Transcript

- Ladies and gentlemen, thank you for joining us, this is going to be the part two of a general review for peripheral nerve disorders. Again, we're joined by Dr. Rob Spinner from Mayo Clinic. Rob thanks again and please proceed.

- Sure, thanks Aaron. I'd like to continue along this review for boards on peripheral nerve subjects that might be of interest. I'd like to now spend the next few minutes talking about nerve entrapments. All examiners have hands so I think different hand postures would be something that you might think about. Let's talk about some basic principles of nerve entrapments. Any nerve can be compressed anywhere along its course. Most nerve compressions occur though at predictable sites namely fibro-osseous or fibromuscular tunnels. In other words, tunnel syndromes. In a true sense entrapments really shouldn't encompass mass lesions because mass lesions could occur anywhere. So for example a buttock level tumor causing sciatic nerve symptoms really isn't piriformis syndrome for example. Now the pathophysiology can either be understood in terms of static or dynamic compression. And I think that's important when you think about provocative maneuvers that we've all learnt. Now there are some clinical features that should be known and are predictable. I'm simple-minded I think that nerves do three things. They do pain fibers, there's muscle fibers and they're sensory fibers and they can all have associated dysfunction and you need to ask about these when you're taking a history and doing a physical exam. But the key is is that the pattern of presentation with these syndromes by definition is largely predictable. I use this analogy from my friend Michelle Cleo who will be in UCSF. I think that the physical exam along with the history and testing are similar to the legs of a table and the more legs of the table you have the more stable the table. So in other words when you're defining any syndrome it's nice when you have four legs history physical exam EMG and then imaging. Now of course you don't need imaging in all cases especially with a routine carpal tunnel. But in some of the rare ones, again, three out of four legs is good, two out of four is okay but once you're less than two for example, you're really not on very stable ground. Nerve blocks can also give some information in my hands I think nerve blocks are also effective when they don't produce a clinical outcome because then you know when it produces an effect that it may not be the nerve that's the problem. Now non-operative measures should always be considered for your oral boards, most likely the patient won't get better so I'm not going to spend a lot of time but in general, what we should think about with any nerve entrapment whether it's carpal tunnel or some of the other ones is a period of rest, avoiding the exacerbating activities or positions, some type of splinting perhaps, physical therapy, non-steroidals and or corticosteroid injections as a whole. Now again surgery is often done especially when you're taking your boards and in this case if they're done the goals would be for a compression syndrome is to eliminate the compression. You wanna ensure that there's a good dead for a nerve let's say like the lateral thermo-cutaneous nerve a sensory nerve you can either do a neurolysis or if it's expendable some people would do a neurectomy that's controversial. The basic principles of surgery would be to be done when there are persistent symptoms after a trial of non-operative therapy, a progressive deficit under your watch, or significant atrophy by the time the patient presents to you. In general, these are very gratifying procedures. So typically good to excellent results in primary cases and good for pain control when you're even doing a revision case under the right circumstances. Let's start with the median nerve, the median nerve is the most commonly entrapped, we all know about carpal tunnel. I think this would be a very fair board question. And I think we're all familiar with carpal tunnel, you need to know what carpal tunnel is, patients will tell you they get tingling in their hand, they may not always tell you that it's the right digits. They may in fact tell you it's all digits but if you third it out it's usually thumb index and middle finger. Classically there are nocturnal symptoms, patients get relief by shaking their hand so you see this and patients will tell you that their symptoms are worse when they drive a car. That history by itself can be correlated with the clinical diagnosis of carpal tunnel syndrome. Now it's unusual that you'll see thenar atrophy like this. This is late, this is may be seen with patients who are elderly who present with pain. Maybe they're not so bothered by the loss of function, the pain is keeping them at wake. So this is rarely seen in lifetime but may be seen on your board exam. Now, on physical exam patients may often have normal testing clinically. So their sensation may be normal when you touch them that you may do two-point sensation like I do and it may be relatively normal. Their strength may be intact. You wanna test in particular abduction of the thumb which is abductor pollicis brevis. You remember the loaf muscles and we'll talk about that in particular. The median nerve sensory distribution is the three and a half digits. Receptor pollicis brevis would be your thumb and you resist it towards your nose. So like that, and your examiner might ask you that. The other muscles the extrinsic finger flexors are proximal to carpal tunnel. You wanna test those but they should be normal. So for example finger flexion, flexor pollicis longus would be normal as would your index finger flexor digitorum profundus. So how I would examine that would be blocking out the other fingers and resisting that. flexor digitorum superficialis, for example those would be normal. The other thing would be checking for a percussion sign at the wrist or doing valence tests or reverse valence test. Those provocative maneuvers put the carpal tunnel under some stress. On your boards and in real life, I get EMGs on any nerve of that's being compressed. Here you want to see that they are positive, the examiner might ask you about sensory latencies being very reliable. Velocities are usually 50 to 60. I remember that just like driving a car in a highway, less than that is slow and that's consistent with the nerve compression. Now carpal tunnel is common. So just because an EMG sees it doesn't mean that that's what's the problem and we all have seen cases of foramen magnum tumors, for example, with EMGs that show carpal tunnel. When non-operative measures fail, then one would consider surgery, there are certain landmarks that you need to know about, the carpal tunnel, the transverse carpal ligament goes from what's considered