Welcome to the Neuro Transmitters, a podcast about everything neurology with the goal of reducing your a phobia. Today, I'm taking a look at medical journal articles and exploring how they can be used to improve clinical practice. We'll start with an article called Acute Epileptiform Abnormalities are the Primary Predictors of Post Stroke Epilepsy: A Matched Case Control Study. Then, we'll move on to a study called A Simple Risk Score for Predicting Neurologic Outcome in Out of Hospital Cardiac Arrest Patients After Targeted Temperature Management. Lastly, we'll look at the Association Between COVID 19 Vaccination, SARS-CoV-2 Infection and Risk of Immune Mediated Neurologic Events: Population-Based Cohort and Self-Controlled Case Series Analysis. This session will be highly relevant to medical professionals, looking to optimize their clinical practice when dealing with post stroke epilepsy, out of hospital cardiac arrest and COVID 19 related neurologic complications.
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Join in on the virtual journal club. Links to articles and books below:

Acute epileptiform abnormalities are the primary predictors of post-stroke epilepsy: a matched, case–control study


A Simple Risk Score for Predicting Neurologic Outcome in Out-of-Hospital Cardiac Arrest Patients After Targeted Temperature Management


Association between covid-19 vaccination, SARS-CoV-2 infection, and risk of immune mediated neurological events: population based cohort and self-controlled case series analysis


The Utility of Quantitative EEG in Detecting Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage


The Diagnosis of Functional Movement Disorder


The Neuroanatomy Riddle Book: Test and Expand Your Knowledge


Twitter: @DrKentris

Email: theneurotransmitterspodcast@gmail.com

The views expressed do not necessarily represent those of any associated organizations. The information in this podcast is for educational and informational purposes only and does not represent specific medical/health advice. Please consult with an appropriate health care professional for any medical/health advice.

Learning objectives

Learning objectives: 1. Understand the clinical relevance of acute epileptiform abnormalities in predicting post stroke epilepsy. 2. Assess the utility of the SLANT risk score for predicting poor neurologic outcome in out-of-hospital cardiac arrest patients after targeted temperature management. 3. Analyze which characteristics are associated with survivors of out-of-hospital cardiac arrest. 4. Discuss the potential implications of the medical nihilism concerning anoxic brain injuries. 5. Explore the association between the COVID-19 vaccination, SARS-CoV-2 infection, and risk of immune-mediated neurologic events.
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Computer generated transcript

The following transcript was generated automatically from the content and has not been checked or corrected manually.

