Great, thanks. Good afternoon, everyone. Welcome to the Neurotrauma Scientific Session at this year's Virtual Double ANS. I'm excited to be here, hoping for an exciting afternoon. Apologies in advance for any technical glitches we may run into. We've been fighting through a few of them, but hopefully we get things sorted out before we get going too far. There's a couple housekeeping things to announce. I'm Sarah Woodrow, the moderator for this session. Just a couple of things to let you know about. First of all, throughout the sessions, if you've got any questions for any of our faculty members, then please enter it into the Q&A box on the right side of your screen. It goes directly to our faculty, and we'll hopefully be able to answer back to you. If you want to engage with your colleagues, there's a chat box on the right-hand side as well that you can chat with your colleagues back and forth. Finally, there'll be some polling questions throughout some of these presentations. To participate, you click on the Q&A box and select the polls option. Hopefully, we'll be able to, if the glitches get sorted out, we'll be able to show you some live results as we go along. At the very end, please don't forget to go to myAANS to submit for CME credits for this. In the interest of trying to keep us on time today, which will be part of my job here, I'd like to get us started by introducing Dr. Joe Maroon, who will introduce our first speaker for us. Thank you very much. It's my great pleasure to introduce the second annual Chuck Knoll Foundation for Brain Injury Research speaker, Dr. Shelley Timmons. What I would like to just take a few minutes and introduce who Chuck Knoll was and what the foundation is all about. Coach Knoll was the four-time Super Bowl champion for the Pittsburgh Steelers, an incredible educator as well as a coach, a great person and human being in his own right. He also was a stimulus for the formation of neurocognitive testing at the University of Pittsburgh with the impact test that we devised at his prodding and recommendation. About four years ago, Mr. Art Rooney founded the Chuck Knoll Foundation for Brain Injury Research with a very generous grant of his own. Subsequently, the vision has been to diminish the impact of sports-related head injuries, focused primarily on sports-related head injuries. The mission is to advance research related to the diagnosis and treatment of injuries to the brain, primarily from athletic injuries. The scientific advisory board, Julian Bales, Rich Haid, Shelley Timmons and Don Whiting meet annually three to four times a year to go over proposals. We have to date given out over $1.66 million in grants. This year, we hope to get it up to $2 million for the projects listed. These are some of the things that we've supported in the past. Phosphorylated tau in patients or in individuals with no history of contact sports. Rudy Castellani is now at Northwestern. Biomarkers for inflammation and saliva biomarkers. Also, a grant to the Carnegie Mellon University, Dr. Polker Grover, on the detection and suppression of brain tsunamis for alleviating brain damage from concussive injuries. We have amount raised thus far over $3 million. We're continuing to be aggressive in raising money for this kind of research. It gives me great pleasure to introduce a friend, a colleague, a board member, Shelley Timmons, professor and chairman at Indiana University and also co-director of the Neuroscience Institute at IU. My alma mater as well. And Shelley has been incredibly active in sports production and all trauma-related injuries, has been a consultant to Homeland Security, the government, the first female president of the AANS, and has been an incredible thought leader, a researcher, and committed to all good things in neurosurgery. So, Shelley, without further ado, thank you and welcome. Well, thank you, Joe, very much, both for involving me in the foundation and for your kind introduction. It is an extreme honor to provide the Chuck Knoll Lecture in Sports Neurotrauma at the annual meeting of the AANS. Today, I will share information on advances in brain injury research related to sports-related TBI and mild TBI in general. My sincerest thank you to the Chuck Knoll Foundation and Mr. Rooney for sponsoring this lectureship. Many will recognize the Hall of Fame coach who led the Pittsburgh Steelers to multiple Super Bowl wins and established the team status as an NFL powerhouse. What many do not know is Coach Knoll's role in enhancing the understanding of concussions and his pioneering efforts in identification of concussions in athletes dating back to 1990, when little was known about this phenomenon. His influence ultimately led to substantial safety changes across many different sports and levels of competition through work with Dr. Joseph Maroon, Steelers neurosurgeon, and University of Pittsburgh faculty member. Joe is also an Indiana University alumnus and was the inaugural Chuck Knoll Lecturer in 2019. Today, we will review current leading topics in sport-related TBI and emphasize the importance of longitudinal studies and those that take into account multifactorial influences on long-term effects of concussion. I serve on the National Science Advisory Board of the Chuck Knoll Foundation and I have also served on the Scientific Advisory Board of the National Football League in the past. I serve as an unaffiliated neurotrauma consultant for the NFL currently. None of these roles results in a conflict of interest for the contents of this presentation. An estimated 214 million children and adults participate in athletics in the United States alone. While there are many, many benefits to be reaped from engaging in sporting activities, there is also a risk of sustaining a traumatic brain injury that is higher in certain sports. About 20 percent of TBIs are thought to result from sports participation, with half of these occurring in children and adolescents. Given the potential impact on learning and lifelong development, this has been an area of increasing research in recent decades. However, surveillance strategies and research studies have been limited in terms of contributing to our understanding of the true prevalence, incidence, and severity of these injuries and with respect to impact on neurologic status and life events. Unfortunately, various forms of bias in the literature have obscured our understanding of the true incidence of sports-related TBI. These include a historical reliance on administrative and billing databases to assess the extent of the problem, reliance on hospital-only datasets, selective publishing, and lack of standardization of datasets. In 2015, a unified set of reporting standards for neuroepidemiology was proposed, and it is hoped that future studies will incorporate more uniform reporting techniques. Up until recent years, there was a widespread lack of cultural awareness of the signs and symptoms of brain injury and the knowledge of the potential short, intermediate, and longer-term impact on people who sustain them. While additional public education efforts and even legislative and regulatory enactments requiring reporting, assessment, and clearance prior to return to play and availability of medical care have resulted in increased awareness and reporting, there is still major geographical and socioeconomic variability in how people report and how they seek care. Patients sustaining milder forms of a concussive injury still often do not seek health care and do not even report these injuries to others, including parents or teammates, trainers, and coaches. Injury surveillance systems can help identify a broader segment of the injured population beyond those presenting to hospital, but they also have limitations, including lack of consistency on sports definitions, data elements, entry processes, and reporting mechanisms. Importantly, consensus needs to be achieved on what constitutes the denominator determining overall exposure for various sports activities and, therefore, a more accurate measure of risk. Recent efforts have begun to focus on more longitudinal studies of athletes who have sustained injuries to assess those factors that might predict intermediate or long-term problems, trajectories of recovery in various domains, and impact on neurological, cognitive, and behavioral functions. One such effort is the CARE Consortium, funded by the National Collegiate Athletic Association and the United States Department of Defense. The aims of this collective are to study the cumulative effects of concussion and repetitive head impact exposure during military service academy and NCAA student-athletes' careers, with specific attention to cognition, psychological health, and life function at the end of their collegiate careers and up to four years later. This group also studies changes in brain structure, function, and neurobiology through advanced neuroimaging, genetic, and proteomic biomarker studies. These goals are accomplished through the enrollment of now more than 41,000 collegiate student-athletes via an established national multi-site consortium and infrastructure. Studies are prospective, longitudinal, and multi-center, with multiple sports being represented. At least 70 peer-reviewed publications and numerous scientific presentations have emanated from this consortium to further advance our understanding. Several other consortia exist and, importantly, a number of brain-banging efforts exist across the world for long-term effects of TBI as well as the study of various forms of dementia. Such tissue-banking efforts have aided in the research of histopathology of long-term effects of traumatic brain injury in general, but also the effects of repetitive concussion and subconcussive injuries. The clinical syndrome of advancing dementia and other neurological dysfunction has been well-known for ages and has been discussed in the medical literature since the early 20th century. Pathological characteristics of boxers sustaining repeated knockout injuries were described by Harrison Martland in 1928. Further characterization of punch-drunk syndromes was published by Critchley in 1949. Since that time, there has been significant controversy about the impact of repetitive head injury on the development of clinical encephalopathy. In an effort to at least come to consensus about the pathological features of chronic traumatic encephalopathy described by Amalou and McKee in the early 2000s, the NIH and NFL partnership launched a major effort to define the neuropathological characteristics of CTE in March 2013. The future directions identified then included advancing our understanding of comorbidities of CTE with other neurodegenerative disorders, clinical correlates, and delayed effects of TBI. The group concluded at that time that the incidence and prevalence of CTE remained unknown. A consensus paper on the pathological characteristics of CTE was published in 2016 highlighting the role of hyperphosphorylated tau protein, or p-tau, in specific brain regions in this pathological entity. In order to come to consensus on this subject, seven blinded, experienced neuropathologists evaluated cases of various tauopathies as listed here and found good correlation of CTE as a distinct pathological entity from the others. Even though nine of ten subjects with this pathological diagnosis were former American football players and one was a former boxer, the question remained at that time whether this was clinically correlated to a history of trauma. The conclusion of the manuscript confirmed that CTE remained a diagnosis that could only be made definitively on neuropathological examination of the brain. The consensus panel identified minimum recommended sampling sites following the National Institute on Aging Alzheimer's Association standards and highlighted the need to include deep-circle regions for cortical sampling in order to detect 80% of pathological CTE cases. P-tau deposition in neurons, astrocytes, and cell processes around small vessels and irregular patterns deep in cortical sulci was the first criterion. Hippocampal atrophy, neuronal loss, dendritic swelling, and the presence of neurofibrillary tangles, all in specific areas, were also part of the diagnostic criteria. Thorny astrocytes in subpial and periventricular regions and grain-like or dot-like structures signaling P-tau also support the diagnosis. Cytoplasmic inclusions were also identified in certain areas. On gross examination, disproportionate enlargement of the third ventricle, septal abnormalities, mammillary body atrophy, and contusions or other evidence of prior injury were notable criteria. So while it has been noted for decades that certain athletes sustaining repeated significant head trauma can develop long-term cognitive and psychomotor sequelae, and there is now consensus that the specific P-tauopathy is a pathological entity distinct from other neurodegenerative disorder patterns, labeled chronic traumatic encephalopathy, the correlation between the clinical syndrome and the pathological constellation of findings needs further validation. This is because correlative studies so far have been done in highly selected subjects. There is therefore a significant need for further highly structured rigorous perspective and longitudinal studies to definitively correlate neurodegenerative diseases with chronic sequelae of traumatic brain injury, repetitive injury, or cumulative subconcussion impacts. Perhaps some of the most exciting research aimed at accomplishing these goals involves the use of novel imaging techniques to determine the pathology of brain injury. These techniques have the potential, once thoroughly investigated and contextualized, to guide interventions such as return to learning, work, and play, to study the effects of various therapies in more sophisticated research protocols, and ultimately to guide therapies in the clinic. While standard MRI techniques can glean information on brain volume, large lesions, ventricular size, and the like, more sophisticated MR techniques are beginning to guide our understanding of regional anatomical and physiological changes occurring in the phase of injury and subconcussive repetitive blows. Such techniques can assess the presence of microhemorrhage, blood oxygen content, and blood flow, amongst others. With further understanding of these anatomical regional changes and their functional correlates, we can begin to understand differences amongst individuals and within individuals over time, as well as their clinical significance. MRS measures peaks in various brain metabolites, such as choline, creatine, myoinositol, and others. It has been used to describe regional differences in concussed and non-concussed athletes compared to age-matched controls in both acute and chronic phases. However, studies have been small in sample size and have shown mixed results. The imaging working group of the Enigma Consortium has published technical specifications that can be used on all commercially available MRI units in an effort to standardize protocols and broaden the potential for clinical and research uses of MRS in a variety of neurological diseases, including TBI. Diffusion tensor imaging has been used to study axonal and myelin integrity. This technique has demonstrated axonal changes in all severities of TBI, but myelin changes only in more severe injuries. Hypothesis-driven studies of selected individuals with cognitive decline in a history of TBI have shown that the same structures and brain regions affected by pathological CTE or p-tauopathy have also demonstrated diffusion abnormalities. CARE Consortium studies have been implemented to study this technique in larger cohorts of athletes with injury, without injury, and with age-matched controls. In Wu et al. 2020, the investigative group showed the changes in white matter on DTE were evident after sports-related concussion as long as six months after injury, but they were not observed in contact sport exposure without concussion. They further showed that these persistent changes correlated with both clinical outcomes and delayed recovery. Interestingly, athletes were cleared to return to play based upon clinical findings, but these imaging findings persisted in some athletes even after being cleared. However, volume of white matter structural abnormalities did decrease over time, suggesting restoration of microstructure and healing. This study was consistent with prior smaller studies of persistent DTI changes after symptom resolution. However, other metrics were different from prior studies. For example, in this study, female athletes had more changes at the long-term study points than males. Other inconsistencies from previous studies involved age and stage of the athletes. Clearly this tool is promising, but more longitudinal work needs to be done to further refine its significance. Multiple radio tracers have now been described that can detect tau and related proteins on PET scanning. Hypothesis-driven studies in selected individuals have again shown similar patterns of activity as seen in pathological CTE and p-tauopathy, but others have shown patterns similar to Alzheimer's disease, highlighting differences in imaging at different stages of disease, different ages of onset, and potential overlaps in diagnosis. As different radioligands are being validated and their sensitivities defined, thoughtful approaches to the utilization of these tests in subjects who will commit to later neuropathological diagnosis through tissue donation will help to bridge the gap between diagnosis in life and diagnosis after death. As alluded to earlier, collaborations among various longitudinal data-gathering efforts in imaging studies like PET will also help to identify imaging characteristics of various dementias, their stages, and any relationships to trauma exposure, as well as confounders in etiologies such as genetics or epigenetic contributions like substance and medication exposure and medical comorbidities. Conectomic studies show promise in this area as well. Challenges to all forms of imaging research after sports-related and other forms of mild TBI include lack of within-subject data, i.e. pre-injury baseline data, as well as lack of normative data atlases across the entire age spectrum. Conectome studies done prior to injury and after injury may yield additional insights into the long-term effects of trauma within subject and will yield additional information for connections prevalent across populations. Magnetoencephalography is a highly sensitive technique that measures magnetic fields produced by the brain's electrical currents. It is not widely available in the setting of traumatic brain injury, its use remains essentially investigative. However, it promises to become a future, more widely used tool for both research and clinical decision-making. Interesting correlations between MEG findings and cognitive deficits and functional status have been observed. In addition to the various imaging modalities discussed, there is a veritable cornucopia of field modalities being developed for prediction of chronic sequelae of TBI and clinical diagnostic testing. These range from a host of biomechanical innovations such as accelerometers and helmets, headgear and mouthguards, to helmets designed to mitigate force application. Acceleration and deceleration, rotational, directional, and other data recordings are being utilized with increasing frequency to formulate computational predictive models not only for development of concussive symptoms, but also to investigate the impact of cumulative sub-concussive events on long-term cognitive and other sequelae. With respect to diagnosis, innovation begins on the sidelines and continues through the clinics. Use of computerized assessment tools, correlation with imaging and neurophysiological data from, for example, evoked potential or eye-tracking methodologies, are increasingly seen in investigative and real-world use. Many of these testing modalities rely on furthering our understanding of the underlying pathophysiology of injury. Neurophysiological methods in the clinic include several interesting approaches using traditional techniques. One such adaptation is the mathematical analysis of EEG waveforms to study changes in the electrical activity of the brain over time. Such quantitative EEG techniques have had early applications in mild TBI and concussion related to sports and may be able to provide diagnosis of injury in asymptomatic patients. Another is the study of cerebral blood flow through multiple techniques, including