Kaplan's cardinal line which is an imaginary line drawn from this inner space across the wrist that suggests where the recurrent branch is but it's also the end of the transverse carpal ligament, the artery from the palmar arch superficial palmar arch is here, very close to that. The proximal end of the carpal tunnel is at the distal crease. A standard incision would be from here to here. You would use the flexed ring finger. For example, that's a good landmark in this direction so that you're avoiding cutaneous branches. When you do your carpal tunnel release, you wanna stay ulnar when you're making your opening in the ligament so as to avoid any chance of injury to this recurrent branch which goes to the thenar muscles, for example. Here would be sort of a standard carpal tunnel release, you could see the landmarks Kaplan's cardinal line the wrist crease in line with a bent ring finger and then typically most people would even use a wrist crease. There are different ways to skin a cat, you can use smaller incisions endoscopic ways. For your boards, I would do a standard release open especially if that's what you do. If you do endoscopic releases in practice, that's fine. We'll talk about results. Here's a standard open release. The one advantage is you can see the nerve and you can see the discoloration of the nerve with an hourglass type deformity. Here you can see the transverse carpal ligament. The key, again, is stay ulnar. The risks of the procedure postoperatively one could injure the palmer cutaneous branch which comes off several centimeters proximal to the wrist people can get pain in the palm. You can get ulnar nerve entrapments if you put or ulnar the nerve symptoms at the wrist if you have a hematoma or the ulnar nerve is just superficial and ulnar so if you see the vessel, you can actually be near the ulnar nerve and that can get retracted with a self-retaining. The injury the recurrent branch was discussed and can be avoided. Now you don't need to know a lot about studies but I do wanna just give you a few related the carpal tunnel and to the ulnar nerve at the elbow since those are most common. I will just tell you for your boards, prospective controlled randomized studies comparing open verse endoscopic show that all techniques are affected. There are some advantages to endoscopic releases. In practice people can return to work somewhat earlier so two to three weeks. Some people suggest it's cost effective maybe because there's fewer incisions there's less scar tenderness and pillar pain and you do get quicker return of grip strength. But there are some disadvantages to endoscopy. It's a new procedure, steep learning curve, we visualize structures less and in this meta-analysis at least one could bear out the increased risk of neurovascular injury. And people in the lab have talked about incomplete ligament release being more common using this that hasn't been borne out clinically. In summary though, the potential benefits are seen only in the first several weeks, but at about three months, the results are the same. Now I do want to talk about median nerve anatomy because there are several things that need to be considered. Again, carpal tunnel is here, so here is your abductor pollicis brevis muscle that I was talking about along with these other loaf muscles which are less important to clinical testing. Opposition you have to be careful because someone could oppose their thumb using trick motions. Abductor policy brevis and thenar bulk are good for thenar muscles. Now, the more proximal innervated nerve injuries or lesions or entrapments can involve the anterior interosseus nerve which is below the elbow and that affects these muscles flexor digitorum profundus, index and middle, flexor pollicis longus and pronator quadratus. We'll talk about that in a moment. Even higher to that, so even proximal, you use your finger flexors. So an anterior neuroses nerve syndrome is not the same as a high or a complete median nerve lesion. Above the level of the elbow. This would give you some sensory loss, the anterior interosseus does not have cutaneous sensation, it provides some sensation only the wrist joint. So that's more of a capsule type of articular pain rather than a cutaneous sensory pattern. The palmer branch that we talked about is given off several centimeters above the wrist. So that would not typically be affected. In other words, it would be normal in patients with carpal tunnel but it could get injured in patients who've had carpal tunnel releases that injured that nerve. Anterior interosseus nerve syndrome is a famous one on the boards, it's a relatively rare syndrome as we've talked about. This is the largest branch of the median nerve that's given off just below the elbow and it innervates these groups of muscles. No sensation to skin. In effect, what you get is the okay sign. People when they're asked to make a fist, they're unable to bend their thumb, they're unable to bend the distal interphalangeal joint of the index finger. So in other words instead of making an O, they have what's called a square pinch as you can see in this drawing. Your examiners have a hand, so they can tell you a patient presents like this even though in truth they may not have seen that patient. Now it used to be thought that the anterior interosseous nerve syndrome was due to entrapment. And various things were described including fibrous bands particularly of some of the forearm muscles. In truth, I believe that most of these so-called entrapments are really due to inflammation from variants of Parsonage-Turner syndrome. And we'll talk about that. Any patient who has an unusual syndrome, anything more unusual than a carpal tunnel or a cubital tunnel, so ulnar nerve at the elbow, I would say image. Image that region with an MRI scan or a high resolution ultrasound. Make sure there's no mass lesion. And of course take a history for trauma. These are the four things that you really need to think about with any unusual nerve entrapment syndrome beginning with this anterior neuroses nerve. The other test question relates to this ligament to struthers. The ligament to struthers is an abnormal bony, it's an abnormal bend associated with the supracondylar process. This is akin to a cervical rib, it's an extra bone. About half a percent of normal people have this. It very very rarely causes symptoms. It could be found on a routine elbow X-ray or a clinical exam with a spur. It's a very rare case of entrapment. But what passes through this is the median nerve above the level of the elbow and the brachial artery so you could get neurovascular syndromes. This is not an anterior interosseous nerve syndrome because the anterior interosseus nerve is here. This is above the level of the elbow. So this could give something that might look like a carpal