Dear Paul Words cant express how thankful i am for your series. You're making better doctors around this world 🌍 and im proud to be one of them. May God richly bless you.
Just a side note: I had a massive hemorrhagic CVA at the age of 24 related to a thalamic AVM. My only presenting symptom was loss of sensation and proprioception on the left side of my body. My FAST assessment was completely negative and I remained verbally fluent. I also didn't have a headache until about 30 minutes after the onset of numbness. Just because they don't look like they are having a stroke doesn't mean they aren't.
Hey Dr Bolin.!! Thank you so so much for your lectures! They are excellent !! :) unfortunately the sound for this doesn’t work :( I would be so greatful if you could reupload it so we can hear it!!!
Great video as always, thank you. Just to comment that the book written by the locked-in syndrome patient is called "The Diving Bell and the Butterfly", and he wrote it using a letter board, as opposed to morse code. It's an amazing book (and a great French movie too!)
Hello. I had two CVA's in 1969. I was 5 years old My strokes were hammorrhagic strokes. From time to yime, I have seizures. I am now 53 years old. Thanks for the video. It was very interesting.
In Benedikt syndrome, i read there is no contralateral hemiplegia. since red nucleus, cn 3, and medial leminiscus are only affected. corticospinal tract is not affected. please confirm it.
"Debate remains about how much red nucleus involvement occurs in Claude's and Benedikt's syndrome. Seo concluded on the basis of clinical and MRI studies that the lesion usually lies just caudal and medial to the red nucleus and that the tremor and ataxia are due to involvement of the cerebellar outflow pathways in the cerebellar peduncle." ("DeJong's The Neurological Examination", p. 337). In practice there is usually some damage which causes contralateral hemiparesis/hemiplegia in patients with Benedikt's syndrome. If the lesion is exactly the way Benedikt originally described it, then there wouldn't be contralateral hemiparesis/hemiplegia. However, one must keep in mind that back in the time when Benedikt practiced, they were much more likely than we are to see tuberculomas and tertiary syphilis as the cause of the neurological defect. Hence, the lesion will be much more confined and lead to much more focal symptoms. Today, and for the purpose of the topic of this discussion, the primary cause of such neurologic defect is ischemic stroke -- which is much less focal. So if you want to be technical and faithful to the original definition, you could remove contralateral hemiparesis/hemiplegia for Benedikt's syndrome. But when stroke is the etiology, there is almost always going to be some level of contralateral motor signs which may range from tremor and ataxia to varying degrees of contralateral weakness. In real life you rarely see stroke patients with syndromes so clearly defined as these. There is usually some overlap with other conditions or symptoms depending on the severity of the ischemic damage.
THANK YOU..I WAS SO CONCERNED WITH MY MOTHERS EYES GOING TO THE RIGHT...A PN TOLD ME ITS NORMAL DUE TO THE STROKE..ITS A LONG RECOVERY FOR HER ...SHE SUFFERED TWO STROKES AND AN ANEURYSM IN ONE NIGHT..I HARDLY WANTED TO GATHER THIS MUCH INFO BUT I NEED TO LEARN ALL I CAN..THANK YOU AGAIN
Love the videos. Question. When explaining eye deviation with MCA stroke, I thought it was attributed to loss of FEF on lesioned side. You explained it as loss of CNIII.
+Corey Kirshner Yes... you're right, thank you - I goofed there. Loss of FEF on the side of the stroke means you lose contralateral gaze ability through loss of input to contralateral PPRF and hence loss of input to (1) the contralateral CN VI and (2) the ipsilateral CN III via MLF. End result is decreased signaling to the contralateral LR and ipsilateral MR which means you have ipsilateral deviation or, in other words, deviation to the same side of the lesion. It's such a complex mechanism to commit to memory, but it's a useful one for remembering internuclear ophthalmoplegia which is a sequela of MS (and can happen with pontine strokes). The explanation I gave with "losing" CN III *is* what happens when losing the ipsilateral FEF, but a lesion to CN III alone doesn't explain why the contralateral eye also deviates towards the lesion side, and that's of course because, as you said, the lesion originates with the frontal cortex rather than the cranial nerve itself and this causes you to lose LR tone. Phew! I think I might have addressed INO and this whole pathway in the neuro-ophthalmology slides, but I'd have to double-check.
