and I have the distinct honor of presenting with some of my colleagues and I'm gonna make a small here. I do not have any disclosures in regards to any financial disclosures. I do work at the Cleveland Clinic, I'm employed there and I am president elect of the American Academy of Physical Medicine and Rehabilitation. The other disclosure I have is that I have the honor of working with my friends. So you'll get to hear a variety, a variety of four of us speaking today and they really are fantastic speakers. So I get to do the first one. Last year, when we did this virtually, we were just talking about this in that morning meeting. Someone said, not on mute. Sorry about that. So back to our presentation, but we had, so when we did this virtually, we had a challenge. We had challenging electrodiagnostic cases and one of the feedback that we got was, these were great cases, but can you share like a simple one or something more common? So that's my role. As I mentioned, I work at the Cleveland Clinic and when I do electrodiagnostic studies, I do them at one of our satellite facilities and we have generally 12 patients that day. We have six in the morning, six in the afternoon. I work with an EMG tech. So we have, she'll be in doing the electrodiagnostic, the nerve conduction studies and I come in and do the needle part of the exam, run over, do my report back and forth. So this was a case back in May of this year and so I just wanted to tell you a story about a gentleman that had severe carpal tunnel or medium neuropathy after a carpal tunnel release. So the history starts back in September of last year. He's a 59 year old right-hand dominant gentleman and he presented to the orthopedic clinic with progressive hand numbness. Like a lot of my patients, he had chronic neck pain. He had a history of cervical spine surgery. He also has nocturnal numbness. He didn't have any weakness at that time and they were reviewing an EMG that was done, it looks like March 11th, 2020. So right before the pandemic started that demonstrated moderate, medium neuropathy. And reviewing the history after I did the study, he had surgery on September 22nd, 2020, right open decompression of the median nerve at the wrist and then follow-up, he had a one month follow-up, three month follow-up and at both of those times, he was continuing to complain of some numbness, tingling in the same distribution. Again, chronic neck pain, chronic pain patient, similar symptoms, not getting better. Sounds like they were reassuring him that things would get better with time. Eventually he was referred for a electrodiagnostic test and this was on May 27th when I saw him. He was extraordinarily, had horrible pain and I'm really not sure how he managed to tolerate some of the nerve conduction studies, but he presented with numbness, sensitivity and dropping things. These are, hopefully you can see this. My studies from May 27th, the nerve conduction studies, he has no median sensory response, no median motor response, normal ulnar and radial sensory responses, as well as a normal ulnar motor response at the wrist and elbow, there was no slowing there. So pretty significant. The needle part of the test really didn't show anything significant aside from he had pretty much no, very atrophied APB and I didn't hear any active units at all and maybe some irritability, but I'm not really sure if that was there or not. As I said, he had a difficult time tolerating the test. So when we're formulating our diagnosis, we also are, we're always reminded that we have to go for the localization, the physiology, the activity that we're hearing, chronicity and then also comment on the severity when we're presenting that report to our referring provider. So in regards to this gentleman, we pulled up the previous data from March, 2020 to provide a more accurate interpretation and some concluding statements to the referring physician. So I have the report from March, 2020. So this was before his surgery and you can see that his median sensory is 6.32 milliseconds, small amplitude. In our lab, 4.1 microvolts compared to an ulnar and radial sensory amplitudes of 14 or 15 microvolts. The distal latencies for the ulnar and radial sensory nerves are normal. Those are on the right-hand side. Median motor is also prolonged 5.6, small amplitude compared with the ulnar. And then we have the temperatures listed there. The needle electro examination a year and a half ago, almost two years ago, showed a little bit of chronic irritability in a few muscles, but really nothing to state definitively that there was a C8 type of acute radiculopathy. So what we did, I tried to compare to give you on the left-hand side of the screen of the March studies and then the study that I did in May of this year. So pretty significant in regards to changes. I suspect not what the patient nor the surgeon anticipated if you have a moderate neuropathy surgery and then not good outcome at that point. So I wrote something to the fact that compared to the previous study from March, the current study shows interval progression of the right median mononeuropathy severe in degree and commented in regards to the absent median sensory motor responses. Also commented that I didn't see any active changes in regards to the cervical radiculopathy. I think from what I recall, he tolerated that part of the test fairly well. And then just to provide a little update, as I said, he had his test on May 27th. He saw his orthopedic hand surgeon thereafter. And then again on June 9th. At that time, looking at the notes, he was referred to occupational therapy and the therapist noted that again, he had hypersensitivity in all of his digits as well as weakness. Didn't know this, but he had a right wrist fusion and he also had limited range of motion of his wrist, which I believe is why they referred him to occupational therapy. From what I recall in looking at the records when I wanted to present this case, he only went to one session of occupational therapy and did continue with his pain management physician. And he's going to have surgery next week. So I will, I don't know whether I reach out to him and say, hey, how are