My name is Evgenia Dworkin-Wininger, and I'm an assistant professor at MetroHealth Medical Center, Case Western School of Medicine. Thank you so much for joining us on this on-demand session. Today we're going to be speaking about electrodiagnosis in patients with cancer, what you really need to know. We have no relevant financial disclosures. So the objectives are as follows. We will recognize the indications for electrodiagnosis. I'm sorry, can we stop? I apologize. but I can't see my slides. I can only see. My name is Evgenia Dvorkin-Wininger. I'm an assistant professor at Metro Health Medical Center at Case Western Reserve University School of Medicine. Thank you so much for joining us on this on-demand session. Today, we're gonna be discussing electrodiagnostic evaluation in patients with cancer, what you really need to know. We have no relevant financial disclosures. The objectives of this talk are the following. We would like to recognize the indications for electrodiagnostic evaluation in cancer patients, establish precautions necessary for safe electrodiagnostic evaluations in patients with cancer, understand the common diagnoses that electrodiagnostic evaluation will, or an electrodiagnostic clinician will encounter in the cancer population, and describe the differential diagnosis and electrodiagnostic evaluation in this particular patient population. So the first thing is what are the indications of EMG and nerve conduction studies? Overall, they're very similar to our general musculoskeletal or neurology population. First, what we wanna do is make a diagnosis. Is there actual nerve injury or neuropathy? Is it related to the cancer, the cancer treatment, or is it unrelated to the cancer at all? Then we wanna make a prognosis, meaning what's the severity of the nerve injury? Is there re-innervation? And altogether, that will help us decide if we need to either order more lab work, imaging, or maybe we decide that we need to repeat the nerve test a few months later. Then all of this will help us with the treatment. For example, if we see that the patient has carpal tunnel, will we refer them to a surgeon or maybe they need an injection? In some patients, they might just experience pain, so we would focus on medication management. Once in a while, the nerve damage could be as a result of either recurrence of the cancer or metastatic disease. And in that case, the patient would need to see their medical or radiation oncologist. All of these things will help us with the function and quality of life. Ultimately, many of these patients go through different treatments, and many of them are quite anxious, so we want to make sure that we educate them if they have a new neuropathy or a new concern. So this is a nice graph from a paper by Dr. Costudio published in 2011, and it describes the different kind of nerve injuries from the actual cancer that can occur. For example, there's brachial plexopathies, lumbar sacral proxopathies, or radiculopathies. The actual nerve test would be similar to a regular musculoskeletal patient. We can see these neuropathies specifically in patients with breast or lung cancer and sometimes lymphoma. Then we have other nerve injuries as a result of the treatments. First, there could be surgical neuropraxic injuries, including unintentional nerve injury, for example, from a GYN cancer, or a plexus injury, also from surgical treatment. And then there could be some intentional nerve sacrifice, for example, in head and neck cancers after radical neck dissection, the accessory nerve is either sacrificed or damaged. Then chemotherapy, something we're all pretty familiar with, can induce peripheral neuropathy. Generally speaking, there's certain groups that do this more than others. For example, there's the vinca-alkaloids, the vincristine, venblastine, often used for solid tumors, leukemias, and lymphomas. Taxanes, so it's just facetaxel, dacetaxel, often used in solid tumors. And the platinum group, cisplatin, excellaplatin, as well as carboplatin, often specifically causes a sensory neuropathy. The third group of treatment is radiation. Radiation, as we will discuss later in this talk, can cause a variety of damage at every level, brain, spinal cord, plexus, nerve roots, as well as skeletal muscle. The next group is perineoplastic neuropathies. Overall, compared to what we just talked about, it's more rare, but it can present often as a first sign of cancer. And if that is found on an electrodiagnosis, further workup would be necessary. One of the more common ones that we are aware, that we know are the sensory neuropathy, is neuropathy especially with small cell lung cancer. One of the most common kind of nerve injuries we actually see in this patient population are the kind of nerve injuries that most of the population has. For example, carpal tunnel, also radiculopathies, ulnar neuropathies. Sometimes we see patients with fibular compression neuropathy after they've had weight loss because of the treatment or because they've been hospitalized. So we'll talk a little bit about some of the risks that go along with doing the nerve or the EMGA test in this patient population. The infection risk, for example. So how to avoid it is the same as with our other patient populations. We wanna wear gloves, clean the area with alcohol swipe, use disposable needles. However, specifically in this population, we need to be aware if the patients are neutropenic, if they're actively being treated. So it is something to consider the risk versus benefit if somebody is neutropenic of how much we really need this test. Likewise, there is a bleeding risk, especially in some patients that are on anticoagulants or have low platelets during the time of their treatments. Overall, there are very few case reports of actual hemorrhage or compartment syndrome. There was one study that looked at hematomas that could occur with patients undergoing EMG, especially in the paraspinal muscles. This looked at over 1,000 patients and less than 1% developed any kind of hematoma. And then there's the patients that have lymphedema or upper or lower extremity. We will discuss this later through our cases, but there is some hypothetical relatively small risk of cellulitis or worsening of lymphedema. Again, there has to be a discussion of risk