Welcome back to the neuro transmitters, a podcast about everything neurology with the goal of reducing your your a phobia. I'm your host, Dr Michael Ken Trees. And today we're talking about journal articles. I thought it might be fun to do a sort of virtual journal club. I've selected a handful of articles that have come out recently that I think have some interesting points to make and hopefully some useful clinical relevance. So the first article I was looking at was called acute epileptiform abnormalities are the primary predictors of post stroke epilepsy. A matched case control study. This is in the annals of clinical and translational neurology by Puny A at all. Um Just to give you a little bit of the abstract here. Stroke patient who underwent continuous eeg eeg monitoring within seven days of presentation and developed post stroke epilepsy. Uh An end of 36 were matched in a 1 to 2 ratio by age and follow up duration with ones who did not. So there are uh in their controls with 72 variables significant on Univ arable analysis, hypertension, smoking, hemorrhagic conversion, pre continuous eeg e convulsive seizures and epilepsy form abnormalities were included in the multi variable logistic model and only the presence of epileptiform abnormalities on eeg remained significant for a post stroke epilepsy predictor with an odds ratio of 11.9 and a range of 1.75 2, 491.6. So, with acute epileptiform abnormalities, independently predicting post stroke epilepsy development. Accounting for their presence may help to tailor post acute symptomatic seizure management and aid anti epileptic genesis therapy trials. So as many listeners probably know, right, we sometimes call them anti epileptic drugs. But in reality, they're more accurately called anti seizure drugs. Since they don't necessarily prevent epileptic genesis, the process of establishing epilepsy after a single isolated seizure or something similar. So, in this study, they did continuous eeg monitoring at least 12 hours within seven days of the last known well time and these were all preceded by a routine 20 minute eeg. So, patient's who had a clinical seizure after hospital discharge were considered to have post stroke epilepsy. They matched these by age at the time of the stroke plus or minus five years and the duration of follow up plus or minus three months. Uh again, in a 1 to 2 ratio, they define their epileptiform abnormalities as electra graphics seizures based on the Salzburg criteria, uh isolated sharp waves, lateralized periodic discharges, lateralized rhythmic delta activity and generalized periodic discharges. And these are based off of the American Clinical Neurophysiology Society nomenclature. Uh the post stroke, epilepsy cases at the time of the acute stroke were less likely to have hypertension. Uh with an odds ratio of 0.33 and ongoing smoking 0.39 more likely to have a hemorrhagic conversion of the stroke 3.92 odds ratio. As you might expect, epileptiform abnormalities were more common among cases of post stroke epilepsy. 58.3% compared to the control of 15.3% with an odds ratio of 15.4. Uh And I thought this was notable, except for generalized periodic discharge, is all individual epileptiform abnormalities, including electra graphics seizures, etcetera were significantly more common in cases. And I think this speaks a little bit to kind of the entity of gpds which uh kind of are a little bit of a confounder overall. We know that they are associated with an increased risk of non convulsive seizures. But they also can be a manifestation of um metabolic or medication effects, other kind of diffuse things. So I I do always view them with a little bit of a grain of salt myself. So how long do we have two monitors? Write these, all these patient's had continuous eeg monitoring. So all of these findings were present on the first day of monitoring. Uh in 85% of cases roughly and nine, which is also about 81% of controls. Uh 16 patient's had their epileptiform findings on the initial 20 minutes, screening eeg and the median time for epileptiform abnormalities to appear was at about 1.65 hours. Now, I'm a little biased because I I am an epileptologist by background, practicing as a neuro hospitalist these days. And I do find continuous eg and critical care eg uh studies probably more interesting than the average neurologist. But I think this has some interesting clinical implications uh in terms of who are the people who are most likely to develop post stroke epilepsy. You know, it's a very common cause of epilepsy, especially in the geriatric population. And if we, you know, have a late seizure after stroke, you know, should we be getting routine eeg es on these patient's obviously, there are some limitations to this study uh in terms of like the sample size being relatively small, but I think it could be very interesting uh if it were able to change our practice and potentially reduce readmission rates and uh keep people from coming back in after a stroke, having another seizure on top of that. Um So I think there is some potentially very good clinical utility. Hopefully they'll continue working on this and bring it up to uh a very large study so that we could have some robust evidence to God our clinical practice. Next, I wanted to talk about a study called a simple risk score for predicting neurologic outcome in out of hospital cardiac arrest, patient's after targeted temperature management uh this was in the journal of Critical care medicine by chunking at all. Uh and this was done primarily in Taiwan it looks like. So this again a little bit of the abstract here. This was aimed to develop a risk score to evaluate individual out of hospital cardiac arrest, patient risk at early admission. After targeted temperature management. Regarding poor neurologic status at discharge, their primary outcome was a good neurological outcome at hospital discharge, which was defined as a cerebral performance