about 20% of patients die. Um, and it always occurs below the level of neurological, the level of injury. And it's correlated to what degree of completeness of spinal cord injury, as well as like cervical and thoracic injuries tend to have a higher prevalence of this over lumbar injuries. And from what I read, it most often occurs in the hip, but it can occur in other spaces and other joints as well. Complications that come with heterotopic ossification are ulcers, difficulty with care, DVTs, decreased range of motion in the joints where these are found. And then another quick definition to give before we jump into what the paper was really about was the difference between primary and secondary prevention of heterotopic ossification or HO. So primary prevention is trying to prevent it from forming in the first place. So primary prevention, secondary prevention, is preventing the recurrence of HO after surgical resection of the bony piece. At the time of the study, NSAIDs had only been trialed as secondary prevention, never as primary prevention. And Adirondate, so like Adirondate, I was fascinated was used, has been shown to reduce the progression of ectopic bone rather than incidence of it forming in the first place. So that's where they were coming out at the beginning of the study. So the study design was a randomized, prospective, double-blind, placebo-controlled trial with a length of treatment of three weeks. There were 33 patients in the study. They had 16 in the experimental arm and 17 in placebo. The experimental group got indomethacin 75 milligrams daily. And because NSAIDs are known to cause gastric upset and gastric bleeds, gastric ulcers, both groups were given mesoprostol 200 micrograms four times a day for gastric ulcer prevention. And because they were given mesoprostol, women were excluded from the studies, females were excluded from the studies due to the abortive active properties of mesoprostol. So, but the two groups were pretty evenly split between the level of spinal cord injury, the ASIA impairment score, and then also like patient age. So, and days post injury were pretty, pretty well split between the two groups. So the methods of the studies, all participants in the study, whether they received the NSAID or placebo were monitored for clinical signs and symptoms of heterotopic ossification. Because that was, those are the first signs that people would get that these were forming. So things like local erythema, swelling, fever, loss of range of motions were monitored for. And if these were detected, ultrasound and radiographs were performed prior to doing bone scintography, which I may be mispronouncing that, I'm going to say it the same way for the entire presentation. But those were used to rule out DVT and trauma before moving to the bone scintography, which can be used to diagnose early stage heterotopic ossification. And so patients with positive bone scintography for HO were then discontinued from the study medication and started on the bisphosphonate, adirondate, 300 milligrams IV for three days, followed by oral for six months. And then they had follow up radiographic exams every two months for six months to test for late stage HO. And so that was the course, if they showed any symptoms and then tested positive on the first scan. And so these were the diagnostic methods I was talking about earlier. So bone scintography are these pictures on the left. And this is a perfusion study from what I understand. So it's like a nuclear study. And so it just shows the uptake with perfusion as it goes on. And then this is a late phase picture within the study, I believe. And so this is used for early detection of heterotopic ossification HO versus late stage can be seen on radiograph, but the late stage can't be seen, or early stage can't be seen on just a regular x-ray. So you have to do this other study first. And then obviously, you want to prevent the late stage. So it's better to do the early stage monitoring as well. So the results that they found in the study was that the endomethasin group had a lower incidence of early stage HO. And it took a longer time to onset of early stage HO versus the placebo group. And the difference was pretty stark with 25% of the endomethasin group getting early stage and 65% of placebo group. And as you can see, the date to onset was longer as well with the NSAIDs taking an average of 32 days and the placebo being about 19. And so then we're going to talk about late stage HO, which is only considered if they were positive in the first stage, in the early stage, I believe. So the endomethasin group, only 12.5% of the NSAID group progressed to late stage HO. So there was less progression. And then in placebo group, 41% progressed to late stage. So even whenever they they both started similar treatments after detection of early stage, and then there was still a higher rate of progression to late stage in the placebo group than the NSAID group. So and then on top of that, the quantity and the quality of HO between the two groups was different on that was found on the radiographic findings. So on x-rays, so the NSAID group endomethasin, only two patients had findings. And there were only solitary lesions that were described in the paper as small islands of bone in the tissue, versus the placebo group, 41% had late findings. Four of those seven had solitary lesions, three of the patients had more than two around two separate joints. And just generally, they were larger bone masses compared to the NSAID group. And then just speaking on adverse effects that can happen from taking endomethasin, abdominal upper abdominal discomfort was what was most reported. There were none of the participants had any signs of GI bleedings, and none of them discontinued the study due to the symptoms. And then the mechanism of NSAIDs in the study, and how do they work to prevent HO, the thought is that it blocks, NSAIDs block COX, which then blocks the formation of