you doing? I don't know if you remember me, but I just wanted to share an example of more of our typical things that we do and maybe less good outcome for this gentleman. Hopefully he will do better after surgery. What we're going to do is I'm going to stop sharing my screen I'm going to turn the mic over to Dr. Farron Williams and then I believe Dr. William Pease and then Eric Ensrud will finish up. These are great, interesting presentations, great studies. And I believe that we'll have some time afterwards to open it up for questions. Thanks. Now we need to stop sharing my screen. Here we go. Hello, I'm Dr. Farron Williams. I'm the clinical professor of physical medicine rehab at Chan Medical School, University of Massachusetts. And I have a case that I'd like to share with you about a patient who had a right shoulder reverse arthroplasty and woke up unable to move her arm. I'm going to stop sharing my screen. I'm having a little trouble advancing this. There it is, 68 year old patient, right-handed. She had a right shoulder arthroplasty with an interscaling block. And on awakening from the surgery, she immediately could not move the right arm and had some altered sensation in the posterior arm and pins and needles from the elbow down the lateral forearm to the thumb. She had no proximal strength, no wrist extension, no thumb or finger extensors and very weak wrist flexion as well as finger and thumb flexors. Also had some decreased light touch over that lateral forearm, especially the extensor surface. I wanted to highlight for you the fact that the nerve conductions do change in the first week after an injury. It's not the same as your needle EMG changes which may take three to four weeks. So if you do nerve conductions within the first week, you can already see motor changes followed later within a few days by sensory changes. And here's a little schematic of that. I actually did do on her some nerve conductions six days after surgery. And at that time, she already had a decreased right radial motor amplitude was a third that of the left side. And you do need to compare it to the contralateral side in these cases. And she had a slightly decreased right radial sensory recording from the thumb. It was about half of the left side with normal median ulnar sensory responses. So it looked at this point more like involvement of the posterior cord of the brachial plexus. Three weeks later, I saw the same patient again and confirmed that she still had no proximal strength. Wrist flexion was slightly improved now three over five but she continued to have no wrist extension. Finger flexors also were improved in strength but ulnar innervated hand muscles were less than antigravity. And again, she had no thumb or hand extensor muscles firing. She had radial sensory slightly decreased more approximately than distally and a decreased right triceps reflex. So at this point she had no functional recovery. She was starting to experience neuropathic pain and started on gabapentin 300 milligrams TID by the surgeon. And I added amitriptyline at night because it would take a little longer for that to be effective. She was not on narcotics. Three weeks later, her radial motor had significantly decreased in amplitude. If you recall, it was one six days after surgery. Now it's 0.2 millivolts and I could no longer get a radial sensory from the thumb. So I studied it from the snuff box and got no response. She continued to have normal amplitude, median and ulnar responses but she had some other decreased amplitude for her sensory, both median and ulnar, only on the right side. And ulnar F waves were slower on the right side. Now I did a needle study of different muscles and found I did a sampling of at least 10 different muscles innervated by different nerves and portions of the brachial plexus, but she had no motor units in the deltoid, the ECR, the EDC and decreased recruitment in the triceps with discrete recruitment in the EIP. So most of the positive findings on the needle study pointed to problems at the level of the posterior cord or the axillary nerve. She did however, have some sensory changes. If you look at this schematic of the brachial plexus, you'll see that at the poster aspect of the poster, at the distal aspect of the posterior cord, where this branches into the axillary nerve and there's also some contributions to the median and sensory nerves that may be where she had some problem from retraction of the surgery. And she also had the intrascaling block. I had to look in the operative notes to try to find out more information about what type of block she had. It's not always so readily available and nor did it say much about if there was any other complication, but the surgery did take longer than some. So she could have had problems because of the retraction, the intrascaling block, or there is documented in the literature of perioperative inflammatory neuritis, which can be treated with short course, high dose steroids. There's not good evidence about how much it helps, but it usually is not harmful. So I put her on those for a week and she didn't think it helped that much. Two months following the surgery, when I saw her again, she had improved strength in her wrist flexion. She started to have some wrist extension and the finger flexors continued to get stronger to the point that she could start to open a jar. Her pain was not that significant and she was not a patient who complained much of pain, but she still had some altered sensation. Her shoulder range of motion was starting to improve and she was able to work on this herself after working for a short time with physical therapy. And they've set her up with a pulley system. She used her other arm for active assistive range of motion and actually had been doing before this, a high level IT job and even questioned whether she might go back to work part-time. This patient I did see on telehealth four months after surgery. And again, the exam is a little bit more challenging, but you can ask people to show you, you know, how much they can raise up their arm. I wasn't sure if there's anything going up on in the deltoid but it looked like her biceps