Good morning, everyone, and welcome to our session, A Game of Clue, where we invite you to help us diagnose the causes of these presenting neck and upper extremity symptoms. I'm really lucky to be working with the same awesome group of presenters that I have at past AAPM conferences, and our goal here is really to bring you clinically focused spine talks that cover relevant topics that you'll see in your everyday physiatry spine practice. This year, we're trying to gamify our approach a bit, inspired by the board game Clue, which is always a huge hit in my household, and we want you to put on your detective caps while we try to sleuth out the causes of these mysterious symptoms. On the agenda, I hope you'll join Dr. DJ Kennedy in figuring out what is causing these occipital headaches, Dr. Aaron Yang in figuring out what can cause sudden arm weakness, Dr. Amit Anagpal in diagnosing the ideology of numb thumb, and wrapping up with Dr. Matt Smoot in helping us all understand what can cause axial neck pain. To begin, I'll start off with a mysterious case of trouble with buttons. My name is Patricia Zheng. I am a clinical assistant professor in the division of PM&R at the University of California, San Francisco, and I have no relevant financial disclosures. My case starts on a windy San Francisco morning when a 77-year-old female comes into my clinic complaining of trouble with buttons. Three months ago, she slipped while out on a walk and fractured her hip, and so she had to go in the hospital, had surgery, and recovery has honestly been slower than expected. She had to go to the skilled nursing facility and just got home when she noticed that she's having more trouble with buttoning her blouse, and her right hand even feels numb, sometimes during the day, sometimes at night. You look through the records, and she does have a history of chronic neck pain, and she's not noticing any specific arm symptoms. I really want to keep this session interactive, and so we're going to start off with a polling question, taking advantage of that capability at this year's AAPM&R. There's no right or wrong answers here. We just don't have yet a lot of information, but what are you suspecting here based on what I just told you? You can use the pop-up window and click your answers. Do you think the reason why my 77-year-old lady is having trouble with buttons, that is she having cervical myelopathy, maybe cervical radiculopathy? Is it carpal tunnel syndrome? I mean, that's just quite common. Where is this? I don't know. I mean, I certainly have trouble with buttons myself. I'm just giving you a couple seconds here. What do you guys think? Yeah, let's close the poll now, because we do have a lot of slides to get through, and I totally agree. You might see here that we're pretty split here. There's some concern for cervical myelopathy, but could it be radiculopathy or carpal tunnel syndrome? I like to also keep my differential really broad. Could this be something central, something arising from the cervical spine? Could it be even a brachial plexopathy, or yeah, a compressive lesion further out, like carpal tunnel syndrome? To be honest, what I'm thinking right now is, yes, it sounds like there's a chronic history of neck pain. This could be coming from the cervical spine, or maybe it is coming from the carpal tunnel, because the main complaint is actually hand symptoms, and I think we just need more information. Let's talk to the patient, examine her, and figure out next steps. When you see the patient and talk to her, she's really noticing worse numbness over the pointer and the long fingers. She tells you she does have a history of diabetes, and when you do your examination, you find that she has a positive Phelan sign, and especially the bolded findings, you're probably thinking, yeah, maybe she has carpal tunnel syndrome. The thing is the distribution of her symptoms seem like it would be consistent with a median nerve. She's telling you about some medical history, and a 2003 systemic review of carpal tunnel syndrome found that there is association specifically with diabetes, where the odds ratio of having carpal tunnel syndrome increases by 2.2, hypothyroidism, rheumatoid arthritis. You did your examination signs for carpal tunnel, and both the Phelan sign and the tunnel test are quite specific, with specificity of more than 70% for carpal tunnel syndrome. I'm not an EMG expert, but sometimes patients like this at EMG will be helpful. I usually start with median and owner CMAPs and SNAPs. For people with some underlying pathologies, maybe like peripheral polyneuropathy, I like to do that combined sensory index, compare the median nerve against another nerve. I only really do EMGs if the median CMAP is abnormal, and if I do, and I'm not thinking could be cervical, I usually just do an APB with an FDI. I remember learning that the grading of severity was actually not advised by AEM, just because many of them are not clinically validated, but the surgeons I work with actually do some sort of grading. For me, mild refers to people with only sensory findings, moderate, I start to see CMAP findings, maybe demyelinating ones, and severe is really if they have axonal loss, maybe even denervation on the EMG studies. The surgeons here like me to grade them, because for milder cases of carpal tunnel, we can think about splinting, and there's some studies which show that if it's mild, then people can really respond to splinting, especially if it's shorter duration of symptoms, less than one year, where less severe nocturnal paresthesia. We do also sometimes offer injections, and there was a really nice 2007 systemic review, and they actually had two high-quality randomized control studies that showed injections can be helpful, especially in the short run. But in general, if people have moderate to severe carpal tunnel, we think about surgical decompression, and the surgical outcomes are really good. I mean, just refer to the JARBEC study, a very great randomized control trial, the outcomes for pain and function are improved for those treated with surgical decompression, especially if it is EMG proven. But let's just mix things up a little bit here, right? So what if instead this patient has worsening trouble with buttons, but instead of just being the second and third digit, it's basically the whole entire hand, and she's actually noticing, yeah, like her neck pain is a lot worse. And the one thing that's interesting that she's telling you as you sit there with her is that every time she puts her neck into flexion, she feels an electric shock-like sensation in her neck radiating into her arms. You guys remember what that's called? This is what we call the Lamiertz sign, right? And especially if I have that in front of me, you know, that's usually something more central. It can sometimes present in, say, like multiple sclerosis, where definitely there's a lesion or compression of the upper cervical spinal cord. And so that's really going to skew my finding towards cervical myelopathy. So let me just kind of show you an MRI here. So here, you know, the way I like to look at MRIs is that on the left side, I have a sagittal T2, and on the right, I have axial T2 as well. And you can see, yeah, there's like kind of multi-level degenerative changes for C4-5, C5-6, and C6-7. And as you're looking through this, I really try to pay attention to the core to look at T2 hyper-intense findings. And then so as you kind of scroll down the axial, you can see, yeah, it gets really tight. You can almost make out some areas where maybe you can start to see some core signal changes, which is called myelomalasia, right? And I have actually a couple other MRIs, and you can scroll through this more. My presentation will be uploaded. In this patient, there's kind of a developmentally narrow canal, right? And then in the next one here, we actually have someone with a developmentally narrow canal, who on top of it has a focal C3-4 disc protrusions. And so when we're looking at, you know, the MRI, I pay specific attention again to the spinal cord itself, looking for T2 hyper-intensities within the cord. And, you know, this is when I see myelomalasia, I would be a little bit more concerned. And on the axial, sometimes this can present as what is called the snake eye sign. Sometimes they're also known as the owl eye sign or the fried egg sign if you're a very imaginative radiologist. And what's surprising to me is actually investigators have reported mixed results when attempting to correlate neurological impairment with these findings. Do I see