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Upper motor neuron

From Wikipedia, the free encyclopedia

Upper motor neuron
The motor tract
Identifiers
FMA84631
Anatomical terminology

Upper motor neurons (UMNs) is a term introduced by William Gowers in 1886. They are found in the cerebral cortex and brainstem and carry information down to activate interneurons and lower motor neurons, which in turn directly signal muscles to contract or relax. UMNs represent the major origin point for voluntary somatic movement.

Upper motor neurons represent the largest pyramidal cells in the motor regions of the cerebral cortex. The major cell type of the UMNs is the Betz cells residing in layer V of the primary motor cortex, located on the precentral gyrus in the posterior frontal lobe. The cell bodies of Betz cell neurons are the largest in the brain, approaching nearly 0.1 mm in diameter. The axons of the upper motor neurons project out of the precentral gyrus travelling through to the brainstem, where they will decussate (intersect) within the lower medulla oblongata to form the lateral corticospinal tract on each side of the spinal cord. The fibers that do not decussate will pass through the medulla and continue on to form the anterior corticospinal tracts.

The upper motor neuron descends in the spinal cord to the level of the appropriate spinal nerve root. At this point, the upper motor neuron synapses with the lower motor neuron or interneurons within the ventral horn of the spinal cord, each of whose axons innervate a fiber of skeletal muscle.[1][2]

These neurons connect the brain to the appropriate level in the spinal cord, from which point nerve signals continue to the muscles by means of the lower motor neurons. The neurotransmitter glutamate transmits the nerve impulses from upper to lower motor neurons, where it is detected by glutamate receptors.

