Hey, good morning, everybody. It's eight o'clock, so we'll go ahead and get started. We've got a big program today, a lot of information to get through, so we'll try to keep everything on time. My name is Dr. John Michael Baratta. I am an assistant professor at the University of North Carolina School of Medicine, where I developed and co-direct our UNC COVID Recovery Clinic. It's so good to have you all in the audience today, and we also have a live stream this morning, which is very exciting, so hello in the cloud. This is the third and final assembly session for Long COVID, and this is really the accumulation of work from the past collaborative, of which AAPMNR has been very supportive, and so we really appreciate that. Today's program is going to be a continuation of the prior sessions, which were on Thursday and Friday, so if you didn't see those but are interested, please tune in on the recording, which should be available on AA Rewind in the coming weeks. So today we're going to start with discussions of autonomic and nervous system disorders, and then discuss central research in PASC, knowledge dissemination of the PASC collaborative, and then future directions of PASC care, as well as the PASC collaborative. To start, we're going to speak about autonomic disorders, and first we have Dr. Svetlana Blitshteyn. She is director and founder of Dysautonomia Clinic in Buffalo, New York. She also serves as a clinical associate professor of neurology at the University at Buffalo Jacobs School of Medicine, and following her will be Dr. David Petrino, who is director of rehabilitation innovation for Mount Sinai Health System, and associate professor of rehabilitation and human performance at the Icahn School of Medicine. Thank you. All right. Thank you very much for this introduction, and thank you for having me over, inviting me as a faculty. So I'm a neurologist who specializes in autonomic disorders for many years. As I always say, I've done that way before the pandemic and way before it was considered cool. So I have no financial disclosures. I'll start with an illustrative case. This is my patient. I'm sure you have similar patients. It's a 51-year-old male physician. He was previously healthy and athletic. He had mild COVID in January and appeared to recover by February. A few weeks later, while shopping with his family, he developed shortness of breath, presyncope, fatigue. And of course, he went to the ER where a pulmonary embolism was ruled out. He also saw his cardiologist. There was no evidence of cardiac disease. Then he went back to work at the hospital. But he noticed that he had difficulty walking from the parking lot to the hospital. The symptoms were fatigue, lightheadedness, and shortness of breath. There were other symptoms as well. He had insomnia, difficulty concentrating. He noticed his heart rate went from 60 supine to 100 beats per minute standing. And while showering, his heart rate would go up to 140. So let's define autonomic nervous system and dysautonomia. And so recall from your neuroanatomy and neurophysiology classes that autonomic nervous system consists of three parts, sympathetic, parasympathetic, and enteric nervous system. And it controls all of the vital organs and functions in the body. Your sympathetic nervous system is, crudely speaking, the flight or fight response. And the parasympathetic calms you down. But also, it's a secretor motor system. And enteric nervous system controls defecation and motility. So dysautonomia is a general term we use for any kind of autonomic dysfunction or autonomic disorders. But I want to call your attention because oftentimes, I see my colleagues referring to dysautonomia, autonomic neuropathy, autonomic dysfunction. Seems like they're similar, but they're actually not. Because the autonomic neuropathy refers to dysfunction of the peripheral autonomic nerves. And we typically like to have some kind of objective confirmation on autonomic function tests that that's indeed the case. So there are common autonomic disorders like postural orthostatic tachycardia syndrome, neurocardiogenic syncope, and neurogenic orthostatic hypotension. And then we have less common autonomic disorder, neurodegenerative ones, multiple system atrophy, pure autonomic failure. When I see these patients in my clinic, that's my bad day because those are very bad disorders with bad prognosis. And then we have this rare kind autoimmune autonomic ganglionopathy, which is a peripheral neuropathy type. There are also rare autonomic disorders, familial dysautonomia, amyloidosis. And very importantly, not every dysautonomia or autonomic dysfunction is an autonomic neuropathy. The neuropathy is for those cases that were reconfirmed by the autonomic function tests. So a few definitions on PASC long COVID, what's that? So patient-led organization defined long COVID. It's coined by Dr. Elisa Perigo. I wanna give her the credit. And it's long-term symptoms after COVID. And shortly after NIH realized that PASC long COVID is a big problem, so they had their own term, PASC, defined as persistent symptoms for four weeks or more after the infection. And then CDC, World Health Organization, weighed in on their definitions. And for CDC, it's post-COVID conditions that are present for four weeks or more, but the World Health Organization also defined that the duration should be at least two months and no other explanation exists. All right, symptoms of PASCs, multisystemic. Most common systems affected are cardiovascular, neurologic, pulmonary, immunologic. And this is a table taken directly from the CDC. As you see, many symptoms, dyspnea, fatigue, post-exertional malaise, brain fog, cough, chest pain, palpitations. So we decided to make sense of it all and how do you assess and treat for autonomic dysfunction. And we met with the PASC collaborative frequently to discuss various recommendations and vote on it. And I was very honored to have been chosen to be the clinical lead on that. The paper was just published, September 28th. And it's also very nice to meet my wonderful co-authors, you know, face-to-face after a couple of years of just interacting on Zoom, though we agree that Zoom is pretty cool too. All right, so assessment. You know, as any evaluation in physiatry and neurology begins with a detailed history of pre-existing symptoms and conditions. And I've outlined a couple that stands out for me in my patients is a history of migraines, dizziness, fainting, fatigue, allergies, and concussion, interestingly enough, in the past. But these people were never disabled. So they were very functional people just with something in the past that happened. And you wanna assess for medications that can cause or worsen tachycardia, hypotension, or orthostatic intolerance. Family history of autonomic and autoimmune diseases, obviously very important, as are features of long COVID that other family members can have. Social history, you wanna ask for caffeine intake because it can raise your heart rate. And then obviously, fluids and salt intake. You wanna see if they can exercise because exercise intolerance is a huge feature of dysautonomia and long COVID both. A lot of people are unemployed. And obviously, as I always say, if you have a chronic illness, you're not gonna be very happy. So secondary anxiety, depression, even PTSD might not be uncommon. So stress is important. For physical exam, you see in red, we recommend a 10-minute stand test with blood pressure and heart rate measurements in supine and standing positions. Now, we're all very busy in the clinic and there was an argument, should it be five? Should it be? You can have your nurse or a medical assistant do this, record vital signs, record symptoms, and then that's one of the criteria for a common autonomic disorders. It's done by a 10-minute stand test. So neurologic exam needs to be done, including sensory exam for small fibroneuropathy, diagnostic tests that we recommend, EKG, pulse ox, Holter monitor, a tilt table test. Now, tilt table test is very important. Should you get it on every patient? Of course not, but you should get it if a stand test is unrevealing and you're still suspect that there is dysautonomia. Autonomic function tests were available because not every city, even not every state, has autonomic function lab. I don't have it in Buffalo, so I have to make do with tilt table test and a skin biopsy and all of the other tests that are available. And blood tests that are on there in the statement is CBC, CMP thyroid function test, vitamin B12, ferritin, morning cortisol, and then of course your autoimmune inflammatory markers, ANA, Cedrate, and CRP. So we go back, we go, finally we reach treatment. You know, there's a big topic in and of itself. Even