MR. Some preliminary studies have shown that CBF changes correlate with early symptomatology, but not necessarily long-term recovery. Cortical spreading depolarizations are pathological depolarizing waves seen in stroke, epilepsy, intracranial hemorrhage, migraine, and TBI. CSD is rooted in glutamate toxicity and metabolic mismatch related to decreased blood flow in the hypermetabolic post-injury states. Links to the mild TBI population at this time are unknown. It has long been thought that there are certain genetic predispositions to recovering well or recovering poorly from traumatic brain injury, just as genetics affect all other pathophysiological processes. As elucidated through the scholarship of my colleague Tom McAllister, the putative mechanisms of influence of genes on outcome from TBI include modulating the extent of injury from any given dose of traumatic force, modulation of innate repair mechanisms, genetic impact on pre-injury traits, and genetics of other conditions influencing domains of outcome after TBI, such as cognition, behavior, headache, balance, coordination, and others. Recent enabling legislation protecting subjects from discriminatory practices, primarily from insurance providers and payers, has resulted in renewed interest on the part of the public in obtaining genetic information regarding their health. Home testing kits have also popularized access to personal genetic information even further. Unfortunately, there is little useful information that can be gleaned to inform the public about the risks for persistent or severe repercussions after TBI. This is in part due to lack of sufficient scientific rigor to draw meaningful conclusions in studies done thus far. Results of preliminary studies have been hampered by problems with reproducibility, inclusion criteria and biases, and statistical power, to name a few. Still, there is some emerging evidence that differential gene expression impacting immunological, inflammatory, and hormonal pathways is seen in pre-injury baseline testing versus testing done acutely and subacutely after injury. While genetic testing remains investigational at this time, it is hoped that large-scale studies, including those with tightly controlled protocols, correlative assessments such as imaging and biomarker testing, and longitudinal designs will help further our understanding of the roles genes play. Much of our knowledge of the molecular processes occurring in sports-related and mild TBI had its genesis and work done in the 20th century on severe TBI. Giza and Havda characterized the new neuro-metabolic cascade of concussion in 2014. They outlined many of the well-established pathophysiological processes seen in more severe forms of TBI and the evidence of their occurrence in even mild TBI. They further postulated associations between several of these phenomena and known sequelae of TBI, citing examples from the literature to support these associations. Finally, they discussed the evidence for transformation from acute processes to chronic to tie together many of the findings discussed in this talk while outlining areas for potential future research. Various interesting molecular and genetic findings have been associated with post-concussive symptoms. In the example of post-traumatic headaches shown here, we see that there are multiple potential contributing factors related to immune processes, electrolyte and hormonal imbalances, and genetic background. For specific post-traumatic symptom domains, a thorough understanding of molecular mechanisms and causality will ultimately help to derive appropriate therapeutic approaches. A natural next step is to search for tests that capitalize on our knowledge of these molecular processes. Biomarkers are, in the traditional sense, identified in assays of body fluids as an indicator of a specific biological process. Current research is aimed at identifying readily accessible and measurable biomarkers from saliva or blood to aid in the diagnosis of TBI. The presence of an intact blood-brain barrier may affect the probability of developing a valid biomarker in these substances, but significant effort has gone into such research. Still, no biomarker yet exists to predict CTE. Multiple potential biomarkers are under investigation as listed for mild TBI. Given the implications of being able to make a rapid diagnosis with a sidelined biomarker assay, several studies have centered on sports-related brain injury. While some early correlations between biomarker levels and degree of symptoms, number of head hits, and related mechanistic factors have been seen, none has yet been validated. Fewer than 100 biomarkers have been validated for clinical use in general, despite hundreds of thousands of manuscripts being published on the subject, so the challenges are not necessarily unique to TBI. Likewise, no pharmacological interventions have been proven to benefit outcomes from TBI in general, despite many clinical trials and severe forms of injury. In sports-related TBI, trials have focused primarily on the use of various medications to target persistent concussive symptoms, and on the use of nutrients and nutraceuticals. Nutraceuticals have multifactorial modes of action and maintenance of homeostasis, and there is at least some preliminary evidence of positive impact. Neuropsychological studies have been a mainstay in the diagnosis and follow-up of sports-related TBI for years. They aid in the objective assessment of cognitive, behavioral, and mood changes after mild TBI. Research has focused on identifying abbreviated and automated assessments that can be deployed to the sports arena, as well as in baseline testing and follow-up. Ideal systems must be valid, sensitive, and specific, and have adequate test-retest reliability while minimizing practice effects. Many of these testing modalities show increased sensitivity and specificity when combined with other diagnostic modalities. Further work is needed to understand which populations benefit most from baseline pre-injury testing. In summary, despite the explosion of interest in and publications about sports-related brain injury and mild TBI in general, there remain many unanswered questions related to the diagnosis of injury, the trajectory of recovery, and the optimal modalities that can be used to follow progress, guide interventions, and connect injuries to long-term neurodegeneration. This remains a fruitful area of research, with exciting advancements occurring, particularly with respect to imaging and large longitudinal studies which track subjects over time. I would like to thank you very sincerely for your time and attention today, and please enjoy the rest of the meeting. Thanks so much, Shelley. Hoping that everyone can hear me. We've been working on some technical issues backstage here. Does anyone have any questions for Dr. Timmons? We have a few minutes before we can move on to the next session. When you put it on the right-hand side of your screen, we should be able to see the questions. I should be able to see it back here and relay them on. Silence is deafening. Shelley, I've got a question for you. With all these biomarkers that we're working on, what do you think the timeline is when we get to a point where clinically we'll actually be using these on a day-to-day basis? I think that the studies that are ongoing now with ALERT-TBI and TRACK-TBI studies, using different portable devices to be able to test them will really propel the research forward, Sarah. As those results are starting to come out, I think it'll probably be in the next year or two that we'll be able to see some results and be able to start to translate those into clinical practice. Well, that's fantastic. We've been talking about this for a while, so it's good to see it progressing through. Exciting. It's really accelerated in the last couple, three years. Yeah, for sure. I don't see any questions. I'm not sure if I'm missing anything on my screens. I'm working two computers here trying to figure out all this technology. Here's one question for Dr. Royberg. Should neurosurgeons advocate against sports where head injury is common? What are your thoughts? I think that's a really personal choice. I think the better thing for neurosurgeons to do in the community and in the public discourse is to really educate and talk about what the risks are so that people can choose to participate in sports that have significant risk or not, and that they can take steps to protect themselves. I think that's reasonable. I'm going to combine a couple of questions here. What do you see as the most important test or most promising biomarkers coming down the line? I think what I'm most excited about the DTI studies that are being done because I think those have shown some significant findings that have enlarged cohorts of athletes compared to normal controls or uninjured controls, and also control groups that have similar exposures in contact sports, but no definite diagnosis. Correlating that with clinical trajectory over time will be important. The more we understand about the white matter changes and the axonal changes on those images, the better we'll be able to counsel people. I'm really most excited about the imaging and DTI studies in particular. One last question. Do you think the cause of CTE is fundamentally ischemia or inflammation? I don't think I know enough about that pathological process to understand it, but certainly because of the areas that are involved in that pathological diagnosis of CTE and the hippocampus and other parts of the temporal lobe, which are most susceptible to ischemia, one has to assume that there is some ischemic component to that, but I don't think that we know the answer to that question yet. Great. Well, thank you so much for joining us today and congratulations on being named this lecture. It was an honor to have you here. Thank you, Sarah, and thank you, Joe. Appreciate it. Great. We're going to move on now to the complex case discussions. I'm going to introduce Dr. Shaw, who will be moderating the next three cases for us. Hello, good afternoon, everyone. I'm Kushal Shaw from the University of Kansas. Appreciate everyone tuning in. We've got three great cases and three great speakers today talking about complications and complex case discussions in neurotrauma. I'll introduce the first speaker, which is Dr. Ryan Kitagawa from UT Health. He's an assistant professor there and he did his residency at Baylor University and then did a fellowship at the University of Miami on neurotrauma and critical care. He's going to be discussing a complex cranial neurotrauma case today. Well, thank you very much for the introduction. As he said, my name is Ryan Kitagawa. I am the director of neurotrauma at UT Houston Memorial Hermann Hospital. I have no disclosures and I'm going to be talking about one of the cases that happened very early in my career that really informed my decision making moving forward. This is an 18-year-old female, status post multiple gunshot wounds throughout the body, including the left face. Upon the neurological examination, there was an obvious left face and eye injury. The right pupil was reactive. The patient was localizing on the left with no movement on the right. In terms of what the next step is in moving forward, these patients in general need to be resuscitated. The biggest issue is in this particular patient, there was 11 different gunshot wounds scattered throughout the body. Obviously, those that affected her hemodynamic status are the ones that should take priority. The patient was resuscitated. A chest tube is placed. Once hemodynamically stable, we move forward with our management of the patient. All other injuries were superficial and orthopedic in nature. Therefore, the most significant was the chest as well as the brain injury. Here we see a CT reconstruction of the skull as well as the entrance wound that we see here. What we see across here, I'll show you several of these studies. Obviously, we want to know what the next step is. We'll go ahead and switch over to the Slido function. I'll read these to you as we do that. What is the next thing that we're going to do with this patient after they've been resuscitated? Is it ICP monitor placement? Is it non-invasive vascular imaging like a CTA? Do we do informal invasive studies such as an angiogram? Do we proceed forward straight to the OR for decompression or do we admit the patient to the ICU for further resuscitation? We'll go ahead and take a minute to see how our audience feels about this. So, it seems that everybody feels strongly about non-invasive vascular imaging, and indeed, that is how we proceeded. Now, a lot of the questions that I'll be going through show what I did in this particular case. And as we'll discover in most penetrating head injuries, you know, there isn't a great amount of literature to guide exactly what the next step is. Now, I've worked very hard at my institution to make it basically protocol. When any patient has any sort of penetrating trauma to the head, when they go to the CT scanner, it's automatically a CT angiogram and a CT venogram to help guide our therapy moving forward. So, here is the vascular imaging. And what we see here is a concern for active extravasation, as well as a potential for an aneurysm within the proximal left ICA. And so, now we know that there is a concern for a vascular injury. What's the next step? We'll go ahead and switch over to the Slido. But do we proceed to the OR for decompression, as well as clipping of the aneurysm? Do we go to the OR, decompress the patient, and then postoperatively go for angiogram? Do we proceed with angiogram to treat the aneurysm first and then to the operating room? Should the patient have an ICP monitor placed and then go to angiogram? Or should they be admitted to the ICU for further resuscitation? Let's go ahead and see what our audience feels about this. Okay, let's see, we're getting a few more answers as we come along here. So what I actually did under this circumstance is the patient went to angiogram for embolization and then the OR for a decompression. Several things about this particular case, the first of which is the imaging studies and the clinical exam was not consistent with overt herniation. And therefore, in this situation, I think we have a little bit of extra time in order to treat the aneurysm. My own experience with post-traumatic aneurysms and penetrating trauma specifically is that managing these aneurysms with clipping is a big, big challenge. They don't behave as they normally would. The walls are very thin, they tend to rupture a lot. And in addition to that, the severe degree of cerebral edema can make it very, very challenging to get access, particularly if they're proximal lesions and not more of the distal MCAs that we see fairly frequently. In this particular case, it actually went extremely quickly in that as the patient was being resuscitated in the emergency room, the IR service was coming together. We have an angio suite that is a hybrid room, and then we're able to convert that immediately to surgical intervention, and therefore it happened very, very quickly. So in my practice, I always am prepared for pseudoaneurysms. Every patient gets noninvasive vascular studies. If there is a lesion, we tend to try to treat the pseudoaneurysm first, particularly if there aren't obvious signs of cerebral herniation. We have a hybrid suite. Now, an alternative would be to go in and be prepared to clip the lesion, but in our particular case, we proceeded forward. Now, the aneurysm was successfully coiled. Now the next step is if we are going to proceed with a decompression, which one of these surgical options would you proceed with? Would you proceed with sort of the traditional reverse question mark incision? Would you do the teed-off incision, like the military style? Would you do a three-quarters coronal incision with a tee-off there, or would you do a terrional incision and teed-off posteriorly? So let's see what the audience thinks. If we could go to the Slido. Doesn't look like we're able to do it via this type of question, but I actually used the third option along the way. Based on the preoperative imaging studies, you know, the frontal sinus is blown apart ipsilateral to that. It goes through the face, and it's something that will likely need to be addressed, the timing of which is something we will discuss. And so in order to be able to do a hemicraniectomy and later on be able to do a bicoronal incision, this is the incision of which I chose. You can do the traditional reverse question mark incision. You really need to cheat anteriorly and then remove the bone from underneath there because when you lay the patient in a supine position to convert to a bicoronal, it can be quite a challenge if the incision is very, very far posteriorly. So the aneurysm is coiled. This is our incision. What kind of surgical intervention would you do? A craniotomy with an aggressive debridement, a hemicraniectomy with ventriculostomy, hemicraniectomy with frontal temporal lobectomy, craniotomy with cranialization of the sinus, or a hemicraniectomy with cranialization of the sinus? Why don't we go ahead and see what our audience feels about this? So which are you going to do? Are you going to put the bone back on? Are you going to address the sinus during the immediate concern or do we just need to get out of the operating room? Okay. It seems to be 50-50 between just a simple hemicraniectomy as well as the cranialization of the sinus. Now, in this particular patient, I proceeded forward with the hemicraniectomy with ventriculostomy placement. Now, in general, when you're dealing with penetrating trauma, particularly if it's an entire hemispheric lesion, a large bony decompression and a small amount of debridement specifically for hemostasis and to remove the fragments that are immediately underneath the surface and accessible is sort of the standard of care these days. Now, in terms of the timing of the cranialization of the sinus, it can be very, very challenging to do this particular kind of complex skull base operation when the brain is obviously very swollen and in the end, the decision was to get him out of the operating room. Now, I do address the sinus during the first operation in that you do want to get a temporary closure to this area utilizing things like gel foam, utilizing things like pieces of the temporalis muscle, placing dura product into in order to seal that off. The only thing that I don't mobilize at this stage is the pericranium. That's something that I want to preserve for my definitive treatment. So I mobilize the pericranium and then tack it down again at the end of the operation so that I have it available for that. So you can see the patient's postoperative imaging. So what kind of antibiotics are we going to use for this particular patient? Let's go ahead and go to the Slido while I talk about each one of them. So number one, none. Number two, your standard postoperative, you know, one dose before incision and one day afterwards with Cefazolin. You're going to extend that with Cefazolin for a week. You're going to use broad spectrum for one day or you're going to use broad spectrum for a week. So let's see what our audience has to say. So we seem to be kind of at various ends of the spectrum, meaning that many would use just your traditional postperioperative antibiotics versus otherwise would go broad spectrum for an entire week. In this particular patient, I did broad spectrum for approximately a week. You know, my antibiotics regimen for these tends to be tailored in a very specific fashion based on how dirty the wound is. In this particular case, it's going through some of the major sinuses. One of the sinuses is actually open and exposed as a result of the trauma. Those are ones where I tend to do the more traditional style of broad spectrum for an entire week. Now, if the patient has just an isolated gunshot wound, they are awake and alert, a mild TBI. You debride it, you wash it out, you close it up. You know, my practice these days is just sort of your standard. So I do it based on the particular method of injury and hopefully we'll have more information at that. You know, as we start wrapping up our talk, there's several other questions along the way. So I will forego the Slido and sort of talk to you about what I did in particular. So screening for pseudoaneurysms. You know, I always screen for pseudoaneurysms. I don't wait for the full six weeks. Now, whether you do it with noninvasive or angiograms sort of depends on your