Hello, everyone. Welcome. Today is the functional and epilepsy session. We have an action-packed afternoon. We have top scientific abstracts. We have our community and social initiative showing Halloween costumes from around the country. We have Professor John Rogers as our invited speaker. We have a session on selective dorsal rhizotomy and more top abstracts. Stay tuned. It's going to be a great afternoon. Welcome. Hello. My name is Monica and I'm a fourth-year medical student at Washington University in St. Louis. Today I'm going to present our work for the Australia lab on characterizing the contributions of ventricle size and early intervention on neurocognitive outcomes in post-hemorrhagic hydrocephalus or PHH. So timing of temporary CSF diversion has been evaluated with the ELVIS trial demonstrating that earlier intervention was associated with lower brain abnormality scores and smaller ventricles on MRIs. Other studies report more revisions, externalizations, or removal procedures, which may decrease long-term cognitive outcomes. However, though the ELVIS trial looked at thresholds for VP Shandang, optimal time for permanent CSF diversion is unknown. And furthermore, in a prior paper from the Australia lab, we evaluated that smaller hippocampal volumes are associated with poor neurocognitive outcomes, but it is unknown how ventricle size or timing of permanent CSF diversion relate to hippocampal volumes. So we aim to address both these previously unanswered clinical questions. So our patient cohort consists of 25 preterm infants with average gestational age of 25 weeks, all had IVH grade 3 or higher, and an average social risk score consisting of patient and family demographics of 2.2. Family scales of infant and toddler development were assessed at 2 years of age with the averages shown here, and patients received either form of temporary intervention with subsequent permanent CSF intervention, and 64% underwent shunt revision prior to 2 years of age. So ventricle size was measured on serial cranial ultrasounds using FOHR, and rather than using a single maximal time point, we aim to understand cumulative ventricle size over time with area under the curve for FOHRs for two different time periods. We had BIR to temporary CSF diversion and BIR to permanent CSF diversion, and the area in blue represents our primary focus in determining the optimal time point for transitioning from temporary CSF diversion to permanent CSF diversion on neurodevelopmental outcomes. So we found that there was no significant correlation between timing of temporary CSF diversion and Bayley motor, cognitive, or language scores. Maximum ventricle size measured by the largest FOHR value recorded on cranial ultrasound prior to temporary CSF diversion and cumulative ventricular size were not significantly associated with Bayley scores. However, earlier time point of permanent CSF diversion and smaller cumulative ventricular sizes prior to permanent CSF diversion were significantly correlated with all motor, cognitive, and language long-term outcomes in our patient cohort. So we subsequently characterized ventricle size one year following permanent CSF diversion and observed that smaller FOHRs assessed at this one-year time point were associated with some increased Bayley scores. Furthermore, with this understanding, we observed that earlier time point of temporary and permanent CSF diversion resulted in smaller ventricle size one year post-permanent intervention. Interestingly, cumulative ventricular size prior to temporary or prior to permanent CSF diversion resulted in smaller ventricle sizes one year post-permanent intervention as well. And lastly, similar to our findings with neurodevelopmental outcomes, when assessing hippocampal volumes that were normalized to intracranial volumes as a ratio, there was no relationship of timing of temporary CSF diversion, but there was a significant relationship with earlier permanent CSF diversion and smaller cumulative ventricular size correlating with larger hippocampal volumes. And so to summarize, in infants with PHH, smaller cumulative ventricular size and shorter time to permanent CSF diversion were associated with improved neurocognitive outcomes, reduced long-term ventriculomegaly, and larger right hippocampal volumes. In future perspective, randomized studies are needed to confirm these findings and to understand the role of complications associated with earlier shunt placement. And I want to acknowledge my PI, Dr. Straley, and everyone else in the Straley Lab, as well as St. Louis Children's Hospital, who helped with this work. Thank you. Hello, my name is Vinit Dharanavu, and I'm a medical student at Northwestern University's Feinberg School of Medicine. Today, I will be presenting on the presentation, management, and outcome of pediatric thoracic outlet syndrome. For background, thoracic outlet syndrome is a rare disorder involving the compression of the brachial plexus, subclavian artery, and subclavian vein, which may present with various symptoms. Neurogenic thoracic outlet syndrome predominantly involves brachial plexus irritation, while vasogenic thoracic outlet syndrome is from subclavian artery or vein compression. With diagnostic imaging improvement, pediatric thoracic outlet syndrome has been found more frequently. The objective of this study is to analyze the presentation, management, and outcome of pediatric thoracic outlet syndrome. The methods used in this study include a retrospective chart review, which was conducted for 43 patients undergoing surgery for thoracic outlet syndrome at Lurie Children's Hospital. Data was collected on demographics, preoperative presentation, perioperative characteristics, and postoperative outcome and follow-up. Mann-Whitney U tests, chi-square tests, and Ohms ratios were used for subgroup comparison. The variables collected in this study can be found on the bottom right of this slide. For results, 43 patients underwent 50 surgeries, 8 of which were done bilaterally. Average age was 15.5 years, with 72% being female. The most common symptoms were numbness and pain with an average duration of 35.2 months and with 58% having a normal physical exam. For imaging, patients most often underwent preoperative x-ray or MRI. 32% of patients used physical therapy preoperatively. A supraclavicular approach was performed in all patients, with anterior scalene resection, rib resection, neurolysis, and intraoperative EMG most often performed. Hospital stay was less than 48 hours for the majority of patients. Lymphatic leak was noted in 2 patients, and all patients had relief of preoperative symptoms. When investigating differences between neurogenic and vasogenic thoracic outlet syndrome, for which we had 36 and 9 cases respectively, we found that there was higher preoperative swelling, decreased symptom duration, higher venogram usage, and higher usage of preoperative thrombolytics in vasogenic compared to neurogenic thoracic outlet syndrome. No laterality differences were found. When investigating operative and postoperative characteristics, we found no differences between neurogenic and vasogenic thoracic outlet syndrome. In conclusion, most pediatric thoracic outlet syndrome patients are female and may have multiple years of symptoms. The supraclavicular approach is effective with a low complication rate. Differences exist in symptom presentation and management of vasogenic and neurogenic thoracic outlet syndrome in pediatric patients. Some of these differences include that vasogenic has higher preoperative swelling and usage of venogram and thrombolytics, but lower symptom duration in comparison to neurogenic thoracic outlet syndrome. Thank you for the opportunity to present at this conference. Surgical outcomes of redo peri-insular hemispherotomy, a single institution experience by Omar Iqbal et al. at Great Ormond Street Hospital for Children, London, United Kingdom. Peri-insular hemispherotomy is a technically challenging, labor-intensive operation. Successful outcomes for peri-insular hemispherotomy have been reported between 70 and 93%. Despite thoughtful patient selection and a well-executed surgical plan, failures of functional hemispherotomy still exist. Redo peri-insular hemispherotomy is complicated by distorted postoperative anatomy with difficulty in distinguishing residual connection from gliosis. We sought to evaluate the outcomes of redo peri-insular hemispherotomy and identify risk factors for recurrence. A retrospective review of all medical records of all children who underwent peri-insular hemispherotomy at Great Ormond Street Hospital for Children was performed. The data collected included patient demographics, diagnosis, initial angle outcome at one year or sooner if seizures return before one year, location of radiographic residual connection, EEG characteristics following index operation, medication requirements, and angle outcome after redo operation. The operations were performed by three surgeons. The majority of the index operations were performed by one surgeon. The surgical technique had evolved over 20 years of performing functional hemispherotomy. The technique of redo hemispherotomy always involved exploring all original locations of disconnections, followed by resection of residual tissue. Workup in the evaluation of redo hemispherotomy included MRI, EEG, with or without ictal spect. DTI was performed for all patients after 2015 following failed hemispherotomy. Between 1998 and 2019, 230 patients underwent peri-insular hemispherotomy. Of these, 25, or 10.9%, underwent redo peri-insular hemispherotomy. 22 of the 25 patients had adequate medical records to be included in the analysis. Five patients had two revisions and one patient had three revisions. The diagnoses recorded are listed here. The age at first operation average was 2.1 years, at a range of 2 months to 8 years. The sex, 15 males. Age at time of last operation, 7.32 years, for a range of 9 months to 16 years. Angle outcomes after index operation are listed here. The mean time to seizure recurrence for all patients was 29 months, at a range of 1 to 96 months. The mean time to seizure recurrence for angle 1 outcome patients was 50 months, for a range of 15 to 96 months. Angle outcome after final revision is listed here. Of note, 55% of patients ended with an angle 1 outcome. 55% of patients ended with an angle 1 outcome. Follow-up of 4.4 years, for a range of 2 months to 15 years. Of the angle 1 patients, 56% remained with an angle 1 after final revision. 0% at angle 2, 22% at angle 3, and 22% at angle 4. Of those patients with multiple revisions, 2 out of 6, or 33%, ended with an angle 1 outcome. Of note, 1 patient with 3 revisions ended with an angle 3 outcome. Seizures can return several years, following initial angle 1 outcome. Long-term follow-up is essential. Greater than 50% of patients undergoing redo, peri-ancillary hemispherotomy can achieve angle 1 outcome. Patients requiring multiple revision operations are less likely to achieve seizure freedom. Thank you. This presentation is entitled, Epilepsy Surgery in Young Children with Tuberous Sclerosis Complex, a Novel Hybrid Multimodal Surgical Approach. My name is Vijay Aravindra, and I'm a pediatric neurosurgeon at Naval Medical Center, San Diego. Tuberous sclerosis complex-related epilepsy. Medically refractory seizures can occur in 55% of children with TSC. Recurrent seizures after epilepsy surgery are of major concern. In TSC, modern data contend that before surgical intervention, more precise diagnostic efforts are needed to identify the offending tuber, as not all tubers are epileptogenic. In this study, we sought to investigate which method of treatment, either traditional open surgical resection or minimally invasive treatment, affords higher rates of seizure freedom and developmental improvement. Our hypothesis is that minimally invasive and traditional open approaches both achieve similar epilepsy control outcomes and serve as complementary techniques. This study was undertaken in children diagnosed and treated for TSC-related epilepsy. This study was undertaken in children diagnosed and treated for TSC-related epilepsy at Texas Children's Hospital from January 2016 through April 2019. They were treated by two senior pediatric epilepsy surgeons. The treatment groups included those that were treated with open surgical diagnostic treatments, including craniotomy for placement of subdural grids, strip electrodes, and or depth electrodes. Minimally invasive diagnostic treatment, which would include patients who underwent robot-assisted stereoelectroencephalography, or stereo EEG. Open therapeutic treatment, which included resection of an epileptogenic zone or seizure focus. And minimally invasive treatment, which consists of magnetic resonance guided laser ablation. The primary outcomes were angle classification and greater than 50% seizure reduction for the targeted seizure type. At Texas Children's Hospital, a multidisciplinary approach is utilized on a weekly basis, which consists of a meeting of neurologists, neurosurgeons, social workers, developmental psychologists, and radiologists who follow the algorithm as presented on this slide. 38 children total, 20 of which were female, were treated during the study period with a mean age of approximately 4. 90% of patients were Caucasian, 87% presented with some form of global developmental delay, and 95% with severe language delay. When looking at the two treatment cohorts, the mean age was higher in the laser ablation cohort, 4.9 years versus 2.4 years, and this finding was significantly different. And seizure frequency was higher in the resection cohort, 4.9 years versus 2.4 years. With respect to outcomes, there were similar rates of seizure reduction seen in both treatment groups, 86% and 88%. The length of stay was slightly longer in the open surgical resection cohort, 5.5 days versus 3.2 days, and the median angle class of two at last follow-up for both groups. With respect to overall seizure outcomes, 87% overall or 33 patients achieved greater than 50% seizure freedom after initial treatment. 