though there are no FDA-approved therapies for long COVID, and there are no FDA-approved therapists for POTS either. But obviously if you diagnose an autonomic disorder, you have to treat it. And then if there is mass cell hyperactivity symptoms and signs, you treat it with antihistamines and low histamine diet. And if there is headache, insomnia, pain, symptomatically based, of course you need to treat that. But what's there? What do we have available for autonomic dysfunction? Because sometimes my colleagues who are not in this field, a lot of neurologists as well, they say, well, what do you do for them? What do you treat them with? Is there anything available? You diagnose them, but what do you have to offer? We have a lot to offer. So we start with non-pharmacologic therapy consisting of fluids. We recommend at least two and a half fluids, two and a half liters of fluids per day. We recommend at least seven grams of sodium chloride, your table salt, compression garments in the form of waist high compression stockings and or abdominal binders. We also use diet, you know, high sodium diet obviously is important, but gluten-free diet can also be helpful as is a low histamine diet. Pacing and mild exercise are on there and Dr. Petrino will talk about that more. And what medications do we have? You know, the staples are beta-blockers, Florinef, Midodrine, Mestinone, but we also have the Vabradin stimulants and low-dose naltrexone. Now patients themselves you'll see are using vitamins, supplements, and that's okay. Again, there are no FDA studies, FDA approval on any of the medications, so why not? If it doesn't cause any harm and the doses are appropriate, I am okay with that. IV saline we use on as needed basis. We try not to end up with peak lines or ports because the risk of infection and blood clots may be higher in this population. And then a short course of oral steroids can be used. IVIG, subcutaneous immunoglobulin for severe refractory cases. Autonomic rehab will be discussed and then biofeedback and supportive therapy. So last slide, I have a table of pharmacotherapy and on that question, well, what do you have to offer? These medications are all used in various forms of autonomic disorders and you can check it out in the paper. But I do want to stress these points. Treatment is necessary for many patients because it reduces severity of symptoms. It improves functional status. Yes, it's a trial and error approach, so of course it's not ideal, but I think it's very important in disease scores because in my experience, I see patients who are extremely sick two years out because they haven't been treated. So I want to stress that we have a lot of things to offer. They're not ideal. They're symptomatic base, but please use these medications and don't hesitate to start the medication without waiting for months for the patient to improve spontaneously. All right, thank you very much for your attention and I'll pass it over to Dr. David Petrina. Thank you. Thank you very much, Svetlana. That was amazing. I always learn a lot when I'm listening to you. So I've been given 10 minutes to talk about rehab for long COVID. And in full respect of 10 minutes to talk about that, I wanted to build on some of what Svetlana spoke about in terms of how we characterize long COVID, because it is very important to think about when we're rehabbing people with long COVID. I'm going to give a disclaimer before I move to the next slide, which is that I have made multiple variations of this slide. And at some point, someone gets angry about this every single time I make it. But I keep adapting it based on feedback. So if this slide makes you angry, give me feedback, and I will adapt it. So as Svetlana mentioned, we say the word long COVID. And it was a patient-derived term. Eliza Perrigo first used the term. And when she first used the term, this is what she meant. Anybody who has symptoms that persist after an acute SARS-CoV-2 infection has long COVID. Now, I feel the need to start to break this diagnosis up into different presentations, because it affects the way we treat. So what you can see in the purple is individuals who have mainstream test results that correlate with their presenting symptoms. So what I mean by that is someone who got a severe COVID pneumonia, they come to you and they say, I've got shortness of breath, exercise intolerance, I can't do things the way I used to. You look at their lungs, you see serious scarring, pulmonary fibrosis. You look at their pulse oximetry, it's not doing what it should do. And they respond well to something like pulmonary rehabilitation. In the blue, you've got individuals who are presenting, and they have severe symptoms, they have severe disability. But their mainstream tests are coming back normal or abnormal in a way that is difficult to interpret. And their symptoms are more syndromic. These are folks that meet diagnostic criteria for ME-CFS, dysautonomia, some autoimmune condition. Post-ICU syndrome, I think, also fits in the blue category. The reason I'm starting to separate these out is because the ones in the purple, although there is overlap between the two groups, so sometimes the folks in the purple may also have syndromic elements to their illness, the ones in the purple may respond well to traditional interventional approaches. You see lung scarring, you see drops in SpO2, you see evidence that this individual is just recovering from a severe pneumonia. They may respond well to traditional pulmonary rehab. The ones in the blue, however, will be harmed by traditional rehab approaches. If you just say, oh, you're deconditioned, so let's get you doing graded exercise therapy, this is going to make these patients worse. We will be doing harm. This needs to be said over and over again, because we've seen too many patients have their disease progressed by bad exercise prescription or thoughtless exercise prescription. And so this is why we need to separate out these two, because we don't want the folks in the purple to not get adequate care, but we don't want the folks in blue to get harmed. And being very intentional about our investigations and our assessments becomes very important. I also just want to point out that also, as covered by Svetlana, but I want to put into a little bit more context, there are people that can get a long COVID diagnosis based on CDC guidelines, so a post-COVID condition diagnosis, that will look syndromic. So they'll come to you with fatigue. They're testing normal. They've got exercise intolerance. They've got post-exertional malaise. But if you diagnose too early, sort of four or six weeks after their acute SARS-CoV-2 infection, these could be individuals who are just taking a long time to recover from their acute COVID infection. And what I worry about here is by diagnosing these folks too early, these folks will just spontaneously recover. And what we want to be careful of is making sure that these individuals don't get caught in the numbers of long COVID because then there is a narrative that, oh, 60% of long COVID cases just recover spontaneously. Again, this is not the case. It's just our need to make sure that when we're diagnosing things, we're diagnosing things correctly. And so that is why I do tend to favor the WHO guidelines, which they actually talk about three months post-acute SARS-CoV-2 with at least two months of symptoms. So for me, that is a much better characterization. And the CDC actually agrees, and they've updated their guidance statement to include the fact that you can start suspecting at four weeks, but diagnosis should occur more toward three months, which I think is sensible. And then I finally just want to touch on individuals who will present with long COVID and I believe that they have long COVID. They meet the diagnostic criteria for long COVID, but they had pre-existing complex chronic illness that has been worsened by their acute COVID infection. And so you need to treat with their prior history of complex chronic illness in mind. So I've lost count of the number of folks with Ehlers-Danlos syndrome, for instance, who have come to our clinic, and their symptoms are just significantly worsened. Now, is their pathobiology of their symptoms distinct to the folks who were perfectly healthy prior to their acute SARS-CoV-2 infection and now have symptoms? We don't know, but I think it's just worth keeping track of these folks and understanding that they exist. They may be slightly different and may respond slightly differently to rehabilitation approaches. And it would do us well to keep us in mind. And then to just add further controversy and confusion to the mix, we also should acknowledge that vaccine injury exists. And folks with vaccine