 Hello friends, let us see why there is hypertonia and exaggerated deep tendon reflexes in umn lesion while hypertonia and lost TTRs in lmn lesion. So, for this first we should know that what is umn and lmn lesion I will do just a quick revision of that topic. So, this simplified line diagram is showing a pyramidal tract where the neuron is arising from the motor cortex passing via internal capsule and at the level of medulla it is crossing over to the other side and then it is descending in the spinal cord and synapsing at the level of the spinal cord. From there another neuron arises which we call alpha motor neuron which supplies the muscle. Now, injury anywhere from alpha motor neuron to the level of the muscle is known as a lower motor neuron injury while injury anywhere from motor cortex internal capsule medulla up to the level of the spinal cord where the first neuron is synapsing is known as a upper motor neuron lesion. So, now both these lesions present with muscle weakness however on examining the patient we find that there are different signs in these lesions like in lmn lesion there is hypotonia and lost deep tendon reflexes and umn lesion which is also presenting with muscle weakness but there is hypotonia and exaggerated deep tendon reflexes. So, why is that occurring? So, to understand that we need to know some basics about a stretch reflex. So, we will consider that not entirely in detail but certain basics we should be aware of. So, let's discuss that see every skeletal muscle has two components one is the extrafusal fibers which are contractile and are supplied by alpha motor neuron which we have seen it is coming from the spinal cord. Now, the other component of a skeletal muscle is intrafusal muscle fibers now these intrafusal muscle fibers they are sensory so a muscle which we always think of as motor has some sensory component also and these intrafusal muscle fibers are supplied by sensory fibers that is they are 1a and 2 fibers which also enter into the spinal cord and go and synapse with the alpha motor neuron. So, these are sensory fibers 1a and 2 and this is the alpha motor neuron which is supplying the extrafusal fibers and causes the contraction of the muscle. Now, apart from this there is another neuron known as the gamma motor neuron which also arises from the spinal cord and it supplies these ends of the intrafusal muscle fibers. So, this intrafusal muscle fiber is sensory but it has contractile ends so the ends can contract and it is supplied by another motor neuron that is the gamma motor neuron. So, what is basically these deep tendon reflexes this is basically the stretch reflex see whenever a muscle stretches that is relaxes or stretches there is increase in the length of the muscle this sensory intrafusal fibers also stretches along with that because it is passive. So, if the extrafusal fibers are stretching the intrafusal fibers will also stretch. Now, this stretching of the intrafusal fiber leads to generation of action potential in this sensory fiber which reach the spinal cord and we have seen that it is synapsing with the alpha motor neuron and this synapses excitatory. So, action potentials from 1a and 2 what will happen that they will excite this alpha motor neuron. Now, when alpha motor neuron gets excited what it will do it will go and supply the extrafusal muscle fiber and cause the shortening of the muscle that is the contraction of the muscle. So, basically what is happening that is stretching of the muscle it is ultimately leading to the contraction of the muscle. So, this is a reflex whenever the muscle stretches it will cause the contraction of the muscle and you see we talk about it further when the muscle will shorten passively intrafusal muscle fibers will also shorten isn't it. So, if this intrafusal muscle fiber shorten then what will happen the stretch is lost and the action potential which were being generated before will also be gone. So, no information is being carried to this spinal cord and hence the excitation of the alpha motor neuron also will be lost. So, it will stop stimulating the muscle. So, what is happening that with contraction it is again causing relaxation of the muscle isn't it. So, this is a reflex but do you think that it actually goes on in our body. If this is happening then we will never be able to make voluntary movement isn't it because whenever we try to contract this action potential will be lost and there will be relaxation of the muscle. So, what happens that when we try to make voluntary movement from pyramidal track there is excitation of the alpha motor neuron and also there is excitation of the gamma motor neuron. So, will it prevent this? Yes, it prevents this. How? So, what happens that with the excitation of the gamma motor neuron these ends contract. So, if they contract see ends are pulling they are contracting. So, it pulls the center right. So, if they pull the center that means the center will stretch ok. So, with excitation of the alpha motor neuron the extrafusal fibers contract they shorten, but due to simultaneous activation of the gamma motor neuron the intrafusal fiber stretch normally when we saw the passive component what we said that when the muscle will contract the intrafusal fibers also will shorten, but with