Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Today, we are going to learn how the medial longitudinal fasciculus is going to coordinate the eye movements for conjugate gas. So you imagine that um you are looking to the right side, like you imagine how I am looking to the right side. When I look to the right side, that is in a rightward gaze, my right eyeball will abduct and my left eyeball will adac which are the muscles that will cause this movement. The right eyeball abduction is caused by the right lateral rectus and the left eyeball abduction is caused by the left medial rectus. So initially, you understood that for a rightward gaze, you need the lateral rectus and medial rectus of the opposite eyes to contract together. Ok. So this is the task uh that is mediated by the meal fasciculus. So the lateral rectus innervation is by abdeen and the medial rectus innervation is by oculomotor nerve. Now, within the brainstem, you know that you have the midbrain, the pons and the mela and within the pons, lower part, you have the abductions nerve nucleus. And in the midbrain upper part, you have the oculomotor nerve nucleus. So if you imagine the right word gaze. This is the brain stem and this is the midline. You need the stimulation of the right abdus nucleus and the left oculomotor nucleus because the left oculomotor uh innervates the left medial rectus and the right abduction nerve innervate the right lateral rectus. So these two nucleus should be stimulated at the same time for a rightward case. This is the task that is mediated by medial log fascicle. Uh what is media log fasciculus. Now, students often confuse medial longitudinal fasciculus and medial lemniscus. Medial lemniscus is a continuation of the dorsal column coming from the spinal cord, medial longitudinal fasciculus or MLF is a heavily myelinated tract that is interconnecting the vestibular nuclear in the brain stem within the lower pons and the mela and the 34 and six cranial nerve nuclear 34 and six, mediate the eye movements and the vestibular nuclear which gets vestibular input. This MF th coordinates the vestibular nuclei with 346 and also interconnects 346. So that is a function of this MLF on a broad sense. So it is through the MLF that the sixth nerve nucleus of the right side and the third nerve nucleus of the left side are yolked together. Basically conjugate movements is a yoking moment. The right lateral rectum is yolked with the left to media rectus to create a rightward conjugate case. So we are going to understand how this is occurring. The right absence nucleus is actually not a completely moor nucleus. It is actually a gaze center. It is a lateral gaze center in the ponds that that's very, very important. So the right uh ABN nucleus, if you look to the cytology of the right absence nucleus, it contains 70% of large motor neurons just like alpha motor neurons that you find in the spinal or in any other mono nuclei. The six nerve nucleus contains 70% of large motor neurons that is going to innervate the right lateral rectus. Ok. So when this nucleus gets stimulated, obviously, the right lateral rectus will get contracted. So it will cause the abduction of the right eye board. It's very clear, but it also contains 30% of small inter neurons. These inter neurons as soon as they emerge, they will cross the midline or decussate. I mentioned in a previous video that any crossing midline is called a decussation because at the similar point you have the opposite pair crossing the midline. So here the axons will cross the midline and it will ascend through the MLF, which is inter connecting the vestibular nuclear and the 346 cranial nerve nuclear. So it just gets into the MLF and it ascends up to the left third nerve nucleus. So thus, the abs nucleus, when it stimulates, it innervates the right lateral rectus as well as through the MLF. It stimulates the third nerve nucleus. So the ML is in a way interconnecting the ABC as well as the oculomotor nuclear of the opposite side. The 30% inter neurons of the ABD no nucleus is crossing the midline and it is ascending up. So the left L left is helping to connect the right ab nucleus and the left oculomotor nucleus. Imagine the similar case. If you attempt the leftward gaze, you have the left ABD nucleus. Always understand the ab nucleus. Actually gaze end up absences nucleus gets stimulated. The person will look to that side. In a similar scenario, the left ab nucleus gets excited, it will cause contraction of the left lateral rectus. The eyeball gets abducted on the left side and through the MLF of the right side, the right oculomotor nerve nucleus also gets stimulated and the eyeball of the right side will be abducted. So left ab distance stimulated leftward gaze, right ab stimulated rightward gaze. This is done through the ML fibers. Now, we're going to the lesions that can affect the circuit which connects the uh six the nerve and the oculomotor nucleus and can affect the lateral release. Uh So if you are not familiar with the functional anatomy of the circuit, I suggest you see the previous video first and then come to this video. Suppose there is a lesion that affects the absence nerve nucleus of the right side. This is the midline, the right absence nerve nucleus is affected by a lesion. What can happen if the right absence of nucleus is affected in a lesion. It will cause a right lateral gaze palsy because the right absence nerve nucleus is actually a gaze center. As I mentioned, it contains the large motor neurons as well as the interneuron that will run through the ML. So it will cause a gaze palsy. So if you have a lesion in the absence of nucleus, it will cause complete paralysis of gaze to the right side. So a person cannot look to the right side, attempted lateral gaze to the right side, it will not materialize. But the gaze to the left side is intact because the left ab distance nucleus is intact. One thing I want to mention here is suppose the lesion is not in the nucleus but in the abundance nerve fascicles that are entering forward, then