injury often look a lot like people with long COVID and often will respond well to similar interventions because they do have dysautonomia, they do have POTS, and we can treat that. OK, so we're going to talk about syndromic long COVID, and we're going to talk about it quickly. But that was a lengthy preamble that I think is very, very important and I hope has cleared things up as opposed to made things more complicated. So in terms of treating, some of the best things we can do and the most powerful things we can do is identifying known triggers and giving people strategies to avoid or mitigate these known triggers. Sometimes we always start with pacing and energy conservation techniques, helping people to identify what their energy envelope looks like and not exceed that energy envelope for the day with the understanding that they may not feel it in the moment, but several days after they will experience a worsening of symptoms if they start to push beyond the energy envelope. So pacing is a strategy that every single physiatrist should be familiar with and should be explaining to long COVID patients as they come in. Because sometimes it's the only thing we can do for very severe cases, and it makes a big difference in symptoms. As Svetlana mentioned, many people will experience anxiety and depression secondary to this new diagnosis of a disability, and they should be made aware that their dysautonomia can be significantly worsened by stressful situations. And so making sure that they're aware of services to assist with emotion regulation strategies or even medication if necessary is very important. Dehydration, Svetlana already mentioned, hydration with electrolytes. Making sure people understand that extreme weather can cause flares in their symptoms is very important, and helping them build a plan to manage weather changes can make a big difference in daily symptom burden. Consuming large meals, this is an autonomic event. You stretch your stomach. It causes a parasympathetic event, and that can trigger symptoms. So having conversations about meal planning and spacing out meals. Alcohol consumption, sadly, usually affects people. So just having that hard conversation. And then individuals, a number of people who menstruate will mention that they experience their premenstrual period causes a lot of worsening of symptoms. Again, similar to any chronic pain patient, we are identifying triggers of pain worsening. Just make sure people are aware of this. Monitor this. Use things, fertility app trackers to look at hormonal levels to see if there is anything that you can treat, because often progesterone levels and estrogen levels are linked to increase in symptom burden. And just conversations about prepping for this. We've had great success with breathwork protocols. We focus on parasympathetic breathing. We've been working with a company called Stasis, but the breathing program is really not so complicated. We published a paper showing that individuals with long COVID have hypocapnia, so they're low levels of CO2. So we focus on increasing systemic CO2 levels and focus on CO2 tolerance. So breathwork has been really helpful for a lot of our patients and is cheap and easy to deploy in the moment when people are experiencing a flare. Autonomic rehab, of course. I wish I could spend a little bit more time on this, but this is basically an hour of a session. Just be aware that this is not graded exercise therapy. There are things like the Levine protocol and the modified CHOP protocol. These are too intense for patients from the day that they step in the clinic. Measure their activity tolerance. And what I'm showing you here is a video of one of our first phases of autonomic rehab. The patient is supine, performing heel slides. So much of autonomic rehabilitation can be non-aerobic in nature if the patient is being exacerbated by aerobic rehab. And I also want to point out that although this is being done in clinic, patients can do without location-based rehab in the early stages. They can do rehab in a tele-rehab environment if their symptoms are too severe that getting them to the clinic is enough of an exertion to cause a flare. So just to be aware of that. I just wanted to share some results of a case series of just over 100 patients that we put through autonomic rehab. I'm a minute over, Svetlana. Almost there. What we see basically here is in three months of rehab, a halving of fatigue and a doubling of activity tolerance. But I really want to point out that people are still symptomatic. So we are easing symptoms. But in only a very select percentage of long COVID patients are we actually completely resolving symptoms. And I think that that's important because this speaks to the underlying pathology that is still present while we're managing their severe symptoms. And so I want to just finish with this as a sort of a zoom in on the 10 meter walk time, so gate speed. And we see that gate speed is increasing over three months of rehab. But it should also tell you here that if you're at the three month mark and people are just, their symptoms aren't moving, rehab is not working. In fact, if you're at the one month mark and you haven't seen some sort of improvement in symptoms in most of your patients, you should consider moving into a second round of treatments, including medications. So not just rehab alone. And we're also starting to investigate things like non-invasive vagus nerve stimulation that can be accompanied with autonomic rehabilitation as well. Lots of resources on the AAPMR website. But I'd also recommend Long COVID Physio. They have enormous amounts of resources. I'd like to acknowledge everyone and sorry for going over. Thank you, Dr. Blitzstein and Dr. Petrino. Those were excellent talks on a very important part of Long COVID. So I am going to transition slightly to talk about central nervous system effects within Long COVID. And I'll be followed by Dr. Weiss, who will describe peripheral nervous system issues. So the objectives will be primarily to describe the main Long COVID effects seen in the CNS, as well as some evaluation and management approaches. There are a wide range of CNS effects that have been reported in the post-acute period, including cognitive and memory issues, headache and migraine disorders, dizziness and balance problems, cerebrovascular disease, and so on. Dizziness and balance problems, cerebrovascular disease, movement and sensory disorders, and others, including mental health concerns. Unfortunately, neurological PASC is a common manifestation. This paper published in Nature Medicine last month shows that there is a 42% increase in the risk of development of neurological symptoms and the diagnosis of them within 30 days to 12 months after COVID. So this is, I completely agree with Dr. Petrino about the timeline, that probably three months is a more appropriate timeline as far as diagnosis of Long COVID. But out of the traditional acute period, so beyond 30 days, there is still an increased risk of development of neurologic diagnoses. And these increased risks are present across different age groups, races, sexes, and other comparison groups, including in both hospitalized and non-hospitalized cohorts. There are a number of potential mechanisms underlying the CNS presentation. These have not been fully defined. And as with other manifestations of PASC, there could be multifactorial components. But neuroinflammation may be a big risk factor, as well as damage to blood vessels. It's also important to note that there has been some documented change to brain structure after COVID illness. The UK has a biobank repository. And in that, there are a number of patients who have baseline MRIs and cognitive testing. The COVID-19 pandemic presented a unique opportunity to examine people with imaging and cognitive testing after their illness. And so they had, in this particular study, about 800 participants who had developed COVID and went back for repeat imaging. And this showed a loss of gray matter thickness, particularly in the orbitofrontal cortex and parahippocampal gyrus, along with smaller overall brain volumes when compared to controls. So this is a particular change to brain structure which should be noted. The degree to which it corresponds with the symptoms seen in CNS-PASC is a little unclear still. So Dr. Fine and others in the PASC collaborative have published a guidance statement which describes cognitive symptoms. This is, I think, one of the most common types of manifestations of CNS-PASC. A lot of patients come in describing brain fog. And this is generally what they're referring to. In studies after 12 weeks, there are In studies after 12 weeks, there are prevalence rates of cognitive symptoms