versus benefit in this patient population. And lastly, given the pandemic, some have also published about COVID-19 precautions. Of course, wearing face masks, hand hygiene. The other point is to try to make the study as efficient as possible to make sure that there's less face-to-face contact with the patient. And for studies that are including facial laryngeal nerves, wearing N95 masks and isolation gowns is very important. So we will go ahead and start with our cases. Thank you. Hi, my name is Cody Andrews. I'm an assistant professor of physical medicine and rehabilitation at the University of Michigan. And I wanted to go through a case with you today of foot drop in a cancer patient. So we have a 63-year-old man. He was previously healthy, but then he was diagnosed with ALL. He did undergo four cycles of induction chemotherapy with the agents here. And also underwent intrathecal methotrexate for prophylaxis. Due to complications, he was hospitalized for 28 days. He had neutropenic fevers and pneumonia. And after that, due to some severe debilitation and weakness, he underwent a 22-day inpatient rehabilitation course with excellent functional improvement, was able to discharge afterwards. He was seen in follow-up in the rehabilitation clinic after he received two more cycles of chemotherapy. Overall, he's still doing well, but he complains now of a new onset bilateral foot drop. So, you know, just looking at him, he's generally well appearing. It looks like he's recovered well from his illness, but then on strength examination, it is noticed that he has a four out of five strength to ankle dorsiflexion, and then three out of five strength to great toe extension. Approximately, he seems very strong. He's able to stand up unassisted, but then whenever he walks, he does have a foot slapping sound. So just to briefly go through, you know, what is on the differential diagnosis here whenever a patient like this is seen. Anytime there's a leukemia, a leptomeningeal disease is on the differential, some kind of lumbosacral radiculopathy, possibly even unrelated to his cancer is on the differential as well. He did receive a lot of neurotoxic chemotherapy, and so neuropathy is definitely a consideration. Critical illness neuropathy and or myopathy is definitely on the differential here. I mean, it could just be a good old-fashioned peritoneal neuropathy. It's far from a comprehensive list, but it kind of gives a flavor for, you know, what could cause an ankle weakness in a patient like this. Just looking, you know, I would say that chemotherapy-induced peripheral neuropathy is pretty high up there on that list. Something like critical illness neuropathy and myopathy is a bit lower because he is a ways out from his critical illness. And then, you know, just because he's a cancer patient doesn't mean he can't have, you know, bread and butter kind of rehab-style weakness with a RIDIC or a neuropathy there. So, of course, an EMG was ordered for this patient. And there were some pretty profound findings. As you can see, there were extensive nerve conductions done in the lower extremities. His sural sensory and his perineal motor recording over the EDB were both not registrable. He had pretty low amplitudes over his anterior tibialis bilaterally for motor nerve conduction studies. And then again, his tibial motor studies were absent. So you can see that distally, we're pretty much getting no responses. And then even proximally, the amplitude of those responses is pretty diminished because this was such striking findings in the lower extremities zone, especially if it's a bit out of proportion to the infamination. We also went into the upper extremities where you can see the median sensory was absent. The ulnar sensory, lowish amplitudes, but obviously much better than the median sensory. And then a little bit more normal with the radial sensory recording a little bit more proximally there in the forearm. So as you can see, the nerve conduction studies here for the first part of his EMG are definitely supporting more of a neuropathy type picture. It's definitely not something focal, something focal like a radiculopathy. It would have to be a pretty extensive polyradic to have these findings. And they'll support a central cause like leptomeningeal disease or something like that. So we're honing in pretty closely onto the chemotherapy peripheral neuropathy here. A brief needle exam was performed just to confirm the diagnosis and to kind of assess how severe the denervation was. So starting in the anterior tibialis muscle in pretty pronounced spontaneous electrical activity with two plus sharp waves and fibrillations there in the anterior tibialis, very significantly reduced recruitment, very polyphasic morphology motor units. And then coming proximally even to the level of the gluteus medius, there were still some denervation changes seen there, which is very striking for somebody with a peripheral neuropathy type picture, especially again, a bit out of proportion to his exam, but a very, very striking EMG study. So given these results, the discussion was had with hematology. Even Christine was held given that it was thought to be the causative agent of his neuropathy for many months, many, many months. And then some soft ankle braces were provided just to prevent him from, you know, tripping and from tiring out. And then of course he was sent to physical therapy to both mitigate his fall risk and kind of provide him some adaptive strategies, but also in order to kind of help strengthen the muscle fibers that weren't denervated and get him as strong as we possibly could. So he actually had quite a remarkable recovery. Over the next 12 months or so, he was, his strengths recovered significantly. He stopped needing the ankle braces. You know, he was even able to restart in Christine after an extensive discussion with his hematologist, though he did have to start it at a decreased dose due to the pretty severe neuropathy developed before. Kind of toward the end of his treatment, he was even able to go out to Utah, go on a five mile hike with his family up in the mountains there. So very remarkable recovery after the, then Christine was discontinued and he was able to get into appropriate therapies. So I want to take a moment to kind of just talk about