prostaglandins, specifically PGE1 and 2. And these PGE1 and 2 simulate bone formation over bone resorption. So by preventing COX and preventing PGE1 and 2, you then halt that bone formation part. And so the discussion paper, part of the paper discussed previous studies that led to them asking this question and then having a study. And like I said earlier, oh, man, I have a typo there, whatever. The previous studies had never looked at this as a primary prevention. But previous studies have shown that Adirondate has been used to preventing the extent of formation of heterotopic bone mass, but it's not in preventing the progression, but not necessarily good as a primary prevention. It's more like, once it's found, it prevents it from getting worse from what I understand. But something else that really spurred the study was that there was a similar study used to as with NSAIDs to prevent HO and total hip arthroplasty that was performed. And it actually had very similar findings to this study in the spinal cord injury patient group, with them having 15% being positive in the NSAID group and 75 in the placebo group. So the conclusion of the paper is that indomethacin is an effective drug for the primary prevention of HO after spinal cord injury. If it started within the first two months of injury, this paper, they started generally in that timeframe. There's a lower incidence of early and late heterotopic classification in both in the indomethacin group, and it influenced the extent of the development as well. So some of the study limitations that I was thinking about is that the initial study had no women in it, had a smaller sample size of 37 participants. And something else that should be considered is that NSAIDs mask a lot of the first clinical symptoms that are used to detect HO, so like the swelling, erythema, and fever. So that could lead to maybe like a later diagnosis, but that's just something to consider. And then the same people who did this study then conducted a study with a COX-2 selective inhibitor in 2004, so three years later, and found similar results that it was still effective, statistically significant that it was effective in preventing HO in spinal cord injury patients. There were still women in the study, but it was still kind of lopsided, their exclusionary criteria, and that one was just a history of public ulcer disease, being pregnant, and then being out of an age, that specific age range of 18 to 60. And I think that's it. Thanks. Awesome. Thank you, Kirsten. Super interesting topic, and loved the way you presented it. Let's punt it over to Dr. Wilson to give us his first thoughts and add some kind of clinical applicability to heterotopic ossification, because I know I haven't, I haven't been able to see this in clinic myself either. So I'll start by saying I read a very nice review article about HO, which apparently was the wrong article. So I don't have all the details of the, you know, just their presentation. So I guess one of the problems with studying something like HO is that it is relatively common, but its clinical significance is really varies, right? That you can find incidental findings, you know, as much as 50% of the time sometimes. So sometimes a study like this would need to be powered pretty, pretty high, you know, a large number of participants to be able to really see, you know, there's really severe kind of ankylosis or neurovascular compromise or those kinds of things. So it's interesting that they found a significant difference with such a, like you said, a smaller study. You know, the risks and the side effects of the NSAIDs, especially the indomethacin, you know, they are significant, you know, our patients have a high rates of GI bleed after a spinal cord injury. And that they're not always that well tolerated. I mean, you're talking about a relatively high dose for three times a day for as much as, you know, maybe months, if you end up finding HO. So it's, it's, it is exciting to have results like this. Classically, we talked about the indomethacin, excuse me, the atigenate as kind of the go-to for treatment and the NSAIDs for prevention. Yeah, this is, I mean, it's a good study. Awesome. Thank you. And then any questions from the audience for Kirsten or Dr. Wilson? So is the indomethacin something that they take like prophylactically, like every spinal cord injury patient does that? Or only if you suspect some concern? So the answer is no, we don't typically give it prophylactically well, we don't give it prophylactically. And I've had a very good conversation a few years back with a group out in Stanford, and they were designing a similar study that was going to be a larger prophylactic study with NSAIDs. And they looked at all the risks versus benefits. But honestly, the surgeons are very concerned about nonunion, you know, lack of poor bone healing, and then also just hematomas and other kind of bleeding risks. So it's not something that we give routinely. It's more for patients that are at a high risk. That's, that's kind of where typically we draw the line that if they've had HO before, if they're, they've got even Dish syndrome or hypertrophic osteoarthritis, you know, some of these kinds of other high risk conditions that you might think about prophylaxis, or if they've already had HO, and they're having a resection, those are certainly people that you wouldn't do prophylaxis on. Should I respond to that, Aiden? Yeah, let me read it out to you first. Has topical versus by mouth NSAID administration for heterotrophic ossification prevention been studied? I don't honestly know. I would be very skeptical that topical NSAIDs would be able to penetrate the tissues to the extent that you need. You know, when you guys take the board exams, eventually, you know, the things you need to know the top hits about HO. One is what we talked about already with NSAIDs versus bisphosphonates. Two is that your first line study is going to be a triple phase bone scan, that's