| Affiliation |
(AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (SF) Class of 2024, Baylor College of Medicine, Houston, Texas |
| Description |
Summary: • Pupil pathways o Afferent pathway: light in o Efferent pathway: motor response • Classic diagram: eyeballs -> optic nerve -> chiasm o Before geniculate body, pupil fibers come off optic tract, go to dorsal midbrain syndrome • Dorsal membrane centers: o Control pupil efferent pathway o Edinger-Wesphal nucleus of cranial nerve 3 -> carry pathway through postsynaptic postganglionic fiber from ciliary ganglion away from pupil o Afferent signal: retinal ganglion cells in retina -> optic nerve -> temporal fiber (uncrossed) -> nasal fibers (crossed) -> pupil fibers from the optic tract -> pre-tectal nuclei in dorsal midbrain -> efferent pathway of cranial nerve 3 • Detecting afferent pathway problems o Relative afferent pupil defect: > Light reaction of right eye: received at Endinger-Wesphal nucleus level by both pupils • Direct and consensual response to light o Detecting RAPD > Swing light to normal/right pupil: constrict both • Right relative afferent pupillary defect: right and left pupil dilates > RAPD: take advantage of relative different in afferent pathway to pupil • Same bilateral involvement of both eyes o Count finger vision in both eyes due to optic neuropathy -> no RAPD > Bilateral, symmetric > No relative difference between eyes > Light near reaction -> light path impaired > Edinger-Wesphal nucleus: receive signal form more rostral midbrain for near reflex • Note: near reflex also generated when blind > Anterior visual pathway disease -> light near dissociation • Light near association: also in efferent pathway disease o Dissociation occur at dorsal midbrain -> disconnect light pathway from near pathway • Argyll Robertson pupil o Neurosyphilis affects pretectal nuclei area o Lead to light reaction impairment but normal near reaction o Pupil accommodates, does not reacts o Not tonic pupil o Does not react to light, react to near o Light near dissociation > Bilateral, small irregular pupil -> tiny to pinpoint o Efferent pathway deficits of third nerve palsy or the ganglion > From ganglion: idiopathic, also Adie's tonic pupil • Adie's tonic pupil: light near dissociation o Initial same for light near dissociation o Tonic near reaction, constriction stays down o Postganglionic fiber or ganglion disruption: nerve regenerate but afferently > Ciliary body pupil control lens > Near and light reaction poor • Ciliary body not really constricting -> pupil constricting • Due to aberrant regeneration of postganglionic fibers in Adie's tonic pupil o Efferent disease and parasympathetic: anisocoria > Edinger-Wesphal nucleus to ganglion > Postganglionic nerve and iris > More in the Horner syndrome video • Summary: pupil has afferent and efferent pathway o Afferent pathway: test with RAPD and bilateral light near dissociation o Efferent pathway: anisocoria, Horner's pathway (sympathetic or parasympathetics), third nerve, or ganglion in postganglionic nerve |
| Transcript |
Today, we're going to be talking about the pupil and there are two pieces: the afferent pathway, which is the light going in,and the efferent pathway, which is the motor response. The classic diagram has it starting with the eyeballs, the optic nerve, and the chiasm. Before it reaches the geniculate body, the pupil fibers come off of the optic tract and go to the dorsal midbrain syndrome. And those dorsal membrane centers control the pupil efferent pathway and that's at the Edinger-Wesphal nucleus of the third cranial nerve. Then, the third cranial nerve carries the pathway to the ciliary ganglion and the postsynaptic postganglionic fiber from the ciliary ganglion carries the rest away to the pupil. So, when we have the afferent signal, it actually starts here in the retina at the level of the retinal ganglion cell and travels along the optic nerve. The temporal fiber remains uncrossed. The nasal fiber crosses, but the pupil fiber then comes off of the optic tract to go to the pre-tectal nuclei in the dorsal midbrain and then to the efferent pathway which is carried on cranial nerve 3. You need to know both the afferent and the efferent pathway when we're discussing pupil problems because, when you have an afferent problem, we have two ways of detecting this. One is a relative afferent pupillary defect, so the light reaction to the right eye is actually received at the level of the Edinger-Wesphal nucleus by both pupils and that means we have both a direct response to light and also a consensual response. In order for us to detect they are RAPD, we're going to swing the light from the normal pupil. In this case, the light reaction to the right pupil constricts both pupils. And when we swing the light to the left, it should normally stay the same. If we swing the light back to the right and there's a right relative afferent pupillary defect, pupil will dilate but, because of the direct and consensual response, the left pupil also dilates. So really, when we have an RAPD, in this example, on the right side, both pupils dilate when we swing the light from the left (the normal eye) to the involved right. When we swing from the right (the involved eye) to the left, both pupils constrict. And, so when we have RAPD, we are actually taking advantage of the relative difference in the afferent pathway to the pupil, and that's what tells us that there's a defect. What if you have bilateral involvement of those eyes and it's the same in both eyes? So let's say both eyes are count fingers vision in both eyes because of an optic neuropathy, then we won't have an RAPD, because relative to the fellow eye, there's no relative difference. In that setting, we can use the near reaction and that is light near dissociation, so the light path will be impaired because the Edinger-Wesphal nucleus can receive signal from the more rostral midbrain for the near reflex. In fact, you can be completely blind and still generate a near reflex. In someone who has no RAPD, because they are bilateral and symmetric, but anterior visual pathway disease, we want to look for light near dissociation. Unfortunately, that light near association can also occur in the efferent pathway disease so the disconnection can occur here at the dorsal midbrain, disconnecting the light pathway from the near pathway. And it doesn't have to be afferent; it can also be efferent. The most prominent is the Argyll Robertson pupil. In this location, neurosyphilis affects this pretectal nuclei area and causes the light reaction to be impaired, but the near reaction is still good and the Argyll Robertson pupil accommodates but it doesn't react. It's bilateral; it's a small irregular pupil that goes from tiny to pinpoint and demonstrates light near dissociation. You can also have efferent pathway deficits from third nerve palsy (it's the pupil involved third) or from the ganglion that's usually idiopathic, which we call Adie's tonic pupil. An Adie's tonic pupil, though, will also be light near dissociation, because the light pathway and the near pathway are the same initially. However, if you have a disruption of the postganglionic fiber or the ganglion, the nerve might regenerate but afferently. So, pupils that used to go to the ciliary body for control of the lens now are going to the pupil. When you think you're doing the near reaction and the light reaction is poor, the ciliary body is thinking it's constricting but, really, the pupil is constricting because of abberant regeneration of the postganglionic fiber in the Adie's tonic pupil so that causes light near dissociation as well. But, the difference between the Argyll Robertson pupil and the tonic pupil is the tonic pupil is tonic. It has a tonic near reaction where its constriction stays down. Argyll Robertson is not a tonic pupil; it doesn't react to light, but it does react to near but it's not tonic. And so, efferent disease usually causes anisocoria if it's the parasympathetic. That's from the Edinger-Wesphal nucleus to the ganglion and the postganglionic nerve and the iris, and you'll have to look at the video on the Horner syndrome to see anisocoria on the sympathetic side. So, in summary, the pupil pathway has an afferent and efferent pathway, the afferent pathway we test for RAPD and bilateral light near dissociation. The efferent pathway is anisocoria, either the Horner's pathway for the sympathetic or for the parasympathetics, the third nerve, or the ganglion in the postganglionic nerve we're going to be looking for light near dissociation. |