this? I'm, you know, I'm on high alert for clinical screening on exam for myelopathy. And so cervical spondylitic myelopathy, it's actually more common than you might imagine in a retrospective study of 585 patients more. And colleagues found that it's the most common cause of spinal cord dysfunction. And onset is usually insidious. Sometimes patients just have difficulties with balance at first. And the progress is actually episodic. So people can be stable for many months, years only to undergo kind of acute decompensations. And so if you look at the Spengling PACE review, 1952, he followed out 21 patients. And one of the more common initial presentations would be clumsiness and steadiness with gait. So let's take this patient. You get more history. You know, she's really reporting that she, once she has a right hand numbness, there's no true sensory loss or definitive weakness. And, you know, she does have some trouble with buttons, trouble with tandem stairs, a tandem walk, but stairs is okay. And really no big issues with bowel and bladder. So what would you do now? Second poll question. You know, you have someone, you're kind of concerned about myelopathy. Is this someone where you would be like, whoa, we need to send this patient to the emergency room right away? Do you say, OK, you go home, take some precautions, but I'm going to arrange for you an expedited outpatient consultation. What should we be talking about? Yeah, OK, we know this. Let's start physical therapy and monitor you closely. I think it's hard. It's hard to come out with the right answer in this case. Let's just close the poll right now and share the results. I think it's, yeah, so I think not a lot of people are sending them to the emergency room, but definitely we need to think about what to do next. And kind of, yeah, 25 percent actually said, OK, to monitor closely. And, you know, the surgeons here, they like to triage patients based on the modified Japanese orthopedic association scale, looking at four domains, motor dysfunction in the upper extremity, motor dysfunction in the lower extremity, sensory dysfunction, as well as sphincter tone dysfunction. If the MGOA is 14 or less, then they need surgery. If it's between 15 to 17, then, yeah, I can support supervised trial structured rehabilitation. And, you know, generally the guidelines do not recommend prophylactic surgery if there's no evidence of myelopathy, so like actually exam findings. And so, you know, you were probably wondering why was I telling you so many different things? Well, one thing is if you just kind of tabulated it out, our lady has a MGOA score of 16. So it was fine to monitor. So, you know, for me, I always like to just get a surgical consultation arranged for these patients, and it's really hard for them, right? So even though she wasn't acutely decompensating, it just worried her that she had these kind of findings, and any time she could progress, and she eventually ended up having surgery and actually did pretty well. So wrapping my part of the talk up, you know, take home points for trouble with buttons. You know, with carpal tunnel, I think my suspicion is raised if there are risk factors for physical exam findings, for, you know, surgical decompression is very successful, but for minor cases, you can think about injection and splinting, and for cervical spondylotic myelopathy, have a good index of suspicion, look for those MRI findings, and you can use the MGOA for triaging, and, you know, there's evidence-based behind that. So we're excited to be efficient. I ask you to enter any questions you may have, some people are already doing that, into the chat box, and we'll tackle them all at the end, and I'm going to wrap my part up and turn over the Zoom spotlight to Dr. D.J. Kennedy. Thank you, Dr. Cheng. Super happy to be here, and, you know, happy to be talking on this, and we'll be talking today about cervicogenic headaches. Disclosures are mainly societal relationships, and I think nothing relevant to what we're discussing today. An overview, we're going to go cervicogenic versus other forms of headaches, anatomy in a differential, key presentations, as much evidence-based as we can, very brief intertreatment options, because the evidence for them is pretty limited, all in a whopping 10 minutes, so hold on to your seats. I will start out with a brief disclaimer. I'm approaching this as a spine specialist, I mean, I generally see people in my clinics that are referred for, or concerned for, upper cervicogenic headaches, cervical occipital headaches, et cetera. I'm not a headache specialist, I mean, we have people like Dr. Brittany Mays on the call that are, and they're seeing people as primary headaches, and, you know, they have forgotten more about some of these things than I know, in terms of differentiating some of the others. But, with that being said, let's go through it. So, how do we differentiate, really, from other headache syndromes, and that's one of the first questions. When someone comes to you with a headache, how are you thinking, is this cervicogenic versus something else? Well, the first criteria were actually published in 1990, and then revised in 1998. Before that, there were really no published diagnostic criteria for a cervicogenic headache. And the original published diagnostic criteria were unilateral headache associated with provocation of pain by movement or pressing on the neck, concurrent pain in the neck, shoulder, or arm, and reduced range of motion in the neck. Sounds pretty reasonable. The only problem is, when they actually looked at this, it's really not unique to cervicogenic headache. These criteria are common in all kinds of diagnosis, and they're not even able to differentiate features in healthy individuals. So we find things like range of motion or arm pain, you know, some of the other features might be present in healthy individuals. So not necessarily the best criteria. Additionally, the inner radar reliability, when we start looking at what is actually reliable, we actually have studies on this. Well, the good news is, as physicians, we can do location. So we can reliably say where the pain radiates to. Boy, that's a lot of medical training just to be able to say pain reliably rotates, radiates to the occiput or to the frontal region. We are also pretty reliable on provocation of pain by neck movement. You ask a patient to move their neck around, it works. This is not us putting them in position or moving them and putting them in position of doing it or manipulating them. This is the patient doing it. But those are reliable. Unfortunately, fairly poor reliable and restricted range of motion and pain on palpation. Both of these findings, which are, you know, hallmarks to a lot of what we do, have very poor reliability in the cervical spine. So the ability, inter-radar reliability, to actually range of motion somebody, even with goniometers and pain on palpation are both challenging. Probably the pain on palpation is because everybody hurts in a lot of places. I mean, if we did an audience poll right now of how many people had neck pain or tender points, we would get a high prevalence. And the restricted range of motion, I mean, we've all seen those cervical fusion patients that you really can't pick up a range of motion deficit in. So that's probably why. Well, what about radiology also? We know no radiographic abnormalities. And patients said to have cervicogenic headaches. We have good studies on that. And we also have radiographic features that overlap with those in healthy individuals, meaning our radiology helps us, but it's not pathognomonic for this, you know, in terms of how we really are diagnosing or treating. There are caveats to radiology, and there's really not much data looking at physiologic patterns, such as STIR positive MRI, especially in the cervical spine is not a lot there, but there's an emerging body of literature suggesting this is something to look at. And there's also even less interest in the C1-2 joint point. I think radiology formal training ignores this as a potential. I rarely see a radiologist ever comment on it. In fact, I had a fortuitous case this week of a patient following up with me, and this is the MRI. And I'll orient you, so this is a midline sagittal, and it's not completely midline because you can see the cord disappears as we go distally. So it's not completely midline, but surgeons, radiologists are generally looking at discs and posteriorly at zygapophyseal joints and I really want you to orient anteriorly and I'm just going to scroll out these are sequential