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Transcription

In this video I'm going to talk about upper motor neurons. So upper motor neurons, which are different than the motor neurons we talked about before, which are the lower motor neurons. Now when we talked about the lower motor neurons, we talked about how they have their somas, either in the brain stem or in the spinal cord, and how they send axons out through nerves in the peripheral nervous system to synapse on and control skeletal muscle cells to tell those skeletal muscle cells when to contract and we talked about that the lower motor neurons that pass through spinal nerves primarily control muscles of the limbs and the trunk, and lower motor neurons that pass through cranial nerves primarily control the skeletal muscles of the head and the neck. But now we're going to talk about the upper motor neurons, because it turns out that while the lower motor neurons are controlling the skeletal muscle cells and telling them when to contract, upper motor neurons are the ones that are controlling the lower motor neurons and controlling their activity. The somas of the upper motor neurons are found mainly up in the cerebral cortex, way up here in the brain on that outside surface of the cerebrum, and their axons descend down to synapse on lower motor neurons in the brain stem or in the spinal cord. And so information flows from up here mainly in the cerebral cortex down these axons to the lower motor neuron somas and then out the axons of the lower motor neurons to actually reach the skeletal muscle cells to determine when they'll contract. And we can divide up the upper motor neurons into some different pathways or tracts, depending on if they go all the way down into the spinal cord to synapse on lower motor neurons or if they go a shorter distance to the brain stem to synapse on lower motor neurons. So first let's look at these longer upper motor neurons that send axons all the way down into the spinal cord. So let's take the brain and the spinal cord here, and I've got a little larger illustration of that. So here we have the cerebrum up top. Here is the brain stem, and behind it is the cerebellum, and then beneath it is the spinal cord. But first let's think about a lower motor neuron here in the higher part of the spinal cord, on the left side. Because we're looking at the front here. So this would be the left side. And the lower motor neuron will have its soma inside the spinal cord and then it'll send it's axon out through spinal nerves and the smaller branches that it branches into until it synapses in some muscle that it's going to control, some of the skeletal muscle cells in that muscle. The upper motor neuron that's going to control this lower motor neuron is going to start somewhere way up in the cerebral cortex here, in that layer of gray matter, on the outside of the cerebrum, and its axon is going to kind of travel down to the deep white matter of the cerebrum and then it's going to travel down through the brain stem through the mid brain, then the pons, then the medulla, and then at this point, where the brain stem meets the spinal cord, at the bottom of the medulla, most of these axons are going to cross over to the other side, and then they're going to travel down the other side of the spinal cord until they reach this lower motor neuron to synapse on it and control it. So this pathway, this collection of axons that are upper motor neurons, traveling from the cerebral cortex to lower motor neurons in the spinal cord, we call this the corticospinal tract. Let me write that out. Cortico, cortico which means it starts in the cerebral cortex, and then spinal, which means that it ends in the spinal cord. So it's going from cerebral cortex to spinal cord, so we call it the corticospinal tract. And a tract is a collection of axons traveling together through the central nervous system. Now because most of the axons that make up the corticospinal tract travel down one side of the brain and then cross over to travel down the other side of the spinal cord, what we see is that if there's dysfunction of these axons of the corticospinal tract on one side of the spinal cord, we usually get weakness of muscles on that same side. But if we see dysfunction of the corticospinal tract on the other side of the brain, either up here in the cerebral hemisphere on this side or on the brain stem on this side, we usually see weakness on the other side of the body, so that the right side of the brain controls the left side of the body in terms of controlling the skeletal muscles. For the most part things get a little more complicated for the lower motor neurons in the brain stem. So let me just draw one lower motor neuron over here on the left side and it's going to send an axon through a cranial nerve to a skeletal muscle in the head or the neck and let me actually draw the same kind of thing on the other side, sending lower motor neuron axons through the same cranial nerve to the other side, to a muscle on the other side of the head or the neck. There are going to be different upper motor neuron somas, up here in the cerebral cortex and many of these are going to send an axon down in a similar way as the corticospinal tract and similarly they're going to cross over and innervate these lower motor neurons on the other side of the brain stem. However, for lot's of these lower motor neurons that pass through cranial nerves, what we actually see is that there is often also upper motor neuron axons that come down and innervate lower motor neurons on the same side. So instead of having most of the upper motor neuron axons cross from one side over the other side, like we see with the corticospinal tract, where a lot of these lower motor neurons that control muscles of the head and neck we see that one side of the cerebral cortex often sends upper motor neurons to both sides of the brain stem. So we give this tract carrying the upper motor neuron axons to lower motor neurons in the brain stem a different name than the corticospinal tract because we're not going to the spinal cord. We're still starting at the cerebral cortex, so we call this pathway, it starts with cortico as well, cortico, but instead of going to the spinal cord, we're going to the brain stem. And it would make sense to call this the cortico brain stem tract. But instead it's got an older name for the brain stem which was the bulb. So we call it the corticobulbar tract. Corticobulbar tract. And that includes these upper motor neuron axons that are going to innervate lower motor neurons in the brain stem and because the wiring is a little bit more complicated in the brain stem, we can get some different patterns of weakness with abnormalities of this pathway. So I'll save some of the details of that for later because it gets a little complicated. Dysfunction of either the lower motor neurons or the upper motor neurons can cause weakness. Because if there's a problem with the lower motor neurons and they're not telling the skeletal muscle cells to contract, then there isn't going to be as much contraction and we can see weakness. But it turns out that if there's a problem with the upper motor neurons and they're not telling the lower motor neurons to tell the skeletal muscle cells to contract, we also don't get as much contraction and we can see weakness. In another video we talked about the lower motor neuron signs. These other things we can see in addition to weakness or even without weakness, if there's some problem with the lower motor neurons. And it turns out there are upper motor neuron signs and just like with the lower motor neuron signs the upper motor neuron signs can occur with weakness or even without weakness if there is abnormalities of these upper motor neurons. And this can help us understand if a patient has weakness whether the problem is in the lower motor neurons or in the upper motor neurons. The first of these upper motor neuron signs we call hyperreflexia. Let me just write that out. Hyperreflexia. And this is an increase in the muscle stretch reflexes. So let me just write MSR for muscle stretch reflexes. So this is actually the opposite of one of the lower motor neuron signs which is hyporeflexia, where we see a decrease in the muscle stretch reflexes. So that if this patient over here had some trouble with their corticospinal tract, their upper motor neurons coming down from the cerebral cortex to the lower motor neurons in the spinal cord, when this doctor right here, taps this patient in the tendon below the kneecap with the little rubber hammer, instead of less response, instead of less contraction of these muscles, we could see more response, we could see this very brisk kicking out of the leg because these muscles kind of over respond to that stimulus. The cause of hyperreflexia with upper motor neuron dysfunction is not totally clear, but apparently when the muscle spindles, these little receptors in skeletal muscle that detect muscle stretch, when they're activated and the somatosensory neurons carry that information back into the spinal cord to excite the lower motor neurons to cause the muscle contraction that is the muscle stretch reflex, apparently without periodic stimulation of the lower motor neurons from the upper motor neurons, the lower motor neurons may become kind of super sensitive, so that the normal excitation of this somatosensory neuron causes this very exaggerated response of the lower motor neuron and you get a bigger reflex. But we definitely don't understand the whole process of why this happens. The next upper motor neuron sign is called clonus. Clonus. And clonus involves rhythmic contraction, rhythmic contraction, of antagonist muscles, antagonist muscles. And those are muscles that have the opposite effect on a joint. So for example on this patient here, and on you, there are muscles in the front of the shin that cause you to pull your toe up like that, pull your foot up, and there are muscles in the back part of the leg here that cause you to push your foot down, like you're pushing on a gas pedal. We call those antagonist muscles because they cause the opposite movement and what we see with upper motor neuron dysfunction is that if this doctor were to grab this patient's foot and rapidly pull it upward, the foot may go into this involuntary movement where it starts coming up and down, and up and down, and up and down, and we call that clonus. And the cause of clonus is probably just hyperreflexia because if the doctor here rapidly pulls up on the foot, there is stretching of these muscles in the back of the leg here and that can activate the muscle stretch reflex causing these muscles to contract which then makes the foot go down and that can actually stretch the muscles on the front of the leg here, triggering their muscle stretch reflex and then the foot comes up and basically each time the foot goes the other direction, it stretches the muscles on the other side so that the muscle stretch reflexes of the antagonist muscles are triggering each other. The next upper motor neuron sign we call hypertonia. Hypertonia. And hypertonia means increased tone of skeletal muscles and this is another one that's an opposite of one of the lower motor neuron signs where we can see hypotonia, we can see decreased tone of skeletal muscles and we really don't understand why we see an increased tone of skeletal muscles when there's upper motor neuron dysfunction. One possibility is that it's related to hyperrlexia, that if this doctor takes this patient's leg and tells them to try to relax it as best they can, and they start moving that leg around, it gives more resistance, it isn't as relaxed as it normally would be. And that might be because the pulling on the muscle stretches them and activates the muscle stretch reflex. But we're not totally sure about this. And the last upper motor neuron sign has a long name, it's called the extensor, extensor plantar, this just refers to the foot, the bottom of the foot, extensor plantar response. And what this long name means is that if you take a hard object, like they're showing in this picture here and what we usually use is the hard end of a reflex hammer and what you do is you scrape up along the bottom of the foot with the hard end. Not really hard, but just enough so that the person can feel it and a normal plantar response is not extensor, it's flexor. So just like they've drawn here, if you normally scrape something hard up along the bottom of the foot, the toes all flex. They come down in the direction of the bottom of the foot like they're showing here. This way. But with upper motor neuron dysfunction, we can see this abnormal extensor plantar response. Where we scrape up along the bottom of the foot and then the toes go into extension. They go the other direction, away from the bottom of the foot. So we call that the extensor plantar response. It also has a person's name, Babinski. So it's called the Babinski sign because this person described this. And we really don't know the mechanism of the extensor plantar response when there is dysfunction of the upper motor neuron, but it is something that we commonly see.