particular institution about the availabilities of angiograms. In general, I usually do a CT angiogram at about one to two weeks. Based on that, I decide, do I need an angiogram? If there is a lot of scatter artifacts from bone and from bullet fragments, I forego the noninvasive and instead proceed forward just with the angiogram. In this particular patient, they're found to have a recurrent aneurysm on CTA, which allowed the endovascular team to plan ahead and treat the patient in a more controlled fashion. Despite that, it was treated with endovascular repair, but did have an intraoperative rupture. They were able to embolize the whole of the aneurysm over the process of the rupture, but this is kind of what the imaging studies that resulted from this. As you can see, a massive hemorrhage within everything, and we're left with this very big challenging problem of this massively swollen brain. When you're dealing with this, it's the usual stuff, and this is important for the board exams. Elevate the head of bed, improve their venous return, hyperventilation, hyperosmolar therapy, intraoperative EVD, but in this particular patient, there's a large ICH. As a result of the large ICH, it's best to go in and to evacuate that lesion. Of course, when do you cranialize the sinus? In this particular patient, I do believe cranialization is necessary because it's penetrating trauma and there's a large defect. I do think it can be repaired in an urgent but not emergent fashion, so certainly prior to discharge is when I repair this particular lesion. This was the order of things, cranialization followed by cranioplasty followed by shunt. The patient did return eight years later with a seizure and a fever. What you see here is actually evidence of an intracranial infection. We performed a craniectomy and took cultures, and those cultures did demonstrate staph aureus. Where did that come from? Based on all of the information that we can glean was that there was probably a small communication with the sinus as a result of the cranioplasty that was abutting right against where the sinus repair was. We did the craniectomy washout. We did antibiotics for three months, six weeks of IV and six weeks of oral based on the ID recommendations, and this time we performed the cranioplasty but left a significant amount of soft tissue between the edge of our implant and the actual repair itself. So I will stop there. Thank you very much for that talk, and we're going to hold off on questions until we're done with all three complex case presentations. Before I introduce the next speaker, I just want to remind everyone, if you're on the web browser on the right side, there's a little box for Slido where you're able to answer questions as the speakers are presenting them in their talk so that it can be interactive, and as you saw, we'll show the results during the presentation as well. So our next speaker is going to be talking about spinal trauma. I'm going to introduce Dr. Anne Parr. She's an Associate Professor at the University of Minnesota. She is the Director of Spinal Neurosurgery there. She did her residency at the University of Manitoba and the University of Toronto, and then did a Complex Spine Fellowship at the University of Miami, and she is going to be discussing a complex spinal trauma case today. Anne, thank you very much. Yes, thank you for asking me to speak here today. I think this is like quite a switch from the previous case. I'm going to be talking about thorax or lumbar trauma, and I think it really does also show or exhibit the breadth of trauma out there and what all the different skills that you need as a trauma surgeon, as a trauma neurosurgeon, and so this is a recent case we had. I wanted to use something that was fairly fresh, and I thought this was particularly interesting, so this is a case borrowed from one of my colleagues, Dr. Stephen Kim, but I thought, again, that it was particularly interesting, and I know that the residents really had a lot to discuss as well, so I'll include some of that discussion during this talk. So, I can't advance the slide. Let me try. Oh, okay. So, this is an 87-year-old female. She lives in assisted living, but she's doing very well, has no real medical comorbidities beyond she has osteoporosis, quite severe, and ankylosing spondylitis. So, she had a ground-level fall one week prior to presentation, so she's ambulatory, and she's a walker. She's totally neurologically intact, but she's had persistent back pain since the fall, and so she presents to the emergency department, and so here's her injury. So, you can see a couple of things here. First of all, on the left side of the screen, you can see the CT scan, and you can see that she clearly has an L1-2 fracture, and it's these. I'm trying to show you here that it's actually a three-column injury. You can also see that she has quite a bit of sagittal imbalance on the images on the right side. So, my first question, and I don't know if you can go to Slido or not, but this is one question, is an MRI really necessary? Because a lot of times when trauma patients come in, they get an MRI for this, and we were asking the question, is it necessary? Yes, no, or is there any other kind of other imaging? We did CT scan and regular x-rays when she presented. So, I don't see the Slido up, so I'll just tell you what we did, and you can just think about these questions. So, in this case, we did not do an MRI, which is a little surprising maybe, but our reasoning was that she was neurologically intact, first of all, so she had no signs of neurological injury. We were worried that it would delay surgery, although remember, she was already one week out, so that was less of a concern. But we were more concerned about manipulating her on the MRI table, further manipulation, and would an MRI really change your decision-making? Because this is really a stabilization procedure, that's how we saw it, and efficient use of resources if it's not gonna change your decision-making. And so here are really our management options. And I guess, like I said, I don't think the Slido is working for this. You can text me if it is, but really our options were this. One is to do nothing. This is an 87-year-old lady. She's had a long, long life. She has very, very poor bone quality. We have to ask the question, is any instrumentation really going to hold? Number two is conservative management with a brace. We could try a TLSO brace or another brace if somebody wanted to suggest something else. Number three is surgical. We could do an anterior approach. Number four, posterior approach, and number five is surgical. Anterior and posterior approach. And again, let me just check. Oh, okay, so the Slido is working. Okay, so that's great. Yeah, so it looks like the posterior approach is leading, and that's, in fact, what we did. So this is the final result of what we did. I took some discussion points. Basically, we used fenestrated screws, and we did a T10 to L4 navigated posterior instrumented fusion with cement augmentation that we used through the fenestrated screws. So this was our final construct, and this is her standing in a brace. So we did give her a brace as well, TLSO. And here's some of the things that we discussed. So first of all, the quality of her bone was some of the worst that I've ever seen. We ended up using a ton of cement through the fenestrated screws. Again, we used about four bags of cement. And another challenge was actually the positioning of the patient. And I don't know if anybody has any suggestions or other options, but because of the osteoporosis, basically, we thought the anterior surgery would create more problems with fixation. And also, we thought if we did an anterior first, then positioned her in the prone position that the screws might have ripped out in the front because the fractured area would have gaped open due to the force created by her ankylosing spondylitis. So in order to prevent that, we would have had to place her in a lateral flexed position to insert screws, which can be very challenging. So at the end, we spent about two hours, our residents spent two hours with Dr. Kim trying to position her on the Jackson table. We had the pro-axis table fully flexed, Wilson frame, gel rolls with blankets underneath, and everything trying to close the fractured gap. And everything failed. So what we ended up deciding to do is to put the patient on the Jackson table, insert the screws, and augment them with the cement. And then we closed the wound and then placed the patient in the lateral but fully flexed position, almost like doing an LP. So the patient was in sort of a fetal position and reopened the wound, placed the rods in that position so that we could then close the gap. And then I put this in as also as a Slido if anybody would have not used the cement or if they didn't think it was helpful. And that's it. So I think, yeah, so I think we're back on time. Dr. Parr, thank you very much. And it's nice to know that the Slido is working. So thank you to those of you who are using the Slido on the right side of the screen. Our last complex case discussion, I'd like to introduce Dr. Kim Harbaugh. She is a professor of neurosurgery at Penn State University where she acts as the chief of the Division of Peripheral Nerve. She did a residency at Dartmouth and did her fellowship at LSU. So today she's gonna be presenting the complex case specific to peripheral nerve. Kim, thank you very much. Thank you, Dr. Shaw. It's a pleasure to be here. And yeah, I just wanna present not a terribly complicated case, but it has some interesting clinical twists that I think highlight some of the difficulties that we run into when we're handling these cases. I work with Dr. Rizek and this is actually his case. So our case is a seven-year-old who was driving her snowmobile around her family's property and managed to go over a 10-foot embankment. As you can imagine, she had significant left lower extremity trauma and at the scene had no movement below the knee. She came into the hospital and had these fractures. So you can see she's got a very complex set of fractures. She's got a tibial plateau, sorry, go back one, tibial plateau fracture, mid-shaft tibial fracture, tibial fracture. So these two could give you a combined tibial and perineal fracture, but then she's also got this horrible displaced femur fracture with a laceration both anteriorly and posterior, so a compound fracture. And the fact that she had zero motion made us think that this was probably the femur was the main, the sciatic nerve was the most likely location for the injury. Not that she couldn't have some additional injuries downstream, but the fact that she had no gastroc motion made us think that it was probably a pie. So the first issue is always a localization of the nerve injury. So our orthopedic, or the orthopedic team that saw her, took her to the operating room, washed out her wound and managed to get her stabilized. And so that brings us to the next question is, what do you do as far as, when do you intervene? And we know we have this great classification scheme that SEDN developed with neuropraxia, axonamnesis, and neuramnesis. In the first category, you don't operate. This last category, if you don't operate, they're not going to get better. And then you have everything in between with the nerves in continuity, but has varying degrees of injury. And so the issue is always like, when do you jump in? If you operate on somebody who's going to get better on their own, you typically, if you have to graft, are not going to give them as good a result. So the first Slido question is, what's the SEDN grade for this? Neuropraxia, axonamnesis, neuramnesis, combined injury, or unclear. And I don't know if we got the Slido there or not. And if not, that's okay too. Oh, there we go. Give that a second. And the issues from as far as the thought processes go, yeah, we thought that basically it was unclear, that you really don't know for sure, right? Patients don't come to your office saying, I have a neuropraxic injury. So a lot of the times these classification systems, until our imaging systems catch up to us, you don't really know for sure. So it's a matter of kind of watching and waiting and using some of your clinical acumen to try and decide what you need to do. We know the rule of threes. If someone has a clean, sharp laceration, glass, knife injury, something like that, that you want to get them operated on within three days or so. If it's a chainsaw injury, blunt laceration, that kind of thing with a bad, dirty wound, you want to give it a couple of weeks so the nerve can kind of declare itself and you're not connecting macerated nerve edges together. But then a lot of these injuries are these injuries in continuity where you're going to have to wait three to six months to get a sense of, is this a grade two, sudden sunderland injury where it's going to get better on its own or not. But if you wait too long, obviously you're going to get into trouble and you're not going to get any recovery. So it sounds straightforward. You do serial examinations, you do EMG studies and you do imaging, but you have to kind of picture in your mind this little kid who comes back to the orthopedic guy's office with a long leg cast. So an examination in this situation is her telling him that, oh, I think I can feel tingling on the top of my foot, but I don't have any motion yet. And that was sort of the degree of her examination. So in his mind, it's like, well, maybe the nerve's coming back. So he kind of watched her for a little bit. She ultimately got her cast off. And with that, he was able to send her for an EMG. And she had an absence of both her sensory and her motor nerve action potentials. She had no voluntary motor units in either the tibialis anterior or the gastroc. So obviously it looks really bad. But again, this is a little kid. She's not tolerating the needle exam at all. They wanted to sample the short head of the biceps to try to really pinpoint the localization above the knee and that sort of thing. They just couldn't do that. So the electromyographer sends a note back to the orthopedic guy saying, oh, just send her back to me in three to 12 months, and maybe we can figure out what the prognosis is. And obviously, as we talked about, that's kind of the wrong thing. You're not going to want to wait 12 months to operate on somebody if they're having this bad of an injury. Well, what about imaging? High definition ultrasound, I think, is going to be a game changer as things go forward. But at this point, early on, she was in a long leg cast, so that wasn't going to be helpful. If they're in the emergency room and you've got these unfixed fractures with edema, loss of normal relationships, things like that, all of these imaging studies can be pretty tough to interpret. She did ultimately, based on that EMG, get her MRI scanned. And of course, the insurance company said, you have to do this close to home. You can't do it at just any scanner. And the guy there reading the study said, oh, the sciatic nerve looks perfectly fine. There's no signal change. There's no mass effect. It looks great. In fact, maybe you should scan her pelvis to try to see what's going on. And it was at this point in the whole management of the case that neurosurgery got involved. So we said, well, we're not comfortable just reading your report. We want to see the actual images. And as you look at this scan, you can see the sciatic nerve coming out between the hamstring muscles here. And then you sort of see the stump of it right here in this callus. Then we thought there was a gap here. And then you sort of pick up the nerve again distally. It kind of where you normally see the bifurcation. And on axial images, that's what you see. There's nerves here kind of stuck to the callus. As you come down, there's this big blank space and then you get to the next part. And this is where you get the bifurcation tibial and the perineal nerves. So in fact, this was a neuromedic injury. And that's very unusual. Most femur fractures, only less than 5% will be associated with a nerve injury at all, let alone having one transected. So it's kind of a no-brainer, right? You've got a neuromedic injury. Ideally, this would have gone to surgery at three weeks, at about three weeks or so, but we're seeing her not at three weeks. In fact, we're seeing her over a year out from her injury. So then the second question comes up, do you do a tendon transfer? Do you nerve transfer? Do you do nerve graft repair? Do you fuse the ankle? Or nope, sorry, there's nothing to do that's too late. So this is kind of the next slide. I'm kind of curious to see what people in the audience would do. Give that a little second. And if it's not working, we can kind of move on and make sure we get done in time. Oh, there you go. A little bit of time. So our logic was that, well, she's young, so she's got time on her side. There really isn't a good tendon transfer that you can do in this situation. If it's an isolated perineal nerve palsy, you can do a tibial transfer, but you can't do that. Nerve transfers, you're gonna be trying to take something from the femoral nerve or whatever. That's really not gonna be ideal. Even though it's a high level injury and she's got a gap, we thought that she had a good chance of getting her gastrocs and her soleus back. And equally important, we thought she could get some sensation back to the bottom of her foot, which is gonna be critical going forward to make sure she doesn't get chronic alterations, osteomyelitis, and potentially amputation, which I've seen in the past. So we definitely offered surgery. When Dr. Rizek triggered the surgery, you saw exactly what you'd expect to see. The proximal stump was stuck up into the bony callus up there. And then the distal stump down by the bifurcation was way down here. These cases are important that you cut back to healthy nerve. It's very anxiety producing because you've already got a gap and you know by making the gap longer, the chance of recovery is even less. But it's really important to make sure you do that. Otherwise you're just creating a Sunderland grade four injury. So you gotta cut back to healthy nerve. He was able to take a seronerve graft and he was able to find a piece of the posterior femoric cutaneous nerve to create, to bridge this gap that was about nine centimeters at the end. So how'd she do? At three years, she did pretty well. She got four over five plantar flexion back, which is what you want. Not much in the way of inversion or dorsiflexion and no eversion, but she did get good sensation at the plantar foot. And she's able to ambulate independently in an orthotic. She had some limb length discrepancies and things like that, but overall she had a fairly good recovery. Was it as good a recovery if we had gotten her three weeks? No, clearly not. I'm sure the gap would have been much smaller. We might've even been able to get an end-to-end anastomosis, but we didn't. So as far as the conclusions with these traumatic injuries, you have to have a high level suspicion to look for these very unusual nerve fracture associated nerve lacerations because you wanna get those early if you can. Most of these are gonna be nerves in continuity. So you're gonna watch, but if they're still have these dense deficits, you don't keep watching them. You gotta get them to surgery if it's in that three to six month period. Ideally, I would like to image people at like three weeks or so that gets you over that acute stage with all of the hematoma and that sort of thing, and then do monthly examinations. And I usually delay the EMG till later, till it's closer to the time where it's gonna change my decision-making to look for these voluntary units. I think the most eye-opening thing for me on this case was the fact that we are doing a very good job as a peripheral nerve group in educating referring physicians in public. There are multiple times along the way where she should have been referred early and she didn't get sent in. So we need to get the word out for that and avoid that wait, wait, wait, up too late kind of situation. Thanks very much. Dr. Harbaugh, thank you very much for that interesting case. And I'm very glad that this young patient was able to see you and your team so you could help her, even though I know you wish you would have met her months before you did. So I just want to take a few minutes and answer any questions. I don't know the best way to have our speakers back for these questions, but Wesley Fowler asked, does literature