tunnel but in truth other muscles should be affected et cetera. The ulnar nerve has been associated with it but it doesn't pass through it. There are some cases of people with this abnormal anatomy having an ulnar nerve lesion as well. The other hand that is good for testing is called the benediction sign. Now, this is confusing and important to understand. With a high median nerve injury, the patient in addition to losing the distal flexion of the thumb and index finger causing the anterior neuroses nerve also loses other muscles including the flexor digitorum superficialis. So if this is a picture of somebody trying to make a fist, this person does not have an anterior interosseous nerve syndrome because you can see he can't bend at the middle joint here. So this is the flexor digitorum profundus level, this is the flexor digitorum superficialis level. So in other words, this patient has a more proximal injury affecting all of this and likelihood the patient would also have sensory loss in the thenar digits and if you examine for pain most likely this patient would have a Tinel sign at the level of the elbow or higher rather than at the wrist with carpal tunnel. Now this benediction sign is the one for the median nerve. It's very important to distinguish this from if everyone looks at my hand, somebody who has clawing of the fourth and fifth digits. This person has clawed here hyper extension at the metacarpal phalanges joints, this patient is trying to extend the fingers. This is me trying to bend and I have a high median nerve injury this is clawing on a nerve injury that could be anywhere along the ulnar nerve. In fact when the clawing is worse, it tends to be at the wrist rather than a more subtle clawing which is usually the ulnar nerve at the elbow. Similar hands, different nerves, important to understand what's happening with both. Let's switch gears now and talk about ulnar neuropathy. Ulnar neuropathy at the elbow is the second most common nerve entrapment. We're all familiar with paresthesias in the ulnar one and a half digits. Hand weakness worse affecting intrinsic, so interossei, first adductor pollicis muscle for example, and sometimes elbow pain. Ask about elbow trauma, either acute or remote. It's important to consider and to distinguish this from a C8 radiculopathy, how to distinguish it and why it's not C8 versus ulnar neuropathy, why it's not a pancoast tumor, why it's not on the nerve at the wrist. These are things that you need to know. Part of it is related to the anatomy. The anatomy again start with your history, does the patient have elbow pain or neck pain? The patient has elbow pain, then it's more likely elbow level problem. The patient uses jackhammers and has wrist pain, think about ulnar problems at the level of the wrist. The patient has provocative maneuvers overhead, it could be thoracic outlet. Patient's a smoker, has weight loss, is coughing, think about a pancoast tumor with pain. So again, history is important. You wanna ask about motor sensory and pain. When you're examining the patient think about motor sensory and pain. How to distinguish an elbow lesion of the ulnar nerve versus the wrist for motor testing. At the elbow, the extrinsic muscles namely the flexor digitorum profundus to the little and ring finger would be affected or could be affected with the flexor carpal nerves. Those are difficult to test clinically and may not be weak because the ulnar fibers that seem to get affected are usually similar to the ones that are affected at the wrist. Namely, the hand intrinsics that are ulnar innervated. But importantly the sensory dermatome would be different. With ulnar nerve at the wrist, you would lose palmer sensation but the dorsum would be unaffected. So in other words the dorsal aspect here would be normal with a wrist level lesion whereas at the elbow this would be abnormal. That could be tested on a nerve conduction study as well as on your clinical exam. So again motor testing sensory abnormality and pain. You always want to test pain. How you can do that here would be provocative maneuvers, elbow flexion test, tunnel sign at the elbow, if you were thinking about the wrist you might tap on the ulnar side of the wrist, you might do provocative tests like carpal tunnel ones or Guyon's canal. You think about thoracic outlet, et cetera. For her spine, you might be thinking about doing a sperling's test and narrowing the foramen. Again the anatomy is such that the dorsal cutaneous branch that I showed you, that gives this, is six to eight centimeters above the wrist. So this branch would be affected with an elbow level lesion but would be normal with a wrist one. That's important. So build up from your history, to physical exam, do an EMG and if you're concerned do imaging. Like I said for carpal tunnel or cubital tunnel, I probably don't routinely image with failed cases I would but for atypical presentations of these lesions or unusual entrapments like the anterior neurosis, posterior neuroses all the other ones I do image and would recommend you do the same. Cubital tunnel syndrome definitely has a dynamic component. The ulnar nerve goes through at the level of the elbow, it goes beneath a retinaculum. Some people talk about Osborne's band. It's a little bit difficult to know exactly where Osborne's band is. So I think this is better terminology, cubital tunnel retinaculum. The nerve goes between the heads of the flexor carpi ulnaris and it gets entrapped right here. When you transpose a nerve, it's not that you're transposing it in order to decompress the nerve because of potential entrapments. In fact 99% of compressions occur right here and that's the concept between the surgical approach doing a simple decompression. This is somewhat controversial. However, when you're transposing a nerve in order to make it go anteriorly, you need to decompress it more widely so that it's free when you move it. You don't wanna cause a man-made or woman-made entrapment. Now mentioned that the ulnar nerve is a dynamic creature. Here you can see the nerve is happy in extension, this is a cadaver specimen. This is work of Dr. Shawn O'driscoll here. And the nerve is flex. When the elbow is flexed as you can see here, the nerve is taut. The pressures go up, we know that from people like Richard Gelberman. So that's why patients get symptoms with elbow flexion. Curling type activities using a cell phone like this can cause problems. So the treatment would be gentle, positioning in a splint like this rather than this. This would be provocative. More and more people are going to in situ decompression. Here you can see proximal and distally. Here's the level of the pubital tunnel retinaculum which has been released. The nerve has been unroofed. It hasn't been circumferentially decompressed. Skin nerves have been