With TN it is hard to know what causes it to go into remission but it is in no way unusual. I don't know if the meds slow healing, I do know some meds can cause rebound pain. Also each of us responds differently. I have meet many who are using only natural methods that have for TN and if the meds are to harsh for you it maybe an option for you.
Hi Laura, I had TN surgery in 2009 and was told to take Neurotin to help control the pain, i was taking 3600mg. a day, plus i was taking Tegretol 600mg. a day, Topamax 50mg at bed time, Fiorset 40mg twice a day, but i still was in pain.Then finally my pain left, after about 2 months. Then in 2012 everything came back and i was operated on again and after that operation i was still taking the same medication for pain for about 6 months, then my Dr. ask me to try BOTOX shots, and i said YES, i'll try anything to relieve the pain, and that was the best thing i ever did cause i haven't had any pain since. I wish you the best of luck Laura!!
Sorry, Aiculsamoth, I don't know what the REZ is, and Dr Google was no help there!, so I can't comment on that, but the myelin sheath would make a difference simply because if it's meant to be there and it isn't, then trouble ensues, as MS proves. I assume, because the explanation is given all the time, that myelin sheath is present on the trigeminal nerve and so its absence is an issue. It acts just like insulation on a cable so you can see why its absence could potentially be so traumatic.
I can't see that the interior of the nerve root would be the same, if the myelin sheath was damaged. Looking at it in the most basic way, no part of the human body remains the same, in either its performance or the results of its performance, if you damage part of it. Think of it with very basic things like cutting your finger. As soon as that breach is made lots of things change, from pain sensors, to skin irritation, to healing, which creates its own changes independently. Likewise, if you take away the gallbladder, for example, although we can all "do without it", as doctors love to say, in reality it changes everything, If you've lost your gallbladder you'll find that out quite quickly - adaptation or no. So, at its most basic, with no more information than that, we can surmise that loss of myelin is, at some level, catastrophic. It could be because myelin is doing more than neurologists currently realise. After all, they only just discovered that there was a blood network in the brain they knew absolutely nothing about!
P.S. Yes, the incidence of TN in MS is significant, much higher than in the ordinary public.
aiculsamoth said:
wwtet,I realise MS is a major demylinating disease, but my question which remains unanswered is why a little bit of myelin sheaf towards the REZ affects, if at all, sensory pain input from the face, bearing in mind we have changed epineurium to myelinin over approx. 3mm, for what reason? Nerve impulses aren't coming back in the same direction The interior of the nerve root remains the same, mylinated/ unmylinated nerves, I would have to say at this point it means little. Is the incidence of TN in MS individuals significant? with the electric teeth said:
Well, Aiculsamoth, MS is a 'straightforward' demyelinating disease, as in that's the major cause/result of the condition. The fact that TN does occur with it gives it at least a strong correlating link, since TN only occurs with two conditions that I know of: MS and shingles, also a nerve aggravating/destroying disease. Interestingly, I've never looked shingles up to see if any demyelination is thought to occur there. If it did, that would certainly strengthen the correlation. Actually, it would be a very interesting thing to do, to compare those two diseases and see if they have any common bonds - maybe if there were any it would give a clue to what causes TN.
aiculsamoth said: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.
Thanks for the info on Raxatrigine, Janet - that's very good to know. And I sympathise with being hypersensitive to anti-convulsants - I've got a list as long as my arm of serious side effects, none of which are giving up even although I am now down to only 100mg of Carbamazepine a day!
Janet McGee said:
I do not have TN, but my daughter did. She died from acute toxicity of medications prescribed to mediate the pain of trigeminal neuropathy. Emily was something of a known quantity in the TN community, as she was one of the founding members of the Young Patients Committee of the National Facial Pain Association (TNA). Many groups have done me a great kindness by inviting me to participate. At first, I participated to honor my daughter. Now, I do it because I feel there is a great need.
Laura, I have taken anti-seizure meds, not for seizures, but for other issues. I still take Klonapen for anxiety, although I have been told that I may not take benzodiazapenes (Depakote, Klonapen, Ativan, etc.) for the long term. For a short period, I was given Gabapentin to control the panic attacks that woke me every morning, because I did not know if Emily was going to have a seizure that day. After she died, the panic attacks went into remission for about 8 weeks. Then they returned, because I knew I was waking to face another day of grieving. At 1800 mg of Gabapentin, I had relief from panic attacks, but I also had allergic reactions. My face looked red and blotchy; it looked like I had some sort of food allergy. Although Gabapentin is sometimes prescribed to relieve tinnitus (ringing in the ears), I had a paradoxical reaction of getting tinnitus from Gabapentin. I will spare you the details of other reactions. I tried working down to a dose that I could tolerate that might give me some relief from the panic attacks. There was no such dose. I just had to wean myself off of Gabapentin.