chemotherapy-induced peripheral neuropathy a bit more generally here. So we talk about these as if they're one big unifying diagnosis, right? So chemotherapy-induced peripheral neuropathy is this big unifying diagnosis where there really, really are some pretty significant differences here between the different chemotherapy agents. I like it when I'm talking to residents or to learners or even the colleagues during lectures that it's a bit like kind of lumping all metabolic neuropathies into just a metabolic neuropathy category. You know, is that technically correct? Yes, because they do all kind of fit into that same category together. But in terms of, you know, you miss then a lot of the nuances in the different diagnoses. So just kind of a broad picture of these. So taxanes, those agents, which are very common in like breast cancer patients, for instance, will get also very common in gynont patients. They, it tends to be a more large fiber predominant situation there. And so it's kind of, you're looking more at proprioception and balance loss. Patient complaints are often relatively vague because they're not having a, a lot of them don't have a significant pain component. And so they're, it's a lot harder to describe, you know, decreased balance, but they'll talk about having trouble walking on like in the sand, if you go to the beach or climbing stairs sometimes, especially in the dark is difficult for them. So it's really a bit management, diagnosis and management of that can be a bit more difficult. It also doesn't show up as well on EMGs often. So moving on to the platinum agents tend to be a kind of just more sensory predominant, not a ton of pain, but it can have a lot of like uncomfortable tingling kind of sensations. It's, you know, these are, this is kind of the more classical peripheral neuropathy that we're all used to seeing in diabetics and those kinds of patients. Moving into the vincas, which is what our patient in our case here had, these can really have a very significant motor component, which is very striking whenever it happens in comparison to other chemotherapy agents. So it's, as you saw with our patient here, he had motor unit changes all the way up to the level of his glute needs. So a very, very proximal, I mean, that's, you know, about as proximal as you can get without going into the trunk. I mean, this is a, that was certainly a striking profound case, but it's certainly something to watch out for. And this is where, you know, us as physiatrists can really add value to these patients because, you know, seeing somebody with a bilateral foot drop, it kind of can tune in our neuromuscular brain to things that the hematologist or oncologist might not be thinking about and management that they might not be able, that they might not think about. In this case, you know, one role of physiatry was to recommend actually a discontinuation of a chemotherapy agent, which, you know, doesn't happen often, but given the severity of the findings, in this case was warranted to the hematology team to read. The last one I want to talk about is bortezomib or Velcade. This is often used for myeloma patients. And this one really has a much more small fiber predominant kind of pain, burning, their feet feel like they're on fire, especially when they're asleep, they might have some aledenia. These it's mostly going to be symptom management in terms of pain to try and get them through. The good thing about the chemotherapy induced neuropathies, a lot of them are reversible with this continuation of the agents. So as we saw in the patient represented here, he was able to make a very, very good recovery given time away from the agent and then going through appropriate therapies. It's not always completed. In fact, it's often not, but I do try to counsel patients that, you know, up to two years or so after you've completed your chemotherapy, you might continue to see some improvements. Just another thing I wanted to briefly touch on, when to order electrodiagnosis for these patients, because just because you suspect a neuropathy doesn't mean that we need to jump right into the electromyography lab. I usually find it most useful. So if you need to confirm a diagnosis that you're not sure about, maybe there's something clinically about them that doesn't quite fit, you want to rule out mimics. So there's a lot of neoplastic diseases that are rare, but very severe that you need to rule out or might need to rule out. Sometimes, like in this case, you need to determine severity for treatment considerations. And so, you know, does this patient really need to come off of the chemotherapy agent? How severe is it? And then sometimes for patients who are having like a slow recovery or maybe concerned about their recovery, you can get a good sense of prognostication, given some time to see, you know, are the motor units healing? Like, does it look like there's some axonal sprouting going on? That can give patients a little bit of a peace of mind. So yeah, that is the end of my portion of the presentation. I appreciate your attention. Hello, my name is Sarah Holtz, and I'm an associate professor at the University of Wisconsin in Madison, and I will be starting our next case. We have a 48-year-old woman who presented with swelling in the anterior neck on the right side for about two to three months. She described the sensation as painful, and the area was enlarging. She also noticed that her shoulder looked different on that side. On exam by her primary care provider, she noticed tenderness over the right anterior neck with a palpable lymph node. A determination was made to do a lymph node biopsy at that time, and it was performed in the posterior triangle. Post-operatively, she developed pain in the upper trapezius and noted that her shoulder was sagging. She was sent to physical therapy and was noted to have trouble with shoulder abduction and rotation and scapular winging. So in a patient who has fullness and pain in the anterior neck, undergoes a node biopsy, and then develops weakness, we wanna think about some of the possible sources of pathology. This particular patient also had a history of rotator cuff surgery on the right side and did a physical labor job. So some of the other things that we wanna consider would be rotator cuff