Andrew in your own opinion, what is a brain aneurysm? Did you have any symptoms? What did you experience while having a brain aneurysm? Did you have any medical treatment or a stay in hospital? How are you now? In your own opinion, is there any way to prevent a brain aneurysm? Andrew, you write crime fiction Novels. What can we expect from these?  Andrew you are the host of the show happy hour podcast with Heather, who is Heather and what can listeners expect from the podcast?  What does 2022 hold for you, you are taking a Clinical Mental Health Counseling program? What does that involve? Where can listeners get in contact with you on Social media? If you would like to contact Andrew Davie: Website: https://andrew-davie.com/ Facebook: https://www.facebook.com/adavieauthor Twitter: https://twitter.com/adavieauthor   Disclaimer: This podcast and website represents the opinions of Wellbeing and Career World and our guests to the show and website.  The content here should not be taken as medical advice, financial advice, career advice, sports coaching, and is for informational purposes only, and because each person is so unique, please consult your healthcare professional for any medical questions or Aviation/Aerospace Employer, Regulator, organization for questions related to you. Views and opinions expressed in the podcast and website are our own and do not represent that of our places of work. While we make every effort to ensure that the information we are sharing is accurate, we welcome any comments, suggestions, or correction of errors.   Privacy is of utmost importance to us. This website or podcast should not be used in any legal capacity.  No guarantee is given regarding the accuracy of any statements or opinions made on the podcast or website. In no way does listening, reading, emailing or interacting on social media with our content establish a, coaching session, employment interview, wellbeing advice, employment advice, doctor-patient relationship. Wellbeing and Career World is based in Dublin, Ireland. If you find any errors in any of the content of this podcast or blogs or would like to get in contact , please send a message to wellbeingandcareerworld@gmail.com This podcast is owned by "Wellbeing and Career World Podcast” If at any time you want to play or stop the podcast, it is at your own discretion. The podcast may contain conversation or opinions you may find unsuitable or against your opinions or beliefs, if you feel you may be uncomfortable, stressed, anxious, worried, concerned, upset, insulted by any of the podcast, we recommend you do not listen to the podcast.

Chris provides a brief update on some of the postulated underlying mechanisms involved in subarachnoid haemorrhage associated brain injury. These mechanisms provide hints to future therapeutic targets that will hopefully expand our currently limited repertoire of options. Subarachnoid haemorrhage is a catastrophic type of stroke. Subarachnoid haemorrhage represents only 5% of the total stroke burden. Notably however, as it is most common in people aged 40-60 years, it has a disproportionate effect from a personal, social and economic perspective. Subarachnoid haemorrhage classically presents as a thunder clap headache and loss of consciousness. Unfortunately, it is associated with high morbidity and mortality rates. There is limited research in this area and there is significant opportunity to improve the way that we manage these cases.  The key is understanding the link between early brain injury and why we develop delayed cerebral ischemia. How can we stop this from happening? How can we better understand why good brains go bad? From #CodaZero Live, Christopher Andersen provides an update on delayed cerebral ischaemia. Join Chris as he looks for future treatment options through the mechanism of brain injury in subarachnoid haemorrhage. For more like this, head to our podcast page. #CodaPodcast 

In this Episode Dr Jonathan Bardgett interviews Dr Murray Blackstock, a Consultant in Intensive Care Medicine and Anaesthesia. He talks about the presentation and management of patients with subarachnoid haemorrhage (SAH) and gives some useful advice on how to refer these patients to neurosurgery and critical care. He refers to NICE guidance and his own personal experience of managing the patient with acute onset headache. NICE Guidelines - https://www.nice.org.uk/guidance/conditions-and-diseases/cardiovascular-conditions/cranial-aneurysms

So this time we're going to be talking about subarachnoid haemorrhage. So this is going to be a short and punchy look at a really important and interesting topic in subarachnoid haemorrhage. We run through the approach to headache and then focus on the specific features and findings that we should be looking for with regards subarachnoid haemorrhage. We then consider who we should be investigating further, what value a CT head brings and the sticky subject of who should be going on to have a lumbar puncture. Finally we consider the the management once the diagnosis of SAH is reached and how we can ensure the best outcomes for our patients. At the time of recording NICE has published its draft version of Subarachnoid Haemorrhage Caused by a Ruptured Aneurysm; diagnosis and management, which will be a great resource once finalised. Once again we'd love to hear any thoughts or feedback either on the website or via twitter @TheResusRoom. Enjoy! Simon, Rob & James

Subarachnoid hemorrhage is a major cause of morbidity and mortality around the world.  The rapid diagnosis and treatment of the underlying source are paramount to ensuring optimal patient outcomes.  This lecture will overview the pathophysiology, risk factors, and immediate diagnostic/treatment priorities when caring for these patients.  Utilizing case studies, a review of possible sequelae with pre-emptive and reactive medical interventions will occur.  