support the use of a TLSO? And this is for Dr. Parr in her complex spinal case. I'm not sure if there's a way we could get our speakers back on to answer a few quick questions. I think we're having a little bit of technical issues getting all of our speakers back in here, so I apologize we won't be able to take any questions today. But I'd like to once again thank our three speakers who prepared great cases Dr Kitagawa, Dr Parr, and Dr Harbaugh. Thank you very much. Right. Hi everyone I'm Hanal Gowdas, I'm one of the current chief residents at UPMC. The title of this five minute talk is going to be the impact of COVID-19 and shutdown on neurotrauma volume in the state of Pennsylvania. So we're obviously all well versed with the COVID pandemic and it has caused and continues to cause a significant stress on our healthcare environment and early on during the pandemic. Stay at home mandates closure of non essential businesses really kind of fueled the social distancing and social isolation craze. So we realized that this is really a unique opportunity to allow us to analyze healthcare delivery in the midst of a pandemic so our goal was to look at the impact of the early wave of the pandemic and stay at home and it's on neurotrauma volumes at level one trauma centers within the state of Pennsylvania. So we use the Pennsylvania trauma outcome study which is part of the Pennsylvania trauma systems foundation to look at retrospective data from four years 2017 2020. And we defined an epic between March 12 and June 5, which really in the state of Pennsylvania is when stay at home mandates were enacted and then multiple counties went into a green phase of reopening. So we looked at this epic at four different years and looked at a number of different variables you can see on the right side there, which will further discuss here. So first in regards to presenting features in the injury type that we noticed during this epic of the pandemic. First and foremost, we noted a 27% absolute reduction in neurotrauma volume in the year 2020, kind of contrary to what we originally anticipated we had more intoxicated neurotrauma presentations during the coven index year than relative compared to prior years. There was no change in elicit drug use and the neurotrauma phenotype was really the same. So there was no change in the relative likelihood of traumatic brain injury spinal cord injury spine fracture skull fracture or any vascular injury during the pandemic. And then an absolute reduction in those just based on sheer volume, but no change in the relative numbers. When we looked at the mechanisms and the places of injuries, more often, for which to occur. We noticed increases in penetrating trauma reductions in blunt trauma, going with that, but then curiously enough increases in cases of gunshot wounds falls at the expense of less motor vehicle accidents. And this all kind of makes sense and you can see that in terms of the location of injury as well, more injuries recurring a private establishments rather than public establishments and less so on the roads, which makes sense that people are you know indeed staying at home during this first wave. In terms of outcomes we were looking at within the Pennsylvania trauma outcome study there was no change in neurologic complications, but there was an increase in mortality across the state 7.7% during this index year for coven versus about six and a half percent pre coven, which we did not realize in Allegheny County or so ourselves where Pittsburgh is but you know we can make some judgments on that. In conclusion, you know on the left side we see we noted an absolute reduction in trauma, a similar neuro traumatic phenotype, a reduction in the role of alcohol and a shift away from car accidents towards things like falls gunshot wounds and recreational vehicle accidents with a mortality increase across the state. You know what we can kind of take away from all this is that indeed stay at home man is we're being followed but more importantly, we're looking at, you know, how does society react to a pandemic and this is really the first piece of the puzzle to kind of understand that that problem. So we looked at this first wave of stay at home mandates but, you know, during the period of reopening a lot of surgeons and traumatologists have anecdotally suggested that there have been surgeon trauma numbers, more so than one would expect and really now with the Delta variant is there even something else to consider a look at so one of our goals is to look at the prolonged impact and the neurotrauma climate that the pandemic may have a lot of additional interesting questions to potentially answer here. So with that happy to take any questions if allowed to do so technically. Hello double NS. My name is Anthony O'Connor, a third year medical student working with the Michael lab in the neurosurgery department at Stony Brook. Today I'll be talking about an exciting new analysis of electroencephalographic recordings to evaluate potential for recovery and patients with disorders of consciousness following traumatic brain injury. Traumatic brain injury is a major cause of death and disability in the United States, severe TBI usually results in loss of consciousness at Stony Brook we received 70 to 80 severe TBI cases per year. Typically most of these patients recover consciousness, and our measure of full recovery is that they can follow commands. However, some patients recover quickly, while others take weeks to months, and still 20% never recover. During the comatose phase. There are a few effective measures to assess neurological functional status and predict whether the patient will recover. The question is, what is different in these patients, and how can we improve their outcomes. The first measure for electrophysiological assessment of comatose patients is the ABCD model. This is a coarsely defined model with widely spaced categories that essentially correlates electrophysiological states with degrees of consciousness, thalamocortical connection, and neocortical function. D indicates a complete loss of corticothalamic integrity, and only has signal in the delta range, while D indicates a full recovery of consciousness with signal in the alpha and beta ranges, while B and C represent states in between. Unfortunately, electrophysiological recordings can be noisy, and it can often be quite difficult to make a clear cut distinction and fit each patient into a discrete category for prognostication. This issue of noise is precisely what Donahue et al was hoping to address with their landmark paper in Nature in 2020. A largely overlooked cause of noise and error has been the confounding effect of so called aperiodic components with periodic components in EEG analysis. Aperiodic components include bandwidth. In this example, it's from 8 to 12 hertz in the alpha range. Center frequency is the apex of this peak, and band power is essentially the height of the peak over this baseline. Aperiodic components include the aperiodic exponent, which is the slope of that baseline, and the offset, which is its y-intercept. Here you can see how an algorithm may assess all four of these images as a reduction in band power, when only the image at the top left is a true reduction. For example, the image at the top right is a broadband shift which shifts the entire power spectrum down, but this can be mistakenly assessed as a reduction of band power in the alpha range, and the same can be said for exponent changes and frequency shifts in the images at the bottom. So what we did in this example created an algorithm for fitting power spectrum with aperiodic and periodic parameters, and in controlling for aperiodic background, validated their function with resting and event related working memory tests in their study of aging. So we use this algorithm for a different purpose. Our project was a retrospective study of 17 patients that presented a Stony Brook University Hospital with severe TBI. The TBEG was extracted from these patients with minimal sendation and analyzed. Frequency analysis was broken down into periodic and aperiodic components using the Donohue et al model, pictured here in this black box. The graph on the left hand side is an example power spectrum that was then fit to determine aperiodic and periodic components as you can see on the right. The k-means clustering of our data revealed two distinct clusters. In this graph, each of the axis represents a band power range of alpha, theta, or beta, and each data point represents the respective band powers of a single patient controlled for aperiodic background. Poor outcomes have a bold outline, good outcomes have no outline. Predicted poor outcomes are colored red and predicted good outcomes are colored green. As you can see here, we achieved a relatively high sensitivity of 87.5%. However, this result was not evident when the data was the whole EEG signal spectrum that was not controlled for aperiodic background. On this slide, the x-axis of each graph represents a favorable versus unfavorable endpoint, an outcome which was the ability to follow commands after 90 days. You can further see here that when we control for aperiodic background, the leftmost graph of data shows a significant difference, while the whole EEG signal adjacent to it shows no such significance. You can see a similar trending for beta signal, which did not achieve significance. In summary, we have shown that controlling for aperiodic background can have a significant impact on the analysis of electrophysiological recordings of patients who suffer from TBI and can be a tool for prognosticating recovery of consciousness in comatose patients. I appreciate the privilege of presenting here today. I could not have done this without the help of my mentors, Drs. Mofakam and Michael. Thank you so much. Good afternoon. My name is Aaron Yango-Khan. I'm a six-year neurosurgeon resident at Vanderbilt, and I'm grateful for the opportunity to present our work titled The Neurosurgical Care and Outcomes for Pediatric ATV and Dirt Bike Crashes, and it's our 10-year experience at our Vanderbilt Children's Hospital. There's no relevant disclosures. I do serve on a scientific advisory board that had no role in this project. ATVs and dirt bikes are a major cause of injury, especially for younger children. Over 100,000 injuries per year in all comers and greater than a quarter of these are in children less than 16 years of age, and there's 16% of all fatalities occur in this age group. Most of these kids are engaging in risky behaviors, riding without helmets, riding with passengers in unofficial seating arrangements, and most importantly, neurosurgery-specific data is infrequently updated, although we see many of these injuries. So the objectives of this study were to better characterize the spectrum of neurosurgical injuries related to ATV and dirt bike crashes and to describe the effectiveness of helmet use in preventing these injuries over a 10-year period. Helmet use, we hypothesized, would be associated with decreased rates of intracranial injuries and reduced needs for neurosurgical intervention. We conducted a retrospective cohort study. We included patients that we saw, that our trauma team saw, between January 2010 and December 2019 at our Pediatric Trauma Center. Patients with unclear helmet status, meaning it wasn't documented in the chart, or competition-related injuries were excluded. Our exposure of interest was the helmet use at the time of the injury, and our primary outcomes were the need for a neurosurgical consult, the presence of intracranial injury, and then whether or not they had a moderate or severe TBI defined by GCS 3-12. Our secondary outcomes, we looked at the length of hospitalization, the need for neurosurgical procedures, and the Glasgow outcome scale follow-up. We ended up including 680 patients. 66% of them did not wear a helmet. 94% of them had just a mild traumatic brain injury, whereas the other 6% had moderate or severe. And you can see that those that were not wearing helmets were older, more likely to be female, and more likely to be riding on an ATV, and passengers were very infrequently helmeted. And then if you notice here that those that weren't wearing a helmet had slightly less severe mechanisms of injury that led to being in the hospital, such as having a higher incidence of rollover accidents. So we used these significant differences in demographics and injury characteristics as covariates. So looking at our univariate analysis, we found that unhelmeted riders more frequently received head imaging, 70 versus about 50%. They more frequently received a neurosurgical consult, almost twice as likely. They more frequently suffered skull fractures by a wide margin and intracranial hemorrhage, and they received more neurosurgical procedures. And it's important to point out that only one neurosurgical procedure was performed on a helmeted patient over the entire 10 years. After accounting for age, sex, vehicle type, driver status, and mechanism, we found that helmet use was associated with 75% reduced odds of neurosurgical consult, 83% reduced odds of intracranial injury, and 76% reduced odds of suffering a moderate or severe TBI. We did not find any difference in the length of stay. The length of stay was short for both groups, a median of two days, and we did not find any difference in the Glasgow outcome scale follow-up, where 98% had a good recovery and minor deficits, GOS-5, in both groups. So, in conclusion, two-thirds of injured patients were not wearing helmets. Helmets are clearly effective, and that continues to be panned out in the data. And this data can be used to support public health efforts and encourage helmet use. We can say things like one brain surgery over 10 years in children wearing helmets, or only four children need to consistently wear their helmet over 10 years to save one intracranial injury. And hopefully, in the future, we can do more granular analysis and look at how helmet use and ATV accidents can save school days missed and improve neurocognitive outcomes for the mostly mild TBIs that we see. Thank you. Thank you so much, gentlemen. Unfortunately, I think we're missing one of our speakers who signed off a bit early, but I'm trying to leave the floor open to the audience now to see if there's any questions. First of all, congratulations to both of you who are on. Your abstracts were chosen at the top of all the ones submitted for neurotrauma, so you're all to be congratulated on that very impressive work in body of water. I'm just keeping an eye on the screen here to see if we've got any questions popping up for me from the audience. One question came in from Dr. Shah for the last speaker. Did you look at the types of helmets that were perhaps used, like a full motocross style versus a bike type or anything like that? So we collected that data when we could, but unfortunately, it's extremely sparsely populated in the chart. And so with the retrospective nature, we're limited by what we could reasonably figure out. Usually, they would just say helmet, unfortunately, in the records. So that's a great point. Yeah. And where do you go with this data next? I mean, obviously, it's something we all know. You wear helmets to protect your noggin, but how do you think? This is one of those projects that the answer is obvious. We knew what we were going to find going into it, but it's a matter of saying every some amount of time, we need to readdress the question and make sure they're still doing something. Now that we have this, we're actually working on doing an analysis by geolocations and where these patients are coming from to see if there's any signal in the noise where we can go to different counties and say, we really need to do helmet education here. We need to reach out to parents. We need to get in the schools and say, even if you're a passenger on ATV, for example, which only about 90% of passengers were unhelmeted. And so that's a really clear area of intervention. So this is kind of pointing out the problem and the solution, and now we just need to apply the solution at a county-by-county, individualized level. Yeah, great. Let's see if I think we may have another question. Oh, someone's asking, are there regulations or laws about helmet use for children on ATVs or dirt bikes in some states that you're aware of? Yes. So in Tennessee, a helmet is required for all riders under 18. And so you'll notice that 66% of our patients were technically breaking the law by riding without helmets. And so even though that we have these laws, we're clearly not able to enforce them very well. Most of these kids are getting injured on their own land, riding their own ATVs, not on public roads. And so it really needs to be down at the individual parent level and community level where people are recognizing that even if you're just riding around the yard on the ATV, you probably should put a helmet on and spare yourself the hospital admission. Yeah. Sorry, I cut you off there. You know, there's certainly laws on many different aspects of ATV and dirt bike riding in Tennessee where the study was conducted, but rarely followed, it seems. Fair enough. There was a question by Yves Sai, but unfortunately it's for the speaker who's already left, signed off on it. So we will have to defer that one for now and perhaps talk about later on in a more general session. Okay, in the interest of time, I think I'm going to close this down for right now. We're going to be taking a break for about half an hour and then we will be back here at 4 p.m. Eastern time to continue on with some discussions on concussion as well as some great debates and our final Marmaroo lecture at the very end. So join us again in about half an hour. Okay, welcome back. This is the neurotrauma session and we're about to begin Advances in Concussion Management and Return to Play panel discussion. Ken Blumenfeld, I'll be moderating. We have three very distinguished and renowned speakers. I would ask that we reserve our questions to the end so we can have a robust discussion. And with that, I'd like to introduce our first speaker, Dr. Alan Sills, Concussion Reduction Strategies. Thanks, Ken. I'm going to go ahead and share my screen here. Hopefully everyone can see that. So I'd like to touch on just a few concepts of what we've done in the NFL around concussion reduction strategies. And I have no relevant disclosures to this. First and foremost, what do we have in the NFL that's at our disposal to attack this problem? We have a large resource of data sources. So we obviously record every concussion, both from our game day personnel. Also, we have recording of the exact exams done and what we call a C3 logic system. And of course, we have video. But then we can combine that with a number of different statistical measures with player participation data. We've got GPS tracking data. We've got equipment data, surface data, and all that gets put into our electronic health records and can be excerpted in conjunction with our epidemiologists and our bioengineers to give us a really comprehensive look at who's being injured and how they're being injured. And so just to cut to the chase of this, I think as we look at an injury reduction strategy, we've sort of looked at it from three different aspects. One is equipment and the infrastructure of our game. Two is around rules and how the game is played. And then thirdly, around education. So sort of diving into that, let me start with the punchline, which is this does work. If you look at this slide, in 2017, we had an all-time high in terms of concussions that were suffered overall in the season. Regular season game concussions were our second highest ever at 178. And we really targeted this and said, you know what, we're going to go in and try to make a targeted reduction of concussions in NFL games and practices. And we were able to do that. If you'll see these game data over the last three years, we've had a sustainable decline in concussions. And that's been around some key rules changes, but also some equipment and other teaching issues that I'm going to outline for you here. So we started by really analyzing on video exactly the nature of these injuries. We have analyzed every concussion in the NFL over five years to say who was being injured, how were they being injured, what was the contact point, what was the point on the helmet, what was the type of play, and really mapped all of these 150 variables against every single one of those concussions. And in doing that, we were able to understand a lot more about the