Understanding Multiple Sclerosis
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Understanding Multiple Sclerosis
CCSVI is just one component of a more global, biomechanical disease process which we call MS. I have outlined a framework for understanding MS which incorporates a multitude of contributions from various sub-disciplines of medicine, including contributions related to CCSVI. Contributions from Schelling, Williams, and others have been included. Please read and consider. Do not hesitate to email me for help, that is what I am here for.
http://www.anothingnobody.com/Content/u ... ing_ms.pdf
http://www.anothingnobody.com/Content/u ... ing_ms.pdf
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Re: Understanding Multiple Sclerosis
No comments? The framework I have outlined specifically accounts for all of the following shortcomings of the autoimmune theory as summarized by Behan and Chaudhuri:
• Age effect of migration
• Geographic variation (higher prevalence in most northern latitudes)
• Maternal contribution to disease risk (Ref. 5)
• Early and extensive grey matter involvement (estimated number of deep grey matter lesions per gram wet weight is higher than in any other brain structure [Ref. 6])
• Progressive brain and spinal cord atrophy, beginning at the stage of clinically isolated demyelinating syndromes (Ref. 7)
• Selective anatomical localization, symmetry and sharp margins of plaques
• Absence of specific immunological marker
• Effect of stress
• General failure of immunotherapies that are highly successful in other organ-specific autoimmune diseases and transplant rejection
• Associations with Charcot-Marie-Tooth disease and neurofibromatosis-1 (Ref. 2)
• Age effect of migration
• Geographic variation (higher prevalence in most northern latitudes)
• Maternal contribution to disease risk (Ref. 5)
• Early and extensive grey matter involvement (estimated number of deep grey matter lesions per gram wet weight is higher than in any other brain structure [Ref. 6])
• Progressive brain and spinal cord atrophy, beginning at the stage of clinically isolated demyelinating syndromes (Ref. 7)
• Selective anatomical localization, symmetry and sharp margins of plaques
• Absence of specific immunological marker
• Effect of stress
• General failure of immunotherapies that are highly successful in other organ-specific autoimmune diseases and transplant rejection
• Associations with Charcot-Marie-Tooth disease and neurofibromatosis-1 (Ref. 2)
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Re: Understanding Multiple Sclerosis
I would also like to add that I am being censored on other forums by moderators. They are removing the link to the write up or are blocking my posts altogether.
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Re: Understanding Multiple Sclerosis
I noticed that you duplicated your post in two forums within TIMS, this technique is frowned upon in many forums as being impolite and disrespectful to other members/readers, and therefore on some forums you will bring attention to yourself as such.ANothingNobody wrote:I would also like to add that I am being censored on other forums by moderators. They are removing the link to the write up or are blocking my posts altogether.
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Re: Understanding Multiple Sclerosis
Hi ANothing---
Great info---looks like you've gotten a lot of stuff from the Upright Doc and our wonderful Dr. Schelling's book. I first met Dr. Schelling via e-mail in 2008 after finding his book online, and later in Bologna in 2009. I was thrilled to know he and Dr. Zamboni had connected. No arguments here, I think you're right on! Just know that we've been discussing all of these issues on here for a few years with Dr. Flanagan and others, so don't be insulted by a lack of response. Also, the only thing that gets folks banned on this forum is disrespect...certainly not out of the box thinking!
Here's the first time we started talking about Dr. Schelling, in 2008 (look down 3 posts)
You can read his reply to my e-mail on this thread, too. (4th post)
http://www.thisisms.com/forum/chronic-c ... c6488.html
Here's Dr. Flanagan's thread--it's 309 pages long
http://www.thisisms.com/forum/chronic-c ... 14005.html
Dr. Flanagan just published an excellent review on the craniocervical junction and CSF. If you haven't read it, it's fantastic--and published!) http://www.hindawi.com/journals/nri/2015/794829/
Marie Rhodes' book really gets into the whole autoimmune issue, inaccuracy of EAE--citing Behan and Chaudhuri. It's really a well-researched, excellent publication. Highly recommended
http://www.amazon.com/CCSVI-Cause-Multi ... 0786460385
Medicalese is also sometimes tough for laypeople to enjoy, can be intimidating. But lots of us are trying to get helpful research into public consciousness.