saved. The area of compression has been relieved. Whether or not to transpose or not to transpose, this is the question. Again, there are enthusiastic supporters and even louder refuters. When we look at the data, what is the best study from the meta-analysis that have been done, it really is surgeon's preference. Many people have been brought up with one being better than the other. And in fact most studies don't show dramatic changes and there really haven't been true statistical differences in by and large. People then faulted those studies as being retrospective. Meta-analysis so now there are several prospective randomized studies and the key is is that despite what you may or may not have been taught, the several studies, several of which are in neurosurgical journals show that there's no statistical difference between clinical and electrophysiological outcomes between patients treated with simple decompression versus transposition procedures. And in fact only P-value is that a simple decompression has less of a complication rate. It's a smaller operation, less wound problems. And here are some references including ones in neurosurgery journals showing the various procedures and the comparisons. Now let's talk about ulnar nerve at Guyon's canal. Of a hundred people with an ulnar neuropathy, 99% or so at the elbow only 1% are at the wrist. But this seems to show up on board exams. Again, start with a good history. The history is very similar to ones at the elbow. Ulnar nerve at the elbow would cause similar findings at the wrist but there are subtle differences. So again take a systematic approach using a good history. So sensation are you numb, yep. Palmerly, what about on the outside? Nope. Hand weakness may be present with either one but here the patient's symptoms would stem from the wrist probably rather than the elbow. And definitely not at the more proximal. We'll talk about combinations whereas people have one or the other rather so patients can have pure atrophy and motor loss without sensory loss. And that's important because this could look like ALS. You wanna take a work related history so if an examiner told you that this was a carpenter or a jackhammer and that's something where you could use the wrist or the elbow but you wanna think about that because, again, that's information that potentially is useful. Just for anatomy, I'm showing the MRI appearance of someone. And the point is is that this is a wrist in the scanner Guyon's canal is superficial and ulnar to the transverse carpal ligament. In fact, Guyon's canal, the floor is the transverse carpal ligament. So in other words, the ulnar nerve can be seen here, the median nerve can be seen here. So you can just get some topographic orientation about where you're putting your retractor, for example, when you're exposing the carpal tunnel and why you want to avoid a deep blade because it's possible to take the ulnar artery along with the nerve while spreading. The other thing that's important is if you release the carpal tunnel in some patients, you see that you could actually be within Guyon's canal and you might even see the artery. Just again, while you're staying ulnar to avoid the recurrent branch, you wanna be mindful of that anatomy. This is taken from Dr. Kline Atlas. I think people exposing it would make some sort of curved incision across a crease. You want the easiest way of finding this anatomy. Again, your carpal tunnel is here while you could get to Guyon's canal from a standard carpal tunnel approach, I think it's easier to find the ulnar nerve next to the ulnar artery right by the flexor carpi ulnaris. Find the nerve, find the ulnar vessels, protect both in vessels and then trace the ulnar nerve into the superficial branch which goes superficial, the deep branch which goes deep. This is important in order to understand that Guyon's canal runs through this part of the nerve territory. You can get a cyst affecting just the deep branch looking like an ALS hand without sensory abdomen. It's important to know so be careful about patients like this otherwise patients presenting in this zone would have motor loss and sensory loss. But again the back of the hand would be normal. So here's a patient. You can see scrubbed in the OR. Lots of atrophy. Here's the first dorsal web space, interossei atrophy. They would have a positive fore man sign and you need to understand again that if they showed you a hand like this with normal sensation, think about ulnar nerve at the wrist along with ALS. Ask about the other hand, ask about the EMG. Again, the EMG in this case, the examiner wouldn't give you the patient was found to have ALS. They would give you some information they'd wanna know if you understood it. But again you would wanna tell the examiner that you're aware that there are electrophysiological criteria for ALS like the limbs or the tongue and you'd want to say ulnar neuropathy at the risk versus ALS. That would give them ammunition to know that you know what you're talking about. And then all of a sudden if you've got the needle exam of the opposite hand that had asymmetric fasciculations, or fibrillations et cetera because it's upper and lower motor neuron disease and you had breast reflexes, again, you wanna think outside the box. Think about the tongue et cetera. So a motor neuropathy that looks like this without sensory problems still could be on the nerve at the wrist that you wanna think about other entities including ALS. Here's a patient who presented, however, with ulnar nerve loss intrinsics. Had some sensory loss that was mild and in fact you could see that here there was terrible compression and this is part of the decompression of the deep branch and you can see how thinned out that area was. This was not well characterized. It's not known why this patient had this abnormality. Another type of incision used where a ganglion cyst was detected on MRI. And again here the key is is, as I mentioned, any patient who presents with an unusual entrapment, I would image. Because here, I would rather know that there was this big ganglion cyst coming from the wrist compressing the ulnar nerve. I'd rather know about it preoperatively and make my plans rather than finding out about it intraoperatively and not knowing what it is or how to deal with it. So ganglia from the wrist joint can compress them secondarily. There's a case the ulnar nerve at Guyon's canal. Here's the deep branch going under there. The patient had just motor loss like an ALS patient. Here's the ganglion cyst. Superficial branch is above it unaffected. And you can see the nerve is then moved, the ganglion is traced to the wrist joint, and resected in this case, the nerve is free. Ulnar symptoms from ulnar neuropathy must be distinguished from thoracic outlet syndrome. Now we're all familiar