Ramoray

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ok i posted in another thread a question and got a couple replies but if ANYONE could help me id really appreciate it. Now forgot my other question or if you know please do tell but i have searched far and wide , virtually every neuro book i can find, internet, medline everything and i cannot find an explanation on how VOR and nystagumus work. I konw there are other types but ill use that specific one. Now this is what i do know or i understand. Now VOR reflex is triggered by opposite side so- left canal is stimulated and that sends signals via left vestib nucleus to contralateral abducens nuclues, which connects via mlf to the left CNIII to cause right horizontal gaze upon head turn to left.

Now i also know that for voluntary horizontal gazes-fast saccades of the eye you iniate a signal from the frontal cortext vision center, which sends a message to contralateral PPRF- which then links to the abducens nuclues right next to it on same side(the abducens ipsi to the pprf, which means both pprf and abducens are contralateral to the inital cortex signal. now that triggers the abducens nerve and via mlf the cnIII medial nerve of the other side to have horizontal gaze.

Now back to VOR, so say after, like above a head turn to left, the eyes go right in horizontal gaze and then a nystagmus move back to left as a fast saccadic move to recenter the eyes

NOW here is the QUESTION, this is the part i dont get- i know the nystagmus is signaled by the cortex frontal eye center, just like the voluntary horizontal gaze but I do not understand the connections. My hypothesis was this:

So back to a left heard turn--> causes a VOR to the right from firing right abducens and left cnIII. Now time for nystagmus, now does the Left frontal cortex send a signal to the RIGHT pprf to inhibit the abudens/mlf/cnIII right horizontal gaze produced by the VOR, which would stop the contraction of those muscles and produce a fast "rebound" of the muscles back to the center( to the left in this case).

Now why i believe this is because according to BRS neuro, in bilateral mlf damage causes a monoocular nystagmus- So again say in bilateral mlf damage you turn head to left and trigger a VOR signal of eyes to right-only the abudecs will fire and cause right eye to look right as usual but due to no mlf the CNIII of left side will not be triggered therefore all youll get with a right horizontal gaze from vor( or any horizontal gaze but in this case is VOR) is your right eye looking laterally. Now brus says that right eye will have a nystagmus action back to the left( just like normally occurs in a vor) but the thing is it is monoocular and the left eye neither moves initially due to mlf damage nor does it have a nystagmus reaction.

Now that tells me that there are 2 possibilities for nystagmus path.
1. continuing with this example, the right eye look right after head turns left followed by left beating fast nystagmus is caused by what i said above- LEFT cortext signal to RIGHT pprf INHIBITING the right abducens which stops the abducens lateral rectus from contracting thus " due to decrease lat. rectus contraction- the right eye moves left back to center.
OR
2. the nystagmus is caused by a signal from teh RIGHT frontal cortext to the LEFT pprf which excites the left abducens and via mlf the right cnII medial rectus (assuming no damage) to move the eyes to the left for the fast nystagmus.. BUT NOW THE PROBLEM- is why thsi path doesnt make sense is back to the bilateral mlf damage- if this were the path that causes nystagmus then with bilateral mlf damage you would indeed have only a right eye move right on left head turn with no movement in left medial rectus BUT you would also have a monoocular nystagmus in the LEFT eye that didnt move at all in teh first place and no nystagmus in the right eye that initally moved since the movement to the left would require excitment of the left abducens triggering left lat rectus and via mlf to the cnIII medial rec. to adduct the right eye back to center causing nystagmus but the mlf is GONE therefore this would be impossible, BUT brs says tha monoocular nystagmus IS in the right eye that moved initally in the VOR and the left eye that never moved, never had a nystagmus.. THEREFORE i can only deduce that my first path is feasible.