pictures as we're orienting anteriorly and this is the AA joint on one side of this patient and this is not a healthy neck as you saw from the midline sagittal but this is the AA joint on this patient and if we come back to midline and go to the other side we get this highly edematous joint that the interesting thing on this particular patient was the surgeon missed it the anesthesiology pain management provider missed it and the radiologist missed it she did have a near complete relief when I injected it actually a complete relief unfortunately it only lasted the duration of the anesthetic she didn't really get much from the steroid on it but it was a missed diagnosis because this is a highly edematous joint and just look anteriorly now you know where to look I think it's a really good pearl because if you're only reading the radiology reports you're probably missing out on this one in particular so if we go back to our clinical criteria for diagnosing a cervicogenic headache now that we know radiology has some utility but not a ton and we know some of the original criterias weren't great this is a more recent one it's at least from this century that it seems to be working and we got some studies validating it but they define it as possible cervicogenic headache if it's unilateral headache without side to side shift meaning it's the right-sided headache it's not shifting right left or bilateral and it pain starts in the neck and sprays to ocular frontal temporal area so it can it can radiate up and around but it does need to start in the neck that's possible it goes to probable if symptoms and signs involve neck involvement pain triggered by neck movement sustained awkward posture external pressures of the posterior neck occipital region ipsilateral neck pain shoulder arm pain reduced range of motion all of those make it probable the other two there are pain episodes of varying duration fluctuating or continuous pain meaning this isn't a standard they're sitting at seven out of ten pain all the time this will fluctuate and this is what you expect from a mobile pattern that probably has some biomechanical features and they usually there are a couple exceptions to this they're moderate non-excruciating pain usually of a non-throbbing nature if you get these really excruciating pain patterns in the absent excluding a c2 neuralgia specifically usually you're thinking is this a migraine or some other type of headache syndrome rather than a cervicogenic headache that's usually we do know we have a broad differential of things in the cervical spine that can really cause this we see a variety of joints nerves including third occipital greater occipital discs and then you have random things sterile pain with such as meningitis can present this way we're not usually seeing that in outpatient spine clinic disaster reactions can very much do that as well arterial dissections are other things that are more rare in a typical outpatient spine clinic but it is a pretty broad differential when we're trying to figure out which of these things the pain patterns are a nice thing to think about but unfortunately they're not terribly helpful meaning they help a little but not a lot we know c1 c2 and c3 spinal nerves all basically converge and they you know by converging these second order neurons it really allows the cervical pain to be referred to regions of the head innervated by the cervical nerves so when we look at our pain patterns these are from several different studies you see c1 c0 they they're all upper occipital upper uh upper neck some radiation and some slight differences but they're they are all over the place the interesting thing is we're not finding pain lower in the cervical spine 5-6 doesn't usually cause c5-6 doesn't usually cause a cervicogenic headache this is really up in an upper cervical spine that we're talking about other features to consider to help you differentiate some of these things you know c0 c1 aa ao versus aa lano occipital versus lano axial joints um we know that the lano occipital does about 15 to 20 degrees of flexion and the lano occipital does a 50 range of motion of the cervical spine in rotation so while i've already said rotation range of motion deficits are hard to find um and the data shows that picking up subtle ones are really hard and poor interrater reliability i've yet to see a really good study specifically on those with reductions thought to be due to the lano axial joint my clinical experience tells me these are easy so people with general range of motion reductions are pretty hard but these patients have a pretty significant uh range of motion deficit given the amount of uh rotation that comes from that lano axial uh joint um we also know the c2 nerve pain there's a picture of it you can see the c2 ganglion right over the c12 facet joint and it is an intermittent lancinating occipital pain associated with lacrimation ciliary injection and rhinorrhea just because of the innervation and another really rare syndrome at least in my clinics is the neck tongue syndrome with a lingual afferent fibers traveling through the hypoglossal nerve the c2 spinal root so they have upper neck pain and half tongue tongue numbness so these are just things to put in the back of your mind as to this can be coming from the upper cervical spine we know the c23 joint has a prevalence of 60 70 percent of whiplash associated cervicogenic headache we don't have a lot of data on other groups outside of whiplash but we do have it within whiplash um and that it's important to note the tenderness to palpation over c23 only has a likelihood ratio of 2.1 which is pretty poor so just because someone's tender over that doesn't mean that they're more or less likely to really have it to a high degree we have limited prevalence data beyond c23 but it's likely that linoaxial and then c34 are are the the next two most common uh prevalence especially in whiplash patients our conservative treatment not a lot there especially for confirmed i mean if you start putting a gold standard diagnosis which is our interventional treatments are conservative for probable cervicogenic headache this is based on the criteria i showed you other earlier exercises with or without manual therapy it seems to be some of the best conservative options um you know there there are a lot of other things and it's really challenging when we start looking because there are a lot of headache syndromes where we're doing all kinds of therapies and injections for them but when we really try to dive down into the cervicogenic headaches we're we're going back almost 20 years for papers for these things our interventional treatment options we have a lot uh with poor evidence on almost all of it so you where there is a joint you can stick steroid prp whatever you want to stick in there uh poor data across the spectrum for that um nerves we can do there's third occipital cervical medial branches c2 nerve root there's thermal ablation for rf which actually has some pretty good data in cervical spine a little bit limited for third occipital nerve um you know leading some insurers to deny it um there are a few small series of pulsed rf or c2 pain discs uh people inject anything imaginable into the discs all with very poor data um so what do i do history and pe i'm really looking for range of motion patterns for aa versus ao um and i'm i'm specifically worried about what dr zhang was just presenting earlier with hyperreflexia and signs of of neurogenic signs i usually do an initial conservative treatment with the exercise based therapy plus or minus manipulation if that's uh failing i get a cervical spine mri i'm specifically looking for stir positive findings in the aa joint which are frequently missed by our radiology colleagues and then if no significant findings on the mri they're really leading me leading me down one rabbit hole i'll do a third occipital knot block uh plus or minus a c23 intra-articular corticosteroid at the same time was built under the same numbers if you do a c23 medial branch block or or do it that way um progressing to rf if if they're meeting criteria for it i consider c34 uh because i do have good treatments for it i have radiofrequency ablation of those medial branches uh versus the lanoaxial joint which actually may have uh more by me slightly more prevalent but i have so many less options for them that are evidence-based um and then everything else beyond that gets pretty rare and with that uh thank you and i will hand this over next uh to my colleague dr aaron yang uh dr yang is an associate professor here with