hi everyone dr. Simon frog from the clinical neurophysiology channel here this video is actually a part of a symposium for the neurology 2020 course of the institute of neurology that's upcoming a couple of years ago I gave a similar lecture and I had an hour to do that so on this occasion I've only got half an hour so we really need to be very focused during the natural course itself and we'll be talking about case based data interpretation of the type of things that you as a neurologist may be coming across on the day to day practice and so that's going to be recorded separately this is actually just a preparatory talking a way to give you a flavor of what your physiology is about it's not just about the numbers just to show you what the tests look like on the screen it's a little bit more interesting rather than just the drawing numbers themselves so I hope you find that interesting and illuminating as to what we actually get up to doing so without much further ado let's dive straight in let's start with an overview of what we're going to be talking about let's talk about the basics let's show you a little bit of the equipment some of the techniques in myelination patterns localization and then a little bit on EMG now if you have a look at my youtube channel the rest of it there's lots of information about any one of these individual points but this is just an overview we'll start with there's a wonderful specimen over here from the Royal College of Physicians if you haven't already been to sit then I would recommend that you do the under the skin exhibition will be closing pretty shortly so make use of the opportunity to see it this is a specimen and that's how an anatomical table from Italy and amazingly they've managed to take the nervous system and squish it into two dimensions and it's really interesting particularly if you want to try and work out which nervous twitch but in terms of what I'm going to be illustrating with this right now is we basically in your physiology have three groups of tests the first group of tests are the nerve conduction tests and EMG and that will basically assess the peripheral nervous system away to the dorsal root ganglion to assess the sensory side of things or to the anterior horn cell in terms of the motor fiber pathways we have the EEG which will assess the cortical signals directly and then we have the evoked potentials which essentially assess the essential pathways in between the peripheral nervous system is of course made up of different types of nerve fibers you can categorize them by their size so some of them are large some of them are small some of them are in between and the important point to remember is actually there's not very much difference between the large and the small fibers we're literally talking about micrometers say the very small nerve fibers are just a couple of micrometers in diameter and the larger ones are in the range of about 20 and you can also describe the nerve fibers and classify them by the degrees of myelination team symptoms for patients may be positive or negative symptoms and these are really important pointers as to working out whether one may be having a large fiber peripheral neuropathy group of symptoms or a small fiber neuropathy group of symptoms so the small fiber one sensor provide more positive symptoms and the large v ones tend to give more negative symptoms so more loss of function importantly in terms of why I'm talking about this right now is the nerve conduction studies basically measure large fibre function and its importance about this in mind of course large fiber dysfunctions will often include a small fiber dysfunction as well so if for example you have a patient who has got a predominantly small fiber dysfunction and ones looking for evidence of this and that is quite difficult to do directly if there is already a large fiber dysfunction then that can certainly cover that too and a small fiber dysfunction either in isolation you know perhaps heralding a more diffuse fiber neuropathy you might start thinking about things like diabetes that the small farm dysfunction can precede a large fiber dysfunction by a couple of years although c5 perhaps alcohol excess again small fiber functions will start first now there are very specific ways in trying to test these small fiber dysfunctions some of these you can actually do with your standard nerve conducting equipment for example the sympathetic sweat responses or the cutaneous silent periods or things you can actually already do with your nerve conduction tests and I've got separate videos on all of those types of things Thermal thresholds are done with very specialized equipments then there's the quantitative sensory and autonomic tests and of course skin biopsy which can all be used to have a look at the small fiber dysfunctions but basically what I'm going to be talking about here and describing over here in this lecture are going to be about the large fibers and those are assessed with enough conduction tests all machines are a variation of the following a method for stimulating the nerve a method for recording from the nerve some form of interface with which three things and then a computer which has to communicate with all of that so if we start with the sensory studies there are a number of different ways in which we can do things I'm going to start by showing you here's a hand over here and these are some ring electrodes and they are over the second finger which is of course median and these electrodes over here over the wrists are also overlying the median nerve now you can actually stimulate and record either direction and this is in this particular setup these ring electrodes are being used to stimulate these pads over here are being used to record the pad in the middle is actually the ground and making the patient electrically neutral to the machine the reason that we need to two electrodes to spread the current from one to the other so generate those currents going forward of course when we're doing nerve conduction tests were actually not interested in trying to stimulate these skin receptors to then send signal along the nerve we're actually depolarizing the nerve directly there are ways of looking at the skin receptors but in terms of what we're doing the charges that we're giving we are directly stimulating the nerve underneath and depolarizing it and then those signals are then being picked up by these two pads the reason