now had some less than anti-gravity strength and her wrist flexion continued to improve as long as well as the wrist extension. She seemed to have anti-gravity thumb and finger flexion, but no thumb or finger extension. And according to the patient, she still had that altered sensation. Now her pain was controlled with just the amitriptyline and she'd required no gabapentin. She did continue to take her short-term disability. She actually had quite good coverage for disability from work. So her physical exam, six and a half months after surgery now showed, this was in person, that she had a trace deltoid, a biceps which was getting stronger as well as triceps and wrist extension too was getting stronger. And if you recall, her wrist and finger flexors were better all along, but now she was starting to have some finger and thumb extension. Again, her radial sensory still was a little off but her reflexes were now symmetrical. So at this point, I did another electrodiagnostic test and now her radial motor was almost two thirds that of the contralateral side and she was starting to have some radial sensory response only from the snuff box. But at three weeks, I got no radial sensory. She now had spontaneous activity on her needle study only in the extensor and disproprius and in a number of different muscles, she had polyphasic long duration motor potentials with decreased recruitment. This included the infraspinatus, the deltoid, triceps and biceps and many of the radial innervated muscles had reduced recruitment. Her shoulder range of motion continued to improve with her doing her usual active assistant range of motion. And now her neuropathic pain was controlled with amitriptyline, which she actually said she wanted to discontinue. And again, she continued on this short-term disability. At eight and a half months after surgery, deltoid hadn't improved that much but there was some strength in all planes and biceps and triceps were improving in strength along with not much improvement in the degree of strength in the extensors of the hand but other muscles were getting to be closer to a normal range such that most muscles had at least up to a great improvement in strength. Again, with some decreased radial sensory in the proximal arm and shoulder active range of motion was to about 45 degrees where it was only about 20 degrees the couple of months before that when I had examined her. And at this point, I did an electrodiagnostic study again which now showed the radial motor being almost the same as the contralateral side three which is what I had gotten for the left radial initially. I should mention though that you can get a normal motor response because of the degree of axonal sprouting and it goes to different motor units and it doesn't necessarily correlate with normal strength. Radial sensory from the thumb was obtainable but very low amplitude. And now the spontaneous activity including in the EIP had resolved and she had more polyphasic longer duration motor units with decreased recruitment in the deltoid as well as other proximal muscles and also the wrist and finger extensors. So the patient, every time I saw her which was every couple of months, it continued to improve. And we didn't do electrodiagnostic studies every time if you recall, sometimes I saw her in clinic and occasionally on telehealth. What is it about this patient though that helped with her recovery? Well, number one, she was highly motivated. She did a lot to maintain and improve her right shoulder range of motion. She had minimal neuropathic pain and she actually at this point told me she wanted to try to go to work. She wanted to try doing four hours a day perhaps limiting her typing up to about 50% of the time because she had an IT job. So being on the computer was a big part of her job and it wasn't that much that she had to limit that was more physically demanding at work but on her restrictions said she couldn't do anything more than 20 pounds. And if you recall, she was 68 years old but she enjoyed her job and she actually wanted to maximize her retirement benefits and work until she's at least 70 for her full social security as well as some other work-related retirement benefits. So she did go back to work at eight months. She also wants to go back to skiing. She has a place in Vermont and she was disappointed that she couldn't ski all last winter and she likes to ride a motorcycle. So at 10 months, I saw her again on a telehealth and her shoulder range of motion continued to improve passively, significantly more than actively up to 160 degrees. Again, she had some pins and needles in the radial nerve distribution, but no significant pain and it didn't bother her that much. And she had started adding some weights to her exercise regimen. And at this point she wanted to work full-time and she did. So I saw her a month after the surgery and everything had improved except the deltoid strength and the extensors in the hand were still in the two over five range, still a little altered sensory but it didn't bother her to any extent, not to the point that she wanted or asked to take any pain medication. And her hand grip was improving and she had near full shoulder range of motion. So I wanted to see how complete her recovery was and did a year later, a follow-up electrodiagnostic study which again showed the radio motor of three millivolts similar to what it was at the prior study with again, very low sensory from the thumb but no spontaneous activity on the needle study and a lot of complex poly-basic units in the deltoid with the better recruitment pattern and just slightly reduced recruitment in the biceps and the extensor indices proprius which went along with her improving strength. At this point, one would say she's reached pretty maximal improvement. And I just have some tables which you can look at on your own. This is not by any means an example of everything we did. I just put these together so you could see how much the decrement and the amplitude of the radio motor was over time and how it improved after about eight months. And the sensory though, never really completely improved to normal levels. And this is