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Nerve Physiology , NCS and Nerve Injury for Orthopaedic Exams
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Nerve Physiology , NCS and Nerve Injury for Orthopaedic Exams
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Segment:0 .
OK good evening, everyone, thank you for joining us to this Wednesday's fa stitching. The presenter today is Rishi dear. He is a consultant, upper limb surgeon in Harlow. He's very active RCS tutor.
He he runs lots, of course. He teaches a lot of courses and he runs his own course. Let's talk Doctor blitz overseas. Quite damp. Very good. Excellent science teacher. And I'm very happy to have him with us. We also have other mentors here. We have schwann, Ranjit Abdullah Fouad, munir Anwar with us to support the session.
Amphoras, I will be moderating. This will try to answer all your questions and to try to get you actively involved. So please, if anyone wants there, would be vivo. And I would urge you all to use this session to have a vivo experience with Rishi. It will be invaluable experience and make the best out of it. So if anyone wants to take part in the vivo questions, there won't be many.
There will be probably only two or three. So if anyone wants to take part, please raise the hand symbol next to your name on the group and the participant list. Or send me a message and I will put you on the list, so please express your interest as possible. Again, just to reiterate that if anyone wants a CPD certificate, please get in touch with me and I will get this sorted for you.
And the video will kindly agreed for us to make it available to you guys later on. And as usual, we only record the lecture. We do not record your vivo answers. OK, so without any further ado, I will leave you with the original thank you for having me first and thank you to all the mentors. Hi, guys. Lovely to meet you all.
Hope you're all not suffering too much with this corona virus, and I hope to teach you tonight about nerves and also nerve injuries. I'll try and make it as relevant to folks as possible. So tonight we're going to look very briefly at nerve anatomy. We're going to look at nerve injuries in particular. How do you classify them and a mechanism for dealing with them as well? And then we'll try and look at some common vivo scenarios as well.
So let's start with nerve anatomy now. The nervous system itself is broken down into three main parts. There's the central nervous system, which consists of the brain and spinal cord. As the peripheral nervous system, which essentially relays information from the periphery to the brain and vice versa. And then there's the autonomic system, which is responsible for sympathetic and parasympathetic function, and this is the peripheral nervous system is really the focus for the exam.
This is what you're going to mainly be tested upon. So the basic functional unit in the nervous system is the neuron, which consists of a number of parts. So you essentially have a cell body and the cell body is kind of the chemical factory. It contains a nucleus. It contains a cytoplasm, which is also known as the axilo plasm and various constituents, such as vesicles, microtubules and the acts endoplasmic reticulum.
And that's mainly needed to maintain the physical and physiological well-being of the axon. So the axon itself is where the impulses travel down to the n-terminal, where they then communicate via synapse with other nerves, and the axon may be surrounded by a myelin sheath, which is a fatty layer. Now, the way that I think about it or break it down is into neural and non neural tissues.
So neural tissues are things like the cell body, the axon, the dendrites, which give a greater surface area for impulse transmission, and also the axon terminal, whereas the non neural tissues are things like glia. And what these do is these essentially are bits of connective tissue, which nourish and support the axons. So glia within the central nervous system are known as oligodendrocytes.
And within the peripheral nervous system, the known as Schwann cells, and these have quite an important function because they produce this fatty layer, which encases the neurons and can increase the speed of impulse transmission. And I'm going to very briefly tell you about how this works in a second. So this is just a quick look at the peripheral nerve anatomy, and with the peripheral nerve anatomy, you essentially have a group of sensory fibers, motor fibers and autonomic fibers, which is surrounded by connective tissue layers.
The motor neuron is situated in the ventral horn of the spinal cord, which is the bit at the front, whereas the sensory cell body resides in the dorsal root ganglion, which is the bits of the bark. And these cell bodies essentially project axons through the dorsal and ventral root, respectively. And they join the spinal nerve as it exits the vertebral foramen. OK now, within these motor and sensory fibers, you've got a group of myelinated and unmyelinated axons, so what I mean by that is surrounded by a fatty layer or not surrounded by a fatty layer.
And that's in the ratio of 14. So you have many more unmyelinated axons than myelinated ones. OK and these myelinated axons, I'll just come to that second. They have various points where they're interrupted, called nodes of Ranvier vein. And one question a lot of trainees ask me or they get asked in the exam is why do impulses conduct more quickly in myelinated axons than unmonitored ones?
And it's often a question, which is not well answered. So people mention this buzzword soul territory conduction. And the question they often say is, Oh well, the impulse is jump from one node to another because the fatty layers impermeable to ions. But impulses don't truly jump. So that's not really an accurate representation of what happens as the buzzword that I want you guys to use in the exam is this thing of active and passive conduction.
OK, so active conduction is an energy requiring process. You get sodium and potassium, ATPs pumps, you get active transport and essentially it's a slower process, whereas passive conduction is a much quicker process. So what happens in myelinated axons is whenever you've got a node of ranveer, you essentially have an impulse, which is produced and action potential, and that's an active process by the sodium potassium ATPase pump.
However, because you've got these fatty layers, the impulses can't be produced across here. So essentially what happens is this action potential will begin to decay all the way across here, and that's a passive process. And then the next impulse will be produced at the next node of wrongdoing. So that's a much quicker process because you get passive conduction.
In the case of an unmonitored axon, you have to keep producing these action potentials again and again and again, and that's an energy requiring process. So it's much slower. So that's the real reason of what happens in Salt conduction. It's not that the impulses jump, it's that you get passive decay of the impulse. So it essentially acts as a capacitor and impulses.
A circuit is being sent between the different nodes of ranvir, so that's just a very quick aside. I wanted to mention that because that's a question I have seen asked in the exam, and it's not answered very well. So just going back to peripheral nerve anatomy at a macroscopic level, the nervous surrounded by a number of coverings which you need to know about.
So each axon is surrounded by a Andoni oreum these under aneurysms, then grouped together in bundles or physicals and are surrounded by something called a perineum. And then lots of these bundles grouped together to form a ulnar nerve trunk, which is surrounded by epimysium. So remember those three buzzwords and new oreum. Meriam and epimysium.
And I suppose this is a clinical exam, it's an application exam, so the way that they may ask you, it is, well, what's the relevance of these clinically? Well, the epimysium protects against compression. It's your outer layer of compression. And so you've got your epimysium, which protects against compression, whereas the epimysium and terenure protect against stretch.
And actually, the perineum is the most critical layer in neurophysiology because it represents a blood nerve barrier, which is created between the inner layers of the perineum and the endothelial cells, which are inside the endon micro vessels. So what I think of as this blood nerve barrier, which is your main resistance to compression, so that's why it's so important. OK, so let's move on to nerve injury, and this is really the crux of my talk nerve injury can be caused by a number of different things.
Most commonly is trauma, but I've created a little mnemonic, which is a nice way of remembering the etiology. So it's remembered by the mnemonic dating me diabetes and drugs. Autoimmune causes traction or trauma, and I've highlighted trauma because that's the most common cause inflammatory, iatrogenic infection, neoplastic causes, general or systemic causes, motor neuron disease.
And finally electrical or thermal causes. So how do we classify nerve injury? OK, so most commonly, my trainees will say to me, OK, classification. I remember Seddon and I remember Sunderland. All right. And Seddon basically breaks up nerve injuries into three main types a newer apraxia or a conduction block, which essentially means that all the neural coverings are intact.
But the nerve has been stretched or distorted in some way, such that it's not working properly. OK, then axon optimises, which basically means that some of the neural coverings has the axons been cut, but some of the neural coverings are intact. So the end your may have gone, the perineum may have gone, but the epimysium is still intact. And then finally, neurons message, which means everything is gone, ok?
Sunderland was a variation of this, which broke it into five main types. OK, so we've mentioned Seddon. Sunderland broke into 1 to five, where one was again a newer apraxia or a conduction block. 5 was a rock Mrs. and two, 3 and four were different variations of accent at methis, depending upon which neural covering had gone. OK, so a 2 basically meant that the basal lamina had gone, but the perineum was intact.
A three basically meant that the sorry to the end in your room had gone, but the basal lamina was intact. Three meant that the end aneurysm and basil had gone, but the terenure was intact a formality and aneurysm. Basal lamina and perineum have gone, but the epimysium is intact and 5 means everything's gone. Now that's the answer, which most people give in the exam. I would use Seddon or Sunderland. But having worked on the peripheral nerve injuries unit in stanmore, one thing that those guys always taught me is actually in reality.
Seddon and Sunderland are not very useful clinically because if you think about it clinically, somebody comes in with a nerve injury and always say is the nerve is not working. We don't know if the nerve has been cut or not. We do not know how many neural coverings have gone, or we don't know if it's been a conduction block unless we look under the microscope, unless we exercise a piece of nerve and look under the microscope.
So actually, these are what I would call anatomical classifications. They don't offer much help clinically. So much better classification for clinical use is this one here called birch and bonnie? And what birch and Bonnie did is they. And that's Rolf birch, who worked on the peripheral nerve injury unit at Stanmore. They basically broke these nerve injuries that broadly into two main types a conduction block, which are the same as a newer apraxia and a degenerative lesion.
And that's because they said, well, actually clinically, you cannot differentiate between an excellent methis and New York Mason, so that all should go into the same group of a degenerative lesion. OK and that's probably more useful clinically. So this is just a sort of slightly more complex table, just shows you the different classification systems, and I don't really want you guys to learn them in detail. Just remember what I said about sedin neuro apraxia axilo, not Mason Europe Mason Sunderland is 1 to 5.
And basically, birch and Bonnie is a conduction block or a degenerative block lesion. OK, so I'm now going to explain this in a bit more detail, and I want you to remember these two characters here the earthworm and the bomb. This will revolutionize your understanding of conduction blocks and degenerative lesions. OK, so the analogy that I think of and I can't say this is my original thought.
I worked on the knee unit at Stanmore and the consultants there used to teach me about this. I have to thank them for this, but it's a great analogy. So the analogy that I can think of is imagine if you have a lit bomb and you put the lit bomb in a puddle of water, the bomb will not go off because it's surrounded by a puddle of water. But if you dry the bomb and you take away the water and you light it, it will then go off and work.
And this is very analogous to what happens in a conduction block or in your apraxia. Essentially, the nerve is all intact, but it's been distorted. There may be a hematoma. There may be some scar tissue. Something is representing the puddle. It's stopping that bum from going off. As soon as you remove that, or it may spontaneously result, then that nerve will start to work again.
OK, but if you leave a conduction block for a period of time because essentially you get a compartment syndrome, you get disruption of the blood nerve barrier, which I mentioned before between the perineum and and ending effectively that will progress on to become a degenerative lesion. The next one is this concept of the earthworm, and the way I want you guys to think of it is imagine if you shop an earthworm in half, what happens?
Well, what you find is the worm doesn't die. One part of it, the tail dies and shrivels away. But actually the bit, which is connected to the brain regenerates and starts to grow a new tail. OK and if you do not know that, try and find an earthworm in your garden. You have my permission to practice that, ok? And that represents exactly what happens in a degenerative lesion or Wallerian degeneration.
And I'm going to just go on to explain that to you. So conduction block, the mechanism that I spoke of is this thing called the blood nerve barrier. And this was something which I didn't really understand until actually after I became a consultant. But it's all to do with this perrineau rhythm and endothelial cells. It's a barrier between those two. And the way that I think of it is that, say, selectively permeable barrier.
So essentially, these cells have got tight junctions, which are impermeable to many different substances, and there's no lymphatic vessels within either the engineering or the perineal. So what that means is it creates an immunologically and biochemically privileged space for peripheral axons and supporting cells. So the two buzzwords I want you to remember are selectively permeable.