Sorry you've been censored on other sites. Just keep getting the info out there, and take care of yourself, too.
Hope you're doing well!
cheer/Joan
Great info---looks like you've gotten a lot of stuff from the Upright Doc and our wonderful Dr. Schelling's book. I first met Dr. Schelling via e-mail in 2008 after finding his book online, and later in Bologna in 2009. I was thrilled to know he and Dr. Zamboni had connected. No arguments here, I think you're right on! Just know that we've been discussing all of these issues on here for a few years with Dr. Flanagan and others, so don't be insulted by a lack of response. Also, the only thing that gets folks banned on this forum is disrespect...certainly not out of the box thinking!
Here's the first time we started talking about Dr. Schelling, in 2008 (look down 3 posts)
You can read his reply to my e-mail on this thread, too. (4th post)
http://www.thisisms.com/forum/chronic-c ... c6488.html
Here's Dr. Flanagan's thread--it's 309 pages long
http://www.thisisms.com/forum/chronic-c ... 14005.html
Dr. Flanagan just published an excellent review on the craniocervical junction and CSF. If you haven't read it, it's fantastic--and published!) http://www.hindawi.com/journals/nri/2015/794829/
Marie Rhodes' book really gets into the whole autoimmune issue, inaccuracy of EAE--citing Behan and Chaudhuri. It's really a well-researched, excellent publication. Highly recommended
http://www.amazon.com/CCSVI-Cause-Multi ... 0786460385
Medicalese is also sometimes tough for laypeople to enjoy, can be intimidating. But lots of us are trying to get helpful research into public consciousness.
Sorry you've been censored on other sites. Just keep getting the info out there, and take care of yourself, too.
Hope you're doing well!
cheer/Joan
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: Understanding Multiple Sclerosis
Sure there have been discussions from uprightdoc and Schelling, but how much discussion has there been about Williams? What else can account for the diffuse axonal injury and global brain damage? Why do MS patients have weak bones and what does that even have to do with autoimmunity?
While supine, extracranial venous drainage is normally through the IJVs which contain a valve just
proximal to their ends at the subclavian veins. The valves are designed for relatively low-pressure blood
flow leaving the cranium propelled along with minimal accelerative force by the windkessel mechanism.
Therefore, when the bruxing episode ends and the cranium contracts, the accumulated volume of blood
is accelerated out under pressures and velocities exceeding the limitations of the IJV valves. When fluid
travelling in a pipe strikes a barrier, a rebound wave is generated (Ref):
sinuses, straight sinus, and eventually the vein of Galen and its tributaries, thus creating the
characteristic perivenous lesions by mechanical impacts and stretching of vein walls. The trauma causes
an inflammatory breakdown of the blood-brain barrier (BBB), edema, and the immune cleanup response
thought to be the cause of MS. There are numerous pathological changes in MS consistent with an event
like this occurring chronically such as diffuse global brain damage, periventricular atrophy, perivenous
lesion spread, and altered collagen expression in the IJVs. Incompetent, thickened, or irregular IJV valves
could present a more robust barrier to venous evacuation thus generating more powerful rebound
waves back into the intracranial space.
While supine, extracranial venous drainage is normally through the IJVs which contain a valve just
proximal to their ends at the subclavian veins. The valves are designed for relatively low-pressure blood
flow leaving the cranium propelled along with minimal accelerative force by the windkessel mechanism.