just a few of the muscles which had more profound changes that I put on this table so you could see how they changed over time. This is only three muscles that we did probably at least 10 different muscles. One year after surgery, the patient had made a near full motor recovery electrodiagnostically, not completely full strength but enough to do the type of work that she did. And she did return to work full time and she had no ongoing pain issues at least nothing that limited what she could do. She did all her activities of daily living by herself and that included driving. And I should note the patient also lived alone. So in the beginning it was challenging and she bought a ski pass for the coming year and looking at what she might wanna do when she does reach age 70 in 2020. And she actually is so optimistic. She had told me she's questioning whether she might wanna have surgery for the left shoulder. And I don't really have any thoughts about that but I was surprised that she would even consider wanting to do the other side. And one reason I also presented this case for you is that I had a medical student last summer when a lot of the labs were closed because of COVID who did a nice retrospective study of 30 of our patients who have had traumatic peripheral nerve injuries and looked at improvements on manual muscle testing also pain issues, analyzed age, gender, smoking, comorbidities, whether they had therapies including physical and occupational therapy or surgery. And we found that all of these patients had some improvement in manual muscle testing and more people now are saying there is a benefit for doing peripheral nerve surgery or doing it sooner rather than later. But in the patients we saw, some of them did have surgery and we didn't really find any statistical significant difference between surgical versus non-surgical because nerves physiologically do often have a fair amount of recovery after trauma but it takes longer as you see in this case, it took up to a year and she's still not maximum strength. The advantage of consulting physiatry early as all of you know though, is not only to evaluate the patient acutely but also to do the consultation and get an electrodiagnostic study when it's appropriate. And in this case, the changes in the nerve conduction were already occurring within that first week. And this can assist with one's diagnosis, prognosis and how to manage the patient and make decisions about the extent of therapy they may or may not need, help with pain management and educate the patient. And I neglected to mention that I do not have any financial disclosures, but I do hope that next year we can do this live. Thank you. Well, thank you, Dr. Williams, and as soon as I can get this, now I'm moving into a more limb case for those of you who've been waiting through the two upper limb cases, but I'm going to continue the theme of serial EMG studies, although in my case, it's studies done in three different facilities for EMG. I have no conflicts of interest to disclose. She was referred to me because of problems related to an unusual gait associated with chronic back pain and Parkinson's disease. 68-year-old woman who'd had a left hip replacement that had no problems, weakness, painless. She had an unusual gait pattern, though, when she stood on her left leg, she leaned to the right and forward, biomechanically, obviously, a position that can only be maintained if you're using a walker because all of her upper body weight was on her upper limbs and on the walker. And so it was a struggle of a gait, even with a rolling walker. Her history included a 2014 lumbar decompression for stenosis, and she did complain of numbness and tingling in the right lower limb. Had some edema in the left ankle and calf. And her previous EMGs were both by board certified electromyographer, one physiatrist, and one neurologist. History includes Hashimoto's thyroiditis. As I mentioned, axial low back pain, at least at first, bilateral knee pain, followed by rheumatology, neurology, first diagnosed Parkinson's disease in 2009, maintained on Sinemet. The lumbar laminectomy follow-up with a spine surgeon in 2019 looked fine, according to the surgeon. She saw an orthopedist about left hip pain first in August of 2019, who was concerned about weakness of the hip girdle muscles, especially the hip abductors on that side. She moved on to a second orthopedist and had her total hip replacement without further delay. On examination, when I saw her, reflexes were normal in the upper limbs. Patellar reflex, absent on the right, normal on the left. Achilles absent bilaterally. Right hip range of motion and strength were normal. Left hip range of motion was limited. There was some tenderness. There was significant weakness of hip abduction and also some weakness of the left hamstrings and ankle dorsiflexors. Her first EMG was in 2011, where she was having some walking problems, and this was part of the evaluation about her Parkinsonism. At that time, the amplitude of the left and right several nerves were symmetrical, but considered abnormally small in the EMG lab where she was studied. When I look back at the report, I was concerned about an asymmetry of the perineal motor nerve conduction studies with a 40 to 50% loss of amplitude on the left side, where I was now seeing ankle dorsiflexor weakness. I thought that might be significant. Although at the time, since it fell in the normal range, it wasn't commented on. The F-wave studies were all normal in 2011. There were abnormalities in the right extensor dige brevis muscle on the foot in 2011. The findings at that time were reduced amplitude sensory nerve action potentials distally, normal motor studies, normal upper limb sensory and motor studies. The needle EMG was said to be of uncertain significance, and the finding was of length-dependent sensory-only neuropathy. MRI in 2013 showed disc extrusion and lumbar stenosis, and they proceeded to that 2014 decompression that I mentioned. It was an additional EMG early in 2020 that found the distal serosensory responses to be normal. The bilateral perineal motor studies to have small amplitudes and reduced conduction