Health in Charlotte. We have four speakers today and we'll address the spectrum of spasticity care from inpatient to outpatient with our cancer populations. I'll be reviewing spasticity basics so other speakers don't have to and I'll focus on inpatient rehab management thereafter. The following speakers will address special topics with outpatient cancer rehab spasticity management just to round up the talk. Dr. Khanna is the Director of Cancer Rehabilitation at Winship Cancer Institute of Emory University and he'll be discussing outpatient head and neck cancer spasticity management. Dr. Gupta is an Assistant Professor at UT MD Anderson Cancer Center in Houston, Texas. She'll be discussing outpatient breast cancer spasticity management as well as insights into virtual spasticity management. And Dr. Kindig is a Physical Therapist and the Director of Quality for the Revital Cancer Rehabilitation Program at Select Medical. She'll highlight key principles and share examples of therapy management of spasticity in outpatient cancer rehab. So let's get started. I don't have any disclosers and we'll go through this outline. Three topics I'll review are spasticity basics, inpatient cancer rehab hurdles, and a case example. So spasticity can be painful, limit range of motion with ADLs by self or caregiver and can manifest as muscle stiffness, spasm, pain, resistance to stretch, repositioning. We've all heard the definition velocity dependent resistance to stretch. And this description is just part of an upper motor neuron syndrome that results in abnormal stretch reflexes primarily due to mismatch of primary afferent inputs. Traditionally, the signal mismatch can be seen after a stroke, traumatic brain injury, spinal cord injury resulting spasticity, but it can also occur with our cancer patients after a non-traumatic brain injury, a non-traumatic spinal cord injury from tumor burden or after chemo or radiation, which can result in nerve damage, radiation necrosis, radiation fibrosis syndromes, which can damage similar neuronal pathways. The differences is the general mechanism of injury and the timing that we see spasticity kick in. For strokes that results in spasticity, they're typically due to cortical strokes, damaging the SMA or supplemental motor area, the brainstem or pyramidal tracts. This results in dissociation of motor responses from sensory input. So the brain heals and reorganizes, and this is theorized to cause the hyperexcitability and spasticity. Spasticity onset is usually gradual, but more likely to be there if you have initial onset of severe paresis. Traumatic brain injuries, spasticity results usually due to pyramidal upper motor neuron disruption and diffuse axonal injury, like to the brainstem if it's severe. And the onset is really variable, but usually within the first few weeks and sometimes before they're admitted to invasion rehab. Spinal cord injuries that result in spasticity are due to uninhibited motor neurons below the level of injury, resulting in increased glutamate signaling. The spasticity onset, if traumatic, occurs after a period of spinal shock, which can last days or several weeks. So the time and onset of spasticity is important to discuss here because our cancer population can often present with strokes, such as if they have hypercoagulability from new or progressive cancers, or sometimes from non-traumatic brain injuries like tumor burden, brain surgery, radiation necrosis. The non-traumatic spinal cord injuries, such as the tumor burden, spinal surgery or radiation fibrosis, all of which can develop spasticity. But in the cancer population with brain tumor or spinal cord tumor that's treated, spasticity tends to develop later than typical for the traumatic brain injuries or the traumatic spinal cord injury patients. And this is theorized because of a cumulative effect of cancer treatments, late effects of surgeries, tumor recurrence, or radiation necrosis, for instance. And later in my talk, I'll give a case example to better illustrate this. So let's talk more about inpatient rehab. When you have a patient in inpatient rehab spasticity, at some point, you'll consider trialing oral medicines such as muscle relaxants. One variable to consider, however, is cancer-related fatigue and the sedation effect that these medications can provide, and which can be a significant barrier to therapy and participation and quality of life. Because these meds are sedating, we might initially trial at lower dose or less frequent and communicate closely with the therapists and nurses to better titrate them slowly before we get to more aggressive dosing. Sometimes we can't hit therapeutic optimization with these oral meds due to side effects, and that's often why we trial botulinum toxin later in care. So botulinum toxin during inpatient rehab is less frequently performed, and there are several reasons for that. If you have newly diagnosed spasticity, it's important that you first trial oral meds and fail so that you can support insurance approval for the expensive drug later. Furthermore, the average inpatient rehab length of stay is around 14 days. You're unlikely to observe the benefit from the first dose during that admission. With respect to outpatient management, there are studies demonstrating safety of botulinum toxin during chemotherapy, and therefore it should be considered. If a patient does transition to hospice, at that time you'd need to clarify reimbursement since some hospice groups may not reimburse that procedure. Another inpatient rehab spasticity insight I'd like to discuss is the use of TENS and NMES with cancer. And there is documented benefits to spasticity and pain, so let's discuss some theoretical risks and benefits. In 2010, a team of Canadian physiotherapists wrote evidence-based guidelines and precautions for using electricity with therapies. With respect to cancer, they had three main points. No e-STEM directly over malignancy, but yes if TENS is used for palliative pain goals, and yes if NMES is for quality of life in advanced disease. The controversy around using electricity comes from mostly animal models and expert opinion, but there's also some supporting evidence with safety too. Electricity either theoretically stimulates DNA synthesis, making tumors grow, or inhibits mitotic spindles formation, stopping or slowing tumor growth. An example of how electricity is used to treat cancer is with GBM, an aggressive brain tumor. The frequency and dose of electricity is different. For instance, a TENS unit is about 200 Hertz, and the frequency used to treat GBMs is about 250 kilohertz. And this has been FDA approved for treatment in recurrent and progressive GBM. If we look to our cancer rehab textbook, in the chapter authored by Dr. Vargo, it states that e-STEM and NMES should be used at discretion of the provider. The key takeaway here is assessing benefit from theoretical harm. For instance, in a hospice or palliative case without future chemo plans, e-STEM or NMES may benefit pain and spasticity and can have a greater benefit at end of life despite the theoretical risk. It's important to point out that not everyone will tolerate NMES. There's a 2013 case series following 18 patients with advanced lung cancer receiving palliative chemotherapy who had limited exercise tolerance, and they were enrolled in the study. They were treated with NMES to the quadriceps and FES biking for about 30 minutes per session, about three days per week. And ultimately only about 50% tolerated the intensity and duration of NMES. But this was in a population who already were unable to tolerate traditional exercise due to fatigue. And so cautiously I interpret these results