me at vanderbilt university medical center where he is the associate residency program director the director of our medical student clerkships he's on the program planning committee for the pmnr and does a wide number of things and we're thrilled to have him talk so he is up next thanks dj for that the nicest introduction you've ever given me so i appreciate that um let me share my screen here okay so hopefully you guys can see this um so again thank you dj i am an associate professor here at vanderbilt and so i'll be talking about arm weakness so i have no relevant financial disclosures my only disclosure is that dr kennedy is my chair and this will be me if i don't do a good job so there's a lot of pressure on me because he's right down the hallway so i really have one main learning objective and that's to distinguish between two of the most common reasons for a patient coming with arm pain and weakness and i really like that dj prefaced that i'm really approaching it from more of an outpatient base setting perhaps in a spine clinic for example as opposed to if you're part of a a a group where you're seeing a lot of brachial plexopathy because that is something that i'll be talking about so i always like to start off with three takeaways and just in case i lose your attention first thing is that not everything that hurts or is weak in the arm is from the cervical spine second you heard dr weinstein say this in the first lecture that he gave for all of us but the mystery is in the history really listen to the patient because you can glean some things from them and lastly atrophy is not a common presentation for cervical radiculopathy and i'll go over some of this in a little bit so this was a case that i had which was someone of a learning case going through it so it was a 45 year old male came to the emergency room initially with left shoulder pain and numbness and tingling in the left arm he had severe pain in the left arm that worsened at night time and increased pain with movement of that arm so when he went to the emergency room the differential per their note was aortic dissection they thought cervical radiculopathy or mi and so they obtained labs they got vitals all within normal limits they also ordered a ct angiogram of the neck and chest which was normal so this patient came the following day into my spine outpatient spine clinic continued to have 10 out of 10 pain predominantly in the shoulder down the left arm it was really in a non-dermatomal fashion he had difficulty using his left arm and laying on the left side an exam was at that time notable for really again not much neck pain with movement he had intact light touch sensation he had some slight weakness with elbow flexion extension he had reduced reflexes in the brachioradialis and triceps you was able to take a look at his ct angiogram i didn't notice you know look like maybe there was a disc osteophyte complex at c56 he had these left arm symptoms so we thought might be more along the lines of a c6 radiculopathy considering his pain levels difficulty sleeping we started him on a course of oral steroids and lyrica and ordered an mri of the cervical spine so he was seen six days later following his mri crazy enough he saw a cardiologist i think that was set up from his emergency room visit and had a cardiac cath which was normal and this time he presented it was different again this was about six days later and he had now numbness that was persistent in the fourth and fifth digit continued to deny any neck pain he also had an exam notable for atrophy along the first dorsal interossei numbness along the fourth digit and full fifth digit i just have one slice here sagittal and axial cut t2 mri he has some moderate foraminal stenosis at c56 but again not severe and he's presenting with now atrophy and numbness predominantly affecting what seems like the c and t1 nerve roots so this imaging here this finding may not be as helpful so really the question is where do we go from here do you order more images do we send for therapy the usual treatments we have in the toolbox so when you think about the differential i'm just going to broaden it not just to the case we discussed but someone who comes in with arm pain some level of weakness some of the more common differential diagnoses are going to be again cervical radiculopathy possible parsonage turner syndrome and in particular our case there could be a peripheral nerve entrapment of the ulnar nerve although specifically for that case that would be less likely considering he had severe shoulder pain at first and then developing symptoms distally another possible but still rare diagnosis could be thoracic outlet syndrome particularly the neurogenic type and then less likely multifocal motor neuropathy als which usually present with painless weakness multifocal motor neuropathy is a demyelinating disease with conduction block it is a slower progressive disease and usually presents asymmetrically the reason i mentioned these is because if we think for example whether it's cervical radiculopathy or even something like parsonage turner they have a period of time where the pain gets better but now they have weakness so they could present with painless weakness by the time they get into your clinic other differentials uh modernized multiplex this is a what was thought as a vascular type ischemia injury to the nerves usually affects the lower extremities and then hereditary neuropathy with pressure palsies again usually affecting peripheral nerves but i really want to focus on what is here in red because again in an outpatient setting these two might be the most common things that you may encounter in clinical practice so we know a lot about cervical radiculopathies and we'll circle back to that but first i want to focus on brachial plexopathy and i just encourage you to watch a great talk by dr hearn who had a on-demand session on electrodiagnostics for brachial plexopathy but i'm going to be focusing on neurologic amyotrophy or parsonage turner the most common reason people have a plexopathy injury will be trauma but i'm going to be talking specifically about this and there are other causes for brachial plexopathies as well so just keeping that in mind so really when should you consider plexopathy in the office setting again patients will usually discuss will usually endorse an abrupt shoulder pain and developing arm pain it's usually worse at nighttime they may hold their arm in a flex and adductive position because pain can get worse with movement of the arm they're usually not discussing or complaining of neck pain or pain worse with neck movements an important thing to especially consider plexopathy is this pattern where you see an intense time of pain initially followed by weakness and atrophy so what you typically see is that weakness can develop within two weeks but as the pain improves weakness becomes more of the prominent symptom so again in this scenario depending on when you see them they may come in and their pain may have been resolved and they may not endorse much pain but it's important to ask that in the history because they may come at that point with painless weakness it's important to know that majority of the time plexopathies and especially the brachial plexopathies affect the upper and middle trunks and you also can affect the long thoracic nerve so it's important to look at the scapula and it's usually not as common to see bilateral involvement in the upper extremities so when you're examining someone what you typically see is more motor nerve involvement as opposed to sensory it's important to think about looking at the scapula if you're even considering a plexopathy you may catch medial winging again typically what you see with the long thoracic nerve involved also to check what we call the okay sign and so that the okay sign is predominantly innervated by the muscles provided by the anterior interosseous nerve in a way I have my residents remember those nerves are the four p's which is the flexor pollicis longus the first two digits of the flexor digitorum profundus and the pronator quadratus. And so again, just two things that you might be able to check in the examination if you're thinking about a plexopathy. You can have sensory loss and it does occur about 66% of the time. But again, patients are not really discussing this because initially pain is the primary complaint. So just a couple of things to remember, the annual incidence varies, but it's about two out of four out of 100,000 cases per year. It's more common in males than females. It is thought to