between 20% to 65%. And the wide variation depends on the cohorts and the types of patients that are enrolled as far as ambulatory at the time of their illness versus hospitalized. But the cognitive symptoms can run across a number of different domains, as listed here. Drs. Fine and Ambrose spoke at the presentation yesterday in detail about the cognitive symptoms and the guidance statements. So I won't go back through all of their presentation, but I did want to include it here for completeness that there are assessment and treatment techniques provided. And if that's of interest to you, please look back at their particular presentation. So moving on to post-COVID headaches and migraine disorders, moving on to post-COVID headaches and migraine disorders, there are increased risks of both of these in the first 12 months after COVID illness. These could represent a new daily or intermittent headache, as well as a worsening of a preexisting headache syndrome. They could start after a delay or as part of the initial infection and just continue from there. Together with other long COVID symptoms, particularly altered smell, these are very frequently seen symptoms. Mostly they are tension-type headaches as opposed to ones with migraines features. The treatment for these headache and migraine disorders should be guided based on the existing protocols for primary headaches with the corresponding phenotypes. So for tension-type and migraine-like headaches, this is probably going to be acetaminophen or NSAIDs as a first-line treatment. Second-line approach for tension-type would be a combination preparation with caffeine and for migraine headaches, triptans. Preventative headache medicines may be used for those with more frequent headache symptoms, and these could include TCAs, SNRIs, and others listed here. For all patients, we should consider recommending a healthy balanced diet, encouraging good sleep hygiene techniques, and regular physical activity. And also considering non-pharmacologic techniques such as acupuncture and breathing and relaxation techniques is appropriate. In the first year after COVID, there's also an increased risk of ischemic stroke, TIAs, hemorrhagic stroke, and also venous thrombosis. And again, this is past 30 days, but before one year. Endotheliopathy is a particular contributor to ischemic stroke, and this has been well-described in acute COVID with a hyper-inflammatory prothrombotic state. But I believe the factors that permit that in the acute COVID illness could persist for a period of time, leading to increased risk of stroke in the post-acute period, too. This is mainly mediated by infection or activation of the endothelium, which can contribute to a thrombus formation and then embolization. Movement disorders are also seen at increased rates after COVID, including tremors, Parkinson-like disease, dystonia, and myoclonus. And the management of these should also be guided based on the general treatment principles for each of these syndromes. And finally, I wanted to touch on mental health concerns. Mental health is a piece of long COVID that we have to be aware of. Many people who are newly disabled, with regards to their long COVID symptoms, have challenges with anxiety and depression, and this should not be forgotten in their overall treatment plan. There are extremely high rates of depressive disorders, adjustment disorders, and anxiety after COVID, particularly in that long COVID period. This can be described based on a biopsychosocial model, perhaps biologically with neuroinflammation, challenges with pain, fatigue, and dyspnea. Psychologically, there could be concerns about loss of livelihood, worries about reinfection, and also the unpredictable nature of long COVID disease course. And socially, I think it's fair to say we've probably all been affected by physical distancing, lockdowns, closures, and I think these challenges are just magnified for people with a new disabling condition, such as long COVID. Evaluation for neuropsychiatric concerns should follow validated symptom screening, but traditional measures, such as the PHQ, are not totally sensitive and have some false positives. There may be reversible causes, and those should be investigated, including nutritional deficiencies, endocrinopathies, and sleep problems. Behavioral management approaches are a consideration, and there are a number of different options to support patients. And finally, medication options can be a good consideration. There are a number of potential classes of meds, such as listed here, many of which treat depression and anxiety. But when selecting one of these medicines, it's important to consider what additional benefits might be conferred upon the patient, including anti-inflammatory effects with a SSRI, activating and concentration effects with bupropion, concentration and focus with some other meds as well. So consider medication options as part of the overall treatment plan. So I've reached the end of my time. I'm going to turn it over to Dr. Weiss. Dr. Lynn Weiss is Chair of PM&R at NYU Langone Hospital Long Island, and she's Professor of Rehabilitation Medicine at NYU Long Island School of Medicine. Thank you. Should I do a dance or a song in between? You don't want to hear that. Okay. So, um, here's my objectives. Um, basically, um, you know, I think that that long COVID PASC has a similar problem to PM&R in that we have too many names. We need a PR person to really consolidate it. It's physiatry, PM&R, rehab, physiatry. And then we have long COVID, um, PASC. We have, uh, too many, too many words where people kind of don't understand. So that's just my long haul post COVID, post acute COVID, post acute sequelae of COVID. So if you can get one thing from this, we need a PR person, both for physiatry and for a PASC to figure out, um, so that everybody's talking about the same thing. Um, but basically we've gone over this, the difference between the World Health Organization definition and the CDC definition. Um, but what are the manifestations? I'm going to be talking about the peripheral nervous system and, um, the most common ones are muscle weakness, myalgias, decreased smell, decreased taste, tinnitus, um, hypesthesia, tremors, dysesthesias. And the mechanism, you know, again, is proposed. We really don't know for sure. We think that in PASC, inflammatory mediators, um, cytokinins, prostaglandins and nerve growth factors are released and these results in peripheral sensitization. And by the way, I want to be clear when I'm talking about the peripheral nervous system, we, I've seen in my practice, my clinical practice, I do mostly electrodiagnostic testing and I've seen so much peripheral neuropathy as well as entrapment neuropathy, um, in these patients. There is stretching of the peripheral nerves. A lot of times these patients have lost a lot of weight and, um, they're more prone to, um, nerve entrapments, um, space occupying lesions. We heard about thrombus formations. And don't forget that blood vessels, um, feed nerves. So, you know, we have so much talk about blood vessel problems, um, you know, in the central nervous system, in the heart, in the lungs, in every place else. Well, we need those same blood vessels to feed the nerves. So when a problem occurs in a, um, the basal nevorum, the nerve can be affected. Um, T-cell abnormalities, endothelial dysfunction, like he was just talking about mast cell activation and prothrombotic state. So there's so many mechanisms that can affect nerves in the peripheral nervous system. Um, neuropathic pain, um, we've all dealt with this. It's usually spontaneous. Patients can have allodynia, hyperalgesia, um, and so, um, patients can also have small fiber neuropathy. And again, the proposed mechanism, it could be immune-mediated inflammatory nerve injury or endotheliitis. Um, the A fibers and unmyelinated C fibers can be affected, and you can get pain and peripheral dysfunction. Um, now there's some studies that say, you know, is post, is PASC, um, in the nervous system somewhat like shingles? Is there a reservoir of, um, COVID sitting in the, in the peripheral nervous system that is reactivated? You know, again, um, we don't think that it's currently, um, in the central nervous system, but maybe it's harboring in the peripheral nervous system. And then, you know, another theory is that, um, that the virus induces neuroinflammatory prothrombotic hypoxic metabolic and cell death cascades. So um, how prevalent is this? And you know, we talked yesterday about how many people have COVID in the world. And if you think about how many people have COVID and how many people, you know, tend to 25% then develop, um, PASC, it's a huge number of patients who potentially can suffer from