category 1 to 2 with the poor defined as 3 to 5. So these cerebral performance category scores were adjudicated retrospectively using provider notes and physical examinations by consensus of neurologists who are blinded to the study. The secondary outcome measure was in hospital mortality and I always have to look this up. So I thought I'd just mention it here, right. So the cerebral performance category CPC score uh CPC one is good performance conscious alert, able to work might have some mild neurologic or psychologic deficits. Grade two moderate cerebral disability conscious, sufficient cerebral function for independent activities of daily life and able to work in a sheltered environment. Uh grade three severe disability conscious, dependent on others for daily support because of impaired brain function uh could be all the way from ambulatory to severe dementia or paralysis. Uh Number four coma or a vegetative state, any degree of coma without the presence of all brain death criteria unawareness, even if appears awake, such as vegetative state without interaction with environment, may have spontaneous eye opening and sleep wake cycles and then grade five is brain death. Uh apnea, areflexia, eg silence and so forth. So, looking at their study here, uh they found that survivors tended to be younger, more likely to be mail and have a higher frequency of co morbidities such as coronary heart disease, arrhythmias, heart failure, uh cerebrovascular disease and connective tissue disease compared with non survivors. So that was already a little bit interesting. Uh They also found those with a good neurologic outcome were less likely to be female and had a higher frequency of coronary heart disease and arrhythmia history compared with those with a poor neurologic outcome. So kind of mirroring that survivor aspect also not very surprising, both non survivors and patient with poor neurologic outcome at discharge, had a lower frequency of a witness collapse and onlooker CPR, they were more likely to have an initially non shock herbal rhythm and noncardiac cause. We're less likely to have received subsequent uh percutaneous cardiac intervention and had a longer resuscitation duration required more administration of adrenaline and had a higher sofa score. It had a longer length of hospital stay. So in this study, they, you know, everyone's trying to make more algorithms, more scores for neurology and try to make things a little more standardized. So they looked at five factors uh and call this new score. A pneumonic called slant slant with the minimum score of zero and a maximum of 21. So, slant stands for initial non shaka ble rhythm, leucocytosis or leukopenia to find as less than four or greater than 12 K per micro leader. A total adrenaline dose of greater than or equal to five mg. A lack of on, that's the end looker, cardiopulmonary resuscitation, uh time of duration, greater than or equal to 20 minutes. And so going down those again, we have the non shock, a ball that was eight points. Uh leukocytosis leukopenia, four points. The greater than five adrenaline is four points. Lack of onlooker CPR is two and the time of resuscitation being more than 20 minutes is three points. So they group these into moderate high and very high risk uh categories and that was moderate is a score of 0 to 7, high risk, 8 to 14, very high risk, 15 to 21. So already within like a non shackle rhythm, you got an eight that's already in the high risk group. If you had like more than a couple of rounds of uh a CLS or things like that where you're getting multiple rounds of epi that's a four, you know, so these points rack up quite quickly. So when they were looking at their data, they found a slant score and a threshold of 6.5 predicted poor neurologic outcome at discharge with the sensitivity of 84.1% and a specificity of 70.9% positive likelihood ratio, 2.89 negative ratio of 0.2 to four. So again, looking back at those moderate high and very high risks, the rate of poor neurologic outcome at discharge was 43.1% 86.9 and 96.6 respectively. And the differences between all of these groups were statistically significant. The limitations they noted in this study, there were institutional variations in uh the targeted temperature management. Uh the duration for potential neurologic recovery, uh whether there was pre existing, do not resuscitate in tension or withdrawal of care amongst survivors and in their population, they also noted a significantly higher proportion of patient's with initial shock, herbal rhythm than usual, which they were concerned may slightly distort their statistical analysis. But overall, you know, there's been this uh push in the neurology literature to not be so defeated with these potential anoxic brain injuries. You know, are we uh jumping the gun too quickly and saying that everything's hopeless. Remember reading in one of the uh issues of continuum in the critical care issue recently where they were talking about medical nihilism, essentially saying if you think that everything is futile and you do nothing, then the outcome is not going to be good, which shouldn't be too surprising for anyone who thinks about it for a second. So it is important to make sure that we're continuing to research this population find out what is the best data because a lot of our data is in the pre hypothermic era. So, does it apply as well? Is there obviously there's the potential for confounding situations. It's not apples to apples. So it is good to see that there's more data coming out in the post cardiac arrest, like sort of neuro prognostication family. So it wouldn't be post 2019 without at least one article about COVID 19 and neurologic complications. Uh So this study was called the association between COVID 19 vaccination. SARS COV two infection and risk of immune mediated neurologic events, population based cohort and self controlled case series analysis. And this was in the British