84% experienced developmental improvement after surgery. The mean time to last follow-up was similar at 1.5 years, and the median angle class was two at last follow-up with similar rates of angle 1 and 2 outcomes among both treatment groups. Limitations of our study is a relatively small sample size. Recurrent seizures and treatment are of special interest in TSC, therefore a longitudinal study is extremely important. And measuring global developmental delay indirectly is definitely a limitation. Further neuropsychiatric testing is warranted. But in conclusion, surgical treatment has become critical in the modern management of TSC-related epilepsy. A hybrid approach of both open surgical and minimally invasive techniques are effective and safe. Iterative treatment of TSC-related epilepsy is required over time, and both open and minimally invasive methods are complementary. I'd like to thank my co-authors at the Texas Children's Hospital Multidisciplinary Epilepsy Team. We'll take any questions. Thirteen patients had prior treatment at other institutions, and we only had information available for six of them. All six underwent craniotomy for a section at outside institutions. Two patients had undergone greater than two resections. Of the six that were treated previously, five were treated with laser ablation and with no re-treatment. One patient underwent open resection at an outside hospital and then underwent a second open resection at our institute. With respect to re-treatment, nine patients underwent a second surgery, and five were treated with laser ablation. With respect to re-treatment, nine patients underwent a second surgery, and two underwent a third. Five patients that were initially treated with MR-guided laser interstitial therapy required additional treatment. Three underwent open resection. One underwent additional laser ablation, and one underwent additional laser ablation followed by an additional resection. Four children who underwent open resection required further treatment. Two laser ablation. One resection, and one laser ablation. There's no difference between treatment methods with respect to the time to the second treatment. Hello, my name is Meg Ryan, and I'm a first-year medical student here to talk to you today about the complications of intervecal backlifting therapy. We do not have any conflicts of interest to disclose. Intervecal backlifting therapy is a proven effective method for treating spasticity. However, it can have various complications. In this study, we reviewed the complications and efficacy of intervecal backlifting therapy in a large series of patients who underwent backlifting pump implantation at our institution. We reviewed the charts of 142 patients who underwent intervecal backlifting therapy. In our review, we included complications of both initial implantations and subsequent revisions, complications not related to surgery, and backlifting drug side effects. We also reviewed preoperative and postoperative side effects. We also included complications related to surgery and backlifting drug side effects. We also included complications related to surgery and backlifting drug side effects. The most common diagnosis on our patients was cerebral palsy, although there was some overlap between diagnoses. The most frequent tone abnormality was spastic quadriparesis. 78% of patients experienced at least one complication. Of these patients, 57% required a revision, and 50% did not require a revision. The most frequent tone abnormality was spastic quadriparesis. Of these patients, 57% required a revision, 13% required a surgery to address an infection such as a wound washout, 8% had a blood patch, and 20% of patients had their pumps removed. Pseudomeningoceles and catheter complications were the most frequent complications by far, although pseudomeningoceles usually resolve spontaneously. We saw as well that postoperative pseudomeningoceles were significantly less frequent when catheters were passed from the back to the abdomen in a subfascial plane than when catheters were passed subcutaneously. We reviewed other complications as well. Infections occurred in 20% of patients and after 11% of surgeries. Percutaneous CSF leaks occurred in 10% of patients and after 5% of implantations, and neurologic deficits occurred in only 1% of patients. We reviewed the differences in complications between catheter models as well. The newest models were associated with significantly fewer complications of any type. The difference in complication rates between newer and older catheter models was even greater for catheter-related complications. Patients who had a VP shunt or a G-tube prior to the pump implantation were no more likely to have a complication than patients who didn't. In fact, patients with VP shunts had a greater lowering of the upper extremity modified Ashworth score, as we can see here on this graph on the left. Pseudomeningoceles and catheter complications were the most frequent complication type. Fortunately, pseudomeningoceles usually resolve spontaneously, and fewer pseudomeningoceles were associated with passing catheters subfascially versus subcutaneously. The newest catheter model was associated with a lower rate of catheter complications than the older models. VP shunts and G-tubes were not associated with higher complication rates. In fact, VP shunts were associated with a decrease in upper extremity modified Ashworth score. Our study had several limitations, such as neurosurgeon experience with implantation surgery, patient length of time with baclofen pump system, and age of catheter models. Neurosurgeon experience and length of time the catheter had been implanted could have affected the complication rates between the newest and older catheter models. Thank you for listening. All right. Thank you to those abstract presenters for those wonderful talks. Really enjoyed those. There have been a couple of questions come up in the chat. I see some of them have been answered already. That's wonderful. Of course, over in the conversation lounge on the remote platform, all of these authors should be available. Please head over there and ask them your questions and engage in this discussion. We'll have about a five minute break to do that and we'll see you back here for the start of the next session. Thanks very much. you Welcome back. We're going to show our sense of community, really the spirit of pediatric neurosurgery. So this year we had a social media challenge with Brainy Halloween 2020. We had entries from all around the country and you're going to see what your colleagues and friends dressed up as for Halloween. After we see these pictures, we're gonna have a live vote. So please pay attention and get ready to vote for your favorite. ♪♪ Thank you, everybody, for voting. That was amazing to see how creative our friends and colleagues are around the country. I hope this is the start of a tradition. I had a ton of fun with this, and I'm glad everybody is so engaged with the voting. So the prize is fame and honor in pediatric neurosurgery, and really, I think just the community spirit, especially in this year, is really prize enough, and it was awesome. So the votes are still coming in. It looks like Lurie Children's Hospital with Trolls is getting the most votes. Brandon Rock just told me this is rigged. The second most votes is the Johns Hopkins Group with the Brain Anatomy, then Mount Sinai Neurosurgery with the Cranial Nerve Anatomy, and then Children's Hospital of Los Angeles with the group dressed as Grease. So I thank everybody for participating in this, and this was a lot of fun. And I'm sure the patients enjoyed it, too. So switching gears, next we're in for a treat. We have our invited speaker, Professor John Rogers from Northwestern University. He has a CV that is way too long to list. He's had education and worked at the who's who of science and engineering, UT Texas at Austin, Harvard University of Illinois at Urbana-Champaign, Bell Labs, and then now Professor at Northwestern University with the highest accolades and actually in multiple departments and doing amazing translational work across engineering, physics, chemistry, and really bringing technology to medicine and helping people. So without further ado, we're so excited that you're here, Dr. Rogers. Thank you so much. Okay, great. Thank you for that introduction, Dr. Lam. I hope this talk lives up to that hype you provided, but I'll do my best. So as was mentioned, you know, I'm an engineer, very interested in biomedical engineering, more specifically. My training is in material science, electronic material science. And so we've attempted over the last 10 years to develop the foundations for sort of skin-like, highly non-invasive wireless biosensors that can kind of reproduce ICU grade vital signs monitoring with a real focus on beginning of life. So pediatric patients, neonates, expecting mothers, some maternal, fetal, neonatal, pediatric health. And that's what I'll share with you today. We're very active kind of at the boundary between engineering and medicine, looking to develop, you know, new academic science, but in the support of technologies that can really have an impact on patients and healthcare more generally, attempting to reduce costs and improve outcomes is kind of what we do. So it's highly interdisciplinary appointments across many departments here at Northwestern, but maybe one of the most important affiliations I have is with the Department of Neurological Surgery because that really ties us in very strongly, not only to the medical school here at Northwestern, but the broader medical community, medical complex here in Chicago. And I'm really fortunate to have deep, productive engagements across many branches of the medical system here. And I'll share with you some of the advances that we've made just in the last few years around devices targeted toward pediatric intensive care. And I hope this kind of resonates with the audience, but to give you a sense of where we are, what kind of devices are being deployed and what's kind of in the pipeline, what's next. And so, you know, what we tried to do from an engineering science standpoint is to create devices that are wearable systems in a sense, but are skin-like and soft and thin in their construction. So moving devices, wearables away from, you know, kind of watch-like platforms that interface loosely with the body at the wrist and are capable of capturing sort of qualitative, maybe not too terribly meaningful metrics around health status, steps, and maybe sleep metrics and so on to full clinical grade ICU data streams that the physicians and nurses understand and know how to interpret and act upon. And this is a picture of a device that we published maybe almost 10 years ago now. It was sort of a platform at that point. I think we began to feel like we understood how to do the engineering, how to build advanced electronic digital systems, radios, power supply systems, skin interface, clinical grade sensors, and so on, into platforms that looked like they could be the realistic foundations of technologies that would allow us to envision a PICU, for example, of the future, one that doesn't rely on tethers and wires and adhesive tapes, but just gentle interfaces through devices that are much like kids' temporary tattoos, as what I'm showing you here, or maybe slightly thicker, depending on the engineering requirements, more like a Band-Aid. So we published the first work back in 2011, got a little bit better in 2014. And since that time, we've really focused on translating these devices into platforms that are addressing real clinical needs and working closely with hospitals and patients to deliver things that have a potential meaningful role in patient care. And so the underlying science is really around how do you take a rigid computer chip type technology that forms the basis of a smartphone or a laptop and reconfigure it, reformulate it into a platform that has soft tissue-like characteristics, and in particular, mechanical properties that are very much like those of the epidermis itself, with the idea that you create almost like a second skin that can very gently, but robustly and intimately, interface with the skin, but without a requirement for strong adhesives that can be damaging to the skin of pediatric patients, and neonates in particular. So it's really a combination of material science, mechanical engineering, electrical engineering. There's some signal analysis that comes into play as well, but configured in close collaboration with nurses, neonatologists, pediatricians, and so on, to deliver devices that can be used in a practical way in a hospital. So that's kind of at a very high level, kind of the architecture and the platforms that we're talking about. They're quite generic in the sense that they can accommodate many different types of sensors. We've looked at precision thermal, you know, characterization of the skin, all kinds of electrical measurements, biopotential, ECG, ENG, EEG, I'll give you a sense of that. We can even capture minute volumes of sweat and biofluids that are emerging from the surface of the skin, and we can route those around and do sort of biochemical analysis. We can measure body sound, strain, motion, modulus, pressure, different kinds of optical measurements. Oximetry is pretty straightforward for us to do. Really kind of a broad toolbox of different types of functionality that can be integrated into a single device of that type, and then you can mount these devices really on the relevant parts of the anatomy without constraint, in a sense, and you can run multiple devices simultaneously in a time-synchronized way. So there's a lot of versatility there that we can bring to bear on real unmet clinical needs, and what we focused on initially, this is going back maybe four years now, is premature babies and thinking about NICU care and how vital signs are monitored today, and I don't need to go through this. This is an expert community, but the wires and the rat's nest of hardware and the adhesive tapes and so on, it's old technology. There's no reason why we should be doing things in that way today because I think, you know, this wireless platform can serve as a really powerful alternative. So this was sort of a Photoshop vision of what we had hoped to do, you know, starting maybe four or five