as being positive. I'd like to wrap up this presentation by presenting my case example. And so here's a patient, a 30 year old male without significant medical history. He developed headaches, malarate-sided weakness, and he came to the emergency room where a head CT revealed a left temporal mass and was diagnosed with the anaplastic astrocytoma. He got debulking surgery and craniotomy. His strength improved and he went home and he completed some outpatient radiation. By three months, he was evaluated by a neurologist and he noted full strength, but he was starting to develop some hyper-reflexivity, no spasticity at this point. By six months, his weakness returned and they rescanned him and he was found to have a recurrence. So he was admitted. He had a renewed craniotomy and debulking tumor and he came to inpatient rehab at that point. So at the six month point, after radiation and two brain surgeries, that's when he started developing spasticity. We trialed him with Baclofen, low dose to start with, and he got a rest in hand splint and an AFO. We trialed some FES biking and he tolerated it really well. The pain got better. His spasticity was well managed at that point. So we discharged him home at about eight months from his initial diagnosis and his spasticity, unfortunately, started to progress even further. Part of this was explained by some noncompliance with stretching and splinting, like a nocturnal wrist splint that the wife was telling us required a lot of encouragement for him to wear. But anyway, we coordinated with his outpatient therapist, titrated up his Baclofen to the point that we were having significant sedation and understandably, we wanted him to be more awake during the day as this was limiting ADLs and quality of life for the wife and the patient. So he was agreeable to botulinum toxin and we were able to get him off the Baclofen. I've seen him every three or four months with some toxin injections. So I didn't want to go too much into the botulinum toxin treatment. I want to leave that to our next speaker to go more in depth with spasticity management. So allow me to pass it off now. Here are my resources and thank you for your time. Hello everyone. My name is Ashish Khanna and I am going to continue our talk here. First of all, I will say that I have no disclosures, but I am open to some if anybody has any. All right. So I'm going to talk a little bit about spasticity in head and neck cancer. Most spasticity that we see in head and neck cancer is secondary to radiation. So I'll just open with a little bit of a brief introduction to that. When patients have been radiated, at that point, they have issues, multiple issues, and this is termed radiation fibrosis syndrome. So basically, radiation can result in an insidious, pathologic, fibrotic tissue sclerosis. It's important to remember that radiation fibrosis syndrome takes months to years to decades to develop. So it's not something that you see in the acute radiation period, when someone says, they're in radiation at the moment and they said, the fibrosis is killing me or something like that. So that's not the case. Radiation fibrosis is really, it's an unpredictable, it's progressive, and it's non-reversible. So really, I call that the trifecta of badness. We don't know how the radiation is going to affect them. It will affect them in unpredictable ways. It is progressive. So patients can potentially progressively get worse as the radiation continues over months to years and decades to continue to sclerose. And anything in the radiation path can become fibrotic and sclerose and scar over time. Ultimately, this is non-reversible as well. And like I said, all the structures in the radiation field can be affected. And this is termed a myeloradiculoplexoneuromyopathy. So this is an all-inclusive term, myelo starting with the spinal cord. From there, we go to the nerve roots, radiculo, then the plexus, plexoneuro, and then ultimately ending in the muscles with myopathy. So I'll talk a little bit about the spasticity, speaking of myopathy. Why do we see muscle rigidity and spasticity? The reason that we see that, that this results in tightness and painful spasms, with a couple of etiologies. The first one really is that it's a certain type of myopathy called a mnemeline rod myopathy. You can see that in the picture here, in the path slide there, in the bright red, you'll see those little rods there. This results in a relative weakness as well as easy fatigability of the muscles. Probably one of the bigger etiologies though, was it's going to be this ectopic firing of the innervating motor nerve. And that results in sort of this volley of neural activity that fires across the neuromuscular junction. And as a result, we have these painful contractions, sometimes superimposed on like a tonic muscle spasticity. So here we're talking about spasms and cramps. Sometimes, like I said, on the background of muscle tightness. And this is actually called a neuromyotonia. So tonic contraction of muscles, of course, requires a high oxygen demand. When a muscle is contracted, you're going to have poor blood flow through that muscle. That combination results in a lot of local acidity as well. And then ultimately, we're going to have hypoxia of the muscle, the acidity cause a low pH. And then that causes sensitization of the pain fibers there. So that's the, you know, our kind of theoretical framework of how that happens. Once you have sensitization of pain fibers, you're going to have more pain. And this kind of creates this cycle. So the question is, how do we break that cycle, right? And I'm going to address that here at the end. One of the most common pathologies that we see with radiation fibrosis is patients with trismus. Trismus is the inability to fully open the mouth or if you want to be fancy about it, we're talking about a decreased aperture of the jaw. Normal mouth opening is 23 to 71 millimeters, sorry. And that's measured between the incisor teeth, top to bottom. For the diagnosis of trismus, we use a cutoff of 35 millimeters. That has a sensitivity of 0.71 and a specificity of 0.98. So we do have measuring devices that you can carry in your white coat that I use all the time to measure the aperture of the jaw. The less scientific way to do it is to just use your three fingers. That's called the three finger test. Basically, you just take your three fingers and you see if you can fit three fingers into your mouth. That's roughly 35 millimeters. So I'll pause while everybody does that. Go ahead. I can fit four in my mouth. That makes me have a big mouth, I guess. All right. Next, we'll talk about the incidence of trismus. That's about 9% immediately post-treatment, and then it can be as high as 28% in head and neck cancer patients one year post-treatment. Trismus will develop in about 45% of patients who receive curative doses of radiation therapy. That's in certain cancer types, of course. It evolves most rapidly one to nine months after completion of radiation therapy. And let's talk a little bit about what we can do about it. Essentially, because we're talking about scar tissue here, in combination with muscle spasticity, the best way to fix trismus is to actually physically stretch the tissues. We do that in therapy and with certain of these jaw opening devices. Our colleagues in speech therapy are particularly adept at treating this issue. Physical therapists have wonderful tools and magic hands, as always. They use manual techniques, and also treatment of lymphedema can go hand-in-hand with trismus and other head and neck cancer issues post-radiation, so they do a wonderful job with that. Medications, we have topical