Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:
What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
Well that depends on whether the compression is the whole picture, Laura. Many people, self included, think there is more to it than that. Autopsies on 'healthy' (i.e. non-TN) people sometimes show exactly the same compressions and problems, yet they have not suffered from TN. It's suggested that you need myelin sheath damage for TN to occur. So it's not the compression, per se, that is the problem. Subsequently the body may manage to repair the sheath for a while, sometimes a long while, or even, if you are lucky, indefinitely, and the TN will go into remission. It's also a possibility that the compression can move and thus put the TN into remission.
Laura said:
Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:
Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
Hi Aiculsamoth, I'm not quite sure I understand what you mean by this: "Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN."
Are you saying that in a healthy person 30% of the nerve fibres are unmyelinated (I'm assuming as opposed to demyelinated)? I was under the impression that ALL nerve fibres had myelin sheaths, otherwise wouldn't people be having TN type nerve pain all the time? Can I ask where you read/heard this?
aiculsamoth said:
Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
Well for what its worth, from an immunology viewpoint the presence of Axonal proteins should be considered. For most that means a collagen problem which effects the myelin sheath. EVERY person with TN in my opinion should have a pretty complete genetic work up. Especially considering the COL5A and COL3A genes. Woman with electric teeth make a good point. the myelin sheaths job is to helps tissues resist deformation. If there is a collagen disorder (Ehlers-Danlos Syndrome is the most common and most frequently undiagnosed) Not only can the nerves collapse but the blood vessels ccan collapse as well. The blood vessels is prolly the most significant forTN.
Everything involved with MVD including just "massaging" the nerves goes toward this kind of deformation. Which is why I have always thought MVD is often effective but inefficient in that there is no predictability in outcomes.
Not that a collagen disorder changes treatment options much, it can explain why Tn (and other neuralgias) come and go and why MVD fails. Or is successful when they don't find the blood vessel issues. Working through whether or not there is a collagen disorder COULD predict surgical outcomes.
That's correct there are both myelinated nerves and nonmyelinted nerves. Here's a pretty good summary. The smaller cranial nerves along with most sensory nervers (those you feel with) are nonmyelinated
http://www.mananatomy.com/basic-anatomy/myelinated-nonmyelinated-nerve-fibers
Woman with the electric teeth said:
Hi Aiculsamoth, I'm not quite sure I understand what you mean by this: "Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN."
Are you saying that in a healthy person 30% of the nerve fibres are unmyelinated (I'm assuming as opposed to demyelinated)? I was under the impression that ALL nerve fibres had myelin sheaths, otherwise wouldn't people be having TN type nerve pain all the time? Can I ask where you read/heard this?
aiculsamoth said:Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
Hi ModS - there are so many interesting ideas in your reply I hardly know where to start. The axonal proteins/immunology comment - are you saying that there could be an autoimmune issue causing proteins to form or collect where they shouldn't - e.g. on or around the neurons? Or are you suggesting something autoimmune is damaging axonal proteins? I know nothing about this area of research so any light you can shed...
Also, collagen problems? I've never heard of a connection of that to TN. Most interesting. I've looked up Ehlers-Danlos Syndrome, but joint hypermobility seems to be a defining feature. I definitely don't have that - quite the opposite. I have a world of joint pain! I do have lots of the other things they list as "minor", like no gut motility and gastric problems, but I suppose they could be something else entirely, although no doctor has yet to find a cause for them (or care much about them).
And what are the COL5A and COL3A genes, and how do they impact on TN?
You've thrown me a ton of new information, sorry; it's a dangerous thing to do!
ModSupport said:
Well for what its worth, from an immunology viewpoint the presence of Axonal proteins should be considered. For most that means a collagen problem which effects the myelin sheath. EVERY person with TN in my opinion should have a pretty complete genetic work up. Especially considering the COL5A and COL3A genes. Woman with electric teeth make a good point. the myelin sheaths job is to helps tissues resist deformation. If there is a collagen disorder (Ehlers-Danlos Syndrome is the most common and most frequently undiagnosed) Not only can the nerves collapse but the blood vessels ccan collapse as well. The blood vessels is prolly the most significant forTN.
Everything involved with MVD including just "massaging" the nerves goes toward this kind of deformation. Which is why I have always thought MVD is often effective but inefficient in that there is no predictability in outcomes.