years ago, which is to replace the wires and all the constraints on the babies and the inability of parents to sort of engage with their babies due to the wires and so on, and the kinds of skin injuries that can arise from application and removal of the adhesive tapes to these skin-like wireless devices, maybe two or three of them, depending on the need and the requirement, and do things that are a lot more patient-friendly and better for the babies, essentially, and so I won't go through the details. It turns out you can do all of that. We published our first paper just last year, but these are battery-free skin-like platforms. There's two devices that you can use to recapitulate all of the vital signs that are being monitored, even at sort of a level four NICU, and we've done all this work in close collaboration with neonatologists, dermatologists, and pediatricians at Lurie Children's Hospital, Princess Women's Hospital here in Chicago. I won't go through the details to just make the argument that you can actually do all of that. We're probably 150 neonates into a set of clinical studies where we're benchmarking the performance against the standard of care, which is these wire-based systems. This is a 31-week-old baby here. You can see the chest unit mounted on the chest. You can see the wires for the ECG leads. This is the standard way that cardiac activities monitor, obviously, but it provides dual data streams where you can do quantitative validation of the devices themselves to establish accuracy. We started in the NICU. Deep into that, folks were fairly happy with the way things were going, and so we've actually expanded into the PICU as well, bigger babies, but still, in many cases, needing that kind of continuous 24-7 vital signs monitoring. This is the baby. You can see the chest unit here, and then we have another unit that goes on the limb, either the foot or the hand, to monitor blood oxygenation. With those two devices operating in a time-synchronized way, you get full vital signs in that manner. So ECG, again, clinical grade, all wireless, continuous monitoring with accuracy and precision that lines up quite nicely with clinical standards. So heart rate, heart rate variability, get an estimation of respiration rate from the depth of the RP. We have a clinical grade temperature sensor as well. You get a skin temperature measurement on the chest, and then the limb unit is doing optical measurement of oximetry. So this is photopleth, and you get blood oxygenation. You also get another estimate of heart rate, and the time-synchronized behavior of these two devices allow you to get pulse wave velocity as well, sometimes can be used as a surrogate for systolic blood pressure. So a lot of these things are possible. That's kind of what we've done to sort of pilot the technology. We were approached by the Gates Foundation, the Save the Children Foundation, to think about deploying those kinds of technologies into parts of the world where there aren't any monitoring systems at all, wired or wireless or otherwise. And so we started working with the Gates Foundation, Save the Children, deploying devices into India, Pakistan, Zambia, Kenya, and Ghana. So we're deep into that process. I spent a couple of weeks in Zambia about six months ago, and it's quite an emotional thing to see, you know, monitoring, sort of, you know, level four NICU monitoring capabilities being brought to that kind of part of the world. We had to change some of the design parameters and the engineering approaches, ruggedize the devices a little bit to allow for use in these remote settings. This is, you know, a paper that we published just earlier this year on the technologies that are being deployed in that way today, just to give you a sense of that. But these devices also offer additional functionality, so there's high bandwidth accelerometers, so you can measure vocal biomarkers, cry time, cry tonality, cry cadence. You can determine body orientation, really thinking about, you know, what kind of future capabilities might be possible by building on these sorts of platforms. This is a really rich range of opportunities here. So we start with the basics, vital signs. There's no reason to stop there because now you have a foothold. You can begin to drop new sensor functionality into these kinds of devices that go far beyond what's done today. Heart sounds, for example, valve openings and closing, you can capture all of that continuously. Same devices. So that's kind of what we're doing, is to give you a sense of what the pipeline looks like. So we have non-invasive devices we develop with folks in neurosurgery here for measuring flow of cerebrospinal fluid through shunted hydrocephalus patients, mostly pediatrics, but that provides a new measurement capability that, you know, doesn't exist today. We can do functional NEARs. I'll show you that in a second. We can do fetal ECG. We can do neonatal EEG. We can also monitor vital signs in the context of surgical recovery. Again, focus on pediatric patients. So going far beyond actigraphy to full vital signs monitoring during that recovery process, and that's working very well also. But let me just give you a sense. This is kind of our latest work. It's in press now, but it's sort of a band-aid-like device that does full-blown NEARs. And so it's multiple photodetectors, multiple LEDs, and so you can get a pretty good picture, clinical-grade assessments of cerebral hemodynamics, but without the wires and in a reusable sort of adhesive patch type format. We've done quite a bit of, you know, initial pilot studies of that device on pediatric patients and actually get better signal-to-noise ratio than what you would see in a standard wired NEARs device. You can see that in the blue and the red is our device is quantitatively accurate. It's actually better because you eliminate a lot of motion artifacts associated with tugging on the devices associated with the wire-based interfaces. A lot of that noise goes away quite naturally. So anyway, that's kind of a summary. I think I'm pretty much out of time, but I just want to highlight, you know, kind of what we're trying to do at a translational level working at the boundaries between engineering and medicine and working in a highly collaborative mode as well. We have deep interfaces to various, you know, expertise in engineering, science, senior collaborators, and then the clinical medicine interface is really important for us, and I list several of the main collaborators we have there. But ultimately, it's an academic group, and those students and postdocs are doing the work. I just get to talk about it. So I always like to conclude by acknowledging their efforts and thanking you for your attention. Thank you so much, Dr. Rogers. That is amazing. Can I just say you are a neurosurgeon's dream come true for collaboration. I mean, the possibilities are endless. I guess I'll start off the questions. What in your mind makes a good collaborator for you? Because you're going to have the huge line virtually in person. I would say, you know, I think physicians who have an interest in technology, you know, those folks tend to be the best collaborators, but probably little patients, you know, because this is all new stuff. You know, I think a certain fraction of the clinical community has expectations that, you know, things coming out of an academic lab are going to be like a commercial product. It's not that way. You kind of have to be willing to work with us and tell us what works, what doesn't, and, you know, there are iterations, and kind of being able to stick with it a little bit is a good thing. You know, all this stuff is really hard, and I think people who understand the level of difficulty that we're talking about here and are willing to kind of go back and forth with us a few times, those folks tend to be the best types of collaborators. But I have to say, overall, great, great experiences. You know, I think, you know, the medical community is very similar in some ways to the engineering community in the sense that we're both very interested in problem solving, you know, and I think the hospital environment is very problem rich, and engineers love to work on problems and try to come up with solutions. So I think it's a great synergy there, and we've had great, you know, sets of collaborations. I can't say that I have any negative experiences, so maybe we've gotten lucky. I don't know, but it's been really wonderful. Great. So since we're in the epilepsy and functional day, we'll ask that we see that that's in your pipeline, neonatal EEG. What are the unique challenges to, I guess, you know, neonatal EEG or, you know, vis-a-vis what you've done with other types of monitoring in babies? Yeah, it's a great question. I mean, ECG is much easier. I mean, the amplitudes are, you know, 100,000 times, 100 or 1,000 times larger. That's kind of the biggest challenge, and I think for amplitude EEG, it's a little bit easier and a little bit more similar, I guess, to the single lead ECG that we're doing. The device that's being shown here is, you know, multi-lead. I think it's eight channels in this case, and that seems to be the strongest pull that we've experienced, and so we've kind of focused on that, the multi-channel. Doing the amplitude is easy from there, and maybe that's useful as well for more routine neurological assessments of, you know, status, but it's really the signal amplitude that makes it much harder. I mean, scaling to multiple leads is not too bad, but dealing with the very low signal amplitudes and, you know, the correspondingly higher significance, I guess, of things like motion artifacts has been the main challenge, but I would say it hasn't been, like, a severe challenge. I mean, I think that this was not something that we focused on initially, and so it's not, you know, just now entering the pipeline because it was impossibly difficult. It's just that we didn't get to it, you know, until, you know, fairly recently. We wanted to knock off the highest priority items, which is the basic vital signs. That seemed like the best place to start, and from there, now we're kind of expanding out, and this is giving you a flavor of some of the things that we're looking at, but we don't have a lot of patient data yet with the neonatal EEG system. We've done adults, and it looks like it lines up very nicely with, you know, clinical state-of-the-art. I don't expect any problems there, but the pandemic has really slowed us down in terms of patient recruitment. I think that's been the biggest bottleneck, well, by far the biggest bottleneck, actually, and so as things loosen up, I think that will move forward very quickly. I don't see any real challenges there. Okay, we'll have one more question on this platform, and then I invite further Q&A on the Remo platform because there are a ton of questions coming in for you. So, our closing question is that actually, Brandon and I, our moderators today, actually have a big interest in global neurosurgery, so we're excited to hear about your work in the developing world. So, I guess for you, what was the most daunting thing that you saw when you went to Africa in terms of your work, and what is the most exciting thing about your work in Africa? Well, I'll start with the second part. I mean, the most exciting thing is the need is tremendous, absolutely off the charts tremendous, you know, and so I think the possibility for making an impact there is very strong. You know, I think it's one thing to make monitoring a little bit better, get rid of the wires, get rid of the adhesive tapes, it's great, there's a lot of interest, we're doing that, but we don't have anything, you know, I think this becomes a whole other level of value proposition, I guess, is the way you can think about it, and I wasn't really aware of the value of monitoring fully until I was there myself, and the real challenge is a dearth of trained health care workers, and so you have the individuals who are spread thin, you know, like at a whole other level, and monitoring allows them to focus their attention on the patients in greatest need, so they can juggle larger numbers of patients effectively, you know, and so that's where sensing comes in. It really allows, you know, those clinics to much more effectively leverage the personnel that they have, so they can oversee larger numbers of patients, but the challenges are just, you know, multi-faceted, I guess, I mean, one thing is there's no reliable source of wall plug power, so, you know, we couldn't use the battery-free device design, we had to embed small rechargeable batteries into these devices themselves, you know, that's number one, there's no reliable internet access either, everything needed to be stored locally in the devices, and you have to use cell phones rather than hospital monitors as user interfaces, it's a whole other world, cost is absolutely dominant consideration, it's a whole other level, so before Gates even kicked this program off, we had to go through cost modeling, and you have to think about it in terms of cost per patient day, so the devices have to be reusable, you have to be able to recharge them, you have to be able to use them a large number of cycles of use in order to amortize the cost of the device out of the overall per day cost structure, so there are a number of technical and economic challenges, but it's been a great engagement, and Gates has a very strong presence in these countries, and so it provides a great vehicle for us to get devices out into the field. Thank you so much, we're going to have to move to the remote platform, because there are so many neurosurgeons who have a lot of questions for you, and want to continue the conversation, so we're thrilled you're here today, and we all learned a lot, we're so excited. Welcome back, welcome back, hope everybody got a chance to chat in the conversation lounge, we're about to start our next batch of abstracts, we've got another set coming now, so without further ado, we'll get those rolling. My name is Jonathan Parker, I'm a six-year neurosurgery resident at Stanford, and I'm going to be sharing with you today some of our work looking at patterns of anti-epileptic drug reduction after pediatric