+Corey Kirshner Okay good - I did explain this in the Neuro-Ophthalmology lecture! For anyone confused by my explanation above, visit this lecture: th-cam.com/video/oHio_R0_NR4/w-d-xo.htmlm58s
Thank you for your slides, I just have a couple of questions. Macula Sparing is the result of branches from the MCA correct? Also, for Weber Syndrome.... wouldn't you get upper motor symptoms to the Corticobulbar tract since Facial nerve come out at the level of Lower Pons/ Upper Medulla... not the bid brain? So you should expect exaggerated gag reflex, spastic dysarthria. Likewise, you say that PCA will not cause motor symptoms but both Weber & Benedict syndromes are both caused by PCA occlusions... If anyone else can explain this I'd appreciate it.
1st Macular is supplied by branches on PCA and MCA therefore we get macular sparing No in CN7 issue we could not see Upper motor symptoms as Cranial nerve GENERALLY have bilateral innervation from corticobulbar tract. Gag reflex and Spastic Dysarthria are CN9 and CN10 probelms not facial nerve(cn7) PCA supplied medial mibrain where the corticospinal and corticobulbar runs so it would cause hemiparesis but by motor symptoms do you mean upper motor neuron signs? it would not cause upper motor neuron sign for cranial nerve as they have bilateral innervation but these symptoms would appear for limbs which only have contralateral innervation hope i made no mistakes
Dr .Paul your videos are very good..but I am confused in the point of bilateral eye deviation towards the side of infarct and how the cranial nerve IV remains intact and also how MCA produces homonymous hemianopsia?please make this clear to me..
In MCA stroke, the *ipsilateral* eye looks toward the side of the lesion because of the physical damage. Why then does the contralateral eye also follow the damaged eye's direction, gazing to the side of the lesion? Is it something to do with the medial longitudinal fasic./a natural function of the eye which maintains alignment of both eyes? Cheers
For the purpose of test-taking, I would entirely remove contralateral hemiplegia as a sign of Benedikt's syndrome. Although in practice, there will likely be some degree of contralateral weakness but not as severe as in Weber's syndrome. As I wrote above, these syndromes were not primarily described in ischemic stroke patients but rather those with masses (i.e., tuberculomas, gummas). Hence, they saw much more defined focal lesions. You should probably remain faithful to their definition for test-taking purposes. But in real life, in stroke patients, bear in mind that it's never this clear-cut.
Apparently this video is lacking sound. Please refer to the earlier version of this video. There are some errors in the video, which I address in the description, so please take note of that.
![BOWKYLION - วิงวอน (ex-change) [Official MV]](http://i.ytimg.com/vi/cLdnZWDaO-w/mqdefault.jpg)
Dear Paul
Words cant express how thankful i am for your series. You're making better doctors around this world 🌍 and im proud to be one of them. May God richly bless you.
Please re upload with sound we love your content!
Just a side note: I had a massive hemorrhagic CVA at the age of 24 related to a thalamic AVM. My only presenting symptom was loss of sensation and proprioception on the left side of my body. My FAST assessment was completely negative and I remained verbally fluent. I also didn't have a headache until about 30 minutes after the onset of numbness. Just because they don't look like they are having a stroke doesn't mean they aren't.
Please re-upload this video. the sound is off
looks like a great lecture
Please reupload this one Dr. Bolin. We would understand this more with the audio.
There is no sound on this video :( Thank you for all of your videos though, they are super helpful!
Doc no audio please reupload
Hey Dr Bolin.!! Thank you so so much for your lectures! They are excellent !! :) unfortunately the sound for this doesn’t work :( I would be so greatful if you could reupload it so we can hear it!!!
I really want to hear this video, but no sound :(
th-cam.com/video/NfST1Vq8skI/w-d-xo.html
Thanks for the work. There's no sound. Can you please re-upload??🥺
I'm a stroke survivor! Enjoyed your video. I have been looking at my CT/MRI imagery on the theory of know your enemy! Thanks for the video!
Me too! Agreed. I want to say thank you too!! xxxx
@paul bolin, M.D. No sound, please re-upload this lecture, thank you.
This one doesn't have sound in it !
No sound in video
no sound please
It seems that some people can hear the audio for this?
Great video as always, thank you. Just to comment that the book written by the locked-in syndrome patient is called "The Diving Bell and the Butterfly", and he wrote it using a letter board, as opposed to morse code. It's an amazing book (and a great French movie too!)
Please sorry there is no audio on this
Audio isn't working. Thanks for the videos.
lecture is good but there is no audio for this lecture
There is some problem in the voice 🙁💔
Plz dr can U correct it because I'm really want to watch this 🙁
Hello. I had two CVA's in 1969. I was 5 years old My strokes were hammorrhagic strokes. From time to yime, I have seizures. I am now 53 years old. Thanks for the video. It was very interesting.