or oral pain medications for pain and spasms. Those medications are the ones that we're all familiar with, baclofen and tizanidine and all those kinds of things. There are also splinting devices. And then lastly, of course, is the botulinum toxin injections. And I'll take a moment just to talk a little bit about that. So for trismus particularly, what we're gonna target are the muscles of mastication, right, the muscles that close the jaw. There are two large muscles, two on each side, I was gonna say four. There's the temporalis and then the masseter. We also have the lateral and medial pterygoids as well. These are actually on the inside edge of the masseter, which can be a difficult muscle to reach. Typically, with the ultrasound, you need to go from the bottom and kind of go this direction to reach those. Those are smaller muscles. I don't typically botox those for trismus unless we have an unusual case. And then typically, I would start with 25 to 30. Units of botulinum toxin A to the temporalis and then maybe a little bit more, 40 or 50 perhaps to the masseter. Of course, that depends on how severe their trismus is. And to what extent that I think that their trismus is due to scar tissue, which of course, botox would not help. We can only use our sort of stretching devices and therapy colleagues for that. Or if we feel like it has a large muscular component, then we will be more aggressive with the botox for that. So the combination of the two generally will be effective because most patients are gonna have a combination of both muscle rigidity, spasticity, as well as scar tissue that's preventing them from opening their jaw all the way. So the treatments are similar for cervical dystonia as well. Cervical dystonia, oftentimes we have neck postural changes. So I have a picture here. You can see with this patient here, she's got a significant, you can see her SCM here from sort of across the room. It does result in pain. It can result in spasms. As you can, the spasms, of course, like I said, are baseline spasms on top of this underlying tonic spasticity or tonic contraction of the muscles. It can result in difficulty with swallowing, difficulty with speaking, definitely can affect activities of daily living. You can imagine this patient here is gonna have a hard time turning her head when she's driving to look out the side view mirrors, for example, and a lot of patients is gonna impact a lot of their work-related tasks as well because they have a decreased range of motion of the neck. Here's the general sort of Botox guide. Most of the time I find the sternocleidomastoid, this is just my experience, sternocleidomastoid is generally the most commonly affected. It does sort of traverse the field where neck dissections are typically done. It's sort of, you know, it's a large muscle and it's sort of right in the way of both radiation and surgeries. So the sternum, it is normally, is spared during surgery, but can become, you know, have that myotonia there. Next most common, in my experience, would be the levator scapulae as well. Sorry, I'm sorry, next most common would be the scalene. Sorry, I rarely do the levator scapulae and the other muscles that you see here. Sometimes the trapezius as well, although the trapezius with radiation becomes weak and the patients can develop a head drop. So we don't wanna typically do too much Botox to the trapezius unless we have a really good reason to do that because that would further weaken the trapezius and therefore further weaken their head drop. Here's another example. I mean, I personally do these injections with ultrasound, which I would encourage if you're an ultrasound person. So next I'll talk about first bite syndrome. This is a relatively rare condition, but it is common in the head and neck cancer population. And it's important for, I feel like for everyone to know because it's a common, commonly, it's a misdiagnosis, an underdiagnosed issue. First bite syndrome, it's a good name for this because basically what happens in this condition is that you get a sharp sort of lancinating pain right in the parotid region. And it generally occurs with the first bite of food. Then it can improve with subsequent bites of food, but literally it's first bite, the first bite of food in severe cases, even if people see a Domino's commercial on TV or something that would make them sort of salivate, that can also create that kind of pain. But typically it's with the first bite of food, particularly acidic foods and things like that, that would cause increased salivation. And this is basically due to the loss of the sympathetic nerve innervation to the parotid gland as a result of surgery or radiation. So here we have a little bit of a diagram. You can see the parotid gland here, the otic ganglion, or I'll start down here. These are the post-ganglionic sympathetic fibers coming up to the parotid gland. And then we have the otic ganglion here, or otic ganglion, which are the parasympathetic fibers. So basically what happens is that we have a loss of the sympathetic nerve innervation. And ultimately that results in a supra-maximal contraction of those myoepithelial cells that are surrounding and within the parotid gland. So we have a supra-maximal painful contraction of the parotid gland with the first bite of food. Here's a diagram. I'll just go through this really quickly. As a person is masticating or eating, generally we have the both parasympathetic as well as the sympathetic nerve innervation. If we lose the sympathetic innervation, then we're gonna have the myoepithelial cells of the parotid gland have a supra-maximal contraction. Whereas if we have the sympathetic nerve innervation, it would generally reduce the contraction of the myoepithelial cells. And because this is a myoepithelial problem, this does work well with Botox as well. So Botox to the parotid, I generally do it in two, maybe three different spots and a total of maybe 40 units, depending. Of course, the side effect of this is going to be dry mouth, as you might imagine. But for many patients, dry mouth is a small price to pay, or you can titrate the amount of Botox to try to decrease the intensity of the first bite syndrome while trying to prevent the xerostomia as much as you can. Another useful thing for doing the Botox for the parotid gland is for the treatment of salaria or where patients have excess saliva. Of course, in head and neck cancer, xerostomia or dry mouth is far more common. The salivary glands generally can become damaged, I believe it's something around 50 gray, which almost every head and neck cancer patient is going to get. So dry mouth is much, much, much more common. The salaria or excess saliva, or what we call anterior spillage, you can see this gentleman here is carrying a napkin in front of his mouth. These days, a lot of patients have them tucked into their mask, they're just constantly absorbing the anterior spillage of saliva, also known as drool. The reason that we have that sort of persistent drooling is not because we have an excess production of saliva, but rather it's a treatment-related dysphagia. So ultimately, they have impaired handling of their secretions. So essentially, they have a dysphagia with a normal amount of saliva, perhaps even lower, who knows. Either way, they're not able to handle that, and so the saliva pools in their mouth. Most commonly, we see this from altered anatomy from oncologic resections, particularly the upper aerodigestive tract or the middle third of the mandible. Many of the patients who have numbness, of course, if you can't feel the saliva in your mouth, you're not going to be able to move that around and do that as