that bone scan, that's that bone syndrome graph. That's got the best sensitivity and specificity. And the location of the HO, so hips, knees, shoulders, elbows. And unfortunately, there's been studies that say they vary slightly in different populations. So you have to memorize different locations for SCI versus TBI. And in the end, it's not that dramatically different, but it is one of those board question kind of things. So I guess I only brought that up because you'd have to rub NSAID gel all over your body every day, three times a day for six months, you know. Other questions for our speaker and our clinician expert? All right, well, we have more questions come up. We also got other kind of times and spots for questions. But for the sake of time, let's go on to our next presenter here. Thank you again, Kirsten. Next up, we have Ravdi Bobaroi. She's a fourth year med student at the Toro College of Osteopathic Medicine out of Harlem, New York, going to talk about the efficacy of amitriptyline for relief of pain and spinal cord injury. The results are a randomized controlled trial. So take it away when you're ready. Thank you, everyone. I'm sorry, can everyone see my screen? You can, indeed. Okay. So thank you for that introduction. So I will be discussing, as you mentioned, the article, the efficacy of amitriptyline for the relief of pain in spinal cord injury. And this was in the journal Pain from April of 2002. So I plan on discussing the clinical indications for amitriptyline, as well as the study design and findings from the article I mentioned and discuss the overlying main points. So amitriptyline is a medication typically known for its indications as an antidepressant. However, it also has been used to treat neuropathic pain. It was discovered in 1960 and it was approved by the U.S. FDA in 1961. So some common indications for its use in neuropathic pain include diabetic neuropathy, post-traumatic neuropathy, fibromyalgia, tension and migraine headaches. And atypical facial pain compared to its use in antidepressant. The doses are around 25 milligrams for neuropathic pain, which is well below the antidepressant dosage. And its mechanism of action is that it basically blocks the reuptake of norepinephrine and, I apologize, it blocks the reuptake of norepinephrine and serotonin, which causes an increase of these concentrations in the synaptic junction. And this is seen in this diagram. So as you can see, the tricyclic antidepressant, also known as amitriptyline in this case, which falls under that class, is going to be blocking the reuptake of these neurotransmitters. So the management of pain in spinal cord injury patients has been, there's multiple approaches to manage the pain in these patients. And some of those medications include antidepressants. So that's amitriptyline, bitium, trazodone, duloxetine. Also antidepressants have been used such as pregabalin, gabapentin, valproate, lamotrigine, and carbamazepine. Opioids have also been used such as morphine and tramadol, and as well as cannabinoids and ketamine and lidocaine. So the current first-line medications include amitriptyline, pregabalin, and gabapentin. So treatment for chronic pain, secondary to the spinal cord injuries, has been an area of interest over the past few years, given the limited clinical studies that are currently available. Multiple studies that had been performed to investigate this topic were included in this slide. So the first study was done in 1987. However, it failed to show any significant benefit of using antidepressants for the treatment of spinal cord injury pain. A few years later, another study was performed in 1992, and this demonstrated a benefit with the use of a combination of amitriptyline with carbamazepine. However, since then, only a few multiple case reports were done that recommended how tricyclic antidepressants can target pain, but no clinical trials have been performed till date. So now I'm going to be discussing the article. So in this article, the participants were screened based on a specific inclusion criteria that included spinal cord injury that lasted more than six months ago, pain that was present for at least three months, and an average pain rating in the last month of at least a numerical score of three on the scale of zero to 10. And participants who were excluded from this study included those who were less than the age of 18 or older than 65 years of age, those with a history of cardiovascular disease, any abnormalities in EKG, any history of seizures, hyperthyroidism, or glycolytoma. If for females, they excluded any women who were pregnant or unwilling to use a contraceptive during the study, and any patients who were on any antidepressant medication, as well as anyone consuming more than two alcoholic beverages, and any patient who met the diagnostic criteria for a major depressive episode. So after the screening, 84 participants with spinal cord injury and chronic pain were then included, and they were randomized to a six-week trial of amitriptyline or an active placebo known as benzotropine medecilate. So this was chosen as the placebo because it's able to produce a very similar side effect that is seen in amitriptyline of producing a dry mouth. And of those 84 participants, 44 subjects were advised to receiving amitriptyline and 40 were given the placebo. The randomization was stratified by level of depressive symptom severity given the concern for patients with a depressive symptom that didn't qualify as a major depressive, didn't meet the criteria for MDD as I mentioned before, because those participants were excluded. So in terms of dosing, amitriptyline was dosed at an increase starting from 10 milligrams per day, and that increased up to 125 over the six-week period. This medication was titrated based on the patient's reported severity of pain. And on the other hand, the placebo benzotropine was kept at a consistent 0.5 milligrams per day dosage throughout the entire study. So