Why does the video have no sound?
sound is not working
Cheers Paul. I've been avoiding learning this for years, this was really helpful.
This video lost its sound.
Where is the sound?
Can turn on the captions until he is made aware of the issue
Audio is not working 😓😓😓
Thanx for the video but audio was not working ...if it is then it was helpful for me alot ..anyhow thanks
In Benedikt syndrome, i read there is no contralateral hemiplegia. since red nucleus, cn 3, and medial leminiscus are only affected.
corticospinal tract is not affected. please confirm it.
"Debate remains about how much red nucleus involvement occurs in Claude's and Benedikt's syndrome. Seo concluded on the basis of clinical and MRI studies that the lesion usually lies just caudal and medial to the red nucleus and that the tremor and ataxia are due to involvement of the cerebellar outflow pathways in the cerebellar peduncle." ("DeJong's The Neurological Examination", p. 337).
In practice there is usually some damage which causes contralateral hemiparesis/hemiplegia in patients with Benedikt's syndrome. If the lesion is exactly the way Benedikt originally described it, then there wouldn't be contralateral hemiparesis/hemiplegia. However, one must keep in mind that back in the time when Benedikt practiced, they were much more likely than we are to see tuberculomas and tertiary syphilis as the cause of the neurological defect. Hence, the lesion will be much more confined and lead to much more focal symptoms. Today, and for the purpose of the topic of this discussion, the primary cause of such neurologic defect is ischemic stroke -- which is much less focal.
So if you want to be technical and faithful to the original definition, you could remove contralateral hemiparesis/hemiplegia for Benedikt's syndrome. But when stroke is the etiology, there is almost always going to be some level of contralateral motor signs which may range from tremor and ataxia to varying degrees of contralateral weakness.
In real life you rarely see stroke patients with syndromes so clearly defined as these. There is usually some overlap with other conditions or symptoms depending on the severity of the ischemic damage.
Thank you very much for clear explannation.
i would really like to appreciate your effort for making these video. Thanks a lot.
I don't know why but I do not hear the audio in this video. Otherwise I love your videos
Thanks Paul for all the videos..
THANK YOU..I WAS SO CONCERNED WITH MY MOTHERS EYES GOING TO THE RIGHT...A PN TOLD ME ITS NORMAL DUE TO THE STROKE..ITS A LONG RECOVERY FOR HER ...SHE SUFFERED TWO STROKES AND AN ANEURYSM IN ONE NIGHT..I HARDLY WANTED TO GATHER THIS MUCH INFO BUT I NEED TO LEARN ALL I CAN..THANK YOU AGAIN
Why isn’t there any sound??
Love the videos. Question. When explaining eye deviation with MCA stroke, I thought it was attributed to loss of FEF on lesioned side. You explained it as loss of CNIII.
+Corey Kirshner Yes... you're right, thank you - I goofed there. Loss of FEF on the side of the stroke means you lose contralateral gaze ability through loss of input to contralateral PPRF and hence loss of input to (1) the contralateral CN VI and (2) the ipsilateral CN III via MLF. End result is decreased signaling to the contralateral LR and ipsilateral MR which means you have ipsilateral deviation or, in other words, deviation to the same side of the lesion. It's such a complex mechanism to commit to memory, but it's a useful one for remembering internuclear ophthalmoplegia which is a sequela of MS (and can happen with pontine strokes). The explanation I gave with "losing" CN III *is* what happens when losing the ipsilateral FEF, but a lesion to CN III alone doesn't explain why the contralateral eye also deviates towards the lesion side, and that's of course because, as you said, the lesion originates with the frontal cortex rather than the cranial nerve itself and this causes you to lose LR tone. Phew!
I think I might have addressed INO and this whole pathway in the neuro-ophthalmology slides, but I'd have to double-check.
+Corey Kirshner Okay good - I did explain this in the Neuro-Ophthalmology lecture! For anyone confused by my explanation above, visit this lecture: th-cam.com/video/oHio_R0_NR4/w-d-xo.htmlm58s
+Paul Bolin, M.D. please when the sound of this vedio l need it so much please😢
hi Dr d you mind uploading this section.I believe this is an important class to understand.Thanks for your classes.You are amazing
Great great work. Love you . keep up the good work cuz you are an inspiration
where is sound
Paul, i love all the work youve done! i always rewatch your videos. Could you reupload this one? the audio doesnt work.
th-cam.com/video/NfST1Vq8skIh/w-d-xo.htmlttps://th-cam.com/video/NfST1Vq8skI/w-d-xo.html
No sound !!!!