well. So it's not only from dysphagia. Also if you have a pretty profound numbness of the mouth, this can occur too. It also results in abnormal salivary flow as well. Radiation can result in abnormal salivary flow. We see it in sialoceles or fistulas and things like that. So what do we do for this? Both of them are going to be, as I mentioned, Botox to the parotid gland, 25 to 50 in two to three spots, like I said, and then one thing we worry about is the dry mouth. If you do an ultrasound with ultrasound guidance, you can do it like this. I tend to do it more in-plane than out-of-plane, but here's an appearance. Here's what the parotid gland looks like on ultrasound, sort of a homogenous type of structure. And then you can see this is the mandible right here. So right to anterior ear and then along the mandible sort of below the ear is probably the best place to go. If you're going to do it blind or palpation guided, then there is something we call the security zone. Basically, you take the corner of the patient's mouth, you draw it to the posterior edge or basically the ear lobe here, and then right below that in the central one-third of the area is where we want to do that. The facial nerve travels through this area, and that's why we call this the security zone. And with that, I will pass it to Dr. Gupta. Hi, everyone. So I'm going to talk a little bit about botulinum toxin in breast cancer patients. Dr. Khanna did a great job in going through etiologies, and so some of that is pretty similar to what we see in breast cancer, obviously different location. So I also have no disclosures, unfortunately. Like Dr. Khanna, I'm also looking for some. But I will start out kind of talking a little bit about what we do know with Botox use in post-mastectomy reconstruction. So in general, when we talk about implants for post-mastectomy, we usually are seeing either sub-pectoral or pre-pectoral implants. This figure shows the difference between the two, especially with reconstruction. So in the top section of the figure, the tissue expander is placed under the pectoral muscle with supportive tissue matrix then attached to the pectoralis major muscle. The final implant will then eventually replace the tissue expander as seen in Part C of the figure. In a pre-pectoral implant, the tissue expander is placed on top of the pectoralis muscle as visualized here. And then the supportive tissue matrix attaches to muscle on top of the expander. And then once again, the final implant replaces the tissue expander. Now not everybody gets a tissue expander. And then patients are also undergoing reconstructions with the muscle-sparing deep inferior epigastric artery perforator or deep flaps. So more and more plastic surgeons are moving towards either pre-pectoral implants or these deep flaps. And that's partially because some of the literature that we've read and seen. So those that undergo post-mastectomy radiation have a three times higher rate of capsular contracture when they have a sub-pectoral implant compared to a pre-pectoral implant. We know that patients that use these tissue expanders, especially in sub-pectoral implants, also have a higher association of muscle spasms, pain, and lateral displacement. This can result in range of motion changes too with shoulder and arm movement. As I mentioned, the deep flaps, we're starting to see more and more of these, but there is no literature yet regarding deep flaps in the use of Botox. So for those who do receive tissue expanders, what does the literature show? There was a study by Gabriel et al. that showed in 30 patients who received 40 units to the pectoralis major muscle. These patients then had an improvement in pain, less narcotic use, and expedited expansions. This was a smaller study, as I mentioned, as was the next study. So Lowe et al. also did a study with 23 patients, but in this study, the patients underwent bilateral mastectomies with 100 units of Botox injected into the pectoralis major on one side versus a placebo on the other side with the tissue expanders. In this study, there were no changes in pain. And then the last study that I would like to briefly mention is the Lemine et al. study. In this study, they looked at 131 patients that were randomized into receiving either 100 units of botulinum toxin to the pectoralis major versus none while undergoing tissue expansion processes with subpectoral implants. So these patients showed that there was no improvement with pain or patient-reported physical well-being when compared to the placebo. However, this study ran over five years, during which the use of supportive tissue matrix changed, and that also changed the impact in terms of the tissue expanders and how patients felt. So this study acknowledges that this is a pretty significant limitation, as well as the changes from paravertebral blocks to interoperative field blocks that occurred during this time period. So that's just a brief kind of overview of what the literature with Botox in tissue expanders is. But I'd like to move on to use of Botox in the post-mastectomy pain syndrome. So this figure kind of shows some of or highlights some of the major muscles that we see that are affected. We're primarily talking about the pectoralis major muscle, but in our patients, we often see other changes as well. So what do we know? Besides tissue expanders and implants, we know that surgery and radiation can cause scar tissue formation, fibrosis, and shortening of soft tissues. Dr. Kenda just reviewed this in our head and neck patients as well. But these can lead to increase in muscle tone and pain, especially in these muscles. As the pectoralis muscles often shorten, they can narrow the semicromial space and also lead to rotator cuff pathology. We can see tightness in the latissimus and trapezius with the latissimus shown here. As standard of care include physical therapy, and Dr. Kenda will be talking about this in the next section, but these can include passive mobilizations, myofascial therapy, stretching, and exercises to try to strengthen muscles. There are other options such as acupuncture, oral medication, and last but not least, Botox. Since our talk in this section is mostly focused on Botox, I wanted to review the main study that uses Botox as a randomized controlled study to compare Botox and physical therapy to a placebo, which was saline and physical therapy for breast cancer patients. These patients actually completed radiation at least three months prior to their enrollment. In general, they were two years out of surgery. I highlight the two years because that's often different or further out than many of us see our patients, but that's not saying that I don't see patients that are five years out from their mastectomy and still suffering from post-mastectomy syndrome and fibrosis of muscles as well as spasms. So in the patients in this study, there were complaints of pain at least three months after surgery, and these patients were followed for six months once enrolled in this trial. The primary outcome measure of the study, and the study was actually published as two separate publications, with one focusing on the primary outcome measure, which was a change in pain, and the second focused on different factors such as evaluating strength, range of motion, and quality of life. So the first publication that reviews these patients showed that there was no significant change in pain at three months. However, the Botox to pectoral muscles with physical therapy did decrease pain intensity at up to six months. However, they reported that this effect size was not clinically relevant. So therefore, the study did say that there is a possible benefit