pathology, frozen shoulder, AC joint pathology, post-op edema, injury to the upper trapezius and soft tissues. And of course, this is an electrodiagnostic assessment, so we wanna talk about nerve disorders. The most common would be an upper trunk like brachial plexopathy, spinal accessory neuropathy. You should also consider cervical radiculopathy. And in some patients, the cervical facet mediated pain could also cause pain and dysfunction in this area. When we saw her approximately four months after her node biopsy, she had a scar in the right sternocleidomastoid and it was posterior to the muscle. She had a positive TINEL sign over the scar. She had atrophy of the right shoulder in the upper trapezius area with sagging of the right shoulder. On cranial nerve exam, there was weakness of the upper trapezius, that was three out of five. The remainder of her strength in cranial nerve exam was normal. She was unable to abduct her arm past 90 degrees and was noted to have scapular winging that was worse with forward flexion. At this time, she also had an ultrasound which showed a post-traumatic neuroma of the spinal accessory nerve. And because she had weakness and was still unable to progress in her job and return to her full activities, it was determined that an electrodiagnostic assessment was needed. So now we're going to look at the nerve conduction studies that were performed. In her, the right median ulnar and radial sensory responses were assessed as well as the ulnar and median motor responses. All of these were normal. In this situation, the axillary and musculocutaneous nerve could be assessed. However, she had no weakness in those muscles or symptoms in those muscles. And since those studies can be technically difficult and challenging and sometimes painful, it was decided that they would not add much to the study. Her EMG examination is noted here. Her first dorsal interosseous of the hand on the right side was assessed as well as her pronator teres, triceps and deltoid, all of which were normal. Her cervical paraspinal muscles were normal as was her infraspinatus muscle. Her right upper trapezius muscle, however, showed three plus positive waves and fibrillations with decreased recruitment and one to two motor units seen. So what we have here is normal nerve conduction studies with an isolated abnormality in the right upper trapezius and a diagnosis of a moderate to severe spinal accessory neuropathy with ongoing denervation. So spinal accessory neuropathy is fairly common when you're looking at surgeries in the neck. There's been reported of an incidence of three to 10%. It used to be even more common due to radical neck dissections. However, new surgical techniques that spare the spinal accessory nerve have become more prevalent. They were noticing that many of those patients were developing shoulder dysfunction following the surgery. So it was determined that better surgical techniques were needed. The outcome for most of these patients is fairly good and we're gonna discuss that in a minute. The diagnosis of spinal accessory neuropathy is fairly easy, as you can tell on an electrodiagnostic evaluation. There's a study by Lena in 2011 that demonstrated that electrodiagnostic evaluation was successful in demonstrating the spinal accessory neuropathy in most cases. So for this patient, the management, we started off with physical therapy. This focused on stretching of the pectoralis muscle, postural training and scapular stabilization. She actually developed some dysfunction of the sternoclavicular and acromioclavicular joints due to forces that were altered because of the atrophy. And we ended up doing a sternoclavicular and acromioclavicular joint injection with steroid, which was quite successful. She also developed a trigger point in her levator scapula, which was compensating for her upper trapezius being weak and that was also successful for her. So despite the fact that we did the physical therapy and we're working to control her pain, we also used medications such as Lyrica and Gabapentin and eventually ended up going to Topamax because those were not successful for her. She still wasn't able to be a full duty at her job and was still having weakness and scapular winging. So it was determined at that point that she undergo a surgical reconstruction. This was about six months after the initial biopsy. Her surgical plan included spinal accessory nerve exploration with intraoperative monitoring and a sural nerve graft. And she actually did very well after this. These surgical reconstructions take a long time to get the full benefit, but at a year post-operatively, she had improvement of her range of motion to 180 degrees of abduction, or sorry, of forward flexion and 120 degrees of abduction. She had less scapular winging and has been able to return to her job. So for surgical reconstruction, there is not a ton of literature. However, there have been studies with nerve reconstructions in the neck and upper extremity, such as this one by Kostas listed here, that have shown some improvement in patient's function after surgical reconstruction. Overall, with the spinal accessory neuropathy, there is a good prognosis. There was a study out of the Mayo Clinic that looked at 106 patients with spinal accessory or long thoracic neuropathy, and most patients did do fairly well. However, some poor prognostic signs included inability to abduct the arm and initial weakness and atrophy, which this patient did have, as well as involvement of the dominant arm. So those all suggest that this patient may have had a worse outcome, but luckily she was able to have a surgical reconstruction, which was very successful for her. Now we will move on to the next case. Oh, hello, this is Mary Vargo from MetroHealth Case Western Reserve University. And our next case has to do with lymphedema and electrodiagnostic issues. So our case today is a 68 year old woman with a history of right breast cancer 10 years earlier, treated with lumpectomy, axillary lymph node dissection, and radiation to the right breast. She also has a history of rheumatoid arthritis and was taking some immunoactive medication. She had had bilateral carpal tunnel releases five years earlier with good clinical response, but no prior electrodiagnostic study available. Her right