And then I want you to remember a privileged environment. That's the buzz word to remember. So what happens is when you compress this nerve, it gradually upsets this blood nerve barrier. It alters the pressure within the vessels, creating an internal compartment syndrome and essentially breakdown of the vasculature, which causes leakage. This then leads to accumulation of various proteins and aggression of inflammatory cells like lymphocytes and macrophages, which otherwise were not able to get in.
And as a result, this initiates an inflammatory response and increases the permeability even further. So it's like a positive feedback cycle. OK, so compression upsets this barrier lessen in the inflammatory cells, the macrophages, the lymphocytes. These cause inflammation. They increase the permeability even more positive feedback cycle.
It all goes downhill. OK, so that's the way to remember it. OK, now the only reason I put this slide in is because just I have heard of examiners saying to people, oh, well, why does the conduction block actually cause the problem? This is what it does. It starts selective permeable. Barrier, which creates an immune, privileged environment. OK and it initially starts as apraxia or a conduction block, and it later progresses to form galarian degeneration.
So that's a little diagram of what I was saying. You start off with changes in the blood nerve barrier. You get compression and edema, which leads to thickening. And essentially what it does is it leads to localized nerve changes. You get an influx of these inflammatory cells, which otherwise we're not able to get inside. They lead to increased permeability and start to cause breakdown in the nerve, and that will eventually progress to Wolverine degeneration.
Now, this is the bit, which I think is more interesting for you guys. So my biggest buzzword when I teach is this word of compartmentalization. I compartmentalize everything. OK, so even if you go into your fridge, you talk about liquids and solids, solids, which are vegetarian me, everything you do now as part of your daily routine.
Compartmentalized, compartmentalized, compartmentalized. Ok? so with Woolery degeneration, I break it up into three main parts the cell body. The proximal segment and the distal segment. So when you cut a nerve. Imagine if you say, OK, I'm doing a carpal tunnel decompression, I accidentally cut the median nerve. And this is a vyver question.
They might give you what is happening at a cellular level. Well, basically, I would say to the examiner, I would break my answer up into three main parts the cell body, the proximal segment and the distal segment. So the first thing that happens is just like the earthworm, the distal segment, because it's disconnected from the cell body, the nutrients can't get in. It will essentially shrivel up and die.
It collapses, and all that is left behind are the Schwann cells, and they form these things called bands of Bumgarner, BU and gene and e-r. So I always think of it as I remember it, like the parties from the old Italian prime minister. OK, so that's the way I remember it. OK and so what happens is they basically become neuro tropic factors and an EU rotr opIc neuro tropic, which means they guide the direction of growth.
They're telling the nerves where to grow into. OK, then what happens is in the cell body, the nucleus moves to one side and it changes its phenotype from being a conductive phenotype to a regenerative phenotype, so increases its activity, mitochondria, et cetera and it becomes a regenerative phenotype. Then, in the proximal segment, you start to get outgrowth of these little finger like projections called really podia.
And these Filipovic podia produce neurotrophic factors spelt trop h I c, which stimulate growth. So at one end, you've got neurotrophic factors which are stimulating growth. At the other end, you've got neurotrophic factors which are telling it where to grow into and when the two meet. It's known as a process called contact guidance, so the analogy I think of is a blind man and his cane.
The nerves are kind of feeling in the dark where to grow, and the factors are telling them where to grow into. And sometimes that process just stops and it will end in something called a neuroma. And when that happens, you have to go in and intervene. So classically, Woolery degeneration is a very predictable process. You typically get a latent period of about 2 to 6 weeks, and that's why nerve conduction studies are useless within the first four to six weeks because of this latent period.
And then the nerve starts to grow at a rate of 1 millimeter a day, the same as hair. And clinically, we can monitor that by something called an advancing 10 hour sign. OK, so when you're in the PMI unit, one thing I always do is I always start distally and then work APR and I feel for a hours tapping over it because that will tell me where the nerve has grown to. So I can say, OK, it's three months with injury.
I can see that the nerve has grown to the mid forearm. I'll see you again in six weeks. I would expect it to have gone, let's say, down to the wrist or whatever it is. OK, if it is, I'm going to continue to observe. I'm not going to do anything about it. If it doesn't, I may need to go in and explore. OK, so that's the way to think about it. Keep it nice and simple.
And some people say to me, Oh well, Rishi. A true tunnels only occurs in a degenerative lesion when the nerve has been cut. So why do we get a tonsils and carpal tunnel syndrome? Because that's not a degenerative lesion. It's not. The nerve hasn't been cut, it's a conduction block. So what we call that is they don't say this in any of the books, but it's something called a pseudo tonsils.
And that's because essentially, when the nerve has been compressed for a long period of time, the myelin sheath has melted away. So essentially, what you've got here is when you tap on here, you're tapping on exposed growth cones because the myelin sheath is essentially melted away. So it's not a true tonsils should actually be called a pseudo tonsils. OK all right now, I think this is another really important thing to understand this, so a common investigation we order is nerve conduction studies, but a lot of people don't really understand what they are.
So I'd really encourage you guys to look at the next time the nerve conduction studies you get and try not to look at the result. Just look at it because that's one way they could give you an exam. They might give you a picture of a nerve conduction study, or they might actually give you a nerve conduction study and say, analyze this. So what do you actually put on a form when you request a nerve conduction study?
Will you request two things? You request the nerve conduction study and you request an EMG and a nerve conduction study looks at the electrical activity in a nerve, either sensory or motor, whereas the EMG looks at the electrical activity in a muscle. All right, so the nerve conduction study consists of four electrodes, which you can see in this diagram.
So you have a stimulating electrode. You have a recording electrode. You have a ground electrode, which essentially earths the patient and stops them being electrocuted. And you have a reference electrode, which essentially gets rid of any sort of background interference activity and gives you a nice, good trace. OK so in the case of a sensory nerve, the stimulating electrode will be distal and the recording electrode will be proximal.
So it's what we call anti-drone impulse transmission, whereas in the case of a motor nerve, the stimulating electrode is proximal and the recording electrode is distal, so it's called orthodontic stimulation. So this particular case, this is the stimulating electrode, and it looks to me like the recording electrode is on the thenar eminence. I think this is probably a medium motor nerve because the stimulating electrode is proximal and the recording electrode is distal, and it's also on the thenar eminence.
And that would be a reasonable question, guys. They might ask you that an exam, because what they want to see is, have you done a nerve conduction study or have you been to a clinic before the stimulating? That's the recording. That's probably either probably a reference electrode, and that's probably just the ground electrode. OK, now the next thing people say to me is, well, how do I actually interpret a nerve conduction study?
So you have to know three main parameters, and those are latency. Amplitude and conduction velocity. And the first two parameters are measured directly. The third one is derived, which means you work it out. OK, so the latency is known as the quality of impulse transmission. It's the time taken to travel between two points, whereas the amplitude is the volume of axons or the quantity of impulse transmission, the conduction velocity, which is in meters per second.
The way that you calculate that is you essentially mark two points on the arc and you basically mark one as M1A1 is beat and then you take a tape measure and you go between those two points. And then you look at the time taken between go between those two points. So that's another thing you can say in the exam. And it's just a way of showing the examiner that you've been to a nerve conduction study.
These are things that they don't say in the books, but these are little tricks that you can put in just because what they want to see in this exam is they want to see clinical experience. They don't want to see just factual knowledge. They want to see clinical experience. So these are lot of things that you can do. Now you do, you need to values for this exam? No, probably.
The only one that I would learn is a average value of 50 meters per second. So 60 minutes per second for the upper limb, 40 for the lower limb, but on average, about 50. But the key thing you do is if they give you a nerve conduction study in the exam and this is often a trick they will play on you is they will say, OK, this is the nerve conduction study and it's the left hand.
The first thing you say and this is a pass/fail answer is you say I cannot I cannot assess this in isolation. I want to see the right side. And that's because somebody could have an underlying problem, like hereditary motor sensory neuropathy. They could have something like MS where they've got universally slowed conduction, but you won't know that until you see both sides In comparison.
Does that make sense? So it's not a case of OK, fine, he's got a nerve conduction conduction velocity of 20 meters per second. He must have a carpal tunnel or a cubital tunnel that may be normal for him if he's got MS or if he's got hereditary motor sensory neuropathy. So you must ask the other side. Nerve conduction studies in isolation are meaningless.
Right? the second thing you need to know is about how to interpret EMG. And an EMG is slightly different because in an emg, you've only got three electrodes, a recording, a ground and a reference electrode. And that's because the patient provides their own stimulus. So the neurophysiologist will often say if the patient, can you move his thumb from me, OK, they're doing APB and opponent's policies, so they are testing the median nerve.
So at rest, a nerve or an EMG should have a flat line. It should have nothing there. The minute you do that, it should suddenly have a motor unit action potential. OK however, if you see somebody at rest on, the nerve has been cut. You will see lots of little v-shaped things. And in the early phases, these are positive things which are called positive sharp waves.
OK upside down VS and then you get fibrillation later on. So not particularly those guys. Remember for simulation is a clinical sign. It's twitching, you get positive sharp waves and you get fibrillation. So that's a sign of denervation. OK, so. Then how do we know if the nerve is regenerating, how do we know it's coming back to life?
Well, the analogy that I think of you get these things called physic units. That's how. So the analogy that I think of as the Indian chief and villages. So you've got the chief and village, a guy who's got eight kids and each of those kids represents a muscle or a motor unit. And the chief represents a motor nerve.
The chief in village B has also got eight motor units. Now what happens is when the chief in village dies, B will take over his kids and his own kids. So instead of supplying eight, he will now supply 16. So as a result, you get a bigger amplitude of stimulus and you get more up and down things which are known as physic units. So poly fascia is a good sign. It's a sign of recovery.
So there are two things of recovery, either clinically, we can look for an advancing 10l sign or newer. Physiologically, we can look for physic units. So a common referral we would have is guys would say, OK, I've done a posterior approach to the hip. I know the sciatic nerve was intact, but the patient's got a foot drop. So we would say to them, OK, is there any evidence of hematoma as in something compressing the nerve to an ultrasound?
OK, no. Is there any pain? No OK, there is no evidence of ongoing compression. Is there evidence of recovery? So we look for a advancing tunnels and we do a nerve conduction study after six weeks. If we could see polyvalent units, if we could see an advancing. We would do nothing.
We were just observe them over a period of time. OK, before we move on from nerve conduction studies, I just want to mention one other thing because a lot of people say to me, oh, well, Rishi, what about the reflex or f waves? They get worried about these things now. These are very rarely used in clinical practice. And in the knee unit. The guys would say they weren't useful at all. But in a nutshell, what happens is the way to think about nerve impulse transmission.
Although I told you guys orthodontic anti-drone, that implies that nerve transmission only goes one way. It doesn't actually goes in two ways. So when you provide a stimulus, the stimulus goes down towards the hand and it goes up towards the neck. All right. So what it does is it basically sends an F wave or a heat reflex where it bounces off the top and it comes back and we record that.
And that's useful in cases where you cannot get above the lesion, such as a nerve root lesion in the neck. So that's what we use reflex or phrase for. We do not use them in practice, really, but that's just if the examiner asks you, it's used for cases where you cannot get above the lesion, ok? So the other question, I think is really relevant clinically and I've kind of alluded to this already is when do we explore, when do we surgically make the decision to explore with these guys?
Well, I've mentioned it. There's two main reasons evidence of ongoing compression. And clinically, we can determine that by a patient having pain, either spontaneous or evoked pain. So by that, I mean spontaneous. They've got pain at rest without any stimulus evoked means you can likely stroke the skin, you can tap on it and they start screaming in pain.