Therefore, when the bruxing episode ends and the cranium contracts, the accumulated volume of blood
is accelerated out under pressures and velocities exceeding the limitations of the IJV valves. When fluid
travelling in a pipe strikes a barrier, a rebound wave is generated (Ref):
When the vented blood strikes the IJV valves, simultaneous rebound waves will travel up the IJVs, duralWhen the leading edge of a water column strikes the closed valve it comes to a halt, but the
water behind it is still in motion and, since it has nowhere to go, it begins to compress. This
compression along the entire length of the column allows a small amount of water to continue
to flow into the pipe even though the leading edge has halted. When flow ceases, its kinetic
energy of motion and that due to compression is transformed into pressure and energy is
conserved. Compression begins at the leading edge of the water column and since the
additional energy it produces cannot continue on past the closed valve, a pressure or shock
wave is generated and travels back upstream.
sinuses, straight sinus, and eventually the vein of Galen and its tributaries, thus creating the
characteristic perivenous lesions by mechanical impacts and stretching of vein walls. The trauma causes
an inflammatory breakdown of the blood-brain barrier (BBB), edema, and the immune cleanup response
thought to be the cause of MS. There are numerous pathological changes in MS consistent with an event
like this occurring chronically such as diffuse global brain damage, periventricular atrophy, perivenous
lesion spread, and altered collagen expression in the IJVs. Incompetent, thickened, or irregular IJV valves
could present a more robust barrier to venous evacuation thus generating more powerful rebound
waves back into the intracranial space.
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Re: Understanding Multiple Sclerosis
How about the gender gap and the before-15 age of effect of migration? All of these can be specifically accounted for by bone density as it relates to the cranial sutures.
One study suggests that a vitamin D deficiency contributes to MS risk only if the deficiency occurs before
the age of 15 (Ref). The before 15 age-effect and gender gap in MS correlate tightly with typical gender
differences regarding skeletal growth (Ref),
prior to this age could have a significant impact on MS disease risk well into adulthood. Since boys have
a later and longer growth spurt and end up with overall greater bone mass, they have a lesser likelihood
of developing MS.
One study suggests that a vitamin D deficiency contributes to MS risk only if the deficiency occurs before
the age of 15 (Ref). The before 15 age-effect and gender gap in MS correlate tightly with typical gender
differences regarding skeletal growth (Ref),
By the age of 15, girls on average will have achieved much of their final adult bone mass and a deficiencyThe onset of puberty corresponds to a skeletal(biological) age of roughly 11 years in girls and 13
years inboys.19,20 The rates of increase in statural height and bone remodeling are greatest in
early puberty followed by progressive decline.21 Consequently, peak vBMD velocity occurs 2
years later, at menarche in girls and late puberty in boys. The growth pattern in boys varies from
girls in two ways: boys have two more years of prepubertal growth because of their later onset
of puberty than girls, and pubertal growth spurt in boys lasts for 4 years compared to 3 years in
girls.5,16,17 These differences widely account for the 10% greater statural height and the 25%
greater PBM achieved by males.
prior to this age could have a significant impact on MS disease risk well into adulthood. Since boys have
a later and longer growth spurt and end up with overall greater bone mass, they have a lesser likelihood
of developing MS.
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Re: Understanding Multiple Sclerosis
How about the rapid periventricular atrophy and ventricular enlargement experienced by RRMS patients? Once again, the brain is compressed from the outside-in by the cranial bones causing the pooled blood to be squeezed out of the intracranial space. Then blood rebounds back in, travels to the veins and capillaries adjacent to the choroid plexus, causing the intaventricular pressure to spike. Thus, you have a profound "squeezing" of the periventricular tissue which leads to rapid atrophy.
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Re: Understanding Multiple Sclerosis
How about explaining the fact that MS patients often wake up with new symptoms? How many stories have you read that start with "I woke this morning and...". This is an indication that the disease mechanism is MOST ACTIVE DURING THE NIGHT while the patient sleeps.
Unfortunately, I had an ms attack 2 weeks ago. I woke up one morning with only 40% vision in
my right eye (this was the same eye that had diplopia in my first attack). I immediately
contacted my ms nurse and went to the hospital for a 3 day course of steroids.