with thoracic outlet syndrome because it's controversial but in general I think for your boards you need to know that for example a young woman with a long neck who had cramping pain in the forearm, cramping with overhead activities, radiating paresthesias, very well could have thoracic outlet syndrome. Now, most patients with thoracic outlet syndrome symptoms have normal findings. They have a normal exam, normal EMGs, maybe they have an extra rib. In fact there's a patient I saw last week who presented with right side symptoms. You can see close up, up here there's a small rib, but in fact on the opposite asymptomatic side there's a bigger cervical rib. Cervical ribs like the supracondylar process are found in approximately one or a little less than 1% of the population. Rarely are they symptomatic, so they're just radiologic findings. Provocative maneuvers that you all know including the adsense test and some of the overhead costoclavicular maneuvers et cetera so here we use what's called the javelin throwers or the east positioning costoclavicular maneuvers overhead cramping et cetera, those are all provocative maneuvers but in fact they could be found in normal patients up to a third or fourth of the time. So the finding that a pulse obliterates or is asymmetric is not enough to make this diagnosis and that's part of the controversy. Patients may have some symptoms, they may have been involved in a car accident, have litigation, they present with these constellation of findings, they have a normal exam then you have to use some poor sense and correlating everything as best as you can come up with an answer. The mainstay is often physical therapy as long as there are no neurological findings. There is an entity of neurogenic thoracic outlet syndrome. This is the real deal. And this is someone who has T1 lower trunk proximal innervated neurologic loss. I show these pictures as a patient I saw last week who had loss looking like a ulnar nerve problem but here on close up there's also phenol wasting. So here you can see hypothenar wasting, interossei that's ulnar. Thenar is median. So combined median and ulnar loss is C8 T1 close to the foramen usually and that's often called a Gilliatt-Sumner hand and that can be surgically decompressed. That's different than a thoracic outlet syndrome where someone has symptoms but without findings. In patients with thoracic outlet symptoms, the EMG is typically normal. This patient clearly would have neurologic loss. Here the patient had fibrillations in the affected muscles including some finger extensors which are C8 and some other finger flexors which are also C8. So here you wanna image, this patient had a rib the patient may not have an extra rib and then the treatment is surgical and there you know about the controversies with decompression either superclavicular, transaxillary both taking out the extra rib taking out the first rib or just doing a decompression. Let's move to some other good testmanship areas involving the radial nerve. Again, the train track of the radial nerve, radial nerve derives from posterior cord. Triceps branches are given off high on the posterior cord to distinguish a radial nerve you test axillary nerve and deltoid. You need to know that triceps are typically normal with a arm level entrapment. Arm level entrapment is usually the site for trauma or cyanide palsy. So it's everything below which would be wrist and finger extensors. So that's the lay of the land. The other thing we mentioned before is the importance of testing the brachioradialis with a arm level lesion. This would be the earliest one that would show some recovery these would be later. An inch a month. Radial nerve entrapment in the arm true entrapment is very rare, I'll show you a case. Compression can occur as in the interossei palsy, that would be a very fair test question I think. Some young kid drinking too much, forgetful with his position of his arm had a bunch of little bottles on the airplane for example, fell asleep in a stuporous state, compressed the arm didn't move and ended up with a radial nerve palsy. Traditionally these are neuropractic lesions. If you remember the neuropraxial ones, don't have to recover by regeneration, they're thought to be more a metabolic type of lesion or a vascular type so they recover quickly. So here cyanide palsies typically have the best outcome. Now the most common radial nerve palsy is not an entrapment, it's a traumatic lesion associated with an arm or a hemo fracture. These are often time treated like the closed stretch injury. Wait three to six months, wait for recovery if there's no recovery then explore. And again with any spontaneous entrapment, like I told you, I would MRI make sure there's no lesion. With a history of trauma, you don't have to get an MRI. Playing films are often helpful but again you wanna take a good history. Here's a patient who's a weightlifter, he presented with a wrist drop, this is the type of exercise he would do routinely. He presented with this characteristic wrist and finger drop. This is not a posterior interosseus nerve palsy. Posterior interosseus nerve palsy did not have a complete wrist drop as is seen here. There's sensory loss and on the thumb they're sensory loss in the autonomous zone, so right here. And here you can see X marks the spot, that's the side of the Tinel sign percussion there. You start distally go along the course of the nerve and here I get a spot that reproduces parasthesias into the back of the hand associated with a wrist and finger drop. Here's the x that's a radian nerve palsy and this was an entrapment. Unusual but good to show you guys. Posterior interosseus nerve lesions are rare. They have a different hand and I think for that reason it's a good exam question. Again, in the past it used to be thought due to entrapment. I think many of the cases of entrapment are not entrapment their inflammation. We'll talk about that again. You wanna rule out compression from a mass. I would image these patients and I would take a history of trauma. Here is the hand of a patient with a posterior interosseous nerve palsy. The wrist can be dorsiflexed actively in a radial deviation so here's the thumb, there's a finger drop. The wrist cannot come up in neutral. This is neutral, this is radial. The reason is is if you learnt the anatomy, the wrist innervated muscles are proximal to the posterior loss interosseous nerve the extensor carpi ulnaris is part of the posterior interosseous nerve. So this patient has none of that so the pull is this way and the fingers are part of the posterior interosseus nerve. Like the anterior interosseous nerve, there is no cutaneous innervation here similar to the anterior interosseous nerve, there are fibers that go to the wrist joint for proprioception but no cutaneous innervation. So