OK, that is a sign of ongoing compression. Or if you do an ultrasound, it shows an expanding hematoma. You will tell the referring center, go back in there and decompress that hematoma. There's not time to refer to the unit. Just go in and decompress it. OK if they don't have these things, if there is no evidence of recovery either clinical in the form of an advancing tonsils or neuro physiologically in the form of physic units, so those are your two reasons to do an operation.
And what kind of operation do we do? So I've created this thing called the ladder of reconstruction. It's a really nice way and easy way of thinking about it. So at the most basic level, you start with a new releases, you go in there, you remove the hematoma, you remove the scar tissue. And that's useful for people who've had neuro apraxia. And actually with the knee unit, when we have people who have very severe plexus lesions, they go in there even if the nerve roots were advanced.
The first thing they do is neutralize them and they might do something afterwards, but they do a new analysis in the most basic level. I remember you can combine procedures together, so if you find that actually the nervous cut, but the distance between the nerve is such that you can bring it together primarily and repair it without tension, then you can do a direct nerve repair and that's always the best.
But remember, guys, the nerve repair must be done under microscopic guidance, either loops or a microscope, and you must have fascicle to fascicle matching. So a common question they've asked before is you've cut the cord. You do carpal tunnel decompression. You cut the median nerve. What do you do?
And the mistake people make is in the age they go, OK, I'd repair the nerve. I wouldn't save up. I would say I would tag the two nerve ends. And my justification for doing that is because I need, first of all, the training microscopic guidance. But secondly, I need fascicle to fascicle matching. And if you do not have the skill set to do that, you're not doing the patient the best service.
And I always used to advise tag to nerve ends do not attempt to repair them. In fact, if you find that, actually, do you know what? And I've actually I've missed out one there. What I should have said is if you find that actually there is a gap between the two ends, because remember when you do a nerve repair or a nerve exploration, you have to take off the serrated bits, the inflamed bits or whatever the damage because you can't just repair end to end.
So once you've excised the two bits, if you find actually you can't bring them together without tension, you can actually put a nerve graft. And that nerve graft could be something like a sewer ulnar nerve and intercostal nerve or some sort of sensory nerve. Or it could be synthetic. Ok? if you find that actually the gap is too big, even with graft, you may have to do something called a nerve transfer where you take a nerve, which is less useful elsewhere, and you basically transfer it to supply function.
I think there's three main transfers that you should know for the exam. OK, so if somebody has, let's say, a upper trunk injury or a yeah, like a C five, C six, your three priorities there is basically want to restore shoulder stability, so you want to get the suprascapular nerve. So I would normally take the spinal accessory nerve to the Super suprascapular nerve.
OK secondly, I want to restore shoulder movement in the form of deltoid, so I do what's called a somesuch transfer. Socom, asac and I'm taking a branch of the radial nerve, which supplies the triceps and I'm putting it into the auxiliary nerve. And finally, I want to restore elbow flexion. So I do what's called an Auberlen transfer OB or alliance, and I take a branch of FCU OFDR supplied by the median.
So it's applied by the ulnar or medial nerve, respectively. And I plug that into the musculocutaneous. I wouldn't learn any other nerve transfers. Those are the three that I think just remember those for the exam. And that's if you're going for a seven or an eight. So don't panic. All right. Obviously, the next thing is with the first three things you have a certain period of time.
The books say one year, but I would say in reality, about six months to a year, and that's because after a period of time, the motor units will die. So even if you restore nerve function, you've got nothing to innovate. So in those cases, you do what's called a tendon transfer where you basically take a functioning muscle tendon unit and you take it into one that's not functioning very well.
And finally, you do what's called a free muscle transfer where it's like a free flap in plastics and you need plastic surgeons to do this where you're essentially taking a muscle from somewhere else. So you might even take something like gastric or chrysalis or whatever it is, and you basically take it with its pedicle and you plummet it into the area. OK, but that's really high end stuff.
So that is the ladder of reconstruction. I would learn that as a way of treating everything, guys. I think you can't go wrong with that, really. OK so tendon transfers, I'm going to very briefly just to end my talk, say something about tendon transfers. OK so we're tendon transfers. I've got a really good way of remembering these rather than memorizing the tendon transfers guys in the exam. I break it up into four bits.
I say, what is your deficit? What actually three bits, what is your surgical priority and what are your options? And that way, what they want to see in this exam, I remember I told you it's clinical application, it's not memorizing it. OK, so they want to see, does this guy or girl, does she? Did they have the sort of wherewithal to understand the principles?
OK, so what's your deficit? Let's say somebody's got a. Let me think of what let's say they've got a low rate. Certainly let's say they've got a low median nerve palsy. OK, so they're deficit. They're they've essentially got it's an anatomy question. All right. So we know where the median nerve runs. The median nerve doesn't give any branches and upper arm.
It basically starts to give branches in the forearm. It gives off four branches of the common flexes FCR PhDs. Paul Morris longest and pronounced Tyrese. It then gives off three branches and dropped nerve to FPL FDP to index the middle and prenatal code writers. And then it basically gives off your hlophe muscles and sensory to the radial 3 and 1/2 digits and also a Palmer cutaneous branch. So with a low median nerve palsy, basically you've just lost your hlophe muscles.
That's your deficit and you've lost sensation to the radial 3 and 1/2 digits. What is your surgical priority? So your surgical priority with a low, medium of palsy is restoring opposition? OK, and then what are your options? So with a. Policy, your options often opponents plastic, you can either use Paul Morris longest, you can use IP, you can use FDS to the ring or you can use abducted digitally minimi known as a Huber's transfer.
OK although remember, that's the pediatric transfer because you lose 75% of the strength. Now the problem with the high median nerve palsy is this time you've essentially got your surgical priority. Here is opposition, but you've also lost some flexion because you've lost FPL. OK, and you've also lost FTP. OK and you've also lost finger flexion to these ones because you've lost FDS and FDP with a high median nerve injury.
So this time you have surgical priorities restoring some flexion. Finger flexion to these two and opposition. So what are your options for opposition? You can't use primaries longer because that's gone with the high medium, the deposit. You can't lose s-vhs because that's gone. You can't use abducted a.m.e. because it's a pediatric transfer.
So your only option is IP. OK, for some flexion, you can use brachial radio less and for finger flexion. You can basically buddy the FDP from the older ones and basically have a mass movement like that. So always break it up into what is your deficit, what is your surgical priority and what are your options? OK and finally, the principles of tendon transfers, now I have to tell a very quick, funny story, if you guys don't mind me.
So I was crashing and burning on one of my questions in the exam and I was desperate to get in principles of tendon transfer. It was like a running joke because in my revision sessions, I would try and get principles of tendon transfers into every single thing. So I kept saying to someone to the examiner, I was like, they were like, well, what are you going to do? And I said, well, there's a number of things you can offer, such as tendon transfers, which have a number of important principles as you did, but you didn't take the bait.
And then again, I say so I could do tendon transfers, which have many important principles. Again, she didn't take the bait. So I think she just got bored of me saying it. So she's like, OK, tell me about the principles of tendon transfer. So, so the key thing is everybody goes on about the eight S's, which I think is one of the books.
Now this question, I subdivided it and I said the principle is a tendon transfer can be divided into patient donor bed and recipient factors. And she literally ticked it and said, move on. So patient factors would be things like, is the patient sufficiently motivated to do the rehab? Are they able to do the rehab? Don't the fact would be, is it a sacrifice about donor?
Did it have sufficient power, at least MRC grade 4 out of 5 because remember, you drop an MLC grade, same line of pool, et cetera so what I'm doing is I'm saying this eight ss, but I'm just subdividing them into those different parts in case I miss one out. So it's just a nice way of doing it, and it's that whole thing of compartmentalization that I was saying to you guys. So finally, we've got some common scenarios, and I think for us, did you want to me to offer these as viable questions to people?
Or I think if you don't mind, we could do it with Aviva practice and if you could then give us your model answers for them? Absolutely I think people will find it useful to give them an opportunity to practice with you. So I think so you've finished your goodness. Yeah, sorry, guys. If that a bit long. No, perfect.
Wonderful wasn't was spot on, actually. Yeah I hope I've not scared you too much because I'm trying to keep this simple. As remember, it's called basic science. It's not called complex science. So it's all about keeping your principles really simple for this exam and stuff, right? Thank you, Michel. I think this is very interesting, a very high standard presentation, as expected from you.
You made this dry topic very interesting. You, you brought it. You brought the clinical significance off of the basic sciences behind the nerves into our clinical practice. And that's exactly the higher order thinking that we're trying to implement in our teaching exactly how you transfer this dry theoretical knowledge to clinical practice.
And that's exactly the level they are looking for in a fast candidate. A lot of buzz words there in the lecture more than I can count. So I think we have to revisit every candidate to really listen to this, learn all these arteries, conduction all this mnemonic dating me. And I think that's very useful, especially when you get stuck in the question and you don't know what to do if you're remembering the words, this mnemonic could get you out of trouble sometimes.
So and and actually the slider of reconstruction you present that day in is actually it's worth gold, really. It's amazing one. So I think in terms of. Questions, I think you covered really everything about nerves, I think people will just have to look at this lecture again. But any comments from any of the mentors and anyone wants to add anything.
And those really well presented a very broken down into its basic from a very complex topic to a very, very public to understand now. Just a reminder to all the candidates that in the exam, don't be frightened by something that looks complex because often the patients that are coming with nerve injury have already had medical procedures done to them. They're not well known to the examiners who are organizing the exam, so they've got lots of different things happening.
Just take a breath, start at the basic and move forward from there, especially in the concessions. Yeah, I think I think, as you said, is what you have to remember is when, when we get a break, let's say a brachial plexus injury is an example. When that comes in a NIPE clinic, we get 30 minutes with that patient. And by the end of the 30 minutes, we often don't have the diagnosis.
We often have to do nerve conduction studies. We have to bring them back. So what they're looking for in the exam, they're not looking for a perfect diagnosis in five minutes. They want, they want. Look, how can you do a general impression or just a general overlook? Is this a plexus injury?
Does it look like it's a high or a low plexus lesion? And what investigations might I do? And just a generic impression? Will I do the same thing? Basically, that's what they're looking for. So as Sean said, I think it's very important. Just keep nice and relax, keep calm and just keep it really, really simple in terms of general principles and things like I can.
I mentioned an experience recently by one of my colleagues who just had the exam, and he felt that question. He had a nerve injury exam, clinical and here because he knew that they will end up with a tendon transfer. So he jumped all the steps and immediately jumped into the tendon transfer. And then he made himself a big, big, big hole and dug himself into it and buried himself.
And I really liked this ladder of management, which is really good if everyone stick to that. So you always start by the simple methods and you slowly make your way up. I really like that. Yeah, you have to remember that you can't get an eight before you can get a six. And I have had guys coming up to me in the like Rishi. I don't understand why I failed.
They got me onto management. I got into evidence. But the reason why you failed is because the sixth is always the safety question. So unless you've demonstrated safety first and safety would be assessing this patient appropriately, assessing them clinically getting appropriate investigations, they might let you jump to the end, but you won't have done well on that question.
So don't just assume because you got into evidence that you've automatically done well and that station cover the basics is all about level four, they consultant. It's not about peripheral nerve injury, unit consultant, level Professor work. Lovely so if everyone is happy, we will move on to the vivisection. We have ATF who was volunteered to go first.