epilepsy surgery. I have no disclosures. As many of you know, there are several existing challenges that plague epilepsy surgery outcomes research. One of these is that clinical studies of pediatric epilepsy surgery often rely on time-consuming, labor-intensive, retrospective manual chart review, or patient-or-family questionnaires to evaluate seizure frequency, anti-epileptic drug use, and other outcome metrics. These surveys can also be subjected to recall bias, which limits their utility. Lastly, existing administrative and billing databases provide an alternative, which has granular access to medication prescription data with resolution at the single drug, patient, and duration level. We set out to use these administrative databases to answer several questions that are pertinent to epilepsy surgery outcome. First, do clinical or surgical variables exist which predict AED freedom in children undergoing epilepsy surgery? How durable is this AED freedom? And finally, are reductions in AEDs associated with changes in healthcare expenditures and utilization? Inclusion criteria for the study were as follows. The patient had to be less than 18 years of age at the time of surgery, and the patient had to have undergone an eligible epilepsy surgical resection procedure, listed here on the right, and also had to have at least one year of outpatient pharmaceutical records. We intentionally excluded patients who underwent complete hemispherectomy or calisotomy, as the intention of these procedures is not a surgical cure of the patient's epilepsy, and we also eliminated those patients who did not have adequate outpatient pharmaceutical records. To define our endpoints, we used an AED free period, which was a 90-day free period without an active AED prescription, and we also defined a stable AED decrease period, which is 90 days with a mean decrease of at least one AED less than the preoperative baseline. To describe our cohort, we only included patients who underwent surgery between 2007 and 2016. This captured 1205 patients who had a qualifying epilepsy resection, however, only 348 patients met all inclusion criteria. Approximately 51 percent underwent intracranial monitoring prior to their epilepsy surgery resection, two-thirds achieved an AED, stable AED reduction, and 43 percent achieved at least one three-month period of AED freedom during their follow-up. We first looked at our cohort in a single variant analysis, looking at the group that did not achieve AED freedom versus the group that did. Although tuberous sclerosis patients only made up eight percent of the cohort, we found that they were overrepresented in the group that did not achieve AED freedom. Additionally, as we expected, the AED freedom group demonstrated increased length of follow-up compared to the did not achieve AED freedom group. Further, looking at resection type, we found that those patients who underwent an epileptic focus resection were overrepresented in the did not achieve AED freedom group versus those who underwent temporal lobectomy, which were overrepresented in the achieved AED freedom group. We next performed a Cox proportional hazards analysis to mitigate the effects of potential covariates in this analysis. We looked at both the patients who achieved an AED free period and those who only achieved a stable AED reduction. We noticed that the patients who carried the diagnosis of tuberous sclerosis had a decreased probability of both achieving AED free period and a stable AED reduction period. However, in the patients that achieved a stable AED reduction, higher preoperative number of anti-epileptic drugs was associated with a higher probability of achieving a stable AED reduction. We next looked at the timing of AED reduction in a visual format using a heat map with increasing color temperature representing increased number of anti-epileptic drugs. As you can see represented in the rows, the type of surgical resection was separated out into four groups. Amongst those children who achieved an AED free period, this occurred on average 20 months after their index surgical resection. AED freedom amongst these patients was durable through follow-up and over 50 percent, and we also secondarily looked at the time to reduction of the first AED, which was not significantly different between the two groups. We then looked at health care costs. Comparing the costs between the two groups, we found that the cost of the index admission was significantly higher and they did not achieve the AED freedom group, most likely representing the underlying complexity of their epilepsy and the surgical modality utilized for treatment. Next, we looked at the pharmaceutical costs, which as we expected were significantly decreased by over 50 percent in the AED freedom group on a per patient per day cost analysis. We found that this was a reduction in over $12 per day compared to the preoperative baseline in pharmaceutical costs. Looking at health care utilization, we found that children who experienced AED freedom had lower rates of readmission and ED visitation, which were both significant, and also a decreased number of neurology visits within the first year after resection, although this did not reach a statistical significance threshold. Finally, we conclude that patients with a higher mean number of preoperative AEDs demonstrated increased probability of reduction in AEDs after surgery. Across this heterogeneous population of children, a diagnosis of tuberous sclerosis was associated with a decreased likelihood of AED freedom and reduction of AEDs. This decreased AED use in children who achieved AED freedom resulted in over a 50 percent decrease in pharmaceutical costs. Lastly, outpatient pharmaceutical records such as those utilized in this study are an attractive data resource that allows for large-scale longitudinal analyses of epilepsy surgery outcome. Critically, further study of pharmaceutical prescription changes in these administrative databases is necessary to validate a potential correlation with patient slash family reported epilepsy surgery outcome measures. We'd like to acknowledge that team that completed this research and our mentors, as well as provide appropriate resources for the current study. Thank you very much for your time. Hello, my name is Nathan Schloben. I am a medical student at the Northwestern University Feinberg School of Medicine and a researcher in the Division of Pediatric Neurosurgery at Ann and Robert H. Lurie Children's Hospital. I will be discussing vagus nerve stimulation after failed colonoscopy. I will be discussing vagus nerve stimulation after failed cranial epilepsy surgery in pediatric patients. So as background, epilepsy affects 0.5 to 1 percent of all children. Vagus nerve stimulation is a neuromodulatory treatment choice for children with refractory epilepsy. However, little is known regarding outcomes after VNS as a last-line therapy in children. We examined our experience with VNS deployed as a last-line treatment after medical management and targeted epilepsy surgery to guide the management of these patients. Moving on to the methods, we conducted a retrospective chart review of patients seen at our institution from January 2010 to January 2020. All pediatric patients age 0 to 18 years old who received VNS after cranial epilepsy surgery were included. We collected variables including demographics, clinical data such as epilepsy characteristic, video EEG findings, and radiographic findings, previous surgeries, and outcomes after VNS. After conducting the study, we included 44 patients age 10.3 plus or minus 4.8 years. 56.8% of patients were right-handed, 25% left-handed, 9.1% ambidextrous, and 9.1% unknown. 6.8% of patients had a family history of epilepsy, 25% had genetic associations, and the etiology was classified as congenital or structural in 47.7%, acquired in 22.7%, and other in 29.5% of children. Seizure type included 97.7% impaired awareness, 97.7% motor, 84.1% generalized, and 34.1% atonic. 75% of patients had abnormal radiographic findings, and video EEG showed 36.4% of patients had multifocal epilepsy, 29.5% generalized, and 27.3% focal. Patients were taking an average of 3.1 plus or minus 1.3 antiepileptic drugs preoperatively. Before VNS, 36.4% had phase 2 monitoring, 31.8% corpus callosotomy, 29.5% lesionectomy, 20.5% MRI guided laser interstitial thermotherapy, 15.9% lobectomy, and 4.5% hemispherectomy. The average time from seizure diagnosis to VNS implantation was 7.6 plus or minus 4.2 years. Seizure outcomes were identified in 56.8% of patients. The mean seizure reduction was 58.4% plus or minus 34.1%, and 64% of patients had at least a 50% seizure reduction, and follow-up length was 5.3 plus or minus 3.4 years. In conclusion, VNS is a palliative therapy option for pediatric patients who fail treatment with other modalities. Nearly two-thirds of patients experience at least a 50% seizure reduction. However, future studies are necessary to identify patients that may benefit from VNS in order to stratify management. Thank you. Thank you very much to the pediatric section for this opportunity to share our work. My name is Andrew Hale, and I'm an MD-PhD student at Vanderbilt, currently applying to neurosurgery residency programs. Cerebral palsy is a heterogeneous and poorly understood disease, and while there have been a number of antenatal, perinatal, and postnatal clinical risk factors that have been identified, far less is known about the genetic basis of the disease. And although targeted approaches, such as candidate gene sequencing or analysis of protein coding variants by exome sequencing, has been performed, no unbiased genome-wide association study has been done, and this severely limits our understanding of potential genetic risk factors. Thus, to start to answer this question, we performed the first genome-wide association study for cerebral palsy, and in fact, the largest genetic study of cerebral palsy to date. And we limited our analysis to patients with the spastic subtype of CP, and of patients of European ancestry. After controlling for covariates, including age, sex, and five principal components, we identify a single SNP reaching genome-wide significance. But how is this SNP contributing risk? And what is the underlying mechanism leading to clinical features of CP? To start to answer this question, we performed expression quantitative trait loci, or EQTL analysis, which is a method to determine what effect a SNP has on gene expression. And this approach mapped this SNP to decreased expression of GRK4 in patients that are heterozygous, shown here by the CT designation, or homozygous, TT, for this SNP. GRK4 is a member of a glutamatergic or canate preferring ligand-gated ion channel family, which has been previously implicated in neurodevelopmental and psychiatric disease. But is this association unique to our population? And does variation in GRK4 and other GRK isoforms more broadly underlying CP risk in an independent cohort? The answer is yes. And here we provide independent replications for additional variants in the GRK4 locus in independent cohorts in the United Kingdom and Finland, totaling just over 1,000 cases. And not shown here, we also observe highly significant variance in other GRK family members, most notably GRK1, suggesting that genetic variation in this receptor family more broadly may confer significant CP risk. But what are the functional consequences of GRK disturbance? And since our lead SNP-reaching genome-wide significance is associated with decreased GRK expression, what are the phenotypes associated with GRK loss of function? So we went to the literature. And we found this paper from the Contractor Lab at Northwestern, who undertook the Herculean task of generating mice lacking all five GRK isoforms. And in this knockout animal designated 5KO in red, they demonstrated reduced amplitude of corticostriatal action potentials, shown here by voltage clamp recordings. They also show decreased number of excitatory synapses, i.e., reduced spine density in the D1 and spiny projection neurons within the striatum in the knockout animals. But most strikingly, the knockout animals display hind limb clasping, contracture, and motor deficits, suggesting that loss of GRK function, as suggested by our GWAS analysis, recapitulates the phenotype seen in human patients with cerebral palsy. So in conclusion, we performed the first genome-wide association study of cerebral palsy in the largest genetic study of the disease to date. EQTL analysis of our top SNP points to decreased expression of GRK4 underlying CP risk. And deletion of GRK isoforms in mice recapitulates features of spastic CP, suggesting that our candidate is a prime target for further study. I'd like to thank my mentors, Dr. Seva Shannon and Rob Naftal for their support, as well as the funding sources listed here, and I'm happy to take any questions. My name is Afshin Salehi. I'm the fellow at St. Louis Children's Hospital, and I'd like to talk about the single-center cost comparison analysis of sero-EG to subdural grids and strip implantation. The preoperative assessment of a child with epilepsy encompasses two methods. The non-invasive method, which includes MRI, video EEG, SPECT, and MEG. And the invasive method, which is indicated for non-lesional imaging or when there's a need to map elephant cortex in relation to epileptic zone. That includes subdural grids, which has long been the gold standard for invasive monitoring, good for 2D surface analysis, and good for mapping language and motor. And the sero-EG that's gaining traction in recent years that's less invasive, easier on the patient, and allows for 3D mapping of the actual discharge. While there has been a number of studies that have talked about the surgical considerations between the two, the complications raised and outcomes, to my knowledge, there has been no direct cost comparison between the two techniques. To that end, we went through our cases from 2013 to 19 and put together two comparable groups with nine patients in each arm that are similar in age range, male to female ratios, and severity of baseline seizures prior to treatments. We have two very different workflow between the two procedures. In the subdural