velocity. Bilateral tibial nerve studies were normal, including the F-waves, and the electromyographer was unable to find EMG activity in the tensor fasciae latae on the left. Determined there were end motor unit changes, amplitude increases, and polyphasicity in the quads and adductors on the right. So they concluded a right L3-4 radiculopathy that was chronic, and bilateral focal-fibular neuropathies near the knee. This was the end of my presentation. I hope you enjoyed it. F-waves, right, tibial F-waves. A little bit complex, but it seems appropriate. When I looked at their perineal F-wave, I had difficulty determining how they actually figured the latency here because it seemed too noisy for me to have been able to mark it if it had been my own study. These were the amplitudes. We had 1.4 left perineal motor, so not dissimilar from what was seen in the first study. And one thing to keep in mind about the amplitude of a motor study, since Dr. Williams just talked about recovery of motor studies, there's going to be distal sprouting re-innervation in a chronic study. If you lose a significant amount of motor amplitude, you've lost a greater proportion of the motor axons than just the amplitude difference you're looking at. And let me clarify that this is my EMG study later in 2020. And the left perineal motor amplitude, the left sural sensory amplitude, 2.3 microvolts in a 68-year-old with an edematous angle. I was happy to record it and find a consistent response, so I considered it pretty normal. Comparing my F-wave in the tibial nerve, 57, to the previous one, or the one 10 years previously at 59, so no significant change there. The waveforms, the perineal motor was somewhat prolonged in duration as well as reduced in amplitude compared to the tibial motor. And you see the sural sensory had a normal duration and the tibial F-wave responses look pretty good. Needle EMG study, I found abnormalities on the left significant with chronic changes, no fibs or positive waves were seen, but motor units reduced and polyphasics increased durations, increased amplitudes in the tibialis anterior, biceps femoris, gluteus medius, and tensor fasciae latae. Although there was a small, it was difficult to find muscle tissue in either of those muscles, especially the gluteus medius. The tensor fasciae latae appeared to have some perhaps compensatory hypertrophy. My conclusions in this abnormal study were a significant left L5 radiculopathy and findings that did not suggest peripheral polyneuropathy to me, either motor or sensory, and minimal residual findings on the right of previous radiculopathy as well. The eight abnormalities I determined were combined effects of these left L5 and probably some S1 radiculopathies from the lumbar stenosis. The weak hamstrings resulted in poor trunk control, affecting hip extension, therefore the ability to hold the trunk upright. And then the weak gluteus medius causing the body to go to the right. She didn't have enough activity in the hip extensors or abductors in order to get her trunk over the left hip like a normal compensated Trendelenburg gait would produce. And of course, the whole pattern was aggravated by her previous gait patterns of hip pain and then the replacement and the hip replacement surgery. The caution here, as the first orthopedic surgeon noted, you got to be careful about replacing a hip when the gluteal muscles are weak. Conclusions and advice for electromyographers everywhere. You should think about radiculopathy rather than peripheral neuropathy when you have asymmetric compound muscle action potential amplitudes in the feet. You should not be thinking peripheral neuropathy when you can record a decent sensory response at an age over 60 years. You shouldn't be thinking peripheral neuropathy when the F waves are normal. And you should watch out for asymmetric needle EMG findings as a clue for radiculopathy. And far as future practice guidelines suggestion, and these are mostly already practice guidelines. It's always a good idea to compare EMG abnormalities for symmetry, since symmetry versus asymmetry is a key to many diagnoses. And don't discard findings as error when they just don't fit. I believe that the first EMG was guilty of confirmation bias in neglecting to consider the absent right knee-jerk reflex or the motor unit potential changes in the left or right extensor digitorum brevis. They simply didn't explain them, and they left with a sensory-only neuropathy, which is a relatively rare condition. And we all know to think horses rather than zebras when we're coming to our diagnoses. And then be aware that the distal effects while airing degeneration following an L5 radiculopathy will look like perineal motor neuropathy because most of the EDB is innervated by the L5 root, and the findings are going to be there from a motor standpoint. Thank you for your attention. Hope you enjoy all of the PM&R Assembly in 2021 and have a wonderful time tomorrow, especially on Physiatry Day. Please feel free to send me your questions, or if we have time, we'll discuss them later. Thank you. Now we'll transfer the microphone to Dr. Insrud. Great. Thanks, Bill. Well, I'm going to be, I guess, batting clean up here. Thanks for all the great talks. My talk is going to transfer nicely over from Bill's because I am going to talk about a case that the unique findings here were really found in the EDB, and I have no disclosures. I hope everybody is in no disclosures. I hope everybody is enjoying a beautiful fall after moving back to the Midwest this year. After many years in the Pacific Northwest, I realized how much I missed the fall, and it's just been a spectacular one this year. So what are we doing here? Again, we're working on designing an EMG study, interpreting the EMG results. Can we say anything about prognosis based on the EMG? We may or may not. And then we want to try and provide for our patients some meaningful recommendations on management. And just to remember that whenever possible, we want to do this following a focused history and exam. Some people add consults onto EMGs, which is a great strategy. If not, to try and do a focused brief history