This is a 48-year-old manual laborer who's been having some difficulty with his hands. He's complaining of dropping things. He's come to see you in your hand clinic. OK I mean, this is a tactic I often use and I tell trainees about is I kind of stop to stop myself from slowing down and the vyver and getting bogged down because I felt that you were getting bogged down a bit then is I almost I almost think of it as like, you're driving along Route 66 and you're trying to get to the rainbow at the end, which is the 8 and having the mind of the back of your mind, where do I need to get the aim?
What is the final question they're going to ask you? And a tip is in the nerve, in any nerve question. Whatever it is, the final question is always going to be tendon transfers. It's always going to be OK. So you need it to get to the opponent's place to get to the 8. So so you need to find a way of getting through it very quickly.
So so I divide it up until I call the five days of deer, which is describe, diagnose, discuss, decide and diagrams to describe as your opening gambit. The first thing that comes out of your mouth is determined if you've got a five, six or a six seven. So this is a clinical photograph of both hands, which shows bilateral fena muscle wasting or thin remnants wasting. You said APB.
We do don't know if it's APB. It's thenar eminence wasting, which is asymmetrical worse on the right compared to the left. OK that's what you say, first of all. All right, so that's described diagnosis. OK I suspect that this is a bilateral carpal tunnel syndrome worse on the right compared to the left. But because this bilateral involvement, I would want to check for a central involvement by checking the cervical spine.
OK describe. Diagnose discuss. What are your concerns and how would you go about addressing those concerns? So I break it up into like a triple assessment clinical, radiological, biochemical and neurophysiological. All right. So I kind of think it to myself.
I think imagine you're driving along the road and you've got bits of shit on the side of the road. You want to acknowledge the shit, but you don't want to get stuck in it. All right. So that's why you want to find a quick way of saying history, examination investigations. So you said I would take a history. Don't say that.
Say I would take a pertinent history asking this, this, this and this, and I always break it up into a risk factor history and a condition history. So how is the condition affecting them? Have they had conservative treatments? And then risk factor history, hypothyroidism, manual activity, pregnancy, et cetera? All right. There's not really any imaging you can offer these guys.
So you then say I would do a neurophysiological assessment and I would look for a prolonged conduction study and also a to conduct velocity and increase latency across the wrist. So that's the buzzword I was looking for. If you look at conduction studies, they always say wrist and elbow. OK and then finally, you want to get on to the operation. So that's the fourth day decide to describe, diagnose, discuss, decide, OK.
And that's going to be talking through the layers. So in an appropriately marked consent to patients supine with an arm table tourniquet and infiltration of local anesthetic to the carpal tunnel, I would mark out four lines. OK, you want to say the lines, Kaplan's card and a line from the base of the abducted thumb to the hook of the helmet, which I do not want to go distal to because it marks the deep Palmer arch, the distal skin crease, which I do not want to go proximal to because of the Palmer cutaneous nerve, the radial border of the ring finger, which marks the line of the carpal tunnel and the real border so of ring finger, the real ball to the middle finger, which marks the recurrent branch of the medial nerve.
OK, and then you just say I would dissect through skin fat coming onto the flexor-pronator Allen. I would make a small neck in a tearing sensation. Use words that show that you've done it before until I can just visualize the median nerve. And then I would use a McDonald's and under direct vision, I would release the nerve proximally and distally and just close skin at the end.
OK and then the last thing they'll say to you is, OK, the patient comes back. They've had no improvement in the function. What are you going to do? And that would be tendon transfers, opponents blasting. So I think those 5D's sorry, the last day I should have said is diagram detective or discussion points. A discussion point can be and I use those 5D's for every Fox question.
It really helps me in my structure of those. So yeah, thank you. That helps. If I could add at did exactly what we had said you. Yeah, I would ask. I would ask. It's not a problem, but there are certain questions that go to help you diagnose and manage this patient. But when we said, what are you going to do, the right decision making process?
That's fine, but you don't need to repeat it a second time, he wasn't tricking you when I hear that, they'll move on. Then they're asking you what you're going to advise does not make sense. Yes, and yes, you do have to discuss all options, including non operative versus thing. The reality is, we should say, what are you going? It's just it just means less responding to a prompt.
Yes I think, as I say, I was at the same point, like he mentioned the same question three times, so that means he wants to take you to the surgical route. So why wait? Yes and I think I think I did, exactly as he said to me, that is it in this patient here? I agree with you shared decision making, of course, but. As a surgeon, if you've got a muscle wasting and severe changes, you want to get in there quickly because otherwise they're going to have a non-functioning hand.
So that's what I was trying to push you just to say, actually, yes, of course you will consult the patient. But in this particular case, I would advise to do this, this and this. It's like if I saw a Jupyter patient who's got a diagnosis or who has a pip contracture of more than 2021, 30 degrees, I would say, look, yes, we could try conservative measures first. But in this case, I know it has a very high risk of recurrence.
It has a very poor response to conservative management. So I'd probably recommend surgery in this particular patient. Yeah thank you. Yeah OK, guys. Well done. And that was just taking you guys to medium nerve anatomy. We don't need to go through that. They'll probably ask you about carpal tunnel anatomy if you're doing very well.
Yeah OK, I'm sorry if what I was going to get onto is, if you did really well is where can the median nerve be compressed with a high median nerve palsy? So I've got a little mnemonic flats, fesa process ligament Struthers aping the biceps pronounced 3 epicondyle process. can learn that if you want the example, OK, I'm just sorry, I really have to emphasize this if it's an easy topic your day to it's bread and butter for you.
If you need to know these details really well, the information is to be described perfectly. The management, the investigations, all of that just needs to be perfect because the more common the operation is, the more in-depth they're going to ask you. Yeah, absolutely, absolutely. Sometimes the difficult ones are the easiest ones to score ET on because you don't have to say much.
OK welcome. Welcome to your first exam. Thank you. This is my table and this is your examiner. He has a question for you. OK hi, Joey. So this is a 35-year-old gentleman who came off a motorbike and did this injury a week ago. He's now come to your fracture clinic.
This is his clinical appearance on the left, and these are some radiographs that you got on the right things there. There was a lot of good stuff. Mm-hmm your initial description, I thought, was very good. You, you, you describe the whole St Louis. You got the diagnosis very well. You keep OK. So initial description you got you described it well, but you just wasted too much time.
OK, so just let literally say this is a clinical photograph of a restaurant and an AP radiograph of the right humerus, which shows a whole St Louis fracture at the junction of the middle, and distal thirds. This is a radial nerve. Halsey just say describe diagnosis nice and quick. All right. Yeah then what you need to do is you need to get through that third day.
You're you're getting stuck in the shit. OK, so just describe it in terms of a triple assessment clinical, radiographic and neurophysiological. OK what you want to say is clinically, as you said, you want to find out about co-morbidities, level of function, dominance, occupation, et cetera. But you also want to know about if there's any evidence of iatrogenic injury, which is what I was, which is what you said, which is fine, but I had to prompt you a little bit.
So you need to say, look, if it's been there after they did the splint, it means it's iatrogenic injury and the nerve is in fact and it obligates exploration. OK, Yeah. Other things you look for clinically is, as you said, you could look for advancing 10 hours. I wouldn't expect to see that after a week. You could also look for pain and you could look for swelling as well, which is a sign of ongoing compression.
OK, radiologic, you talked about a newer physiologically, it's useless before six weeks because of a latency period, but you can mention it anyway. Now you mentioned about. You got into a controversial area in the whole St Lewis structure is very regularly asked because it trips people up. And this question about whether you fix it or don't fix it, I agree with you.
So g tenodesis paper showed that 90% of cases the nerve recovers in three months. But the problem with that is the way to say this is we don't really care about the nerve injury. If it's not iatrogenic, we know it's going to recover. But the problem with these is in 30% of cases because of the deforming force of triceps. They basically go into muscle union or they get incredibly stiff elbows.
So a way to avoid the controversy is to say, look, this is a young, active patient. I deliberately made him young for you. 35 years that I would counsel the patient, I would expect the nerve injury to recover. I know that the recovery of 90% of the cases, so my decision making is based upon the fracture. And I know with these distal third fractures because of the deformity force of triceps to have a high rate of mild union and they get elbow stiffness.
And my rationale will be to fix this to allow early mobilization of the elbow, because what you do is you tell me, OK, fine, I'm going to get nerve conduction studies, I'm going to do serial examinations. So I'll say to you, OK, it's three weeks. What are you going to do now? OK, I'll examine him again. OK, six weeks.
And you said I wouldn't even do nerve conduction until three months. So you're just going to keep going and going and going. And it's what I call a lot of risk for very little reward. It's like the pink pulseless hand in the Super con La fracture. Yes, we know that can wait till the next morning. But the new both guidelines have said if there's any evidence of impaired muscularity, including purposelessness, take them in the middle of the NIPE.
So it's a way to sidestep the controversy because what you want to think to yourself is I need to get onto the operation. I need to get onto posterior approach. I need to get on to plating extra articular locking plate. I need to get on to tendon transfers. If you're not going near that, you're not scoring a 7 at all and you're lucky to score a six. So you've got to think, how do I get through that initial crap as quick as possible by 1 and 1/2 minutes?
You should be in theater. Yeah, so little things like triple assessments, like talking about clinical neurophysiological that just gets you through that crap as quick as possible and sidestepping the controversies. I mean, what do you guys think? Is that? Is that fair? Or I think I think you're percent?
Yeah, absolutely. The only concern I always have with because I've seen this among some of the guys who are preparing for exams and they've come back and said, this to me after they've done the exams, is that in the rush to get to the tendon transfer, they didn't cover the basics and I absolutely agree with you. We must get to that level of discussion, but cover the basics.
Well, what are the basics? Well, yeah, yeah, a common question, wholesale Lewis that came up in my exam because it's an area that can trip people up, they want a question that is potentially controversial, that can because it does discriminate. This discriminates between someone who is 6 and an 8. It's a good discriminating question. So you wanted to.
Oh yeah, the same X-ray can be oxygen in a basic science table or in a trauma table. So we need to be mindful of which table it's going to be because if it's at a basic science table, they're probably going to take into bone healing or no injuries. So we shouldn't spend a lot of time describing the x-rays. We need to catch the go into that first. But in case it's a trauma table, then we need to imagine as if we are seeing on day one and these questions need to be answered without the examiner asking like day one, what are you going to do with splintered and fractures when you are going to do next, when you're going to see the patient next?
So the six week mark and at that time, what are you going to do? And next, when are you going to see next? So it should be like a sequence thing as if you're sitting in a clinic and that should come without the examiner prompting you. So that's the important bit that I want to add. Yeah, I agree with Ajit. I think with this common, predictable scenarios, it is possible that you could talk the whole five minutes without having.
I have to ask you many questions. This is one of those predictable scenarios where you can just take the examiner from clinical representation history into the further the management, you know, you know what they're getting to, and that's something the level required for that. If our case, you can just take the examiner through the whole journey easily. But yeah, that's what I want to say.
Thank you. I agree with you. Grateful to lovely students and thank Welton to all the guys who volunteered. It's not an easy thing, you know, lots of courage and that's good I like, but that's a really good attitude as well. So Yeah. Well, of course, everyone to try to come forward, thank you very much.
We appreciate your presence. We're very privileged and guys, thank you very much for having me and really grateful. And yeah, really lovely session. Thank you, Alicia. We hope. We know you are very busy with your clinical practice and with your courses and teaching. But we would love to have you again.
I would love to. Absolute pleasure. It's really enjoyable and well-done once again. For those guys volunteering, that's really difficult for them to do. But keep doing it because it will help you a lot. Thank you for being with us this evening and hopefully we look forward to seeing you again. Thank all the mentors.
One Abdullah Fawad Ranjit Anwar for being here. Appreciate your input and we'll see you guys again next time next week next Wednesday. Thank you, everyone. Thank you. Thank you. Thank you.