Now i am sorry i hope someone was kind enough to follow this nonsense and i know this was long but this is really driving me mad and id relaly appreciate some feedback of the nystagmus path with an example.. Thanks so much
 

NR117

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Ramoray,

The abducting nystagmus that you see in the eye contralateral to the MLF lesion has an entirely different pathogenesis than vestibular nystagmus. With vestibular nystagmus, the problem is a slow phase abnormality resulting in a slow drift, followed by a refixation movement(fast phase).
What happens in internuclear ophthalmolplegia(that's the clinical name for an MLF lesion) is different and is believed to be an adaptive response to the medial rectus paresis. To understand this further, you need to know about two cardinal laws of extraocular motility:
1- Hering's Law which states that yoke muscles (e.g. right medial rectus and and left lateral rectus for left gaze) receive equal innervation.
2- Sherrington's Law which states that when an extraocular muscle is innervated, its antagonist is inhibited.
When you have medial rectus paresis, there is increased innervation going to that muscle (to compensate for weakness). Based on Hering's Law, this means that its yoke (the contralateral lateral rectus) will receive an equal amount of increase in its innervation. That creates what is called a pulse-step mismatch and this is believed to be the underlying mechanism for the abducting nystagmus in MLF lesions. Please note that I've discussed a unilateral MLF lesion here for simplicity but when you have bilateral MLF lesions, the same principles apply. You get nystagmus in the ABDUCTING eye.

All this to say that you cannot apply the pathophysiology of vestibular nystagmus to abducting nystagmus of internuclear ophthalmoplegia. There are many different kinds of nystagmus with different underlying mechanisms.

Hope that was of help.
 
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NR117 said:
Ramoray,

The abducting nystagmus that you see in the eye contralateral to the MLF lesion has an entirely different pathogenesis than vestibular nystagmus. With vestibular nystagmus, the problem is a slow phase abnormality resulting in a slow drift, followed by a refixation movement(fast phase).
What happens in internuclear ophthalmolplegia(that's the clinical name for an MLF lesion) is different and is believed to be an adaptive response to the medial rectus paresis. To understand this further, you need to know about two cardinal laws of extraocular motility:
1- Hering's Law which states that yoke muscles (e.g. right medial rectus and and left lateral rectus for left gaze) receive equal innervation.
2- Sherrington's Law which states that when an extraocular muscle is innervated, its antagonist is inhibited.
When you have medial rectus paresis, there is increased innervation going to that muscle (to compensate for weakness). Based on Hering's Law, this means that its yoke (the contralateral lateral rectus) will receive an equal amount of increase in its innervation. That creates what is called a pulse-step mismatch and this is believed to be the underlying mechanism for the abducting nystagmus in MLF lesions. Please note that I've discussed a unilateral MLF lesion here for simplicity but when you have bilateral MLF lesions, the same principles apply. You get nystagmus in the ABDUCTING eye.

All this to say that you cannot apply the pathophysiology of vestibular nystagmus to abducting nystagmus of internuclear ophthalmoplegia. There are many different kinds of nystagmus with different underlying mechanisms.

Hope that was of help.
Thanks so much nr, that was really helpful so obiiously i was extrapolating from what i knew but that doesnt work eh. sounds like you konw a ****laod, are u a medstudent or how such a great neuro knowledge? that was great, if by chance you could tell me about the nystagmus in a typical VOR reponse, like the pathway of it that would be great as i havent been able to find that or any other paths for nystagmus.. do you have a good detailed neuro book that you suggest? I have and learned most neuro from Nolte and Hanes but as my interest grows i find they jsut arent detailed enough and was lookign for a more comprehensive neuro book but wasnt sure what to get, so if you have any suggestions that would be great! thanks so much for your help!
 

NR117

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You're welcome. Ocular motility is a special interest of mine, so anytime... :)

When you say nystagmus in VOR response, I assume you mean when you do caloric testing, right? Let's leave that aside for now and go over the VOR pathway first: There is a direct excitatory projection from the horizontal semicircular canals to the vestibular nucleus, then to the ipsilateral medial rectus subnucleus through the ascending tract of Deiter's (ATD), which is just lateral to the MLF. Another direct excitatory pathway projects to contralateral abducens nucleus which contains both motorneurons to the lateral rectus muscle AND interneurons that project in the contralateral MLF to the medial rectus motorneurons. That is how conjugate gaze is controlled.

When you do caloric testing, cold water injected into one ear creates convection currents in the endolymph of the horizontal semicircular canals and inhibits the ipsilateral vestibular system. A normal response is the eyes moving slowly and conjugately to the tested ear, followed by a fast corrective phase in the opposite direction to reset the eyes. Then the cycle repeats. The slow phase is produced by the VOR connections from the unopposed contralateral ear and the fast phase is mediated by the frontal eye fields. The direction of the response is the fast phase, that's where the mnemonic COWS comes in.

