Sorry for a few minutes of delay, so we won't have any question and answer today, I'm just kidding. We have got a great session, I mean, on, we've got two excellent speakers, co-speakers, and Dr. Sridhar and, Professor Sridhar and Professor Williams, we're going to be presenting on PM&R investigations, which you can do in the office if you're doing EMGs, and how you can use ultrasound with it and correlate with the conditions. So Professor Sridhar, he's the Director of Electrodiagnostic Center at Moss Rehab, he's Professor of Clinical Rehabilitation Medicine, he is and was my mentor when we were at Moss sometime back in Philadelphia, he's also a gifted teacher, he's taught all over the world and also he's part of the AANEM lectures and DVDs and videos, you'll come across them. And we have Professor Williams, who's a clinical professor at UMass Medical School in Worcester, that was one of the schools I did my fellowship earlier, and she's also a great teacher and we have been co-speakers at multiple conferences, and she is also a teacher at the AANEM. I'm myself, Amit Bhargav, I'm Medical Director at Advanced Interventional Pain and Sports Medicine Center in Baltimore region, and I usually put some of the sessions for a long time and this has been kind of bringing the two investigations we have in our field together and putting them how we can use it in the office. So welcome for the session and please silence your cell phones. For all sessions, the audio recording is taking place within this room and would request you to fill in the evaluation forms as they will help for the future planning if you want some more sessions like this. And please visit the pavilion where there are other things which you can learn. Good morning. I don't have any disclosures for this talk. What I want to talk about is the electrodiagnostic evaluation of peroneal neuropathy. Now, peroneal neuropathy, you think about is basically what you're thinking about is foot drop. In the foot drop, you have a lot of different considerations. We'll talk about some of those in a bit. So what I want to do is I want to present a case to you. And then we'll talk about how we can differentiate between different causes for foot drop. And then you can think about what kind of study you want to do as a clinician in the office. Here's a patient who is a 54-year-old male with right lower limb weakness and numbness for four months. He has radicular pain for maybe 15, 20 years and had spinal stenosis, spinal cord stimulator, two years ago. Good relief of pain. However, about 18 months ago, he started having some new ankle weakness. And in the past month, right foot drop, multiple falls. He had 90-pound weight loss with a sleeve gastrectomy, valgus deformity of the right knee. The weakness is in the right peroneal distribution. No atrophy. He had decreased light touch sensation in superficial peroneal nerve distribution. There was hypertrophy of the right peroneal nerve over the fibular neck. So here is the nerve conduction studies. One of the considerations I want to bring in when you're talking about nerve conduction study is majority of the times in a lot of the laboratories, you do the recording from the EDB. However, what we are trying to evaluate is a foot drop, not necessarily toe drop. EDB tells you about toe drop, not about the foot drop. So you want to really do the recording over the tibialis anterior, because that is the target muscle. And that would help you to assess what's happening with the peroneal nerve function of the ankle dorsiflexion function. So here you see the left side, the common peroneal nerve conduction to tibialis anterior. The latency was normal, and the compound muscle action potential amplitude was pretty similar, both proximally and distally, with a good conduction velocity. On the right side, what you notice is you have the compound muscle action potential distal to the fibular head is pretty similar to, or even probably a little bit better than the left side. And then proximally, it decreased by almost 90%, significantly small, with a conduction velocity which was very, very, very slow. Now, when you look at conduction velocity in a situation like this, we have to be very careful. Is that due to demyelination? Or is it because you are not recording from the same fibers, both distally and proximally? And so we'll talk about that in a second. And the superficial peroneal nerve was pretty good, good amplitude and conduction velocity. And the right tibial nerve was evaluated. CMAP amplitude was somewhat small. Conduction velocity was OK. So remember, this guy has also spinal stenosis. Here are the needle EMG findings. So there was small fibrillations and positive waves in the tibialis anterior and peroneus longus, with moderate to severe decrease in recruitment. And the multi-unit potential characteristics, however, were normal. There was no needle abnormalities in gastrocnemius, vastus medialis, and tensile fasciae latae. So there are a few considerations I want you to think about here. The size of the fibrillations and positive shock waves. Why would there be small fibrillations and positive shock waves? Remember, the fibrillations and positive waves are really