body parts involved, a lot more about the technique that was involved, and again, a lot more about the equipment that was involved. We also reviewed 100,000 non-injury impacts to look at the differences in all these variables. And from that, our engineers were able to note some important trends. First, who's being injured? This is a slide suggesting that it's our linemen, offensive linemen most particularly. And you can see it's not just a problem in games, but it's a problem in practices as well where offensive linemen are being injured. And a lot of this data now has led to more advanced equipment changes. We've also been using instrumented mouth guards to supplement this video database. You see in the center of the screen here a typical mouth guard. We've been able to put sensors within this mouth guard to actually, again, measure direction force and total impacts and understand who's being hit and in what manner. And the data from the video plus these instrumented mouth guards has actually led to the development of the first position-specific helmet. This year, the one you see on the bottom right is an offensive lineman-specific helmet that's being marketed. And it is reflecting the fact that offensive linemen tend to have these impacts in the front of the helmet with this sort of face-to-face, head-to-head contact as they initiate blocks. So further beyond that, our engineers, as they looked at all these concussions, noted the posture plays an important role. And on this slide, you can see that as you pitch over and assume this posture where the back's parallel to the ground as this person's tackling and initiating contact, dramatically increased risk of concussion injury and also neck injury. No surprise to us as neurosurgeons when you get these axial forces. And so all of this work between the sensor data and the biomechanical video analysis led to us to change a rule around lowering the head, making it illegal to lower your head and initiate contact in the lead. We've started calling that foul over the past couple of years if you watched NFL games. And you can see that this behavior is decreasing. We measure and monitor that, and we can see fewer of these types of impacts. They're certainly not gone, but now everyone recognizes that posture at the top right of the slide is not the way that we want to be contacting. We're trying to get towards this more upright posture for not only tackling but also for blocking behavior. And again, some of the things that we revealed from this data was it wasn't just the person who was being tackled, it's the person who is doing the tackling that tends to be injured. Here you can see up to five times the injury risk of the person doing the tackling when they lead with the head or the head is the first point of contact. So a big point of emphasis on education has been this isn't just about the person getting hit, this is a risk to the person doing the tackling. And again, we've tried to work with coaches and others to fundamentally change that behavior. We've also worked a lot on the helmets themselves. Many of you are familiar in the NFL with our helmet testing methodologies. Again, we've taken all of this data from these video reconstructions and gone to the lab and created models that test helmets under the same conditions that we have for NFL concussions. And from that, we rank helmets. As you see on the right-hand side of the slide, we rank helmets from best performing to worst performing. And you can see a dramatic trend over the last six years in the league where green are the highest performing, dark green, red are the below standard, ones we've actually outlawed. And we've gone from where only about half the league in 2015 wore a good performing helmet to last year, all but one player in the NFL wore one of these top performing helmets. This is a remarkable story of adoption and of education, but we think it's also contributed to this drop in concussions because better equipment is certainly protective. We have to also at the same time say better helmets don't mean use your head as a weapon. The idea is not that you can go out and weaponize your head because you're wearing a safer helmet. It's much like having a car with good airbags and anti-lock brakes and so forth. Those safety measures are protective to a point, but you still don't want to put the car in a dangerous situation to start with. And thankfully, we've been able to correlate how helmets perform in the lab with how they do on field. We tag every helmet with an RFID chip. And so we know that those helmets that test better in the lab actually show lower on field rates of concussion, which has helped us, I think, with this adoption. And just this summer, we've made a renewed emphasis on helmet add-ons, the so-called guardian cap. You'll see these plastic shells, protective shells, foam shells that go over the helmet. We emphasize that our testing did reveal that they reduce force by about 10%. And so we've been emphasizing that and we have a number of our clubs that are using them, if you're looking at preseason practice footage this year. So we've still got more work to do. We're really focusing now on blocking techniques and mobile blocks, how we can not only reduce concussions, but also the frequency of head impacts. And I think that's going to be our next big frontier is not just focusing on concussion reduction, but actually how can we study and measure the number of head impacts and reduce those as we go along. So a lot of work to be done here. Again, it's a very collaborative effort, not only between our physicians, but our bioengineers, our statisticians and epidemiologists, but most important, our coaches and our players themselves, who are really active participants in this work. And I do think that we're seeing a new era in football and we're going to continue to see this evolve because I think everyone wants to see this type of head contact continue to go down. And as we're able to quantify it, measure it with these instrumented mouth guards, I think we'll see that reduction continue to occur, which will obviously translate into fewer concussion injuries overall. So I'm going to stop there and toss it back to you, Ken. Thanks. Thank you for that, Dr. Sills. Our next speaker will be Dr. Joseph Maroon. He will be speaking on the role of biometric monitoring for concussion management. Dr. Maroon. All right. Let me just share my screen here. And sorry. So when I first got into neurosurgical sports medicine quite a few years ago, we recognized concussions as primarily loss of consciousness. And then we realized there were different phenotypes than subconcussions in 212. And then what Alan was talking about, biometric monitoring, to determine really in terms of the subconcussions, the number of hits, the forces of the hits, and is it possible to have a dosimetry badge, so to speak, for concussion management. So we all know the HISS system was introduced in 2000 or so with accelerometers placed various positions in the head. But it was recognized that it did not agree with video observed impact locations in up to 36% of the cases. So what resulted from that was the HISS system, a recognition or a popularization of American HISS, 62 car crashes in a game, thousands of blows per year. It takes its toll on the brain. And as young as nine years of age have 500 impacts per season, clearly alarming. And the question, though, and then it came out with additional papers that this data may be used for the development of youth-specific protective designs. Well, the question is, and Alan knows this, in the NFL, does the HISS system really accurately measure forces as we would like? Well, we recognized in 2003 that mouthpieces provide the best coupling. And as Alan mentioned, BioCorps and also Prevent Biometrics, a Cleveland Clinic-started company, looked at the accuracy and the repeatability of the hits from the HISS system. And they, in the laboratory, looked at the hits versus the mouthpiece. And you can see the scattergram here from the HISS system showing how it's much more than a third less accurate, is very inaccurate. And the linear is the mouthpiece showing the forces that are consistent in a linear fashion. And when helmets were instrumented with both the HISS system and the mouthpiece, we could see that the HISS system consistently showed much higher G-forces. Well, the problem is, is this is the data that was used showing that in a HISS system helmet, 652 versus 60. So the question is, does the HISS data incite fear and uncertainty and lead to unforeseen and unwanted circumstances? So in youth football, we see there's a marked decline, 27%, 30% decline. And the perceived dangers are certainly popularized by people like Brett Farr, who says it's just not worth the risk for kids to play football before high school or virtually any contact sport. Well, we know also that Brett suffered, as he said, 90% of tackles, a concussion. He was a sissy if he didn't play after a ding. And after 20 years, 326 games, sack pipe, 120. If I had that kind of a concussion history, I think I probably would not want my kid to play football either. But I don't think he's considered in what he's saying, the new rules, the changes, the equipment and everything we're talking about in this conference. So these are a few papers that you won't hear much about. And this is a study from the Mayo Clinic in 2012. I'd like to interrupt you for one second. We're not seeing your slides. I think you need to hit the share. You're not seeing the slides? Yeah. So just want to interrupt you to see if you can hit the share. I hit the share. I'm sorry. Try one more time. I can't believe it. No, I don't see the share here. I can't believe it. It's fine. Can you see them now? We cannot. Are you seeing the slides on your screen? Yes. The green button at the bottom, Joe, share screen. I don't I don't I don't see it here. You might want to reduce your window size. You might not be seeing those buttons at the bottom. Share screen. I can't believe it. Share. There. Now hit power to the PowerPoint icon at the bottom, Joe. It was just up right there, the orange icon on the PowerPoint. Just hit that one. Right there. Come right up. There you go. Start slideshow from current slide. You're all set. OK, I'm sorry. No, you're fine. You're a very enthusiastic speaker. So basically, let me go through just a second. So I'm sorry. So I mentioned Brett Farr, you know, such and such. So the paper for the Mayo Clinic, the next four papers to save time all looked at kids, looked at adults who had played football or hockey. And they looked back in 1946 to 56 in this case. And they asked the question, did these older adults who participated in football suffer from neurodegenerative disease? And clearly, the answer in all of these papers from Gary Solomon and Alan Sills from the Mayo Clinic, from Barry Willer and all and also from Grant Iverson just this year, did not have a higher prevalence of anxiety, depression or significant difference in those elderly or older patients who had played youth football earlier. So the point I'm trying to make, obviously, is that the data has been used maybe inappropriately. And of course, the paper by Willie Stewart from Glasgow and 60 leading international neuroscientists is a failure to recognize the disease, CTE, how to assess it, no clear understanding of the link and or the specific symptoms. So what I'm trying to get at, are we there yet for a dosimetry badge for concussions to measure the location, the forces and the number of hits in a cumulative fashion to give an individual some idea about the possibility of subconcussive hits as well as big hits? Well, I think we're very close, as Alan alluded to, at the Wake Forest, Cleveland Clinic, Stanford, BioCorps. What I think we're going to be seeing and clearly open to debate is the eye in the sky or the parent in the stands is going to have a mouthpiece telemetried with the data to the eye in the sky and picking a number, which in the study in Glasgow that was done this past year on rugby players, 50 Gs and over resulted in concussions, not significantly below that. So that what I think we're going to be seeing is we're going to have accelerometers in the mouthpieces and there's going to be a number, probably 40 to 50 Gs and that will signal an alarm. A call will be made down from the parent to the coach or the eye in the sky to the doctor on the sideline saying, at least look at this athlete who's had a 40 or 50 G hit and examine him. And then to take it one step further into the future, of course, a finger prick looking at Ampar receptors or biomarkers that might or might not conform a concussive injury. So futuristic, but we're getting close, I think. And then not to forget what Douglas MacArthur, the commandant at the West Point said, this plaque facing the friendly fields of football, basketball, and soccer. On the fields of friendly strife are sown the seeds that on other days and other fields will bear the fruits of victory. We're losing this in the conversations that we hear every day relative to contact sports. Thank you. Thank you very much, Dr. Maroon. Our final speaker is Nicholas Theodore. He will be speaking on return to play following concussion. Dr. Theodore. Thank you. All right, so we don't run into problems here. All right, do we see that? Great. So very quickly, I'm gonna try to just fly through this. The reality is that, you know, not just in sports, but in the military is a perfect segue from Joe's comments. Obviously, this really has become a, you know, a national calling for us to really figure out how we can decrease the number of concussions, not just in sports, but also in the military. When we go back, this is a problem that really has been around for a while. When we look at this is Homer Winslow's classic painting from 1865, a little bit more rougher than we have today when you can actually bludgeon your opponent. And when we look at football through the ages in the 1880s and early 1900s, the game was almost gone because of the number of sports-related injuries that happened, including deaths, multiple deaths. In 1905, 18 people died playing the game of football. This is a, this Richard Ron Albert Gammon had a severe concussion, ultimately died. His mother actually really saved the game of football by writing to the governor and saying, you know, kids die climbing rocks, riding bikes, why do we have to outlaw one sport? And we realized that the number of concussions now, because of awareness, I think, is at the forefront of everything that we see. And, you know, probably more than 300,000 concussions now are reported annually. And the question is, you know, when it comes to return to play, that's what we'll talk about here for the last few minutes. Looking at in sports, football, wrestling, we can see it actually occurs in any sport. Alan very nicely talked about concussion reduction. And in the NFL, we have the concussion protocol, which really guides us with how we look at concussion, how we diagnose concussion, how we return patients back to play. And when there's a very intricate checklist that happens on the day of any given game, we have unaffiliated neurotrauma specialists, one on each side, one up in this stand, watching for concussion. Anybody can report a concussion. Once the player is actually taken out, we realize that we put into play a diagnostic algorithm that takes us through whether or not somebody can return to play and when they return to play. And that's what we'll focus on here. And that those things happen, you know, really in real time at the sideline. So again, during the game, a lot of moving parts, but when somebody is identified, the first question is, can he return immediately? If they're losing consciousness or have any of these significant risk factors, fencing, posturing, staggering when they get up, they're out, they're done. This is a no-go criteria. They're gonna go to the back. They're going to the locker room. We take their helmet off. We get them basically now evaluated. This is Alan evaluating a patient in the blue tent. This is off the sidelines. We have a very scripted way to do this now. And really at a high level, I can tell you that really designed to make sure that we are not missing anything. And again, if it's benign and we look at the replay and the player clears, he can actually be returned at the same time. There's any inconclusive aspect to this. The player goes to the locker room and undergoes more formal testing. So this is all laid out. This in and of itself has been a significant driver, especially in organized football with safety. And again, once they go to the locker room, they go through a complete neurologic examination and a more formal assessment. If that's normal, they could theoretically return to play. Once the diagnosis of concussion is made, the player stays in the locker room and then gets follow-up examinations. The next question is again, when do they return to participation? And there's a scripted way we are handling this down in the NFL. And I think this will carry through and does carry through the sports with some rest and recovery for the first 24 hours, then slowly increasing the player back into some light aerobic activity and then increased aerobic activity then into some football specific activities and then ultimately fully clear. And this protocol is published. The reality is it makes perfect sense. And I think this is the difference from the game of yesteryear when the players were dusted off and put back in the game. They are now very carefully brought through this protocol and ultimately have to be cleared by an independent neurotrauma consultant. They're seen by neuropsychology and ultimately everybody has to agree and the patient has to be completely symptom-free before they return to replay. I don't wanna belabor the point. I think there's really, there's not a lot that guides us rather than symptoms and taking players through this. But again, on average, the player is not returning to play for seven days until the following week in most cases. And we're looking at that data now about to publish this. There's a beautiful article written about structural brain injury. I don't wanna, we're running short on time. The reality is it's interesting that advice changes depending on the level of play, whether somebody is playing at a high school or collegiate level, we have to take that into account. And again, giving the player a chance to recover from their injury. When we look at that for brain injury where there is a structural problem, even then the experts don't agree. Ultimately, we want the player to be asymptomatic, their neuropsychological testing to be back to baseline, thorough neurologic evaluation and return to baseline and then imaging as it's needed, which is it's not needed in most cases of concussion. So the return to play paradigm, I think we're learning a lot. We're now looking at this data. Ultimately prevention still is really one of the most important cornerstones of this. But I'd like to thank you for opportunity to speak today, Alan and Joe, again, taking us through where we are right now with concussion, thanks. Well, thank you for three very provocative and informational talks. I am not seeing a ton of questions coming through in Slido, but I certainly have many. This is sort of open for the whole panel, but it was hit on a little bit, but we've learned so much with football. But as you know, there's so many other sports, whether it be boxing, rugby, soccer, hockey. How could we take the information that you've come up with in football and apply it to these other sports? Yeah, I can start, Ken. I mean, I think the principles are the same. I think obviously each sport has nuances of equipment and rules and style of play, but I think the principles are the same and taking that same data-driven approach is really what's important. But I think it starts with a comprehensive understanding, again, of who's being hurt and how they're being injured. But you're absolutely correct. I often tell people, in my practice, I see almost as many women soccer players each fall as I do football players, for example. They have a really high incidence of concussion injury during sport. So as I think Nick pointed out, this can happen in any sport, from cheerleading to rodeo to wrestling. And so I think that there is opportunity within each sport, but each one is unique. And I'll give you another quick example. I've had a chance to work some with equestrian sports. A lot of the focus there has been on equipment because people's head