to Botox, but more research is needed. In the same study, they also mentioned that quality of life did not show any significant improvement, and this is further reviewed in the second part of the study. So the second part of the study looked at shoulder range of motion with improvement in both groups for forward flexion, but no significant difference between the two. Interestingly, they did not assess adduction, which is the primary function of the pectoralis muscles. They did look at abduction, which an asbestic pectoralis muscle we would hope would improve with Botox normally. Unfortunately, this did not show any significant change between the groups, nor did they notice any significant change in biomechanics as measured by the chromium table index, pectoralis minor index, and scapular upward rotation. Both groups did show improved shoulder function with the DASH questionnaire, but no significant change occurred between these groups. Upper limb strength was measured by hand grip strength, and this did not change significantly. The other caveats to this study or limitations were that they had no way to follow up on the home exercise program to ensure adherence. So these patients initially had their first three months monitored by physical therapists with exercises that may include a variety of modalities, and then the second three months were supposed to be a home exercise program where the patients did their exercises twice daily. So there was no way to monitor the adherence, and so it's difficult to know if Botox patients consistently did their exercises and whether this may have contributed to some of the differences between the two patients, or I'm sorry, some of the lack of differences between the two patients. So in terms of applications for Botox for my patients, I usually mention to them the results of this study, and I think what's tricky is that I normally do not look at hand grip strength as my primary measurement of strength in my patients, and I also look at the variables of pain and range of motion specifically with adduction and abduction. Scapular mechanics can be variable and do not always correlate to upper limb dysfunction as well. In addition, as many of you have probably experienced, each of our patients is unique, so we have to look at all causes of spasticity in patients as well. In my experience, I have done Botox for patients with a poor response, and I have found in these patients there may be other etiologies contributing. So I always say that it's important to examine your patient thoroughly and consider imaging such as cervical spine imaging when they do not respond to spasticity management. So the second part of my talk is actually how to do spasticity management virtually. As many of us went to virtual visits, we had to figure out strategies to best assess patients objectively and also correlate this with subjective complaints over video. This was definitely a change in our standard of care from pre-COVID to post-COVID, or during COVID as we are right now. So I would often ask patients to point to areas of pain and tightness and request that they show me their incisions and palpate to see if any spots were particularly tender. I would also ask them to perform their cervical spine range of motion in addition to arm range of motion. Then I would compare the affected side to the unaffected side for those with unilateral mastectomy. I found this to be very helpful. I also ask patients if they felt that any topical interventions, massage, and or physical therapy that they had done prior to our visit had helped with their pain or relaxation of muscles. I think it's important to continue to educate our patients on the importance of these interventions and modalities, especially when our in-person visits were quite limited. So what was the process for injections for our patients at MD Anderson? So I think that when COVID-19 really spiked in Texas, we actually initially canceled all injections due to our clinics being transitioned to being entirely virtual. So at this point, the home-based physical therapy exercise program became even more important. For those that telemedicine was allowed for, which as many of you know, changed over time, initially we started out doing telemedicine to Texas patients, then we expanded to doing it to all patients, whether or not we could bill just to make sure that patient care was managed appropriately and our patients were not suffering unnecessarily. Later on, certain states started approving virtual visits, and therefore this was followed closely by our staff. So for those that we could do these telemedicine visits for, we would actually try to evaluate our patients over video, order the Botox with insurance approval, and then encourage those patients to continue with their either home-based or in-person physical therapy and exercise programs locally. So once we resumed injections, which was about two to three months into COVID, we would then do a second visit for injections. Our institution did not require a COVID test, but we would have the screening questionnaire for patients. For patients that were coming in from out of town, sometimes this process was actually a little bit different. So for those patients, we would often do a simultaneous approval for Botox from insurance. Generally, I would tentatively request about 100 units, and then I would do an in-person evaluation as well as a possible injection. I think this was a change that both our patients and providers really appreciated in order to maximize their visits, as they usually were flying in three days prior to their visits, getting COVID tested, getting cleared, and then coming in in-person to MD Anderson. So in addition to this time phase, the three-day visitation limitation, patients at that time were also mostly pleased with our COVID precautions. We had our providers bring gowns, gloves, masks, and face shields. In addition, we were limiting the number of people in the procedure room to limit exposure. Now as we have become more familiar with COVID, I would say that some of this has changed. We no longer require the three-day limitation. Out-of-town patients are able to fly in. Once again, they are asked a screening questionnaire, as is any local patient. What are our pearls for a future pandemic? Well, I think that the main takeaway would be that telemedicine can provide adequate information, and especially while we may have modified the way we assess patients initially, we really learned from this pandemic how to not affect patient care, meaning we really learned that we can see our patients, provide comfort, provide education, teach them how to do different physical therapy, home-based exercise programs, and still educate them on the effects of botulinum toxin and how this may benefit them. I think that we have plans in the cases of a future pandemic in order to be able to provide them with the injections, and in addition, despite what the literature says, every single one of our patients is unique, and so we have to acknowledge that Botox is an intervention that may provide relief as long as the patient understands risks and benefits. And I think my next slide are my references, and then we'll move on to the next presenter. Thank you, Dr. Gupta. My name is Tiffany Kendig, and I'd like to wrap up our talk today by discussing therapy management in the setting of cancer-related, or asbestos in the setting of cancer rehab, specifically, I'll cover some best practices and provide two brief case examples. I have no formal disclosures. I am an employee and do draw a salary from Select Medical, however. So, in the absence of clinical practice guidelines specific to