(Ref),
I was diagnosed with ms about a month ago. My first symptom was a sharp stabbing pain in the
side of my head right above my ear. I then started getting a general headache and ringing in my
ears. I also noticed a throbbing pain in one spot in my right thigh. I woke up the next morning
with the sensation like i just looked into the flash of a camera, and also found out i had
developed two severe blind spots in both eyes. Things have been improving until tonight. I
layed down on my bed, on my stomach, and when i tried to lift my head to look up, i got this
loud ringing in my ears and this whooshing sound, like my heartbeat maybe, or blood pumping,
and my head felt really heavy. But as soon as i moved my head and laid back down flat the noise
was gone. Now i feel like im getting the same weird vision problem i had the first time, and pain
in the exact same spot in my head, and the throbbing in my right thigh. Has anyone had
anything like this happen?
49
(Ref),
However, the last couple days I now have numbness spreading down my right arm, where I had
none before. confused I guess this is a new relapse? I'm scared of what I'll wake up with
tomorrow morning... and if it will ever go away. Being a long weekend, there is no one I can
call.
(Ref),
This was very fortunate because just before my appointment was due I woke up one morning
numb from the waist down. It was incredibly frightening. An MRI scan showed lesions - like
white spots - in my brain and neck, and I was told this indicated swelling on my nerves that
could be MS. The neurologist explained that he would give me high-dose steroids for five days
to stop the swelling and only if I had a relapse would he be able to confirm the diagnosis.
(Ref),
In the years since, Frye has remained cognizant of how the disease could affect him and is a bit
more strategic in planning for each hunt. “Sometimes I wake up in the morning and don’t feel
right, so I don’t go hunting on those days,” he explained. He also tries to arrange his Rebif
injections to accommodate his hunting schedule, and as often as possible makes sure he has
someone hunting with him.
(Ref),
My last MRI was only 2 months ago, that's why I'm not in a big hurry to go back to the
neurologist. The only meds I take now is Amantadine for the fatigue, which has been very
helpful until a few weeks ago when the fatigue started getting stronger than the prescription, I
guess. My muscles are sore when I wake up in the morning - my forearms and my inner things
- as if they have been spasming during the night. My exercise routine hasn't changed in a while,
so I don't think it is that. The jaw pain has been an issue off and on, and I am not sure whether it
is stress (dentist has said I'm grinding yes so I wear a night guard) or the trigeminal nerve
wreaking havoc (I get both the sore muscles and the electric shocks).
(Ref),
Anyways, I am not asking for opinion on the likely hood of MS or if you think I have it. What I am
asking is, when you get a relapse, are your symptoms bad 100% of the time during that relapse,
or do they symptoms sometimes come and go? The only symptom that hasn't disappeared since
this all started is my fatigue. But the limb weakness, it's not always super apparent. And it is
often worse at night. Is that common with MS? Symptoms being worse at night?
Unfortunately, I had an ms attack 2 weeks ago. I woke up one morning with only 40% vision in
my right eye (this was the same eye that had diplopia in my first attack). I immediately
contacted my ms nurse and went to the hospital for a 3 day course of steroids.
(Ref),
I was diagnosed with ms about a month ago. My first symptom was a sharp stabbing pain in the
side of my head right above my ear. I then started getting a general headache and ringing in my
ears. I also noticed a throbbing pain in one spot in my right thigh. I woke up the next morning
with the sensation like i just looked into the flash of a camera, and also found out i had
developed two severe blind spots in both eyes. Things have been improving until tonight. I
layed down on my bed, on my stomach, and when i tried to lift my head to look up, i got this
loud ringing in my ears and this whooshing sound, like my heartbeat maybe, or blood pumping,
and my head felt really heavy. But as soon as i moved my head and laid back down flat the noise
was gone. Now i feel like im getting the same weird vision problem i had the first time, and pain
in the exact same spot in my head, and the throbbing in my right thigh. Has anyone had
anything like this happen?
49
(Ref),
However, the last couple days I now have numbness spreading down my right arm, where I had
none before. confused I guess this is a new relapse? I'm scared of what I'll wake up with
tomorrow morning... and if it will ever go away. Being a long weekend, there is no one I can
call.
(Ref),
This was very fortunate because just before my appointment was due I woke up one morning
numb from the waist down. It was incredibly frightening. An MRI scan showed lesions - like
white spots - in my brain and neck, and I was told this indicated swelling on my nerves that
could be MS. The neurologist explained that he would give me high-dose steroids for five days
to stop the swelling and only if I had a relapse would he be able to confirm the diagnosis.