and very brief focused exam before we start shocking people and putting needles in them. So this patient, the reason for consultation was a history of a fall and a right radius fracture, and they were referred for question of weakness and ataxia. This is a 74-year-old female who's had multiple falls over about the past decade due to balance problems. And two weeks ago, she was climbing stairs, fell backwards, fractured her right radius, which was casted. She didn't have any change in level of consciousness with the fall or loss of consciousness subsequent to the fall, but she did hit her head. She denies any numbness. At 74, she continues to be a very active harpist and piano teacher. And her spouse notes that she cruises a lot to walk around the house. She supports herself on furniture when she's walking around the house. However, she denied any weakness. She does have a history of breast cancer about a decade ago and was treated with cisplatinum and Taxol. And at that time, she had some hand numbness and was given the diagnosis of peripheral neuropathy from hand numbness, and that resolved. And like I said, she's still a very avid harp performer. If I could find where I packed my CD player, I'd play the CD that she gave me. But she says she's having some mild difficulty with harp pedals. They press on pedals to change the tension of the strings to go from flat to sharp and so on. But she kind of brushes that off and says that she's 74 and just taking some Norco for the pain from the radius fracture. So the examination, and this is always, even though I like EMG, I would say I've had to pick a favorite part of assessing a patient. The exam is where some of the most meaningful findings are found. So her mental status is within normal limits. And just something I noticed this year, I used to do attention by asking people who were the past presidents were, and that just raises so many comments on either side that I don't bother. It's kind of sad, but the cranial nerves are normal. And then taking a look at the bulk, she has quite a bit of atrophy in the distal lower extremities, both anterior and posteriorly. But I always look at the EDB and she has great bulk in the EDB. If you look at the right there, the EDB, there's a real easy metric you can do on exam. And when the muscle is contracted, it should be equal to or greater than the size of half of the green grape. And I was about to say seedless grape, but I see the seed in that picture. So I'm going to back off of that. But at that size, if you can feel that it's half of a green grape, you're going to see on your perineal to EDB motor study, it's going to be greater than two millivolts almost always, which is the lower limit of normal in most labs. And as Bill was saying, it's highly L5. So that's a great metric for asymmetry, say if a patient has some low back pain radiating down into the leg and you see an asymmetry with a smaller EDB on that side and a normal bulk on the asymptomatic side, that's a great clue that you could be looking at an L5 radiculopathy. You could also see atrophy there with the perineal neuropathy. And we know that some people don't have EDBs and they often atrophy bilaterally due to external pressure, but just you can learn a lot from the EDB. So she's got no fasciculations and reported some mild decreased light touch and pinprick in the distal legs on exam. Her vibratory sense was normal and her reflexes were absent at the ankle, but normal elsewhere. So here's her motor exam and her neck extension is normal. You can see that her upper extremities are normal. And then in the lower extremities, proximal hip flexion, abduction, adduction, knee extension and flexion. She really has great strength, but when you go distal to the knee, we encountered that she has pretty profound decreased strength. Ankle dorsiflexion was four minus and foot inversion was four minus. Always check that to make sure to look for whether we're seeing a perineal neuropathy at the fibular head. And then manual ankle plantar flexion. I like to text plantar flexion because it's the only muscle in the body that you can lift. Many people, if not most, can lift their whole body weight several times with one unilateral ankle plantar flexor. But if I'm checking it manually, I don't use the MRC squares. I feel like that doesn't correlate well with such a strong muscle. And so I just say, I can't break it with manual force, can break it with mild manual force, moderate manual force or maximum manual force. And so this is quite profound decreased muscle force here that it's breakable with mild manual force on both sides. So how do we design this study? So she has a leg problem. So we're going to look at the tibial motor studies and our standard perineal to EDB and sensory studies. I'm going to look at the searls and plan to look at those bilaterally. And again, kind of along the lines of what Bill was saying, I'd never want to over-interpret a low or abnormal searl. You know, it's very small potential that can be really affected by lower extremity edema or a connective tissue. So I certainly, unless it's going to be real high on one side, would always check both sides and then the upper extremities, why or why not? So these are just things to think about. I don't know if there's a right answer. She didn't have any symptoms in the upper extremities. She didn't have anything on exam, but I was concerned about a more diffuse process. So we did look at an arm as well. And then things to think about in this patient, and this wasn't a, you know, a super time-consuming exam, a quick focused exam, but the EDB bulk was very robust, but the distal lower extremities, including the tibans, were atrophic. So that's kind of unusual, isn't it? So we decided to add the perineal to tibialis anterior motor studies. Why or why not? So why would be to see if we have a slowing across the fibular head to see if the amplitudes are really low to the tibialis anterior. I've always hoped that I'd be able to pull something out of doing this study along with the study to the EDB, kind of along the lines of that. There's a great Larry Robinson paper that looked at how people did after ulnar