A question I can't shake

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LegaultMD

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While I was studying for my day in ophthalmology, I came by this little paragraph in the Guyton textbook. And it has literally have been driving me crazy for days.

"The final nerve fibers in the pathway through the pre-tectal area to the Edinger-Westphal nucleus are mostly of the inhibitory type. When their inhibitory effect is lost, the nucleus becomes chronically active, causing the pupils to remain mostly constricted, in addition to their failure to respond to light."

The pupilary light reflex begins with the photosensitive retinal ganglion cells, which send impulses to the pretectal olivary nucleus in the mesencephalon. The stimulation is proportional to the light intensity.
Then the pretectal olivary nucleus stimulates both Edinger-Westphal nuceli, which sends parasympathetic fibers to the ciliary ganglion and then to the iris constrictor.

HOWEVER, according to the Guyton textbook, the pre-tectal area sends inhibitory signals to the Edinger-Westphal. After researching this for a couple of hours, I only found one paper which suggested that the pretectal olivary nucleus was inhibitory. (http://www.ncbi.nlm.nih.gov/pubmed/9125451) I thought it might be because of the ambiguity of the Edinger Westphal nucleus (structures with the same name) but the other one isn't parasympathetic and goes to another place altogether.
I tried looking for some conditions that took advantage of this mechanism. The closest thing I could find was the Argyll Robertson pupil, whose physiopathology is not well known and a focal lesion hasn't been described.
I also tried to asume that maybe, maaaaaaaybe the Guyton was wrong. However, the failure of this inhibitory mechanism was constantly brought up in various places and pathologies such as pontine hemorrhaging and tumors, which coincidentally affect the pretectal area.
The only explanation I've been able to come up with, and also the most logical one, is that there are various kinds of fibers coming out of the pre-tectal area. In favor of this argument is the fact that the textbook doesn't pinpoint a particular nucleus. Some papers I found suggest something of sorts, mentioning cortical and other pontine sources of inhibition of the Edinger Westphal nucleus. The closest I could find was the locus coeruleus (Pupil dynamics during bistable motion perception, Hupé JM et al), however this nucleus is not part of the pre-tectal nucleus as far as my understanding goes. This would also mean that the inhibition has to come from somewhere in that same area. Since my OCD and this question has been driving me crazy for days, I figured I could ask here. Please help me, I really want to go to sleep. 😴

Think of it as a nice challenge. Thanks in advance.
 
I see your dilemma here. If the olivary pretectal nucleus (OPN) sends mostly inhibitory fibers to the E-W nucleus, how is it then that stimulation of the OPN by light causes pupillary constriction? Interesting question, not sure what the answer is here.
 
Not sure if this is correct,but this is how I always understood what was happening:
Normally, sympathetic tone dominates the eye, and the OPN is not being stimulated by the postganglionic retinal fibers. So without light, the fibers that are traveling from the OPN to the EWN which are inhibitory are active on the EWN, thus no stimulation of the ciliary ganglion, no pupil constriction.(The EWN starts a new circuit in the light response by sending preganglionic efferent fibers to the ciliary ganglion.)
If light hits the retina, postganglionic fibers travel down the optic nerve to the visual cortex and stimulate the OPN, resulting in disinhibition of the EWN, which allows the fibers from the EWN to the ciliary ganglion to initiate pupillary constriction.
 
So essentialy, there are two pathways from the OPN to the EWN, one inhibitory that is always active, and another one that is excitatory that is sensible to light?
 
There is one pathway from OPN to EWN. Without photo stimulation of the fibers to the OPN, the pathway (ending on EWN) is in a state of inhibition. Light causes stimulation of the OPN which leads to disinhibition of those and thus activation of the EWN and pupil constriction.
 
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