we have two pads I'm not going to go into into details over here it's called differential amplification is to remove biological noise from the signal and to have a good signal to noise ratio so that's all we have two pads now over here I'm actually using a stim troller or you can use bar electrodes so it's another way of delivering that charge and because we are sending the current in this direction up the arm in the direction that the sensory responses would normally be sent this is called the authored Romek direction if we were to do it the other way round against the usual way in which a signal is transmitted then that is the anti chromic direction this tends to be the modus operandi in the United States this is what we tend to do in the United Kingdom now when we send the signal the first thing I want to show you over here is that you can see a big line at the very beginning that is the stimulator artifact that's the point of time that the stimulator is actually discharging then there's a period of time as the signal propagates along the nerve and then as the signal goes underneath the recording pads it generates this action potential for the sensory nerves it's called the sensory nerve action potential or a snap now there's a difference in how we actually pick up these different responses in terms of the sizes and the cleanliness of the signals whether you do or third ramiro anteed sramek if you do it in the anti-heroic direction then actually one ends up having on the whole while the large response is however because you're stimulating over here you're actually not only stimulating the sensory fibers that will end up going to the finger you also stimulated some of the motor fibers too and therefore one may have some muscle artifacts terminating the signal now this is a relatively clean signal but one can often have quite a bit of movement as a result can actually make the response quite untidy and there's one of the reasons that we don't really like doing that here in the UK so this is what we tend to you to use here in the UK the author drainback stimulations you can see here quite clearly is much smaller than the anti drainback stimulation and the reason for this is actually remarkably simple over here the recording pads are actually within millimeters of the underlying nerves the digital nerves that run are on either side however at the wrist they're already buried under a fair bit of subcutaneous tissues and are therefore in being insulated from being able to send the signal forth upwards to the recording pad so the recording pads are somewhat insensitive to the currents going underneath them and therefore there's this attenuating effect and so that's why they're actually smaller if we have a look at this example over here this is actually from someone who's got carpal tunnel the green response over here is the side in question which happens to be the right side and what we do over here is we mark up the sensory nerve response so the first marker over here is the onset and that's the peak and that's the end of it over there and we actually physically measure the distance between the stimulation points and the recording point we measure the time difference and therefore we can work out the velocity in meters per second in this example here it's going at 42 meters per second between this point and that point there and you can see compared to the other side it's shifted across a little bit in time it's signals being delayed and that's what 1/2 that's what happens in carpal tunnel syndrome what the earliest thing that happens is that sensory sponsors start to become delayed let's have a look at the motor studies say with the motor studies we perform them in a slightly different way to the sensories we we don't have the luxury of sending singles up or down and recording directly over the nerve itself instead we are actually stimulating over the nerve and recording over the muscle and what that means is that not only are you recording the signal over the nerve itself there's also neuromuscular Junction and the time it takes for the muscle to depolarize to so it's not quite as pure as with a sensory sighs when was trying to work out the velocities particularly for the distal ones so again we're sending the signal this is a stimulation artifact over there and over here this is the time it takes to reach the muscle after the muscle to begin to depolarize the green one over here is the muscle in question and it's taken five point four milliseconds for the signal to reach the muscle and for it to become depolarized you can see if we were comparing it to the contralateral side that this is occurring at a later time point than the left side would and this is again what happens in carpal tunnel once it's already a little bit more moderate and there's involvement of the motor fibers to let us now talk about the F waves we all know that a nerve will enter a refractory period once it has been T polarized by voltage and time gating mechanisms and that's to ensure that signal transmission is unidirectional so usually we think we are going to be moving via our brain that sends a signal down the spinal cord and then at that point the signal will then start moving its way down into the foot now these were first described in the foot that's why they're called F waves but if you were to stimulate someone's nerve down over here for example the tibial nerve not only will the fibers going distally to for example the abductor hallucis be stimulated but some of the signal will be travelling up as well and it will also be depolarizing some of the anterior horn cells tickles them a little bit sets them off and then they in turn send a signal back down again roughly about 10% of the anterior horn cells will be stimulated by doing that and one will therefore get and after contraction of about 10% of the entirety of the contraction so when artificial stimulation occurs the depolarization goes in both directions and this particular property of the motor nerves allows that conduction to be assessed across the entire motor pathway to the anterior horn cell so this is what it looks like in real life the first thing that happens is of course one hats the signal gain to the distal point occurring so one has the emwave the muscle motor wave over there and then sometime later one has an F wave which is a as I said as about 2/10 of the original M wave and this is an upper limb study it takes about 30 milliseconds