Learning more about types of headaches, treatment options, and when to be concerned. Guest is a board certified neurologist, Dr. Rajani R. Caesar.

Subarachnoid haemorrhage (SAH) is the sudden leaking of a blood vessel in the subarachnoid space in the brain. We chat to Dr Teresa Withers the director of neurosurgery at GCUH and Angelly Martinez, ICU Intensivist about all things SAH. We follow a case study from medical history, presentation, interventions and management in ICU. We were really looking forward to this chat and it did not disappoint. We hope you can learn a few things from this one and it can shed some light on the management of SAH and why it is so important. Enjoy 

Subarachnoid hemorrhage. It's a mouthful and it sounds terrifying. Join host Eryn Martin as she talks about the subarachnoid hemorrhage that she experienced in  May of 2020 in the midst of the US Covid quarantine. Out of nowhere, Eryn was struck by an uncontrollable headache and vomiting after completing an at-home workout. After being rushed to the hospital, she was told by neurologists that she had suffered from a perimesencephalic subarachnoid hemorrhage, meaning that she had experienced a spontaneous venous rupture in her brain. Eryn was rushed from her local hospital in New Hampshire to the neurological intensive care unit at Massachusetts General Hospital in Boston, where she spent seven days recovering. Eryn talks about her time in the hospital, her return home, what her recovery journey has been like, and the hurdles and surprises along the way. HELP US SPREAD THE WORD!   If you dug this episode head on over to Apple Podcasts and kindlyhttps://podcasts.apple.com/us/podcast/making-headway/id1534964037 ( leave us a rating, a review and subscribe!) Ways to subscribe to the Making Headway Podcast: https://podcasts.apple.com/us/podcast/making-headway/id1534964037 (Click here to subscribe via Apple Podcasts) https://open.spotify.com/show/4Ishnxgh8xbJfV8BtbCtZw (Click here to subscribe via Spotify) https://making-headway.captivate.fm/listen (Click here to subscribe via RSS) https://www.stitcher.com/podcast/making-headway (You can also subscribe via Stitcher)   https://www.makingheadwaypodcast.com/ (Visit the Making Headway Podcast website) to learn more about Eryn and Mariah and our journey to podcasting. Follow us onhttps://www.instagram.com/makingheadwaypodcast/ ( Instagram) orhttps://www.facebook.com/makingheadwaypodcast ( Facebook).

In this episode, we finish our 2-part episode on treating a significant subarachnoid bleed in the critical care realm. Hope you enjoy. reach out to me and let me know what you want to hear about! kisercpr@gmail.com #HEMS #FOAMed #EMS #Airmedical #PHIairmedical #coffeebreakHEMS #criticalcare #flightparamedic #flightnurse #emergencymedicine

This first part is a look into the ED care of a 50's female with subarachnoid hemorrhage following a ruptured aneurysm. These are incredibly dynamic patient's and give way for many different treatment modalities. Let me know what you think and be on the lookout for Part II in a few days (that's the part where the patient starts to give you a mental and logistical workout). #HEMS #FOAMed #airmedical #criticalcare #coffeebreakHEMS #flightparamedic #flightnurse #phiairmedical #emergencymedicine Reach me at: kisercpr@gmail.com

Ten quick fire questions on Subarachnoid Haemorrhage to kick off the weekend !

