Questions I have after reading article on Something New in Myelin Research

General General TN & GPN (Old Site)
1

Hello All,

First of all, I am a science idiot, meaning that it is not an easy subject for me. So, please be gentle with me :) I read the article mentioned in the subject line because I was excited about any progress for MS, as I have a daughter with MS. I immediately sent her the article. She found it interesting as well and could understand it better than I could because she is an RN (currently on disability).

On my journey to find out what was causing my facial pain, I was tested for MS (brain imaging and spinal tap). After the testing, I was told that I did not have MS. I was found to have only one brain lesion and one Oligoclonal band. At the time I was told that normal was not to have any Oligoclonal bands. So I questioned why I had one. I was just brushed off and told not to worry about it.

Now, with the understanding that TN involves the Myelin Sheath, I am starting to wonder if there is anything to the one band. I generally don't consider myself to have typical TN but I do have periods of what feels like lightening strikes in my face. I just have the other type of pain more often.

In addition, I do have what is called Connective Tissue Disease, which is an auto-immune disorder. In addition to having a daughter with MS, I also have a daughter with Lupus and a niece with Lupus.

So, if anyone understands this question, I'm not even sure it makes sense, please help me understand :)

Thanks to all of you,

Cathy In MD

2

Cathy, a Wikipedia article on monoclonal bands includes the following statement concerning their significance:

"The presence of one band (a monoclonal band) may be considered serious, such as lymphoproliferative disease, or may simply be normal—it must be interpreted in the context of each specific patient. More bands may reflect the presence of a disease. The bands tend to disappear from the cerebrospinal fluid as a person recovers from the neurological disease."

Likewise, "connective tissue disease" is not a single medical entity. It's a class of nearly 200 disorders that may include Ehlers-Danlos syndrome (EDS), Epidermolysis bullosa (EB), Marfan syndrome, Osteogenesis imperfecta, and several others. See the following for authoritative discussion:

http://www.webmd.com/a-to-z-guides/connective-tissue-disease

Go in Peace and Power

Red

3

I can't answer your question, but with regards to TN and the myelin sheath, considering many patients after microvascular compression gain almost immediate relief, I can't see how the myelin is a component of the issue, it doesn't rebuild over night

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Moth: Myelin doesn't rebuild quickly, but removal of the stimulus of a vascular pulse on a section of damaged myelin compressed by an artery or vein seems to produce almost instantaneous relief in the majority of patients who undergo MVD. Others experience relief over a period of weeks to perhaps as long as a year. Peter Janetta's papers demonstrated a better than 90% success rate in a consecutive series of over 1200 patients with typical TN symptoms. Other surgeons have reported lower rates of success when pain is of a more mixed nature, with neuropathic components. It would appear that the neuropathic (atypical TN) components result from a different mechanism or a different type of damage to both the myelin layer and deeper fibers in the nerve.

Regards,

5

Red,

Between you and myself, I stand to seem argumentative, it is not my intention but I am trying to reach a level of understanding. Burchiel states a theory of minimal compression and demyelination, so removal of compression, if myelin was also responsible it wouldn't mean near immediate cessation of symptoms, after all MS shows symptoms of demyelination without compression,and I'm not talking TN due to MS.

Not looking to hijack, Cathy in MD's post. I accept aypical TN has symptomatic element of neuropathic pain, but according to classification neuropathic TN has a defined cause.

K Burchiel states atypical, TN2 to be a continuation of TN1, so considering TN to be progressive why is the medical profession not advocating MVD for all, after all at circa $25000 dollars it would seem to be quite a cash cow. It would seem to me that tn2 if a progression of TN1 would be a more severe compression, with a less likely hood of MVD success due to a more severe compression, even so why leave the compression, with the patient at a loss. The fact that MVD is treating atypical, although at smaller rate of success, would suggest the medical profession is accepting Burchiels concept of continuation. So why not MVD every TNer, it would seem the medical profession has it's doubts as the aetiology of TN.

6

Moth,
I accept that you're not trying to be argumentative just to be argumentative. We all learn in different ways, and the Socratic method is alive and well.