you only have a lateral rectus palsy of the right side and not a gaze palsy. A gaze palsy will occur only if the absence nucleus is affected. So, the typical difference in this can be found in a Millard Gobbler syndrome where you have the absence nerve fascicles involvement, but the absence of nucleus will be spared in MLL Gobbler syndrome. On a rightward gaze, left eyeball will add that but the right eyeball will not abduct due to lateral rectal palsy, but the left to gaze will be completely intact. Ok. This is a Millar Gobbler syndrome where you have a pure lateral rectal palsy. But suppose you have a lesion of the absence nerve nucleus classical in a fovea syndrome. In a Fois syndrome, when the ab nerve nucleus is affected, you will have a right lateral gaze pals because the ab nerve nucleus is a gay. Now, we're going to another lesion. This lesion is affecting only the right MLF. Understand that the right ML is carrying the inter neuronal fibers on the left absence nucleus. So when the right ML is affected, we'll, we'll think what can happen. The person will have an intact right lateral case because the right absence nucleus is fine. It is interconnecting with the left ocular motor nucleus. It's innervation to the right lateral. It is also fine. So the right and the left eyeball will cause a rightward gaze. But when the person attempts the leftward gaze, the left eyeball will abduct that is intact because the left ab dis nucleus is innervating the left at a. So this is fine, but the a yoking tract towards oculomotor nucleus is affected and that will cause an absence of abduction of the right eyeball. This is called an internuclear ophthalmoplegia. Example, the right ML is affected, it will cause affliction of the abduction of the right eyeball. Since the right eyeball is not going for reduction, the left eyeball can have a nystagmus. The complete uh mechanism is not clear, but it's probably a compensatory mechanism because this is not getting adducted. By definition, the right ML left lesion will cause a right eye, no, in a right eye. No, the right eyeball fails to go AUC. So the abduction of the right eyeball is affected in a right eye know, ok. Now we are going into more extensive lesion where the right MLF and the right ab nerve nucleus is affected inhalation. What can happen? Always remember when the ab nerve nucleus is affected inhalation, it should cause a lateral gaze palsy. So when this extensive lesion affects the right ab nucleus, it should cause a right gaze palsy. It also affects right MLF. So that will add the component for right eye, you know. So in that case, the person will have a complete loss of right word gaze. Then that person, when he attempts the leftward gaze, the left eyeball will go for abduction, but the right eyeball will not go for abduction. So this is called a 1.5 syndrome because one complete gaze is affected and half of the left toward gaze is affected. So that creates a fancy name 1.5 syndrome. Now, just for completion, I need to add two more structures to complete this lateral gay circuit. One is the PRF para pot reticular formation, parap reticular formation is just close to the ab dis nuclear. OK. So you have two ABD nerve nucleus in the lower points just close to that you have the PRF. When the PRF get stimulated, it will stimulate the ABD dis nucleus. So a lesion in the PPR F will cause the same effect as a lesion in the ABD nerve nucleus. Now, the R gets its influences from higher gaze centers. I'll give you one gaze center, which is clinically important. That is the frontal I field. You have two frontal I fields in the frontal cortices. OK. In front of the precentral gyrus Roman area number six and a part of eight will have the frontal I fields which is going to influence the para formation. So imagine the left frontal I field, the left frontal I field will stimulate the right P pr which will in turn stimulate the right ABD nerve nucleus. So it's actually a chain. Ok. You imagine that you want to look to the right side. So the beginning of that process begins from the frontal eye field, the frontal eye field will stimulate the para reticular formation. The par reticular formation will in turn stimulate the ABD nerve nucleus which will cause the gaze to the right side by the mechanism which I mentioned. Now, we are going to think about what are lesions can affect the circuit and how it can affect gaze. Suppose you have an irritative focus of the frontal eye field. You think about a a gliosis here, a scar here causing a seizure focus. So during a seizure, the eyes will tend to shift drift towards the opposite side. Suppose there is a destructive lesion in the frontal eye field the frontal eye field is destroyed. You don't get the input from the frontal eye field. So that will cause the eyes to have a less gaze preference towards the right side. So the eyes will 10 to drift towards the left side because it is not getting the stimulation from the frontal eye field. One of my teachers used to say a pneumonic that is when this has an irritative focus, you you have an excess stimulus from here. The eyes will tend to look to the opposite side but no stimulus from that side, the eye will look up why the stimulus is not coming. Ok. So this pneumonic is pretty useful to understand irritative and destructive fossa in the uh frontal eye field of the left side. Suppose you have a lesion in the right ponds that is affecting the para po and articular formation or the ABD nerve nucleus. It will cause the right lateral gaze palsy. Imagine about the lesions that can affect the ML. The most common lesions are an infarct, localized infarct over there or a multiple sclerosis plaque because I mentioned that MLF is a heavily myelinated tract, uh localized MS plaque that is affecting the right ML can cause a right I no in the space. So these are some common lesions that can affect and cause horizontal gaze manifestations. So this is the functional anatomy and the clinical anatomy of the gaze circuits that will mediate horizontal release. Thank you.