be immune mediated, although we're not quite sure. And the reason we think that is that some studies show that about 50% of people report some type of antecedent event, whether that is some type of infection or et cetera. That's why it's thought maybe it could be immune mediated. So it's important to know that it's a clinical diagnosis and you have some diagnostic tests available. And again, you're really thinking this if a patient comes in with severe and sudden pain, usually in the shoulder followed by muscle atrophy. And why in this case with atrophy, why are you not usually thinking about the cervical spine? Part of that is because you have overlap of myotomes that affect your muscles. And so if you're treating a lot of spine cases, it's as you know, it's not very often where you see multiple myotomes affected at the same time simultaneously. So when you do see that, you start thinking more peripheral pathologies like a plexopathy. So in terms of diagnostic tests, you have electrodiagnostic studies, which I would say is the primary way we diagnose this. You have MRI or MR neurography that you can obtain in which you may see increased T2 signal intensity along the nerve. However, the sensitivity varies around 40 to 50%. And the labs are usually normal unless it's associated with some type of greater disease, such as something systemic or infection. But again, usually the first step will be electrodiagnostic studies. So again, I encourage you to watch the on-demand session by Dr. Hearn, because I'm not going to go in depth into this. But again, the tests that you're going to usually add in addition to your usual routine nerve conduction studies are you're checking the lateral antebrachial cutaneous, particularly because that's a very common sensory nerve involved. The medial antebrachial cutaneous, again, your usual median ulnar, but also including the F responses, the median ulnar responses. And when you're doing the needle EMG, again, you're checking different muscles to help delineate whether you're along the upper, middle, or lower parts of the trunk or the medial lateral cords. Not going to really go much into this because there's not a whole lot of evidence of what type of treatments actually reduce the degree of impairment or even affecting the prognosis. Steroids are usually the most go-to medication that is done on the outpatient side, and it can reduce the degree of pain, but has not shown to really alter the course of disease. In terms of physical therapy, it's usually done to reduce more secondary complications such as shoulder immobility in this case. And again, in terms of prognosis, prognosis usually improves over time, and it is a slower process. We do see that majority improve, but it could take up to three years. Usually that recovery starts to happen when there's improvement in pain. Now, it seems that most people have their intense pain symptoms improve over the course of about a week. In my case, that patient's pain was very intense in the beginning, but got better after a few days. And usually if the upper plexus is involved, it tends to recover more rapidly than distal part of the plexus. So in terms of recurrence, it's uncommon, but there is a small percentage that they may have repeated episodes, and there is a autosomal dominant, a hereditary form of brachial plexopathies that can occur. But again, in general, for most people, it's going to be pretty rare. Now let's circle back to what we may see more commonly. What about cervical radiculopathy? What may be different? So again, the typical radiating pain from the neck, pain worse with movements of the neck, possibly a positive Sperling's maneuver. What about concordant myotomes, dermatomes, and reflexes? So really do pain referral patterns help, especially in this scenario? So if someone comes in with pain rating down the arm in a certain distribution, how often is that accurate? How often does it change our sort of next steps? So I wanted to share just two studies before I close. So this was an interesting study that was done in 2018. It looked at 239 patients who had a one-level ACDF, so one-level cervical decompression surgery. They had 75% relief at six months postoperatively. And it was a retrospective study looking at these patients preoperatively and where they described their symptoms and compared it to Netter's diagram. And so what they saw was that about 54% in general for all their patients followed that dermatome pattern based on Netter's diagram. If you look at the most common levels that are often operated on, C5-6 and C6-7, about 50% of the time did it follow that standard Netter's diagram pattern. What they did see is that patients with, for example, a right-sided cervical radiculopathy would have right-sided neck pain about 81% of the time. We really wanted to pay attention to this because about almost 20% of the time they may not complain of any neck pain at all. They may just have distal arm symptoms without any neck pain. So really my main takeaway is dermatome patterns and using that to help diagnose is not always helpful. Very rarely does it always follow the specific dermatome pattern all the way to the hands. So it's important to just keep your differential open in this case. What about painless weakness coming from the cervical spine? Can that happen? And it can, but it's pretty rare. So this was a study in 2018, looking at 788 patients and 31 of them had what they say were painless compressive cervical radiculopathies, meaning they had no pain into the extremity, but they had muscle atrophy in the extremity. And it was interesting to note that 83% of those patients were smokers and majority had anterior nerve root compression as you can see in these photos here at the neural foramen. So it can happen where you can have painless weakness in the extremity from the cervical spine, but it's not as common. So really to close up some pearls, again with parsonage, Turner or brachial plexopathy, the big things that you may see are atrophy. Atrophy, especially out of proportion to cervical stenosis as we saw in my case. If you're even thinking about plexopathies, check the scapula, look for winging, do the okay sign. In terms of thoracic outlet syndrome, which I not talk a lot about, it is a rare entity. Oftentimes you wanna rule out cervical radiculopathy or ulnar monopathy first. It is a slower process. It's not abrupt like a brachial plexopathy. It usually affects the C8 and T1 fibers. So it's important to check the hands, especially thumb abduction, which is preferentially affected. And in terms of cervical radiculopathies, again, we talked about the common things. Worse with neck movements, like Dr. Kennedy mentioned, prevalence of neck pain is high. So you can't just say it because you have neck pain. This is all always from cervical radiculopathy. You wanna interpret referral pain patterns and presence of neck pain as we saw with these prior studies with caution. And really reflexes are going to be your most objective finding. So my final takeaways, shoulder pain, weakness should raise your spidey sense. Arm weakness followed with atrophy should raise your spidey sense. Think about other ideologies. Don't think about the cervical spine all the time. And pain pattern distribution in terms of cervical radicular pain patterns may not be as reliable as we thought, especially in the upper extremities. Electrodiagnostic testing can really help us. All right. We'll take some questions at the end. Appreciate your attention here. I'm going to have Dr. Nagpal, who is an associate professor at UT San Antonio, present his next topic. Good morning, everybody. I am excited to present my topic for you. And I'm excited to be with this great group of physicians today speaking on these musculoskeletal conditions that may be difficult to diagnose. My section is going to be on numb thumb. It's actually based upon a patient that I saw. I mean, I'm going to say five or six years ago. And the patient came to my clinic simply with numb thumb and frankly, with a little bit of pain in that thumb too, for purposes of this particular topic. For purposes of this particular, for this particular presentation, I'm going to just leave out the fact that it was a little bit painful. But this is a 45-year-old female who came to the clinic complaining of 18-month history. The palmar surface of the distal portion of her right first digit, the thumb, had decreased in sensation and she also had constant paresthesias. Associated symptoms included mild neck pain that was also constant and was one out of 10 in intensity. The symptoms