| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (AL) Class of 2022, Baylor College of Medicine, Houston, Texas |
| Transcript |
Today we're going to talk about the sixth nerve, and there are six syndromes of the sixth nerve. I'll just draw for you a quick diagram here of the pons. The sixth nerve begins at its nucleus at the caudal portion of the pons. The nucleus of VI is interesting because it supplies both the sixth nerve itself as well as the connecting interneuron to the third nerve nucleus - specifically the medial rectus subnucleus via the medial longitudinal fasciculus. So if we ding out the sixth nerve nucleus, we don't just get a sixth nerve palsy - we get both an abduction deficit from the lateral rectus weakness, but also because the contralateral third via the medial longitudinal fasciculus to the medial rectus is out; that produces a horizontal gaze palsy. So a nuclear sixth, the first syndrome that we are going to talk about, produces a horizontal gaze palsy, not an isolated abduction deficit. The nerve itself travels as a fascicle, which is this little tiny piece inside the pons itself and exits the root exit zone of the pons and it's tethered there. Tt has to go up this bone, which is called the clivus. And clivus means slope, so this sloping bone. Then it turns 90 degrees here, at that location it is also tethered at the petroclinoid ligament. It's tethered at two locations: the root exit zone at the pons, and at the petroclinoid ligament. That means things that cause increase or decrease of intracranial pressure affecting this subarachnoid segment can result in what we would call a non-localizing side of increased intracranial pressure or decreased intracranial pressure. A non-localizing sixth nerve palsy, for example in pseudotumor cerebri or really any cause of increased intracranial pressure. As the sixth nerve makes the bend here, it enters into the substance of the cavernous sinus rather than the wall. In coronal cross section this is the cavernous sinus, this is the internal carotid artery. In the wall of the cavernous sinus, our III, IV, V subdivision 1, and little bit posterior V subdivision 2. But the sixth nerve lives in the substance of the cavernous sinus. In the cavernous sinus, the sixth is in the substance of the cavernous sinus, and then passes through the superior orbital fissure to reach its target organ the lateral rectus muscle. The six syndromes started with nucleus and fascicle, which passes by important structures in the brainstem; you can imagine that a sixth nerve palsy can be associated with a contralateral hemiparesis from corticospinal tract involvement, the Raymond syndrome, or Millard-Gubler, or involves VII because the fascicle of VII wraps around the nucleus of VI, and so the brainstem syndromes are defined by the company they keep. These fascicular syndromes can have hemisensory loss, Horner's syndromes, seventh nerve palsies, or hemiparesis. I already mentioned to you the third syndrome which is in the subarachnoid space. That's increased intracranial pressure as a non-localizing finding. You've got the clivus, which is this bone right here. So the sloping bone, the clivus. And the most common tumors here are meningioma, chordoma, or chondrosarcoma. The cavernous sinus syndromes are number five that affect the substance of the cavernous sinus rather than the wall. So those would be things like cavernous sinus tumors, carotid cavernous fistulas. And then finally through the superior orbital fissure to the orbit. So, if you just knew the anatomy of VI, you would know the six syndromes. Nucleus, fascicle, subarachnoid space, clivus, cavernous space, or orbit/superior orbital fissure. |