cancer-related spasticity, we can draw on related clinical practice guidelines and integrate principles of spasticity management and cancer rehab to best manage our patients. So, over the course of the next few minutes, I'll briefly review our understanding of spasticity from the previous presenters, management, and clinical practice guidelines, and then we'll layer on the principles of cancer rehab to appreciate the nuanced needs, highly clinical presentations, and complexity of this patient population. So, with respect to spasticity, as the previous presenters have pointed out, we understand and appreciate that spasticity is dynamic. It can change over time, and as Dr. Mitchell pointed out in the beginning of the talk, it often occurs later after a cancer diagnosis or, as Dr. Khanna talked about, as a result of some treatment and can be more of a late and lasting effect. Spasticity, in general, can have cascading effects, and this is of interest to us as therapists because we understand that spasticity results in motor impairment, which can inherently contribute to pain and contracture and ultimately task interference and activity limitations that limit one's ability to fully participate in the important life roles that are meaningful to them and can have a negative impact on quality of life. So, in order to help an individual who is experiencing spasticity and potential functional consequences of it, we need to understand the clinical practice guidelines and best practices that are out there. So, here are a few of them. Here, we see a comprehensive patient-centered approach to adult spastic paresis. This is a consensus-based framework where the authors outlined common symptoms or impairments and consequent activities and functional limitations that can result in the setting of spastic paresis, as well as goal areas for rehabilitation management. So, common symptoms or impairments in the setting of spasticity would include pain and discomfort, which we would work to address the spasticity-related symptoms with goals specifically related to pain and decreasing discomfort due to stiffness. Involuntary movements that can occur in the setting of spasticity, we would work in therapy to decrease unwanted involuntary movements during the use of other limbs, including associated reactions or spasms or dystonic movements. And finally, contracture prevention in the setting of sustained muscle shortening, adaptive muscle shortening. We would be working to improve range of movement with the prevention of contractures and deformity and splint tolerance. From the activity and participation side, in order to reduce functional limitations, we can categorize these into active and passive functions. Passive function would include caring for the effective limb, and goals would include optimizing ease of caring for the limb, ability to perform independent hygiene of the effective limb, optimize skin integrity, and then be able to perform dressing and positioning, application of splints or other modalities as needed. With respect to active function, we're talking about the ability to effectively use the affected limb. Examples, if the upper extremity was affected, would be the ability to reach, grasp, or manipulate objects, or working to optimize dexterity and one's ability to lift or carry objects. Functional use would be incorporation of those tasks into activities of daily living, optimize one's ability to perform personal activities such as eating or drinking, self-care, dressing, bathing, grooming, and occupational tasks such as those related to one's work or recreation. And lastly, mobility. Goals related to optimizing mobility with respect to ease of transfers, optimizing balance and standing and walking in order to access one's environment. There were several clinical keys that were really highlighted in this framework for the management of spastic paraparesis, and these included a patient-centered approach with intervention centered on the patient's priorities and agreed upon with the rehabilitation team, including goal setting, negotiation, and formal recording of agreed-upon SMART goals based on those priorities, and discussion about what's really realistic for for the individual to achieve, and use of a goal attainment of goal attainment scaling to measure progress towards those goals throughout the episode of care. Consideration given to the patient and family capacity to effectively help self-manage in the setting of a chronic condition that's going to require ongoing self-management strategies and self-rehabilitation and ways to optimize the ability of the patient or the caregiver to do so, and considering the impact of any neuropsychological, cognitive, or potential behavioral deficits that may coexist, especially in the setting of spasticity due to CNS dysfunction. Interventions recognized in the framework were those specified for postural management and exercise and retraining. Those focusing on postural management that are often integrated into therapy include splinting or orthoses, supports or slings to optimize positioning and reduce injury risk, serial casting, which could be to have a prolonged stretch and optimize range of movement, and positioning to optimize mechanics. Exercise and retraining approaches would include passive stretch manually applied by the therapist, electrical stimulation as Dr. Mitchell talked about earlier, strength training especially for agonist muscle groups if there's pharmacologic management involved that would allow for the quote-unquote unmasking of strength potential in agonist muscle groups, cardiovascular and aerobic training because decreased mobility may lead to deconditioning, task practice, so carry over into functional tasks with repeated practice is a recurring theme throughout the guidelines as you'll see, and balance training to optimize mobility and safety as well. A separate publication reviewed optimal management for spasticity in individuals with spinal cord damage and presented a clinical care pathway for the assessment and treatment decision making from the Ability Network. Several key points in this pathway were assessment that needed to focus on the nature, severity, and impact of spasticity to best determine the treatment plan. Identification of collaborative goals with the patient, very similar to what we heard in the last practice guideline, and selection of appropriate outcome measures. These authors emphasize the importance of PROs, patient-reported outcomes, so that we can use those in conjunction with some of our objective exam-based measures and really understand the impact that this is having on some more of the activity and participation aspects of the patient's life and health-related quality of life. They suggest use of a health-related quality of life measure, such as the SF-36, in addition to condition-specific or spasticity-specific measures to really gauge how a patient is doing in progression through therapy. Management key components included identification and treatment of any secondary contributors, pharmacologic management, as was discussed previously, and physical modalities, such as prolonged stretching, positioning, range of motion, bracing and splinting, or serial casting. We see a lot of overlap here. Again, a patient-centered approach is key because the patient plays an important role in ongoing self-management over time. Coordinated interdisciplinary care, especially if pharmacologic interventions are used, ideally that should be followed by therapy to optimize functional carryover and optimize gains from the use of those agents. The patient involved in goal setting to optimize therapeutic alliance, efficacy, and meaningful