these problems. So the most frequently reported, um, peripheral nervous system is sensory motor deficits, 91%, and then disorders of smell and taste at 58%. And this was a survey online of, um, you know, almost 4,000 participants. This is six months after the acute disease. There's another study of 165, um, patients who have had COVID, and this is six months after hospitalization. And again, you see a lot of, um, problems in the peripheral nervous system, um, numbness, tingling, um, you know, sensory motor deficits. Um, and then here's a very large sample, um, again, six months after this was looking at electronic medical records, um, nerve and root, and nerve root and plexus disorders in 2.9%. Okay, 2.9% is not a lot, but when you multiply that by millions of patients who've had long COVID, uh, or PASC, it's, it's a lot of people. And you have to be aware. You have to say, when you're looking at your patient, you know, and we've talked about this throughout, um, these three days or three sessions, you know, you have to ask the right questions. You have to say, um, you know, are you experiencing any weakness? Are you experiencing numbness? Because a lot of times they're just so overwhelmed by the fatigue or the breathing problems that they don't even notice it. Neuromuscular junction problems, um, in half a percent. And then Guillain-Barre is, you know, we were, everybody was worried about Guillain-Barre in the beginning because it's very common in viral conditions. Um, but, um, it's actually, there's been less Guillain-Barre than in influenza. And there were some concerns about, um, Guillain-Barre when, um, the vaccines first came out that think the Johnson and Johnson was the most prevalent, but really there has been very, very low incidence of Guillain-Barre. Myalgias, um, noted in 22% of patients, um, after 12 months of follow-up, again, very significant number of patients. Small fiber neuropathy, um, this can be confirmed by, um, skin biopsy and, um, may be related to some of the paresthesis that the patients are helping. Um, Svetlana talked about the autonomic dysfunction, so I'm, I'm not going to talk about that because we only have 10 minutes to talk about the entire peripheral nervous system. Um, but there is a higher occurrence of pain and peripheral neuropathy, um, in patients, um, with PASC. So, um, you know, this was another study that looked at pain and neuropathy symptoms. And one in 16 patients had persistent symptoms. The control group without this had nearly threefold lower. So there is a large, I, I, again, my take-home message, if I haven't already said it, is look for peripheral neuropathy in patients with PASC. Um, and in patients with pre-existing chronic pain or pre-existing neuropathy, um, there was a higher portion of patients reporting, um, worsening of symptoms compared to controls. So bottom line, you know, why does, um, PASC affect the central nervous system? We don't know. Um, or we don't know enough, I should say. So, um, so what are the symptoms that would make you think your patient has a peripheral nerve injury? Um, numbness, weakness, anything lower motor neurons, so, um, decreased reflexes, looking for atrophy. Um, and these are things, again, good history and physical. Um, like any, anything else, your history and your physical are going to give you 90% of your information. Um, EMG testing is very, very important to confirm either a, um, a peripheral neuropathy or an entrapment neuropathy. So, um, you know, sending these patients for EMG testing, um, if you suspect it is important to confirm. Um, differentiating between a general neuropathy and a, um, isolated nerve injury. In peripheral neuropathy, it's going to be distal and usually it's going to be symmetrical. Whereas in, if you have, you know, we've seen a lot of, um, fibular neuropathy due to weight loss, due to positioning, due to immobility, it's going to be asymmetrical and it's going to be in a specific, um, nerve root, dermatoma, or myotomal distribution. In terms of laboratory testing, um, like we've been talking about, you want to rule out anything that, that, um, may be treatable or a little bit easier treatable or differently treatable. Um, so you want to rule out autoimmune disorders. You want to look for inflammatory mediators. So all of these, um, laboratory testing, you know, are important. Um, the rehabilitation of these patients, um, so, okay, now you've diagnosed that the patient has a peripheral neuropathy or an entrapment neuropathy, um, sometimes bracing is needed. Um, I've had a lot of patients with foot drop. Um, a lot of patients, it's not necessarily from past, but, um, leftover, they've had ECMO and they have femoral neuropathies or, um, things like that. Um, physical therapy, again, um, you want to make sure that the muscle's not atrophied by the time re-innovation occurs. Um, and so, um, you know, like we talked about, you do want to make sure that the patient does exercise, but you don't want to fatigue the patient. You don't want to do too much. Occupational therapy is important and assistive devices so that they can compensate for their, um, peripheral nerve disorders. Prognosticating, um, nerves grow about an inch a month in the peripheral nervous system. Um, so you can say, you know, your, your nerve problem is in the brachial plexus or, and I've seen a lot of plexopathies, um, both in the, um, lumbosacral plexus and the, um, brachial plexus. Um, so, um, nerves can regenerate from the peripheral nervous system, um, and you can say, you know, this is about how much recovery you'll have depending on how far along it is and how distant the nerves that have to innervate are. Um, and then you can also, you know, the reason why EMG testing is important also is to quantify the amount and type of injury. Um, if it's neuropraxia, then it's a localized area of conduction block, which the body remyelinates very quickly and you can tell the person, you know, you have very good recovery. Axonotmesis, where the, the axon is affected and therefore, um, it's going to take longer to recover. Um, and then neurotmesis, which is a complete lesion of the myelin, the nerve, the axon and the surrounding structures where really surgical intervention is required. We do have treatments, um, and most of them unfortunately are, um, symptomatic treatments, but, um, we do have medications like gabapentin, pregabalin, um, you know, antidepressants, anti-seizure medications, um, desensitization therapies. Sometimes, um, you know, these can be very disabling and they can interfere with therapy, so you want to make sure to address their pain. Um, capsaicin and lidocaine patches don't work great, um, but they are there if the patient, especially if the patient can't tolerate medications. You want to really optimize glycemic control because, um, glucose can have a very bad effect on the nerves. Obviously, lifestyle and risk factor modifications, you want to talk to the patients about blood pressure, weight, um, avoiding alcohol and tobacco. Physical therapy, like we spoke of, is extremely important, not only to, um, make sure that the, there's no atrophy so that when there is re-innervation that the muscles are there, but also to maintain, um, your strength. TENS is, um, very good for pain control. Sometimes acupuncture, and then in rare cases, if the pain is unbearable, spinal cord stimulators. So, thank you. Thank you, Dr. Weiss. Next, we have a discussion of critical research in PASC. Dr. Monica Verduzco Gutierrez will be, uh, leading that. She is professor and chair of the Department of Rehabilitation Medicine at the Long School of Medicine at UT Health San Antonio. Thank you for being here, for listening virtually or in person. And I also like to call my session, what we know and what we don't know about PASC, because there's still, you know, there's stuff that we know and what we don't know and where the research is going and what treatment options. Because I think in the end is what we want to know is how do we treat these patients best with the tools that we have or what we will be having. So, for pathogenesis, this is a nice slide that shows all roads lead to long COVID, that, you know, what there, we know exactly what's happening. And I think as we see more and more research, that one person may not, or PASC may not just be one thing going on, but there is going to be people that are having autoimmunity. There's going to be the micro clots, the micro thrombi. There is the immune response and the inflammation that not all, in some studies, not all patients have. Viral reactivation, not every patient has had EBV or viral reactivation, but that's driving some of the long COVID. And I think one of the big questions of what we don't know yet is still