the assessment for this study was basically the primary outcome was subject reported average pain intensity, basically what the subject reported their pain to be on a scale of zero to 10. And this was assessed three times every week and a baseline of their pain level was also obtained prior to treatment. And other secondary outcomes were also assessed during the study, which I've included in this slide. So T-test and Chi-square tests were used to create the statistical analysis. And the Chi-square test was used to compare the presence of symptoms as well as the frequency of side effects for both the placebo and the imitriptyline groups. Eight subjects in the imitriptyline group and three subjects in the placebo group had discontinued medication, but this difference was not statistically significant. The median percent of doses missed was 2%. So the results from this study showed that no significant differences between imitriptyline and the active placebo group were noted for any of the outcome measures, except for a satisfication with life scale, which was seen to be higher in the placebo group. And a regression analysis was performed to predict each outcome variable at post-treatment, adjusting for the pretreatment scores on the variable. In each case, the pretreatment scores explained a large and statistically significant proportion of the variance in post-treatment scores, and the medication group did not make a significant additional contribution. So in other words, if values were seen to be higher during the post-treatment score assessment, when compared to their given pretreatment scores, it basically explained for that difference. I've included the results in this. This is the chart that was provided in the article. And as you can see, the only significant difference between the imitriptyline group for the pre- and post-outcome measure scores compared to the placebo group would be the SWLS, which was the quality of life that I mentioned before. And I think this can be expected because imitriptyline is associated with many side effects. So since this is a subjective finding, it can be understandable why that discomfort would cause patients to report a lower quality of life. So as I mentioned before, there was no statistically significant difference between those on imitriptyline and those on the placebo in terms of side effects and severity. The most common side effects reported by those on imitriptyline listed in a decreasing order of frequency were the same as those reported by those on the placebo, and that is as follows. So you have dry mouth, drowsiness, tiredness, fatigue, constipation, spasticity, urinary retention, and sweating. 79 of those total 84 participants did report one or more side effects or increased severity of an existing symptom during the study, and of the 79, 43 were in the imitriptyline group and 36 were in the placebo group. So in conclusion, the results indicated that imitriptyline was not effective in reducing the chronic pain or disability or improving quality of life in these participants. So what this article taught me was basically, this was the first placebo-controlled trial to examine the efficacy of tricyclic antidepressants, specifically imitriptyline and the treatment of chronic SCI pain. The previous literature that I had mentioned did not specifically target imitriptyline. It would either include it with other agents, just carbamazepine, or there was a lack of a control group that signified the benefit of imitriptyline alone. And so this was the first to have singled out imitriptyline as an agent. The multiple side effects that were reported could have been present in participants prior to enrollment in the trial. So despite this being a negative study, that this could be one of the reasons why there was no improvement in the quality of life in those that were treated with imitriptyline. Many studies have demonstrated the efficacy of imitriptyline with the treatment of peripheral neuropathy and it is possible that changes produced by SCI alters the effects of the action of imitriptyline. So as I mentioned in the background slides, imitriptyline is used to treat, for example, diabetic neuropathy, which is a peripheral neuropathy condition. And it's possible that although that agent is beneficial in those conditions, it is not as beneficial in a patient who has an SCI because the damage from the SCI may make the effects of imitriptyline reduced and therefore not alleviate the pain. Some of the limitations of this study that were discussed were that one may argue the trial period was insufficient, that six weeks are not necessary. I apologize, six weeks are not sufficient to provide a proper assessment of pain relief. However, most studies of antidepressants for other chronic pain conditions demonstrated improvements within one to three weeks. Another limitation was that subjects of this study had different types or subsets of chronic pain. So this study did not specify or have an assessment to differentiate between a true spinal cord injury pain versus a musculoskeletal related pain. And that may show different findings. And the last limitation would be that the sample size was relatively small. So perhaps another study with a larger sample size may be more beneficial. And that concludes my presentation. Awesome. Thank you. Thank you for that. It was a very in-depth look at amitriptyline. I know I got some questions, but I'll punt it over to Dr. Wilson to give his thoughts first here. Well, you know, I'm really glad we're doing a negative study. You know, we don't talk about these that much. And so it's nice to kind of highlight it a little bit. You know, I would agree that the idea that they mixed in all different kinds of chronic spinal cord injury related pain in one study is probably a significant limitation. I really agree with the premise from the study that there are different kinds of neuropathic pain, right? The idea that you get a peripheral diabetic