grids, patients undergo grids and strip placement, followed by one to two days of ICU stay, and then to the EMU for monitoring until sufficient data is collected during seizure events, and then back to the OR for grids removal and the resective surgery. This is then followed by ICU and floor for recovery phase and discharge home. In contrast, in the sero-EG, the patients undergo procedure for a sero-EG implantations, they'll skip the ICU and go directly to the EMU for monitoring until sufficient data is collected during seizure events, and then back to the OR for removal of the electrodes and discharge home. Then the epileptologist and the neurosurgeons review the data, and once a decision has been made at a later date, the patient is brought back to the OR for the resective procedures, followed by the ICU and floor for the recovery phase, and then discharge home. There's a two inpatient hospitalization for a sero-EG. Our data shows, including the two hospitalizations for a sero-EG, that there is a statistically significant longer duration of ICU stay in the subdural grid. This is because the sero-EG implantation does not require ICU stay afterward. There is similar duration of invasive monitoring and total length of stay between the two groups. Outcomes were favorable with no 30-day readmissions. Due to the fact that we send patients home between the sero-EG implantations and the resective surgery, we have significantly longer time from monitoring to epilepsy surgery in the sero-EG. We had two complications in the subdural grids, which included a minor wound dehiscence that resolved with oral antibiotics, and immediate post-op weakness that came back with a short course of steroids. The inflation-adjusted costs are shown here. Like most places, we had a shift towards sero-EG in recent years, and therefore we had to take into account inflation adjustment for a more accurate comparison. The grand total cost between sero-EG and subdural grids were similar, with statistically significant higher seen in the neurosurgical fees, likely due to the fact that sero-EG is essentially three procedures while subdural grids is two, and significant lower fees in neurology for sero-EG. In summary, we retrospectively reviewed our experience from 2013 to 19, using nine sero-EG patients and nine subdural grids patients. We showed that subdural grids had longer ICU stay and shorter time to resection. Showed that overall fees and costs adjusted for inflation was the same for both sero-EG and subdural grids, and the fees for neurosurgery was higher due to the fact that there was three OR events, and the fees for neurology was less, likely due to the fact that there's, on average, shorter EMU stay. Good afternoon, thank you for the opportunity to present this work today. These are our disclosures. Drug-resistant epilepsy is a large-scale problem. As you can see, the number of patients treated with epilepsy surgery is dwarfed by the total number of patients with drug-resistant epilepsy. This represents an opportunity for innovation and improved treatment. RNS is a neuromodulatory treatment for drug-resistant epilepsy that has been deployed for the treatment of adults. However, pediatric applications are not yet FDA approved, so the device can only be used off-label. Pediatric epilepsy is commonly extratemporal, non-lesional, or multifocal, and associated with underlying congenital malformations. While disconnective and resective surgeries are effective under the right circumstances, there are many patients who do not achieve maximal relief with these interventions. Furthermore, the ability to modulate therapy without taking an irreversible destructive approach is appealing to families and practitioners alike. We maintain a prospective single-center database of pediatric RNS cases. This study consists of a retrospective review of this database in which we collected additional data regarding the response to treatment and complications. Children ranged in age from seven to 17 years and were evenly divided between boys and girls. Mean follow-up was almost two years. Syndromic and multifocal epilepsy etiologies predominated. Stereo EEG was the primary localization technique, and seizure foci identified by intracranial monitoring were spread widely within the cerebral hemispheres, as you can see here. Here we have the annual implants over the course of the last several years and demonstrate that the connected leads were widely spread but approximately 50% of them were either mesial-temporal or parietal, and thalamic leads comprised approximately 20% of the connected leads. 10% of patients were seizure-free during the follow-up period, and 65% achieved a greater than or equal to 50% seizure reduction. Importantly, a large number also experienced reductions in their seizure duration or severity or had improvements in their post-ictal recovery. Complications were rare, and only one patient's device could not be salvaged. The other three infection-related complications could be salvaged with either local wound care, antibiotics, or partial debridement. There were no major neurologic complications of placement. We demonstrate here that RNS placement in the pediatric population can be safe in our series with a low rate of operative complications. There was no relationship between age and complications. Many patients experienced dramatic reductions in seizure frequency as well as severity, demonstrating the efficacy of this intervention in the first six months to four years after placement, which was covered in our follow-up period. We acknowledge that this retrospective study has its limitations, including its relatively small size and lack of other measured quality-of-life outcomes. We would also benefit from longer follow-up to monitor seizure outcomes over time with the device in place. Further study will help us elucidate the efficacy of this device over longer treatment durations, as we have seen the seizure control in these patients evolve as the device's settings are gradually calibrated. We would also like to explore more granular neuropsychological changes and effects on quality of life. Ultimately, we expect, based on this early data, that RNS will become an important tool in the treatment of pediatric epilepsy and hopefully expand our ability to treat these patients with drug-resistant epilepsy. Thank you for your attention and time, and thank you to my colleagues and co-authors in the Mount Sinai Epilepsy Program. I look forward to your questions. All right, that's an excellent session of abstracts. I see some questions appearing in the Q&A. I encourage everyone to pop over to the Remo Conversation Lounge for a few minutes to ask the presenters in person, in person-ish. But please come back on time for our next session. We're gonna have a fascinating discussion of technical aspects of selective dorsal rhizotomy. Come back on time. It'll be 3.28 Eastern time. All right, welcome back. Our next session features four experts, expert pediatric neurosurgeons, that will be showing us their technique for performing selective dorsal rhizotomy. This is an operation that a lot of us do. There's quite a bit published about it. Outcomes are pretty similar across all of the published series, but there's a wide variety in technical nuance for how this operation is performed. So we have four fairly different techniques that we're gonna demonstrate today. And I encourage everyone to stay and ask questions of the presenters live. In this session, we'll have about 10 minutes to ask questions in person. I'll read them out to the presenters after the videos have played. So get ready to see Dr. Partington, Dr. Bolo, Dr. Browd, and Dr. Wilkinson, and how they perform dorsal rhizotomy. Bony exposure consists of a T12 through L2 laminotomy hinged at the top. I take T12 in order to be sure that I can see the L1 root intradurally. The intradural exposure involves opening dura high enough up to see the L1 root as it exits because it will be dissected at the foramen like in the peacock model. And the remainder of the rootlets are done from there down on the dorsal side only all the way to the tip of the cone is similar to the Taesung Park procedure. As stated at the L1 root, we're doing this at the foramen, but divided down to about three or four rootlets cutting anything that has a pathological EMG response. This is usually one or two out of four rootlets. At the other levels, separate the dorsal roots from the ventral roots, create three bunches of these rootlets and upper lumbar, lower lumbar and sacral set. I then do stimulus to find pathologic threshold for each bundle and then dissect and test and cut the roots in each bundle as a group. They're dissected to about a one or two millimeter diameter and we cut those with abnormal EMG or clinical activity. Simple reflex ones are kept as are those that activate sphincter only. Abnormal EMG means multi-segment or bilateral spread or bizarre responses. We do something like 40 rootlets per side, about 80 total, cutting 25 to 45%. Laminotomy is then suture repaired. The bony exposure is dependent upon the level of the conus on the preoperative MRI. Typically involves just L1 but may extend from T12 to L1 or L1 to L2. The level of the nerve dissection is at the conus and proximal caudal quina with exposure of L1 and sometimes L2 exiting the fecal sac laterally. After the patient is positioned, we place a spinal needle based on bony landmarks and get an intraoperative x-ray to correlate with the preoperative MRI to determine the skin incision and bony opening. The skin incision is made after infiltration of local anesthetic and prepping the field and the bony work is then done for epidural exposure. Ultrasound is used to confirm exposure of the conus and proximal caudal quina and the dura is then opened and tented laterally. Next, we isolate L1 exiting the fecal sac laterally, separate motor from sensory, confirm this with stimulation, separate the sensory root into rootlets and cut the most abnormal rootlets. We then isolate the small sensory roots coming off the distal caudal quina from the remainder of the sensory roots and the ventral roots using the conus as a guide to separate dorsal from ventral. We then place a background underneath the dorsal roots from L2 to S1, confirm this, clip it to the dura on the contralateral side and then proceed from lateral to medial or proximal to distal, confirming each root is sensory, separating it into four to six rootlets, stimulating each and cutting the most abnormal, typically 50 to 60% for an ambulatory patient and 70% for a non-ambulatory palliative case. We then remove the cotinoid isolating that root from the remainder of the dorsal roots and proceed to the next. Again, we confirm it's sensory, place a cotinoid between it and the remainder of the dorsal roots, separate it into four to six rootlets, stimulate each and cut the most abnormal rootlets. We then proceed in a similar fashion with the contralateral side. Once we have proceeded down through S1 and start to see sphincter activation, we stop to avoid injury to the bladder or bowel structures. We then irrigate, close the dura, supplement our epidural hemostasis with liquid gel foam, place an epidural catheter tunneled laterally and then superior to our bony opening. We then supplement our dural closure with fibrin glue and close the posterior spinal musculature, fascia, deep dermis and skin in layers. This is Sam Brown, I'm at Seattle Children's and at the University of Washington. Appreciate the opportunity to talk about the infraconus approach for rhizotomy. We've been doing this for about 10 years now at our institution. We published a paper in 2016 describing our technique for those interested. A few pearls before I show the video. The difference in this technique is we're below the conus, so we place a silastic band around the ventral and dorsal roots of the cauda quina. We establish a threshold for ventral and dorsal stimulation. During the case, we're cutting 50% of the nerves that go to target muscles and up to 75% for nerves that have abnormal electrophysiologic responses. I never bipolar during the case on the nerves themselves and we never section the phylum because we're so close to the cones. This video will demonstrate the technique as we do it here in Seattle. So we'll do standard opening. We'll tent back the dura, open up the arachnoid. This is demonstrating now how we will place the silastic band around all of the nerves that's fastened to one side of the dura to keep it secure during the case. What we do after this is we go through and we establish threshold stimulation for ventral versus dorsal nerves. They're usually about a tenfold difference. And then once we identify dorsal nerves that we're interested in, we will cut them. One thing I do differently as I've evolved my practice is I don't divide up the nerve rootlets extensively. I will randomly cut them when I identify a grouping that are meeting criteria for sectioning. Here you can see us cutting two of three rootlets. I find this to be much more efficient. We do these cases generally in under three hours, skin to skin. So what we'll do is we'll just go through one by one and test. Ventral nerves are preserved. Dorsal nerves that meet criteria are sectioned. Again, you see that we will randomly go through and cut the rootlets versus teasing every one of these out. The reason we do it this way is I've found that the more manipulation, the more you change the stimulation thresholds, and it's a more gentle way of performing the operation. When we've dealt with a particular nerve root, it's tucked behind the silastic band. Ventral nerves are typically deeper, and when we find those again, they're just tucked behind. When we're done, typically the L2 exiting roots are outside of our initial field. So we visually identify those and test them in a standard fashion and cut the dorsal component accordingly. When we're done, standard hemostasis, irrigation of the interthecal space, and then we'll close in a standard fashion with a 4-0 Neuralon suture. We don't replace the lamina. Appreciate Dr. Nina Mirapudi for helping make that video a number of years ago. So we think the benefits of this approach, it's quite straightforward, it's