Medical Journal by Lee at all. So the abstract here, they were looking to study the association between the COVID 19 vaccines SARS COV two infection and what is the potential risk for immune mediated neurological events. So, one of the most impressive things to me was the sheer amount of data that they were able to bring to bear in this analysis. Um uh listen to the participants 8,333,497 people who received at least one dose of COVID 19 vaccines. And they looked at the chat ox one and COVID 19 BNT 16 to be too, um which I'm just going to refer to buy the brand name because they're much easier going forward. So they also looked at uh and this was during the rollout of the initial vaccination campaigns from May 2021 in the UK and in June of 2021 in Spain. And they also included a cohort of 735,870 unvaccinated individuals with a first uh positive PCR uh test for SARS CO pay two from September 2020. So essentially, they're looking at the outcome of a few different neurologic entities, specifically Bell's Palsy encephalomyelitis, Guillain Barre syndrome, and transverse myelitis. So they looked at the incidence rates uh in the 1st 21 days after the first vaccine dose and 90 days after a positive test result for uh COVID. And they also compared this to a period between 2017 to 2019 to use that as a sort of internal control, looking at the background rates in the general population cohort. So just to break that down a little bit. So we've got 4 million, 376,000, 535 people who received astrazeneca. Uh I'm going to round off a little bit here. 3.5 million who received the Pfizer Biontech, uh 244,000 who received Moderna and 100 and 20,000 who received the Johnson and Johnson. And then we've got to get about 735,000 who got the SARS COV two infection. And we looked at 14.3 million from the general population, 20% overall of the British population and 80% of the population of Catalonia spain. Now, it was interesting, at least to me was that the number of cases of post vaccine Bell's palsy encephalomyelitis and GBS were consistent with the expected background rates. So this was not really what I expected given that we've had some early reports uh during the pandemic of Bell's palsy potentially being more common. Uh some of the vaccines and things like that. But um they give an example here in the data from the UK, the standardized incidents ratio for Bell's palsy was 1.33 for encephalomyelitis 6.89 and for GBS 3.53 transverse myelitis was too rare, less than five events in all vaccinated cohorts and as such could not be analyzed. Well, so overall, uh they didn't detect any safety signals in the COVID 19 vaccines related to these for neurologic entities, which is I thought very interesting and might change some of the counseling. Um You know, especially with things like Guillain Barre where we avoid certain types of vaccinations. Uh Does that mean that these people could safely have the COVID vaccine? Now, it would seem at least that this data is suggesting that is a possibility. They also make a point of saying that you are more likely in this population to see these three of these entities. Bell's palsy encephalomyelitis and green beret after COVID 19 itself at a significantly higher rate than from the vaccine and the general population. So what are the limitations that we're looking at here? So they only had primary care data from the UK. So they were suggesting that maybe some in patient diagnoses were not captured, although they do think that the system had the robustness that that was a low risk. The vaccinated population also tended to have more co morbidities uh including things like autoimmune disease, cancer, diabetes, obesity, heart disease and renal impairment. Uh So there was some concern about that as a possible confounder. Third, comparisons between vaccinated and historical cohorts might be limited because of changes over time, including seasonal variations. Although again, that was thought to be uh less of a factor overall. Uh They excluded individuals with a recent history of the same immune mediated neurologic events. Uh So they're not generalize about two people with chronic relapsing conditions such as multiple sclerosis or devic's disease or neuromyelitis optica. So, unfortunately, there still is that lingering question mark about how safe can you be in these people who are susceptible to acute relapses and flares of their disease? But you can still make the same argument that the risk from the infection itself is still significantly higher than it would be from the vaccine. So it's probably still going to be kind of one of those counseling situations where you have to weigh the pluses and minuses. So this study again, last limitation. They mentioned here focused on short term adverse events after vaccination using similar time periods to other studies. The time at risk after vaccination was defined according to the shortest recommended interval between 1st and 2nd vaccine doses, even in the single dose vaccines, um they use that same time period to kind of standardize the observation. So, and they're basically recommending further evidence is required as as it always is in most studies uh to understand the long term adverse events of vaccination and SARS COVID two infection. So definitely some interesting findings there. Um You wonder will the the FDA or the CDC be revising any of those things like the Bell's palsy side effects and so on and so forth uh as uh warnings with any of the vaccines. So it could be interesting going forward to see how the data develops on that. All right. So you'll have to forgive me. I have a second eg article here that just happens to be my particular brand of neurology. So this one is called the utility of quantitative eeg in detecting delayed severe olesky me a after aneurysmal subarachnoid hemorrhage. And this was in the journal of Clinical Neurophysiology by bang at all a little bit of the abstract here. Uh In this