neuropathy versus a stroke and brain injury versus even a spinal cord injury. There are three different types of nerves. There are three different types of pain. Why do we assume that? Just because it works for one population and it works for another. So I guess my question would be, how does this impact your care? Are we all no longer using amitriptyline or using it with the understanding that this study didn't show it worked or what do we do with this? And I think you're muted and rubbed deep if you're trying to respond. I can't tell though. Okay, can you hear me now? Yep, yep. Okay, that's it. That's a good point. I think the study just shows that further research needs to be done to show that, okay, if amitriptyline should be used to treat chronic pain, then it hasn't been evidence-based as of yet. So if not, perhaps, I mean, it does not exacerbate the pain. So although it may not alleviate it, it may have indications, but it may also open doors to trying a different class of medication. Yeah. So, I mean, you're right. We don't have that many options. You know, it's either a seizure med or an antidepressant or a narcotic with a few other things in between. Amitriptyline is definitely not a benign medicine. It definitely has risks and side effects to it chronically and acutely. So about five years after this article came out, there was another article that came out that compared gabapentin and amitriptyline for neuropathic pain. And that one showed that amitriptyline was better than gabapentin in neuropathic pain. So, you know, that's why we end up with meta-analyses. Unfortunately for spinal cord injury, we just have a small population that's not well-funded. So we don't have that many RTCs to work with to get to the point of having meta-analyses. Yeah, it's one data point. And it definitely, it's compelling in a lot of ways, but it's just one sample in a large population. Awesome. And then questions from the audience. I know I got the one for sure for you, Rob Deep. I just found it was interesting that they used that benzopine as that placebo. But did you find it kind of curious that they didn't raise the dosage of the benzopine? Because I thought that kind of might compromise the placebo effect that you might have. Again, I'm not super familiar with amitriptyline if it's like a dose effect response in terms of the side effect of dry mouth that they were trying to control for, but I'm not sure that that's the case. In terms of the side effect of dry mouth that they were trying to control for. But I just thought it was interesting that they didn't make the attempt to raise the benzopine or what their thought process on that was, if you had any insight on that. Yeah, they didn't mention as to why they kept it constantly at that dose. But that's, I'm not too sure to be honest. I thought the taper up was interesting, but I think if you count it out and they do a six week study, that if you get to the top dose, you're only on it for about a week before the end of the study. So I think that'd be the only time criticism in terms of how long the study lasts. And maybe high dose amitriptyline works well, but we just never got there. All right. Well, thank you, Rob. I'm happy to drop the share and then want to thank you for that great presentation. That was a good look into an important topic because these SCI folks definitely have pain, so we got to look at some good options to control that pain. Next up, we got Daniel Persson. Let me give you the good intro you deserve here, Dan. He's our third-year med student out of the Ohio University Heritage College of Osteopathic Medicine from the Athens Division. He's going to talk about the safety of every other day fasting and the treatment of spinal cord injury, a randomized controlled trial. Take it away, Dan. Thanks for the introduction, Nathan. I appreciate it. Let's just get into it. Today for the presentation, quick agenda topics. First, I'm going to briefly touch on the pathophysiology of spinal cord injuries, then talk about the research of dietary restrictions and every other day fasting, then review the article, and then have a discussion and go over some questions at the end. The pathophysiology of spinal cord injuries, super complex, a lot of different biomedical, like different pathways going on, but I want to look at it a broad lens. We don't get too focused in on one thing. As you can see from the slide, there is two forms of injury with a spinal cord injury. There's the primary injury and then the secondary injury. The primary injury is like the actual force that occurs on the spine to make that first lesion. This needs to be some car accident or something with a high and a big enough force to cause damage to the actual spine. Then following that initial, that primary injury, then we have secondary injury. This is a cascade of physiologic, intranet, extracellular, biochemical insults that occur to the tissue surrounding that primary injury. One important byproduct of that secondary injury is the formation of reactive oxygen species through the release of potent pro-apoptotic signals and recruitment of regional microbial, super interesting. These reactive oxygen species continue to cause cell death in that surrounding tissue. This specific byproduct of that secondary injury is going to come into play in my next slide. Just keep that in the back of your mind right now. In regards to diets and every other day fasting, we're going to take a look at these right now. The first one is in human research, dietary restriction regimens have been shown over and over again about to be super beneficial in several human diseases. Preventing and treating cardiovascular diseases, preventing cancer and assisting with neurodegenerative diseases, and the list goes on and on and on. Then in addition, specifically with spinal cords, there was some research done that showed that dietary restrictions following a spinal cord injury has shown to improve functional recovery. Us