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.15.152108v1?rss=1 Authors: Ezra, M., Garry, P., Rowland, M., Mitsis, G. D., Pattinson, K. Abstract: Aneurysmal subarachnoid haemorrhage (SAH) is a devastating subset of stroke. One of the major determinates of morbidity is the development of delayed cerebral ischemia (DCI). Disruption of the nitric oxide (NO) pathway and consequently the control of cerebral blood flow (CBF), known as cerebral autoregulation, is believed to play a role in its pathophysiology. Through the pharmacological manipulation of in vivo NO levels using an exogenous NO donor we sought to explore this relationship. Phase synchronisation index (PSI), an expression of the interdependence between CBF and arterial blood pressure (ABP) and thus cerebral autoregulation, was calculated before and during sodium nitrite administration in 10 high-grade SAH patients acutely post-rupture. In patients that did not develop DCI, there was a significant increase in PSI around 0.1 Hz during the administration of sodium nitrite (33%; p-value 0.006). In patients that developed DCI, PSI did not change significantly. Synchronisation between ABP and CBF at 0.1 Hz has been proposed as a mechanism by which organ perfusion is maintained, during periods of physiological stress. These findings suggest that functional NO depletion plays a role in impaired cerebral autoregulation during EBI, but the development of DCI may have a distinct pathophysiological aetiology. Copy rights belong to original authors. Visit the link for more info

In this episode I cover subarachnoid haemorrhage.If you want to follow along with written notes on subarachnoid haemorrhage go to https://zerotofinals.com/medicine/neurology/subarachnoidhaemorrhage/ or the neurology section in the Zero to Finals medicine book.This episode covers pathophysiology, presentation, investigations, diagnosis and management of subarachnoid haemorrhage. The audio in the episode was expertly edited by Harry Watchman.

Musings from our annual trip to the exact same cottage, exactly one year later. The brain of an average 50 year-old.

Gratitude for what I have and its "sufficiency" (Dayenu) and grieving for what I've lost, and sharing with others.

New thoughts on lingering deficits and "marks," a sweet tooth, my good fortune and links to other's misfortune - the not so final episode.

When nearly dying doesn't suck - or the good (and sometimes humorous) things that can come from nearly dying.

On living now, on being present, and learnings in the ICU and from the ICU nurses and patients.

On understanding others and how they I see things through clearer eyes. And as my final episode a thank you to family and friends for all their unbelievable love and support.

A discussion on how messages do matter, and the impact they had on my recovery.

This episode addresses hemorrhagic stroke, building of off Episode #2 of the podcast which was on ischemic stroke. We discuss both different types of hemorrhages including symptoms, diagnosis and treatment!Hypertensive HemorrhageLenticulostriate vesselsSubarachnoid Hemorrhage DiagramAneurysm CoilingAneurysm ClippingIntro/Outro Music: Pinecrest by The Loyalist (Used with permission of the artist)Speakers are employees of Mayo Clinic. The views/opinions expressed in the podcast are solely those of the speakers and do not represent those of Mayo Clinic or its subsidiaries.The Neuro Knowledge Podcast on Facebook!

In this episode I talk about how the road to recovery looks when you're on it, and also share an ode to the love of family and friends.

The first of my post injury Musings, about what you wish for, and about the Beatles.

Introduction and setting the scene - who, where and what is going on.

Episode 2, where I describe the sensations of the initial injury and the visit to the first local hospital.

In this episode I describe my girlfriend's drive to the hospital, my initial hospital experiences, and being on the brink...

Subarachnoid hemorrhage is the king of life-threatening headaches and is on my differential every time. This episode will cover how to take the history, exam, testing and treatment of this devastating diagnosis.

Today Amanda Chats to Neurosurgeon Dr. Mitch Hansen about Subarachnoid Haemorrhage. The after hours call to see neurosurgical patients is one that often instils dread, so we hope that these handy tips, and a good approach will help you approach this daunting condition! 

Author: Peter Bakes, M.D Educational Pearls Intracerebral hemorrhage is an intracranial bleed within the brain tissue or ventricles. Subarachnoid aneurysm causes about 50% of all ICH. Amyloid deposition can lead to ICH in elderly patients. Hypertension is another common cause of atraumatic ICH, commonly leading to pontine, cerebellar, or basal ganglial bleeding. Bleeding in other locations is suggestive of a different etiology. ICH will often present with depressed mental status, but specifically a patient with a systolic BP > 220 is suggestive of hypertensive ICH. CT is the first diagnostic step. CTA should be considered when the bleeding is in an atypical area. Significant edema on imaging can be suggestive of a tumor. Treatment should include hemostatic measures and BP control. Transfuse platelets if necessary and reverse any anticoagulation. BP target is

We are back with a quick dose of high quality, high yield emergency medicine board review. Episode 4 touches on Ascending cholangitis, NEXUS, SSS, Subarachnoid hemorrhage, Anticholinergic syndrome, Lead poisoning...and many mnemonics. The post Podcast Ep 4: Mnemonics, SSS, Subarachnoid Hemorrhage, & More appeared first on RoshReview.com.