and that's that that's a normal time for the signal to have gone all the way up particularly answer your horn cells and then all the way back down again we also have something called the H reflex and that's the electrical equivalent to the ankle jerk over here I'm doing it over this soleus and what one's doing is one stimulating at the popliteal fossa and one is getting a signal out of the soleus of course but the initial stages of what will happen is ones actually sending signal of course in both directions but over here one is actually going to stimulate the anterior horn cells at the s1 level and they will actually start to send their contractive signals to the Solaris it will start to contract and then what will happen is as the impulses increase and I'll show you this momentarily there will be some degree of collision and those will come off and the motor responses will become more prominent and it's quite a useful technique particular if I was looking s1 routes or early guillain-barré a or just as a double check perhaps when the reflexes are clinically absent one can often detect them electrically as a more subtle event this is what I was talking about so here's a stimulator artifact over there and basically as one's increasing the current and therefore the stimulation the first thing that happens is those anterior horn cells s1 level are becoming stimulated they are actually causing the soleus over here to be depolarize and to stop contracting and that's generating a signal over here as one increases the amount of stimulation that will increase in amplitude and then at some point one starts getting collision of signals up and down and the EM wave the motor response from the actual muscle cell directly will increase in size quite dramatically in amplitude and the H reflex the H responses will reduce in amplitude so that's the H reflex and H fool Hoffman who first described it in terms of EMG it's very straight forward we're popping in a concentric needle electrode into a variety of muscles over here this is an EDC one can spend time and do quantitative studies as well and actually isolate individual motor unit action potentials and mu apps Maps as we tend to call them and what can do cloud analysis to looking at turns and amplitude and I'm not going to be dwelling on the quantitative techniques so here's me having a bit of fun doing some motivating potentials you can seem stimulating my motor cortex over here the contralateral arm you can see the recording electrodes over the APB and here we go you see my hand contracting I wouldn't recommend that you ever do these standing up because it's so easy to get your legs to go if you can't aim it entirely precisely without seeing exactly what you're doing as I discovered so I wouldn't recommend getting your legs giving away from underneath you but fortunately I don't have that believer to share and what happens over here is you can see these are the motor responses being recorded and then basically what you will then do is mark up these responses and then you can work out exactly the cortical latency and you can also you know stimulate it over the brachial plexus for example or over the neck and make variety of calculations that work out what proximal conduction is looking like now we're going to go through a little bit of terminology here in terms of our studies our sensory nerve action potentials we call those snaps and for our compound motor action potentials we call those C Maps so the axons give us the amplitude of any of these responses for sensory or motor our myelin is responsible for assuring our conduction velocities so for the sensory nerves those are the sensory nerve conduction velocities and for the motor nerves they have the motor nerve conduction velocities so in an EXO neural neuropathy what one will be seeing is a reduction in the amplitude one will have an essentially preserve velocity with that obviously there are always exceptions to things particularly with vasculitis but as EXO no loss increases one will have something called fast fine but drop out and then the conduction velocities can fall too in terms of the demyelinating neuropathies we will expect to see a reduction in the conduction velocity with an initially preserved amplitude and when everything to does fall and need that's generally later that's often due to failure of saltatory conductance subsequently sane we'll loss there are an important caveat I'd just like to mention now particularly for some of the Gion Berets for a man acute matrix n1r up there is an acute motor and sensory neuropathy versus early Gambari sometimes that one can have very distal conduction block and that can look like an a man or a namsun and in terms of prognosis one often has a poorer prognosis with those entities and for some of those patients they can actually just be a very early presentation of they can't borrow and so it's worthwhile making sure that one repeats the studies usually about two weeks later just to double-check in short and being sure that it really wasn't a man or an am saying that it wasn't taking a Barker's in it can be a far more positive for a patient's outcome let's talk a little bit more about demyelination so of course we've got the focal demyelinating neuropathies which you'll commonly come across and see and treat which are the carpal tunnels and the cubital tunnel x' let's now get into defused imagination patterns so really important point to appreciate is the fact that nerve fibers aren't single cables that are actually made up of numerous different fascicles with individual fiber balls inside each having their own unique properties some will be larger some of these smaller someone have more Miley and someone have less smiling and as such conduction velocities will vary and so in the normal situation you have a standard distribution effectively of some of those nerve fibers conducting a little bit faster if they're larger and more myelinated so they'll be sending their signals at the fastest and some of them will be slower because they are smaller and diameter less myelinated and there'll be a whole cost around about the middle and this is essentially how you have these curves that we see with the sensory nerve action potentials and all similarly also with the motor action potentials too when one has demanding process there's Damona ting processes are often quite patchy some nerves are affected more than others particularly more myelinated