easy to teach. I feel that my criteria for cutting and how much are very objective. We have good outcomes that meet or exceed what's published in the literature. I think the one downside to this is it's very neuromonitoring intensive, trying to separate ventral and dorsal. There's not always a huge separation and stimulation current to ascertain those. But with a good team, this is a, I think, a great way to do this case. Just wanted to thank Jack Walker. Jack was the first to show me a rhizotomy during residency. This picture goes back quite a ways now when I was actually somewhat in shape. But I appreciate Jack, and Jack learned this from TS. So we live in a small world where all these procedures are handed down over time. So I just want to thank Jack for all of his influence on my career and certainly introducing me to rhizotomy. Thanks so much. Recently, after two cases of late spinal cord tethering following rhizotomies through shorter exposures, we've been doing more L1 through L5 osteoplastic laminectomies, in sectioning L2 through S1 and sometimes S2 nerve rootlets near where they exit the dura. The posterior elements are held out of the field by hitching them to a self-retaining retractor. Inside the dura, every nerve root on each side is identified and briefly dissected from the arachnoid before stimulating any nerve roots. Here, we are dissecting the right L5 root. S1 has already been dissected. The S2 root can be accessed at the bottom of the exposure. Each root exits the dura above its corresponding pedicle. Note that the L5 and S1 roots exit the dura closer together than do the L4 and L5 roots. The L2 root is accessed at the top of the exposure. Although there is less room to work here than at lower levels, dissecting and stimulating are entirely doable. Once all nerve roots are identified, we return to work on each one individually. The first step is to confirm that the ventral root is really the motor root, and that the ventral root is to confirm that the ventral root is really the motor root by assessing its stimulation threshold. The dorsal root is confirmed to be the sensory root in the same way. A vessel loop is placed between the motor and sensory roots. Note that at lower levels, sensory roots are much thicker than their accompanying motor roots. The sensory root is divided into two to eight rootlets, depending on the size of the root and how easily its rootlets separate. Each sensory rootlet is then stimulated with a superthreshold train of impulses, and the rootlets that have the most abnormal EMG responses are sectioned. EMG responses are evaluated concerning both type of waveform and spread. After each rootlet is stimulated, it is marked and gently retracted using a narrow length of colored background material as the next rootlet is stimulated. The last two rootlets to be stimulated are not marked this way. One is held by the stimulating hooks while we decide which rootlets to section, whereas the other is the only other root not marked with background material. This sensory root has been divided into four rootlets. Therefore, we are only using two pieces of background material. Rootlets are bipolar, using low current before being sectioned. We usually section between 30% and 65% of the total cross-sectional areas of sensory nerve roots. Thank you to our presenters for this great series of videos. I'll open it up to questions from the audience here. We'll start out with a question about neuromonitoring. Is there a neurologist involved, or is it neuromonitoring technologists? How do you guys handle the monitoring in the case? I have a neurophysiologist, and we have a physiatrist in the room as well, a rehab doc. And they both monitor. They both interpret the EMGs jointly. No neurology involved. Similarly, go ahead, Rob. I would just say I did the same thing. We have our neurophysiologist who does all of our interoperative monitoring for neurosurgical procedures. And then the physiatrist, we have two different physiatrists who know the patients well, who have a lot of experience with SDR. And together, they monitor. We do the same in our practice. Our neurophysiologists pair experience in these cases, which I find to be very helpful. And we also have the rehab providers familiar with that patient in the room. So it's a team approach as we're deciding what to cut. Is there also a physical exam during this case? Does anyone have perhaps a physical therapist who's feeling the legs with contraction during the stimulation for that part of your procedure? Our physiatrist is doing it. I would say the same thing. And also bear in mind, sometimes when you don't have a discernible electrical response and the clinical response can be helpful. So occasionally, when they pick up the other leg contracting or firing a muscle group, that might be the only clue. We did this initially in our practice. And we actually went away from having them examining the patient. A lot of times when you do the stimulation, you're at the table. You can actually feel and get a sense of what's going on just in the operating field. So we don't do that in our practice. I would echo what Dr. Browd said. We've moved away from that over time. Occasionally, we'll tent the drapes. And occasionally, they'll pull the leg out and occasionally, they'll put a hand on the leg underneath. But we rely more on the electrophysiological response. There's a question about percentage of nerve roots cut. And how does that correlate with outcomes? There seems to be a good bit of variation amongst the panelists, some as low as 25%, some as much as 75%. You guys talk about how that affects outcomes and how you think it might affect outcomes? I'm happy to go ahead. Yeah, Rob, go ahead, please. I think that the early trials in the 90s from Vancouver and Seattle showed a clear dose response. And so I think one issue you can get into with this procedure, especially with an inexperienced team doing the monitoring and helping you make decisions, if you don't do enough, you're not going to get a good clinical outcome. And so they're where you are. Ross, Dr. Bogle. Maybe I can jump in for a second. So I'd echo what Rob was saying. There was a study that came out of Seattle quite a while ago. And the number of nerve roots that were cut was quite low. And they didn't show a difference between rehabilitation alone and physical therapy versus rhizotomy. Normal electrophysiologically, but where the patient needs us to be more aggressive. Yeah, sorry for the overlap on the tech there. But we've been quite aggressive in what we do in terms of cutting the nerve roots here. Rob, I was just echoing what you said in the early experience in Seattle prior to my arrival. They didn't really show any difference between rehabilitation, physical therapy, and rhizotomy if you cut a very small number of nerve roots. So we tend to cut quite a bit in our practice. If it goes to a targeted muscle, even though we don't see an abnormal response, we'll still cut 50% of that nerve. And the ones that go and show really abnormal response will cut at least 75%. So we're quite aggressive. And I've evolved that actually over time in my practice. I think when you first start, you're pretty nervous about how many you're cutting. And I think you get a bit emboldened as you go on and see the results. I've actually backed away from cutting quite so many. I often used to cut like 67%. I had one patient who had a little bit of hypotonia. Maybe it was related to cutting so many nerve rootlets, but I've since backed down to more like 50% for a lot of the levels. We'll still cut more at levels where we think the patient needs it more. I would add, I think my experience, both doing this at Gillette and then more recently in Kansas City with the same paradigm, I've never counted or aimed for a given percentage and have been surprised just by going through the limits of how we make decisions. So we have built in things like from motion analysis experience in Gillette, we always did L1 because it contributes to hip flexor spasticity. And we don't do S2 if you've done most of S1. This is very obvious when you're at the foramen, less so when you do it at the CONUS. But if you just kind of forget how many am I doing and just monitor and make decisions, it seems to work out that kids with less, the GMFCS2s and the better end of the threes, they're gonna be getting 25 to 40 something percent. Ours, the average is around 40 something, much more, much tighter. The not so good GMFCS3 that we still call spastic diplegic is gonna be closer to 55 or 60. And also most of the time, the tighter side winds up with a higher percentage, not 100%. I'd say probably eight out of 10 times you do more on the tighter side and you do more for people who have clinically significant or worse spasticity. So it seems to me it's sort of a natural history of that's where they land if you do it based on responses only. Another question following up on that, how important are L1 and S2 at the extremes of the exposure, which for Dr. Brown's approach, perhaps it may be a little bit difficult to reach L1. Can you guys speak about that? I'll repeat what I just said, basically. So from Jim Gage and others had published this looking at follow-up on kids who are getting sort of the classic Mark Peacock L2 through S1 done in St. Paul. And then they were finding that there was still residual hip spasticity, changed the paradigm to add L1 and did better with it after that. The addition of S2 is a problem with late breakdown of the midfoot, particularly like with the teenage growth spurts. When you're doing them as four-year-olds, you know, we don't, you don't know this, but they found in tenure plus follow-up that kids who'd had aggressive distal sectioning wound up with foot collapse. So if we did more than 50% of the S1 route, we didn't do S2, we did less, we kept going. So that sort of defined the range in that report and in that practice. So I can just comment on our experience. So we generally don't see L1. We tend to have, you know, equivalent results and don't see this issue coming up with the late spasticity of the hip. So it seems to work well the way we're doing it, but fair comments. Very fair. We don't usually see L1 as well. Sometimes I do S2. It depends on how much, like Mike said, how much we do at S1 and how much anal sphincter activity there is at S2. I would just say, because we're doing an isolated CONUS operation, you know, we don't, it's difficult, we try to exclude the small sacral roots from the CONUS, but if we get into significant sphincter activity, we don't section those roots. And we probably rely more on that than on an anatomic definition at that level. I want to thank all of you, the speakers, for your work on this segment, and thanks to the audience for your engagement and your questions. I think we've really nicely demonstrated the variability in this operation. So I appreciate all of your work, guys. Thank you very much. Thank you. Thank you. Thank you. Now stay tuned. We'll begin our next section of abstracts starting right now. My name is Scott Seaman and I'm presenting on improvement in cognitive and psychological functioning after surgical decompression for Chiari malformation 1, a prospective study as part of a multidisciplinary team. We have no relevant disclosures. In addition to valsalva induced headaches and syringomyelia from altered CSF flow, herniated tonsils can also cause compression of the brainstem resulting in bulbar symptoms. These symptoms often improve after posterior fossa decompression surgery. Increasing evidence implicate the role of the cerebellum and its afferent and efferent connections through the brainstem and cognition. However, little is known about how cognition is affected in CM1 patients. Moreover, it is unclear whether surgical intervention has any effect on cognitive or psychological function. We therefore sought to perform a prospective study comprehensively characterizing the cognitive and psychological profiles in CM1 and analyze how posterior fossa decompression affects performance on a wide range of cognitive measures and psychological assessment. We included patients age seven and older who had cerebellar tonsil descent more than five millimeters below the Framen-Magnum who were symptomatic on clinical history and neurologic exam. We excluded any patients with potential cognitive confounders. After patients elected for surgery, they then underwent neuropsychological testing. Then within several days underwent surgery and underwent repeat neuropsych testing approximately 12 months later. This chronic epoch of follow-up testing was chosen to limit the effects of opioid analgesics, affects secondary anesthetics, short test-retest interval that may complicate interpretation of the post-operative assessment and interval changes. Patients were then broadly assessed according to the domains defined in the field of neuropsychology. Furthermore, evaluations of mood, affect, and pain were assessed to further control for psychological compounds and cognition. All test measures were converted to Z-scores based on normative data controlling for age and education and multivariate analysis was used to identify significant deviations from zero on baseline evaluation and post-operatively to evaluate for significant changes from baseline, adjusting for changes in mood and motor function performance. Nonparametric analysis lastly was used to evaluate overall performance change. There were 36 patients in the total population and there were 25 patients who completed pre- and post-op testing with a mean follow-up time of 14 months. The mean tonsil herniation was 14 millimeters below the frame of magnum and all patients had valsalva-induced headaches and the distribution of bulbar symptoms as listed. Of note, no patients suffered any complications throughout follow-up. There was significantly lower performance in complex figure copy and complex figure recall, tasks of visual perception and visual-spatial construction and memory, with significantly lower performance in groove pegboard, a task of motor performance that had no relationship with the presence or absence of syringomyelia. In the remainder of the tests, there was no above-normal performance in this