PM&R enthusiasts are really, really big about improving quality of life and function, super cool. Then specifically, let's talk about every other day fasting. For this, there's been a lot of rat research. One of the studies showed that rats treated with EODF after a spinal cord injury showed an increase or a greater number of neurons in the surrounding injury site, and then also a 45% reduction in the lesion size. Pretty fascinating. Then another study showed that the EODF-induced ketogenic metabolism could reduce the oxidative damage by those reactive oxygen species in the spinal cord tissue following the acute damage. Once again, we can see that there is some evidence behind every other day fasting, but there's not a lot of evidence with this type of dietary regimen in humans, and therefore, we have this study, safety of every other day fasting in treatment of spinal cord injury, a randomized controlled trial. All right, so brief introduction to the study. We know that spinal cord injuries are chronic, life-changing injuries that impact almost every single aspect of the patient's life. It's important to take into consideration all these different ways that we can help to alleviate those injuries or treat them as best as we can. More and more physicians nowadays are taking a holistic approach where they're thinking of all the different aspects of a patient's life and how we can impact those parts to better their treatment. And one of those ways is to focus on diet and the amounts of nutrients that someone is taking in, and therefore, leads us to dietary restrictions, a.k.a. the one we're focusing on today, every other day fasting. So what is the study objectives? Because this is the first study of its kind, the main objective is to see if EODF is safe for spinal cord injury patients. We want to see if it exacerbates any function or sensory issues that they're having. Does it cause malnutrition in the patients? Does it cause infection or does anything get worse? That's the main goal. Side objectives are, is there an improvement in sensory and motor function? Changes in blood glucose and changes in body weight were also examined. So the diagnostic criteria, you have to have signs and symptoms of spinal cord dysfunction. You had to go undergo a CT or MRI to confirm the spinal cord injury, and you have to have decreased sensory and motor function below the level of injury. Pretty straightforward things. And then in regards to the inclusion criteria for the actual study, you need to be diagnosed with an SCI at first admissions, and all of these were traumatic cases. You have to be cooperative, ages 18 through 60, can understand and execute instructions, no other organ injury, and you have to have a level A, B, or C spinal cord injury according to the Asia Impairment Scale. And so we're going to take a brief pause and go through some questions. So using your chat function or just coming off mic and speaking, what is the difference between a complete and incomplete spinal cord injury? Wish we had some Jeopardy music playing in the background. Don't be shy. I don't mind taking a whack at it. So I'm going to just go with that. A complete spinal cord injury is when the spinal cord below the area of the lesion is completely out, whereas an incomplete means that there is still a function beyond that lesion. Am I correct? You are correct, Jacqueline. So yes, a complete refers to any spinal cord injury that results in the complete loss of function below the point of injury, and then incomplete refers to some sensation or movement still evident below the point of injury. And so a little follow-up question, and now, Jacqueline, you can't answer, is Brown-Saccard syndrome considered complete or incomplete? It shows up on boards all the time. I also don't know. I don't think I can pull up the chat, so if someone can just let me know what the chat is saying. I got you, Dan. So we got our buddy Sam saying it's incomplete, along with Lizeth Caldera as well. So we got a few saying incomplete. I think those people are correct. And just a, yes, it is incomplete. And just a reminder, Brown-Saccard syndrome is a, And just a reminder, Brown-Saccard syndrome is an injury to one half, one side of the spinal cord, and it causes paralysis and loss of proprioception on the ipsilateral side, and then loss of pain and temperature on the opposite side, contralateral side. And this is for you guys to reference in regards to the American Spinal Injury Association Impairment Scale and the way it's graded. Grade A is a complete injury, and then E is normal, and then B, C, and D in the middle are incomplete. And they all vary based off of the amount of strength that it takes. Yeah, you can see on C, you have to have 50% of your key muscles have a strength grade of below three, and it sort of works like that. I don't want to focus on this too much, so if you have more questions and want to learn a little bit more, there is a link to the bottom. I don't know if I can send this. Maybe I'll send you guys this presentation afterwards so you can have that link. Daniel, I'm going to jump in just real quick, just because you had that up there. To be clear, a complete versus an incomplete injury really has to do with the lowest section of the spinal cord, right? So when it says there, no motor or sensory function preserved at S45, S45, dermatoma, and myotoma are basically your rectal exam. So what we're worried about or we're thinking about is if there's signals making it from your brain all the way down to your bottom, then there's something getting through, and so it's incomplete. So you can have, you know, like an injury up at your neck, but still be able to wiggle your toes, or maybe not your toes, but there might be some function preserved below the injury. But if it doesn't make it all the way down to the end of the spinal cord, then that's a completed injury. It's a little bit more of a nuance, but yeah. Otherwise, everything's good. Awesome. I