directly related to their muscle fiber potentials. So the size of them would be related to the size of the muscle fibers itself. When you have chronic pathology, when there is atrophy, then the fibrillations and positive waves becomes much smaller. And I think that's a good way to think about old versus new. However, you have to be certain that you're close enough to the muscle fiber. If you move away from the muscle fiber, you'll have somewhat smaller amplitude. But when you're looking at generally what's happening when you move with multiple areas, all of them are small. Slightly, they're going to be small. That talks to you about the chronicity of the pathology. What's interesting is with all of that said and done, the motor unit potential here, the characteristics were normal. There was no polyphasicity. There was no large or wide units. So let's think about causes of the foot drop. You could see foot drop in upper motor neuron pathologies and then a lot of lower motor neuron pathologies, right? So you have anti-Hahn cell disease, lumbo-alpha radiculopathy, lumbo-sacral plexopathy, sciatic neuropathy, peroneal neuropathy, and disorders of neuromuscular junction and diseases of the muscles. So you can see it in the foot drop. You can see it in the diseases of the muscles. So you can see it in every one of them. So what electrodiagnostic study will help you is to kind of differentiate between all of these things, right? And that's the key thing which you want to think about. Say if CMAP amplitude of the peroneal nerve you're looking at in the foot drop, think about the amplitude for axon loss. If you're comparing to the opposite side, and if it is smaller, then you have to think about an axon loss lesion or muscle fiber loss. And that's a very important thing. And then you see in anti-Hahn cell disease, lumbo-sacral plexus lesions, radiculopathies, sciatic neuropathy, and peroneal neuropathy with axon loss are disorders of the neuromuscular junction or muscle fiber loss. You'll have smaller amplitude, right? So it tells you about axon loss, the amplitude. Now, when you look at the amplitude which is normal compared to the opposite side, you can think about upper motor neuron lesion or conduction block lesion at the root level, sciatic nerve or peroneal nerve. If you have foot drop and you have normal amplitude, then you've got to think about either one way or the other, right? And same thing with the snap amplitude. So if you have normal amplitude compared to the opposite side, you think about a pre-ganglionic lesion, which could be upper motor neuron lesion, root level, anti-Hahn cell disease, or conduction block lesion at the peroneal nerve or the sciatic, and disorders of the neuromuscular junction or the muscle. When it's decreased compared to the opposite side, it has to be a post-ganglionic lesion, decreased, or peripheral neuropathy could do that as well. When you're doing these studies, when you see tibialis anterior is abnormal, so what do you want to do next? So you want to kind of differentiate between what are the pathologies you're going to see here, right? So check for tibialis posterior. If that is abnormal, it could be a root plexus pathology or sciatic pathology. If it is a conduction block lesion or a peroneal neuropathy, there would be no abnormality in the tibialis posterior. Check, make sure that peroneus longus is normal. That differentiate between deep peroneal and superficial peroneal neuropathies. But it would be abnormal in common peroneal neuropathy. Looking at proximal muscles, which is a non-sciatic muscle, gluteus medius, for instance, a fascia, that would be abnormal in proximal lesions, L5, lumbosacral plexus. But it's normal in common peroneal neuropathy or sciatic neuropathy, right? So basically, what you're thinking about is you're thinking about the anatomy of the plexus anatomy of the sciatic nerve. And majority of the times, you have to think about doing, most of the time, if tibialis anterior is abnormal, you want to think about looking at a non-sciatic innervated muscle to help diagnose an L5 radiculopathy or plexopathy. And paraspinals, of course, are going to be abnormal in a radiculopathy, but normal in lumbosacral plexopathy. So you're gradually going from a distal muscle to a proximal muscle. So one of the ways I always think about is if you're thinking about evaluating for a peripheral neuropathy, you start with the tibialis anterior and go distally to look at the muscles. If you're thinking about a proximal pathology, you start at tibialis anterior and look at proximal, right? And so that's the key thing. The tibialis posterior is a good muscle because it's at about the same level as the tibialis anterior. And because it's at the same level, what would happen is it would be abnormal in patients with sciatic neuropathy or peripheral neuropathy, right? So that would be a good muscle to check in that situation. So if every muscle is abnormal, what you have checked. Now we have to think about looking at opposite side and proximal muscles and keep going higher up to make sure that there is no anti-Hansel disease. So let's go to the next thing, which we want to think about, which is a difficult