(Ref),
In the years since, Frye has remained cognizant of how the disease could affect him and is a bit
more strategic in planning for each hunt. “Sometimes I wake up in the morning and don’t feel
right, so I don’t go hunting on those days,” he explained. He also tries to arrange his Rebif
injections to accommodate his hunting schedule, and as often as possible makes sure he has
someone hunting with him.
(Ref),
My last MRI was only 2 months ago, that's why I'm not in a big hurry to go back to the
neurologist. The only meds I take now is Amantadine for the fatigue, which has been very
helpful until a few weeks ago when the fatigue started getting stronger than the prescription, I
guess. My muscles are sore when I wake up in the morning - my forearms and my inner things
- as if they have been spasming during the night. My exercise routine hasn't changed in a while,
so I don't think it is that. The jaw pain has been an issue off and on, and I am not sure whether it
is stress (dentist has said I'm grinding yes so I wear a night guard) or the trigeminal nerve
wreaking havoc (I get both the sore muscles and the electric shocks).
(Ref),
Anyways, I am not asking for opinion on the likely hood of MS or if you think I have it. What I am
asking is, when you get a relapse, are your symptoms bad 100% of the time during that relapse,
or do they symptoms sometimes come and go? The only symptom that hasn't disappeared since
this all started is my fatigue. But the limb weakness, it's not always super apparent. And it is
often worse at night. Is that common with MS? Symptoms being worse at night?
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Re: Understanding Multiple Sclerosis
I have made some very specific hypotheses within the context of a "big picture" understanding of MS, with a lot of supporting data. Most of the essential aspects of MS are accounted for.
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Re: Understanding Multiple Sclerosis
How about the peculiar protective effect of pregnancy? Estrogen levels skyrocket during pregnancy, and estrogen is crucial to maintaining the structural integrity of the sutures. Thus, when women get a boost of estrogen, their sutures temporarily harden up and they see relief from their MS. Once estrogen levels fall and the sutures weaken, the MS disease activity returns to normal.
In summation, in this study we sought to correlate estrogen signaling with mouse cranial suture
fusion, a process of endochondral ossification [4]. We found that ERα gene transcript abundance
temporally coincides with PF suture fusion. Moreover, immunohistochemistry detected ER
protein primarily within osteocytes and chondrocytes in cranial suture mesenchyme. Via
analysis of ER knockout mice, functional ERα but not ERβ was found to be necessary for normal
suture fusion. In vitro cell culture of suture-derived mesenchymal cell (SMCs) suggested that 17-
β estradiol (E2) enhanced both osteogenic and chondrogenic differentiation within the PF
suture. Finally, in vivo blockade of ER signaling in the developing calvaria via Fulvestrant
inhibited suture fusion and led to severely diminished calvarial osteogenesis.
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Re: Understanding Multiple Sclerosis
Schelling was on the right track with venous reflux causing the perivenous lesions. The question always was: What force(s) can cause such turbulent reflux into cerebral veins? Isolated, unilateral venous reflux from thoracic veins can't be the cause because the blood will just harmlessly descend back down the contralateral IJV. What is need is something that can produce reflux SIMULTANEOUSLY and BILATERALLY in the IJVs, thus leaving no option for the refluxing blood to go anywhere but into the straight sinus. Again, temporary expansions and contractions of the cranial cavity is the only force that could produce such a phenomenon. This also happens to jive very well with all the Vitamin D, global brain damage, poor bone health, TMD, and other data that has been accumulated over the decades.
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Re: Understanding Multiple Sclerosis
Yes, symptoms can come and go. Sleep/head position makes a difference, and can exacerbate symptoms-by compromising jugular flow, which would correlate to worse night time/morning issues.ANothingNobody wrote: Anyways, I am not asking for opinion on the likely hood of MS or if you think I have it. What I am
asking is, when you get a relapse, are your symptoms bad 100% of the time during that relapse,
or do they symptoms sometimes come and go? The only symptom that hasn't disappeared since
this all started is my fatigue. But the limb weakness, it's not always super apparent. And it is
often worse at night. Is that common with MS? Symptoms being worse at night?