worsened with cervical rotation when she was asleep and the symptoms had been worsening. She was pre-diabetic. Now, I added this part, admittedly, for, I don't know, for humor and making things a little more contemporary. But I've had a lot of patients over this pandemic come in who didn't have problems before and suddenly develop problems because they've been working from home and ergonomically their workplace is not set up appropriately. So for purposes of adding a little bit of fiction to my nonfiction work, we'll say that she was an administrative assistant, but let's say that she also had these symptoms begin right after she was converted to work from home. So on exam, there was no atrophy noted. There was mild tenderness along her right cervical paraspinals. She had full range of motion of the cervical spine. She had symmetric reflexes that were normal. Normal strength in both upper and lower extremities, but four out of five right thumb abduction, abduction. She had a pinprick decrement in the palmar surface of the distal phalanx of the right thumb with a negative Sperling test, positive Durkin test over the right wrist and a positive Tenel test in the right supraclavicular fossa. Now I'll say, I had intended to speak a little bit about these exam maneuvers. Some of my colleagues have done a great job describing them. I'll just point out that the Durkin test is one that's not commonly discussed, but essentially it's the same as a Tenel test, but with the exception that you're holding pressure over the carpal tunnel rather than tapping. The classical teaching has been that the Durkin test is the most sensitive and specific of all the physical exam maneuvers for diagnosing carpal tunnel syndrome using physical exam, more so than Tenel's, more so than Phalen's, which is depicted in this cartoon here, and more so than reverse Phalen's, which is simply the opposite process. And again, I say that is the classical teaching. It's also how I taught it until a few years ago. There have been recent studies that indicate that maybe that's not necessarily the case. And ultimately it all comes down to how you determine your sensitivity and specificity relative to what your gold standard test is that you're using as the comparator. If we look at things like EMG as the comparator, the sensitivity and specificity goes down. So nevertheless, I think classically, we believe that Durkin is a better exam maneuver, but that may not be true as more studies come out about that and maybe none of them are that good, to be honest with you. This is also true of Sperling's test, which was just discussed in a bit of detail. And so I won't go too deep into that, but recall that the original description of Sperling's test was that the patient would first extend their neck. And if they had radicular symptoms, it was positive and you stop. They then laterally rotate the neck. And if they had radicular symptoms, then you stop and the test is positive. They then perform side bending on the side that's affected. And that's the third maneuver within it, the Sperling test. And if it's positive, you stop. And the fourth component is pressing down on the head. And if at any one point during the four components of the Sperling's test, there are radicular symptoms that reproduce the patient's pain, it would be positive. We misuse the Sperling's test in today's day and age quite often. So that was the original description. It's still not a great sensitivity and specificity, but if you do it that way, it does increase the sensitivity and specificity. There's also the brachial plexus tension sign, which is shown in this image where the patient's actually pulls the head away from the brachial plexus and that puts tension on the plexus and that may be consistent with a radicular pattern pain. Of note, physical therapists quite commonly use this tension sign as almost a desensitization treatment for radiculopathy. They call it nerve flossing, but nevertheless... So in that case, sometimes it's used as a treatment. We don't know what the number needed to treat for nerve flossing is to improve a patient's condition from their radiculopathy. So we have these symptoms and signs. We have the findings we have. So what should we do? I would say, at this point, it's just the distal portion of the thumb. It's a little bit confusing. So I did order at that time and performed an EMG. I also thought about an MRI, but I had to think of, well, what am I gonna get the MRI of? And geez, it's just her thumb. Should we really go down this rabbit hole? But she does have the neck pain. She has neck tenderness, but in the weird rare chances might be a brachial plexopathy, you may consider an MRI of the brachial plexus. I did not. I would not. But MRI of the cervical spine is not out of the question either. And so I performed nerve conduction studies and this is what I found. And in the interest of time, I'll just say, hey, look, the peak latency for the right median nerve was high, but everything else was normal. I also ran lateral endobrachial cutaneous nerve tests on my sensory nerve conduction study to rule out what I didn't believe the patient to have, which is a brachial plexopathy. Well, we kind of can think of the lack, as everybody does, we all do, as being a nerve that kind of innervates, gives us sensation in the, let's say radial aspect of the forearm. But it actually has some communicating branches that go to the palmar cutaneous branch of the median nerve and some other communicating branches to other parts of the radial nerve too, which is why we think of radial sensation deficits. But there are branches that go to the volar portion of the thumb. So in a non-thumb situation, you may want to check the lack. In this patient's case, they're both normal. And of course, the sensitivity, the reliability, let me say, of the lack as an EMG test is probably not great. It depends on the examiner. I have to say, just like Dr. Zhang said, I'm not a great electromyographer. So I, and I've since subsequently, I don't perform this test anymore, but at least if I find a normal finding, then I think it's probably legitimate. On motor nerve conduction study, again, I won't, in the interest of time, everything was normal for this patient on the median and the ulnar side. On EMG, I did a radiculopathy screen. There were a lot of comments earlier about whether insurers will pay for nerve conduction studies without EMG. And that's a real problem in our system right now. And so a lot of times an EMG is required to get reimbursed for the work you're doing. In this case, I didn't know what was causing the patient's pain. I thought it was reasonable to at least rule out radiculopathy because of the neck pain and the non-thumb. Everything was normal though. And again, a normal EMG does not rule out a radiculopathy, right? So this is a very high negative predictive value test. So, sorry, a low negative predictive value test, excuse me. So now what? So I've got the EMG. I don't, I think, hey, I've got this right here as Dr. Zhang described, this would be classified based on the classification that we kind of don't use all the time as a sensory only mild carpal tunnel syndrome, but it's just the thumb. So I did go ahead and get a cervical MRI. The lateral view and our sagittal view was normal, but I did have a C5, C6 disc herniation that was compressing on the nerve root. So I was a little, I didn't know, could this also be associated with a radiculopathy? And that left me with this differential diagnosis of carpal tunnel syndrome, cervical radiculopathy, and way low on my list, almost zero, but still is brachial plexopathy. I have no reason to suspect this patient has a brachial plexopathy, but nevertheless I put it on the differential diagnosis for completeness. Now I look at, if you look at the sensory territory of the median nerve, we know that there's a palmar sensory cutaneous branch as well as palmar digital branches. We also have some innervation on the back of the hand, but this is probably over, this cartoon is probably overestimating how much of the sensory territory the median nerve really has. Most of this might probably be radial innervation, right? We probably know that. One thing I'll also note is I kind of, we need to discuss, well, what's the normal distribution of somebody who has carpal tunnel syndrome? And this is from 1990. So Dr. Kennedy was talking about studies from different centuries, and here I am showing another one, but the most common classical diagnosis for carpal tunnel. These are sort of the patterns. You can see it to all five fingers a lot