nerve decompression at the elbow, and actually the slowing across the elbow on the ulnar motor study to the FDI was the best predictor, better than to the ADM. And I've never been able to assess anything out of that, but in this case, I thought we should do those. And is there any point of doing the superficial perineal sensory? Well, why or why not? I would, in this case, say why because she's 74 years old and there's going to be absolutely no negative predictive value of this test. So we elected to do the perineal motor studies to the tibialis anterior, but not do the superficial perineal sensories. And I'm not here to tell you there's a right way or a wrong way, but the important thing to do is to think about it. And so the NCS results, and we kept her warm for the test. Fortunately, this study was done in August, so it was very hot in the room. So the tibial motor studies, you can see we've got good latencies. We've got low amplitudes. I will use two as the lower limit of normal for a tibial amplitude and microvolts. And this is below that, although the conduction velocities are good. One side is 41, but that's not screaming demyelinating, particularly with a low amplitude. And then we did the perineal to EDB studies. And if you look at these, the latencies are good, but look at those amplitudes, 3.8 and 3.2 in a 74-year-old. Those are very good amplitudes. Usually labs use 2.0 as the lower limit of normal. And she's got a drop on the right there across the fibular head of 15 and does not have one on the left. So we look like we've got some slowing on the right across the fibular head, but not at the left, but great amplitudes. So then we added on the perineal tibialis anterior study. And I'd be cautious about having two set of an amplitude for this muscle, the tibialis anterior, kind of similar to the deltoid. But in general, if it's less than three or four millivolts, I would start thinking that there could be some axonal loss or atrophy of the muscle. And certainly at 0.9 and 1.6, those are quite low. So we've got this disconnect to the tibialis anterior that we didn't see to the EDV. Again, we've got slowing across the fibular head on the right at 38, but normal on the left. And then the serosensory studies were great for a 74-year-old. Remember the great paper by Ginny Tavis that looked at asymptomatic patients in that age range and found that the paper of that, the conclusion of that paper was that you really can't say anything from age 75 and above as to the absence of serosensories as to whether there's a neuropathy. So that certainly starts before then. It's not certainly at 75 you drop off a cliff. So these are great amplitudes. And the upper extremities she had left CTS, but otherwise her motor and sensory were normal. So then needle EMG results. I just pulled out part of them, but you can see that more distantly in the leg, we've got a lot of decreased recruitment, decreased or increased amplitude and increased duration. Just a trace of fibs in the left tibialis anterior, but otherwise not a lot of insertional activity. So how can we interpret this? It doesn't look like a neuropathy on NCS because the EDB was normal, but tibialis anterior and tibial motor had reduced amplitudes and the serosensories were normal. The needle EMG, however, appears neurogenic marked reinnervation. So this is something I wanted to highlight that don't forget that if you lose a lot of muscle fibers in a motor unit from a dystrophic process, the remaining motor units fire faster and look longer from marked fiber splitting. You can also see this as inclusion body myositis. So could this be a dystrophy? And then not to forget the focal neuropathies that were kind of incidentally found here. So can we say anything about prognosis? Well, sometimes we can't say a lot. That's a tough one here, but there's not much active ongoing denervation. So it implies there's not an active rapidly progressive process. She's had slow progression, but she's got a long history of falls worsening and she had a fracture from the last fall. Unfortunately, it wasn't a hip fracture, which would have been more problematic than the radius fracture. So can we provide some meaningful recommendations here? Well, how about a further workup of weakness? And now we can do free genetic testing. So the muscular dystrophy panel was sent on her. We thought about sending the comprehensive neuropathies panel because it just seemed a little unusual. If her EDBs were low, we would have thought she had CMT perhaps. We checked a CK. It was normal. MRI can be very helpful in muscle problems. That was not done. Didn't want to forget about the CTS because remember she's a harpist. She used her hands, started her with a splint, talked with her about possible release. And then it turned out she, like many people, crosses her legs at the knees and usually the right over the left and talked with her about stopping doing that. So frequent falls. And one thing I'll just say about crossing the knees really quickly is I'm still learning a lot and I'm sure I'll continue as long as I'm practicing. But I finally found a way to get people to stop doing that. As you tell their spouse or someone they live with to determine a monetary amount that they'll have to pay them every time they point out that they're crossing their legs that way, like the grandkids or something. And it's so irritating that the irritation is a lot more motivating for the patient. So importantly, frequent falls for ankle plantar flexion weakness is a lot more destabilizing the ankle dorsiflexion weakness. So in this case, consider ground reaction force, AFOs that are graphite and carbon fiber. They have a really high acceptance and benefit. This is a great paper from 2017 looking at a large number of patients with neuromuscular disease using these. And they found that 89% of the neuromuscular patients were very happy with these off-the-shelf graphite AFOs. They're inexpensive, about a sixth of the cost of a custom molded. They provide very importantly to a greater extent than a plastic AFO ankle plantar flexion support. And very importantly, most insurances pay for an AFO once every five