Segment:0 .
OK good evening, everyone, thank you for joining us to this Wednesday's fa stitching. The presenter today is Rishi dear. He is a consultant, upper limb surgeon in Harlow. He's very active RCS tutor.
He he runs lots, of course. He teaches a lot of courses and he runs his own course. Let's talk Doctor blitz overseas. Quite damp. Very good. Excellent science teacher. And I'm very happy to have him with us. We also have other mentors here. We have schwann, Ranjit Abdullah Fouad, munir Anwar with us to support the session.
Amphoras, I will be moderating. This will try to answer all your questions and to try to get you actively involved. So please, if anyone wants there, would be vivo. And I would urge you all to use this session to have a vivo experience with Rishi. It will be invaluable experience and make the best out of it. So if anyone wants to take part in the vivo questions, there won't be many.
There will be probably only two or three. So if anyone wants to take part, please raise the hand symbol next to your name on the group and the participant list. Or send me a message and I will put you on the list, so please express your interest as possible. Again, just to reiterate that if anyone wants a CPD certificate, please get in touch with me and I will get this sorted for you.
And the video will kindly agreed for us to make it available to you guys later on. And as usual, we only record the lecture. We do not record your vivo answers. OK, so without any further ado, I will leave you with the original thank you for having me first and thank you to all the mentors. Hi, guys. Lovely to meet you all.
Hope you're all not suffering too much with this corona virus, and I hope to teach you tonight about nerves and also nerve injuries. I'll try and make it as relevant to folks as possible. So tonight we're going to look very briefly at nerve anatomy. We're going to look at nerve injuries in particular. How do you classify them and a mechanism for dealing with them as well? And then we'll try and look at some common vivo scenarios as well.
So let's start with nerve anatomy now. The nervous system itself is broken down into three main parts. There's the central nervous system, which consists of the brain and spinal cord. As the peripheral nervous system, which essentially relays information from the periphery to the brain and vice versa. And then there's the autonomic system, which is responsible for sympathetic and parasympathetic function, and this is the peripheral nervous system is really the focus for the exam.
This is what you're going to mainly be tested upon. So the basic functional unit in the nervous system is the neuron, which consists of a number of parts. So you essentially have a cell body and the cell body is kind of the chemical factory. It contains a nucleus. It contains a cytoplasm, which is also known as the axilo plasm and various constituents, such as vesicles, microtubules and the acts endoplasmic reticulum.
And that's mainly needed to maintain the physical and physiological well-being of the axon. So the axon itself is where the impulses travel down to the n-terminal, where they then communicate via synapse with other nerves, and the axon may be surrounded by a myelin sheath, which is a fatty layer. Now, the way that I think about it or break it down is into neural and non neural tissues.
So neural tissues are things like the cell body, the axon, the dendrites, which give a greater surface area for impulse transmission, and also the axon terminal, whereas the non neural tissues are things like glia. And what these do is these essentially are bits of connective tissue, which nourish and support the axons. So glia within the central nervous system are known as oligodendrocytes.
And within the peripheral nervous system, the known as Schwann cells, and these have quite an important function because they produce this fatty layer, which encases the neurons and can increase the speed of impulse transmission. And I'm going to very briefly tell you about how this works in a second. So this is just a quick look at the peripheral nerve anatomy, and with the peripheral nerve anatomy, you essentially have a group of sensory fibers, motor fibers and autonomic fibers, which is surrounded by connective tissue layers.
The motor neuron is situated in the ventral horn of the spinal cord, which is the bit at the front, whereas the sensory cell body resides in the dorsal root ganglion, which is the bits of the bark. And these cell bodies essentially project axons through the dorsal and ventral root, respectively. And they join the spinal nerve as it exits the vertebral foramen. OK now, within these motor and sensory fibers, you've got a group of myelinated and unmyelinated axons, so what I mean by that is surrounded by a fatty layer or not surrounded by a fatty layer.
And that's in the ratio of 14. So you have many more unmyelinated axons than myelinated ones. OK and these myelinated axons, I'll just come to that second. They have various points where they're interrupted, called nodes of Ranvier vein. And one question a lot of trainees ask me or they get asked in the exam is why do impulses conduct more quickly in myelinated axons than unmonitored ones?
And it's often a question, which is not well answered. So people mention this buzzword soul territory conduction. And the question they often say is, Oh well, the impulse is jump from one node to another because the fatty layers impermeable to ions. But impulses don't truly jump. So that's not really an accurate representation of what happens as the buzzword that I want you guys to use in the exam is this thing of active and passive conduction.
OK, so active conduction is an energy requiring process. You get sodium and potassium, ATPs pumps, you get active transport and essentially it's a slower process, whereas passive conduction is a much quicker process. So what happens in myelinated axons is whenever you've got a node of ranveer, you essentially have an impulse, which is produced and action potential, and that's an active process by the sodium potassium ATPase pump.
However, because you've got these fatty layers, the impulses can't be produced across here. So essentially what happens is this action potential will begin to decay all the way across here, and that's a passive process. And then the next impulse will be produced at the next node of wrongdoing. So that's a much quicker process because you get passive conduction.
In the case of an unmonitored axon, you have to keep producing these action potentials again and again and again, and that's an energy requiring process. So it's much slower. So that's the real reason of what happens in Salt conduction. It's not that the impulses jump, it's that you get passive decay of the impulse. So it essentially acts as a capacitor and impulses.
A circuit is being sent between the different nodes of ranvir, so that's just a very quick aside. I wanted to mention that because that's a question I have seen asked in the exam, and it's not answered very well. So just going back to peripheral nerve anatomy at a macroscopic level, the nervous surrounded by a number of coverings which you need to know about.
So each axon is surrounded by a Andoni oreum these under aneurysms, then grouped together in bundles or physicals and are surrounded by something called a perineum. And then lots of these bundles grouped together to form a ulnar nerve trunk, which is surrounded by epimysium. So remember those three buzzwords and new oreum. Meriam and epimysium.
And I suppose this is a clinical exam, it's an application exam, so the way that they may ask you, it is, well, what's the relevance of these clinically? Well, the epimysium protects against compression. It's your outer layer of compression. And so you've got your epimysium, which protects against compression, whereas the epimysium and terenure protect against stretch.
And actually, the perineum is the most critical layer in neurophysiology because it represents a blood nerve barrier, which is created between the inner layers of the perineum and the endothelial cells, which are inside the endon micro vessels. So what I think of as this blood nerve barrier, which is your main resistance to compression, so that's why it's so important. OK, so let's move on to nerve injury, and this is really the crux of my talk nerve injury can be caused by a number of different things.
Most commonly is trauma, but I've created a little mnemonic, which is a nice way of remembering the etiology. So it's remembered by the mnemonic dating me diabetes and drugs. Autoimmune causes traction or trauma, and I've highlighted trauma because that's the most common cause inflammatory, iatrogenic infection, neoplastic causes, general or systemic causes, motor neuron disease.
And finally electrical or thermal causes. So how do we classify nerve injury? OK, so most commonly, my trainees will say to me, OK, classification. I remember Seddon and I remember Sunderland. All right. And Seddon basically breaks up nerve injuries into three main types a newer apraxia or a conduction block, which essentially means that all the neural coverings are intact.
But the nerve has been stretched or distorted in some way, such that it's not working properly. OK, then axon optimises, which basically means that some of the neural coverings has the axons been cut, but some of the neural coverings are intact. So the end your may have gone, the perineum may have gone, but the epimysium is still intact. And then finally, neurons message, which means everything is gone, ok?
Sunderland was a variation of this, which broke it into five main types. OK, so we've mentioned Seddon. Sunderland broke into 1 to five, where one was again a newer apraxia or a conduction block. 5 was a rock Mrs. and two, 3 and four were different variations of accent at methis, depending upon which neural covering had gone. OK, so a 2 basically meant that the basal lamina had gone, but the perineum was intact.
A three basically meant that the sorry to the end in your room had gone, but the basal lamina was intact. Three meant that the end aneurysm and basil had gone, but the terenure was intact a formality and aneurysm. Basal lamina and perineum have gone, but the epimysium is intact and 5 means everything's gone. Now that's the answer, which most people give in the exam. I would use Seddon or Sunderland. But having worked on the peripheral nerve injuries unit in stanmore, one thing that those guys always taught me is actually in reality.
Seddon and Sunderland are not very useful clinically because if you think about it clinically, somebody comes in with a nerve injury and always say is the nerve is not working. We don't know if the nerve has been cut or not. We do not know how many neural coverings have gone, or we don't know if it's been a conduction block unless we look under the microscope, unless we exercise a piece of nerve and look under the microscope.
So actually, these are what I would call anatomical classifications. They don't offer much help clinically. So much better classification for clinical use is this one here called birch and bonnie? And what birch and Bonnie did is they. And that's Rolf birch, who worked on the peripheral nerve injury unit at Stanmore. They basically broke these nerve injuries that broadly into two main types a conduction block, which are the same as a newer apraxia and a degenerative lesion.
And that's because they said, well, actually clinically, you cannot differentiate between an excellent methis and New York Mason, so that all should go into the same group of a degenerative lesion. OK and that's probably more useful clinically. So this is just a sort of slightly more complex table, just shows you the different classification systems, and I don't really want you guys to learn them in detail. Just remember what I said about sedin neuro apraxia axilo, not Mason Europe Mason Sunderland is 1 to 5.
And basically, birch and Bonnie is a conduction block or a degenerative block lesion. OK, so I'm now going to explain this in a bit more detail, and I want you to remember these two characters here the earthworm and the bomb. This will revolutionize your understanding of conduction blocks and degenerative lesions. OK, so the analogy that I think of and I can't say this is my original thought.
I worked on the knee unit at Stanmore and the consultants there used to teach me about this. I have to thank them for this, but it's a great analogy. So the analogy that I can think of is imagine if you have a lit bomb and you put the lit bomb in a puddle of water, the bomb will not go off because it's surrounded by a puddle of water. But if you dry the bomb and you take away the water and you light it, it will then go off and work.
And this is very analogous to what happens in a conduction block or in your apraxia. Essentially, the nerve is all intact, but it's been distorted. There may be a hematoma. There may be some scar tissue. Something is representing the puddle. It's stopping that bum from going off. As soon as you remove that, or it may spontaneously result, then that nerve will start to work again.
OK, but if you leave a conduction block for a period of time because essentially you get a compartment syndrome, you get disruption of the blood nerve barrier, which I mentioned before between the perineum and and ending effectively that will progress on to become a degenerative lesion. The next one is this concept of the earthworm, and the way I want you guys to think of it is imagine if you shop an earthworm in half, what happens?
Well, what you find is the worm doesn't die. One part of it, the tail dies and shrivels away. But actually the bit, which is connected to the brain regenerates and starts to grow a new tail. OK and if you do not know that, try and find an earthworm in your garden. You have my permission to practice that, ok? And that represents exactly what happens in a degenerative lesion or Wallerian degeneration.
And I'm going to just go on to explain that to you. So conduction block, the mechanism that I spoke of is this thing called the blood nerve barrier. And this was something which I didn't really understand until actually after I became a consultant. But it's all to do with this perrineau rhythm and endothelial cells. It's a barrier between those two. And the way that I think of it is that, say, selectively permeable barrier.
So essentially, these cells have got tight junctions, which are impermeable to many different substances, and there's no lymphatic vessels within either the engineering or the perineal. So what that means is it creates an immunologically and biochemically privileged space for peripheral axons and supporting cells. So the two buzzwords I want you to remember are selectively permeable.