thing in a lot of the situations to do a conduction study. What I'll do is I'll present a case, and then I will show you how I do the study of the lateral femoral cutaneous nerve. It's from a DVD, which I helped produce for the AA and EM. So here is a patient who is a 52-year-old, right lower limb pain and tingling for one year. Now he had syncope one year ago. And I don't know what the relevance of that is, but I just put it in there. Low back pain for 10 years with bulging discs, no ball or bladder incontinence, post-medical history of diabetes, anxiety, and chronic low back pain. Truck driver, normal gait, no muscle atrophy. He had decreased light touch sensation in the superficial peroneal nerve distribution and lateral femoral cutaneous nerve distribution. His stretch reflexes were symmetric with normal strength in the lower limb. So here is the recording from the lateral femoral cutaneous nerve and superficial peroneal nerve. So one of the things you notice is I always do two recordings of the same thing to make certain that what you're getting is really the response what you're looking at, right? If you don't do that, you are not certain, right? And you do two of them, superimpose them, make certain that they're similar, and that actually makes it better for your recording purposes, right? So the facet is the superficial peroneal nerve, and then you have the lateral femoral cutaneous nerve responses. The last one is from the opposite side, and the third one is a recording from the side where he had involvement. And the sural nerve was also there, right? So if you look at the conduction studies, the right lateral femoral cutaneous nerve had latency which was longer, 2.8 compared to the left side. And then the snap amplitude was almost 60%, 70% less than the opposite side, 14.5 on one side and 4.3 on the other side. Superficial peroneal nerve, sural nerve were pretty good, and there was no problem with the tibial peroneal nerves. So nearly empty findings, a few polyphasics, some large and wide units in the distal muscles. I think that's due to diabetes. Other muscle studies in the right and left lower limb were normal. So here is the technique which I use. The lateral femoral cutaneous nerve is a nerve which runs right next to the anterior superior iliac spine. The way to record it is by identifying the anterior superior iliac spine and an area 14 centimeter distal to the anterior superior iliac spine in a line which runs from the anterior superior iliac spine to the lateral patella. And once that area is marked, you can stimulate the nerve at that area to localize the nerve. And as the stimulation is increased, and you ask the patient about the spread of the stimulus, and now the patient is feeling the spread of the stimulus, and so we know exactly where the nerve is. And the needle electrode is placed in the area of the nerve. The needle electrodes are basically anodized needle electrode which has a larger area of recording, which has a flatter surface. And the needle electrode is placed perpendicular to the nerve right near it rather than in it. And the reference electrode has a larger area than the recording electrode to obtain the response and to decrease the resistance. Now the needles are in place for recording from the lateral femoral cutaneous nerve. These are sensory needle electrodes which are ionized needles. And the recording electrode and the reference electrode are placed under the skin with the ground in the medial thigh. And the stimulation is done just medial to the anterior superior iliac spine. 14 centimeters distally is the recording electrodes. Now the stimulation starts, and it's gradually increased to obtain a sensory response. And as we increase the stimulus, around 18 or 20 milliamp stimulation, we are getting a sensory response. And that's a very reasonable response. And we should actually average it such that we know that the response is stable. And then we can use another average response to superimpose to obtain definite response. And then we can measure the latencies and amplitudes. And if they're superimposed, they are exactly the same responses. And the latency is 2.05 millisecond with an amplitude of 5 microvolts. And the response is a very clean response with a conduction velocity which should be 68.3 milliseconds. And we can measure the meters per second at 14 centimeters distance. This technique is useful in patients who have myralgia parasitica, that is the burning sensation in the lateral part of the thigh. It is technically somewhat challenging stimulation. Usually with needle stimulation and needle recording. However, in this situation, we are able to obtain it with surface stimulation and needle recording. Use of needle recording usually makes the responses much better and cleaner than the surface recording. So one of the points I want to make is this. I don't do needle recording all the time. I stimulate the lateral thigh so that way I can localize the nerve. You can go anterior or posteriorly and ask the patient, you know. The lateral femoral cutaneous nerve is a nerve which. OK. So I use the surface recording and surface stimulation sometimes. Sometimes I go with needle stimulation because the