the SARS-CoV persistence. And is there some viral? Well, yes, there's been found to be viral antigen persistence, but is that driving the long COVID symptoms that patients are having? This is a slide if Dr. Friedley knows, notices that I stole it from her, but I love it. So, I will give her the acknowledgement for it. And part of the, what we know, what we don't know is, you know, why is it that we see these patients, and sometimes we send them for EMGs and the EMG might be normal, and we get them, they have an echo and they've had a CT scan, and those things are normal, yet they're having all these symptoms that we know are related to inflammation, disrupted immunity, nervous system dysfunction that we don't have good tests for yet, and that we can't test for micro clots yet. And so, I think that's a big of what we don't know and what we, you know, ties into, we know these are real, we know people are suffering, but we still need to get the right test for them. So, what do we know for treatments? And not everyone anymore has all these really bad COVID lungs because people are getting less severe disease. So, this is Dr. Deak's paper where he kind of was looking at pathogenesis of long COVID. So, a lot of these slides are also from some work that Dr. Deak's did, and it goes through what are a possible mechanism that may be driving long COVID and what could be some possible treatments that we have. And so, the first one is, okay, you have acute viral infection, you have irreversible tissue damage. So, these are the people who get very severe myopathies, lung disease, cardiomyopathies, they get interstitial lung disease, and, you know, how do we treat that? We know prevention. Please, you know, try to get your vaccine, try to wear masks, social distance, et cetera, et cetera. Antivirals, we know that we have antivirals now actually to use, anti-inflammatory drugs. Rehabilitation, this is where we have, where we know traditional, if it's pulmonary driven, traditional pulmonary rehab will work for those patients. And so, those are possible therapeutic strategies. And inpatient rehab is also something that there's more and more data on, but these are on the traditional long COVID patients that are the PICs, the post-intensive care syndrome patients. So, these are ones that were hospitalized, they had severe disease, and yes, there's now more data showing that they benefit from inpatient rehabilitation. So, this was a prospective study, patients got 32 days of inpatient rehab, and they, you know, did better with exercise capacity, muscle strength, ADLs. These are two other studies, one from Journal of Intensive Care Society, again, prospective study evaluation of 26 acute hospitals in England, and patients more were referred to inpatient rehab versus community, and community-based rehab. And so, there was, you know, it was also positive for them to have rehab. This is from Korea, and this is a study, 37 patients, comprehensive rehab management, improved their muscle mass, muscle strength, and physical performance. The more they got, the better they did. So, these are for the hospitalized ICU patients. Please make sure that you're fighting for them to get into your inpatient rehab. Outpatient long COVID rehab, you know, it's been talked about before, so again, it's different, it's not traditional. You have to think about autonomic reconditioning, breathing exercises, avoiding post-screening, and avoiding post-exertional malaise. The World Health Organization now has a clinical management of COVID-19. They have living guidelines. This is the most recent one that came out last month. There is a whole section on rehabilitation, and so it's great. It says that it has to be multidisciplinary. Please look for red flags, including, you know, if there's exertional symptoms or cardiac impairment, you have to make sure nothing's going on with their heart before you just say it's, you know, it's not that, and continue to do your exercise. Please look for post-exertional symptom exacerbation, or screen for orthostatic intolerance, because a lot of them will have it, and then graduated return to work and life. Please use validated measures. That's another thing. I would say these are going to be the symptom measurement when you're seeing these patients. Maybe the difference between a patient getting disability or not getting disability, and so there's some list of, you know, scales that you can use for these patients who you're seeing. You heard about triggers, support your patients for disability and work accommodations. We know we've done this before as physiatrists and other specialties to say, you know, patients need a graduated return to work, just like my brain injury patients used to need a graduated return to work, and now the long COVID patients need similar graduated return to work and accommodations. They have relapses. They're going to get overwhelmed by sound, by a lot of people in the room. We've seen this before, and we're able to prescribe this and make these accommodations for patients who have fatigue and brain fog. So what is another, you know, what we don't know, or what may be a possible therapeutic strategy? So if we think that there's, and this I would love to know, is there persistent viral infection? Is there like EBV kind of dormant? Is it like varicella, one day we're going to get shingles, but the COVID shingles or something, I don't know, or worse, like post polio? And is this persistent viral, you know, driving inflammation, driving tissue harm? And so there are going to be studies, and even in the NIH recover trial, they'll probably look at trialing some of the antivirals for longer than five days in some of the past patients to see if it helps. Virus monoclonal antibodies, therapeutic vaccine. Those are some of the things that are being considered. This is a slide that just shows that there have been studies that what happens to past patients after they get COVID vaccines? Some of them have a resolution of their symptoms and feel better. Some get better. A small percentage get worse. And so in these studies, it's, you know, is it triggering our immune system to fight the, you know, remnants that are in our system? Is it good, just like a helpful immune jump to help some of our patients feel better? I do, some patients feel much, much worse too, so I'm kind of cautious in which ones that I'm really, really pushing the vaccine on. But for the most part, I'm encouraging vaccines. Inflammation, we've talked about. It's so hard, because it's like, we know there's inflammation going on, but I can't test all that. I don't know how to, I can't order your interferon and your other types of tests to show you and prove that there is inflammation. And it's either direct from the infection or indirect. Gut dysbiosis, EBV, et cetera. And so, should we be giving patients anti-inflammatories? And these are some studies that may be done. Steroids, colchicine, the antihistamines. Again, that's for some of the mass cell dysfunction that's happening. JAK inhibitors that they use in rheumatoid arthritis and cancer. Those are probably some of the big ones that should be or will be trialed or considered as well. Some of the monoclonal antibodies against all of these, you know, ones that you use for autoimmune disease, but it's against all these inflammatory markers. IVIG and treating viral reactivations. All right, the next one, autoimmune is, you know, considering IVIG and some of the B-cell directed therapies. So, these are some of the autoimmune considerations. I already talked about, you know, monoclonal antibodies, anakinra, infliximab, these, the JAK inhibitors that are DMARDs, naltrexone, and I'll go into that a little bit more because some of the stuff is like, well, I can't really order this in my patients for now and we're waiting for the trials to be done. That's why we don't know. But what are some of the things that can be ordered? Sometimes IVIG, especially if you find, you know, decreased immunoglobulins or some kind of autoimmune that would, and the insurance allows them to get IVIG. So, low-dose naltrexone, it's been used in chronic pain. I actually learned it from my chronic pain friends here in PM&R and then they also use it in ME-CFS and now it's starting to be used also in long COVID. So again, it's not the high dose of, you know, this is the anti-abuse medication, but it's in very, very low doses. It's toll-like receptor four antagonism, opioid growth factor antagonism. It works at ion channels and helps with pain, inflammation, autoimmunity, and very little side effects related to this. So there is a study where they've done, looked at low-dose naltrexone in the past. There was even a more recent one as well, showing it was helping