And then I want you to remember a privileged environment. That's the buzz word to remember. So what happens is when you compress this nerve, it gradually upsets this blood nerve barrier. It alters the pressure within the vessels, creating an internal compartment syndrome and essentially breakdown of the vasculature, which causes leakage. This then leads to accumulation of various proteins and aggression of inflammatory cells like lymphocytes and macrophages, which otherwise were not able to get in.
And as a result, this initiates an inflammatory response and increases the permeability even further. So it's like a positive feedback cycle. OK, so compression upsets this barrier lessen in the inflammatory cells, the macrophages, the lymphocytes. These cause inflammation. They increase the permeability even more positive feedback cycle.
It all goes downhill. OK, so that's the way to remember it. OK, now the only reason I put this slide in is because just I have heard of examiners saying to people, oh, well, why does the conduction block actually cause the problem? This is what it does. It starts selective permeable. Barrier, which creates an immune, privileged environment. OK and it initially starts as apraxia or a conduction block, and it later progresses to form galarian degeneration.
So that's a little diagram of what I was saying. You start off with changes in the blood nerve barrier. You get compression and edema, which leads to thickening. And essentially what it does is it leads to localized nerve changes. You get an influx of these inflammatory cells, which otherwise we're not able to get inside. They lead to increased permeability and start to cause breakdown in the nerve, and that will eventually progress to Wolverine degeneration.
Now, this is the bit, which I think is more interesting for you guys. So my biggest buzzword when I teach is this word of compartmentalization. I compartmentalize everything. OK, so even if you go into your fridge, you talk about liquids and solids, solids, which are vegetarian me, everything you do now as part of your daily routine.
Compartmentalized, compartmentalized, compartmentalized. Ok? so with Woolery degeneration, I break it up into three main parts the cell body. The proximal segment and the distal segment. So when you cut a nerve. Imagine if you say, OK, I'm doing a carpal tunnel decompression, I accidentally cut the median nerve. And this is a vyver question.
They might give you what is happening at a cellular level. Well, basically, I would say to the examiner, I would break my answer up into three main parts the cell body, the proximal segment and the distal segment. So the first thing that happens is just like the earthworm, the distal segment, because it's disconnected from the cell body, the nutrients can't get in. It will essentially shrivel up and die.
It collapses, and all that is left behind are the Schwann cells, and they form these things called bands of Bumgarner, BU and gene and e-r. So I always think of it as I remember it, like the parties from the old Italian prime minister. OK, so that's the way I remember it. OK and so what happens is they basically become neuro tropic factors and an EU rotr opIc neuro tropic, which means they guide the direction of growth.
They're telling the nerves where to grow into. OK, then what happens is in the cell body, the nucleus moves to one side and it changes its phenotype from being a conductive phenotype to a regenerative phenotype, so increases its activity, mitochondria, et cetera and it becomes a regenerative phenotype. Then, in the proximal segment, you start to get outgrowth of these little finger like projections called really podia.
And these Filipovic podia produce neurotrophic factors spelt trop h I c, which stimulate growth. So at one end, you've got neurotrophic factors which are stimulating growth. At the other end, you've got neurotrophic factors which are telling it where to grow into and when the two meet. It's known as a process called contact guidance, so the analogy I think of is a blind man and his cane.
The nerves are kind of feeling in the dark where to grow, and the factors are telling them where to grow into. And sometimes that process just stops and it will end in something called a neuroma. And when that happens, you have to go in and intervene. So classically, Woolery degeneration is a very predictable process. You typically get a latent period of about 2 to 6 weeks, and that's why nerve conduction studies are useless within the first four to six weeks because of this latent period.
And then the nerve starts to grow at a rate of 1 millimeter a day, the same as hair. And clinically, we can monitor that by something called an advancing 10 hour sign. OK, so when you're in the PMI unit, one thing I always do is I always start distally and then work APR and I feel for a hours tapping over it because that will tell me where the nerve has grown to. So I can say, OK, it's three months with injury.
I can see that the nerve has grown to the mid forearm. I'll see you again in six weeks. I would expect it to have gone, let's say, down to the wrist or whatever it is. OK, if it is, I'm going to continue to observe. I'm not going to do anything about it. If it doesn't, I may need to go in and explore. OK, so that's the way to think about it. Keep it nice and simple.
And some people say to me, Oh well, Rishi. A true tunnels only occurs in a degenerative lesion when the nerve has been cut. So why do we get a tonsils and carpal tunnel syndrome? Because that's not a degenerative lesion. It's not. The nerve hasn't been cut, it's a conduction block. So what we call that is they don't say this in any of the books, but it's something called a pseudo tonsils.
And that's because essentially, when the nerve has been compressed for a long period of time, the myelin sheath has melted away. So essentially, what you've got here is when you tap on here, you're tapping on exposed growth cones because the myelin sheath is essentially melted away. So it's not a true tonsils should actually be called a pseudo tonsils. OK all right now, I think this is another really important thing to understand this, so a common investigation we order is nerve conduction studies, but a lot of people don't really understand what they are.
So I'd really encourage you guys to look at the next time the nerve conduction studies you get and try not to look at the result. Just look at it because that's one way they could give you an exam. They might give you a picture of a nerve conduction study, or they might actually give you a nerve conduction study and say, analyze this. So what do you actually put on a form when you request a nerve conduction study?
Will you request two things? You request the nerve conduction study and you request an EMG and a nerve conduction study looks at the electrical activity in a nerve, either sensory or motor, whereas the EMG looks at the electrical activity in a muscle. All right, so the nerve conduction study consists of four electrodes, which you can see in this diagram.
So you have a stimulating electrode. You have a recording electrode. You have a ground electrode, which essentially earths the patient and stops them being electrocuted. And you have a reference electrode, which essentially gets rid of any sort of background interference activity and gives you a nice, good trace. OK so in the case of a sensory nerve, the stimulating electrode will be distal and the recording electrode will be proximal.
So it's what we call anti-drone impulse transmission, whereas in the case of a motor nerve, the stimulating electrode is proximal and the recording electrode is distal, so it's called orthodontic stimulation. So this particular case, this is the stimulating electrode, and it looks to me like the recording electrode is on the thenar eminence. I think this is probably a medium motor nerve because the stimulating electrode is proximal and the recording electrode is distal, and it's also on the thenar eminence.
And that would be a reasonable question, guys. They might ask you that an exam, because what they want to see is, have you done a nerve conduction study or have you been to a clinic before the stimulating? That's the recording. That's probably either probably a reference electrode, and that's probably just the ground electrode. OK, now the next thing people say to me is, well, how do I actually interpret a nerve conduction study?
So you have to know three main parameters, and those are latency. Amplitude and conduction velocity. And the first two parameters are measured directly. The third one is derived, which means you work it out. OK, so the latency is known as the quality of impulse transmission. It's the time taken to travel between two points, whereas the amplitude is the volume of axons or the quantity of impulse transmission, the conduction velocity, which is in meters per second.
The way that you calculate that is you essentially mark two points on the arc and you basically mark one as M1A1 is beat and then you take a tape measure and you go between those two points. And then you look at the time taken between go between those two points. So that's another thing you can say in the exam. And it's just a way of showing the examiner that you've been to a nerve conduction study.
These are things that they don't say in the books, but these are little tricks that you can put in just because what they want to see in this exam is they want to see clinical experience. They don't want to see just factual knowledge. They want to see clinical experience. So these are lot of things that you can do. Now you do, you need to values for this exam? No, probably.
The only one that I would learn is a average value of 50 meters per second. So 60 minutes per second for the upper limb, 40 for the lower limb, but on average, about 50. But the key thing you do is if they give you a nerve conduction study in the exam and this is often a trick they will play on you is they will say, OK, this is the nerve conduction study and it's the left hand.
The first thing you say and this is a pass/fail answer is you say I cannot I cannot assess this in isolation. I want to see the right side. And that's because somebody could have an underlying problem, like hereditary motor sensory neuropathy. They could have something like MS where they've got universally slowed conduction, but you won't know that until you see both sides In comparison.
Does that make sense? So it's not a case of OK, fine, he's got a nerve conduction conduction velocity of 20 meters per second. He must have a carpal tunnel or a cubital tunnel that may be normal for him if he's got MS or if he's got hereditary motor sensory neuropathy. So you must ask the other side. Nerve conduction studies in isolation are meaningless.
Right? the second thing you need to know is about how to interpret EMG. And an EMG is slightly different because in an emg, you've only got three electrodes, a recording, a ground and a reference electrode. And that's because the patient provides their own stimulus. So the neurophysiologist will often say if the patient, can you move his thumb from me, OK, they're doing APB and opponent's policies, so they are testing the median nerve.
So at rest, a nerve or an EMG should have a flat line. It should have nothing there. The minute you do that, it should suddenly have a motor unit action potential. OK however, if you see somebody at rest on, the nerve has been cut. You will see lots of little v-shaped things. And in the early phases, these are positive things which are called positive sharp waves.
OK upside down VS and then you get fibrillation later on. So not particularly those guys. Remember for simulation is a clinical sign. It's twitching, you get positive sharp waves and you get fibrillation. So that's a sign of denervation. OK, so. Then how do we know if the nerve is regenerating, how do we know it's coming back to life?
Well, the analogy that I think of you get these things called physic units. That's how. So the analogy that I think of as the Indian chief and villages. So you've got the chief and village, a guy who's got eight kids and each of those kids represents a muscle or a motor unit. And the chief represents a motor nerve.
The chief in village B has also got eight motor units. Now what happens is when the chief in village dies, B will take over his kids and his own kids. So instead of supplying eight, he will now supply 16. So as a result, you get a bigger amplitude of stimulus and you get more up and down things which are known as physic units. So poly fascia is a good sign. It's a sign of recovery.
So there are two things of recovery, either clinically, we can look for an advancing 10l sign or newer. Physiologically, we can look for physic units. So a common referral we would have is guys would say, OK, I've done a posterior approach to the hip. I know the sciatic nerve was intact, but the patient's got a foot drop. So we would say to them, OK, is there any evidence of hematoma as in something compressing the nerve to an ultrasound?
OK, no. Is there any pain? No OK, there is no evidence of ongoing compression. Is there evidence of recovery? So we look for a advancing tunnels and we do a nerve conduction study after six weeks. If we could see polyvalent units, if we could see an advancing. We would do nothing.
We were just observe them over a period of time. OK, before we move on from nerve conduction studies, I just want to mention one other thing because a lot of people say to me, oh, well, Rishi, what about the reflex or f waves? They get worried about these things now. These are very rarely used in clinical practice. And in the knee unit. The guys would say they weren't useful at all. But in a nutshell, what happens is the way to think about nerve impulse transmission.
Although I told you guys orthodontic anti-drone, that implies that nerve transmission only goes one way. It doesn't actually goes in two ways. So when you provide a stimulus, the stimulus goes down towards the hand and it goes up towards the neck. All right. So what it does is it basically sends an F wave or a heat reflex where it bounces off the top and it comes back and we record that.
And that's useful in cases where you cannot get above the lesion, such as a nerve root lesion in the neck. So that's what we use reflex or phrase for. We do not use them in practice, really, but that's just if the examiner asks you, it's used for cases where you cannot get above the lesion, ok? So the other question, I think is really relevant clinically and I've kind of alluded to this already is when do we explore, when do we surgically make the decision to explore with these guys?
Well, I've mentioned it. There's two main reasons evidence of ongoing compression. And clinically, we can determine that by a patient having pain, either spontaneous or evoked pain. So by that, I mean spontaneous. They've got pain at rest without any stimulus evoked means you can likely stroke the skin, you can tap on it and they start screaming in pain.