nerve is deeper there, right under the inguinal ligament. And record surface. So that would help for you to kind of differentiate. We can talk about the technique a little bit later, I think, if there is any questions about it at all. Thank you. Thank you, Professor Shridhar. So we kind of decided on covering two nerves. So if we can, instead of putting all the nerves and trying to give everything together. Sorry about the technical glitch there. So I'm going to cover the two nerves for the lower limb first. And then once we do the upper limb, we'll cover those. I have no disclosures. And most of the research is on median nerves. So we'll be covering a lot of median nerve when we get to it. It's a focus of ultrasound for focal neuropathies if you're looking at them. Electrodiagnostic testing is the gold standard. And it cannot provide the anatomical information. So you can see the nerve gets pinched at a place, and it swells proximally to it. So that's the short axis and the long axis. The short axis is on the top. And you'll find this kind of images all along. So you can see where the probe is placed and how we are looking at that. So for myralgia parasitica, its origin is dorsal divisions of L2 and 3 nerve from lumbar plexus. It courses medial to the anteosopial iliac spine. And when it comes into this, it passes through, or it most of the time under it. But it may pass through the ilioinguinal ligament. And it gives the sensory supply to the ante and lateral aspect of the thigh. It's lying between the sartorius and tensor facialata. It's a very small nerve, very difficult to see if it's a normal nerve. And that's why you see Dr. Sridhar mentioned using needle electrodes. So if you're trying to find it, it's very difficult to see as a small nerve. And if it's affected by any condition, then it becomes a little swollen and larger as we talked about in entrapment neuropathy. So here you can see that there's a bone spur sticking into the nerve and the fascicles. It's very clearly seen. And so the study in this study had 28 patients. And what they concluded was in the myralgia parasthetica, the distance between the anteosopial iliac spine and the nerve was around 0.5 centimeters. That's a half a centimeter distance in patients with myralgia parasthetica, whereas control patients had over 1 and 1 half centimeters distance. So the closer it was, it was affecting the nerve. For injection, if you're doing the injection and that's a position, you can come from lateral to medial side. And you're unlikely to find any vital structures. If you see a femoral artery or vein in your path, you're way off, of course. So it's simple. You can put the needle under the nerve and inject it. When you're doing ultrasound, it may be easier to look at the nerve distally and then move proximally instead of start trying to find it exactly at that spot. So that may be one of the pulls which I learned. For common peroneal nerve, the anatomy, it comes posteriorly and it crosses over the neck of fibula. So it's very close to the neck of fibula. If you see here, the distance between, if this is about a centimeter, the distance between the nerve and the neck of fibula is about a millimeter or two millimeters. So any change in that anatomy can ding that nerve. That was a technical term, ding. And it's easier for me to see the nerve when you move the probe. So you can see the move probe instead of just putting the probe at one place. Then you can see how it goes across. So first patient, it's a 44-year-old male with a fracture of right tibia fibula. This was a twisting injury, so it fractured the tibia distally and the fibula proximally. And they fixed it by intermediary rod. Patient had weakness of the right great toe, numbness. And so there was decreased sensation on the toe with ankle dorsiflexion and EHL weakness. On the EMG, there was no response on the EDB. There was no sensory response. And there were denervation potentials in the tibialis ante and extensor hallucinus longus. So usually, I don't diagnose nonunion by ultrasound. But when a patient was there, so we just looked at that. So you can see the breaks in the bone still persisting. And on the right image, there's the reverberation effect of the screws. So you can see the screws for the rod. But the fracture site is right there. But when you looked at the fibula at the same time, so the fibula had united. But you can see the callus across. And the nerve was coming proximally. And it was right in the path. The callus was right in the path. So that's one of the ways to look at it. And you can tell the surgeon that this is the spot where you can look at it and if they want to consider the EMG and the ultrasound findings together. The second patient was 64 years old with a left foot drop, burning sensation in the toes. One day, he got up in the morning. And he says, I can't put on the socks because the foot doesn't come up when you're trying to put on the socks. And he had a foot drop. So he had decreased sensation on the foot and also muscle weakness of the ankle dorsiflexion and EHL. The EM nerve conduction studies was no amplitude there. But also, the patient had some delayed latency and conduction velocity with