I've talked with Dr. Kim Burchiel from time to time in TNA Conferences. He also provided external professional validation of my re-write of the TN Fact Sheet at the US National Institutes for Neurological Disorder and Stroke, a couple of years ago. He developed his classification terminology for TN in part out of dissatisfaction with the use of the term "pre-trigeminal neuralgia" as a replacement for "atypical trigeminal neuralgia". It's fairly common to see TN-2 emerge before TN-1, or to see low-grade neurological symptoms like parasthesia and numbness as a precursor to either one or both. So I think it would be fair to note that many practitioners believe that either form of TN can "progress" into the other.

In some patients, some of the time, both patterns of pain might be expressions of some central nervous system sensitization process. But it's clear that while some elements seem to be shared between the two patterns, other elements aren't as much so. Vascular compression near the brain stem is clearly the primary mechanism in typical TN (TN-1), and decompression is clearly the most successful avenue of treatment for long-term medication-free pain relief. The same cannot be said of atypical TN (TN-2) or trigeminal neuropathic pain. While some cases of TN-2 can be attributed to discrete trauma (particularly dental procedures and direct administration of anesthetic into the Lingual nerve), it isn't always clear that neuropathic pain has a discrete and attributable cause.

So yes, there is still ambiguity on both the aetiology of TN-1 in its original presentation, and the mechanisms by which it recurs or transforms into TN-2 or neuropathic pain of a less defined or attributable nature.

There is also a sort of logic for delaying the use of MVD: When done in young people, there is on the order of a 30 to 50% chance of pain recurrence down stream after 12 to 15 years or more. So doctors recommend managing pain medically until it appears that pain is becoming resistant to meds -- and only THEN doing an MVD.

However, Peter Janetta once told me that if TN-1 persists and is not well controlled for about nine years, then he has seen lowered probability of good outcomes from MVD. That figure once appeared in "Striking Back -- The Trigeminal Neuralgia Handbook" by Ken Casey. I'm not sure if it's in the current edition.

Nobody is particularly satisfied with making a decision for or against surgery on the basis of "professional opinion". But that is rather often what occurs, unless patients absolutely demand that MVD be performed. Even then, quite a lot of neurosurgeons are uncomfortable with invading the skull space unless all other viable medical alternatives have been attempted.

FYI, in the US, the cost of MVD is more on the order of $125,000 dollars rather than $25,000.

While we are here: I also corresponded with a neurosurgeon whom I've known for over 15 years who has long treated TN patients. I won't reveal his name because I don't have his permission to do so. However, with a couple of minor editing clean-ups of his short-hand notes, here is what he had to say:

============

Well [there is] a bit of confusion over [whiplash versus TN].

1) Some 25% of TN patients of all types, report trauma within six months of onset of pain (all trauma, including that of procedures, surgeries, as well as MVA, falls,etc.)

2) There is a cervical nexus,wherein the C2,C3 lamina Rexed layers overlie the descending trigeminal nucleus. So excessive activity in the nucleus oxalis specially, can produce neck pain in the region of the often mis-diagnosed occipital nerve. This is why so many people report symptoms in the back of the head, and after a failed block, stimulator, nerve resection or whatnot, still have pain. The blocks do nothing to aid the therapeutic possibilities, but they do generate money for the doctors.

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If there is a bottom line in all of this discussion thread, it may be that both TN patients AND their doctors deal with ambiguities of understanding in the fundamental mechanisms involved in both emergence of TN and its treatments. Even the terminology is squishy at times. So sometimes -- no matter how much we want a definitive answer or treatment or cure for a truly horrific medical disorder -- the final answers just aren't obvious to the best practitioners in the field. OR to patients themselves. So we all do the best we can, and sometimes we grope in the dark.


Go in Peace and Power

Red Lawhern, Ph.D.

Moderator and Resident Research Analyst

Living With TN

7

Thanks for the responses,

I just want to say that I would not even give MVD any consideration. I have read about too many people that have had it done after dental injury, only to find themselves in a worse state than they were in before they had the surgery. That's just my take from where I'm standing.

Red, my diagnosis is actually Undifferentiated Connective Tissue Disease, which I realize doesn't tell you much more. My blood test - the ANA, tested positive for Lupus and RA but I did not have all of the proteins to be diagnosed with either according to my doctor. Unfortunately, the doctor doesn't explain very much and doesn't answer questions either. She just told me that I was "Lupus like". I have decided to get a second opinion; I have an appointment in December. I feel that I really need to because my joints are progressively getting worse. I was just interested in the myelin part when I read about it and remembered having all the tests done. I actually have copies of all of those reports so I will just take them with me.