arm had subclinical to very mild lymphedema, which she managed with a semi-consistent conservative regimen. She had had recurrent episodes of right arm cellulitis several times in the past, and she was referred by her plastic surgeon for EMG study due to symptoms of hand pain at the first web, lateral forearm pain, and neck pain. Looking at her studies, first the sensory nerve conduction. Mild delay contralaterally in the median fibers. In the motor fibers, she also had bilateral median delay, with preserved motor amplitudes. However, in the ulnar studies, there were moderately reduced CMAP amplitudes, which was unexpected. Because it was unclear, given her history of the prior surgery and the ulnar findings and her symptom pattern, it wasn't clear that the diagnosis of carpal tunnel explained everything. So with the patient's consent, it was agreed to proceed with the needle examination, which turned out to be within normal limits for her. So the conclusions were bilateral median mononeuropathy at the wrist in the moderate range of severity, and it was really indeterminate whether this was a true recurrence versus residual effect of her prior carpal tunnel syndrome and surgery. Subsequently, she had a rather interesting course. She followed up with her plastic surgeon, who used the phrase, discussed the conundrum with the patient, and after exploration of options, she agreed to a Kenalog injection to the wrist area with a good clinical response. And then she went on to have another corticosteroid injection a month after that to her right first CMC joint. And over the several months after that, she did in fact have a couple of episodes of right arm cellulitis. But she recovered well without aggravation of the lymphedema, and even over the next few years, went on to have several surgeries to her right arm. So what kinds of questions does this raise? And EMG in the setting of lymphedema in general, what kinds of questions are raised? So the most common one that we talk about is precautions, especially for the needle examination, the concern of onset or worsening of lymphedema or provoking infection. There can also be technical challenges in any swollen limb, especially for nerve conductions. Although surprising to me, this was actually a literature gap and I was not able to find any studies on this. And a third question would be whether certain neuromuscular conditions might be more common in the setting of lymphedema. Starting with the needle stick issue, there's really no research on EMG exam specifically, but there is some emerging evidence for similar needle stick related clinical situations. And as to EMG and cellulitis specifically, there's no reports in the era of disposable needles or in the setting of lymphedema. There is one case report of necrotizing fasciitis of thigh muscle during intraoperative monitoring during spine surgery, which would have presumably been a more lengthy needle exposure. And there was a review by Gatesheff looking at iatrogenic complications of EMG and incidence of infection was estimated at one in 10,000, which was their lowest frequency category. There have been a variety of published guidelines regarding needle sticks and lymphedema. Several are summarized here. A clinical practice guideline by Harris et al for post-mastectomy lymphedema. There's also the... Now... Generally say that needle sticks should be... For the procedure to be considered... Benefits versus risks. And sometimes may proceed with precautionary strategies. So there was a comprehensive review by Asdorian in 2016 reviewing 31 studies on this topic. Many were case reports or small case series. There was a preponderance of case reports, which were older from the era when more radical surgeries were done. And there were also concerns of recall bias and confounding factors such as weight gain. I would like to review one of the studies, however, which was one of the more recent and larger studies by Ferguson looking prospectively at 632 post-mastectomy patients. And they screened the patients at baseline and at every few months post-operatively for a change in limb volumes. They did find that 6% of their population developed cellulitis at some point, about half soon after the surgery. Nearly 8% were clinically diagnosed with lymphedema over a two-year period after surgery. Of note, this population had relatively less extensive surgery in general, with about 80% having either sentinel node biopsy or no axillary surgery, and about 20% having had axillary lymph node dissection. And here's their univariate. This is change in limb volumes and blood draw, no blood draw, injection, no injection. So you can see that there was, you know, really no significant effect of those interventions. There were no significant change in limb volumes with blood draw or injections. However, looking about two thirds of the way down, that data point on the right is cellulitis, which was the most significantly associated variable in terms of change in limb, increase in limb volumes that was seen in this study. And then their multivariate analysis, cellulitis remained their most highly associated variable. It's that point on the bottom there furthest to the right, with the other factors being axillary lymph node dissection, BMI greater than 25, and regional lymph node radiation. So we can see from this that the needle stick itself probably presents negligible concern, but cellulitis, you know, is probably a more significant concern. Moving on to the question of whether neuromuscular conditions are more common in the setting of lymphedema. There's not much, likely be a concern due to the weight of the limb or pressure within the limb or even possible neuropathic effects of toxic metabolites in lymph fluid. But there's really limited data. There's also multiple other reasons why somebody with a history of cancer treatment might have neuromuscular diagnoses. And also there can be age or comorbidity effects going on concurrently that may predispose to neuropathies such as entrapments. With regard to the question of carpal tunnel syndrome, there are a couple of studies. There's an older study by Gainell from 1979, a series of post-mastectomy patients. And it was found that there was a higher incidence of carpal tunnel findings and also brachial plexopathy findings on