appreciate it, Dr. Wilson. Okay. Some more questions to keep you guys engaged. And we're going to take these one by one. So what dermatome level is associated with the following? Big toe, thumb, nipple, umbilicus. So we're going to start with the big toe. Either shout it out or put it in the chat. You guys got this. I believe in you. So we got one guess for S1 then. Okay. Any others? L5. Good. So I've always been taught that it's L4. Some of the resources I've looked at specifically for this question showed L5. I've always remembered it big toe, L4. That's just something that stuck with me. I don't know if Dr. Wilson or someone else wants to chime in, and maybe it is one way or the other. I've always known it as L4 personally. So for the spinal cord world, we have very specific spots that we check on the body. And so in the foot, we're actually checking the medial ankle, like the medial malleolus, and then the third digit, and then the lateral heel. And so we kind of skipped the toe because it might vary a little bit. I would say it's more S4. But, yeah, you know, it's a little bit of a gray zone. Dr. Wilson, did you mean, say, S4 or L4? I meant to say L4. Okay. I just wanted to make sure I didn't put a big typo in here. Okay. Appreciate it. Okay. So what about the thumb? The dermatome for the thumb. We got a C6 for you, Dan. Yes, C6. I remember it because if you do a thumbs up, it kind of looks like a 6. And what about the nipple? You got a T4, Dan. Correct. T4 and then the umbilicus. We got the T10. Beautiful. Okay. One last question for you guys. What is the innervation of the muscle, if impaired, that can cause a Trendelenburg gait? And for extra bonus points, if you give me the muscle and the level of the innervation. anyone the superior gluteal nerve yes superior gluteal nerve and then what do you know what what the what's the muscle uh gluteus medius yes and then do you happen to remember the uh the level spinal levels is it l4-s1 yeah holy crap wow well done yep great job um okay so now let's get back to the study uh so here this is how the the dietary restriction worked so for day one you had free access to food all the way up until 9 p.m and then after 9 p.m you were not allowed to have any more food and then on day two you had restricted access aka no food all the way until dinner time where you got 30 of your daily intake and this is repeated for eight weeks and then what was tested before and after uh was the albumin prealbumin potassium sodium and calcium these are all nutrient markers that uh that the that the researchers were looking at to see if this type of diet was causing any type of malnutrition uh they also tested blood glucose and also measured that before dinner on the second day before yes on the second day before dinner and uh blood weight body weights bmi sensory and motor function as well and so the results they showed no significant differences in the nutrient markers or in sensory or motor function but there in there were was significant differences in body weight and blood glucose and so if you look to the table on the right you can see that the vast majority of things were not significant but you can see on the body weight the circled um the circled results that the eodf post-treatment um participants had a large reduction or a statistically significant reduction in body weight yeah another thing i want to throw out to you is um while these results aren't necessarily statistically significant they are worth noting that some of the eodf patients um were were not included or they stopped participating in the study due to the presence of hypoglycemia and one that was not able to continue the study due to hunger demands uh while they weren't statistically significant they are worth noting and then also um both groups had patients that had infections that caused them to not continue with the study and both groups had participants who experienced severe irritability and one patient that um that had nausea however those five participants still continued with the study it's just worth noting that those were one of the the outcomes and so in conclusion eodf and spinal cord injury patients presented with only moderate adverse reactions like hypoglycemia hunger weight loss irritability and nausea there were no significant changes in the nutrient factors therefore indicating that eodf could be considered a safe and feasible approach to spinal cord injury patients some of the limitations in the study sample size was relatively small the duration was only eight weeks who knows if potential adverse reactions were going to happen after 10 weeks or 12 weeks or however long we continue the diet and then also who knows that maybe there would be better functionality or improved uh motor or sensory um yeah if if the uh uh the the sensory or the motor functions increased or became more um adamant over time who knows day two timing it was a little unclear they called it dinner and they never specified a specific time when the participants would eat on that second meal on that second day so potentially could impact the results and some confounding variables physical activity where some participants going through physical therapy or occupational therapy causing them to burn more calories they never touched upon that and then also the specific foods participants were allowed to eat whatever they wanted and therefore the micro macro nutrients might not line up and therefore potentially could have an implication maybe for uh future research and so moving forward as physicians it is our duty to use every single treatment or remedy that we can to help reduce the severity of spinal cord injury and food is an option nutrition is medicine this type of research opens doors for further research for this form of fasting and then potentially other dietary restriction options that can be used as spinal cord patients and sort of helps us bridge the connection between functionality and food i want to thank everyone