This video has no sound !
just to clarify - the eyelid will be down and out with a PCA stroke, not an MCA, right?
Thank you for your slides, I just have a couple of questions.
Macula Sparing is the result of branches from the MCA correct?
Also, for Weber Syndrome.... wouldn't you get upper motor symptoms to the Corticobulbar tract since Facial nerve come out at the level of Lower Pons/ Upper Medulla... not the bid brain? So you should expect exaggerated gag reflex, spastic dysarthria.
Likewise, you say that PCA will not cause motor symptoms but both Weber & Benedict syndromes are both caused by PCA occlusions...
If anyone else can explain this I'd appreciate it.
1st Macular is supplied by branches on PCA and MCA therefore we get macular sparing
No in CN7 issue we could not see Upper motor symptoms as Cranial nerve GENERALLY have bilateral innervation from corticobulbar tract.
Gag reflex and Spastic Dysarthria are CN9 and CN10 probelms not facial nerve(cn7)
PCA supplied medial mibrain where the corticospinal and corticobulbar runs so it would cause hemiparesis but by motor symptoms do you mean upper motor neuron signs?
it would not cause upper motor neuron sign for cranial nerve as they have bilateral innervation but these symptoms would appear for limbs which only have contralateral innervation
hope i made no mistakes
Dr .Paul your videos are very good..but I am confused in the point of bilateral eye deviation towards the side of infarct and how the cranial nerve IV remains intact and also how MCA produces homonymous hemianopsia?please make this clear to me..
In MCA stroke, the *ipsilateral* eye looks toward the side of the lesion because of the physical damage.
Why then does the contralateral eye also follow the damaged eye's direction, gazing to the side of the lesion?
Is it something to do with the medial longitudinal fasic./a natural function of the eye which maintains alignment of both eyes?
Cheers
If Weber's and Benedikt's are caused by infarct in branches arising from the PCA, then why wouldn't a PCA stroke cause the CN III palsy?
24:00 -- *PCA* supplies "Visual Cortex" which *affects vision* (sensory) *not eye movement* (motor)
Thanks doctor paul you are simply a fantastic doctor ! Gotta love the US amazing country with amazing people
I wish this had sound
Dr.Bolin, no sound!
I have treated a child who was 4 years old and had a stroke but she had moya mots. sad case
This video really needs sound :(
I was asked have you been drinking and what pills have you taken. 🤯
woow. no sound. thanks anyway. very helpful
is the eye deviation different in hemorrhagic versus ischemic strokes?
please where is the sound😢😢
Where's the sound?????
Awesome lecture, thank you!
No voice
At 29:57 you meant to say "spinal trigeminal tract"
Muted?
Please I really want to hear this video could you fix it
Reload please
3 years later....
th-cam.com/video/NfST1Vq8skI/w-d-xo.html&t
Canu please upload this with sound
No sound:(
No sound??
oooohhhh plz this vedio have no sound 😑😑😑😑😑😑your explantion soiooo goood
facial nerve is present in pons , how come facial palsy ?
Sad,no sounds.
excellent lec...thankuuu so so much
Terima kasih.
no sound
Worked with captions
Congratulations educational videos .
Thanks sir.
thanks
Audio
Yes, the audio seems to be missing.
For the purpose of test-taking, I would entirely remove contralateral hemiplegia as a sign of Benedikt's syndrome. Although in practice, there will likely be some degree of contralateral weakness but not as severe as in Weber's syndrome. As I wrote above, these syndromes were not primarily described in ischemic stroke patients but rather those with masses (i.e., tuberculomas, gummas). Hence, they saw much more defined focal lesions. You should probably remain faithful to their definition for test-taking purposes. But in real life, in stroke patients, bear in mind that it's never this clear-cut.
Hello, I hope u can re-upload the video or check it's audio? cause it is not working now! Thanks in advance ^^
Paul Bolin, M.D. It's not clear cut in test taking either. Guidelines vs what the test writer wants.
Sir sound is not there can u plz re upload it
Apparently this video is lacking sound. Please refer to the earlier version of this video. There are some errors in the video, which I address in the description, so please take note of that.
sorry. moya moya
For the updated/condensed version: th-cam.com/video/nBhfQCCANMc/w-d-xo.html
You can watch this video with audio here:
th-cam.com/video/NfST1Vq8skI/w-d-xo.html
No sound