Multiple Sclerosis

Today, we're going to be talking about the neuro-ophthalmology things that we see in patients who have multiple sclerosis. And as you know multiple sclerosis is defined by lesions separated in both space, different locations, and in time. And that can be separated radiographically in space and time with an MRI, because we can see old lesions and new lesions. The new lesions are characterized by enhancements. The old lesions might be black holes ont1, and then you've got the whole spectrum of t2-weighted image imaging abnormalities. For neuro-ophthalmology though we're really talking about two systems: the afferent pathway and the efferent pathway. And on the afferent side the most common presentation is optic neuritis, and that's because the optic nerve is very long. And so we have the eyeballs here the optic nerve, the chiasm, and the track to the geniculate body, and so this part is central nervous system. So the optic nerve, cranial nerve number two, even though it's called the cranial nerve is really central nervous system, and that means demyelinating disease has a very long chance of getting attacked on the optic nerve, producing the clinical finding of optic neuritis. Now, demyelination can occur in the chiasm and can also occur in the optic tract, but these are a lot less common than optic neuritis. And in fact, most optic neuritis is usually the longest segment of the optic nerve, which is the intraorbital portion, rather than the intraocular, the intracanalicular, or the intracranial portion, that's the longest segment. And it's really important on the MRI scan that we do the orbit and do fat suppression and gadolinium, because what we're looking for is longitudinally extensive enhancement. So, if we see longitudinally long enhancement that could be MS, but the longer the enhancement the more likely we're going to be thinking about NMO and MOG, the MS like illnesses, which are demyelinating but antibody-mediated. On the efferent side, the most common thing that we see is INO, an internuclear ophthalmoplegia. The inter is between and the nuclei that is causing the ophthalmoplegia, the weakness, are cranial nerve nuclei for cranial nerve 6 and 3. And, what that means is, when you have a lesion in your brainstem, which is central nervous system, it can be of the nucleus which is cranial nerve 6 nucleus. But that's rare, because the fascicle is the central nervous system component of cranial nerve number 6. The MS lesion really can only affect it in the pons. Once it leaves the route exit zone here this becomes a peripheral cranial nerve 6, and multiple sclerosis is a central nervous system demyelinating disease. And so, six nerve palsy is not a very common presentation of MS and the MLF runs from the sixth nerve nucleus all the way rostrally to the midbrain, and in that location it's trying to reach the cranial nerve three. And so that thing is also a fascicle called the medial longitudinal fasciculus. Fascicle is the central nervous system part, and just like the optic nerve which is very long, the MLF is very long because it runs longitudinally from the cranial nerve 6 nucleus all the way up to the midbrain to the cranial nerve three nucleus. And that's what it's why it's called the internuclear ophthalmoplegia. The other thing that's important is because this MLF is medial, a single demyelinating lesion in the dorsal pons or in the dorsal membrane can knock out both MLFs. And so that is called a bilateral internuclear ophthalmoplegia. And in the old days, we would call that a wall-eyed bilateral nuclear ophthalmoplegia because the patient will be XT because they're looking XT like this. This is obviously outdated and slightly pejorative. So, I just prefer the term bilateral internuclear ophthalmoplegia with exotropia. So, you might change the wall-eye here to with exotropia, bilateral internuclear ophthalmoplegia(BINO)and that way we can keep the name without insulting the patient as being wall-eyed. So, the other thing on the efferent side that you need to know about is nystagmus. So, because the ocular motor nuclei live in the midbrain for 3 & 4 and in the pons for 6,again all the connections between the vestibular nuclei for vestibular input on a central basis, the cerebellar afferent and efferent and all the way rostrally into the midbrain that's a lot of real estate. And so those nerves are very long as well, and so you can get nystagmus. So new onset optic neuritis, acute unilateral loss of vision with optic neuropathy in a young person, new onset binocular diplopia, INO, which is exotropia, and adduction deficit, or less commonly 6 nerve nucleus esotropia abduction deficit, all could be the myelinating disease, of which multiple sclerosis is the most common. And likewise on the efferent side, new onset nystagmus in a young patient should be considered to be multiple sclerosis until proven otherwise, and you need todo an MRI to look for those white matter lesions.