Can u explain why near reflex is present in case of amaurotic light reflex....as the lesion in optic tract which is afferent for both light and near reflex ?
Hi Thanks for your informative videos I have a question can someone accommodation deficit as early as thirties? Or we need to think about brain lesions ( problem identified while seeing through ophthalmoscope) Background is myopia 5.5
LND has always puzzled me a little. Are you saying that a CG lesion is associated with LND because there is aberrant regeneration of the accommodative fibers into the iris sphincter so that a near (but not light ) stimulus produces miosis?
Yes I think that is correct, the hypothesis is that the presynaptic fibres basically get randomised, and as accommodative fibres to the ciliary body make up the vast majority of the pre- and post-synaptic neurons, the result is that both outputs of the CG (ciliary body and sphincter pupillae) are functionally only innervated by accommodative fibres.
Great video. Question: @4:15 you've mentioned that a lesion in the ciliary ganglion can cause a light-near dissociation. My understanding is that if the ciliary ganglion is lesioned then the EFFERENT pathway is interrupted, hence the loss of ability to stimulate the pupil to constrict. So how would a ciliary ganglion lesion present as light-near dissociation, shouldn't both the light and accommodation reflex be affected? Thank you!
You may have already figured it out, but firstly Dr Lee has an older video on light-near dissociation that explains the concept of aberrant regeneration better, and secondly the the Adie syndrome article on the NORD website very nicely explains aberrant regeneration, finally the best explanation comes from the person who actually came up with the idea, Irene Loewenfeld, which you can read on the ciliary ganglion Wikipedia page. I would link them all to you but comments with links sometimes get automatically deleted by RUclips - sorry! The majority of neurons in the ciliary ganglion innervate the ciliary body, which only fires during the near/accommodation reflex. Only a small proportion innervate the sphincter pupillae, which fires during the accommodation AND the light reflex. Ciliary ganglion gets damaged -> over time, the neurons can regenerate -> however in aberrant regeneration the neurons all get jumbled up. The presynaptic neurons destined for the ciliary body under normal circumstances end up innervating some of the postsynaptic neurons that go on to innervate the sphincter pupillae. So the postsynaptic fibres that travel to the sphincter pupillae are now only innervated by presynaptic fibres originally destined for the ciliary body, and will only fire when the brain attempts to signal for the ciliary body to contract i.e. during the accommodation reflex. So the light reflex is lost, but during the accommodation reflex, when the ciliary body muscle is activated, there is concomitant activation of the sphincter pupillae, because of aberrant regeneration. This allows miosis to still occur (although not very well - see Dr Lee's video on Adie pupils for more details). Voila - you now have LND. Edit: but I suppose yes for a short while after the ciliary ganglion is damaged you would lose both pathways - until (aberrant) regeneration can occur.
@@HaemDream Wow thank you so much for your reply. I apologize for the late reply. Also, I haven't figured it out until I read your comment haha. P.S. cool name
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you deserve a bigger whiteboard
He deserves the world 🥺
😂
needs bigger whiteboard
Fantastic clarity, thank you
wow, never knew dr andrew was the Hand of the King
Very nicely explained... thank you sir
Got here looking up a Death Note clip.
so concise! thanks so much prof
Greatings sir !💞💞💯
I wish if there is video for these types of movements too
So helpfull ..thanks
Shout out to our favorite neuro-ophtho!! Woot Woot!
Great video. How then do we differentiate between CNIII and Edinger Westphal nucleus lesions ?
0,1% pilocarpine test - miosis = pupilotony, if no reaction is present with low concentration, proceed with 2% pilo - if miosis, then it's III.palsy
Thank u so much
Great
Do you have any tips for testing pupils in the dark who have dark irides, please? I find it hard to see...
Can u explain why near reflex is present in case of amaurotic light reflex....as the lesion in optic tract which is afferent for both light and near reflex ?
Hi
Thanks for your informative videos
I have a question can someone accommodation deficit as early as thirties? Or we need to think about brain lesions ( problem identified while seeing through ophthalmoscope)
Background is myopia 5.5
LND has always puzzled me a little. Are you saying that a CG lesion is associated with LND because there is aberrant regeneration of the accommodative fibers into the iris sphincter so that a near (but not light ) stimulus produces miosis?
Yes I think that is correct, the hypothesis is that the presynaptic fibres basically get randomised, and as accommodative fibres to the ciliary body make up the vast majority of the pre- and post-synaptic neurons, the result is that both outputs of the CG (ciliary body and sphincter pupillae) are functionally only innervated by accommodative fibres.
Thank you sir
Great video. Question: @4:15 you've mentioned that a lesion in the ciliary ganglion can cause a light-near dissociation. My understanding is that if the ciliary ganglion is lesioned then the EFFERENT pathway is interrupted, hence the loss of ability to stimulate the pupil to constrict. So how would a ciliary ganglion lesion present as light-near dissociation, shouldn't both the light and accommodation reflex be affected?
Thank you!
Hashem ciliary ganglion doesn’t effect the accommodation on convergence so the pupil will constrict on convergence hence the light near dissociation
You may have already figured it out, but firstly Dr Lee has an older video on light-near dissociation that explains the concept of aberrant regeneration better, and secondly the the Adie syndrome article on the NORD website very nicely explains aberrant regeneration, finally the best explanation comes from the person who actually came up with the idea, Irene Loewenfeld, which you can read on the ciliary ganglion Wikipedia page. I would link them all to you but comments with links sometimes get automatically deleted by RUclips - sorry!
The majority of neurons in the ciliary ganglion innervate the ciliary body, which only fires during the near/accommodation reflex. Only a small proportion innervate the sphincter pupillae, which fires during the accommodation AND the light reflex. Ciliary ganglion gets damaged -> over time, the neurons can regenerate -> however in aberrant regeneration the neurons all get jumbled up. The presynaptic neurons destined for the ciliary body under normal circumstances end up innervating some of the postsynaptic neurons that go on to innervate the sphincter pupillae. So the postsynaptic fibres that travel to the sphincter pupillae are now only innervated by presynaptic fibres originally destined for the ciliary body, and will only fire when the brain attempts to signal for the ciliary body to contract i.e. during the accommodation reflex.
So the light reflex is lost, but during the accommodation reflex, when the ciliary body muscle is activated, there is concomitant activation of the sphincter pupillae, because of aberrant regeneration. This allows miosis to still occur (although not very well - see Dr Lee's video on Adie pupils for more details). Voila - you now have LND.
Edit: but I suppose yes for a short while after the ciliary ganglion is damaged you would lose both pathways - until (aberrant) regeneration can occur.
@@HaemDream Wow thank you so much for your reply. I apologize for the late reply. Also, I haven't figured it out until I read your comment haha.
P.S. cool name
Hashem haha thank you and no worries, glad it helped, I spent way too long figuring it out to not tell others about it!
@@HaemDream You're awesome!