Review Your brain is held inside your skull by a tri-layer membrane called the meninges.  These membranes and all the other structures in your brain are nourished by blood vessels, and different circumstances will make these vessels at risk of rupturing. *ALL BRAIN BLEEDS REQUIRE MEDICAL ATTENTION!*  Brain bleeds are classified based on the membrane they are closest to.  They can be caused by physiological malformations, stroke or aneurism from age or disease, or trauma. From the outside in Extracranial bleed: (extra = external; cranial = cranium = skull bones), between your skin and your skull.  Doesn't affect your brain, there is more room for it to stretch. Intracranial bleed: (intra = internal); bleeds inside the skull increase the intracranial pressure and requires medical intervention.  Main goal is to reduce intracranial pressure so brain cells aren't pressed on and damaged. Epidural (yep, that place they put the anesthesia for women having babies, except it's in the spinal cord): Epi = above, Dural = Dura mater, that topmost, durable layer of the meninges.  Between the skull and the dura mater. Subdural: Sub = under; blood leaks in between the dura mater and the arachnoid mater, which are normally in close contact, so the separation causes pain. Subarachnoid: under the arachnoid mater. Normally, under the arachnoid layer is the subarachnoid space which contain cerebral spinal fluid (CSF).  People who have had a subarachnoid bleed and survived, describe hearing a “thunderclap”.  Officially called a “thunderclap headache”.  It's like they can hear the blood vessel pop and experience extreme pain all over their head all at once.  Described as “the worst headache of my entire life”.  Because the pia mater under the subarachnoid space lays directly on top of the brain cells and follows all the grooves and wrinkles of the brain, this type of bleed will require emergent attention and possible surgery. Intracerebral: cerebral = cerebrum, the main part of your brain Intraparenchymal: Parenchyma = organ tissue, means it's right up against the brain cells Intraventricular: Ventricles = pockets inside the brain that make, hold, and reabsorb CSF.  The deepest part of the brain. *ALL BRAIN BLEEDS REQUIRE MEDICAL ATTENTION!*  Connect with me Support us on Patreon *NEW* Join the Pharmacist Answers Podcast Community on Facebook Subscribe: iTunes, Stitcher, GooglePlay, TuneIn Radio Like the Facebook page Music Credits:  “Radio Martini” Kevin MacLeod (incompetech.com)  Licensed under Creative Commons: By Attribution 3.0  http://creativecommons.org/licenses/by/3.0/

Membranes Basics Meninges are a triple-layer membrane that helps hold your brain in place. The inside of your skull bones have many boney processes protruding out.  The meninges surround the brain and provide a cushioning layer around it, and anchor to these processes.  This allows the brain to be suspended inside the skull and not touch the top, sides, or bottom. This setup is partly contributes to concussions.  When the head experiences a large enough impact, the suspended brain crashes into the bone of the skull. Meninges encase your brain and spinal cord to protect them. Three layers Dura mater (mah-ter, not may-ter): durable and thick, contains large blood vessels.  This is the layer that anchors directly to the skull bones.  Membrane that divides hemispheres, separates a few lobes, and coats glands near the brain. Arachnoid mater (yes, like spiders): wispy like spider webs - thin & transparent. Directly in contact with Dura mater, but has cellular pillars that connect it to the Pia mater.  The cerebrospinal fluid flows around these pillars. Also overs the outside of the part of the brain as a whole. Pia mater - delicate, contains the capillaries that nourish the brain.  Is in direct contact with brain cells - following all the contours and wrinkles of the brain. Subarachnoid space - hold cerebrospinal fluid (a closed fluid system that insulates and cushions the brain and spinal cord).  Doesn't mix with blood or lymph system. Connect with me Support us on Patreon *NEW* Join the Pharmacist Answers Podcast Community on Facebook Subscribe: iTunes, Stitcher, GooglePlay, TuneIn Radio Like the Facebook page Music Credits:  “Radio Martini” Kevin MacLeod (incompetech.com)  Licensed under Creative Commons: By Attribution 3.0  http://creativecommons.org/licenses/by/3.0/

A panel of neurocritical care fanatics discuss the nuances of managing aneurysmal subarachnoid haemorrhage (SAH) from pre-hospital through ED to ICU. This is a fascinating insight into international practice variations and the justification for these. It's very unusual to have such a panel of experts all in the same room speaking so frankly. This was recorded live at the SMACCBRAIN workshop in Chicago 2015.