I seem to be a walking text book of adverse drug reactions, and your story so strikes a chord with me. I have had adverse reactions to every SSRI that was ever prescribed to me for depression. I lost 15 pounds while taking Celexa, but it is not a diet plan I could recommend. I also had an adverse reaction to Cymbalta (more ear-ringing). My psychiatrist asked me if Cymbalta had improved my mood. Thank goodness for her sense of humor! I said, "How could I tell, with all that ear-ringing going on?" She laughed, which just proves that she is a rare psychiatrist, indeed. How many psychiatrists do you know who have a good sense of humor? Because I had that adverse reaction to Cymbalta, I am presumed to be a poor candidate for Effexor (amitriptyline). I'm not sure I would even dare try it!
I don't even want to think about what trazodone did to me. It was not pretty. It landed me in the ER three days after I quit taking it, and I hadn't even worked up to a beginning adult dose. Are you beginning to get a picture here? I'm a tough patient to medicate. Whenever I get sick, the person I feel the worst for is my doctor, because I know she has a hard job in front of her.
I do know that no two people respond the same way to the same drug that affects the central nervous system (CNS). Since TN is such a rare disease, until recently, no drug was developed to target TN, specifically. People who have TN have had to "make do" with medications that were found to provide pain relief when they were prescribed for other ailments, like seizures.
Do the drugs prescribed for TN inhibit natural reparations? I do not know that anyone has researched the question. Since anti-seizure meds and opiates are all metabolized in the liver, and some fatty substances are manufactured in the liver, it could be that the medications interfere with the body's own attempts to generate the fatty substances that, in part, protect the trigeminal nerve bundle. But, I cannot say that with any degree of certainty. It's a question in need of research.
The research into that particular question, however, may be eclisped by research into Drug #802, with the preliminary name of Raxatrigine. Raxatrigine was developed specifically for the treatment of TN and has undergone rigorous trials in Europe, where initial findings are promising. It addresses the pain of TN without causing dizziness or memory lapses and has shown no damage to the heart or liver. The FDA has only recently given approval to Dr. Joanna Zakrzewska to conduct trials in the U.S. for Drug #802. I will get her e-mail address for anyone interested in participating in U.S. trials.
TN stinks. The drugs used to treat it stink. The surgical options carry their own risks. Raxatrigine is the first medication developed specifically for the treatment of TN. I will dig up that e-mail address, which I thought I had. Back to the drawing board!
Hello Laura - were you under the supervision of a doctor to stop all drugs "cold turkey?" To me, that would through you into a seizure & you should never increase or decrease your dosages of meds without your doctor!! Who told you to do this? I like the idea that our bodies could repair themselves without the meds. Have you asked Red Lawhern this question. He is extremely knowledgeable about TN. I sure would like to be out of pain for 4 months though. Let us know what happens! Nancy
Why does damage to myelin in the middle affect the opposite end input?
Basically, it doesn’t. The sensory end is unchanged.
Think of an electric cord. The plug is the sensory end. Now strip the cord of its plastic and insulation down to bare wires and throw it in the bathtub. The plug isn’t doing anything. The insulation is gone and allows the transmission of the electric to be short circuited. Our our bodies only know where that nerve ends so all of the extra transmission is determined to be pain from the end. …not the middle.
Thanks, Lee - a good analogy. But it does throw open the possibility that the actual problem may be occurring somewhere else on the nerve other than where we think, or for other reasons. It would be ironic, but not surprising, if the compressions, per se, had little to do with TN and were merely red herrings. It would also account for the variable responses of people to MVD ops and why many healthy corpses (an oxymoron!) have compressions but no history of TN.
LeeS773 said:
Why does damage to myelin in the middle affect the opposite end input?
Basically, it doesn't. The sensory end is unchanged.
Think of an electric cord. The plug is the sensory end. Now strip the cord of its plastic and insulation down to bare wires and throw it in the bathtub. The plug isn't doing anything. The insulation is gone and allows the transmission of the electric to be short circuited. Our our bodies only know where that nerve ends so all of the extra transmission is determined to be pain from the end. ....not the middle.
Exactly!