Pathways

Upper motor neurons travel in several neural pathways through the central nervous system (CNS):

Tract Pathway Function
corticospinal tract from the motor cortex to lower motor neurons in the ventral horn of the spinal cord The major function of this pathway is fine voluntary motor control of the limbs. The pathway also controls voluntary body posture adjustments.
corticobulbar tract from the motor cortex to several nuclei in the pons and medulla oblongata Involved in control of facial and jaw musculature, swallowing and tongue movements.
colliculospinal tract (tectospinal tract) from the superior colliculus to lower motor neurons Involved in involuntary adjustment of head position in response to visual information.
rubrospinal tract from red nucleus to lower motor neurons Involved in involuntary adjustment of arm position in response to balance information; support of the body.
vestibulospinal tract from vestibular nuclei, which processes stimuli from semicircular canals It is responsible for adjusting posture to maintain balance.
reticulospinal tract from reticular formation Regulates various involuntary motor activities and assists in balance.

Lesions

Any upper motor neuron lesion, also known as pyramidal insufficiency, occurs in the neural pathway above the anterior horn of the spinal cord. Such lesions can arise as a result of stroke, multiple sclerosis, spinal cord injury or other acquired brain injury. The resulting changes in muscle performance that can be wide and varied are described overall as upper motor neuron syndrome. Symptoms can include muscle weakness, decreased motor control including a loss of the ability to perform fine movements, increased vigor (and decreased threshold) of spinal reflexes including spasticity, clonus (involuntary, successive cycles of contraction/relaxation of a muscle), and an extensor plantar response known as the Babinski sign.[3]

See also

References

  1. ^ Saladin, Kenneth S. Anatomy & Physiology: The Unity of Form and Function. Dubuque: McGraw-Hill, 2010. Print.
  2. ^ "Frontal Lobe". Rice University Web Calendar. 26 June 2000. Web. 06 Dec. 2010. <"Frontal Lobe". Archived from the original on 2010-07-26. Retrieved 2010-12-07.>.
  3. ^ Purves, Dale; Augustine, George J.; Fitzpatrick, David; Katz, Lawrence C.; LaMantia, Anthony-Samuel; McNamara, James O.; Williams, S. Mark (9 May 2018). "Damage to Descending Motor Pathways: The Upper Motor Neuron Syndrome". Archived from the original on 3 May 2018. Retrieved 9 May 2018 – via www.ncbi.nlm.nih.gov. {{cite journal}}: Cite journal requires |journal= (help)

External links

This page was last edited on 5 December 2023, at 19:47
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