Andy Naidech gives a fascinating and powerful short talk on controversies in management of aneurysmal subarachnoid haemorrhage, followed by discussion from the panel of experts and questions from the crowd. This was recorded at the neuro workshop for SMACC Chicago and was a very popular session.

Tom Bleck - Subarachnoid haemorrhage: what matters? Tom Bleck gives an overview of the pertinent facts regarding the complications and management of aneurysmal subarachnoid haemorrhage (SAH). The complications of aneurysmal SAH can be divided into immediate, early and late. The risk of re-bleeding is maximal on the first day, it is fatal in 75% of patients and the best management is to secure the aneurysm by coiling or clipping. Blood pressure control is utilised widely but parameters are arbitrary and the data is scarce. Early complications (days 1 - 3) include early brain injury in its various forms, stress cardiomyopathy, neurogenic pulmonary oedema and cerebral salt wasting. The most important late complication (day 4 onwards) is vasospasm. Tom briefly discusses the mechanisms and manifestations of SAH-associated brain injury including ischaemia, blood brain barrier breakdown, sustained depolarisation, hydrocephalus, vasospasm, seizures, hyperglycaemia and fever. He goes on to discuss in more detail the management of vasospasm, the associated evidence and the importance of distinguishing between clinically detectable and subclinical vasospasm.

After laying the foundations in the previous podcast, we dive below the dura mater in part 2 of the TBI series and take a look at subarachnoid, intraventricular, and intracerebral (parenchymal) hemorrhages as well as specific treatments for each.See omnystudio.com/listener for privacy information.

After laying the foundations in the previous podcast, we dive below the dura mater in part 2 of the TBI series and take a look at subarachnoid, intraventricular, and intracerebral (parenchymal) hemorrhages as well as specific treatments for each.

Neurotrauma – How to Put Humpty together again Humpty is a 23 year old egg, who fancied himself as a bit of a Hipster. Little did poor old Humpty know that his day was about to end in tears and he was to join the 1000 other Australians who annually have a severe head injury.  The talk focuses on Traumatic Brain Injury. There is particular emphasis on Traumatic Subarachnoid Haemorrhage and Transfusion Thresholds in Traumatic Brain Injury. The discussion explores the incidence and patterns of vasospasm following tSAH and the role, if any, of nimodipine and other therapies usually reserved for the aneurysm SAH population  The optimal target haemoglobin concentration following TBI is unknown. The discussion looks at the literature and explores the pathophysiology of anaemia in this setting.  A blood conservation strategy for patients with TBI is outlined  

In this episode of The FlightBridgeED Podcast, creeping and crawling, silently weaving a web of destruction a small, venomous disease unleashes its deadly bite on an unsuspecting woman. Join Eric and the flight crew as they pull down the webs of confusion and unravel the secrets of The Subarachnoid Bleed.See omnystudio.com/listener for privacy information.

[Full Audio] Oli Flower discusses the tricky issue of prognostication in neuro disasters. This includes intracerrebral haemorrhage, traumatic brain injury, subarachnoid haemorrhage and ischaemic stroke. From Bedside Critical Care 2013 in Cairns. Go to Intensive Care Network for the audio and much more.

Background: Acute non-traumatic focal subarachnoid haemorrhage (fSAH) is a rare transient ischaemic attack (TIA)-mimic. MRI is considered to be indispensable by some authors in order to avoid misdiagnosis, and subsequent improper therapy. We therefore evaluated the role of CT and MRI in the diagnosis of fSAH patients by comparing our cases to those from the literature. Methods: From 01/2010 to 12/2012 we retrospectively identified seven patients with transient neurological episodes due to fSAH, who had received unenhanced thin-sliced multiplanar CT and subsequent MRI within 3 days on a 1.5 T scanner. MRI protocol included at least fast-field-echo (FFE), diffusion-weighted imaging (DWI), T2-weighted fluid-attenuated inversion recovery (FLAIR) and time-of-flight (TOF) MRA sequences. By using MRI as gold-standard, we re-evaluated images and data from recent publications regarding the sensitivity to detect fSAH in unenhanced CT. Results: fSAH was detected by CT and by FFE and FLAIR on MRI in all of our own cases. However, DWI and T2w-spinecho sequences revealed fSAH in 3 of 7 and 4 of 6 cases respectively. Vascular imaging was negative in all cases. FFE-MRI revealed additional multiple microbleeds and superficial siderosis in 4 of 7 patients and 5 of 7 patients respectively. Including data from recently published literature CT scans delivered positive results for fSAH in 95 of 100 cases (95%), whereas MRI was positive for fSAH in 69 of 69 cases (100%). Conclusions: Thin-sliced unenhanced CT is a valuable emergency diagnostic tool to rule out intracranial haemorrhage including fSAH in patients with acute transient neurological episodes if immediate MRI is not available. However, MRI work-up is crucial and mandatorily has to be completed within the next 24-72 hours.