statistically significant in some of these chest pain, tightness, cough, joint pains, low mood, personality change. And so this is something that I can order for a patient and have it sent to a compounding pharmacy. It'd be less than $50 for them and they get a lot of help from it. Then microvascular disease, microclots, endothelial dysfunction. So those are rather like, we don't know, this may be one of the pathophysiologies of it. And what are some of the potential treatments? Anticoagulants, you know, there is Dr. Pistorius in South Africa who is looking at microclots and some of the patients she's treating is getting apheresis or they're getting triple therapy. Some patients even can buy natokinase or streptokinase that is a supplement that helps on these microclots. And then for endothelial dysfunction, enhanced external counterpulsation is something that they've used before for cardiac disease and for angina. And I'm using that in some of my patients with good effectiveness and is covered by some insurances for long COVID. Is there mitochondrial dysfunction? There are mitochondrial supplements that some patients, that people can get over the counter. And then there's ones that are in study that are working on to being used as well. AXA 1125 is one of those that will also be probably looked at by the recovered trial. So again, I want it to be community-based. I want it to start early if they're hospitalized, inpatient rehab, you know, autonomic reconditioning, pacing, pacing, pacing, education, mental health services, and there'll be more to come. And always my take-home message, would good enough be good enough for you when you see these patients with PASC? Thank you. Thank you. Thank you, Dr. Verduzco Gutierrez. Next, we're going to talk about disseminating the collective knowledge of the PASC Collaborative. Dr. Jana Freedley will be speaking on this. She is professor in the Department of Rehabilitation Medicine at the University of Washington, where she also serves as the executive director of the UW Post-COVID Rehabilitation and Recovery Clinic, and Dr. Freedley is also the editor-in-chief of PM&R. And to the technical staff, I'm getting a lot of messages that the livestream is broken, just so you know. Great, thank you very much, and thank you for joining us today. So I have the pleasure of talking about disseminating the work of the PASC Collaborative. So I have a fairly unique perspective in that I'm a member of the PASC Collaborative, so I have been participating in the collaborative. I see patients in our post-COVID clinic at UW for the last two and a half years, and then I also serve as the editor-in-chief of PM&R. So I really have seen things from start to finish in terms of disseminating the knowledge that we've learned. So many of you have heard over the last few days and even longer about these consensus guidance statements that have been published in PM&R. There's now seven that have been published, and there's several more in the works that will be published soon. And these have really been very important consensus guidance statements that have helped to shape the field, that have really been critical in disseminating information to clinicians about how to treat the various symptoms. So these are just a few examples of some of the ones that have been published. There was an initial one that was published that described the methodology used to develop the consensus guidance statements, and then they really started with the most impactful symptoms that were impacting patients and felt to be of highest importance. So fatigue was the first one that was published, but there have been a number of other ones. So I just want to spend a moment talking about how these consensus guidance statements were developed so that you understand what kind of work went into these. And I just want to take a moment to acknowledge just how much work went into these consensus guidance statements, and it really is incredible to see how this collaborative has accomplished as much as it has over the last couple of years. So I can't understate, I can't overstate how much work has gone into these. So these guidance statements really started with discussion at the collaborative level, so bringing a national group of people together who are working in this space, both clinically and on the research side, to discuss the different symptoms and establish which symptoms are most important and some of the concepts that are important. And then they formed work groups that were writing work groups, so smaller groups that could focus on the particular topic. And all along the way, there has been patient input, and I think that's been really critically important to make sure that these are grounded in what's important to patients and getting their perspective. And so once the writing groups were formed and the initial discussions were held in the collaborative, the writing groups then came up with a list of candidate recommendations based on all of that input. And from there, they then sent out surveys to the past collaborative members to try to get consensus about which recommendations were most important, which ones were not felt to be important, or that there was disagreement about what the recommendation should be. And those with more than 80% consensus were retained in the statements. And then those that had some consensus, so 60 to 80% of people agreed that they should be the final recommendations, there was further discussion and refinement and clarification to try to get consensus on those. And that's really how the consensus guidance statements were created. And once we had consensus about the recommendations, the writing group then went back and finalized the statements with the detail needed for publication. And then from there, they were submitted to PM&R and went through our standard double-blind peer review process in PM&R. So most of the consensus guidance statements then went through an additional, at least two revisions based on feedback from the peer reviews before publication. So a very rigorous process. You've seen these tables before, even earlier today. I just wanna point out that the tables with the recommendations are available on the AAPM&R website and through the journal. And these are really good, very brief summaries and I think very helpful for people to get a quick snapshot of what those recommendations are from each of the guidance statements. And then I just wanna point out, this is a table of our top 10 most downloaded articles in the history of PM&R. And you can see that by far and away, the number one most highly downloaded manuscript in PM&R is that guidance statement, that initial guidance statement on fatigue. And so I think this really speaks to the importance of the guidance statements and the reach and how important this has been for the public. So there are other ways that we're disseminating information in addition to the publications in PM&R. They're on the CDC website and there's actually a link to the collaborative. And so this is the first one that you'll see in terms of COVID resources at the CDC, which is really nice to see. And so that's one way that we are also disseminating information. And then the CDC also hosts COCA calls, the Clinician Outreach and Communication Activity calls. And these have also featured a number of our past collaborative members and speaking about the different symptoms and the guidance statements as well. So this has been another way that our collaborative has been disseminating information, which has been really nice to see. And then the other forms for dissemination in addition to publication and through the CDC, there are a number of popular websites that are featuring some of the work that is being done on the past collaborative. This is one from the Bateman Horn Center, which is a very popular website. They highlight a couple of things on this website that I think are important to point out. On the right-hand side, they have direct links to our guidance statements. And so patients are able to access them that way. And then they also highlight the Project ECHO, Project ECHOs that are going on. And so for those of you who aren't familiar with Project ECHO, these are webinars that are case-based learning. People bring in cases of patients that get discussed with a panel of experts. And then there's usually a short educational component, a speaker that talks on a different topic. And it's a way to really educate the community at large. And so there are two that are featured here, one with a partnership with the University of Utah and the Bateman Horn Center, and then another one that is a CDC-funded study, actually, that is being led by the Family Health Centers of San Diego and the