Thank you for allowing me to go off-topic, well sort of anyway. I find medical information to be confusing and appreciate how well you explain things.

Cathy In MD

8

Cathy, I'm glad to hear you are getting a second opinion. "Undifferentiated Connective Tissue Disease" has the flavor of a place-holder rather than any concrete or actionable diagnosis. That said, however, I'm sure you are aware that most of the treatments in this class of genetic disorders address primarily symptoms.

For others: each patient must reach their own conclusions concerning whether MVD is an appropriate procedure. If your symptoms are dominated by primarily typical TN with its volleys of electric-shock stabs, then the weight of medical evidence is toward MVD as a solution unless for some other reason (perhaps a history of stroke or heart problems) you aren't considered to be a good candidate. When TN-1 emerges after a dental injury or blunt force trauma, the picture is more complicated and you might not get full relief of symptoms from either MVD or RF Rhizotomy. The trend in neurosurgery practice seems to be away from destructive procedures which create a deliberate lesion on the nerve to block pain, and toward use of surgically implanted peripheral nerve stimulators.

Regards all,

Red

9

Red,

After speaking to your neurosurgeon, what is the confusion you mention, over whiplash and TN or any trauma for that matter?

No. 2 makes very little sense, can you give your take on no.2 and what the surgeon said? Is he talking occipital nerve blocks or cervical nerve blocks?

I am assuming you put the questions to him. I would, in the light of this thread, would have liked you to have asked him his opinion on cervicogenic trigeminal neuralgia. Due to your reply I assume you didn't.

Regards,

Moth

10

The question as I posed to the doctor is as follows:

We're having a protracted member discussion on Living With TN concerning TN being possibly caused by cervical dysfunction in the neck. Literature has been quoted as indicating that about 25% of all cases of TN emerge after whiplash injury. Is that accurate? And do you see a plausible basis for proposing that nerve damage in the cervical spine can cause chronic face pain -- or that treating it with nerve blocks can manage chronic face pain? If you could send a definitive reference or your own thoughts, that may be helpful.

===============

My reading is indeed that the doctor was referring to occipital and cervical nerve blocks, which he considers ineffective for TN. He also indicates that it is inaccurate to say that whiplash injury to the spine is implicated in 25% of cases of TN, given that many different forms of trauma that contribute to the figure. Some cases doubtless begin with whiplash alone. But not as high a proportion as 25%.

If I'm reading him correctly, the physiology is such that pain in the neck may be related to TN rather than to cervical dysfunction itself. The roots of the 5th cranial nerve do overlap the upper cervical region in C2-C3 in what is called the nucleus oralis [there was a misspelling in his text -- doctors do that too, sometimes]. So over-activity in the trigeminal nerve can be felt as pain in the neck.

Regards, Red

11

Red, thank you for your response, I didn't say the literature said whiplash was responsible for 25% of TN, that trauma was, probably quoting your said neurosurgeon.

So TN can cause neck pain but not the other way round, although the physiology would be the same, why would that be? Your DR accordingly doesn't answer the question "do you see a plausible basis for proposing that nerve damage in the cervical spine can cause chronic face pain"

Hen's teeth spring to mind.

Thank you for your time and effort, as you said we may as draw a line under the discussion of neck related TN. Everyone seems to be ambiguous without mentioning the possibility,as though we can't say it. I could put my cynic hat on, but feel it inappropriate in the forum setting.

I find it extremely sad given the impact of TN on individuals, their finances, relationships etc. I have no vested interest financially, I have spent considerable time over the last 6 months, 7000+ abstracts in addition to further reading. The evidence is there to include it as a differential diagnosis.

Red, with all due respect to your considerable efforts, whilst I realise your field, (this is not meant to be a criticism, but for want of a better word a direction,which I am sure sounds some what..well?) when addressing the issue of facial pain, which you have over some twenty plus years, listening to patient narrative which bearing in mind the forum, you have more opportunity than most, is paramount. I feel many involved with the treatment of TN, fixated by MVD and as such there is no need to investigate alternatives. There are surgeons who state MVC can't be the full picture. I also feel that consideration of the anatomy of the trigeminal complex is paramount. If neuros listened to the patient as opposed to concentrating on the patient's symptoms, on the basis of headache classification by the International Headache society many presently diagnosed with TN1 or 2 would not have been.

I appreciate you time and effort in your responses

Sincerely