Not that a collagen disorder changes treatment options much, it can explain why Tn (and other neuralgias) come and go and why MVD fails. Or is successful when they don't find the blood vessel issues. Working through whether or not there is a collagen disorder COULD predict surgical outcomes.
Not suggesting you know the answer, if the purpose of myelination, in addition to conduction is protection, nature being pretty clever, why is central myelination not seen along the whole of the sensory root? Because it isn't, to me it would suggest more of an 'overspill' from the CNS , peripheral to central what would be is it's role? I know very little about it but regardless of genetics I understand the majority of genetic manifestations outside of birth (maybe even then) require a trigger, epigenetics or something similar?
Well now, who knew?! Not me, obviously! I see though that they all have a neurolemmal sheath, whether they are non-myelinated or not. So maybe that could be the culprit? Aside from that though, am I not right in thinking the Trigeminal Nerve would be myelinated since it is a major nerve and not one of the "thinner axons"?
ModSupport said:
That's correct there are both myelinated nerves and nonmyelinted nerves. Here's a pretty good summary. The smaller cranial nerves along with most sensory nervers (those you feel with) are nonmyelinated
http://www.mananatomy.com/basic-anatomy/myelinated-nonmyelinated-ne...
Woman with the electric teeth said:Hi Aiculsamoth, I'm not quite sure I understand what you mean by this: "Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN."
Are you saying that in a healthy person 30% of the nerve fibres are unmyelinated (I'm assuming as opposed to demyelinated)? I was under the impression that ALL nerve fibres had myelin sheaths, otherwise wouldn't people be having TN type nerve pain all the time? Can I ask where you read/heard this?
aiculsamoth said:Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
I think the answer is if you need X amount of collagen and have y and x<y the distribution won't be linear but rather short in some areas. I have an autoimmune arthritis which is a seronegative HLA B27 type which indeed needs a trigger to get going. Yet what is effected varies. This year its been in my neck and cervical area causing what at least one doc called TN (junk TN diagnoses) last year it destroyed a shoulder (I really like my new one)
There are a number of forms of EDS Tooth woman (love your name but its a long one for these old fingers to type) The hypermobility type is the hot one right now but not all EDS has joint hypermobility. There are 7 types of EDS. FWIW Abnormal electrophoretic mobility is found often times with TN and it is also present in EVERY case of Classical EDS. (Joint pain is as well)
I'm not suggesting anyone would have EDS instead of TN or that EDS is the cause. But the myelination disorders across all (including MS) is to significant in my old head to ignore. Even Dr. Casey admits to them.
BUT what if that was the cause of someone's TN shouldn't it be eliminated along with other Auotimmune disorders before drilling holes in someones head?
aiculsamoth said:
Not suggesting you know the answer, if the purpose of myelination, in addition to conduction is protection, nature being pretty clever, why is central myelination not seen along the whole of the sensory root? Because it isn't, to me it would suggest more of an 'overspill' from the CNS , peripheral to central what would be is it's role? I know very little about it but regardless of genetics I understand the majority of genetic manifestations outside of birth (maybe even then) require a trigger, epigenetics or something similar?
I hope I'm not being crass, but the best example I can give of why the axons could be a problem (although I agree that myelination of the bigger nerves a problem) is that if you ever see a guy who has been kicked in family jewels HARD, he grabs right below his rib cage shortly there after because THAT is where the pain goes. It travels from the smaller axons to the myelinated nerves that end up there. (in fact thats where the testes form and travel down to the scrotum shortly before or shortly after birth not that that has anything to do with anything) Our nervous system is designed to disperse strong pain. A bit different than referred pain stimulus
Woman with the electric teeth said:
Well now, who knew?! Not me, obviously! I see though that they all have a neurolemmal sheath, whether they are non-myelinated or not. So maybe that could be the culprit? Aside from that though, am I not right in thinking the Trigeminal Nerve would be myelinated since it is a major nerve and not one of the "thinner axons"?
ModSupport said:That's correct there are both myelinated nerves and nonmyelinted nerves. Here's a pretty good summary. The smaller cranial nerves along with most sensory nervers (those you feel with) are nonmyelinated
http://www.mananatomy.com/basic-anatomy/myelinated-nonmyelinated-ne...
