2 quest on neuro/eye:

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Vizsla

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1. Can ptosis result from paralysis of either the Levator Palpebrae or the Orbicularis Oculi? (so from CN III or VII?) I thought it was only CN III but I saw a description of bell's palsy somewhere that included ptosis

2. second question concerns MLF syndrome. Apparently with a unilateral lesion of MLF, you get medial rectus palsy while attempting lateral gaze (this part I get) but also nystagmus of the abducting eye (this part Im not getting). Shouldnt the nystagmus be present in the adducting eye, for which the MLF fibers have been disrupted by the lesion?

thanks for the help
 
I'll try to answer your first question. Levator palpebrae superioris and the superior tarsal muscle are the two muscles that raise your eyelid. If there is damage to either muscle's innervation as in Horner's syndrome (sympathetic innervation damaged = no superior tarsal muscle) or a CNIII palsy (= no levator palpebrae) then you can get drooping of the eyelid. In contrast, orbicularis oculi close the eyelid, as well as tense the area around the eye. Thus, with damage to the innervation (CNVII) to orbicularis oculi as in Bell's palsy, the area around the eye droops but the actual eyelid does not. Although a drooping brow (brow ptosis) and lower lid from Bell's palsy can mimic eyelid ptosis, damage to CNVII doesn't technically cause "ptosis" as we think of it--only damage to CNIII or the sympathetics result in eyelid ptosis.
 
I'll try to answer your first question. Levator palpebrae superioris and the superior tarsal muscle are the two muscles that raise your eyelid. If there is damage to either muscle's innervation as in Horner's syndrome (sympathetic innervation damaged = no superior tarsal muscle) or a CNIII palsy (= no levator palpebrae) then you can get drooping of the eyelid. In contrast, orbicularis oculi close the eyelid, as well as tense the area around the eye. Thus, with damage to the innervation (CNVII) to orbicularis oculi as in Bell's palsy, the area around the eye droops but the actual eyelid does not. Although a drooping brow (brow ptosis) and lower lid from Bell's palsy can mimic eyelid ptosis, damage to CNVII doesn't technically cause "ptosis" as we think of it--only damage to CNIII or the sympathetics result in eyelid ptosis.

thanks!
 
I'll try to tackle the second question.

Let's say the lesion is to the left MLF. The leftward gaze is not affected because the left abducens nucleus (hence the right MLF) is responsible for those movements.

The rightward gaze sollicitates the left medial rectus (adducting) and the right lateral rectus (abducting). There is left medial rectus palsy (ipsilateral to the MLF lesion) as you stated.
Because of that, the left eye does not move. There is no nystagmus because no movement is initiated (altought according to my neuro tutor, a very low amplitude nystagmus could be observed because the antagonists muscles relax therefore allowing the eye to adduct then abduct as the antagonists muscles contract again, but I'm not sure it really happens...)

Now, intuitively the right eye should abduct normaly because the fibers innervating the lateral rectus are lesion free, but a nystagmus is observed.
Reasons for that are uncertain. One hypothesis is that there is a mechanism trying to bring back the eye in alignment with the straight ("paralysed") one, which makes somewhat sense.
 
2. second question concerns MLF syndrome. Apparently with a unilateral lesion of MLF, you get medial rectus palsy while attempting lateral gaze (this part I get) but also nystagmus of the abducting eye (this part Im not getting). Shouldnt the nystagmus be present in the adducting eye, for which the MLF fibers have been disrupted by the lesion?

thanks for the help

Ah yes, MILF syndrome. :meanie: Lol, couldn't help it, had to. And sorry I don't have a real answer either. I'm not required to know anything until this fall! At which point I will become a studybot like ya'll. 🙁
 
I'll try to tackle the second question.

Let's say the lesion is to the left MLF. The leftward gaze is not affected because the left abducens nucleus (hence the right MLF) is responsible for those movements.

The rightward gaze sollicitates the left medial rectus (adducting) and the right lateral rectus (abducting). There is left medial rectus palsy (ipsilateral to the MLF lesion) as you stated.
Because of that, the left eye does not move. There is no nystagmus because no movement is initiated (altought according to my neuro tutor, a very low amplitude nystagmus could be observed because the antagonists muscles relax therefore allowing the eye to adduct then abduct as the antagonists muscles contract again, but I'm not sure it really happens...)

Now, intuitively the right eye should abduct normaly because the fibers innervating the lateral rectus are lesion free, but a nystagmus is observed.
Reasons for that are uncertain. One hypothesis is that there is a mechanism trying to bring back the eye in alignment with the straight ("paralysed") one, which makes somewhat sense.

ahh....got it. thanks a lot
 
Ah yes, MILF syndrome. :meanie: Lol, couldn't help it, had to. And sorry I don't have a real answer either. I'm not required to know anything until this fall! At which point I will become a studybot like ya'll. 🙁

😀 i expected this one a lot sooner...someone had to do it
 
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