gamma motor activation the stretching of the end contraction of the end is actually stretching the intrafusal muscle fibers thus the stretch of the intrafusal muscle fibers is maintained during voluntary contraction. Ok. So, this is very fundamental of stretch reflex just one more thing before we proceed that apart from receiving this excitatory input from top when we want to make voluntary movement normally this gamma motor neuron is kept actually inhibited. So, there is both the inhibitory and excitatory input right. So, normally it is kept inhibited only when we want to make a voluntary movement this inhibition goes off and there is activation of the gamma motor neuron ok. So, now let us see that why UMN and LMN lesion lead to respective signs and symptoms ok. So, let us see first UMN lesion. So, this is the basic diagram you should remember that this reflex is operating when we are not making voluntary movement and gamma motor neuron is kept inhibited when we are not making voluntary movement. Now, this stretch reflex you see our muscle is always having some length is not it. So, always this alpha motor neuron some activity is always there and that is responsible for the basal tone of the muscle, basal level of the contraction of the muscle. Now, in UMN injury that is upper motor neuron injury this we are telling that the top neuron is injured right. So, if the top neuron is injured what will happen that at rest that inhibition of the gamma motor neuron is lost see. So, the baseline activity of gamma motor neuron increases. So, that means now with passive stretch of the muscle what will happen this also will stretch more compared to what was present in normal physiological condition isn't it. So, when we stretch the muscle as in deep tendon reflex when we strike the tendon with a hammer what is happening actually we are stretching the muscle ok. So, when we stretch the muscle this intrafusal fiber stretches more this leads to more number of action potentials in these afferents which go and excite this alpha motor neuron more causing increase in the contraction of the muscle. So, stretch now causes increased contraction. So, we are talking about the reflex component only here stretch is causing increased contraction and that is what that is exaggerated deep tendon reflexes. So, in simple terms I can say that in upper motor neuron injury the inhibitory influence on the gamma motor neuron is lost this leads to exaggerated deep tendon reflexes. Now, with the same logic we can explain that why there is hypotonia in upper motor neuron lesion. See I told you that this reflex is important for maintaining the basal tone of the muscle that means the basal length of the muscle is causing some action potentials in afferent and it is keeping the muscle somewhat contracted state at rest. Now, with the loss of the inhibition of the gamma motor neuron since the stretch of the intrafusal fiber that is the baseline stretch of the intrafusal fiber is more since gamma motor neuron has become active isn't it. So, it will lead to more action potential and obviously more alpha motor neuron activity and increase in the basal tone of the muscle. So, it is the same mechanism that is causing the hypotonia as well as exaggerated deep tendon reflexes in upper motor neuron lesion. Okay, so now let us see why there is a loss of deep tendon reflexes and hypotonia in lower motor neuron lesion. Low motor neuron lesion as I told you before it is from the alpha motor neuron to the muscle. So, what is happening suppose if there is an injury to this alpha motor neuron. So, here the injury is somewhere here. So, the final common pathway by which this muscle can contract is lost okay. So, if this is gone it doesn't matter how many action potentials are coming via afferent to the alpha motor neuron thing is that this alpha motor neuron will not be able to excite the muscle. So, if alpha motor neuron is not exciting the muscle in a baseline condition like at rest. So, obviously that length of the muscle will not cause will cause will not cause any contraction of the muscle. So, the basal tone is lost right. So, that is known as hypotonia then similarly in deep tendon reflexes even if we stretch the muscle. So, even if we stretch the muscle by hitting with a hammer what happens there will be stretch of the intrafusal fibers. However, same thing action potential will go, but the alpha motor neuron is inactive isn't it. So, it will not lead to contraction of the muscle. So, that means the reflex will not work. So, it will lead to lost deep tendon reflexes. So, hopefully now you have understood that what is the reason for different signs in upper motor neuron and lower motor neuron lesion especially regarding the tone of the muscle and the deep tendon reflexes. In 1.9 if I say in upper motor neuron lesion the inhibitory input to the gamma motor neuron is lost which leads to increased reflex and increased tone and in lower motor neuron lesion the final common pathway is affected. So, that the input to the muscle itself is gone and leads to hypotonia and lost deep tendon reflexes. So, friends thanks for watching the video. If you liked it do press the like button and share the video with others and don't forget to subscribe to the channel Physiology Open. Thank you.