the mastectomy side compared to the non-operated side. They also reported that for those patients with lymphedema compared to those patients whose operated side was not affected by lymphedema, that those with lymphedema had a higher incidence of these neuromuscular findings. However, there was no statistical analysis and they also did not give the denominators of how many patients were in each category. So it's a little bit difficult to interpret with certainty. More recently, there was a case series by one of our co-presenters in this talk, Dr. Stubblefield, looking at 19 patients. So the 38 limbs of those patients with post-mastectomy lymphedema and found that there was no difference between the limbs affected by lymphedema versus the contralateral limbs in terms of carpal tunnel syndrome. They also noted that... So not much on other conditions. There was a small case series reported as thoracic outlet syndrome diagnosed by ultrasound, no electrodiagnostic study. However, it was noted to respond to lymphedema treatment. And there was also a single case report of radial nerve injury from a compression garment. In conclusion, the available evidence regarding needle sticks is mostly reassuring. It does not directly assess EMG. And also very notably, it's virtually entirely confined to the post-mastectomy upper limb scenario. But it does appear that needle exam has a negligible chance of provoking lymphedema. More extensive, those with more radical surgery are possibly at higher risk. We know very little about the severity or prognosis when it does happen. Is it a small perturbation of control that's quickly restored versus a more serious event? Cellulitis is really the bigger worry, which is virtually not reported after EMG. There is a thinking in general that clean medical procedures may be less of a concern than dirtier community exposures. We have that literature gap that I mentioned on the impact of swelling, on diagnostic accuracy of nerve conductions. And there's really weak evidence in the area of lymphedema itself causing neuromuscular outcomes. So what to do? We come back to that phrase, discuss the conundrum with the patient. It does come down to that individualized risk versus benefit, but in an underlying low risk context. One piece of advice when you're on the referring end for EMG it can be helpful if you feel strongly that you really want that needle exam, or if you don't feel so strongly, to indicate that in the referral to give the electromyographer some guidance. With respect to this case, as I mentioned before, it was not clear that the carpal tunnel findings explained everything. And also importantly, this was a patient very much in the loop with the decision-making. So it did appear reasonable to proceed with the study despite her risk factors. So empirically, what can be done is increased attention to antiseptic precautions, also attention to minimize any trauma such as using a monopolar needle, examining the fewest possible muscles, and then being gentle with technique, and also incorporate the patient awareness for surveillance and possibly to temporarily step up their usual regimen. So with that, I will say thank you and on to our next speaker. Hi there, I'm Dr. Michael Stubblefield. I'm the Medical Director for Cancer Rehabilitation at the Kessler Institute for Rehabilitation. I'm also the National Medical Director for Select Medical's Revital Cancer Rehab Program and all their other cancer rehab programs across the country and I'm a professor of Rehabilitation Medicine at Rutgers New Jersey Medical School. And I get the pleasure, I'm so happy to join all my colleagues here talking about electrodiagnosis in patients with radiation fibrosis symptoms. So it's critical in this situation to understand a little bit about radiation to be able to accurately assess these patients. I'm gonna give a commercial ahead of time. I'm actually don't do a ton of studies on these patients anymore, because frankly, it's so obvious in most of them that I'm not trying to decide between competing diagnoses. So if it's not gonna change things, I don't do it. That being said, if it's new to you, I recommend really kind of becoming familiar with these faces and what their EMGs look like. So the first thing you need to know when we're talking about radiation, we're really just talking about high energy. It comes in the form of photons and protons when used clinically in this group of patients and that is an important difference. Depending on where you are, you're gonna start seeing more protons used clinically. I'm starting to see a lot of that here in the New Jersey, New York tri-state area. So photons are very much like bullets. They're fired from the gun, they hit a peak velocity, and then they immediately start losing energy, which means that when they hit a target, like the human body, that energy starts coming out of the photons and they slow down, which means they have a very high entry energy and go off to zero as they lose that energy. Protons are very different. I liken them to torpedoes. They certainly will leave a mark when they're initially fired because they're a big heavy object, in this case, particles, but they are really designed in such a way that they're gonna release their energy precipitously at a certain area. So the idea there is you have less entry energy and more energy deposited right at the tumor that you're trying to treat. Now, that sounds great. And there's a lot of excitement. There's a lot of emerging data on the use of protons, but I gotta tell you, some of the worst radiation injuries I've ever seen have been from protons either used as the primary treatment or used following failure of photons in other therapies in a cancer patient. So don't think just because they got protons, everything's fine. It is not. So when we're talking about radiation fibrosis, we're talking about that insidious tissue fibrosis that occurs as a result of radiation. It's an immortalized process, meaning it goes on forever. It never goes away. It will just continue to get worse over time. We used to say 20 years. Honestly, I've seen patients now 50 years plus out from radiation who continue to have issues. Radiation fibrosis syndrome are those complications, those clinical manifestations, nerve injury, for instance, that