denervation potentials. So the patient already had an MRI before that. So that's the images of the MRI on the left. And one can see that's a fluid or cyst area, which is along the neck of fibula, right going close to the fibula. And it was originating from the superior tibiofibular joint. So it slowly, slowly grew till it came across and put pressure on the nerve. And one can see the nerve in this area here. And when you move the probe down distally, you can see that the fluid is pushing on the nerve and causing that. So the surgeons took that out. But he had a recurrence of that cyst later. Now, if you think, no, I'm going to take that fluid out with a needle, OK? So there are two things. First of all, make sure it's not an intraneural ganglion. The other thing is you want to know where the nerve is. And one more point I'll add is that the fluid in that is almost like Jell-O, OK? So if you try taking out Jell-O with a needle, you know, it better be a very big needle. And patient was not going to stay there seeing the needle. So it's like a Jell-O. So it's difficult to take this out. I mean, if you want to attempt it, there's reason not to do surgery or something, maybe attempt. But this is not to take out with a needle. And I will end my talk right here. We'll come back to the upper limb. I'll request Professor Williams. Oh, okay. Welcome, everyone. I'm gonna go through this fairly quickly because of time and having time at the end to have Emmett, who was gracious enough to invite me to present, go over some of the ultrasounds. So to start with, we're gonna look at the ulnar nerve. Remember, it has multiple entrapment sites. Anyway, these are the problems that you might detect from. and that was correlated with her physical exam. Mild diabetes, but nothing too significant. But if you look here at her ulnar motor, and I. proximal versus just a Guillen's canal, and you will see the recording on the first, third, and fifth tracings, which is from the ADM, you have a significant drop in her amplitude at the elbow, below the elbow, and above, and the same for the first recording from the first dorsolunar osseous. And that does not happen on the right side, and Dr. Shatara also pointed out the importance of looking at the contralateral side. You can just see in this tabular form how significantly her amplitude changes, and she correspondingly had about a 50% drop in the conduction velocity, but latencies and slowing alone can be problematic because they can be so subject to measurement error. So she had a significant drop, also dorsal cutaneous, as well as ulnar to the little finger, and the dorsal cutaneous is a branch that comes off slightly more proximally. ulnar innervated flexor digitorum profundus. problem, a right-handed 50-year-old male who had some right-handed weakness, and it really occurred pretty much within a day or less after the person had excessively gripped an instrument with his right hand. And he noted weakness, specifically difficulty buttoning and manipulating small objects, and did have the hand intrinsic muscle weakness, thought it was. And if you look here at his ulnar motor. It's going to be a little bit longer, bigger hand. Thank you, Professor Williams. So most of the literature in the published literature for ultrasound for the nerves is on median nerve. But let's finish with the ulnar nerve first. So we looked at the slide earlier with the narrowing of the, at the cubital tunnel and increase in size of the nerve proximally where the compression is. There are various numbers mentioned. This is nine millimeters. There's also a 7.5 square millimeter of the cross-sectional of the nerve at the cubital tunnel as being significant for ulnar nerve pathology. But I think the EMG is the one to go for. One other additional factor is you can look for dislocation of the ulnar nerve. So if you, but make sure your probe is not pressing on the medial epicondyle. So when the patient flexes and extends, you can see that. It's seen in 20% of the asymptomatic individuals and they may have it on both sides. So it by itself, it's not a problem. But if it's, there's a problem clinically and the EMG, then you can mention this in your report. Distally, the Gaens canal, the nerve, ulnar nerve is superficial to the transverse carpal ligament. And you can see the ulnar nerve artery. So the relationship is the ulnar nerve is medial to the artery and pisiform is medial to the nerve. So on ultrasound, when you place the probe across, you can see the ulnar artery, the nerve, and the pisiform bone. And distally, you may go a little distal and this is the hook of hammet. And the ulnar nerve goes just superficial to that. So if there's a problem, especially a fall on outstretched hand and you're looking for that, you can evaluate the nerve distally at that spot. So this is another patient who is 74 years old complaining of numbness in the little finger for three months and had weakness of all fingers on muscle cell. But the finger abduction and adduction was the main one on clinical examination. But clinically, there was no sensory deficit. The EMG showed that patient had slowing of the nerve. There was conduction velocity decreased across the elbow and motor