there's no dermatomal loss with a pure posterior interosseous nerve. So here there's a finger drop, triceps would be normal. The wrist most importantly would be radial deviated and in fact fairly strong in this manner. But the patient cannot dorsiflex neutral or ulnar and has a complete finger drop posterior interosseous nerve is just below the level of the ulnar. You don't have to get out all fingers so in fact not everyone reads the books. There are partial lesions that are posterior interosseous nerve, this patient you can't see very well but has a radial deviated wrist as a finger drop of the ulnar sided digits, this one still works. As I told you get an EMG, get an MRI, this patient has a mass, this mass is the same as the fat, this is a lipoma. You can see the terminal branches and this is entrapped at the level of the arcade of Frohse. This is not an intraneural tumor. This is an extraneural tumor. We'll talk about tumors in a few minutes. Here's the level of the elbow the radial nerve, superficial branch and then the deep branch and deep branches being compressed and all you do is find the nerves and then you move them out of their way and you take out the tumor. Here's the nerve being compressed by an extraneural mass. And there's the benign lipoma. This can be diagnosed readily and planned for preoperatively. Again, an MRI in unusual cases. In the past though, there's been some mention about entrapment. In fact, this is some of the work of my father's describing the arcade of Frohse. The arcade of Frohse is a good test question. It's where the deep branch of the radial nerve turns into the posterior interosseous nerve just beneath the two heads of the supinator the posterior interosseous nerve gets torqued on and with rotation of the forearm there can be some mechanical changes in pressure whether or not this is actually causing the entrapment is disputed. In fact many of these cases that in the past have been thought to be due to this arcade of Frohse and entrapment may in fact be inflammation Parsonage-Turner syndrome that gets better with or without surgery over time as we'll talk about. But this is the anatomy that you may get tested on. Now there are various surgical approaches that you need to know. Everyone asks about surgical approaches, I show you a very easy one. This is the elbow joint. There's a very easy way of making sort of a gentle S either here to find the radial nerve. So the interval is between the brachialis and the brachial radialis if this is taken upwards you can get to the arm, the spiral glue. If it's taken distally, you can find this and then find the radial nerve. Superficial and deep branches posterior interosseous nerve, and go anterior in this interval. The brachial radialis is separated by the pronator teres. Very nice operation. The superficial branch is beneath the brachioradialis. You find that, you trace it up to this. Again, you'll see neighboring contiguous muscular branches, those are the reasons again why there's radial deviation and the PIN is affected because these are still working. The radial pull of the wrist extensors. Now if you go this way, this is easy to get to the radial nerve. But if you take it medially, you can get to the median nerve and the brachial artery. Same interval and then here you have the service fibrosis or the biceps aponeurosis beneath that is the median nerve and the brachial artery. And this is a nice way if you need to explore the median nerve. Again that's a rare sight of injury or entrapment. Lastly with the radial nerve, you can get an isolated sensory symptom. Most motion and muscle testing is normal, this patient has sensory loss in the thumb. The compression is actually the wristband. This can occur with handcuffs, so-called handcuffed neuropathy. It can occur from a lesion from a K-wire such as done for fixing wrist fractures like all these fractures. Plating, small operations like deca veins tendonitis. The superficial radial nerve branch or branches are right here and are particularly superficial and vulnerable and painful. Another thing that you might wanna look at is winged scapula. There's a patient I saw last week who has a very pronounced winged scapula. You can see she's provoking the scapular winging by putting her arm outstretched against the ceiling here, or I'm sorry, against the wall in front of her. Also this is actually the range of her abduction and forward flexion it's about 100 degrees. She can't get it up further than that because her scapula is so unstable. This is serratus anterior palsy. Other things that can cause a winged scapula are trapezius atrophy and even rhomboid problems. This is the most common, as you'll see and as we'll discuss, long thoracic neuropathy is typically synonymous with an inflammatory condition such as seeing with Parsonage-Turner syndrome. Parsonage-Turner syndrome goes by many names as you all know including idiopathic brachial plexitis meaning we don't know what causes it. Neuralgic amyotrophy and even serum neuritis. It's poorly understood as best as we know it's thought to be inflammatory. May be immune mediated. You need to take a good history because often time you'll get something in the history suggesting a concurrent infection, patient or his family may have had the flu, there may have been an immunization, there may have been some trauma but unrelated to the shoulder. In fact, it's often curious because patients may give you a history of trauma such as from a golfing injury or golfing activities, for example, but in fact the avid golfers and they did nothing differently that day but in fact to take a history and their child had a flu that was terrible the week before and that's when they got their body. Surgery can be the trigger and this is thought to be an immune mediated process causing inflammatory mechanism. If you think about some of the thoughts about Bell's palsy many of the same aren't thought about either, pregnancy can also be a trigger. Now the presentation often takes a classic clinical triad. Pain, first then shoulder and arm weakness with a vague sensory abnormality. Typically the shoulder pain is severe and occurs periscapular lasts a week then goes away and then the patient may have the arm or shoulder weakness. Now certain nerves are affected. We've talked about the long thoracic nerve, we've talked about the anterior or posterior interosseous nerves. Other nerves that could be affected include the shoulder girdle ones including superscapular or axillary nerves. Now they can be in isolation like a winged scapula or they could be in combination where the winged scapula occurs with other things. So for example a very fair question would be somebody who has a winged scapula but also has an anterior interosseous nerve palsy that's isolated. That combination would be very good for