As far as books go, almost any major neuro-ophthalmology text like Glaser's or Walsh and Hoyt's will have a lot of good info but I don't know that it'll be practical for you. One book you should check out is Review of Neuro-Ophthalmology by Bajandas and Kline. It's a small book you should be able to find in most libraries and has really nice anatomy diagrams you could go over quickly. If it's detail you want, then go for the ocular motility bible: The Neurology of Eye Movements by David Zee and John Leigh. That's my all-time favourite! I believe a new edition will be coming out in a year or so; if you are leaning towards neurology or ophthalmology (are you?) and are interested in the interface (neuro-ophthalmology of course!), wait and buy the new edition.

Good luck...
 
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NR117 said:
You're welcome. Ocular motility is a special interest of mine, so anytime... :)

When you say nystagmus in VOR response, I assume you mean when you do caloric testing, right? Let's leave that aside for now and go over the VOR pathway first: There is a direct excitatory projection from the horizontal semicircular canals to the vestibular nucleus, then to the ipsilateral medial rectus subnucleus through the ascending tract of Deiter's (ATD), which is just lateral to the MLF. Another direct excitatory pathway projects to contralateral abducens nucleus which contains both motorneurons to the lateral rectus muscle AND interneurons that project in the contralateral MLF to the medial rectus motorneurons. That is how conjugate gaze is controlled.

When you do caloric testing, cold water injected into one ear creates convection currents in the endolymph of the horizontal semicircular canals and inhibits the ipsilateral vestibular system. A normal response is the eyes moving slowly and conjugately to the tested ear, followed by a fast corrective phase in the opposite direction to reset the eyes. Then the cycle repeats. The slow phase is produced by the VOR connections from the unopposed contralateral ear and the fast phase is mediated by the frontal eye fields. The direction of the response is the fast phase, that's where the mnemonic COWS comes in.

As far as books go, almost any major neuro-ophthalmology text like Glaser's or Walsh and Hoyt's will have a lot of good info but I don't know that it'll be practical for you. One book you should check out is Review of Neuro-Ophthalmology by Bajandas and Kline. It's a small book you should be able to find in most libraries and has really nice anatomy diagrams you could go over quickly. If it's detail you want, then go for the ocular motility bible: The Neurology of Eye Movements by David Zee and John Leigh. That's my all-time favourite! I believe a new edition will be coming out in a year or so; if you are leaning towards neurology or ophthalmology (are you?) and are interested in the interface (neuro-ophthalmology of course!), wait and buy the new edition.

Good luck...
Dude you rock, that makes alot of sense, much appreciated. Alot of sources would just assume you knew a few basics so not a one would define and explain some of those fundamental things and i couldnt find them anywhere. The caloric thing was good, since you seem to understand it, do you have input on my previous question about why say cold water in a left ear would cause past pointing and falling to the ipsi ear, when yould thing that if cold water is inhibiting it, then it would be as if the right ear vestibular would be unopposed so its basically simulating turning a head to a right ( like if you were doing rotary instead) and by self testing of spinning myself and even brs neuro for rotar testing says that ie. spinning a person to the right causes past pointing to the right and falling to the RIGHT... which if you think about it so should cold calorics in the LEFT.. should cause a spinning to the right effect in my thought process but maybe the mechanisms are differnet.. Thanks for reading all my babble much apreciated. I am really interesteed in neuro, not so much spec. optho but neuro is fasintating and i love it.
 

NR117

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When you use cold water in the one ear, that would create the illusion that one is turning in the opposite direction. So if I got cold water in my left ear, I would think that I were rotating in a rightward direction, and in order to compensate for it I would pastpoint toward the left. Makes sense, right?

By the way I'm not a dude; I'm a gal... ;)
 
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NR117 said:
When you use cold water in the one ear, that would create the illusion that one is turning in the opposite direction. So if I got cold water in my left ear, I would think that I were rotating in a rightward direction, and in order to compensate for it I would pastpoint toward the left. Makes sense, right?

By the way I'm not a dude; I'm a gal... ;)
ha sorry yes i guess nothing about nr117 indicates a guy huh! i promise no more questions but your answers were all very helpful, i have spent the last few days searchign and searching for info on this stuff but now is alot more clear so thanks again! good luck on your optho endevours! oh yes and thanks for the book recs. ill check them out!
 

NR117

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No problem at all; please feel free to PM me if you think of any other questions.
Good luck with your neuro career; I, too, think neurology is fascinating.