and sensory. And the sensory was also decreased distally with the denervation potentials in first torsional and trotious muscle. So there was a combination of things. But trying to evaluate the nerve, what we looked at on the, this is a normal cross section. So you can see the artery nerve and the vein. And on this patient, the pisiform is on the medial side. The nerve, there's an echoic area which is a ganglion extending to the joint and the artery is distal. So it's, the nerve is getting compressed between the ganglion and the pisiform bone in this patient. And you can't, actually you could not feel the ganglion or see the ganglion clinically. And this was a good find to give to the physician so that this can be released immediately. Moving on to the carpal tunnel, this is the most common entrapment neuropathy. This is more than $2 billion annually. The data was before inflation. So this is carpal tunnel. So in a clinical structure, this is a different, there's an anatomical structure than a cartoon and the ultrasound image is correlation. So you have a transverse carpal ligament, the median nerve passes through it. And you have nine tendons, FBL, superficialis, profundus and the median nerve. And over the scaphoid, flexor capi radialis and the artery, ulnar artery and nerve which is superficial to the transverse carpal ligament. And you can see the ultrasound image, it correlates with the nerve. The nine tendons here, FBL is here, flexor capi radialis, ulnar artery and nerve. So what is the proposition for measurements and what they taught the data? So you have a long axis and the short axis and you have to have a freehand demarcation to measure the cross section instead of using the ellipse. So where do you want to measure? So the nerve usually swells at the site of the compression. So it'll swell at that spot and there are studies which say you measure at just proximal to the tunnel, a little at the quadratus level, at through, within the carpal tunnel and distal to the carpal tunnel. There are various studies on this. One of the studies says you measure both proximally, proximal to the carpal tunnel at the crease and then through the, where the quadratus lumborum upper border is. So that's one of the, and the long axis. So we'll come to this study where they're comparing everything to itself. What are the numbers measured? So this was a systematic review and meta-analysis. They had definite numbers here, mild, moderate, and severe as almost just under 12, under 14, and just under 17. They gave these numbers as having mild, moderate, and severe, but then you come across other studies and say they don't correlate, okay, mild, moderate, and severe with electrodiagnostic study. They don't correlate. So you can be grading based on its severity. This is a comment by Karachi and he does a lot of literature on the nerve measurements. So he said, I mean, it's, in severe and old cases the nerves may, vesicles may reshuffle and they may be smaller than what they were before. Also, they may saw that they were big cross-sectional area in normal patients. So it's kind of muddying the water now and you're getting different numbers. Another study said, you know, they gave a number of 10 square millimeters as a cross-sectional area considering positive. But they also mentioned that if you do a CTS-6 score, which is highly correlated, so that CTS-6 score is considering pain, tingling, numbness, and the symptoms in daytime and nighttime. This was a study guidelines from the neurologist, sorry, excuse me, rheumatologist. I don't think so they do the electrodiagnostic study. So their guidelines says first you do the ultrasound. And if you structure of the nerve, surrounding structures, anatomical variance. And if the patient is not getting better, then you do an electrodiagnostic study and they also have a number of 10 square millimeters. Now, this is the guidelines from the AANEM. They said, it's a great tool to measure and accurately measure the nerve. It may be offered as a diagnostic test. It adds value. So it's not the value, it adds value to the electrodiagnostic study and can be used for screening for structural abnormalities across. And then we had the American Academy of Orthopedic Surgeons. This, I presented this earlier. They had a, on their website, they had 10 square millimeters few years ago. And this is an updated version in which they say there is limited recommendation for ultrasound guidance. But they did mention that if it's more than 12 to 13, they didn't choose one number. But if it's more than 12 to 13, it may be strongly correlated with electrodiagnostic studies and less than eight rules out carpal tunnels. But they said it's a limited recommendation for diagnosing carpal tunnel. And to further muddy the water, this was a study between two countries, the Asian Indians and the Netherlands. And if they looked at the study with the controlling for age, height and weight, there was a significant difference between the two countries, people from two countries. And the conclusion was each lab, we have, you know, in us, for electrodiagnostic study, we have different numbers for taking into consideration male, female, we have, you know, age. So