Parsonage-Turner syndrome, it would be very difficult to pinpoint that to either peripheral nerves or spinal nerves. So if you know the distribution, you can predict that this is an inflammatory case, the treatments are different. You also need to know that occasionally non-plexal nerves like the phrenic or even cranial nerves like spinal accessory nerves can be affected. One or so percent of the time they can be bilateral, they can be hereditary. So those are things to store up your seed. But again patients may have what looks like an anterior interosseous nerve palsy or even a partial median nerve palsy and the bottom line is you need to take a history this patient had a tetanus shot, this patient had a flu. Now EMG can be helpful. The first thing is as it rules out other disease. Secondly, is it can reveal subclinical findings. So for example you may not detect any weakness in muscles but there may be sensory abnormality, sensory or motor abnormalities that miss your exam and the motor findings may be present on an EMG, this may allow you to find this for example. Oftentimes the serratus anterior may be very subtle and there may not be winging. EMGs may not be done of that side, you may want them to do the opposite side, bilateral be particularly helpful. CSF is often normal when it's done. MRI is being done more and more for this type of condition. While the findings for Parsonage-Turner may be non-specific, you do see muscle denervation and in fact you can see muscle denervation beyond what we find on EMG. So for example patchy denervation in a big muscle like the triceps may not be detected on an EMG of one head of the triceps. But when they look at the whole triceps, you may see patchy innervation in one part of the triceps and then you may see abnormalities in another muscle and then all of a sudden you have patchy denervation this is consistent with patchy process separatory immunomediated process Parsonage-Turner syndrome, MRI of the neck for example may exclude other pathology that's treatable such as a disc. But again if you see a winged scapula, I wouldn't be thinking about cervical disease in my top five. Newer techniques really do show nerve abnormalities but those are beyond what you need to know for your advantage. Parsonage-Turner as you can imagine looks like many different diseases. I think the temptation is to try to operate on their spine, many people taking their boards are very comfortable doing several level PCDFs. Again, be careful because the parameter they show you are probably not very tight and you're getting nervous before you know it you're doing several level anterior corpectomy for somebody with winged scapula would be better off treated non-operable. Other neuropathies must be considered, shoulder pathology, rotator cuff always needs to be thought about. The treatment here presuming it's an inflammation is observation. A multi-center actually the meta-analysis from cochlear view may show some subtle difference in giving steroids but most people still are not giving steroids, they'll treat the pain with non-steroidals, they'll watch the patient. Therapy is important. If you do operate, in fact like the anterior interosseous nerve palsies it would be difficult to prove whether or not you're decompressing a compression or an entrapment or in fact if a natural history is favorable. I remember early in my career I operated on someone with PIN palsy, I talked to them about all this, I didn't find anything at the arcade of Frohse. I was reluctant to see and hesitant to see the patient back because I really didn't see the patient's operative, I didn't see any abnormalities in the nerve at surgery. Patient came back thinking I was a hero and patient got better. It's easy to take the credit but in fact it's the natural history. So in fact people are looking for entrapments of the long thoracic nerve, they've talked about a spot in the scaling medius and they're decompressing that, this is deep, this is controversial. Again, most people will follow this and deal with it. There are some people where some biopsy specimens have been done of various nerves and as best as we can see there is some evidence to reinforce or to support the inflammatory nature. Again, late deformities can often be reconstructed using the salvage technique of tendon transfers. Especially for one scapular there's a very good tender transference. Overall, 70 to 80% of patients have a favorable prognosis. It doesn't always have to happen. It may take several years up to two years. The winging may always be a remnant, there may be improvement but it may not go away. And it's unknown whether or not patients with this are predisposed to additional musculoskeletal trauma, patients want to know that. Another favorite entrapment is superscapular neuropathy. Again, beware of these in isolation because as I mentioned before, this could be one of the ones that is affected with parsons turner syndrome. But still there's a subgroup of patients like overhead baseball throwers, volleyball players who seem to be predisposed to injury in a superscapular nerve above the level of the scapular spine where the suprascapular nerve comes from anterior to posterior underneath the ligament and beneath the notch. And there, there's a well-known set of papers by Setti Rengachary describing the surgery. Again this occurs in isolation leading to supraspinatus and infraspinatus atrophy weakness. Supraspinatus is the first arc of motion of abduction. The deltoid can kick in by itself but there would be less resistance to motion. Secondly, infraspinatus external rotation is often affected without an associated sensory abnormality. You need to know about this entrapment and how to do the operation, most people would go posterior prone with an incision just above the level of the scapular spine. The coracoid from anterior is a good spot to find where the level of the ligament is from anterior to posterior, find the coracoid my coracoid is here. That tells me where my superscapular notch is posteriorly and then you can plan an incision at that level posteriorly with the patient prone or seated or semi seated and here's the ligament curly white. I've elevated or split the trapezius. I then reflect the supraspinatus down. Scapular spine is here, there's the ligament, bring in the operative microscope and then cut the ligament and you're looking at the decompressed nerve and that's all you need to do. Is cut the ligament. Now as I mentioned you do wanna get an image because some of these patients may look like they have rotator cuff disease they may also have that but there are people who have ganglion cysts. Again, I'd rather know about a ganglion cyst occurring in this spot before surgery than at surgery. Here the appearance at surgery, I knew about it, I did an appropriate operation. In