Dr Maiken Nedergaard, discoverer of the brain's lymphatic clearance during sleep, has published on the fact that sleep position affects drainage.
http://neurosciencenews.com/lateral-sle ... logy-2363/Sleeping in the lateral, or side position, as compared to sleeping on one’s back or stomach, may more effectively remove brain waste and prove to be an important practice to help reduce the chances of developing Alzheimer’s, Parkinson’s and other neurological diseases, according to researchers at Stony Brook University.
You sure know a lot for being recently diagnosed! Your first flare sounded very dramatic and scary, so sorry---but you're being really proactive. Keep moving, eat well, get UV/vitamin D, find things that work for you--and keep sharing! Interested to learn more about William's research.
My husband is now almost 9 years past diagnosis and still jogging, no MS progression, and remyelination of lesions and reversal of brain atrophy, on MRI. So, there is hope of disease reversal.
Here's the program he's followed http://ccsvi.org/index.php/helping-myse ... ial-health
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: Understanding Multiple Sclerosis
I suffered with a PPMS-like condition for almost five years, but cured myself with proper sunlight exposure, halting masturbation, and removing the mechanical circumstances/habits/practices that caused fluid shifts in my spinal canal (damaging my cord).
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Re: Understanding Multiple Sclerosis
What about the frequency of optic neuritis in MS? Flanagan has written about caudal displacements of the entire brain during CSF hypovolemia, but what circumstances could permit such an occurrence? Why is ON seen so frequently in RRMS, but hardly at all in PPMS? Again, it has all to do with the degree of cranial expansion and contraction. When the cranium expands, this functionally induces hypovolemia. Unilateral ON can also be explained by cranial asymmetry and/or a functional jaw imbalance. The forces during contraction would likewise be asymmetrical, often leading to ON in only one eye.
Acute optic neuritis (ON) appears in at least 50% of MS cases during the disease course and is the
presenting symptom in about 20% of cases. The most likely cause of acute ON in MS is due to direct
compression of the optic nerve by the brain. The diameter of the optic nerve sheath has been observed
to decrease during CSF hypovolemia (Ref). Given that an acute endocranial expansion functionally
induces CSF hypovolemia, one could hypothesize that the brain will initially sink in the cranial vault
when clenching begins. When clenching ceases, the brain will once again be forced caudally within the
cranial vault. Depending on the case-specific anatomy and particular forces involved, the caudal
displacement of the brain may be sufficient to directly compress the optic nerve sheath resulting in
acute ON. If the expansion is markedly asymmetrical, displacement of the brain would likewise be
asymmetrical which would explain frequent unilateral ON. Asymmetrical symptomatology is more
common in the RRMS/SPMS pattern due to the inherent volatility of the disease mechanism whereas
the pattern of symptoms and damage is more consistently bilateral in PPMS which features a more
uniform and subtle disease process.
Acute optic neuritis (ON) appears in at least 50% of MS cases during the disease course and is the
presenting symptom in about 20% of cases. The most likely cause of acute ON in MS is due to direct
compression of the optic nerve by the brain. The diameter of the optic nerve sheath has been observed
to decrease during CSF hypovolemia (Ref). Given that an acute endocranial expansion functionally
induces CSF hypovolemia, one could hypothesize that the brain will initially sink in the cranial vault
when clenching begins. When clenching ceases, the brain will once again be forced caudally within the
cranial vault. Depending on the case-specific anatomy and particular forces involved, the caudal
displacement of the brain may be sufficient to directly compress the optic nerve sheath resulting in
acute ON. If the expansion is markedly asymmetrical, displacement of the brain would likewise be
asymmetrical which would explain frequent unilateral ON. Asymmetrical symptomatology is more
common in the RRMS/SPMS pattern due to the inherent volatility of the disease mechanism whereas
the pattern of symptoms and damage is more consistently bilateral in PPMS which features a more
uniform and subtle disease process.
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