we have different numbers. We take that into consideration when giving the result. Here they are mentioning one number, 10 square millimeters, 11, 12. So, I mean, that it's not going to fit into everybody. So we talked about this presentation before. So this one came out closer study and one measurement was done at the proximal crease, just proximal to the carpal tunnel weights, the nerve was more swollen and then just proximal or at the level of the proximal board of quadratus, pronator quadratus. So you got two numbers of the cross section you also looked at in the long axis. They said if the difference between the two cross section was two square, more than two square millimeters, then it correlated it had a high sensitivity and specificity. So that's what's the number they use in closer study. So I do use this study and when I make a report, but I don't mention carpal tunnel, I just say the nerve is enlarged based on this study. There were other things which they have mentioned if how much it's bulging, the nerve is bulging, is the increased vascularity a notch sign if the nerve is getting pinched somewhere. The correlation with the movement is that nerve adherent to the tendon when it's moving. And obviously we mentioned about the blood flow. Bifid nerve can be seen up to 50% of the patients here. You have bifid nerve and also one can see a persistent median artery. So it'll be a good help to the surgeon to let them know there's a bifid nerve and you may have a persistent median artery if you're doing any surgery. So a few questions arise if you're only doing ultrasound and not doing the nerve conduction studies EMG. First of all, how do we correlate it with the acute denervation, chronic changes or the cervical radiculopathy? How do we account for the structure of everybody? We have endomorphs, mesomorphs, and ectomorphs. We have already used this in sports medicine. How do we use it for our studies? So moving proximally, if you're looking at anti-atrocious nerve and it supplies the FPL. So this is the FPL, that's a passive movement and FDS, FDP here and FDS on the superficial. So you can see the normal FDS with the starry-skied appearance with hypoechoic muscles, which are affected. Now, if you had to put a needle in this, this was Dr. Haig's study for lower limb. So in his study, they said of all the needle insertions, which they put blindly, 10%, almost 10% were in the structure you don't want it to be in. And almost 10% were within five millimeter. Okay, so pretty close. So that means one in, that's about 20%, that's one in five, you're putting a needle close to the thing which you don't want to be in. And with the ultrasound, so it helps out putting a needle if you're putting, so the needle, you're avoiding the nerve and putting it in exactly where the nerve, if FPL, you're trying to put a needle in FPL. One can also look at the muscles just by, so normal starry-sky appearance, hypoechoic. We looked at the previous study and this is FPL tendon. One can see the masses around it. Now, the masses may not be on the nerve itself. There's a distance between the nerve and this is the nerve here, the mass is here. But the mass can push the tendon and the tendon can push the nerve. It's altering the course of the nerve even though not directly. The fluid from the joints, so in the carpal tunnel, if there's some fluid, the fluid is under pressure, it's gonna push on the tendon, which is gonna push on the nerve. This is a bigger, greater amount of fluid which itself may push on the nerve. We didn't cover some of the things, okay? We just covered a couple of other nerves. We can't do an ultrasound. This is a Mulder's sign for Morton's neuroma. And so you can, so that's the ultrasound Mulder's sign. And the other things also in literature for polyneuropathies and this is, I mean, if you're looking for this, the gastrocnemius looks affected and the soleus looks normal, but one can see a fasciculation here. So you can say that the soleus is also affected there. So it's useful to make diagnosis in certain cases. One can look at the structure and the surrounding anatomy. So it's useful as another additional feature by itself. It's not something you should use. I'm not, you can use, but I wouldn't say not to use. But electrodiagnosis, it's a combination of things for certain studies. Those are my references. Thank you. They should be. Question for Dr. Sridhara. I'm curious about the needle recording for the lateral femoral cutaneous nerve. And I'm wondering, given that the distance between the needle and the nerve, as in the recording needle and the nerve, might make a difference for amplitude, how do you handle that with the side-side comparisons? Oh, that's a good question. Generally, you try to go as close as you can to the nerve and maximize the amplitude. So you maximize the amplitude as you're doing the recording, and then look at the opposite side. That's how I try to do it. As I was mentioning, a lot of the times I do surface, basically because of that issue. And I stimulate the nerve in the thigh to localize the nerve. So which makes it actually better, in a sense, because I know now where the nerve is. I can put the recording electrode