OK, that is a sign of ongoing compression. Or if you do an ultrasound, it shows an expanding hematoma. You will tell the referring center, go back in there and decompress that hematoma. There's not time to refer to the unit. Just go in and decompress it. OK if they don't have these things, if there is no evidence of recovery either clinical in the form of an advancing tonsils or neuro physiologically in the form of physic units, so those are your two reasons to do an operation.
And what kind of operation do we do? So I've created this thing called the ladder of reconstruction. It's a really nice way and easy way of thinking about it. So at the most basic level, you start with a new releases, you go in there, you remove the hematoma, you remove the scar tissue. And that's useful for people who've had neuro apraxia. And actually with the knee unit, when we have people who have very severe plexus lesions, they go in there even if the nerve roots were advanced.
The first thing they do is neutralize them and they might do something afterwards, but they do a new analysis in the most basic level. I remember you can combine procedures together, so if you find that actually the nervous cut, but the distance between the nerve is such that you can bring it together primarily and repair it without tension, then you can do a direct nerve repair and that's always the best.
But remember, guys, the nerve repair must be done under microscopic guidance, either loops or a microscope, and you must have fascicle to fascicle matching. So a common question they've asked before is you've cut the cord. You do carpal tunnel decompression. You cut the median nerve. What do you do?
And the mistake people make is in the age they go, OK, I'd repair the nerve. I wouldn't save up. I would say I would tag the two nerve ends. And my justification for doing that is because I need, first of all, the training microscopic guidance. But secondly, I need fascicle to fascicle matching. And if you do not have the skill set to do that, you're not doing the patient the best service.
And I always used to advise tag to nerve ends do not attempt to repair them. In fact, if you find that, actually, do you know what? And I've actually I've missed out one there. What I should have said is if you find that actually there is a gap between the two ends, because remember when you do a nerve repair or a nerve exploration, you have to take off the serrated bits, the inflamed bits or whatever the damage because you can't just repair end to end.
So once you've excised the two bits, if you find actually you can't bring them together without tension, you can actually put a nerve graft. And that nerve graft could be something like a sewer ulnar nerve and intercostal nerve or some sort of sensory nerve. Or it could be synthetic. Ok? if you find that actually the gap is too big, even with graft, you may have to do something called a nerve transfer where you take a nerve, which is less useful elsewhere, and you basically transfer it to supply function.
I think there's three main transfers that you should know for the exam. OK, so if somebody has, let's say, a upper trunk injury or a yeah, like a C five, C six, your three priorities there is basically want to restore shoulder stability, so you want to get the suprascapular nerve. So I would normally take the spinal accessory nerve to the Super suprascapular nerve.
OK secondly, I want to restore shoulder movement in the form of deltoid, so I do what's called a somesuch transfer. Socom, asac and I'm taking a branch of the radial nerve, which supplies the triceps and I'm putting it into the auxiliary nerve. And finally, I want to restore elbow flexion. So I do what's called an Auberlen transfer OB or alliance, and I take a branch of FCU OFDR supplied by the median.
So it's applied by the ulnar or medial nerve, respectively. And I plug that into the musculocutaneous. I wouldn't learn any other nerve transfers. Those are the three that I think just remember those for the exam. And that's if you're going for a seven or an eight. So don't panic. All right. Obviously, the next thing is with the first three things you have a certain period of time.
The books say one year, but I would say in reality, about six months to a year, and that's because after a period of time, the motor units will die. So even if you restore nerve function, you've got nothing to innovate. So in those cases, you do what's called a tendon transfer where you basically take a functioning muscle tendon unit and you take it into one that's not functioning very well.
And finally, you do what's called a free muscle transfer where it's like a free flap in plastics and you need plastic surgeons to do this where you're essentially taking a muscle from somewhere else. So you might even take something like gastric or chrysalis or whatever it is, and you basically take it with its pedicle and you plummet it into the area. OK, but that's really high end stuff.
So that is the ladder of reconstruction. I would learn that as a way of treating everything, guys. I think you can't go wrong with that, really. OK so tendon transfers, I'm going to very briefly just to end my talk, say something about tendon transfers. OK so we're tendon transfers. I've got a really good way of remembering these rather than memorizing the tendon transfers guys in the exam. I break it up into four bits.
I say, what is your deficit? What actually three bits, what is your surgical priority and what are your options? And that way, what they want to see in this exam, I remember I told you it's clinical application, it's not memorizing it. OK, so they want to see, does this guy or girl, does she? Did they have the sort of wherewithal to understand the principles?
OK, so what's your deficit? Let's say somebody's got a. Let me think of what let's say they've got a low rate. Certainly let's say they've got a low median nerve palsy. OK, so they're deficit. They're they've essentially got it's an anatomy question. All right. So we know where the median nerve runs. The median nerve doesn't give any branches and upper arm.
It basically starts to give branches in the forearm. It gives off four branches of the common flexes FCR PhDs. Paul Morris longest and pronounced Tyrese. It then gives off three branches and dropped nerve to FPL FDP to index the middle and prenatal code writers. And then it basically gives off your hlophe muscles and sensory to the radial 3 and 1/2 digits and also a Palmer cutaneous branch. So with a low median nerve palsy, basically you've just lost your hlophe muscles.
That's your deficit and you've lost sensation to the radial 3 and 1/2 digits. What is your surgical priority? So your surgical priority with a low, medium of palsy is restoring opposition? OK, and then what are your options? So with a. Policy, your options often opponents plastic, you can either use Paul Morris longest, you can use IP, you can use FDS to the ring or you can use abducted digitally minimi known as a Huber's transfer.
OK although remember, that's the pediatric transfer because you lose 75% of the strength. Now the problem with the high median nerve palsy is this time you've essentially got your surgical priority. Here is opposition, but you've also lost some flexion because you've lost FPL. OK, and you've also lost FTP. OK and you've also lost finger flexion to these ones because you've lost FDS and FDP with a high median nerve injury.
So this time you have surgical priorities restoring some flexion. Finger flexion to these two and opposition. So what are your options for opposition? You can't use primaries longer because that's gone with the high medium, the deposit. You can't lose s-vhs because that's gone. You can't use abducted a.m.e. because it's a pediatric transfer.
So your only option is IP. OK, for some flexion, you can use brachial radio less and for finger flexion. You can basically buddy the FDP from the older ones and basically have a mass movement like that. So always break it up into what is your deficit, what is your surgical priority and what are your options? OK and finally, the principles of tendon transfers, now I have to tell a very quick, funny story, if you guys don't mind me.
So I was crashing and burning on one of my questions in the exam and I was desperate to get in principles of tendon transfer. It was like a running joke because in my revision sessions, I would try and get principles of tendon transfers into every single thing. So I kept saying to someone to the examiner, I was like, they were like, well, what are you going to do? And I said, well, there's a number of things you can offer, such as tendon transfers, which have a number of important principles as you did, but you didn't take the bait.
And then again, I say so I could do tendon transfers, which have many important principles. Again, she didn't take the bait. So I think she just got bored of me saying it. So she's like, OK, tell me about the principles of tendon transfer. So, so the key thing is everybody goes on about the eight S's, which I think is one of the books.
Now this question, I subdivided it and I said the principle is a tendon transfer can be divided into patient donor bed and recipient factors. And she literally ticked it and said, move on. So patient factors would be things like, is the patient sufficiently motivated to do the rehab? Are they able to do the rehab? Don't the fact would be, is it a sacrifice about donor?
Did it have sufficient power, at least MRC grade 4 out of 5 because remember, you drop an MLC grade, same line of pool, et cetera so what I'm doing is I'm saying this eight ss, but I'm just subdividing them into those different parts in case I miss one out. So it's just a nice way of doing it, and it's that whole thing of compartmentalization that I was saying to you guys. So finally, we've got some common scenarios, and I think for us, did you want to me to offer these as viable questions to people?
Or I think if you don't mind, we could do it with Aviva practice and if you could then give us your model answers for them? Absolutely I think people will find it useful to give them an opportunity to practice with you. So I think so you've finished your goodness. Yeah, sorry, guys. If that a bit long. No, perfect.
Wonderful wasn't was spot on, actually. Yeah I hope I've not scared you too much because I'm trying to keep this simple. As remember, it's called basic science. It's not called complex science. So it's all about keeping your principles really simple for this exam and stuff, right? Thank you, Michel. I think this is very interesting, a very high standard presentation, as expected from you.
You made this dry topic very interesting. You, you brought it. You brought the clinical significance off of the basic sciences behind the nerves into our clinical practice. And that's exactly the higher order thinking that we're trying to implement in our teaching exactly how you transfer this dry theoretical knowledge to clinical practice.
And that's exactly the level they are looking for in a fast candidate. A lot of buzz words there in the lecture more than I can count. So I think we have to revisit every candidate to really listen to this, learn all these arteries, conduction all this mnemonic dating me. And I think that's very useful, especially when you get stuck in the question and you don't know what to do if you're remembering the words, this mnemonic could get you out of trouble sometimes.
So and and actually the slider of reconstruction you present that day in is actually it's worth gold, really. It's amazing one. So I think in terms of. Questions, I think you covered really everything about nerves, I think people will just have to look at this lecture again. But any comments from any of the mentors and anyone wants to add anything.
And those really well presented a very broken down into its basic from a very complex topic to a very, very public to understand now. Just a reminder to all the candidates that in the exam, don't be frightened by something that looks complex because often the patients that are coming with nerve injury have already had medical procedures done to them. They're not well known to the examiners who are organizing the exam, so they've got lots of different things happening.
Just take a breath, start at the basic and move forward from there, especially in the concessions. Yeah, I think I think, as you said, is what you have to remember is when, when we get a break, let's say a brachial plexus injury is an example. When that comes in a NIPE clinic, we get 30 minutes with that patient. And by the end of the 30 minutes, we often don't have the diagnosis.
We often have to do nerve conduction studies. We have to bring them back. So what they're looking for in the exam, they're not looking for a perfect diagnosis in five minutes. They want, they want. Look, how can you do a general impression or just a general overlook? Is this a plexus injury?
Does it look like it's a high or a low plexus lesion? And what investigations might I do? And just a generic impression? Will I do the same thing? Basically, that's what they're looking for. So as Sean said, I think it's very important. Just keep nice and relax, keep calm and just keep it really, really simple in terms of general principles and things like I can.
I mentioned an experience recently by one of my colleagues who just had the exam, and he felt that question. He had a nerve injury exam, clinical and here because he knew that they will end up with a tendon transfer. So he jumped all the steps and immediately jumped into the tendon transfer. And then he made himself a big, big, big hole and dug himself into it and buried himself.
And I really liked this ladder of management, which is really good if everyone stick to that. So you always start by the simple methods and you slowly make your way up. I really like that. Yeah, you have to remember that you can't get an eight before you can get a six. And I have had guys coming up to me in the like Rishi. I don't understand why I failed.
They got me onto management. I got into evidence. But the reason why you failed is because the sixth is always the safety question. So unless you've demonstrated safety first and safety would be assessing this patient appropriately, assessing them clinically getting appropriate investigations, they might let you jump to the end, but you won't have done well on that question.
So don't just assume because you got into evidence that you've automatically done well and that station cover the basics is all about level four, they consultant. It's not about peripheral nerve injury, unit consultant, level Professor work. Lovely so if everyone is happy, we will move on to the vivisection. We have ATF who was volunteered to go first.
This is a 48-year-old manual laborer who's been having some difficulty with his hands. He's complaining of dropping things. He's come to see you in your hand clinic. OK I mean, this is a tactic I often use and I tell trainees about is I kind of stop to stop myself from slowing down and the vyver and getting bogged down because I felt that you were getting bogged down a bit then is I almost I almost think of it as like, you're driving along Route 66 and you're trying to get to the rainbow at the end, which is the 8 and having the mind of the back of your mind, where do I need to get the aim?