The REZ , is the root entry zone, the area where the Trigeminal nerve enters the pons, it is this quarter of the nerve that is myelinated, the other three quarters is not myelinated. Blood vessel contact occurs anywhere along the nerve root ie including the unmyelinated portion. Thirty percentish of the nerve fibres within the root are unmyelinated. Pretty sure this is correct, so my question was essentially how is erosion of myelin the issue in TN or it's remission, like the neuros state?
As far as, the theory of blood vessel, brain sagging with age as an issue I am sure I have read this is very unlikely in that we would expect a far higher incidence of TN than we see in an aging population it also doesn't address remission in younger folk
That's a good point, Aiculsamoth, but if you look at my post above, answering Lee, you'll see that the blood vessel contact may not be the issue, if that's not what's actually causing the problem. The compression theory is really still a theory, despite them lifting compressions in the MVD operation. As I said to Lee, the problem may actually be occurring elsewhere, or for another reason, and the compression may be a red herring. So the myelin sheath could still be playing a role, either directly (for example any damage on the sheath, even if it's not where the compression is, allows the nerves to touch and 'short-circuit') or indirectly, as in it is performing a function of which we are not aware and therefore damage to it anywhere along the nerve makes the nerve misbehave. Perhaps it's the combination of compression, myelin damage and something else, mystery ingredient X, that makes TN occur.
I agree absolutely that the 'ageing causing sagging' thoery seems unlikely. That said, what ModSupport said earlier seems more likely, that it is a collagen issue. So yes, 'sagging', as you would get in ageing, but also it could occur in young people. It's also worth remembering that ageing is actually not entirely to do with physical age, but to do with cell damage. So perhaps TN sufferers have all experienced unusual levels of cell damage (or a specific type of cell damage), or their repair mechanisms are not working correctly.
If it helps, from my own personal experience, my body was getting no fat for around three years. I believe this did two things: it greatly impaired brain regeneration, as it needs a great deal of fat to function correctly, and it also caused a chronic B12 shortage (and doubtless other nutritionally influential problems). I believe those two things 'triggered' my TN. So you can see how individual 'ageing' factors might cause problems although, as in my case, I wasn't, say 70, certain aspects of my body kind of were!
aiculsamoth said:
The REZ , is the root entry zone, the area where the Trigeminal nerve enters the pons, it is this quarter of the nerve that is myelinated, the other three quarters is not myelinated. Blood vessel contact occurs anywhere along the nerve root ie including the unmyelinated portion. Thirty percentish of the nerve fibres within the root are unmyelinated. Pretty sure this is correct, so my question was essentially how is erosion of myelin the issue in TN or it's remission, like the neuros state?
As far as, the theory of blood vessel, brain sagging with age as an issue I am sure I have read this is very unlikely in that we would expect a far higher incidence of TN than we see in an aging population it also doesn't address remission in younger folk
Galli,
I, for one appreciate your humor. It has also occurred to me that my age-clock only goes forward. It's not all bad; there are some decades I would rather not repeat!
At TNA's National Conference, one of the speakers did say that, in inherited TN, the elastin in blood vessels decreases and they begin to sag. Then, just as you described, one of the vessels compresses against the trigeminal nerve, causing an indentation in the nerve structure where it becomes demyelinated. You called it!
Janet
galli said:
What about something as simple as gravity-I look in the mirror and it appears that my face is sliding off. OK not really-but there are sure jowels around my chin that were not there 35 yrs ago. So a blood vessal sags a little with age and a little gravity and is now sitting on my trigeminal nerve. As my heart beats in a regular fashion it irritates the protective coating and I am in pain. Big time pain. As I continue to age ( we never get younger, do we) the blood vessal continues to sag a tiny bit more. Just enough that it is no longer sitting on the nerve but has slid off a bit.
There is a lot of nerve surface to travel and a lot of blood beating through those vessals. The tiniest movement of one or the other along the paths can cause new compressions and resolve others, allowing the cycle to continue or go into remission for awhile, or not. Very over simplified, but you get the general idea. At 67, everything else is sagging, why not a blood vessel. We are talking about a very tiny amount to make a big difference, not the huge amounts that have seemed to have taken over much of my body. Ever try jogging with your head exploding in pain.
I am not making light of anyone's pain. I am bilateral for over 15 yrs. You have my greatest empathy as we travel this very rough road. I thought a touch of humor directed at myself, would not hurt and may make someone smile. Prayers and love to each of you as we go through this.