right on the top of the surface electrode, and then I use a needle stimulation. It's the reverse of what I was showing. But it could be a combination of different things. If I have a 300-pounder, I have to do differently than if I have a young lady who's very thin. So it depends on what my patient is to decide on how I'm going to approach the patient. Got it, thanks so much. Thanks for the presentation, everyone. Thank you. My question's regarding perineal neuropathies at the fibular head. You listed some various causes there. With these newer medications that are leading to more weight loss in people, I've started to notice in people who've had significant weight loss that they're having more perineal neuropathies at the fibular head. And the reasons for that are varied. The traditional thought is they're losing some subcutaneous tissue, and that's exposing the nerve to some more pressure. But there are some metabolic reasons for that that they haven't fully elucidated. And so just your thoughts on that and studies to look into that. So just the weight loss itself, when you lose a lot of the subcutaneous fat, brings the nerve closer to the bone. So the chances of getting compressed are much higher, just like when you do the bariatric surgeries and patients with sudden quick loss of weight. In fact, there have been studies which talk about the causes of perineal neuropathy in the hospital generally is weight loss, right? You know, you lose a lot of weight. The patients are positioned laterally, cause compression of the perineal nerve. So I think that's probably the thing. However, I haven't really come across any literature which would talk about the metabolic causes of the medication itself and causing any kind of neuropathy, which was one of your questions there. You know, I haven't come across anything. Dr. Hearn might have something. Yes, no? I haven't come across anything definitive. I've come across theory also. Okay, all right. Thank you. Any other questions? Just one other comment about the carpal tunnel that maybe we didn't talk about is sometimes you get these cases, you know, that have had surgery, maybe a few years down the road and now they have symptoms again. The ultrasound can be really helpful cause sometimes your nerve conductions can still be a little bit slowed and the ultrasound can help you actually visualize the extent of decompression and how well the nerve moves within that space. So it can help you differentiate sometimes whether it's really a recurrent carpal tunnel versus some other problem. Yeah, as Dr. Bargo was mentioning, you know, the ultrasound is great for looking at the anatomical variants, scar tissue, which I can't really do with the electrodiagnostic study. He can look at it and look at the movement, look at the tumors. He can look at, you know, small intraneural tumors and persistent median artery and or a muscle in the brain. A muscle which is extending into the carpal tunnel. I think those are great reasons why you want to do ultrasound for the carpal tunnel syndrome or other things. The one which he was showing about the fracture and the nerve being pinched by the chalice, which you may or may not be able to pick up, you know, when palpating the nerve. One of the things you want to think about in peroneal nerve is the fact that some of these could be conduction block lesions. You know, conduction block lesions, you have very good prognosis. In patients with slowing of conduction velocity, you have to think about, and especially when you have conduction block, the conduction velocity is not a true conduction velocity. Remember, when you are looking at the distal nerve, you have 100% of the nerve and all of the fibers are conducting and your fastest fibers are still giving you the latency. As you go approximately, when you have 90% of the fibers or 80% of the fibers are blocked, you don't know what fibers are conducting from there. Our way of thinking is we are picking up from the same fiber and that's why we calculate the conduction velocity. And a lot of the times, the conduction velocity slowing in patients with the conduction block is really two different set of fibers which you are getting from. So the conduction velocity could be very, very slow because all the fast fibers are blocked. Now your distal latency is gonna be shorter. Proximal latency is gonna be longer. Your conduction velocity is gonna be slow. It's not due to true demyelination. It is due to the differential of the conduction velocity between the fast and slow fibers between distal and proximal area. And that's a good point to think about anytime. And of course, I always point out to my residents that slowing of conduction velocity doesn't mean loss of function. Loss of function happens only with axon loss and conduction block. So that's a very good point to think about also. Thank you. So I'm also getting polls all the time when presenting with Dr. Sridhar and Dr. Williams. And any questions? Other? Otherwise, it's gonna be lunchtime. Thank you.

PM&R investigations

ultrasound

peroneal neuropathy

carpal tunnel syndrome

electrodiagnostic evaluation

foot drop

nerve conduction studies

ulnar nerve

anatomy

neuropathy diagnosis