||So we are going to be talking about light and near for the pupil. And normally the light and the near reaction are similar, so you don't have to check both of them. And there's an efferent pathway and an afferent pathway for the light and the near pathway. So when light enters into the eye, it hits the retina, travels down the optic nerve, crosses the chiasm, meets its uncrossed temporal fiber, but before we reach the lateral geniculate body (LGB), the pupil fiber comes off the tract and comes in to meet the efferent pathway, and that is at the level of the dorsal midbrain. So at the level of the dorsal midbrain, the afferent pupillary pathway meets the efferent pupillary pathway. And the efferent pupillary pathway begins at the Edinger-Westphal (EW) nucleus, travels with the fascicule of CNIII and then travels all the way to the orbit through the cavernous sinus and superior orbital fissure to its ganglion, the ciliary ganglion (CG). That ciliary ganglion is what is providing the input in terms of post-ganglionic fibers to the iris. So when we have a light reaction, we should have an equal near reaction; the light reaction should be equal between the two eyes. And so when we're detecting a problem in the afferent pathway, normally we're going to rely upon the swinging flashlight test, which is used to detect a defect in your pupil pathway on the afferent side relative to the fellow eye, and we call that a rapid afferent pupillary defect (RAPD). So we shine a light to the right, we swing to the left, and we should be able to have equal reaction in both eyes. There will not be a dilation of the pupil when we swing from the right to left. If we did have that, that would a RAPD, a whole YouTube on that. But when we have light-near dissociation, what that means is that the light reaction is impaired or nil, and the near reaction is good, and that's because you don't need the afferent pathway to activate the near response. So we can literally tell the Edinger-Westphal nucleus that we want to constrict the pupils without any light response, and that happens at near because it's a synkinetic process. When we look at near, we converge, our pupils get smaller, and we accommodate our lens, and that miosis of the pupil can occur in blind people. So even if you are no light perception, you still know where your nose is, you can converge your eyes and make your pupils constrict. So in patients who have bilateral afferent disease, because they are no light perception, because you have bilateral optic atrophy or bilateral retinal detachments, even though their light reaction is poor, we can still test their near reaction. And if the near reaction is good, that is light-near dissociation. And in this example, the light-near dissociation is caused by afferent disease; no light perception (NLP) vision in both eyes. So one cause of light-near dissociation is bilateral or unilateral afferent disease. Usually in the unilateral, we can rely on the RAPD because it's relative. We don't have to use a light-near dissociation. But a bilateral, you have use the light-near dissociation to assess the afferent pathway because you don't have a RAPD, because it's bilateral and symmetrical. However, light-near dissociation can also occur from efferent disease in the motor pathway. And it means it can occur here in the Edinger-Westphal nucleus. So the light reaction is poor, but we have the near reaction that is still able to talk to the Edinger-Westphal nucleus. So if you have lesions in the pretectal pathway, for example, Parinaud dorsal midbrain syndrome, you might have a compressive lesion pressing here at the dorsal midbrain. It disrupts the afferent pathway to both pupils, and that is that part of the dorsal midbrain syndrome, light-near dissociation. And then the other place of course is the third nerve (CNIII). The light reaction is carried on the efferent pathway to the nerve, but you might have aberrant regeneration for near, and that might allow the pupil to constrict. Or, more commonly, the lesion is in the ganglion, and usually there's no cause for that, and that we call Adie's tonic pupil. So the pupil is dilated, it doesn't react properly to light, but it does react to near, because the ciliary ganglion has more fibers going to the ciliary body than the iris, so you're activating the near response, but because of aberrant regeneration, again, it is firing the pupil, and that's usually called Adie's tonic pupil when there's no cause. But anything that damages the ciliary ganglion can produce light-near dissociation in that pupil. And it's Adie's tonic pupil when it's idiopathic. So you should know that light-near dissociation of the pupils can occur from both the afferent side and the efferent side. We normally don't need light-near dissociation to judge afferent disease, because we have a relative afferent pupillary defect. However, whenever you have a bilateral afferent disease, you have to do the light-near dissociation to detect that afferent problem and prove that the efferent pathway is intact with the normal near response. You can have dissociation of the light-near pathway at the dorsal midbrain from any cause of dorsal midbrain syndrome, or things like syphilis. We call this the Argyll-Robertson pupil when it's syphilis at this location. And you can could have it from aberrant regeneration either in CNIII or from the ciliary ganglion and its post-ganglionic fiber. If it's post-ganglionic and it's idiopathic, we call that Adie's tonic pupil. So you do need to know a little bit about light-near dissociation. And basically you should test the near reaction anytime the light reaction is impaired.