| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (KS) Class of 2022, Baylor College of Medicine, Houston, Texas |
| Transcript |
So, we're gonna be talking about internuclear ophthalmoplegia, and you should watch the video on INO. And just to remind you what a regular INO is, a regular INO is an internuclear ophthalmoplegia. It's an ophthalmoplegia that arises from the interneuron between the two nuclei, in this case, the sixth nerve nucleus and the medial longitudinal fasciculus, which is traveling to the third nerve nucleus in the mid-brain. And so, in a regular internuclear ophthalmoplegia, you get an A-D-duction adduction deficit. And the reason there's an adduction deficit is because the medial longitudinal fasciculus is carrying the signal from the sixth nerve nucleus to the contralateral third nerve, which is innervating the medial rectus muscle, versus the sixth nerve which is innervating the lateral rectus muscle. And so, when you have a sixth nerve nuclear lesion, you can get a horizontal gaze palsy. If you have an INO, you get an adduction deficit and because the lateral rectus is still firing, you get a horizontal dissociated A-B-ducting nystagmus from the firing of the lateral rectus on a gaze towards the side of the lead and away from the INO. However, when you have an abduction (not an adduction) problem, that's the lateral rectus, not the medial rectus. And if you have the adducting nystagmus, it'll look like the reverse of an INO. So in an INO, we have an adduction deficit and an A-B-ducting horizontal nystagmus, but sometimes it's an abduction nystagmus and an A-D-ducting nystagmus, but it's the same principle. In the abducting problem, that's the innervation to the lateral rectus. The adduction is still intact and that's why the medial rectus is firing, because it's not a medial longitudinal fasciculus, it's an interneuron that is in the pons. And that interneuron is from the para pontine reticular formation to the sixth nerve nucleus, which is the final common pathway for horizontal gaze. And so, you can get disruption and interruption of the signal, but not from the MLF to the contralateral medial rectus muscle, but from the signal telling the lateral rectus to fire. And because the signal is still intact to tell the medial rectus to fire, you'll have an abduction deficit which looks like a sixth, but then there'll be an adducting nystagmus from the continued firing of the medial rectus. And that dissociation occurs in the interneuron communicating between the para pontine reticular formation and the sixth nerve nucleus. So, all of these pontine lesions make sense if you just know which is the eye that isn't moving, and which is the eye that is moving too much. In a sixth nerve nuclear lesion, you get a horizontal gaze palsy because you're knocking out both the signal to the sixth and the contralateral MLF to the contralateral medial rectus, and that is called an INO when it's the MLF. If you just have a fascicle of sixth, you'll get an abduction deficit and then esotropia and is concomitant, but you will not be involving the contralateral medial longitudinal fasciculus. If however, you get an abduction deficit and an adduction nystagmus, that is an interneuron problem, but instead of calling it just an INO we call it the posterior INO of Lutz. |