Background: The specificity of computed tomography (CT) for subarachnoid haemorrhage (SAH) is very high. However, physicians should be aware of rare false positive findings, also referred to as "pseudo-SAH". We present an unusual case in which such a finding was caused by chronic hypoxaemia. Case presentation: A 37-year-old male patient presented with headaches. His CT-scan showed multiple confluent subarachnoid hyperattenuations, which mimicked SAH. However, the headache was chronic and had no features typical for SAH. The patient suffered from severe chronic hypoxaemia due to congenital heart failure. On CT-angiography diffuse intracranial vessel proliferation was found and laboratory results revealed a highly raised level of haematocrit, which had both probably developed as compensatory mechanisms. A combination of these findings explained the subarachnoid hyperdensities. Magnetic resonance imaging (MRI) showed no signs of SAH and visualized hypoxaemia in cerebral veins. A diagnosis of pseudo-SAH was made. The patient's symptoms were likely due to a secondary headache attributed to hypoxia and/or hypercapnia. Therapy was symptomatic. Conclusions: Severe chronic hypoxaemia should be recognised as a rare cause of pseudo-SAH. Clinical evaluation and MRI help differentiate SAH from pseudo-SAH.

The latest NCEPOD (National Confidential Enquiry into Patient Outcome and Death) report examines the management of aneurysmal subarachnoid haemorrhage, in England's National Health Service. Two of the report's clinical co-ordinators, Mike Gough, a vascular surgeon at Leeds General Hospital, and Alex Goodwin, anaesthetist at the Royal United Hospital in Bath, join us to discuss the reports findings and recommendations. Read the full report: http://www.ncepod.org.uk/sah.htm

A Pecha Kucha introducing the topic of aneurysmal subarachnoid haemorrhage. This includes some epidemiology, the initial management and some treatment options. This is the first of five Pecha Kuchas on this topic.

A Pecha Kucha discussing the intensive care management of aneurysmal subarachnoid haemorrhage. This includes glycaemic control, haemoglobin targets, venous thromboembolism, fever, volume monitoring and fluid therapy. This is the 2nd of 5 PK's.

A Pecha Kucha discussing vasospasm following aneurysmal subarachnoid haemorrhage. The terminology, pathology, risk factors, diagnosis and management are discussed within the limitations of a PK. This is the 3rd of 5 PK's.

A Pecha Kucha discussing the complications that may follow aneurysmal subarachnoid haemorrhage. This includes causes of a neurological deterioration, seizures, hyponatraemia, cardiac complications, re-bleeding and hydrocephalus. This is the 4th of 5 Pecha Kuchas on this topic.

A Pecha Kucha discussing prognostication following aneurysmal subarachnoid haemorrhage. This includes discussion of the various grading scales used and other factors that impact upon prognosis. This is the 5th of 5 Pecha Kuchas on this topic.

Tue, 1 Jan 2013 12:00:00 +0100 https://epub.ub.uni-muenchen.de/25829/1/Cerebrospinal_fluid_analyses.pdf Uhr, Manfred; Wick, Manfred; Petzold, Axel; Tumani, Hayrettin; Skagervik, Ina; Nagy, Karin

This is an article published in the last year in the British Medical Journal that looked at the sensitivity of modern CT scanners in detecting subarachnoid hemorrhage. This article made a lot of waves because it suggested that a head CT within 6 hours of headache onset is 100% sensitive for subarachnoid hemorrhage.  Some have called it a practice changer that allows us to avoid doing a lumbar puncture so its important to read it for yourself and decide if it should change your practice.

We see patients with headache all the time in the ED. Most patients with headache don't have a life threatening diagnosis but its our job to pick up that small percentage of patients that do. In this episode we'll go through how to take a good headache history, how to catch the red flags, the workup, and treatment of headache in the ED. There's also an extended bonus section that will review how to do an LP along with a few tricks of the trade.