for giving me this opportunity to share this uh really interesting article with you and let's open up the floor for some questions and a discussion with dr wilson um so i thought it was a neat article um i'm curious i don't understand the chinese rehabilitation system so i don't know really where these people are in their uh time course you know is this right after injury is this six months after injury um that would be interesting for me to figure out i'm not uh bothered by the smaller sample size what i am a little bit bothered by is that they didn't do any kind of uh power analysis beforehand so they have all that data on other populations that they be able to tell um you know how to how big of a sample you need to get to be able to show a difference in their glucose levels um but they didn't really share any part of that answer that is because their primary outcome was really safety and so it would be harder to power a study for safety like that um i think all of the data that they talked about in terms of neurologic recovery was in rats or other animals um so we always want to be careful about trying to translate animals into humans because it's just those studies kind of fail so often um but um but yeah otherwise you know it's it's um an interesting twist on uh diet you know i think a lot of the advantage of this this particular form is that it's easy to follow right that they it's more regimented that you skip two meals and you cut back on dinner you don't have to really count your calories that um i'm not sure whether they really uh talked about you know that's the other thing that everyone was in the hospital so they all had a controlled diet which worked a lot better for them and would be maybe harder to roll out in the general population but yeah and and just to uh let you know they they did look at uh like the time course um or their disease course and it seems like it was all prior to like one year um for both the eodf participants and the controls yeah awesome any questions from the rest of the crew i have a quick question first of all a great great um presentation loved your enthusiasm that was awesome um i might have missed this or just not heard did they measure at all like quality of life reported by the patients to your knowledge they did not okay um i guess to you like would you if like would you think that that would be something that should be incorporated like what's your opinion on that yeah i definitely think so i think um from from my my brief research it seems like a lot of the um there's there's the quote time is spine and so everyone's trying to do as much as they can as soon as possible to be able to reduce the severity of the injury and i think in a perfect world this type of diet if it is safe and effective in the future after more research comes out then maybe this wouldn't be a continued diet that you would do forever but more so um a quick treatment at the beginning where first couple months to try to sort of get ahead of the injury rather than this is something you continue for a long time but i can imagine that the quality of life would not be the best on that type of diet because food is great yeah i agree so for typical uh pattern for spinal cord patients is they have their injury they often lose weight because they're hypermetabolic they're going through trauma there's inflammation they're losing bone mineral density they're losing muscle mass um and then chronically they're at an increased risk for obesity so because their metabolic rate is lower they're um they have late satiety their hormones and their their nerve fibers all these things have changed um and it's often truncal obesity because again they've lost muscle mass in their legs and so their relative bmi is supposed to be lower than everyone else um so the oxidative risks and some of the things that they talked about for the the animal studies in terms of that uh secondary prevention that would be really exciting if that if that works that'd be great i mean like they said there's no real treatments for spinal cord injury and so this would be a treatment for that um i would be a little bit nervous about restricting diets in order you know if they're the main thing they showed was loss of weight and decreased glucose levels which i think are both great chronically but acutely um i'm not sure that's something that we we need unless they also have those other neurologic benefits that makes a lot of sense yeah all right so we're at the nine o'clock mark i want to leave it still open for questions if we have any last minute ones going once going tice all right well i want to take the time to thank our speakers um i got a real quick plug that really helped me out before i got on my spinal cord injury rotation that dan kind of got us starting down that route so this is a great link toward the um asia spinal cord injury site that i just put in the chat for y'all to look at if you're going into third year fourth year second year first year it's something that's a great resource just to be able to do before you even get on an sci rotation it kind of gives you familiar with kind of how things are done in sci rotation so it's an awesome resource um just want to put it out there because it helped me a ton um so i want to thank everyone for coming i want to thank dan rob deep and kirsten for great presentations i want to thank dr wilson for the great insights into kind of the spinal cord world i know it's a population that as med students we're not able to get a ton of exposure to until we get on audition so i want to thank him for kind of giving us a little piece of that tonight um so i thank you all for coming and we'll see you all next month for cancer rehabilitation as our next topic so thank you all for coming thanks everyone night thank you

safety

every other day fasting

spinal cord injuries

pathophysiology

research

dietary restrictions

randomized controlled trial

nutrient markers

sensory and motor function