Woman with the electric teeth said:Hi Aiculsamoth, I'm not quite sure I understand what you mean by this: "Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN."
Are you saying that in a healthy person 30% of the nerve fibres are unmyelinated (I'm assuming as opposed to demyelinated)? I was under the impression that ALL nerve fibres had myelin sheaths, otherwise wouldn't people be having TN type nerve pain all the time? Can I ask where you read/heard this?
aiculsamoth said:Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
I'm sure you're asking Mod, not me, Aiculsamoth, but yes, you need a trigger for a genetic predisposition. It's usually an environmental trigger, like diet or lifestyle. Some genetic diseases, though, are foregone conclusions, no trigger required - but TN isn't one of those, I'd say.
aiculsamoth said:
Not suggesting you know the answer, if the purpose of myelination, in addition to conduction is protection, nature being pretty clever, why is central myelination not seen along the whole of the sensory root? Because it isn't, to me it would suggest more of an 'overspill' from the CNS , peripheral to central what would be is it's role? I know very little about it but regardless of genetics I understand the majority of genetic manifestations outside of birth (maybe even then) require a trigger, epigenetics or something similar?
Agreed discount EVERYTHING before drilling holes, I just don't see how peripheral to central can be affected by a central change in anatomy, and for what reason. There must be many neck manifestations of various illnesses that can could cause Tn including the likes of say anky spondylosis and more, anyone with such, HLA B27 might want to consider the tn basics tab regarding cervicogenic TN.
About 5% of TN is genetic though..... An interesting read BTW is the Koebner Phenomenon thought to trigger some arthritis. I wonder some times if TN doesn't trigger other things some have a genetic predisposition for like your joint issue
Woman with the electric teeth said:
I'm sure you're asking Mod, not me, Aiculsamoth, but yes, you need a trigger for a genetic predisposition. It's usually an environmental trigger, like diet or lifestyle. Some genetic diseases, though, are foregone conclusions, no trigger required - but TN isn't one of those, I'd say.
aiculsamoth said:Not suggesting you know the answer, if the purpose of myelination, in addition to conduction is protection, nature being pretty clever, why is central myelination not seen along the whole of the sensory root? Because it isn't, to me it would suggest more of an 'overspill' from the CNS , peripheral to central what would be is it's role? I know very little about it but regardless of genetics I understand the majority of genetic manifestations outside of birth (maybe even then) require a trigger, epigenetics or something similar?
Yes, ModS, I thought of arthritis as soon as you mentioned the autoimmune thing. And I did have a look through all the forms of EDS but could only see that unifying factor of hypermobility. Thanks for the FWIW Abnormal electrophoretic mobility tip. I'll look into that and have a more thorough look through the EDS varieties - there's certainly plenty of them!
I couldn't agree more with the relationship to MS. The fact that MS patients often get TN should be all we need to know - with a big caveat: that's correlation, not causation, as they say. Nevertheless it at least gives a springing off point. This has particular significance for me because my TN (of fourteen months standing, with no anticonvulsant able to clear it) was sent into remission by B12 shots. As B12 plays a significant part in remyelination, you will appreciate why I am personally convinced myelin problems play a causative role. And you are absolutely right, all avenues of cause should be investigated before going down the Frankenstein patched-up brain approach. Sadly, that 'incurable and degenerative' label makes a lot of doctors sloppy/lazy or defeatist - sometimes all three.
ModSupport said:
I think the answer is if you need X amount of collagen and have y and x<y the distribution won't be linear but rather short in some areas. I have an autoimmune arthritis which is a seronegative HLA B27 type which indeed needs a trigger to get going. Yet what is effected varies. This year its been in my neck and cervical area causing what at least one doc called TN (junk TN diagnoses) last year it destroyed a shoulder (I really like my new one)
There are a number of forms of EDS Tooth woman (love your name but its a long one for these old fingers to type) The hypermobility type is the hot one right now but not all EDS has joint hypermobility. There are 7 types of EDS. FWIW Abnormal electrophoretic mobility is found often times with TN and it is also present in EVERY case of Classical EDS. (Joint pain is as well)
I'm not suggesting anyone would have EDS instead of TN or that EDS is the cause. But the myelination disorders across all (including MS) is to significant in my old head to ignore. Even Dr. Casey admits to them.