of the time, not just necessarily the median distribution. And then when we get into the ones over here in C, which look clearly pretty ulnar or maybe even a little bit radial, those are unlikely to be carpal tunnel syndrome. What we don't see is just thumb anywhere. But you know, my EMG, my nerve conduction study was consistent with carpal tunnel. But, and if I look at the pattern associated with C6 radiculopathy, well, yeah, that would also involve the thumb, but man, why would it just be the thumb? It was a little bit of a diagnostic mystery to me. And I wound up doing a carpal tunnel injection on the patient and she had 100% relief of her numb thumb for two months. So I felt it could have been placebo, could have been placebo, but I don't think it was. And I did that first because I'd rather do that than a cervical epidural steroid injection. So in summary for numb thumb, at least, which is, man, it's hard to find anything that would tell you what really would be causing it. History and physical aren't perfect, nerve conduction study isn't perfect, EMG isn't perfect, MRI isn't perfect, and it's difficult to diagnose. And I think that we always have to go back to the old adage of the way that we diagnose some of our musculoskeletal conditions shouldn't really be grounded in history and physical as much as we've long thought it should be. And for a long period of time, I suspect that we've all kind of thought that's how we should do it, but truth be told, serial diagnostic blockade of different structures may be the best way to diagnose. So I know I rushed through that, but I know we're also up against the clock. So I thank you all for your time. If you have any questions, you can email me or send me anything through social media. I'm gonna turn it over at this point to Dr. Smook, who is the Chief of Physical Medicine Rehabilitation at Stanford University, and he is a professor in the Orthopedic Surgery Department. Thank you. Thanks, Amit. So I'm gonna take us to the finish line by talking about pain in the neck. My disclosures are listed here. None of them are relevant to this talk. Our case involves somebody with neck pain. It was a 50-year-old male, sedentary and overweight with episodic prior neck pain for about five years. But over the past six months, the pain's become persistent and he rates it between four and seven on a 10-point scale. Pain's in the right neck in the location shown here on the pain drawing. Occasionally radiates down the scapular border and over into the proximal shoulder. Pain's better on weekends when he's not commuting and spending less time on the computer and worse with movement and persists despite oral medications and PT prescribed by his primary physician. And for sake of this talk, let's assume the PT that the patient received was very appropriate for the condition. On your exam, you find tenderness in the right neck in the area shown on the image and the patient has forward head posture, but otherwise the exam's unremarkable in all other forms. And he comes with this X-ray that was obtained by the primary care physician and the patient wants to know what's wrong and how do I get better? Common questions by patients like this. So that's some clues here. What are we gonna do? How do we answer the patient's question? Well, neck pain's common as we all know, but what about the sources of neck pain? If we're gonna try to answer the question about what's wrong, what are the possibilities? Epidemiologic studies have shown that facet joint pain and myofascial pain are the two most common types of neck pain and that's largely what I'm gonna focus on for the remainder of the talk. But I do wanna just point out that there are uncommon sources of neck pain that we have to be aware of and you've heard about some of the things you need to look out for, but for neck pain alone, meningeal irritation and sometimes even vascular issues can present as neck pain. So just be alert of those things. But when it comes down to facet versus myofascial, this can be a challenging thing to figure out. So what kind of workup, what additional tests are we gonna do in order to figure out this patient's pain? Is it facet pain? Is it myofascial pain? Let's assume there's no red flags or other issues that we're concerned about. Well, what about advanced imaging? Does advanced imaging help us to confirm the diagnosis? This is our patient, same patient I showed you before. You can see the same degenerative changes predominantly is C5-6 and C6-7. The midline axial cut doesn't show any compression of the spinal cord. As you scroll over to the right side, you see the facet joints on the T2 image in the middle of the screen. They don't look particularly degenerated. One level doesn't necessarily look worse than the other. And as you look at that same location on the STR, you don't see any increased signal on STR, meaning unlikely to be any inflammation anywhere. So this doesn't really give us any clues about what the cause is, but let's say it did. Let's say that you had a lot of STR signal increase around the C5-6 or the C6-7 facet joint at the levels where the patient has some degenerative findings. Does that clinch the diagnosis? Or let's say that you have a SPECT-CT or SPECT-MRI that lights up in one of the facet joints. Does that confirm the diagnosis? Well, I'll venture to say at this point that it doesn't. It might increase your pretest probability of this being something coming from the facet joint. And there's certainly case reports and anecdotes out there that these things are important, but they're not pathognomonic and they don't necessarily tell us the full picture. So what about physical exam? Can we use our physiatric skills in order to help determine the difference here, whether this is facet versus myofascial pain? The location of the pain is important, but it also doesn't give us a full picture. On the left side of the screen, you see the Trevell and Simons image of levator scapula trigger points. The center is obviously our patient whose pain looks similar to that, but it also looks similar to what's shown on the right side of the screen, which is Dwyer, April and Bogduck's dimetomal maps of cervical facet joint pain. And the pain here overlaps best with C5-6, but could include C4-5 or C6-7. So is this myofascial pain or facet pain? We can't really tell from the location. What about a manual exam? Well, the first publication that used manual exam to determine cervical facet joint pain was published by doctors Joel Bogduck and Marsland in 1988, and reported a 100% sensitivity and specificity for facet joint pain, not just diagnosing facet pain, but choosing the actual facet joint that was the cause of the pain. 100% sensitivity and specificity. Now you don't hear Dr. Bogduck go around and talk about this study much because he realized that it was a small study, a pilot, and he did a much larger study with other colleagues that use the same approach and defined a sensitivity and specificity of 89% and 50%. Now taken together, these two studies, however, do show that manual exam sensitivity for diagnosing cervical facet joint pain and the joint that hurts is between 90 to 100% essentially. So this becomes a very good screening tool. And if you're out there and you're wondering what I'm talking about and you feel like you don't have a good manual exam for neck pain, you probably owe it to yourself to learn to do that because this becomes a very good screening test. If it's positive, then you need to go down the path of diagnostic blocks to determine, is this a treatable facet joint problem? How about using our hands for diagnosing myofascial pain? Here it's much murkier and there's a lot more research on it, by the way. There are some studies showing some decent inter-rater reliability and such, but when you put the studies together, it really shows that manual exam and palpation for myofascial trigger points has a lot of room for improvement. So that makes this more challenging to diagnose. I also wanna just briefly point out that there are physical exam findings that you can use that are analogous to the Waddell signs in the lumbar spine. So these are the non-organic signs for neck pain, but don't make the mistake of saying non-organic causes. It's not called non-organic causes, it's called non-organic signs. These simply point to the fact that the patient's condition is likely more complicated. It doesn't mean they have a non-organic cause for their pain. That's incorrect and a misuse of these signs. And when you find them, just be aware that you need to take that part of things