ones are going to take more of a hit and so basically the clustering of the individual conduction velocities will start to splay out that's temporal dispersion and in this example over here this is someone's to be able to sense here muscle these are actually apart from the fact that they are very small in amplitude they're actually really really broad and usually this type of response would only really cover about three boxes at most and here it's basically taking up five say it's it's definitely splayed outwards the other phenomena to talk about is something called conduction blocks a assault Ettore conductance fails a variety of these vesicles are going to stop being able to send their signals all together so if we knock out half of these for example one will actually significantly reduce the motor amplitudes and that's conduction block so you can see over here in this example this is Tom's wrist so conduction there's working okay but over here in the elbow segment its conduction block because one's actually got a significant reduction here in the ability for the nerves in the forearm to send the signal along so that's where the demyelination is occurring and it's quite significant so in terms of patterns of demyelination we are looking for slowing of conduction which might be focal particularly for the focal neuropathies might be multifocal which might be different nerves and or even patches within the same nerve or Maps more generalized laying of conduction and of course conduction block itself and temporal dispersion so how do we do our lesion localization so we do multiple nerve testing we test them in multiple locations and then we have a look for pre and post ganglionic differentiation so what I'm talking about pre and post ganglionic visions as follows for the sensory studies we are effectively testing the sensory fibers to their primary cell so in the case of the sensory nerves that's the dorsal root ganglion so we can test the nerves up to the dorsal root ganglion it does not cover the distance between there's also root ganglion and its way into the spinal cord before making its way up so the primary cell body is well out sighs that's a anything that happens to a sensory nerve must be occurring from the from its primary cell body outwards however with the motor fibers its primary cell body is actually within the spinal cord itself and so we can differentiate between pre and post ganglionic lesions when there is a discordance between sensory impairment and motor fibres impairment say just to just look at this again in a little bit more detail for a sensory fiber you can stimulate anywhere along it you can record anywhere along it as well as long as you can get your recording powers or perhaps a recording electrode near enough to the nerve and you can test it all the way up to its primary cell body which is that also root ganglia when you're stimulating it starts at time zero we then have the time it takes to arrive at the recording point and then wow one has the response over the recording area and so what we measure is the latency over here we speed is distance divided by time so whatever that distance is between the stimulating point and the recording point we divided by the time and we get our meters per second for the conduction velocity over here we determine our amplitude between the baseline and P you get there are different ways of determining you know what you're you measuring but over here this will be the sensory nerve action potential in how I'm choosing to show that to you at this moment in time in terms of the motor fibers again just to show you skin that see the anterior horn service a primary cell body with electricians we can test along the circuit all the way to the primary cell body that's living within the spinal cord itself so a pre ganglionic process as a process occurring before the dorsal root ganglion will be affecting the motor fibers but it will not be affecting the sensory responses so a sensory response will be unaffected by a pre ganglionic process however a post ganglionic process a peripheral neuropathy the sensory responses will be reduced by it again for the motor studies we stimulate over the nerve itself signal goes along hits the neuromuscular Junction signal transmission has to occur and then will record over the muscle membrane itself again we have the time it takes from stimulation to the point that the muscle starts to contract now we're very exact people in your physiology and the time it takes between the point of stimulation distally to the point that the motor responses are being recorded all is a very short time period it's just a couple of milliseconds neuromuscular Junction transmission is about one millisecond so there could be a fair bit of error in trying to work out and also guess worked at for an individual to work out what the exact conduction velocity might be at the distal point so what we do is we literally just record the distal motor latency rather than trying to calculate a distal conduction velocity as we move more proximally and we stimulate more proximally so we then get a more of an intermediate latency and then we just simply have to work out the difference in the distance between the distal and the more proximal stimulation and do such a similar calculation with the time difference as well and then we can actually work out a exact conduction velocity for all the more proximal segments as we work backwards so for the for the most distal parts of conduction we rely on the distal motor latency for more proximal stimulation we can actually get the conduction of velocities motor nerve conduction velocity is calculated from any of those individual points the F wave just to show you again as we stimulate at any point over here the depolarization will spread in both directions the first thing will happen is getting the M response directly from the muscle itself at some later point one's getting the comeback tickle as it were from the anterior horn cells which then go and stimulate the muscle fibers again and that's about 10% of the response for the event potentials we can either have a look at the central pathway so the central somatosensory pathways via SSC PS that's a somatosensory rate potentials or we can look at the motor pathways with the CMC TS say that's when you stimulate magnetically over the cortex stimulates the central pathways to the answer a horn cell and then one can basically subtract off via the F