you see as a result of the use of radiation in cancer treatment. So several things will determine how bad it is. One is the field. When we're talking about the field, we're talking about that part of the body where the radiation was given. So if it was a sarcoma in an arm, it was that area of the arm that was treated. If it's head and neck cancer, it may be a very large field extending from, you know, the cervical lymph nodes or higher all the way down to the mid chest, depending, and there may be some scatter, and it's gonna go out to the sides. I'll show you that in a minute. Other things we worry about are the total dose, like how much dose did the patient give? Again, and standard radiation for head and neck cancer say is about 70 gray to the primary disease, about 50, 54 gray, I'll show you what that means in a minute, to the neck. The problem is that's not the whole story. We're so good and sophisticated with giving radiation now that we can give like radiosurgery, which is high dose radiation in one treatment. So you wanna know the total dose, but you also wanna know the size of the fraction and the number of fractions that the patient received. You wanna know the tissue that was radiated. You wanna know what surgeries, chemotherapy, other things the patient have, and all of that put together will help you to determine if you're dealing with radiation fibrosis and radiation fibrosis syndrome. A very important thing in neuromuscular evaluation is for this to be radiation fibrosis, it has to be either in the radiation field or due to a structure traversing the radiation field. So for instance, you can have specific damage in the head and neck region, but you can also have atrophy of the hand from damage because those nerves may be traversing that field. So that is very critical to understand because you have head and neck radiation doesn't mean that you're gonna have atrophy of your foot necessarily as a result of it. That probably would not be radiation fibrosis syndrome. So the basic unit that we're using currently is the gray or the center gray, which is, you'll hear them on both terms. Older we would use rats, there's an error on this. I'm sorry, a gray is 100 centigrade and 100 rats. So a typical dose for head and neck cancer of say 70 gray would be 70,000 or 7,000 centigrade and 7,000 rats. This is important because when you're starting to see these patients, you should try to understand how much radiation they got. 50 gray is sort of the standard used in breast cancer. When you start going up on that, or you go up on the dose per fraction, those patients start having a much higher likelihood of having nerve injury. There is difference in the sensitivity of the tissues. This is also important. Nerve is relatively resistant, but it is not without the ability to be damaged as I think we all know. Things like lung really are very sensitive and will melt and a lot of things are in between here. All right, so now having put that beside us, let's talk about a case. 57 year old man with a history of largely right-sided nasal pharyngeal cancer diagnosed in 2002, treated with 5-FU and IMRT, so no neurotoxic chemotherapy. The IMRT, which is intensity modulated radiation therapy is a way of giving the radiation therapy conformally. So the idea is it helps protect the parotid glands and it also sculpts around the spinal cord, which I'll show you here in a minute. But you know what? The nerves, they're all right smack dab in the middle of the field and they will certainly become damaged. So this guy comes in with upper extremity weakness and pain. I saw him a long time ago. He's just a really illustrative thing because he didn't have surgery. Everything you're looking at is absolutely due to the radiation. So if you see the tattoos, if you see the tattoos on him are way down on his chest there. I don't know how well it protects to you. You see the marked atrophy of the neck, right? You see the trapezius and the sternocleidomastoid are both atrophy and that shoulder is very depressed on the right side. You see his pec is atrophic. So that's not, you know, that really has to start getting the pectoral nerves and the plexus to do that. He has lateral winging of the right scapula, which you can see here. If when you test his strength, he's very weak, particularly in the proximal muscles, the trapezius, the deltoid and biceps. And his reflexes are depressed and really the C5-6, the biceps and brachioradialis distribution, but, you know, maybe relatively preserved in the triceps. So the differential here, again, I'm not doing as many EMGs. When a guy walks into my office like that, that's pretty much radiation fibrosis. Certainly it's a bias because I get these patients from all over. But you might think about rotator cuff pathology. Usually that's a secondary problem to the radiation and not the cause of what you're seeing. Same with adhesive capsulitis. You might start thinking of a number of neuromuscular disorders like motor neuron disease, or you might even start thinking about fascial, skeletal or humeral muscular dystrophy. And not for head and neck, but for like Hodgkin lymphoma survivors treated. I've had more patients than I recall who have been given inaccurate neuromuscular diagnosis. You might start thinking of cervical radic, brachial plexopathy or various mononeuropathies. In these cases, you'd actually be right because the patient has pretty much all of those neuromuscular things. Those of you who've heard me talk about this in talks just about radiation fibrosis, this patient has a myeloradiculoplexoneuromyopathy. In his case, the spinal cord dysfunction is less severe, but the nerve root plexus, peripheral nerves that were in the radiation field and the muscles in the radiation field are really subject to injury. So this is just showing you myeloradiculoplexoneuromyopathy. Look, see, this is IMRT. These are different patients, but it really illustrates nicely. And you see that red is where they get the full dose of radiation. So in the neck at this level, it might be 5,000 or 5,400 centigrade. Up higher in the neck, it's usually 70 centigrade or as high as that. I've seen higher. And you see the nerve root, the plexus, all the nerves that are in that, like the spinal accessory nerve, the dorsal scapula nerve, we're gonna