into account as well. So to answer the patient's question, to figure out the clues, what are you gonna do next? A trigger point injection, a medial branch block. I didn't give you the findings from the manual exam. I can tell you that in my clinic, if the manual exam is isolating to one or two cervical levels, then I'm likely to proceed down the medial branch block path first, even if they have a lot of myofascial tenderness, because I rarely meet a patient with neck pain that doesn't have myofascial tenderness. If there is, if the manual exam is not specific, then I'm likely to consider it myofascial pain predominantly and treat it that way first. But sometimes wind up treating it like it's facetogenic pain. Your answer to this question is as good as mine because we don't have, other than what I presented here, any good evidence to help us make a distinction one way or the other. So thank you all for attending today's session and for all of the previous speakers for their excellent talks. I think we're past the time, so we may or may not be able to take any questions. Thank you, Dr. Smook, and thank you to everyone for attending this session. We actually have a lot of good questions that's been posed in the chat, but I also respect people's time. And so usually we're allowed to go a couple minutes over. What I might do is, one, if you have any pressing questions that we're not able to get to in this Q&A, please feel free to reach out to us individually. Our emails are all listed on the AAPMR website. What we might want to do then is, because there's so many questions, we might just, for each presenter, just address the first question that's been posed. So if you have any other questions, you can write it here, but you can also email us afterwards. So for my presentation, sorry, I kind of led to some discussions about billing. I'm kind of lucky here that I don't do my own billing, so I was actually not aware of that. But one of the questions that came up was, is there evidence for hand therapy for mild to maybe even moderate carpal tunnel? And there is some. I would point you to the Mueller Review article where they were looking at multiple studies over the years. And there's been more studies for splinting or splinting with hand therapy than just hand therapy alone. But I think there was one by Tal Akabi that actually did look at carpal bone mobilization and nerve blights for carpal tunnel and actually was able to show that decreased pain more than no treatment. So our next presenter then would be Dr. Kennedy. And Dr. Kennedy certainly brought up a very interesting subject where there were many questions, but just taking the first one. So for his first case, for the patient you injected who only got relief from the anesthetic and not the cortisone, what was your next step for treatment? I'll actually be able to run through a couple of these questions because they relate. One, beyond that, we're already in not evidence-based land when we're doing a corticosteroid and the C1-2 joint, but it's not that invasive for a lot of reasons. I consider it a dorsal root ganglia and pulse radiofrequency. That goes to one of the other questions. I don't have as much experience with thermal radiofrequency and it does have skin innervation. And I worry about truly de-innervating it from that way. There are a couple of case reports of thermal radiofrequency of the dorsal root ganglia in there. It's not something we're doing regularly, but I actually sent her to some colleagues that consider doing that. I don't do a lot of pulse radiofrequency, so I sent her over. They decided to do myofascial trigger points because as Dr. Smoot said, everybody has myofascial pain on top of these things, which also didn't do anything for the patient. I saw her back fortuitously. This was a year ago when I was treating her for this. This was no longer her main complaint. She unfortunately has metastatic melanoma at this point and I'm dealing with that. But that was still a problem, just not there. The other quick questions regarding to people with bilateral headaches after a motor vehicle accident, that is certainly possible. The data is really focused on unilateral and I don't know if that was a selection bias of the data to keep a very clean study because we are going back 30 years for a lot of that. But the data is on unilateral. I do think bilateral can absolutely happen, but there's just not as much data on it. And the other one, if you treat patients with a greater occipital nerve injection, but short-lived, how quickly do you go? Usually by the time they get to me, they've already had a greater occipital nerve injection that's distal to the third occipital nerve from the innervation. So I'm actually pretty quick to going to a third occipital nerve. I don't think greater occipital nerve is, there's a lot of data on it for other headache syndromes, not a lot. It doesn't make sense for a cervicogenic headache. A true cervical origin, if you're splitting hairs, shouldn't be a greater occipital nerve and that would be distal to anything. And it's mostly skin innervation at that point. So I have a very low threshold to going to a third occipital nerve at that point and progressing to a radiofrequency if needed. Hopefully that answered everybody's questions. Thank you, Dr. Kennedy, always efficient. And then so for Dr. Aaron Yen, he's actually been answering some of these questions via chat, but one thing that was brought up was that for the atrophy case, it was quite rapid. And so was there some thought of using diagnostic ultrasound to rule out masses or other causes of plexopathy? To be honest, not really in that case. I mean, part of it just could be my familiarity looking at nerves and looking for structures diagnostically. But again, by the time I saw that patient, the atrophy was so rapid, I decided that it would probably be best to move forward with an electrodiagnostic study, which answers the other question. I tend to lean more towards electrodiagnostic study as opposed to an imaging study because of the low sensitivity of MRIs. And so I probably would not, it's a good thought, but not something that was at the forefront when I was treating that patient. Thank you, Dr. Yang. And for Dr. Nagpal, he's also been answering these questions. I think there were some thoughts about just the nerve conduction study and maybe using diagnostic ultrasound of the median nerve. Do you want to comment on that? Yeah, when this patient was my patient, we didn't really have diagnostic ultrasound as an option in our institution. We would probably consider it at this stage. But again, I think I knew the answer because of the fact that there was prolonged latency on the sensory median nerve conduction study. And the only way to, I guess, differentiate, and the other thing I didn't talk about is maybe it's a double crush injury, right? Maybe it's a C6 radiculopathy and a carpal tunnel syndrome, but the fact that it's just the thumb and the only weakness in the thumb and so on really made me think it was carpal tunnel in a really unusual presentation. There's no harm in getting that ultrasound, but I feel pretty confident that I prefer using diagnostic blocks as my technique of deciding whether somebody has a particular syndrome, and that's what I went with. Thank you. And maybe one final question for Dr. Smook. Just what manual exam maneuvers do you commonly use? Matt, you're on mute. The exam maneuver that I use is similar to what was used in the publications I described, and that's the osteopathic style manual therapy exam of the neck, where generally you isolate the AA joint, then isolate the AO joint in range of motion testing, and then palpate from C2 down to the bottom of the neck, mobilizing each segment, looking for tenderness and restrictions in movement. I predominantly base my findings on the tenderness part of it rather than relying on the restriction in motion, because that part's not as sensitive when you compare it between raters. And I learned to do that through a weekend course of osteopathic manual exam. Thank you. And thank you to all the presenters and all the attendees. If you have any other questions, feel free to ping us individually. We hope you have a great rest of your APMR conference, as well as a great Friday. Take care. Bye. Thanks, Patricia. Bye, everybody.

musculoskeletal conditions

difficulty with buttons

numbness in right hand

cervical myelopathy

cervical radiculopathy

carpal tunnel syndrome

cervicogenic headaches

arm weakness

brachial plexopathy

thoracic outlet syndrome

multifocal motor neuropathy