gear has typically been more about style and looks than it has been protection. So each sport is unique, but I think the principles are the same across all. And we just have to think that this is a much bigger problem than just football. And let's tackle that. I think fundamentally, again, two things, diagnosis and then the treatment. And giving the player in any sport the chance to recover after a traumatic brain injury and putting them through a systematic process where we can sort of reevaluate them and making sure they're symptom-free, that in and of itself, if you think about it from 20 years ago, has been a revelation in the way we treat these patients. And I think that's part and parcel of why the horrible outcomes we'll see are gonna drop significantly based on that paradigm alone. I think that's the greatest advance we've made, Nick, in preventing individuals from going back too soon before the brain has healed. Okay, another general question. I have an orthopedic colleague who happens to be a true cowboy and he goes to all the bull riding contests and he puts accelerometers on those fellows and it's just phenomenal what type of readings he gets. And so I was fascinated by the magic number of 50 that I just heard in your talk, Dr. Maroon. So, you know, when it comes to the different, you know, sort of G-forces that you're seeing and also the biomarkers, where are we going with that? Is that a very reliable measure to be used for other sports? I think, as Alan knows from BioCorps and Nick does, using the HIT data, the numbers of G-forces that were used were all over the place. I think with the mouthpieces, we are getting to a point where we are accurately able to monitor the G-forces. And in the study of 700 athletes in world rugby done last year in Europe, they found that that was the number above which the athletes should be looked at, at least, and evaluated. So I think we're getting closer to a number that we can pick, 40, 50, that if they register that, you should look at the athlete. The blood biomarkers, I think, is another issue. I think we have a little way to go on that. But I think with the accelerometers and the mouthpieces, I think we're very close to instituting that in different sports. All right, well, we don't have much time left, but I have one more question, which is, in my career, I've seen our colleagues fall into two camps, those that think we should get rid of certain sports and others who feel like our job is to make those sports safer. Sometimes that comes across in a question like, would you let your kid play football? I will put my cards on the table. I've always felt that our job is to try to make sports safer, not ban the sports. And I'm just curious, your own personal views based on your experiences. You know, I think Joe's final line really summed it up. There's so much positive energy and aspect to playing organized sports. We owe it to the next generation to make that sport activity as safe as possible. And I think the wholesale outline, and I think is just a bad idea on so many fronts. Forget the teamwork, forget the positive benefits for health and welfare. And a lot of studies have shown that the participation in those sports really does make individuals healthier and does teach them a lot of values that aren't gonna be taught in any other way. So, you know, we have to strive to make it safer. And I would argue that we have, we have ways to go for sure. And I think in the future, with what Joe and Alan and myself have been working on, we're gonna continue to get safer. But the worst thing I think we could do is to eliminate this and just say that we can't do it anymore. Okay. Amen. Thank you, gentlemen. Totally agree. Hello, welcome to the debate section of the neurotrauma session. And for this portion, we're going to have two case presentations. And this will be followed by people presenting varying opinions on management. So our first case is a spinal cord injury case. And so this comes in at a very convenient time, midnight on a Saturday night. And a 34-year-old male motorcyclist lost control, was ejected at high speed, helmeted. On arrival, his blood pressure is 90 over 50. He's tachycardic to 110. He has a right distal radius fracture as well. On his neurologic exam, his GCS is 15. And he has preserved sensation below C5, intact deltoid strength. But below that level in his arms and legs, he's anywhere from zero to two out of five strength. His CT scan on arrival shows C4, C5 vertebral body fracture. His facet joints are well aligned, but he does have this kyphotic deformity. Due to his MRI, or due to his neurologic exam, you decide to get an MRI. And you see here on the STIR and T2 sequences that this patient has ALL disruption. He has interspinous ligament injury posteriorly and edema in the C4, 5 joints bilaterally. So in summary, this is a 34 year old male, and this is an Asia C spinal cord injury with a C4, 5 teardrop fracture. It is now 2 a.m. on a Saturday night after you've finished getting all the imaging. And when do you take this person to the OR? So to discuss this first, we'll have Dr. Paul Arnold discuss early surgery and spinal cord injury. What do I do here? And then we'll have Dr. Tsai discuss ultra early surgery and spinal cord injury. And I'll turn it over to them now. Thank you for the opportunity to give this presentation. I think we'd all agree that early surgery is best compared to late surgery. The two main issues that confront us in terms of early surgery is what really is early surgery and how can we improve time to get there? And I'm gonna go through this in about four or five minutes to go through some of the barriers that it would take to get someone to the OR within six hours versus 24 hours and whether that really makes a difference. And my premise would be that I don't think we really know because there's no studies that are really good to compare six hours versus 24 hours. And of course, there's no randomized trials that look at this. There's only sort of a few prospective trials which I'll go through. So the main obstacles to hyper early surgery which would be six hours or transport. A lot of times the patients go to another hospital before they get to a definitive hospital where they can get taken care of. And sometimes there's a long gamut of issues that the patients have to face. They have to get stabilized, they have to get imaging. And they have to get ready to go to the OR and make sure they're stabilized before they can actually get to the OR. So actually getting some of the OR in six hours is starting to stretch the limits of what's possible. Even if sort of the patient broke their neck in the parking lot of your hospital, they need to get stabilized medically. They need to make sure all their other traumatic injuries are evaluated. They need to get several imaging studies and then you need to get them ready to go to the OR. So these are the main transport issues are that often the patients go somewhere else before they come to the hospital that's gonna ultimately operate on the patients. So studies have shown that in less than 50% of the cases are patients able to get to the OR within 24 hours or less, let alone in six hours. And even Eve is a co-author on a recent paper that we can see this point. The barriers to early surgery again are the intermediate transfers, older age is an independent risk factor. Also we're getting patients to early surgery, which could be due to a lot of their medical comorbidities. In a recent study in the Montreal group showed that surgical planning access to the OR and delays in transfer were the main issues in getting patients to the OR. And again, we also know that patients have to get stabilized in the operating room before they can actually get to the OR. They have to get examined and their neurologic exam documented, which sometimes could take more than just a few minutes that we, a lot of us perform studies in the ER. And the attending has to get to the hospital in time to see the patient. A lot of times you have to the residents and the patients. So there's, again, there's a lot of sequential time that sort of adds up that even if you try to go faster in some of the other steps, time is run out and you can't get the patients to the OR. So the other issue is what is hyper early surgery? So, so the main question is what is hyper early surgery? If we're defining it as six hours, no studies really are able to get the patient to the operating room in that time period. Most of them have been within 24 hours. You know, 10 years ago it was within 48 hours. Now it's, I think we'd all agree that 24 hours is early surgery. Some people would argue that 12 hours is early surgery. There's different criteria for evaluating every aspect of the patient's care, including their neurologic status, the type of injury they have, the other injuries they have, and the ability to get the patient to the OR on time. There's also selection bias, interpretation bias, and confounding variables of all the studies that have been that have been published. So again, I'll skip through this because then we have time so the early before let's say 2010, there are 10 or 11 studies that all look at trying to get basis to your within a reasonable timeframe, or even, or even versus two weeks, four days 24 hours is sort of pushing it up till about 10 years ago. And then when we finally within a review of patients with central core syndrome, 24 hours is defined as early surgery and these patients did better if they had surgery within within 24 hours in a review of patients with central core center, a little bit about this patient has because if you'll notice there isn't a lot of compression on the patient's spinal cord in this particular case, most of the most of the patients, neurologic deficits due to the big contusion and signal change in the spinal cord itself rather than the actual compression. And then finally the stats study came along in 2010 which is a prospect study. And again, early surgery was defined as 24 hours. This is a prospective cohort study. And this, this study showed that patients that could get to the OR within 24 hours did better than if they than if they didn't complications were a little bit less than the 24 hour group. And the take home message for that was an early surgery within 24 hours was was associated with improved neurological outcomes. And then finally, these are the most recent studies that have looked at all this in the last in the last two or three years, and some of them have shown that that getting the patient within 12 hours is helpful but not six hours, sometimes. And again, none of these, none of these clinical trials, really only one study looked at whether getting patients to the OR in six hours made any difference in this case they really didn't. And so finally, the take home message is the latest and best data to date suggests early surgery improves neurological outcome. And that for right now is probably still defined as 24 hours, based on all the data that we have. So the condition of early surgery keeps on improving because it used to be 72 hours or 48 hours and 24 hours now it's 12 hours. And now, once you get towards six hours, even, even if you compare the sort of stroke data we're getting, you know, door to puncture is, you know, after just a CAT scan, getting someone to the operating room in six hours is starting to push up against the, the actual limits like, like the, like a four minute mile or three minute mile, the, what's, what's, what's possible, humanly possible in terms of getting patients to the OR. And the biggest barrier then would be where probably where you're injured, because it may require a second transfer to another hospital, the ability to stabilize the patient normalize the blood pressure and make sure that all their other traumatic injuries are stabilized, getting them to the MRI, making sure the OR is available and then having surgeon availability, getting that done within six hours is really pushing the limits of where we're at right now. So my argument would be that six hours is, it's very, very unrealistic based on the data for 90% of all the patients that get injured. So we ought to continue to focus on getting patients to the OR as soon as possible, but recognizing that, that six hours is starting to bump up against the limit of what, of what we're, what's possible right now in 2021. Thank you very much for your time and I look forward to Eve sort of trashing this, my argument and see what she's got to say. So thanks again for the invitation, I appreciate it. And while Dr. Tsai is switching over, I'll just remind you again, if you have any questions, the right of the screen, feel free to type those in there and we can try to take those at the end. Eve, you're on mute. Thanks. I've been tasked, thanks. I've been tasked to give the, take the argument of ultra early surgery. And so I'm going to do my best to make the case for that. I have no significant disclosures with respect to this. So Dr. Arnold is amazing. He's very smart guy. He's a professor of neurosurgery, he's a chair, he's a clinical investigator, he's one of Castle Connelly regional top doctors. But what I want you to not do is fall for his smoke and mirrors and try not to believe all the kind of smoke and mirrors that he's, he's producing. So, you know, he's touched upon this, you know, we can't take, we can't take the patients to the OR, the timing, it's too hard, you know, we have to work on transferring them, it's too hard, you have to get them to the MRI, it's too hard, the operating room is too hard, you know, these patients who are older, it's too hard. And the reality is that that's all smoke and mirrors, because if we really wanted to get them there, we could get them there. And I, you know, Dr. Arnold has talked about the stroke issues. I mean, in the past, it was like, oh, it's too hard to get them to the angio suite, it's too hard to identify them, it's too hard to bring them in. Well, you know, when, when they actually showed there was a benefit, we can make it happen. And so why, what is the holdup and getting them to the OR? Well, the question is, does it really work? So Dr. Arnold presented the STASCA study. And, you know, it was a great study, it was one of the best we have so far, but it was a prospective cohort study. Okay, there were 313 patients. And it wasn't a randomized control study, there were differences between the different groups, particularly with respect to age and severity. And, you know, what they found was a decompression less than 24 hours is associated with a three, two, sorry, should be two grade AIS improvement at six months. Well, you know, that's great, that should support our argument. However, you know, there are people who are coming up and one of the, criticizing it, and one of the critical arguments was presented by Dr. Mittendorf in the letter to the editor in the Spine Journal. And they said, well, you know, why is there a significant difference for a two-point ASIA impairment scale grade improvement, but not a one-point ASIA impairment scale grade improvement? That doesn't make sense. If you're going to improve them, how can we improve them by two grades, but you can't improve them by one grade? And so what he did was he looked at this and actually did an unadjusted AIS score. And what he found was that when you actually compared ASIA A, B, and C, there was no statistical difference. And so because of that, then, the idea, again, that draws into question as to whether or not there's really a difference. And so if you don't really believe there's a difference, you're not really going to make it work. Now, the other big paper is one by Burke et al. And what they looked at was, well, ultra early surgery, less than 12 hours. And so in that study, again, it was a retrospective cohort data on 48 patients. And in this study, they defined ultra early as less than 12 hours, early as 12 to 24 hours, and late as greater than 24 hours. And they did a two-tailed Fisher's exact test. And what they found was that an AIS grade improvement was 1.3 for ultra early and 0.5 for early. But again, they didn't find a difference between early and late, whereas the Staskis study found there was a difference between early and late. So why is there this question? Like, it doesn't make sense. And again, 89% converted to a higher AIS in the ultra early group and only 31% in the early and late group converted. So again, that calls into question, we should be doing this. Why don't we do early surgery? I think this is the key figure in that paper of ultra early and late. And the reason why I think people are jumping on this with both feet into the pool is because you can see in the late group, there's some people that improved. The late group, there were some people that deteriorated. And I think the reality is that we've all been in situations where we've seen the patient, where, you know, even as a resident, you saw the patient the night before, and they were Asia A. And by the time the staff person saw them, you know, a few hours later, they weren't Asia A anymore. And so the question is, well, you know, are these people really Asia A? Are we really making a difference? Are we really improving these patients? And so what I think one of the questions is, are we even identifying these patients properly? And so maybe we have a biased population. And that's why all those studies that Dr. Arnold presented, where some showed some improvement, some didn't show some improvement, some showed some with early, some didn't show some with early. I think the reality is because we aren't able to actually assess these patients. Dr. Burns et al. did a great study where they assessed patients within 48 hours. Okay. And what they found was that within 48 hours, even within 48 hours, not to mention six hours, half the patients, they were unable to reliably assess them. They either were on mechanical ventilation, they were intoxicated, they had sedation, they were closed head injuries, psychiatric illness, all these other things. And so if we can't properly identify these patients, then any trial that's presented, or any study that's presented, we're not, we're questioning whether or not there's actually improvement with early surgery. So let's take all this data that, you know, we're not sure if it's really early versus late, and let's take it with respect to our patient. And the idea is decompression with those studies, what is actual decompression? If we look at the patient that's in our study, what is there really to decompress? It doesn't look so bad. If we were to just look at the CT scan, it doesn't look like there's anything to decompress. However, this is great. We actually got an MR scan. And here we can see there's a lesion. And here we can actually see there's edema. And even though the canal doesn't look like it's all that squished, we can see that the cord is swollen to the point where we've lost the cervical spinal fluid. And so when we talk about decompression, our effect, our actual surgery, we usually talk about just bony decompression. We're not actually talking about true decompression. And true decompression by that, I mean, is there enough perfusion of the spinal cord? Are we monitoring the spinal cord? Is there dural decompression? How many people would actually do a decompressive craniotomy on a patient with an intracranial bleed and not open the dura? But we're implying that if we just take off the bone in a spinal cord, we decompress them properly. What about actual spinal cord decompression, actual removal of any kind of blood in the spinal cord? So I'm going to go briefly, spinal cord perfusion monitoring, Papadopoulos et al have done a lot of work on this. And one of the things they found that was fascinating was that when we think we've done the decompression, so when they did a bony decompression and they put a probe in and measured the perfusion pressure in the spinal cord, especially in the thoracic region, we're actually making them worse. Because when we took out the bones, what happens is that patients are nursed on their back and the pressure from the back and the bed actually pushes on the spinal cord and actually worsens the perfusion. So one of the things we should do if we're actually going to do decompression is if we do a laminectomy, we should actually put them on some kind of a ring pillow so that we're not actually causing perfusion to be worse. But the other thing too is how do we know perfusion is worse if we don't monitor? The other thing they found was that there's a subgroup of patients where when they put