What is the final question they're going to ask you? And a tip is in the nerve, in any nerve question. Whatever it is, the final question is always going to be tendon transfers. It's always going to be OK. So you need it to get to the opponent's place to get to the 8. So so you need to find a way of getting through it very quickly.
So so I divide it up until I call the five days of deer, which is describe, diagnose, discuss, decide and diagrams to describe as your opening gambit. The first thing that comes out of your mouth is determined if you've got a five, six or a six seven. So this is a clinical photograph of both hands, which shows bilateral fena muscle wasting or thin remnants wasting. You said APB.
We do don't know if it's APB. It's thenar eminence wasting, which is asymmetrical worse on the right compared to the left. OK that's what you say, first of all. All right, so that's described diagnosis. OK I suspect that this is a bilateral carpal tunnel syndrome worse on the right compared to the left. But because this bilateral involvement, I would want to check for a central involvement by checking the cervical spine.
OK describe. Diagnose discuss. What are your concerns and how would you go about addressing those concerns? So I break it up into like a triple assessment clinical, radiological, biochemical and neurophysiological. All right. So I kind of think it to myself.
I think imagine you're driving along the road and you've got bits of shit on the side of the road. You want to acknowledge the shit, but you don't want to get stuck in it. All right. So that's why you want to find a quick way of saying history, examination investigations. So you said I would take a history. Don't say that.
Say I would take a pertinent history asking this, this, this and this, and I always break it up into a risk factor history and a condition history. So how is the condition affecting them? Have they had conservative treatments? And then risk factor history, hypothyroidism, manual activity, pregnancy, et cetera? All right. There's not really any imaging you can offer these guys.
So you then say I would do a neurophysiological assessment and I would look for a prolonged conduction study and also a to conduct velocity and increase latency across the wrist. So that's the buzzword I was looking for. If you look at conduction studies, they always say wrist and elbow. OK and then finally, you want to get on to the operation. So that's the fourth day decide to describe, diagnose, discuss, decide, OK.
And that's going to be talking through the layers. So in an appropriately marked consent to patients supine with an arm table tourniquet and infiltration of local anesthetic to the carpal tunnel, I would mark out four lines. OK, you want to say the lines, Kaplan's card and a line from the base of the abducted thumb to the hook of the helmet, which I do not want to go distal to because it marks the deep Palmer arch, the distal skin crease, which I do not want to go proximal to because of the Palmer cutaneous nerve, the radial border of the ring finger, which marks the line of the carpal tunnel and the real border so of ring finger, the real ball to the middle finger, which marks the recurrent branch of the medial nerve.
OK, and then you just say I would dissect through skin fat coming onto the flexor-pronator Allen. I would make a small neck in a tearing sensation. Use words that show that you've done it before until I can just visualize the median nerve. And then I would use a McDonald's and under direct vision, I would release the nerve proximally and distally and just close skin at the end.
OK and then the last thing they'll say to you is, OK, the patient comes back. They've had no improvement in the function. What are you going to do? And that would be tendon transfers, opponents blasting. So I think those 5D's sorry, the last day I should have said is diagram detective or discussion points. A discussion point can be and I use those 5D's for every Fox question.
It really helps me in my structure of those. So yeah, thank you. That helps. If I could add at did exactly what we had said you. Yeah, I would ask. I would ask. It's not a problem, but there are certain questions that go to help you diagnose and manage this patient. But when we said, what are you going to do, the right decision making process?
That's fine, but you don't need to repeat it a second time, he wasn't tricking you when I hear that, they'll move on. Then they're asking you what you're going to advise does not make sense. Yes, and yes, you do have to discuss all options, including non operative versus thing. The reality is, we should say, what are you going? It's just it just means less responding to a prompt.
Yes I think, as I say, I was at the same point, like he mentioned the same question three times, so that means he wants to take you to the surgical route. So why wait? Yes and I think I think I did, exactly as he said to me, that is it in this patient here? I agree with you shared decision making, of course, but. As a surgeon, if you've got a muscle wasting and severe changes, you want to get in there quickly because otherwise they're going to have a non-functioning hand.
So that's what I was trying to push you just to say, actually, yes, of course you will consult the patient. But in this particular case, I would advise to do this, this and this. It's like if I saw a Jupyter patient who's got a diagnosis or who has a pip contracture of more than 2021, 30 degrees, I would say, look, yes, we could try conservative measures first. But in this case, I know it has a very high risk of recurrence.
It has a very poor response to conservative management. So I'd probably recommend surgery in this particular patient. Yeah thank you. Yeah OK, guys. Well done. And that was just taking you guys to medium nerve anatomy. We don't need to go through that. They'll probably ask you about carpal tunnel anatomy if you're doing very well.
Yeah OK, I'm sorry if what I was going to get onto is, if you did really well is where can the median nerve be compressed with a high median nerve palsy? So I've got a little mnemonic flats, fesa process ligament Struthers aping the biceps pronounced 3 epicondyle process. can learn that if you want the example, OK, I'm just sorry, I really have to emphasize this if it's an easy topic your day to it's bread and butter for you.
If you need to know these details really well, the information is to be described perfectly. The management, the investigations, all of that just needs to be perfect because the more common the operation is, the more in-depth they're going to ask you. Yeah, absolutely, absolutely. Sometimes the difficult ones are the easiest ones to score ET on because you don't have to say much.
OK welcome. Welcome to your first exam. Thank you. This is my table and this is your examiner. He has a question for you. OK hi, Joey. So this is a 35-year-old gentleman who came off a motorbike and did this injury a week ago. He's now come to your fracture clinic.
This is his clinical appearance on the left, and these are some radiographs that you got on the right things there. There was a lot of good stuff. Mm-hmm your initial description, I thought, was very good. You, you, you describe the whole St Louis. You got the diagnosis very well. You keep OK. So initial description you got you described it well, but you just wasted too much time.
OK, so just let literally say this is a clinical photograph of a restaurant and an AP radiograph of the right humerus, which shows a whole St Louis fracture at the junction of the middle, and distal thirds. This is a radial nerve. Halsey just say describe diagnosis nice and quick. All right. Yeah then what you need to do is you need to get through that third day.
You're you're getting stuck in the shit. OK, so just describe it in terms of a triple assessment clinical, radiographic and neurophysiological. OK what you want to say is clinically, as you said, you want to find out about co-morbidities, level of function, dominance, occupation, et cetera. But you also want to know about if there's any evidence of iatrogenic injury, which is what I was, which is what you said, which is fine, but I had to prompt you a little bit.
So you need to say, look, if it's been there after they did the splint, it means it's iatrogenic injury and the nerve is in fact and it obligates exploration. OK, Yeah. Other things you look for clinically is, as you said, you could look for advancing 10 hours. I wouldn't expect to see that after a week. You could also look for pain and you could look for swelling as well, which is a sign of ongoing compression.
OK, radiologic, you talked about a newer physiologically, it's useless before six weeks because of a latency period, but you can mention it anyway. Now you mentioned about. You got into a controversial area in the whole St Lewis structure is very regularly asked because it trips people up. And this question about whether you fix it or don't fix it, I agree with you.
So g tenodesis paper showed that 90% of cases the nerve recovers in three months. But the problem with that is the way to say this is we don't really care about the nerve injury. If it's not iatrogenic, we know it's going to recover. But the problem with these is in 30% of cases because of the deforming force of triceps. They basically go into muscle union or they get incredibly stiff elbows.
So a way to avoid the controversy is to say, look, this is a young, active patient. I deliberately made him young for you. 35 years that I would counsel the patient, I would expect the nerve injury to recover. I know that the recovery of 90% of the cases, so my decision making is based upon the fracture. And I know with these distal third fractures because of the deformity force of triceps to have a high rate of mild union and they get elbow stiffness.
And my rationale will be to fix this to allow early mobilization of the elbow, because what you do is you tell me, OK, fine, I'm going to get nerve conduction studies, I'm going to do serial examinations. So I'll say to you, OK, it's three weeks. What are you going to do now? OK, I'll examine him again. OK, six weeks.
And you said I wouldn't even do nerve conduction until three months. So you're just going to keep going and going and going. And it's what I call a lot of risk for very little reward. It's like the pink pulseless hand in the Super con La fracture. Yes, we know that can wait till the next morning. But the new both guidelines have said if there's any evidence of impaired muscularity, including purposelessness, take them in the middle of the NIPE.
So it's a way to sidestep the controversy because what you want to think to yourself is I need to get onto the operation. I need to get onto posterior approach. I need to get on to plating extra articular locking plate. I need to get on to tendon transfers. If you're not going near that, you're not scoring a 7 at all and you're lucky to score a six. So you've got to think, how do I get through that initial crap as quick as possible by 1 and 1/2 minutes?
You should be in theater. Yeah, so little things like triple assessments, like talking about clinical neurophysiological that just gets you through that crap as quick as possible and sidestepping the controversies. I mean, what do you guys think? Is that? Is that fair? Or I think I think you're percent?
Yeah, absolutely. The only concern I always have with because I've seen this among some of the guys who are preparing for exams and they've come back and said, this to me after they've done the exams, is that in the rush to get to the tendon transfer, they didn't cover the basics and I absolutely agree with you. We must get to that level of discussion, but cover the basics.
Well, what are the basics? Well, yeah, yeah, a common question, wholesale Lewis that came up in my exam because it's an area that can trip people up, they want a question that is potentially controversial, that can because it does discriminate. This discriminates between someone who is 6 and an 8. It's a good discriminating question. So you wanted to.
Oh yeah, the same X-ray can be oxygen in a basic science table or in a trauma table. So we need to be mindful of which table it's going to be because if it's at a basic science table, they're probably going to take into bone healing or no injuries. So we shouldn't spend a lot of time describing the x-rays. We need to catch the go into that first. But in case it's a trauma table, then we need to imagine as if we are seeing on day one and these questions need to be answered without the examiner asking like day one, what are you going to do with splintered and fractures when you are going to do next, when you're going to see the patient next?
So the six week mark and at that time, what are you going to do? And next, when are you going to see next? So it should be like a sequence thing as if you're sitting in a clinic and that should come without the examiner prompting you. So that's the important bit that I want to add. Yeah, I agree with Ajit. I think with this common, predictable scenarios, it is possible that you could talk the whole five minutes without having.
I have to ask you many questions. This is one of those predictable scenarios where you can just take the examiner from clinical representation history into the further the management, you know, you know what they're getting to, and that's something the level required for that. If our case, you can just take the examiner through the whole journey easily. But yeah, that's what I want to say.
Thank you. I agree with you. Grateful to lovely students and thank Welton to all the guys who volunteered. It's not an easy thing, you know, lots of courage and that's good I like, but that's a really good attitude as well. So Yeah. Well, of course, everyone to try to come forward, thank you very much.
We appreciate your presence. We're very privileged and guys, thank you very much for having me and really grateful. And yeah, really lovely session. Thank you, Alicia. We hope. We know you are very busy with your clinical practice and with your courses and teaching. But we would love to have you again.
I would love to. Absolute pleasure. It's really enjoyable and well-done once again. For those guys volunteering, that's really difficult for them to do. But keep doing it because it will help you a lot. Thank you for being with us this evening and hopefully we look forward to seeing you again. Thank all the mentors.
One Abdullah Fawad Ranjit Anwar for being here. Appreciate your input and we'll see you guys again next time next week next Wednesday. Thank you, everyone. Thank you. Thank you. Thank you.
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