review, we discussed the utility of quantitative eeg parameters for the detection of delayed cerebral ischemia abbreviated DC I after aneurysmal subarachnoid hemorrhage in the context of the complex pathophysiology of DC I and limitations of current diagnostic methods. So, you know, they compare a little bit uh Ben eg literature about looking at this DC I. Um you know, historically may have heard of Bezos spasm and it has actually some pretty robust data, but um there are some issues with implementation still. So specifically, some of the criteria that we look at on a quantitative eeg for this looks at alpha power relative alpha variability, alpha delta ratio. Uh because all of these tend to show reliable detection of DC I. And this has been in multiple previous studies, recent studies on epileptiform abnormalities suggest they also have the potential for the detection of DC I. So this is a promising continuous noninvasive monitoring modality. Um So a little background, aneurysmal subarachnoid hemorrhage, 3% of stroke types DC I occurs in 33 to 50% of aneurysmal subarachnoid hemorrhages with the peak incidence between 3 to 14 days. So all pretty basic background information thus far. So why we care about DC I? It can cause strokes, it can cause cause re bleeding, uh seizures, hydrocephalus, it can cause, you know, worsening clinical outcomes in all these different ways. So, historically, they looked at transcranial dopplers. So sonographic radiographic as well in terms of CT angiograms or uh direct digital catheter angiograms, uh looking at uh evidence of change in vessel caliber. Um but they're not able to be done real time, obviously, especially with catheters. So, um it's been kind of a developing science's right. We used to be caused like Bezos spasm, but there appears to be some cortical spreading to polarization, uh impaired cerebral auto regulation, uh some micro circulatory dysfunction, micro thrombosis and neuro inflammation. Essentially, they're recommending an automated detection alarm system using these quantitative eeg parameters uh to be developed. Um However, this is a problem, right? A lot of eg anyone who's ready. GS knows there's a a lot of noise compared to that signal. So it is highly susceptible, especially in like an ICU setting, lots of electro uh electromagnetic interference than movements, things like that. So a lot of noise even more than in the outpatient clinic setting on that eeg and that uh inhibits the development of the algorithm as well as just the organic pathology, you know, increased I cps, hydrocephalus, surgical placements, uh medication changes. So all of these things require usually more hands on approach. Uh I think it's some of the other dcieg studies they've been looking at uh they would have people checking. You can't get a baseline. You look at all these different variables that we mentioned earlier and you compare that sequentially over like every 4 to 6 hours, which is a pretty labor intensive uh undertaking. But you know, it can capture things pretty well. And the uh the detection is pretty amazing. So the question will be, can we automate it with an algorithm that will make it so that it can be available to a more widespread population because not only are we talking about continuous eeg, which is something that is already not available at many smaller hospitals in the country but quantitative eg which if again, you're automating it, that's one thing. But if you are able to watch it remotely, uh, could that help with keeping people in smaller hospitals? Again, that's a debatable points if you need the neuro critical care level of care that these patient's do. But uh just anecdotally, I know that uh it is like in our hospital here, you know, it's around 400 beds. We only have three eeg machines here and we wouldn't necessarily have the resources to uh put every person who had an aneurysmal subarachnoid hemorrhage on, you know, two weeks of continuous eeg monitoring, you know, depending on their relative risks and so forth. Um Just resource wise, uh the hospital doesn't have the resources to do that. And I'm sure there are many other places in the country that would be in a similar boat. So hopefully they are able to develop that algorithm over time as that would be pretty amazing and provide some early warning systems and probably change outcomes on a lot of people. The last study I wanted to mention today uh was called the diagnosis of functional movement disorder. Uh And this was by doctors Gilmore Lid Stone and Lang in practical neurology. And this was a little bit more of a review article. They were having a bit of an issue about functional neurologic disorders. So, you know, if you're like me as a non movement specialist, uh, I always feel like I know what I see a functional movement disorder, but I'm like, I hope I'm not missing some bizarre dystonia or something like that. Um, but let's dive into their background a little bit here. They kind of give an excellent background and you'll have to check out the article. Um And I'll link all the articles in the show notes as well, but um some good line drawings and a very extensive table of all these different uh neurologic symptoms. So a little background here. Functional movement disorders encompassing abnormal movements and weakness is a common subtype of functional neurologic symptom disorder with a motor dominant presentation seen in 61% of a cohort of people with FND. So that functional neurologic disorder. So uh Functional Movement disorder FMD accounts for 2 to 20% of referrals to movement disorder clinics. So there are a lot of socioeconomic repercussions to function. A neurologic disorders with about a third being unemployed, uh significant fraction uh collecting disability. And again, I'm just extrapolating from the PNES data. Uh the longer that you were on disability, the less likely were to go into remission once you started treatment. Uh I don't know if that