the perfusion pressure monitoring and they didn't open the dura, they could find that the cord swelled to the point where it actually cut off blood supply. And so if you cut off your perfusion pressure, again, even if you do a bony decompression, that's not going to work. And so what they've recommended is to do a dural patch. And so if we look at our patient, if we were to do a decompression, and by decompression meaning just the bony decompression, that's not going to work for our patient. They've got edema, they've got blood, they've got swelling. And if we really wanted to do decompression, we should really take off the bone and actually open the dura and potentially even remove the cord, the hematoma. And so, oh, people are like, oh, we don't want to open up the cord. Well, you know, we've got some data from another study, the INSPIRE study, which actually helps us with this. And what this study is... I'm running a little short on time. Sorry. The actual study was to actually have to put in a little piece of implant. And what they found was that when they opened up, there's actually blood and it actually decompresses the cord. And this is a fascinating video that was presented. And what they did was they did a midline myelotomy. And watch this. When they opened up the pressure within the cord, you can see the amount of necrotic debris coming out. They actually ultimately irrigated this and then put their implanting. So, you know, if we all we have, and this is what we usually have with the spine, is just a CT scan. Would you wait? Would you operate on this patient and say you need to do decompression? Well, what about if you got a CT scan, actually saw the intracellular structures? Would you operate here? Look, it looks like it's under pressure. Well, what about here when you actually got a blood clot in there? Would you actually wait for more than 12 hours to evacuate this? The patient's going to be not very good. And so here we've got our patient. Usually people only get a CT scan. We're lucky in this case, we got an MRI in this case. And here, so what do we do? Why don't we do a real decompression and we should do it as soon as possible. And so I'm going to just leave off with this. They talk about the Lancet. If we adopt the concept that time is fine, and I hope I presented some evidence suggesting that in this case, in this patient, it is. Optimization of logistics will be necessary. Stroke patients are nowadays sent to hospitals, receive immediate care. Why should this not be possible for spinal cord injury patients, especially with its effects to younger people with a serious lifelong disability? And so I hope you don't fall for Dr. Arnold's smoke and mirrors, and I hope you vote early. But no, not early. Vote for ultra early. Thank you very much. So, now, to the audience, so it's two a.m. after you've gotten all your imaging, when do you take the patient to the OR? You can vote on the slide on the on the side of the screen or in Slido. So it looks like the majority of our audience is leaning towards at 8 a.m. So early, but not ultra early. Can I just make a point about that? This case is a little bit unfair because Eve brings up a lot of good points that are, you know, really, you know, on the cutting edge and experimental. The patient, you could argue in this particular patient that 90% of people who wouldn't open up the dura, who, you know, wouldn't, you know, put one of the scaffolds in, the patient doesn't have a lot of compression. You could probably put the patient in traction and a shoulder roll under the neck and their kyphosis would go away and you'd probably get everything realigned. And you may, some, a lot of people would never even open the, open the dura at all on this. But, you know, most people would not. It would be one thing if they had like a fracture dislocation with significant pressure that I think you might get a different answer. But here, you know, and again, there are studies that show, you know, even whatever the smoke and mirrors I'm playing here with, there are studies that show that the operations at six hours or earlier is going to make any difference. We just don't have that data yet. So like I said, we're tasked with this point. And I think what I was trying to, and I think Dr. Arnold's been great. What we're trying to do is just highlight some of the potential things that people should think about. Because again, it's a debate for a reason. There's different points of view. And I think what we were trying to work on is trying to educate and really bring different points of view to this topic. Yeah, I think you brought up some excellent points. I'm glad you brought that because the debate that we would have had is nobody would disagree that the earlier you do anything, the better. And, you know, I think what you highlight what may be coming in the next five or 10 years in terms of spinal cord injury management. Yeah, I think we need to make a diagnosis. And I think that's the goal for this is to improve our diagnosis, like we've done with head injury, like we've done with stroke and like we've done with all this. Do you routinely monitor spinal cord pressure? I don't. But I have opened the juror on patients with spinal cord injury. And, you know, sometimes it's swollen and sometimes it's not. And I have done a duroplasty I haven't had one that's so swollen that I've actually had to decompress the cord. Do you have to do a posterior operation, even though, even if you'd like, they might do better with the failure of like if they might need a vertebrae, would you then flip them and do this when there's a front and back operation or just only one. In the cases that I've done so far, they've usually only required just a posterior but sometimes, you know, if that case comes about, I do the decompression and if you know I couldn't get it, flip them at the time I delay that because I think the most important issue is to decompress the cord, as opposed to, you know, stabilize the spine. Thank you very much. Sorry, it's a very difficult topic to cover in 10 minutes. I mean, there's so much new thoughts about this, but we'll now move to our next group of presentations for closed head injury. Hold on, let me just, I think my screen sharing is just interrupted. Okay, so here's that case. 54-year-old female, ejected, high-speed MVC, found unresponsive at the scene, intubated in the field. On arrival, her blood pressure is 140 over 80, heart rate is 90, and there's external signs of neurologic trauma with scalp lacerations. Her neurologic exam, pupils are equal reactive, she has a gag, she's withdrawing in all of her extremities, but eyes are closed and intubated. Her other injury, she has a chest tube placed because of chest trauma and a humerus fracture. The CT scan shows a diffused subarachnoid hemorrhage, multiple small contusions in the bifrontal bitemporal area, a small amount of pneumocephalus, and no midline shift, the basal cisterns do appear tight. So in summary, this is a GCS6T polytrauma with diffused TBI, and the question here is, what form of ICP monitoring should be used for this patient? So our first presenter will be Dr. Emily Sieg, talking about brain tissue oxygen monitoring, and then our second presenter would be Dr. Maya Babu talking about ICP monitoring. So I'll hand it over. Thank you so much for having us. My name's Emily Sieg, I'm the Director of Neurotrauma at University of Louisville, and I will be presenting the side of PBT02-directed therapy in the setting of severe TBI. So as we all know, in a setting of severe TBI, GCS less than eight, outcome can be significantly impacted by decreasing secondary injury to the brain. So what is our goal? It's to prevent secondary injury and to improve neurological outcomes in our patients. As we know, cerebral ischemia can lead to significant secondary injury. It can be caused by things like hypotension, intracranial hypertension, impaired auto-regulation, and hyperventilation. So why not just use ICP? Well, because we know that ICP control does not improve outcomes. Every class two study that we recount in the Brain Trauma Foundation guideline does not show any improvement in neurologic outcomes. Every one of these three studies shows only an improvement in mortality. We know that CTP may not correlate with cerebral blood flow or oxygen consumption in the setting of severe TBI. PBT02 is a more direct predictor of cerebral ischemia and hypoxia. Sorry, I'm having a little bit of a, hearing myself in double. Hopefully you guys can hear me. We do not yet have a randomized control trial that shows that PBT02 improves outcome, but we have a number of studies that do not meet our rigid guidelines that are hopeful. This study from neurosurgery shows that PBT02 is a safe and reliable method for talking about cerebral oxygenation, which we know leads to secondary injury. This 2009 study in critical care shows that hypoxic episodes may be independent of an elevated ICP. And thus, if we are only treating ICP, we may be missing ischemia. This study, again, underscores the importance of cerebral hypoxia with neurological outcomes. Finally, this literature review that shows an odds ratio of 2.1 in favor of ICP and CPP, in addition to PBT02-based therapy, is associated with better outcomes when compared to simply ICP and CPP-based therapy alone. Everyone here has seen the BOOST2 trial. We know that it was stopped early due to a significant likelihood of improvement in the PBT02 group. So I urge you to consider using PBT02 until the completion of BOOST3, which is currently enrolling. Excellent. We can now switch over to Dr. Babu's presentation. Great, thank you. In the interest of time, I'm just gonna hit the highlights. I think Dr. Sieg did an excellent job of going in depth with the literature and kind of where we stand in terms of, you know, awaiting the results of BOOST3. So in terms of when we're making the decision between an ICP monitor versus a Lycox, and, you know, I think we had both spoken prior to this presentation, certainly an external ventricular drain gives us the opportunity to also treat elevated ICPs. So that would be a modality that we would, I think, favor both of us to have at play. But in terms of the purposes of this debate, looking specifically at a Lycox versus an ICP monitor, you know, certainly factors such as cost are important for institutions. The clinical classic or vanilla ICP monitor tends to be a lower cost than some of the monitors with additional modalities like the Lycox. We certainly have more long-term experience. We kind of know what we're dealing with, and we also know how to interpret the information we get. I think there's definitely a predilection towards if there's newer information or just a newer piece of technology, we may not necessarily know what all the data means, but we, you know, it's novel and it's something of interest and we try it, which is certainly favorable in terms of innovation, but we don't necessarily always know what the data is and how to interpret it clinically and help patient care. Brain tissue oxygenation, as was mentioned, you know, there is some debate and really that's why further study is occurring as to whether are we monitoring the effects locally where the monitor is? Are we able to provide more global interpretation or analysis for the entire brain parenchyma? We do have studies pending and we are still trying to understand how we can utilize this information to help with treatment. And we all know too, some of the challenges with monitoring that monitors do require replacement after several days or if the monitoring signal becomes blunted. So we certainly deal with these challenges on an ongoing basis. We continue to look at other things like microdialysis as well to see if we can get adjunct information to help us guide care. Excellent. We do have a minute. I don't know if Dr. Sieg has any rebuttals and in the meantime, I can pull up our poll question. I think we had decided to kind of skip the rebuttal in the essence of trying to get us back on time. Excellent. So when you are in practice and you're seeing this patient, of course, we mentioned many of us would be seeing this patient Of course, we mentioned many of us would use an external ventricular drain, but let's take that out of the equation because we certainly don't have time to talk about all the modalities. What form of monitoring would you use for this patient? A Lycox monitor, a bolt or no monitoring at all? And if you vote just on the right side of the screen, you should be able to see those options. And it seems like the audience is favoring bolt over Lycox. Perhaps after boost three, maybe people will change their management or perhaps it won't change anything at all. It also may be due to availability of these monitoring modalities. But yes, excellent discussion. And certainly we could spend probably a whole hour for discussing this. So I will now, it does seem the audience favors bolt. I will hand it over to Dr. Tsai to introduce the next lecture. Thank you. Hi, so I've been given the honor to introduce Anne-Christine Tina DeHaim as the 2021 Anthony Marmaru speaker. Dr. DeHaim was initially invited to give this lecture in 2020, which would have been particularly fitting since she would have been speaking from her home field in Boston, where until earlier this year, she was the director of pediatric neurosurgery at MGH and continues as the Nicholas T. Zervas Professor of Neurosurgery at Harvard Medical School. Tina graduated from Brown University in 1977, majoring in experimental psychology. After flirting with the idea of being a psychologist, she decided to pursue a medical degree at the University of Pennsylvania. There she remained to complete a residency in neurosurgery, followed by a pediatric fellowship at CHOP. After a brief stint as an assistant professor at the University of Florida Shands Hospital, she returned to CHOP in 1989, establishing an NIH-funded pediatric neurotrauma laboratory, where she cultivated her research interest in the mechanisms of injury and recovery in immature brain. In 2001, she was recruited to Dartmouth, where she became the first dedicated pediatric neurosurgeon at the Children's Hospital at Dartmouth-Hitchcock. Since joining MGH in 2010, Dr. DeHaim has continued her work on traumatic brain injury, brain plasticity, and neurogenesis. She is the author of more than 150 publications in this area. She made a personal pivot in 2015-2016, serving as a fellow of the Radcliffe Institute for Advanced Study and working on a project entitled Neurobiology of Award Circuitry and its relevance to pro-environmental behavior, tying together her longstanding interests in brain function, behavior, plasticity, and global issues. Her interest in sustainability extends beyond the classroom. She serves as an associate editor for the Journal of Climate Change and Health and associate director for the Massachusetts General Center for the Environment and Health. She has also been helping to design a prototype for a green biophilic pediatric hospital. In 2019, she was named to the Board of Directors at the Obedon Society of Rhode Island. I can think of no one more fitting to honor the memory of Anthony Marmaru. While perhaps known as the authority on fluid dynamics in the brain and spinal cord, he conducted equally important basic research targeting mechanisms of cellular injury following traumatic brain injury. Through her commitment to research focused on understanding injury to the immature brain and to translating those gains into bettering the lives of our patients, Dr. DeHaim epitomizes Dr. Marmaru's mantra that patients should explore all their options because there is always hope. Please join me in welcoming Dr. Tina DeHaim, who will be speaking today on the topic of injury response, repair, and plasticity, insights from the young brain. Thank you so much, Dr. Tsai. That was a wonderful introduction. I know we're short on time. I'm going to tell you from the get-go that this is going to be mostly entertainment. You've had a long day of lots of science. We're going to touch on a little bit of science, but in this short time, what I hope to be able to do is inspire especially some of the younger researchers about what it is about being a neurosurgeon that helps us really be motivated to solve some of these mysteries and what we get out of it as well. I want to tip my hat to the Marmaru family, if Christina is in our audience. Tony was just like an incredible person, biomedical engineer, creative lifelong learner, an expert as was mentioned in TBI as well as hydrocephalus. He was a true model scientific collaborator with clinicians and a generous lover of life. If you went to a meeting where Tony was there, it was always more fun. He would take you under his wing, take you around. I hope I've learned some tips about how to be a wonderful mentor from him. As you mentioned, there is always hope. We'll get back to that in a minute. Thank you to Dr. Marmaru for his career. What we're going to talk about in this talk today is the age-dependent response to injury. When I started in my career, I was mostly focusing on acute and subacute response to injury and I've gotten more interested over time in the chronic. Perhaps that's just because as you get further in your career, you follow patients for longer and you see what happens over the long haul. This has led to an interest in what we can learn from animal and other models about repair and recovery processes and the age-dependence of those processes. I've become increasingly convinced that as was mentioned all along today's sessions by Shelly Timmons talking about genomics, by Ryan Kiligawa talking about gunshot wounds, by Aaron Yongo-Khan talking about ATV injuries and helmets, and all of the speakers today have touched on these host factors as well as inherent processes in the brain that we have in common. I think that as you get further in your career, these things start to mesh together because you follow patients and it's the patients and their stories that inspire you. That's what I hope to leave you with today. Neurosurgery has been called a front row seat and it really is a privilege. I know that when I worked with Maya, we talked about many head injury patients and you really get to see the brain up close like nobody else gets to see and it's an extraordinary experience. I've sometimes characterized pediatric neurosurgery as a front row seat on a roller coaster because kids change so much and they're traveling through different countries during their maturation. Literally, they go from being babies to toddlers to young kids to adolescents in a blink of an eye. But during those times, they are changing in their brains in dramatic ways that affects their response to injury, but also their repair and recovery. So what you get to see from the front row seat is a patient who shows up. The debates that we've had, the patient shows up and it's your job to deal with that patient. You take the observations about the patient to the laboratory and you try to model the kinds of injuries that you see on your scans. You may do biomechanical modeling that I collaborated with people doing. You may do animal modeling in imaging and histology and tissue properties. And then we are inspired by the recoveries of our patients. And on the left side of your screen, you see a child who was a crush injury. And as he recovers, you see the lights come back on and you see his personality come back and his abilities and his strength. And what is it that does that? I have just always in my career been totally fascinated by watching kids recover from their injuries and then trying to go to the lab and figure out what is it that they do? How do they do it? Why does it differ from one kid to the next? And we've touched on things like abortive neurogenesis that may lead to post-traumatic epilepsy and other forms of neuronal migration that may lead to changes in who you are on a neural basis. So our main question over the decades I've been in this line of work is whether the brain responds differently to injury, depending on the age at which the injury occurs. And, you know, we see in pediatric neurosurgery, kids at every stage of development up to late adolescence. But it also may vary among different types of injuries. And if you're going to try to answer this question, you have to have a broad net because, of course, one injury is not like another. And I've been increasingly interested about types of patients. So the boy all the way on the right side of your screen, we'll see him later because he's an example of the