response what the central pathway conduction is like with the central somatosensory pathways one can actually track the signal going up with putting electrodes a variety of different places and you can actually have a look directly at the central somatosensory conduction times let's move on to EMG I've got separate videos on EMG itself basically we use a concentric needle a needle within a needle to record the potential differences we record the muscle motor unit action potentials the MU apps just call them ups it's a bit easy to say we can see exactly how the muscle is controlled that's the recruitment we can see how much muscle fiber is being sort of brought in and so therefore how much muscle fibers are present and that's the interference pattern that's the degree of how much muscle contraction and therefore electrical representation is is making the screen busy and we can have a look at the all characteristics of the muscle and therefore determine whether they might be a myopathy or a nerve lesion and we can have a look at the degree of external continuity if there are nerve lesions and we can also have looked for signs of recovery videos and all of that separately they're very fundamental for a myopathy is if this is the recording field that is open to a concentric needle electrode there are a variety of different muscle fibers within that as a muscle becomes sick with a myopathy that will shrink down these individual muscle fibers and therefore one have a small amplitude response out of them because you've got lots of them now clustering around natural needle itself they will become polyphasic also because they're not able to generate generate force very well because they're small and they're very sick the brain will be recruiting more of those to join in and generate force and therefore they'll be rapidly recruiting and so on ends up having a full interference pattern with submaximal effort and let me just show you over here so these muscle fibers are recruiting very very rapidly and over here enough to suppose it is it fiddly and these are small polyphasic units let's now move on to the basics of EMG again this is a complex topic and there's lots of different parts to this but in terms of the basics let's just work through a chronic state so if this is the recording field over here and now I've highlighted muscle fibrils which have been innovated by different motor units so if we have a neuropathic process that's occurred we've wiped out a whole bunch of different muscle fibrils over here and terminal sprouting has occurred and then some of the motor fibers will now be converted as it were and are now sort of sucked into the remaining motor unit so if example if we take this motor fireball over here it's now parts of this motor unit or for example this one over here is now converted into part of this motor unit and so therefore there are more motor fibers contributing to the motor unit so it becomes a larger in amplitude they become quite wide as well because the enamel dispersed and if a further away from the needle electrode the recruitment will be abnormal because once lost out the orderly accumulation of fibers of increasingly larger size of Hanneman principle and of course the interference pattern will be reduced because there are fewer motor fibers to be recruited in so this is what they look like large polyphasic units and they're basically sound like popcorn it's a very simple way in terms of the spontaneous activities which we may see with EMG you may have heard of increased insertion activity and that's when you stick the pen in there's some muscle membrane instability someone's getting some discharges which are non sustaining occurring for a brief period of time those that can be the earlier signs of some active process occurring there may be positive sharp waves of fibrillation or complex repetitive discharges I have separate videos on those you can have a look at those in your own time and there may be things such as myotonia that's purely generated from the muscle themselves in terms of nerve spontaneous activities for circulations and my Crimea our nerve origin of spontaneous activities and fasciculations are super important particularly for differentiating between entities such as motor neuron disease and inclusion body myositis that's a super important clue particularly in the earlier stages so in terms of pre and post ganglionic differentiation so for a post ganglionic process for a peripheral you're looking for reduced or absent sensory responses if the motor fibers are involved as well there may be reduced or absent and again similarly in terms of the EMG if motor fibers are involved than the EMG may be abnormal it says of preganglionic which is either root level or anterior horn cell one will be expecting to have normal sensory responses because their primary cell body is away and from where the pathology is the motor responses may reduce are absent and you would be expecting abnormal EMG so in terms of what we're looking for we are trying to see the type of problem affecting the nerves is EXO nor is it demyelinating is it something which is mixed is it something which is affecting a single nerve multiple nerves all the nerves and then we know which no fibers are being affected sensory motor possibly autonomic or all the above and so we're looking for an overall pattern as to what's going on are we looking at just focal compression sites and Trackman neuropathies are we looking at distal neuropathy is length dependent neuropathies generalized neuropathies multifocal northey's proximal neuropathies i'll variety over there and they can all give you a clues to what's going on now one of the misnomers which i think is important to correct and to point out is that neurophysiology is clinical neurophysiology it's a clinical specialty it's all about the history it's not just about the electrics so one has to look for the clinical clues looking for congenital issues where there are acquired issues maybe trauma should often very obvious inflammatory infective neoplastic metabolic vascular degenerative you have to be able to integrate all of those together so it's not just about the actual data itself it all has to be put together and packaged up thank you for watching I hope you found this video useful and I really do value your support please do support the channel by liking sharing and above all subscribing many thanks and I'll see you in the next part shortly