outcomes. Assessment and outcome measures with good clinical utility and feasibility. Finally, an individualized approach due to the different impacts of spasticity and how that can manifest on an individual's function. Lastly, I wanted to review a synthesis and appraisal of clinical practice guidelines, consensus statements, and Cochrane reviews for the management of focal spasticity in adults and children. These authors presented many clinical keys that were echoed in the previous guidelines, although looking at focal spasticity here. They pointed out that management needs to be multidisciplinary, patient-centered, and goal-directed, with routine measurement of impairment and activity, so taking measures of domains across the ICF model from impairment level, using measures such as the modified Ashworth scale, to the activity and participation level. Measures on the participation level would include something like the COPM. Pharmacologic management should be part of an integrated approach, again, emphasizing that therapy should be utilized to maximize function and optimize benefits after injections. Outlined interventions by these authors were education, including treatment options and the risks and benefits of those options, as Dr. Gupta previously discussed. Task practice, again, the intensive task-specific training, and this really does need to be quite intense and over a prolonged amount of time, which is why there's an emphasis on integration of family or caregiver assistance as appropriate, and because while there's a gap in the evidence or inconsistencies in terms of the frequency and duration of task-specific practice, we do know that large blocks over time do tend to yield the most benefit, and these can be done with or without an orthoses. Strengthening, again, to optimize the potential of motor function and general strengthening in the affected muscles as well as non-affected muscles, casting, splinting, and orthoses, stretching, and electrical stimulation, especially post-injection. So, understanding the clinical practice guidelines gives us a really good sense of where we can start and elements of patient management that we need to consider in our therapy plan, and when we're looking at spasticity in the setting of cancer rehabilitation, overlaying the principles of cancer rehab can be very helpful. So, reminding ourselves that just like spasticity is dynamic, we are working with individuals affected by cancer that are also in a dynamic situation. We know that cancer and its treatments can contribute to multi-system impairments that accumulate over time, manifesting in potential functional limitations or disability that can range from mild to severe, and even the same, you know, two individuals with the same type of cancer, the same type of treatment, can have completely different functional limitations or functional consequences as a result. So, it's important to remember that we're looking at spasticity and that spasticity is dynamic, and we need to consider all of the cancer treatment that is also associated in the clinical picture and can contribute to comorbid impairments, and that those cancer-related effects can last, you know, not only during treatment, but we can have late and lasting effects that can come on after the discontinuation of treatment or start during treatment and persist. Principles of cancer rehab that are important and parallel those for spasticity management is that really is the job of the entire team. We talked about the goal of rehab with spasticity management to optimize function, minimize negative consequences such as pain and contracture. With cancer rehab, the big picture is really working as a team to improve overall function, improve participation and work in meaningful life activities, reducing the risk of late effects, and improving overall quality of life. And there are some special considerations with respect to spasticity management and application of the clinical practice guidelines and best practices we discussed specific to the cancer population. Some examples of those would be use of modalities. So, as was discussed before, that, you know, the use of modality and modalities such as electrical stimulation, electrical stimulation, there has been, there is thought that that could contribute to spreading of cancer. So, there needs to be conversation with the medical team and with the patient to clearly assess the risk versus benefit of any modality that will be used in the population and agreement on that before it's tried. Bony integrity, so if there are bony metastases or decreased bony integrity due to previous treatments, osteopenia or osteoporosis, we need to consider this when we're considering manual interventions as well as bracing to consider the load that will be pacing on bones and consider avoiding the use of bracing or high loads over compromised bone. In the setting of radiation fibrosis or radiation changes or chemo-induced neuropathy, impaired sensation can be a potential issue that we need to consider when thinking about bracing and modalities. Thrombocytopenia for those who are undergoing active treatment, of course, would be something that we need to consider with manual therapies as well as the use of any bracing or dynamic bracing agents, for example. Again, we need to consider the fact that very often our patients are presenting with complex histories and multi-system impairments that accumulate over time and that they may experience treatment-related effects throughout the cancer continuum that again are changing or have the potential to change, so we need to be frequently assessing our patients, screening for any later lasting effects of their cancer treatment as well as for changes in their spasticity that could cue us into some secondary factors that are exacerbating it or in the setting of cancers that are potentially metastatic to the central nervous system that could be cluing us into a potential sign of recurrence. So I'd like to wrap up just by highlighting two cases from the outpatient cancer rehab setting that kind of demonstrate some of the principles that we just talked about, the clinical practice guideline in practice, and highlight the variety of clinical presentations but great outcomes that we can get in the cancer rehab setting. So the first case, I'll be discussing an individual that presented with left upper and lower extremity spasticity following treatment for a right frontal glioma many, many years ago. The spasticity, the onset of the spasticity was, occurred after the initial resection. Several years later, the patient did have a recurrence and had another resection. They were able to keep the spasticity relatively well controlled and maintained, and then many years after that, they noticed tumor growth and therefore did proton radiation as well as chemotherapy after they noticed the growth of that tumor. This was a relatively young individual who was highly active and especially enjoyed activities such as tennis. So their goal was to continue with these kind of high intensity sports and a very active lifestyle, generally independent even in the setting of the spastic hemiparesis over the years, but did report some slowness of activity and ADL. And again, one of the main goals was getting, getting on and staying on the tennis court. So pharmacologic management for a long term was Botox injections, completed generally speaking around every three months, and within days after those injections, we were generally seeing the patient on the therapy side. Therapeutic interventions included a lot of the interventions that we heard about in the clinical practice guidelines. Prolonged muscle, muscle