years. They adapt to further atrophy as the Velcro straps can be adjusted, whereas you're not maintained on that particular posterior curve like you are with the molded plastic AFO. So follow up on that testing, the neuropathy panel is negative. The muscle panel showed a variant of unknown significance. And you know, if anything, these genetic tests, while we're using them more, we're all variants of unknown significance. But we have to look at them and see, is this one that could be meaningful? So it's in the sarcoglycan delta gene. And this is associated, you want to make sure you read everything, not just the first page if you get these. This is associated with autosomal recessive LGMBR4. Used to be called 2F. Why did they change it? Because as we're doing more genetic testing, we're discovering that there's more than 26, for example, recessive limb-girdle muscular dystrophies. And it used to be that one was dominant and two was recessive. And then the letters signify the different types. That's been flipped around. So the first one means dominant, two means recessive. And then we can use this, or excuse me, D is dominant now, R is recessive. And then we can use as many numbers as needed as more are discovered. But it's also associated with autosomal dominant dilated cardiomyopathy. So quickly, how to pursue this? Start with the web. And you know, this doesn't take much time. Honestly, in this patient, it took maybe five minutes to look up SGCD and discover that it includes the sarcolemma transmembrane glycoprotein. It's one of four psychoglarkin proteins that are highly expressed in cardiac and skeletal muscle. And they associate at the membrane. If you look at that picture below there, they're the bright red things that are right on the plasma membrane. The blue is extracellular and the tan is intracellular. So that's the dystrophin associated glycoprotein complex. And it's what creates the structure and the muscle. So when you have an abnormality, you get a muscular dystrophy. And then quickly found that in a group of 52 patients, there was a novel mutation found in two patients who presented with a relatively mild dilated cardiomyopathy and late onset. So could this be a new positive mutation? So what do we do based on learning this? We refer her for a cardiology evaluation, and then we consider a muscle biopsy with sarcoglycan staining with immunofluorescent. And you can see on the right there, these proteins are along the cell membrane. So if they're present, they'll immunofluoresce. Like this is a normal biopsy there. So the follow-up, she was given the diagnosis of possible sarcoglycanopathy. We don't know that. And you could differ as to whether you want to say possible or probable. She got bilateral ground reaction force AFOs with custom molded footbeds. Those can be very helpful making those comfortable. And you're going to max out with the two of those right around $1,000 versus $6,000 per say molded fiberglass AFOs. She's very happy with them, much more stable. She's now got a rollator walker that she uses outside the home. She's thinking about a muscle biopsy. She's not sure she wants one. That's up to her. We're not there to get her to do something. We're just there to inform her. CARDS evaluation is pleasant, pending. And most importantly, as we see on the right here, she's back actively playing the harp, going to her different functions and not falling. So we don't know exactly what she has. We have an idea, but as physiatrists, we were able to help. Thank you. There's one question for you, Eric. Yep. It says, what about nerve conductions and EMGs? What leads you to worry about an S1 and the TA? So not worried about an S1. She doesn't have any radiate. She doesn't have low back pain or pain radiating down the leg. So was not concerned about yet. I believe that we are out of time. Happy Veterans Day. Enjoy the session. There's contact information. It should be online if you want to reach out to Dr. Williams, Dr. Pease, Dr. Ensard, or certainly myself. It looks like there's one other question. Let me see. Second presentation. This goes to Farron. Bicep weakness with posterior cord injury. You often may see some other muscles affected with, because she had prolonged retraction during surgery and most likely some additional swelling or bleeding. And if you looked at that one schematic of where the posterior cord might be involved, you see that some of the fibers that go involved, you see that some of the fibers that go to the musculocutaneous are in that same vicinity. So we don't always see lesions that are completely localizable to only one segment of the cord. We often have a few other changes and that did resolve much more quickly than her deltoid problems and the problems with her other bradial innervated muscles. I'm always impressed, Farron, with your ability to have somebody come back multiple times for studies. Sometimes it works and sometimes we're too excited about doing that. Maybe one last question here. Dr. Williams, was there consideration of MRI of the plexus to look for iatrogenic hematoma from scalene block? That was not done and I'm not sure how it would help with the management of the patient. But I do think that everyone talks about the problem being from the surgery or an inflammatory neuritis, but that we are seeing maybe some of these neurological problems following different types of blocks. And now more and more of them are being used just for pain management, like with joint replacements or whatever. I think you need to look at what type of block did anesthesia do and could that contribute to the problem. But I'm not sure how much, unless she had persistent symptoms, how much more the MRI would help you because she was seen regularly by the surgeon. Yeah. Well, thank you again, everyone. We appreciate, well, it's always a thrill to be with my friends, even virtually. So thanks so much for your time. Have a great meeting and we'll see you in Baltimore.

EMG studies

carpal tunnel syndrome

needle EMG test

right shoulder reverse arthroplasty

radial motor amplitude

radial sensory nerve

abnormalities in muscles

right radius fracture

tibialis anterior

workup