applies to FMD at large, but it is something that's been reported in the the psychogenic non epileptic spell population uh just to extrapolate a skosh. So the tricky bit with uh functional movement disorders and functional neurologic disorders in general, there is this thought that lingers in the neurologic community at least uh to my eye where we tend to think of it as a diagnosis of exclusion. And there is a very robust push in the literature that it is not exclusionary. Rather, it is a rule in based on positive signs rather than the absence of other primary neurologic disorders. And the really difficult part is that it frequently will coexist with other neurologic disorders. Um A large multi center study found that neurologic disorders were present in 22% of people with functional movement disorders. So that even if you suspect a functional disorder, you still have to keep your antenna up looking for a new neurologic disorder that might be riding along. So some key points of the functional movement disorder history is that they will often experience a sudden onset of symptoms, uh frequently occurrent at the time or shortly after a physical injury, which is usually kind of out of proportion, usually a minor injury or an illness or other neurologic symptoms. Uh the symptoms will usually progress to maximal severity rapidly or maximal at onset rather than a typical uh gradual progression seen in many movement disorders. Um If more than one functional symptom is present, it's common that multiple symptoms accumulate then wax and wane over time including pain, fatigue and cognitive symptoms. Careful history, differentiates between symptom accumulation over time versus progression of an individual symptom. And it is common for those with FMD to notice variability with quote unquote good days and bad days and some spontaneous remission. So the key things in terms of the clinical presentation is variable abnormal movements throughout the assessment that are distractible and enhance when attention is drawn to them. Mixed movement, phenomenology, czar common and paroxysmal attacks may occur in the clinic. I can't speak anecdotally to that very often it would seem and these can occasionally be triggered with suggestion which again kind of just extrapolating from my experience in the non epileptic spell world. Uh suggestibility is kind of a key feature. So I like that they broke it down into uh a few categories here. Um weakness, tremors, cranial dystonia, fixed dystonia, paroxysmal dystonia. Um Can I just mention that uh I find estonia's vaccine uh neurologic problem to identify uh jerks and myoclonus ticks, gait disorders and parkinsonism. So, there is some interesting literature out there about evaluation of tremors in terms of surface E MG uh where you can look at the frequency and burst and things like that. Uh I've never worked unfortunately, any place that is able to offer that testing, you can also do things like uh dopamine dat testing pet scans and things like that to evaluate for any underlying primary neurologic disorder. So, ultimately, functional neurologic functional movement disorders is a psychiatric diagnosis and so it is in the DSM five. So FND criteria, we've got four here. So 11 or more symptoms of altered voluntary motor or sensory function. Two, clinical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions. Three, the symptom or deficit is not better explained by another medical or mental disorder. And four, the symptom or deficit causes clinically significant distress or impairment in social, occupational or other important areas of functioning or warrants medical evaluation. So, one of the key points from the DSM four to the five is that they removed the requirement for a quote, recent psychological stress, er, as well as the quote need to exclude feigning uh faking if you will when it comes to diagnosing FND. So, so that is something that I, I have seen where some doctors just think that they're faking it. Uh And unfortunately, I think that attitude is still very prevalent in medicine at large. Um And again, they emphasize rule this in with positive signs rather than keeping it as a diagnosis of exclusion. And this is an analogy. Uh again, something from the PNES uh literature is communicating the diagnosis. Well, I I've read a lot of papers where you just literally what phrases work the best. And uh one of the ones that I've become fond of is uh software versus hardware problems, right? So this is more of a software issue where it's not communicating with your hardware correctly. Um It also can help to demonstrate the abnormal movement findings from the exam and explain what they mean. And uh there is an excellent website as well, neuro symptoms dot org which talks through a lot of these different symptoms uh in a layperson language and it can be very helpful. So those are the articles I had selected for today. I hope you found it educational and not too boring. Uh Hopefully I kept it just to the brief amount that will be helpful. Uh I also had one little bonus thing. I recently bought a book that came on sale. I saw on Twitter, um the Neuroanatomy Riddle book by Doctor James Dull Bow and Doctor Neil Photo Odor. I apologize if I'm mispronouncing your name's. Uh I just wanted to read uh one of these riddles here uh for all the nerds in the audience of which I'm sure there are many, uh the smallest but the longest from the back I come to play though. My goal maybe oblique without me, you'll tilt away to get the answer. You'll have to buy their book. I've included a link to all the articles from today as well as the book in the show notes. As always, if you enjoy this podcast, please leave us a review on Apple itunes, Spotify or wherever you get your podcasts and don't forget to share and subscribe for future episodes. You can reach me on Twitter at Doctor Ken Trees. That's Kentris or by email at the Neuro Transmitters podcast at gmail dot com.