stretching, neuromuscular re-education with facilitatory techniques, including joint approximation to improve muscle recruitment, weight bearing, NDT and PNF strategies, inhibition techniques, and task oriented motor learning exercise. So for this individual, pre-gay, pre-running tennis type activities were extremely important and integrated into the care plan pretty intensely. One interesting thing, and Dr. Mitchell talked about it, that really helped propel this patient to the next level was after a lot of conversation with her physiatrist, the patient, and the neuro-oncologist, one thing that was very helpful to the patient in decreasing spasticity and increasing mobility specific to the tasks of tennis was the use of a neuroprosthetic device or functional simulation on the lower extremity to decrease spasticity, improve dorsiflexion and clearance, allowing her to be more agile, nimble, and run on the tennis court, which really improved quality of life. The second case that I'd like to wrap up with kind of speaks to the different etiologies or causes of spasticity in the cancer rehab setting. So this particular individual was many, many years status post-treatment for head and neck cancer and had cervical dystonia in the setting of radiation fibrosis-related changes. So the patient presented to us with painful spasm and contracture of the anterior neck. In this case, as you can see, the SCM was primarily affected, and we know that there was the muscular overactivity in the setting of dystonia, but we were also working with the changes to the tendons, ligaments, and skin and fibrotic changes in the setting of radiation changes that were also contributing to this aberrant head position and limited movement. The patient did have significant cervical degenerative disc disease with pain and radicular symptoms and paresthesia with dystonia, and it was very troubling for this patient, limiting their ability to eat, communicate, specifically make eye contact in order to carry on a conversation. Being able to lay down in bed to sleep was extremely painful and difficult for this patient, and they also reported it was harder to breathe when they tried to sleep. Driving, as was discussed before, grooming, and turning the head to scan the environment while walking down the street was something that was very difficult for the patient and been really limited, and then the overall impact on mobility. The individual was very cautious and had a slow gait speed, and if you think about the impact of cervical dystonia and the limitations it would have on head writing responses and the impact on overall balance and mobility, it's easy to see why this would be an area that we would need to work on with this individual. This individual, too, did have Botox therapy and, again, coordinated timing with therapy. They also had a number of additional needs that we needed to address in therapy that perhaps weren't necessarily related to spasticity but could be exacerbated by spasticity, and that additional therapy interventions would help. These included lymphedema management, which in the setting of spasticity can be an, you know, ongoing inflammation, can be an exacerbating factor, and lymphedema therapy can help with decreasing that inflammation as well as minimizing fibrotic changes in the setting of chronic edema, so it could possibly impact outcomes that we're trying to achieve through our spasticity management strategies as well. Fatigue management, cardiovascular fitness, general conditioning, and speech and swallowing needs, so here we're seeing some of the common cancer and cancer treatment-related effects also overlapping with some of those negative cascading effects of spasticity, really highlighting the need and the role for ongoing therapy, multidisciplinary therapy for this patient. Therapeutic intervention included a lot of postural re-education, positioning, use of a collar not for support but to give some proprioceptive input to the patient did help her to feel more comfortable. Motor learning exercise, we did a lot focusing on cervical cephalic proprioception, and the patient did report feeling decreased stiffness and decreased pain and feeling more, more cervical mobility with those types of exercises. Stretching and strengthening, a lot of manual and myofascial techniques to combat the, the concurrent scarring and fibrosis that was going on. Mobilization techniques, functional training, relaxation, and one thing that was particularly helpful to this patient that is consistent with practice guidelines we talked about was, was serial splinting. So serial splints for a prolonged stretch applied to the neck very carefully with a lot of follow-up with the therapist to maximize skin integrity and make sure that there were no risks there helped this patient quite a bit. By the time we were done working with this individual, the most important outcome was that they felt they were able to get a decent night's sleep and to lay down in bed without feeling pain so that they could get that night's sleep, which helps them to feel like they could function throughout the day a lot better. So it was a really positive outcome that we focused on because of the, the shared goal-making. So through these cases and the clinical practice guidelines discussed, I'm sure as we all know there are highly variable etiologies and presentations for spasticity in the cancer rehab setting, but the bottom line that boils down to is that we know the cancer related treatment effects and impairments as well as spasticity can contribute to functional limitations and our job and our role is to provide evidence-based interventions to optimize function and the ability to participate in one's day-to-day activities to optimize quality of life. So that's what we're focused on. We have a lot of tools in our kit to do so. So in summary for, for the presentation, Dr. Mitchell kicked us off with key points, including spasticity in the cancer population often presenting weeks to months after a cancer diagnosis to the cumulative effect of surgery, radiation, chemotherapy, and or disease progression. Cancer-related fatigue can be a significant barrier to tolerating oral muscle relaxers. Dr. Khanna talked about radiation fibrosis as an insidious progressive tissue sclerosis that develops over years to decades and can affect all tissues in the radiation field in unpredictable ways. Radiated muscles are prone to spasticity, which can manifest as tightness or dystonia and even painful spasms. Botox can be very effective in this population as we just saw. And Dr. Gupta highlighting that while most recent RCT may not show improvement with Botox for range of motion or quality of life, there is improvement with pain at six months post injections, and that each patient is unique. And while this pandemic has modified the way we use technology to assist in patient care, we should not modify the way we practice medicine to ensure all patients receive the best possible care. And lastly, the application of principles and best practices related to spasticity management and cancer rehab will facilitate effective intervention and rehab management to optimize function and quality of life. And that rehab interventions should be multidisciplinary, incorporate best practices and clinical practice guidelines, and emphasize a patient-centered approach. So with that, on behalf of the speakers and the panel tonight, we'd like to thank you for joining us on this talk. Thank you.

spasticity care

cancer populations

patient-centered approach

medication

physical therapy

botox injections

function improvement

tailored interventions

assessment

multidisciplinary approach