cohort. Univariate analysis showed significant improvement in tasks of attention, verbal processing speed and constructional memory, and multivariate analysis showed improvement in constructional memory independent of mood or mood and motor performance. There were significantly more tests that improved, indicating overall improved cognitive performance. In conclusion, preoperatively, CM1 has poorer performance in tasks requiring visual-spatial perception, construction and memory with possible deficits in processing speed. Postoperatively, CM1 had improved cognitive and psychological function, and when controlling for mood and motor performance changes, visual-spatial construction and memory independently improved. These findings further implicate the cerebellum in cognition. These findings may result as a consequence of cerebellar and or brain stone compression that alters normal functionality of cerebellar projections to cognitive networks. Natural questions arise. As CM1 is heterogeneous in a larger sample, what will subgroup analysis reveal? Which patients are more likely to have deficits or improve in certain techniques better than others? Should every CM1 undergo neuropsych testing at baseline, and should follow-up testing be done to trend over time? Does early diagnosis and intervention portend better cognitive outcomes? And do cases with normal exam findings but decreased cognitive performance warrant surgery? All these questions are worthy of study. Thank you. Good afternoon. My name is Kevin Kumar. I'm a PGY-5 resident at Stanford. Today, I will be presenting my laboratory work entitled Microglia Replacement as a Novel Cellular Delivery Platform for Neurodevelopmental Disorders. Microglia are tissue resident macrophages of the central nervous system. They function in development, particularly in synaptic pruning and regulating neurogenesis. In addition, there are a distinct subset of microglia associated with neurodegeneration. Microglia function to dynamically survey the brain parenchyma, with an even distribution throughout the CNS. They are derived from yolk sac chomatopoiesis and populate the brain during early development. However, they are long-lived and not exchanged from peripheral blood under normal physiologic conditions. Of note, incorporation of wild-type circulation-derived myeloid cells, or CDMCs, can be achieved using bone marrow transplantation, but this is a low-efficiency variable process. The goal of my project was to characterize engraftment of CDMCs into the brain, improve efficiency of microglia replacement in mouse models, and apply this technology for potential therapeutic use in both aging and Gaucher's disease. As previously mentioned, microglia replacement after bone marrow transplantation is slow, inefficient, and variable. Here's an outline of the conventional protocol, where mice are treated with busulfan, a myeloablative agent, then undergo bone marrow transplantation. In the lower panel, you can see that while there is a high degree of chimerism of GFP-positive CDMCs in the peripheral blood, there was a low degree of chimerism within the brain. We then discovered that if we deplete the endogenous microglial niches by treating with the CSF1R inhibitor, PLX5622, after bone marrow transplantation, the efficiency increased to greater than 90% brain chimerism. We then investigated which hematopoietic progenitors had the highest capacity to efficiently engraft into the brain, revealing that hematopoietic stem cells, HSCs, had the greatest potential. This is of particular interest since they can be cultured in vitro and engineered for various applications. We then sought to evaluate if transplantation from young to old mice could rejuvenate the aged brain. Surprisingly, we found that the aged brain conferred an aged expression profile and morphology onto the transplanted CDMCs, suggesting that the brain microenvironment plays a major role in microglial function. However, microglial replacement was an efficient cellular delivery strategy, so we thought to apply this in the context of Gaucher's disease, the most common lysosomal storage disorder. Type 2 and 3 Gaucher's disease is characterized by progressive neurodegenerative symptoms, which are recalcitrant to therapy. We utilized the PSAPNA-GBA1 mouse model of Gaucher's disease that contained a mutation in the gene prosapazin, as well as a point mutation in glucocerebrosidase. RNA-seq data from our aging experiment revealed that CDMCs express both PSAP and GBA1. Thus, we hypothesized that replacement of mutant microglia with transplanted wild-type CDMCs may ameliorate motor and behavioral phenotypes in these mice. Thus far, we have several cohorts of transplanted mice and are currently performing behavioral characterization with some promising preliminary results on motor function. Lastly, one barrier to application of this technique to a wider array of neurological conditions is the use of busulfan, which permeabilizes the blood-brain barrier. We sought to explore whether MR-guided focused ultrasound could be used as an alternative. Here, we demonstrate that the use of FBUS allows CDMCs to efficiently engraft in the treated hemisphere compared to the control hemisphere. In conclusion, we've developed a high-efficiency BMT protocol to repopulate microglia. This is a novel cellular delivery platform to the brain. Transplanted CDMCs from young-to-age mice adopt an age-brain signature. Our current efforts seek to apply this technology to a mouse model of Gaucher's disease. Lastly, MR-guided focused ultrasound has the ability to eliminate toxicity of busulfan, increasing the translational potential of this technique. Thank you. I would like to thank my mentor, Dr. Marius Wernig, the members of our lab, as well as our collaborators at Stanford and Cincinnati Children's Hospital. Hello, my name's Luke McVeigh, and I'm a current medical student at Indiana University School of Medicine. And today, we will be discussing spinal column shortening for tethered cord syndrome. Regarding tethered cord syndrome, as many of you may be familiar, the current gold standard treatment is a tethered cord release. And while this procedure is very effective at relieving neurological symptoms, there are some severe shortcomings, one of which is a high rate of retethering and recurrence, primarily due to scar tissue formation, surrounding the spinal cord. To avoid these complications, we've begun investigating an alternative treatment of spinal column shortening, which alleviates spinal cord tension without requiring entry into the dura. To investigate spinal column shortening, we performed a case series in 41 children and transitional adults, most of which had at least one prior tethered cord release. The surgical technique we used was a one and a half centimeter vertebral column resection, which involved a five level spinal fusion including two levels above and two levels below the osteotomy, as seen here in the CT and x-ray images. Regarding our patient demographics, our average age was 16 years old. However, we did perform this procedure on children as young as five. Our mean follow-up time was 22 and a half months, and our most common etiology for our patients was amyelomeningozole. The most common location of osteotomy was at T12, followed by L1. As you can see here, there were no complications of new neurological deficit, cerebral spinal fluid leak, infection, or death in our series. For our outcomes of the study, we observed successful spinal fusion in all 30 patients with at least 12 months of follow-up. Additionally, we evaluated subjective clinical symptoms, and for those patients with at least 12 months of follow-up, we saw significant improvement in patients with preoperative pain, preoperative weakness, and preoperative bowel and bladder dysfunction. For our patient-reported outcomes, we used a PEDS QL questionnaire that involved both patient-reported and parent-reported surveys, and for the 19 patients with pre- and post-operative scores, we saw a median improvement of plus 5 on a 100-point scale for both patient-reported and parent-reported scores. This was a statistically significant improvement for the patient scores. However, this was not quite significant for the parent scores. Lastly, we evaluated urodynamic outcomes, and we classified patients based on their urodynamic parameters into having either normal, safe, intermediate, or hostile bladder conditions, and for the 17 patients with pre- and post-operative evaluation, we saw a median improvement of one classification category. Key takeaways are, first, that spinal column shortening is safe, as we've had no significant complications or reoperations needed to date. Secondly, the subjective clinical outcomes are similar to those reported for traditional tethered cord release in the literature, as it's been reported that 80 percent of patients with pain improve, and 50 percent of patients with urological symptoms improve with a traditional tethered cord release. Urodynamics also had similar results as those reported in the literature, as tethered cord release has shown to improve about 50 percent of patients' urodynamics. Lastly, we did see a significant improvement in child-reported outcomes, while we did not see a significant improvement in parent-reported outcomes, although this is not entirely uncommon, as parents are often slightly more critical of their child's health. Regarding risks and limitation, there are continued risks with growing skeleton of young children, as well as growth retardation associated with spinal fusion of these children. However, we have not experienced any complications with these risks at this time. Additionally, there is need for longer-term follow-up, and future studies are needed for direct comparison of spinal column shortening with tethered cord release. Lastly, our take-home message is that spinal column shortening represents a safe and efficacious alternative to traditional untethering in children and young adults, especially those with prior untethering procedures. Hello, everyone. My name is Yasunaga Hama. I'm currently a pediatric neurosurgery fellow at Children's Hospital Colorado. I'll be presenting Responsible Neurostimulation in Pediatric Epilepsy, a multi-center retrospective study. We have no conflict of interest report regarding this topic. Responsible Neurostimulation, or RNS, has been shown to be effective and safe in the adult patient population, and has been FDA approved for patients who are 18 years of age or older. Despite growing of label use of RNS in pediatric patients, the literature on pediatric RNS has been limited. Unique considerations in the pediatric RNS use include growth of skull, which is known to be quite rapid, especially in the first two years of life. A prior multi-center double-blind randomized study has shown mean and median percentage reduction in disabling clinical seizures of about 40 to 50 percent within the first one to two years of RNS use. The responder rate, defined as the ratio of patients achieving 50 percent greater seizure reduction, has been shown to be about 40 to 50 percent in one to two years, with infection rate of about 4 percent. A single institution retrospective study from the Mount Sinai group involving 27 pediatric patients reported a responder rate of 73 percent and infection rate of 11 percent. We conducted a multi-center retrospective study involving pediatric epilepsy programs at UCLA and Children's Hospital Colorado to examine the efficacy and safety of pediatric RNS in patients with child onset epilepsy who underwent RNS implantation before April 2020. Seizure outcomes and complications were defined as described here. 18 patients were included in the study with mean age of 16.4 years with age range of 30 to 22 and with 10 of these patients under 18 years of age. All the patients underwent intracranial EEG prior to RNS placement, including 7 patients with intracranial EEG, 10 patients with craniotomy for subdural and defectural placement, and one patient with both. The 18 patients on average had 2.6 RNS leads implanted and 3 of the patients underwent concurrent seizure focus resection. The patients underwent RNS implantation for indications listed here. One patient in the series suffered infection requiring explantation of the entire system. Another patient with concurrent seizure focus resection became seizure-free without RNS ever being turned on for stimulation. Out of the 16 patients who received RNS stimulation therapy, one patient achieved 90% or greater seizure reduction, while 7 patients achieved 50% or greater seizure reduction. One of the patients in the series was a three-year-old girl who underwent RNS implantation for multifocal epilepsy. Postoperative imaging studies shown here demonstrated appropriate placement of RNS leads as well as an RNS generator, which as you can see is following the contour of the skull quite nicely. This patient had achieved less than 50% seizure reduction and recently underwent left frontal seizure focus resection as well as rearrangement of the RNS leads, achieving 90% or greater seizure reduction for the last one month after the most recent surgery. In conclusion, this study showed that the RNS is safe and effective in the pediatric population and 50% or greater seizure reduction was noted in half the patients in this series. RNS could be considered in patients as young as three years of age. RNS can be flexibly used in a variety of clinical situations after intracranial EEG studies. A future prospective study involving larger number of patients with longer follow-ups will be needed. We'd like to thank Kim for management of the IRB at the Children's Hospital Colorado. Thank you very much for your attention. Thank you. That was another set of great abstracts and talks. Now we have a couple minute break and we're going to resume the last batch of talks at 4 11 p.m. If you have questions for the speakers, go to the Remo lounge and you can engage with the speakers there. Hi, this is Dr. Douglas Brockmeyer and I'd like to invite you to the 50th annual meeting of the AANS-CNS Joint Section on Pediatric Neurological Surgery to be held December 7th through 10th, 2021 in Salt Lake City, Utah. On behalf of my partners, Dr. John Kessel, Dr. Rob