fact many of these people are now being treated arthroscopically by shoulder surgeons without the nerve being looked at. Let's move to the lower extremity now. We've talked about upper extremity entrapments, we've talked about Parsonage-Turner syndrome, we've talked about different roles of imaging and entrapments. Let's continue that trend in some of the more common ones that you might be asked about or might see in real life in the lower extremity. Lateral femoral cutaneous nerve is a sensory nerve. You may all be familiar with this, this is so-called neuralgia paresthetic. Patients have lateral thigh paresthesias. It's lateral, it's not anterior, it's not medial, there's no weakness, there's no low back pain. Those findings and symptoms by themselves distinguish them from lower back pain with an LPB that would go anterior and medial perhaps, L4 goes below the knee, L3 radiculopathies would have weakness, they would have pain coming from the back, they'd have reverse straight leg raises. Lateral thermocuteness would have a Tinel sign near the ASIS. Different diseases different presentations that are each and themselves characteristic. Now if you had a patient who presented with lateral thigh parasthesias and you did a work up of the back that's fine. In fact, that probably would be part of standard care. If you don't see anything you can rest assured you might see a little bit of permanent stenosis but again take a good history, do a good physical exam and then correlate it with an EMG. You can do a nerve conduction study of the lateral chromocontinuous. You can do a nerve block and you might do some imaging. Imaging of the back would rule out anything that you talked about. Treatment, weight reduction, avoiding constrictive belts like policemen for example. Wayfish supermodels can get it from their tight pants. All those things should be avoided as best as possible. Medical treatment, oftentimes enough or observation. In my experience only one in 10 patients require surgery. I like to do a nerve block beforehand. Again, the role of blocks is controversial. It's seldom in my experience is long-lasting but on the other hand it does give patients a feeling of what it is to be numb. That's often helpful especially in this nerve where I'm thinking about doing amerectomy rather than a neurolysis though whether you do a neurolysis or a neuropathy is controversial. Finding the nerve, it's medial to the asis by about a sonometer that's why you take your bone graft laterally. Your thenar vessels are down here. Your sartorius is your key landmark this crosses over the sartorius. You need to make one opening in the sartorius fascia, you find a big nerve and you trace it and decompress it through the inguinal ligament. That's the compression site. If you stay lateral on the inguinal ligament, you don't have to worry about hernias. The hernias occur when you stay medially and you're dealing with this typical sites as in general surgery days. Here, hug the bone, stay on the nerve, decompress it and if you wanna cut the nerve, you would cut the nerve and place it into the pelvis away from muscles deep to everything. Femoral neuropathy. Again, this is a rare syndrome, this is different than lateral thermocutaneous nerve. Femoral nerve is L2, 3, 4. Again, you would wanna know how these patients differ from here, the distinction could be an L3 or an L4 radiculopathy. History would be different. Patients femoral nerves are uncommonly injured. One usually thinks about retroperitoneal hematomas in the psoas muscle you can think about yatrogenic lesions following other anterior retroperitoneal approaches around the psoas muscle. Tumors can do anything. But here in general, the distinction is between a femoral nerve palsy and a radiculopathy. And besides history of thigh pain, there's back pain. Talk about motor sensory pain. Sensory would be different because again L4 numbness goes into the sartorius distribution that's medial and anterior it's distant to the knee. For an L4, that might be similar to a femoral nerve but the saphenous nerve wouldn't be affected with an L3. The adductor muscles can be tested again these are L2, 3, 4 but they're obturator innervated. Those would be unaffected with a thermal nerve that would be affected with an L3 or four that is knob. Foot drop, you'll hear a lot about this in my various reviews and in other people's reviews. Perennial nerve palsy at the level of a fibular neck is relatively common. It's most common entrapment at the level of the, in the lower extremities. You've heard about it with dieters, people don't know what that's related to, it might be a nutritional thing, it might be crossing your leg. The point is is the common perineal nerve as it crosses over the fibular neck is somewhat vulnerable to compressing as it goes beneath the fibrous arch or the perineus longus. Take a look at that anatomy, know the difference between deep and superficial perineal innervated muscles. The deep are the ones that cause you to have a foot drop. You need to know the differential diagnosis of a foot drop all the way from a tendon level injury going proximally to the brain. So in that for example the foot drop would be to the ALS anterior tendon, it could be the deep perineal nerve, it could be the common peroneal nerve. It could be the sciatic nerve in the thigh or in the buttock. There you need to think about a common tibial innervated function which may be partially affected or not. Then you need to go into the pelvis, lumbosacral plexus, caudal quina L4 or L5 depending on how people are wired. Conus lesions can give a foot drop when you're talking about upper motor neuron, patterns in the spinal cord. And then finally contralateral brain. Now part of the workup would also include diabetes and other neuropathies you need to think about that as part of your differential. When distinguishing an L5 root problem from a common perineal nerve, you want to particularly test the posterior tibialis. This is an L5 muscle, L5 innervated muscle. You test it by testing the foot down and in. You can feel the tendon on the opposite side. If it's normal, it's not an L5 lesion. And you can also check it electrophysiologically if you don't trust your own exam. If it's abnormal, then it's not a common peroneal nerve lesion. So that's a very good part of taking your motor testing, sensation between many of these would be typical and would be similar. Provocative maneuvers pain related testing would be different. If you found an L sign at the level of a fibular neck that would be good for a perineal nerve if you found a straight leg raise, that would be good for an L5, if you were thinking it's a sciatic nerve, then trace it along the course of the body. Make sure there's no Tinel sign there.

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