BUT what if that was the cause of someone's TN shouldn't it be eliminated along with other Auotimmune disorders before drilling holes in someones head?
aiculsamoth said:Not suggesting you know the answer, if the purpose of myelination, in addition to conduction is protection, nature being pretty clever, why is central myelination not seen along the whole of the sensory root? Because it isn't, to me it would suggest more of an 'overspill' from the CNS , peripheral to central what would be is it's role? I know very little about it but regardless of genetics I understand the majority of genetic manifestations outside of birth (maybe even then) require a trigger, epigenetics or something similar?
That's a very interesting point, ModS - one I hadn't thought of. I need to go and look at some cutaway drawings of the trigeminal nerve and see how the nerves and axons play out in it. I've heard TN described as over-excitable nerves - after all that's why anti-convulsants work, because they slow down the nerve impulses (and everything else, sadly), but I've also heard the theory posited that the nerves are actually touching and short-circuiting, as it were.
Sometimes it frightens me how little we know here. Basically we don't even know what's actually happening, let alone why it's happening!
ModSupport said:
I hope I'm not being crass, but the best example I can give of why the axons could be a problem (although I agree that myelination of the bigger nerves a problem) is that if you ever see a guy who has been kicked in family jewels HARD, he grabs right below his rib cage shortly there after because THAT is where the pain goes. It travels from the smaller axons to the myelinated nerves that end up there. (in fact thats where the testes form and travel down to the scrotum shortly before or shortly after birth not that that has anything to do with anything) Our nervous system is designed to disperse strong pain. A bit different than referred pain stimulus
Woman with the electric teeth said:Well now, who knew?! Not me, obviously! I see though that they all have a neurolemmal sheath, whether they are non-myelinated or not. So maybe that could be the culprit? Aside from that though, am I not right in thinking the Trigeminal Nerve would be myelinated since it is a major nerve and not one of the "thinner axons"?
ModSupport said:That's correct there are both myelinated nerves and nonmyelinted nerves. Here's a pretty good summary. The smaller cranial nerves along with most sensory nervers (those you feel with) are nonmyelinated
http://www.mananatomy.com/basic-anatomy/myelinated-nonmyelinated-ne...
Woman with the electric teeth said:Hi Aiculsamoth, I'm not quite sure I understand what you mean by this: "Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN."
Are you saying that in a healthy person 30% of the nerve fibres are unmyelinated (I'm assuming as opposed to demyelinated)? I was under the impression that ALL nerve fibres had myelin sheaths, otherwise wouldn't people be having TN type nerve pain all the time? Can I ask where you read/heard this?
aiculsamoth said:Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
It explains electric teeth....................
Woman with the electric teeth said:
That's a very interesting point, ModS - one I hadn't thought of. I need to go and look at some cutaway drawings of the trigeminal nerve and see how the nerves and axons play out in it. I've heard TN described as over-excitable nerves - after all that's why anti-convulsants work, because they slow down the nerve impulses (and everything else, sadly), but I've also heard the theory posited that the nerves are actually touching and short-circuiting, as it were.
Sometimes it frightens me how little we know here. Basically we don't even know what's actually happening, let alone why it's happening!
ModSupport said:I hope I'm not being crass, but the best example I can give of why the axons could be a problem (although I agree that myelination of the bigger nerves a problem) is that if you ever see a guy who has been kicked in family jewels HARD, he grabs right below his rib cage shortly there after because THAT is where the pain goes. It travels from the smaller axons to the myelinated nerves that end up there. (in fact thats where the testes form and travel down to the scrotum shortly before or shortly after birth not that that has anything to do with anything) Our nervous system is designed to disperse strong pain. A bit different than referred pain stimulus
Woman with the electric teeth said:Well now, who knew?! Not me, obviously! I see though that they all have a neurolemmal sheath, whether they are non-myelinated or not. So maybe that could be the culprit? Aside from that though, am I not right in thinking the Trigeminal Nerve would be myelinated since it is a major nerve and not one of the "thinner axons"?
ModSupport said:That's correct there are both myelinated nerves and nonmyelinted nerves. Here's a pretty good summary. The smaller cranial nerves along with most sensory nervers (those you feel with) are nonmyelinated
http://www.mananatomy.com/basic-anatomy/myelinated-nonmyelinated-ne...