Age-related vessel sagging occurs in inherited cases of TN, so no, there is a limited occurrence of this rare disease in the general population. The gene that triggers TN occurs in only about 5% of cases, so that inheritance is only a small part of the picture. Aiculsamoth, did you mean to say that blood vessel sagging does not address the "occurrence," rather than "remission" of TN in younger patients?
aiculsamoth said:
The REZ , is the root entry zone, the area where the Trigeminal nerve enters the pons, it is this quarter of the nerve that is myelinated, the other three quarters is not myelinated. Blood vessel contact occurs anywhere along the nerve root ie including the unmyelinated portion. Thirty percentish of the nerve fibres within the root are unmyelinated. Pretty sure this is correct, so my question was essentially how is erosion of myelin the issue in TN or it's remission, like the neuros state?
As far as, the theory of blood vessel, brain sagging with age as an issue I am sure I have read this is very unlikely in that we would expect a far higher incidence of TN than we see in an aging population it also doesn't address remission in younger folk
That doesn't eliminate collagen disorders...... Anybody have varicose veins? or veins "showing" Its the same thing........ Sometimes age related sometimes not.
Janet
Both given the one post that initially introduced the idea. I have no knowledge of the genetics of TN, what gene are you referring to when you mention the 5%?
Woman with the electric teeth, interesting " It would be ironic, but not surprising, if the compressions, per se, had little to do with TN and were merely red herrings. It would also account for the variable responses of people to MVD ops and why many healthy corpses (an oxymoron!) have compressions but no history of TN." Sounds like the possible basis for a John Grisham novel.
After some research;
Jennetta states- "The vascular compression theory of TN proposes that compression of or proximal to the central-peripheral myelin transitional of the trigeminal nerve by a vessel is the central cause of TN", yet he states compression occurs along the whole of the nerve root as a cause, would appear the neuros are as confused as I am.
Peker S and co conclude " If trigeminal neuralgia is caused exclusively by vascular compression of the central myelin, the problem vessel would always have to be located in this region. However, it is well known that pain from trigeminal neuralgia can resolve after vascular decompression at more distal sites. This suggests that the effects of surgical decompression are caused by another mechanism." http://www.ncbi.nlm.nih.gov/pubmed/16883175
Ariai and others.. "Facial pain outcomes after MVD in patients with suspected MS-related TN are poor compared with outcomes for patients with idiopathic TN. This study provides further support that many patients with MS-related TN have pain that is centrally mediated, reducing the effectiveness of procedures performed on the trigeminal root, ganglion, or divisions." http://www.ncbi.nlm.nih.gov/pubmed/24056218
Yes, that sounds about like how it has gone for me. The medications (Tegretol, tramadol, cyclobenzaprine) work to make the pain disappear, but the Tegretol interferes with my ability to walk, and all three of them together make me have a hangover 24/7. Since I live alone, I really need to be able to think and to get around, so when I can't stand the medicine any more I stop the Tegretol and the cyclobenzaprine (I take the tramadol to sleep). It is just like you said - I have relatively no pain for months, and then it slowly starts to increase again. It increases to the point where I have to start the regimen again. My neurologist has told me to keep taking the Tegretol regardless, but I just can't, I just can't. However, as you well know, the pain wins every time.
XOXOXOXO, Pat
Hello, Pat,
I'm so sorry that you have to endure those side effects. As I live alone, I can well appreciate how difficult it must be for you. It would be scary to feel wobbly on my feet. Best of luck to you. I hope that the researchers come up with a medication that you will be able to tolerate.
Janet
I was not referring to a specific gene. I was referring to Page 25 of Striking Back. On that page, Dr. Jannetta said that he estimated that 5% or more of TN patients had a family history of the disease. He further stated that TN starts in younger ages in succeeding generations. Moreover, bilateral TN seems to be more common in patients having a family history of TN. No gene was specified.
aiculsamoth said:
Janet
Both given the one post that initially introduced the idea. I have no knowledge of the genetics of TN, what gene are you referring to when you mention the 5%?
Thanks Janet,
Like I said I am unaware of the genetics/ genetics full stop. Thank you for taking your time to respond.
No problem! When the Facial Pain Research Foundation announced their research projects involving the genetics angle, the Facial Pain Quarterly simply mentioned the 5% figure. I can always take a peek at the Research Foundation's Facebook page to see if they've gotten down to specifics in the information posted there. I highly recommend that you visit their page, as well. They're doing fantastic work.
I've been maintaining my membership in the National Facial Pain Association since Emily's death. They're fighting a worthy cause, and I'm glad to be helping out. I also find their publications and monthly "TNA Newswires" that come via e-mail to be very informative.
Janet