take a hit as well as directly to not only the cervical musculature, but the shoulder girdle musculature. And you can see here a very similar tumor as the patient here to give you the idea that it's a myeloradiculoplexone in both cervical and brachial. Those of you who've forgotten about the cervical plexus, it's absolutely damaged in these faces and a big cause of anterior dysesthetic pain, which you can easily test by testing the four branches. Not enough time for me to go into that for you. And then multiple mononeuropathy, it's cranial, recurrent laryngeal, dorsal scapula, suprascapular phrenic, and then myopathy, the muscle becomes damaged in the radiation field. So when you start doing EMGs, and again, this is not, this is a kind of a guide to EMGs and not to a specific patient. Things that you're gonna see. Well, the spinal accessory nerve, you're gonna see that as atrophic. That's a tough nerve to test or testing it for a nerve's point. You will actually sometimes see a conduction block through herbs point or through anything that's going through the radiation. That is reflecting slowing of conduction through those demyelinated nerves, which might not be out and out dead, but really just dysfunctional because they're poorly myelinated. Same thing with the axillary musculocutaneous. These are not the standard nerves we do, but when you compare them particularly side to side, remember the other side also have radiation, so it may be dysfunctional, just less so. I would commonly see a big drop off in amplitude there. The nerves that are coming off south of the radiation, radial, median, ulnar, they'll generally be normal. And when you're doing your sensory, you're really doing a plexus study largely. So in head and neck where it's the upper nerve roots, upper cervical nerve roots and upper plexus that are more generally affected, you're gonna see that typical sort of drop off from the lateral brachiocutaneous, radial, maybe a little affected. Median, ulnar would tend to be less affected unless the radiation had a wider field. So in the needle EMG, this is really interesting. And this is one of the reasons if you haven't done EMGs on this population, I encourage you to get a little bit of clinical practice before like me, you just kind of stop doing them unless there's a real reason to. Very interesting in that you get a mixed population of myopathic motor units. You have what is a nemaline rod myopathy in the distribution of the radiation. And that'll be right next to these big, large, polyphasic neuropathic motor units. That is extremely common to see a mixed population that may vary depending on how affected the muscle is. Often the severely one that feels like balsam wood when you're going in, it's just soft and noiseless and fibrotic and you don't really hear anything. Out of the field, you're not gonna see the myopathic changes, but you may see neuropathic changes in those nerves that have run through the radiation field. So it's very important for you to understand what's in field and then what's out of field that has a nerve running through the field. In terms of management, this is the gift that keeps on giving. You can't cure radiation fibrosis. So the prognosis ultimately is that it's gonna progress. You can help them symptomatically, but we cannot currently change the underlying progress or pathophysiology of the radiation. So you're treating their pain, which they often have, nerve stabilizers, sometimes opioids. I will often use botulinum toxin in head and neck cancer patients who have dystonia. And that is often very effective. A lot of therapy emphasizing myofascial release and neuromuscular reeducation, postural retraining and other modalities, absolutely critical to have therapists who really have experience in this. And that's just for kind of the shoulder. I also have OTs and SLPs. We're treating lymphedema, dysphagia, dysarthria, and those things. Sometimes a cervical collar for those patients who have trouble holding their head up, particularly those who get weakness from it, and they may not wear it all the time. Jaw stretching devices for trismets, along with therapy and Botox into the masseter usually. And then there's a lot of medical issues in these patients. So I find myself ordering a lot of Carotid Dopplers and other medical exams because I still consider that part of my rehabilitation intervention to keep these patients as healthy as possible. So, you know, the conclusion here is accurately diagnosed in these patients is critical to function and quality of life. I don't know that EMG is necessary in all cases, but they're certainly interesting. And I think it's good for people to do it to understand the full pathophysiology. You need to look at other causes of compression and other causes of neurodysfunction like neuropathy. You need to be aware that there are multiple competing impairments. Myelopathy, radiculopathy, plexopathy, mononeuropathy is in the field, and then myopathy, if I didn't already say that. You need to look at, you know, other things like lymphedema, et cetera. That's it, I'll pass it on to the next speaker. Okay, so in conclusion, thank you for everyone who presented their cases. They were very interesting. So as everyone saw, we had different, a variety of different nerve and muscle injuries from related to lymphedema or related to radiation or chemotherapy. So in conclusion, again, the purpose of nerve conduction studies and EMGs is to diagnose, prognose, to treat and improve the quality of life of our cancer patients and cancer survivors with a variety of nerve injuries and musculoskeletal complaints. As we saw, you can have nerve compression by tumor, by nerve injury from surgery, chemotherapy-induced neuropathy, or a variety of nerve injuries or muscle injuries due to radiation. Overall, the risk of EMG and nerve conduction studies are very, very low. However, there is quite a literature gap, especially when it comes to EMGs and lymphedema. Same goes along with cellulitis as well. Thank you very much. And you can get in contact with us if you have any further questions.

electrodiagnosis

cancer patients

nerve injury

neuropathy

treatment decisions

brachial plexopathies

chemotherapy-induced peripheral neuropathy

radiation-induced damage

precautions

quality of life