Woman with the electric teeth said:Hi Aiculsamoth, I'm not quite sure I understand what you mean by this: "Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN."
Are you saying that in a healthy person 30% of the nerve fibres are unmyelinated (I'm assuming as opposed to demyelinated)? I was under the impression that ALL nerve fibres had myelin sheaths, otherwise wouldn't people be having TN type nerve pain all the time? Can I ask where you read/heard this?
aiculsamoth said:Laura,
On the subject of remission I understand the compression and surely it is always there? confussion. If vascular compression is the cause, which I doubt, then the explanation is given by the respected surgeon Ken Casey in the neuropathic tides of pain video on this site (under video tab on this site), where it is stated that natural healing of the myelin sheaf (at the root entry zone? )occurs and so there is remmision, before compression then again gets the better of the healing process. This would suggest the bodies innate propensity to heal. In which case why do neuros not address this, in promoting good life style changes?
The quarter distance central myelin which occcurs along the trigeminal sensory root is often held responsible by these neuros, altered myelin function by vascular compression is the reason for remission/ cause is the stated hypothesis.
Sensory afferents of pain are from the peripheral areas i.e. face to the central nervous system for processing there is no return impulse involved. So why would a sensory afferent gain anything to be subjected to an extra bit of 'central' myelination proximally to the CNS, what is it modifying, only what is already there, and for what purpose?
Vascular compression is seen along the whole nerve root, not just the quarter that is centrally myelinated. Within the sensory nerve root some circa 30% of nerve fibres are unmyelinated, and these include pain fibres, so what is the significance of de/ myelination in TN. I haven't come up with an answer besides none. This though drives costly research into genetics and myelin. I would suggest there must be an alternative to myelin degeneration as a cause for remission/ cause, but I have yet to hear it, but I could hypothesise.
Laura said:Well why do you think it goes into remission? If there is something compressing the nerve then you would think it would always be there???
Babym12 said:What my doctor had told me is that over time it is possible that TN will go into remission. However, he also said that its no guarantee that it wouldn't come back!
My pain comes and goes. I went several months without any pain although I stayed on 300 mg of gabapentin. Then while in Europe in the cold weather, it came back and despite being on pain meds, I had pain again for 5 months. Then out of the blue, pain has gone away again. I am clueless about what causes episodes but I take those pain free days any time I can get them. I am afraid to not take my meds for fear I will get the severe pain when it was onset.
Hello Laura,
This thread gets pretty complex so please pardon me if I am missing clues here but seems to me you have not yet had MVD surgery, correct? All that I have heard from doctors is that TN almost never improves with time, almost always gets worse with time, and is not as easy to treat with MVD if you have already been through multiple other procedures prior to really getting on the operating table. I've also heard that the younger you are with the MVD surgery the better, and waiting is not a good idea. In my own case, I waited ten years. I went through over-medicating myself into oblivion and that not even touching it, to having months with no meds or symptoms, to all of a sudden screaming and in the ER, to back on the meds, and I did this rat wheel for a decade before getting the MVD. I had my MVD surgery in June of this year. I have right side TN, most of my face was affected on the right side. I was told I would likely have numbness in 50% or more of my face and it could take months to a year to subside. I came out of surgery TN free and with numbness in most of the right side of my head including my gums, tongue and sinus. It's now October. I have 25% numbness still but otherwise I am rock'n it and very glad I did the MVD surgery. I have not had any meds since my surgery was over. They wanted me to stay on the Tegretol after my surgery but I insisted on immediate transition off of all meds. Never looked back. I'm having a beer as I type this and I don't need a straw to drink it! Cheers! Nicole in VT PS: wanted to add that I did not get a plate over the hole, they sutured me back up muscle over the top of the hole without any screwed in covering and my doctor said it was a healthier way to go. I had an 8 inch incision that healed very quickly and I can't even feel a depression back there. Surgery felt like falling asleep and waking right back up, it was over faster than many other procedures I've had over the years. From my perspective there is no reason at all to work yourself up over this MVD surgery. It's a snap.
We know MS individuals have an increased risk of tn, but it does not mean it is due to demyelination, despite research which does not take into account the lifestyle of a MS patient and associated factors, MS patients whilst having a larger incidence of TN it is still rather small compared to the general population which could be a factor of any number of reasons. Unless of course there is research to the contrary.