kind of patient that as a clinician makes you wonder if you really can lump things together in the way you are taught by your training in school. So this was my first clue that kids were different. This was a child. I was a junior attending at CHOP at this time. And this was a two year old who sustained a point blank gunshot wound to her forehead. She came in, brought by, I don't know whether it was a police car or an ambulance, but she was in full cardiac arrest. People were doing CPR on her as they brought her into the ED. She had fixed dilated pupils. And we didn't have time for a CAT scan because she was an extremist. But I did ask for a cross table lateral when they did their chest X-ray for intubation. And in the cross table lateral on the skull film, you could see that this was a through and through gunshot wound that went through one hemisphere, through the deep gray matter and out the back of the head, catching the lateral aspect of the pons. And in the image down at the bottom of the screen, you'll see the exit wound that was almost in the middle of her head, but off center a little bit. And I told the folks in the ED to call this code. Don't do it. Stop. She she is hopeless. Don't do anything. And of course, because I'm trying to do this talk very quickly, I didn't have a surprise slide. So you see what happened. I was wrong. And the chief of surgery who came down and overrode me because he wanted the residents to get some practice was right in the fact that this was not an unsalvageable injury. And I'm not going to say she didn't have serious deficits because you all can see that she did. But she recovered her consciousness and her ability to function, though, with some true deficits. But this is the kind of injury that should have been fatal by everything I had ever been taught and anything I had ever read. And this is the boy you saw in the previous slide. This is a youngster who had was struck by a car while skateboarding, and he had a horrendous injury, came in with a fixed dilated pupil, terrible injury with decompression. This one slice doesn't really show the whole thing. The family, as he gradually recovered, didn't want any rehab. And I was like, of course you have to have rehab. But it was a good family and they wanted to take him home and recover him at home. And they insisted on this. And they got a whole community around them to help this kid recover at home. They were not professionals in health care, but they just were dedicated parents. And this went against anything that I had ever been taught. You must have inpatient rehab if you're this badly injured and it's going to be terrible. And there, of course, is the punch line. You know, he actually did much, much better than I would have expected. This was not just a frontal injury. There were other parts of his brain that were injured as well. And I would have predicted a much worse outcome. So when I was early in my career, my mentors, including Tony Marmaru, but others like Tom Gennarelli and Tom Langford and many others, we were at that time really focused on the biomechanics perspective. And the idea was that you could program in an injury if you understood the forces. And this gets a little to our earlier talk on concussions and helmets. And if you just understood the forces, you could predict virtually 100 percent what would happen to that patient. And the idea was, if you understood the forces, it would be sort of a direct line to the resulting injury. Our surgery and our medical management treatments would maybe have some effect. But I have come to feel more strongly over time, both by patient observation and by our research and that of many, many others, that the host factors play a huge role and that the repair and recovery factors also play a huge role. And that just knowing the forces does not totally predict the injury. There are other factors involved that may play as big a role. In children, of course, there are some injury patterns that only happen at specific ages, and I've spent a lot of my career studying the one on the bottom row, which is most commonly seen with inflicted, that is, child abuse injuries, but not always. The same exact thing can happen if it happens to the right kid at the right time in their life and the right circumstances exist to cause this so-called what we used to call big black brain. We now call panhemispheric damage. And this has been a mystery that we've been trying to solve for a long time. But even apart from that particular injury, other kinds of injuries happen in kids that are exclusive on the top row. The second image from the left shows a classic pediatric injury, which is a skull fracture, fall from height where the skull sweeps in and lacerates the cortex almost all the way to the ventricle, pops back out. And unless you know to look for that brain laceration, you're going to miss it because the child may not look that ill. So in the lab, we have spent decades trying to understand the age dependency of the response to some of these injuries, both focal injuries and rotational injuries. And I think the data suggests very strongly that there are age dependent specific responses. The immature brain tends to be much more resistant to focal mechanical trauma, like a contusion injury when it's younger. But it may be slightly more sensitive to rotational injury when it's younger at certain ages and not orders of magnitude just a little bit. Whereas to focal injury, it's quite different. And there is different patterns and time courses of swelling, atrophy and so on that affect what happens to kids. And while these are large brain animal models, we've seen the same in children. We've spent a lot of time, as I mentioned, looking at combined injuries because because children are resistant to certain kinds of injury, to get these really devastating injuries often requires combined insults. So we've been trying to pick apart what are those insults? Is it hypoxia? Is it apnea? Is it seizures? And as was mentioned in one of the talks today about the EEG patterns, we have come to believe that there is a lot that's going on that we are still starting to learn about with respect to electrical activity and neurophysiologic activity that requires specific ways of studying it, things like spreading depolarization. But with a lot of work, my colleague Beth Costine-Bartell has gotten this model further than I could get on my own. And we are now able to pretty much wipe out one hemisphere and spare the other like the children get. But this pattern is age dependent and only happens in human, usually not only, but typically happens in human children who are slightly older than the kids to get the bilateral form. And the same thing happens in piglet models of this same constellation of injuries. But we, as I mentioned, have become increasingly interested in how and which kids make which kinds of recoveries. So this is work that came from Simeon Misios, Sabrina Taylor and Beth Costine-Bartell in my lab and now in Beth's lab, independent of mine. And Beth and others painstakingly looked at how does how does a trauma in the immature brain at different ages cause neurogenesis and migration? And what we had also tried to study with functional MRI in the piglet was what we all have heard of as plasticity, but what we can subdivide into horizontal plasticity. That's what's shown in the middle of this slide. That is, you have a function. In this case, it's the somatosensory function of the snout that you can see before an injury. You can cause an injury and wipe it out. And then you can see over time how other areas of the cortex that are not injury, not injured, can take over that function. This has been shown, you know, for many, many, many years in many models, including primates. But there is another concept that may be more relevant in young people. And we don't know to what extent in adults. And this is a concept called vertical plasticity. And this is not just the adjacent area of your cortex, but this may be entire networks where even subcortical structures may come into play in attempts to repair and regenerate damage to the cortical structures. And this is an area that Beth had studied a little bit with animal. Oh, I'm sorry, I just heard from the from the organizers. OK, I hope that everyone can still hear me. OK. All right. That's not a problem. But in any event, these migratory streams that are particularly prevalent at certain ages and still present in adults, although in in less robust ways, may direct neurons that are already present neuro blasts that are already present into other entirely different layers of the cortex, entirely different areas of the cortex. And this may be particularly in young people, part of what children use and and perhaps adolescents and adults to some extent to recover their function. We've also been particularly struck by pre-morbid or so-called host factors on outcome, and we notice this in our patients in the TRAC-TBI pediatric study that much to our surprise, I was quite convinced that the that the imaging findings, particularly high detail MRI, would predict the outcome and that would be the main predictor. But in fact, what we found was that what you were like going into the injury was a better predictor than imaging findings in many instances. And if you were a kid who already had emotional problems, already had cognitive problems, already had learning problems, already had so socioeconomic constraints, those kids just didn't do as well. And those predictors were much stronger and played a much bigger role in the kind of recoveries that we saw at six months, one year and even longer now with the TRAC-LONG study than we were expecting to find. And this is not a new idea. This group from Michigan, you know, this idea of cognitive reserve that if you are, you know, more able, particularly in academic skills for kids up front, you have more emotional reserves, you have a supportive family. These things may play a bigger role in your outcome than we really were expecting in the days when we thought if you knew the forces, you could predict the outcome and the injury. So for the rest of the talk, I'm just going to tell you a story. It's late in the day, but I was inspired by this story and wanted to share it with the audience today. So this gets at what we are as neurosurgeons, what we do, what we encounter, what we tell families, how we manage things, and it has many of the factors I've talked about rolled into this one story. This was a 15-year-old kid, not wearing a helmet, he should have been. He was going down a hill near his neighborhood with a skateboard where you have one foot on each skateboard. He's a 15-year-old boy and he wiped out, and he was found unresponsive in the road by a pastor. Actually, there was a neighbor who actually saw it happen, and it was a pretty high-velocity injury. He came into us with a GCS averaging around five, depending on who saw him. Immediately, you can see on the CAT scan, this is a big focal injury at least because he's got a big skull fracture going from stem to stern, a lot of scalp swelling. His CAT scan, which was done very early after his injury, shows a subdural and some contusions. You can see the MRI, which was after his surgery, shows the extent of these contusions. There are other images on flare that show it even more. But this is the kind that breaks your heart when you go to the OR. His family wasn't here. We didn't even know his name. We got him to the OR. This is a view looking at his left hemisphere. The arrow shows the sylvian fissure to orient you. The temporal lobe is inferior. This is his sylvian fissure and his temporal lobe, just a mess. This was not superficial plot. This was contusion with pia that was bursting through the pia and just terrible cortical contusions all over the surface of his dominant hemisphere. This is the kind that you just feel as a surgeon. Darn, I wish that hadn't happened. I wish that kid had had a helmet on. This is just some pictures that his family provided. They've given me permission to share these. Obviously, as neurosurgeons, you all know what this looks like. He's got the long-term monitoring on in the ICU. He's intubated. He's got all the treatments that we gave. He's got ICP monitoring and other multimodality monitoring. In the middle on the top, you can see now the LTM is off. Now he's getting the collection of fluid under the decompressant site. On the top right, what you can see is now he's extubated. He's on his way to rehab in this photo. As he woke up, it was clear as I predicted, and luckily prepared the family for that he was going to have global aphasia. He couldn't understand anything we were saying. He could produce no words. As his words came back, the first words were curse words. His mother would call him sweet boy, and I was like, doesn't look so sweet to me. All he does is curse. But of course, I knew that that was his injury. But he would rip at things and punch people and pull at things, and it was really quite dramatic. The lower left, you can see this is rehabilitation, Spaulding Rehabilitation inpatient. He's got a net bed because otherwise he'll climb out, he'll pull at things. He pulled his NG tube out that couldn't stay in. You can see even though he looks better, he's awake. He had global aphasia and severe agitation at this point. This was a very hard time for the family. We put his bone flap back fairly early as soon as the swelling went down. What I didn't tell you is that this kid was a really smart kid. But in particular, his talent was music. He played multiple instruments, he was in multiple bands, he had traveled with the travel bands, and he knew classical music, but he also composed jazz. While he was a good student, he wasn't quite sure on his career path, but he thought it would involve music and apparently was very talented. The family wanted to know how is this injury going to affect his music because this is what the kid lives for. He also was athletic, he skied, he played soccer, he did many things, but music was his passion. Here's in your lower right-hand corner is an image from a study by Barrett in NeuroImage in 2020. I tried to find something relevant to the family. This was actually an fMRI of a known and prominent jazz composer. She did a bunch of tasks in the fMRI scanner and they tried to figure out where is composing, where is music production, music creation. Of course, it's not a definitive answer, it's one person, but it's a widely distributed trait. Music is also widely distributed. I told the family we just couldn't predict about his musical abilities. Here he is in rehab. I think this is after his skull flap is back. He's still densely aphasic, both receptive and expressive, so he gets very frustrated. You can see what the music therapist wrote. He's frustrated that he can't come up with his musical knowledge, but his ear and fine motor muscle memory, he had some early weakness, but that gradually improved. I want to share this little video with you. It may be loud, so watch out for your ears. He can barely talk at this point, but I want you to pay attention to his facial expressions. He knows he's making a video and he hits a chord and he looks at you like I did a cool chord, so I just want to share this with you. Here we go. You can see he can't talk, but he's expressing himself. He knew he messed up. He and the music therapist were going back and forth about that. Here he is home, very thin, but string bass is one of his favorite instruments, so he was very happy to get back to that, but he was still quite aphasic. This is November now at this time. His injury was in September. I'm home with my family on Christmas Eve and I get a text message. I want to share this with you. What I'm trying to share with you is the recovery. You've all seen this, but I remain amazed by recovery and I never am tired of watching it. I want you to pay attention to his halting speech and where it works and where it doesn't. The colloquial expressions come back sooner than the word finding, but you may enjoy this. I'm not going to go through his playing the piano, but I want to hear the message that I got, probably one of the best Christmas presents I ever got. Here you go. Hello, Dr. DeHaan. I was just going to show you a video of me playing the piano because I remember we talked about George Gershwin, who played Prelude I and Prelude II. Definitely, both of those songs are my hardest songs and I took the most time to learn them. But then after my accident, I couldn't remember how to play them anymore. So I spent a month, a bit more than a month, in my house trying to play these songs. And yeah, I can't do them and I can play them now. And so that's why I'm showing you this video and I hope you have a good Christmas. So, I mean, could you get anything better on Christmas Eve? It was just a wonderful thing. This one's really loud. This is July, so he's getting better. This is playing the upright bass. I'm just going to go through just a tiny bit of this. Okay, so you can see he's definitely improving, but he isn't unscathed from this injury. This was a neuropsych test two years after his injury and they say he has issues with processing speed, challenges in verbal fluency, divided attention in simultaneous processing, the time he takes to require tasks, particularly verbal tasks, are much above that for other students his age. Nonetheless, he managed to graduate high school with honors. And, you know, with respect to host factors, this kid had it all. He had pre-morbidly, he was smart, he had a wonderful family, he had a great attitude. Is his recovery because of horizontal plasticity, vertical plasticity, host factors, genomics, you know, all of the above? I don't think we really know. So in conclusion, I'll just sum up by saying, you know, our studies, our observations, and that of many, many other people, suggest that age does make a difference. Can we tap into what it is that makes, you know, children better able to recover and apply those molecular strategies to people in the older age ranges? Obviously, it varies with injury type, the evolution of the injury and recovery, and there's correlation with maturation studies that I can't get into in great detail, but things like neurotransmitter changes over time. Plasticity and recovery, we still have a lot to learn at the cellular, molecular, and genetic level, all things that were touched on by earlier lectures, age factors, and as mentioned, horizontal and vertical plasticity, which I think is an unstudied, understudied possible strategy. And then the host factors, I think probably play a bigger role than we thought, both with patients who do worse than we expect and patients who do better than we expect, and there's a lot to learn from those as well. So finally, there are many, many people that contributed to this. I know this was a short talk. I want to thank the neurotrauma section, and I want to, again, quote Tony Marmaru by saying the reason that you do what you do and we do what we do is we always are hoping that there's always hope. So with that, I'll end. Thank you. Thank you so much, Dr. Duhaime. It's been an honor having you here with us, and thank you for such an inspirational, exciting talk. And I just want to let the audience know that you'll be giving a full-length lecture on neuro-U later in the fall, so to keep their eyes open for that, because I think you really are a trailblazer in this area, and we can learn so much from what you've learned, and obviously by keeping a close eye and being observant of many of these things. So thank you for sharing your time with us. And then I just wanted to conclude this session by running a few minutes over. Unfortunately, we don't have any time for questions, but I wanted to thank the audience for joining us today. It's really been an exciting afternoon. Thank all of our speakers and participants who put time and effort in, and of course, thank the AANS and the AANS staff in particular, who's had to deal with a bit of a moving target in the last couple of weeks, but have really made lemonade out of lemons and delivered us a great virtual conference that hopefully we can all learn a thing or two from. So thank you once again, and hopefully we'll see you in person the next time around.

7-year-old patient

lower extremity fractures

snowmobile accident

sciatic nerve injury

nerve function

close monitoring

appropriate intervention

recovery

ultra-early surgery

spinal cord injury

neurological outcomes

early surgical intervention

compressive lesions

stabilization of the spine

virtual session