Bolo, and Dr. Sam Cheshire, we invite you to join us. We are looking forward to the opportunity to host you while providing the highest level of scientific and educational content. Our host hotel is the Grand America, a wonderful facility centrally located in the downtown area and near all of Salt Lake City's wonderful restaurants and world-famous attractions. The Grand America is truly a five-star luxury hotel. We have guaranteed run-of-the-house with ample meeting and exhibition space. While you're here, we hope you enjoy the hotel's dining facilities and wonderful amenities. Once you arrive, absorb yourself in the latest scientific content in the field of pediatric neurosurgery. Learn more about cutting-edge technical advances from our vendor partners, and of course, mingle and network with your friends and associates. And last but not least, soak in Utah's legendary hospitality. So, save the date, December 7th through 10th, 2021, to attend the 50th annual meeting of the AANS-CNS Joint Section on Pediatric Neurological Surgery. We hope you come to learn, but stay to play and recreate. And let's definitely hope that we can all meet in person next year in Salt Lake City. Here we go with our last session of abstracts. There'll be a couple more, and then we can all meet together in the conversation lounge after this. Here they go. Good afternoon. My name is Natalie Limoge. I am presenting today on the neurologic and clinical outcomes of infants and children with a fetal diagnosis of AVID complex. AVID is an acronym that describes a constellation of imaging findings standing for asymmetric ventriculomegaly, interhemispheric cyst, and degenesis of the corpus callosum. AVID was first described as a series of imaging findings as a fetal diagnosis by OHSU in 2012. They presented 20 cases. All 20 cases fit a Barkovich type 1a cyst pattern. In 2018, the authors presented the clinical outcomes of 15 fetuses diagnosed prenatally with AVID. Eight survived past infancy and all had neurodevelopmental disabilities, including significant motor and language deficits, a wide range of visual defects, craniofacial abnormalities, and medical comorbidities. Initially, these children were identified postnatally with a head ultrasound due to macrocephaly. Advances in fetal MRI has allowed us to more clearly see these constellations of imaging findings and differentiate them from other developmental anomalies, such as aqueductal stenosis, porencephaly, and hydroencephaly. Here we can see there is severe degenesis of the corpus callosum and there's a large interhemispheric cyst in communication with the left lateral ventricle. We evaluated our cohort of patients that met the imaging findings of AVID complex and looked at their clinical and neurologic outcomes. We queried our fetal imaging database and identified 41 maternal infant dyads with fetal imaging consistent with AVID complex. We then reviewed the medical records for the mothers and infants looking at prenatal and postnatal variables. The median age of diagnosis was 29 weeks. The median gestational age of delivery was 36 weeks. 18 of the fetuses had fetal MRI. A slight majority of fetuses were male. The most common delivery type was cesarean section. 10 were born vaginally and two pregnancies were terminated. The most common cause for cesarean delivery was increased macrocephaly and breech positioning. 22 of the fetuses were born prematurely. The most common cause of preterm delivery was congenital or fetal anomalies charted as increasing macrocephaly. Three infants were delivered prematurely due to breech presentation and fetal distress. One case was listed as premature delivery due to fetal demise. 32 of the fetuses were live-born. 15 of the fetuses had died at the time of this study with the majority passing away in the first year of life. There were eight cases of fetal demise and four additional cases of neonatal demise defined as death before 28 days of life. One infant died at seven months old from respiratory failure. One child died at seven years old from ARDS secondary to overwhelming sepsis. The most common cause of fetal and neonatal deaths were reported as apnea, birth defects, and intracranial anomalies. Overall, 25 children were treated for hydrocephalus. 23 received treatment within the first 28 days of life. 24 were treated with a ventricular peritoneal shunt. One infant was successfully treated with an endoscopic third ventriculostomy. There were 25 children at two-year follow-up. 16 had some form of expressive language. 16 were tolerating floral feeds. 14 could sit independently. 11 were diagnosed with epilepsy. Six were in mainstream schools with two of those six having individualized education plans. One child was diagnosed with panhypopituitarism, and seven had visual deficits secondary to optic sheath abnormalities. Our cohort of patients is more optimistic than prior reports. Of our 41 patients, 32 were live born, and 27, or 66 percent, survived past age one, while in the prior case series only 53 percent survived infancy. Of those that survived, several children had positive outcomes, including full oral feeds, expressive language, sitting independently, and attending a mainstream school. Our data appears that neurologic and developmental outcomes of these children, while still guarded, are better than previously reported. This additional data may help us in future prenatal counseling of parents with a fetal diagnosis of avid complex. Thank you for your time and the opportunity to present. Hello, my name is Nicholas Sater, and I'm a fifth-year nursery resident at the University of Calgary. I'll be discussing the quality of life and satisfaction in surgical versus conservative treatment of non-syndromic children with craniosynostosis. We received grant funding from the Alberta Children's Hospital Research Institute for this project. This group, in particular, is familiar that craniosynostosis is the second most common reason for referral to pediatric neurosurgery. These infants are at risk for neurodevelopmental disabilities, and studies vary, but many have demonstrated alarming findings such as a 15 percent chance of raised ICP and diminished cognitive scores. Craniofacial surgery is the treatment of choice, however approximately 15 percent of Canadian families choose not to undergo surgery. The quality of life and neurodevelopmental impact of leaving this physical disorder uncorrected has not been definitively established. Our specific aims were to identify all children treated within Alberta over the last five years for non-syndromic single suture craniosynostosis and determine the proportion which were managed surgically versus conservatively, as well to compare the quality of life between those treated surgically versus conservatively. This multi-centre cross-sectional study had the inclusion criteria of being less than 24 months at surgery and seen at clinics at the two pediatric neurosurgery centres in Alberta over the last five years for non-syndromic single suture craniosynostosis. Children were excluded if they had genetic abnormalities or more than one suture affected. The exposure was allocated treatment. The outcome was that Pediatric Quality of Life Inventory, or PQL, which is a validated measure of quality of life. Caregivers were also asked reasons for selected management and satisfaction with treatment decision and final head shape appearance. We used a Likert scale with zero being extremely dissatisfied and ten being extremely satisfied. We classified eight, nine, or ten as satisfied. 114 children met the inclusion criteria, 52% in Calgary and 48% in Edmonton. 22% of children had conservative treatment. The median age at consult and surgery was four months and was 3.5 years at the time of the study. 25% were female and 75% were male. The most common affected suture overall and in the surgical group was sagittal and in the conservative group was metopic. There is a statistically significant relationship between severity and surgery. There is a natural cut point, as you can see, between mild versus moderate and severe. This was true for both parents and surgeons. There was overall high satisfaction regarding final head shape and treatment decision, which did not differ between management groups. On univariate analysis, it appeared that the conservative group had a statistically higher total median scale scores compared to the surgical group in all three scales. However, we wondered if the following three confounders confounded that relationship, age at consult, mild versus moderate and severe, and suture type. So we looked at each individually. All three were significantly associated with treatment type. However, when we looked at these potential confounders and the relationship with quality of life, age at consult and severity but not suture were related. Therefore, we found at least severity and age were confounding. When we ran the multivariate, there was no longer an association between management type and quality of life. In conclusion, Alberta families have a high number of children with craniosynostosis treated with conservative management. We found no association between treatment allocation and quality of life when adjusted for important patient factors. A limitation in this retrospective cohort is how consecutive was the sample. These findings will be used as pilot evidence for a prospective study, including all 14 Canadian pediatric neurosurgery centers. I want to thank the patients and the patient families involved in the project, Dr. Eva Cameron and Dr. Mehta for their mentorship and the rest of the collaborating authors for their help and assistance with the project. Thank you. Hi, my name is Eric Montgomery. I'm a medical student at UT Southwestern in Dallas. Thank you for taking the time to attend this talk on the radiographic predictors of clinical presentation and outcomes in Chiari malformation type 1. My co-authors and I have nothing to disclose. Chiari malformation is classically diagnosed radiographically by the caudal descent of the cerebellar tonsils below the foramen magnum. However, prior studies have yet to find an association with its trademark finding to clinical symptoms or outcomes. Recently, other radiographic measurements have been studied and proposed as stronger correlates than tonsil length, such as pliable axial angle and PBC2 measurement. Earlier this year in JNS-PEDS, Haller et al. demonstrated that ob-exposition had a more robust association with syrinx headaches and CSI grade postoperatively, as well as surgeon decision making than tonsil length. As you can see on the left, maintaining a normal ob-exposition while increasing the severity of the tonsil position did not exhibit an increased frequency of syringomyelia. However, the converse, maintaining tonsil position while increasing the severity of the ob-exposition did correlate with increased frequency of syringomyelia. This corroborated on the right, where there is little difference in the severity of the tonsil position between headache and non-headache patients, as well as low and high grade CSI, where there is variance between each group in the ob-exposition. So the objective of this study is to characterize the association of multiple radiographic metrics with clinical presentation and outcomes. A consecutive series of 391 pediatric patients from 2001 to 2019, we measured on pre-operative MRI, cerebellar tonsil length, foramen magnum width, distance from posterior pistae into spinal cord, clivo-axial angle, PBC2, and syrinx when applicable. The mean age was 8.3 years with 49.6% male and the follow-up was 32 months. Overall, patients were fairly homogeneous, with females presenting with greater rates of headache as well as syrinx. Radiographically, there was also little difference, except for females demonstrating a very slightly decreased clivo-axial angle. At clinical presentation, decreased clivo-axial angle was associated with brain stem and spinal cord symptoms. Increased distance from posterior pistae into spinal cord was associated with headache, while decreased distance was associated with cranial nerve symptoms, and the same was true for foramen magnum width. Decreased foramen magnum width was also associated with hydrocephalus. Post-operatively, although syrinx or symptom improvement did not associate with any radiographic variable, decreased distance from the posterior pistae into spinal cord was associated with both re-operation and CSF-related complications. In conclusion, our study corroborated that tonsil length does not demonstrate a significant association with any clinical presentation or surgery. However, we did demonstrate that there are multiple other radiographic variables that may be more clinically relevant, as they show specific associations with certain symptoms or post-operative outcomes in QRA malformation patients. Thank you for your time. Thank you again to our speakers. Those are great presentations. Thank you again to our speakers. Those are great abstracts, and thank you to everybody who's attended this session. Looks like we had over 200 people watching this today. That's a really great turnout. Please head over to the Remo room to talk to our speakers and to mix and mingle. The conversation lounge that you have been attending up till now is going to close in about five minutes, so just go ahead and maybe move over to the Meet the Leadership Remo room. That's a different link. It should be in your program, a relatively new link. It should be in your program and relatively easy to access. So again, thank you all for attending today's session. This has been awesome. We heard from our colleagues. We heard from our trainees who are the future of neurosurgery. We heard from colleagues from different disciplines. I think we had a really great mix of programming, and it's been exciting and just energizing. I hope you enjoyed it as much as we did. Thank you, everybody. Have a great Meet the Leadership session.

St. Louis Children's Hospital

study

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stereo-EEG

subdural grid

strip implantation

preoperative assessment

children with epilepsy

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cost-effectiveness

less invasive

efficient method