So, if there's any questions, I'll try and answer them. You know, I'm sorry about all that hoarseness. Last week was a bad week when they prerecorded this, this week a lot better. But if there's any questions, I'll go through it now. So, you know, so there were two papers that came out probably 10 or 15 years ago now. One Wilbur and Morgan and one Wilbur and Gilead. And they put the rest, they put to rest the idea of the double hit hypothesis. And at the same time, you can see two separate lesions. So you can have someone that has a C8 radiculopathy and an ulnar neuropathy at the same time. Say a diabetic that then hurts their neck, they might have bilateral ulnar neuropathies and bilateral carpal tunnel syndrome, which we see a lot in diabetics. They're more susceptible to compression neuropathies. And then they just happen to get a C8. So in the history, you may recognize right away that you're dealing with a radiculopathy because they may say, you know, I have really bad right-sided neck pain and that pain radiates down my arm. And so it has the features of a radiculopathy. Pain is the most pronounced feature often. And then they have sensory changes in the dermatome for that root and weakness in the myotome of that root, which would include the median C8, the ulnar C8, and the radial C8. Clinically, it'd be fairly easy to tease out, but on EMG, it's even easier. So what you would expect to find is ulnar sensory abnormalities. So when you have the ulnar sensory abnormalities on part one of the EMG study, the sensory nerve conduction studies, you know that it's a ganglionic or postganglionic lesion. And then on the motors, if the radial motor response recording EI is abnormal, then you know it's supercurricular. It may not be. So on the needle exam, you'll see abnormalities outside of the ulnar nerve distribution. So you'll see abnormalities in the radial C8s and in the median C8s. So median C8s, APB, which is more T1, but has C8, and other median hand-intrinsic muscles. But the flexor pulsus longus is another C8 T1. So you would see C8 median, C8 ulnar, all the ulnar nerve innervated muscles get C8. And then the radial, so the eccentric interstitial, eccentric pulsus brevis. And so you would know that you had a C8 root lesion, but because of the ulnar sensory, you know there's also a concomitant ulnar neuropathy. And then you would add the DUC to see where that ulnar is. The other thing you might notice is that on needle exam, there might be two populations of abnormalities. You know, there may be abnormalities related to timing. So say this diabetic had a long history of an ulnar neuropathy. So the ulnar innervated muscles might have a lot of chronic change and no fibrillations or sparse fibrillations. But then all the C8 innervated muscles have high amplitude fibrillations, implying that that lesion is new. And then the ulnar would be overlapped. So ulnar nerve innervated C8 muscles might have low amplitude fibrillations and high amplitude, but the C8 radial and C8 medians would have only high amplitude. So you wind up having to stick a lot of muscles and do a lot of side-to-side comparison when you have lesions that overlap each other like that. And sometimes you just have to say that, you know, more than one explanation is possible, but the most likely explanation is as follows. So sometimes in my report, I'll put that introductory comment and then put number one, you know, left C8 radiculopathy, number two, left ulnar neuropathy. And that would be another time when the EMG, which works independently throughout the test, can then be coupled with clinical findings at the end. So when I first start, I do my initial clinical assessment, it's very focused. And then I'm EMG from that point forward. And then once I'm done, I can't answer anything else with EMG, then I may correlate it clinically when I think that might help. So if this person had 10 L's at the ulnar groove on the symptomatic side, but not the other side, that would also support a lesion at that level. So it's hard when you have lesions that are pre-ganglionic and post-ganglionic in the same PNF segment, so a C8 root and an ulnar nerve. And then I see another question. The mean line of brachial cutaneous is going to be abnormal in a lower trunk and a medial cord. The only time you might see a discrepancy is when the lesion's at the anterior primary ramus level, proximal to the lower trunk, where the C8 and T1 anterior primary ramus or root fibers have separated. So in that case, if you had a C8 anterior primary ramus lesion, it would be expected to spare the MABC, but because the ulnar sensory axons run through C8, the ulnar sensory response is going to be abnormal. So they're both affected with medial cord and lower trunk, and the difference is proximal to the lower trunk where you may see one or the other. Or if you have a specific lesion like Trunagent Thoracic Outlet Syndrome that happens to be at the lower trunk level, because that pathology is from below, that band pushes up on the brachial plexus from below, and so the T1 anterior primary ramus and lower trunk get deflected the most, and then the C8 less. And so that's another time when you see a discrepancy, T1 more than C8. So the second lumbar hole, for some reason it just seems to be the last to go out. Maybe it's better protected. You know, depending on the fascia growth inside the median nerve, it might be that the motor axons of the second lumbar hole just don't get compressed as easy. So they tend to be the last to go. So I always check that last, you know, when I'm desperate. When the sensory response is out and the motor is out, I know I have a median neuropathy somewhere distal to the axilla. I can tease it out on needle. I can check hand intrinsics, and if they're abnormal and the flexor palsus longest and the pronator teres are normal, then I know I have a lesion somewhere, you know, distal to the flexor palsus longest branch point. But if I do the median second lumbar hole and it's still there, then like in that case, 1C, there was quite a delay, but the amplitude was pretty robust. And so it was obviously a demyelinating lesion, and now I can conclude that it's distal to the stimulation site, which was the wrist, and proximal to the second lumbar hole branch. And so I was able to say, I was able to better localize it with the second lumbar hole rather than say it's somewhere distal to the axilla, I can say it's distal to the wrist, and based on those clinical features, we know that it's carpal tunnel syndrome. I haven't noticed significant asymmetries when I record the radial EI. You know, in order to be abnormal, it has to be a 50% difference, and although if we can go back in time, it seems like a 40% difference is easily reproduced as well. But in our lab, we don't call it unless it's more than 50%, and then you just have to rely on the needle exam. And I haven't noticed any side-to-side asymmetries that were outside of normal. So I wouldn't think a technical would give you a greater than 50% side-to-side asymmetry. The problem is, if you do make a technical error and you don't know it, and then the other side you do ideally, you may see a greater asymmetry than is really there. So we always double-check, either the big one's too big or the small one's too small. And more likely, it's going to be that the small one is too small. So if I see a side-to-side difference that doesn't make sense, I just repeat it myself. And then I may or may not repeat the other side. But sometimes, there are technical errors, but by double-checking, you can pick them up. In the end, everything should make sense. The localization that the sensories generate should be the same as what the motors have to say, which should be the same as what the needle has to say, which should be the same as the clinical findings. So really, everything should be in harmony. And when two things point in different directions, something's not right, and you just have to double-check the most likely thing that's not right. And again, really sorry about the hoarseness. It's almost gone now, but I still have some. But even though I was having a hard time understanding myself. Anyway, if you want, someone asked for the slides, those pathway slides. If you email me, I put my email in the chat box, but it's just my initials, M-A-F-M-D, the number one at gmail.com. If you email me for those, I can send them to you. All right, thank you. Hopefully, next time it'll be face-to-face. Although I did enjoy front row seats as an attendee, but still, I think that it's better face-to-face. Have a good rest of the day.

double hit hypothesis

diagnosing conditions

C8 radiculopathy

ulnar neuropathy

ganglionic and postganglionic lesions