University of Washington participates in that, where they're actually comparing whether the outcomes for patients are better in communities that use the Project ECHO as the primary way to treat patients and to disseminate information about long COVID versus a multidisciplinary clinic like ours at the University of Washington, which is actually the control group for this study, because they believe that they can get more outreach and better outcomes with a Project ECHO-style forum than a treatment of individual patients at a multidisciplinary clinic. So it'll be an interesting study to see what the outcomes are. And then there are also, as you have heard, probably over the last few days, lots of press releases and media events that our past collaborative have been participating in that have helped to disseminate the information about the work that has been done. And then finally, I'll have to give kudos, of course, to Dr. Rodusco Gutierrez for her social media involvement and many of the past collaborative have been disseminating information via social media, which is another important way that the information has been disseminated. So I encourage all of you to continue to do that, to get the word out about what the collaborative has been doing. So I'll end there. Thank you. Thank you, Dr. Friedley. With our remaining time, we'll be speaking about future direction and needs of the past collaborative. Dr. Benjamin Abramoff is coming up now. He is assistant professor of PM&R at the University of Pennsylvania, Perlman School of Medicine, founder and director of Penn's post-COVID clinic and he's co-chair of the past collaborative. And also Dr. Stephen Flanagan, professor and chair of rehabilitation medicine and president-elect of AAPM&R. Thanks. Thank you, John. I think Dr. Flanagan is mostly gonna be emotional support, but if any comments at the end, I'm sure he'll be up to coming up and sharing them. So no offense to my neurology colleagues, my co-chairs. So I'm gonna be talking a little bit about next steps, where we go from here. And so no offense to my neurology colleagues or my pulmonology or primary care co-fellows, co-chairs, but I think physiatry is a very good home for care of the patients with long COVID. Long COVID is a complex multi-system disease, similar to brain injury, similar to spinal cord injury. There's a focus that we have on function. How do we get patients back to the activities that they wanna do? Whether that's school, whether that's work, I think that's very important. We focus on symptoms. So we might not always have the pill, like a, excuse me, a pill to treat hypertension or diabetes. We have to treat the symptoms. What is causing the patients to feel poorly? And we look at holistic care. We troubleshoot. We think about how, you know, we may not have one way of doing things. We have to look at the individual patient, their lives, and how do we give a treatment that works for them? We focus on interdisciplinary care. So we work with our therapy colleagues, our other specialists throughout the health system, primary care doctors, to make sure that we're all working together to come up with a good plan for our patients. We focus on disability care. For many, long COVID is a disability, and we have to think about how do we give them workplace or other accommodations? And then finally, we have AAPMNR, which has been extremely supportive for all of our long COVID efforts. From the top down, Dr. Flanagan, Dr. Vennessy, have really made this a priority. And the collaborative has really become a real leader in getting information and resources to doctors to help treat their patients. Dr. Ferdusco-Guerrero has already spoke on this, but research is a key step moving forward. We have to, of course, understand the underlying pathophysiologic mechanisms. Patients want a treatment that targets the underlying cause of their illness. We don't have that yet. Right now, we're still looking to treat the symptoms. But I think there are other research that we have to lead in. What clinical models are effective? Is it long COVID clinics? Is it primary care models? Is it medical homes? These are really important questions, and there's financial implications. There's government funding implications. Rehabilitation. Patients are getting a lot of rehabilitation. We're using it often. Dr. Petrino went into a lot of great detail about them, but we need to know, does it work? We have to do trials like Dr. Petrino is doing to understand and prove it so we get, insurance covers it and we get the support for as long as the patients need it. There's a lot of treatments that are being used. Again, we have to test those treatments. We have to do better at sharing our outcome measures. We say we're helping the patients, but we have to prove it. And we have to work together on trials. I think another step moving forward is education. The group here, this forum is a great way to teach other clinicians about long COVID, but medical students, residents, fellows, they're not getting much exposure to long COVID in most cases. And so we have to think of ways, how do we teach them about it? How do we give them the tools so that moving forward, this very common disorder in long COVID, but also related post-viral syndromes get the care that they need. I think we have to come together more to focus on long COVID, continue reaching out in terms of discussing new articles, new research that comes out in the literature. And as AAPM&R is doing, we have to focus on advocacy, getting funding for novel solutions, grants to develop the creation of more long COVID clinics. And also as it's becoming more and more apparent, sustaining the clinics that already exist. Because there are clinics that are shutting down even now due to not getting the funding that they need and the support that they need. This is a lot of work. There's a lot of work outside of seeing the patients that needs to be appropriately reimbursed. Telehealth is key for a lot of our clinics. And as we see, that's getting pulled back from a funding perspective. Patients often have extreme fatigue. They can't come to clinic visits week after week or month after month. So being able to meet them in their home, see their home environment is really important. Making sure we have equitable access. I think lots of us kind of anecdotally note that we're not seeing those underserved patients from minority groups. And whatever the reason that is, we know that those communities were hit hardest by COVID acutely. And I think we're missing a lot of them in the treatment of long COVID. Patient care, again, continue to disseminate best practices, continue not only developing new guidance statements, but pretty soon we'll have to start going back and revising our initial guidance statements to make sure we update the guidance statements to fit the new literature that comes out. We are developing and continuing to develop clinician toolkits, smart phrases, decision-making algorithms, rehabilitation protocols to make it easy for any physiatrist or clinician out there who's not maybe seeing a ton of long COVID patients to treat their patients. We're developing a model for centers of excellence so we can get our patients to clinics that know how to treat their specific illnesses. So that's just a brief overview of steps moving forward. This really couldn't have happened without Kavitha, Michael, and Sarah from AAPM&R. I was surprised to learn. I was saying, you know, I thought, that I was surprised to see that they have other jobs besides just helping with a long COVID collaborative because it seems like they give it that much attention. And so when they have other things that are running off to it at the meeting, I was like, it's like seeing your teacher outside of school when you think that all they do is be your elementary school teacher. We're always looking for more members of the collaborative. So feel free to reach out to me. That's my email. Kavitha, I know is happy to kind of give you more information and we'd love to have you. And if you have other suggestions, any other ways you think that we can help treat your patients or improve our work, please don't hesitate to reach out to us. So thank you. It's been three really excellent sessions on long COVID. If you haven't seen any, they should all be available after a few days to review. There's all the symptoms of long COVID have been addressed, some of the big picture topics. So hope for you guys to have the chance to look at those. Thank you.

Long COVID

neurological effects

central nervous system

peripheral nervous system

cognitive symptoms

brain fog

memory issues

post-COVID headaches

migraine disorders

treatment options

peripheral sensitization

nerve damage