It's odd you should say that, Mama. I've often thought the opposite - that some day someone will hit on exactly what causes TN, and it will be something so blindingly obvious future generations will be completely disbelieving that we missed it!
mamaof2 said:
Thanks for everyone's input on this topic. As someone above mentioned I too wonder what causes the excruciating pain and then just stops suddenly? Everything about this disease is so confusing that we might not ever understand it all.
Hi Ksimager. Your dad's history really sounds like it might have stemmed form an injury of some sort, doesn't it? Getting it so young, before any brain deterioration could have occurred, really makes me think of trauma of some sort....
ksimager said:
My dad developed TN in high school, so 50+ years ago, but wasn't diagnosed until his 30s. He has had off an on flair ups for for the whole time, and I think they have increased with age. Tegratol is the only medicine that works; his docs check his liver enzymes regularly. He says he has not figured out any specific triggers, including stress. I know he has been able to get off the Tegratol numerous times, but goes back on it at the first sign of tingling. A major flair up last fall had him going in for his second balloon compression in December. The surgeon said the surgery "failed" due to unexpected swelling, but amazingly a couple of days after surgery, his pain went away and hasn't returned.
Hi GP, I see you are another B12 success story. B12 injections sent my TN into remission. I am currently trying (very slowly!) to get off Tegretol completely. I am now down to only 300mg a day and the B12 is still coping, but it's getting a little 'sensitive' now. However, I am still hopeful I might make it!
GP said:
Amazing how everyone is so different... My TN started in 2004; came with Winter and disappeared with Summer for 6 years.
I used Tegretol at different amounts, depending on the pain levels. Then the 7th year it did not come at all. The next four years it came on and off Summer & Winter, whenever it felt like it; but cold always made it worse.... Last year I was on Tegretol most of the year, sometime 800mg/day for months. Any higher I get drug induced Lupus. But I had also started taking B12 1000mg/day and it really did help; as it built up the pain lessened.
Then in December I starting sniffing some essential (anfi-inflam) oils, when the pain started - it seemed to relax me, so I did not tighten up the face muscles and it get worse... I have lost about 7kg in weight (now 60kg) - have been trying to do this for several years, but with the Tegretol and eating to have something on my stomach before taking tablets did not help me lose weight.
We got 3 very hot days in February and it just went away... you can feel the relief when it does.
I still take my B12 1000mg but now 3 times a week ... TN has not returned and we are in mid Winter and its a cold one too. I am keeping warm, using my hot water bottle, staying out of the cold winds, etc
I am sooo delighted and hope its not just a passing whim and comes back next month, next year or so...
One can hope!! But I have all my energy as I do not have to take the tegretol and I am enjoying it & hoping it lasts...
I still get little twinges, (both sides of face & on my nose) but they do not become a full attack..... wonderful..
It is like the nerve is now not touching the blood vessel...
I too have had some very stressful times, but TN I cannot associate with these stressful times...
But I do keep very busy and I am good at blocking out the pain, because I have other things to do and concentrate on them. My neurologist said when you can concentrate on something, your brain can actually block out other things like pain... that is how I have been able to manage it. But I do admit that I know from past experiences that I do have a very high pain threshold, which can help.
Regards
In Type I (really, Stage 1) TN, remissions are to be expected. It is believed that remissions occur when the body is able to repair the lost myelin sheathing. It is now believed that glial cells are responsible for the production and distribution of lost myelin.
Hi Janet. Why do you say "really stage 1" when you refer to TN1? Do you believe it becomes or moves onto something else? Also, I was curious about what you said about remissions being repair to myelin. There doesn't seem to be any surety at all that the myelin sheath is even damaged in TN, or that a myelin sheath problem is what causes TN in the first place. My doc certainly doesn't believe in it! Could you tell me where you read this; I would be most interested to read it.
Thanks, Chancery
Janet McGee said:
In Type I (really, Stage 1) TN, remissions are to be expected. It is believed that remissions occur when the body is able to repair the lost myelin sheathing. It is now believed that glial cells are responsible for the production and distribution of lost myelin.
Hi again, Janet. Just got this reply from you, but there's nothing in it! Has it eaten your answer or did you hit reply too soon? (Done that one myself!) Hoping to hear from you....
Janet McGee said:
I was asked to comment on remissions for TN. In all candor, I don't think anybody knows with confidence what causes remissions -- any more than we know what causes many cases of TN itself. Some cases appear to be associated with blunt force trauma to the face, whiplash injury in car accidents, or anesthesia mis-administered during dental work. But a lot of cases are called "ideopathic" because the pain emerges "of itself", for no apparent external cause.
Similarly, some people associate remissions with particular treatments they've undergone or conducted themselves. B12 shots or pills are often discussed, though there doesn't appear to be any consistent medical evidence for B12 in the literature. People report that stress sometimes caused them breakthrough pain, and reduction of stress seems to help with whatever else they are doing to manage pain. Some people get long remissions after chiropractic treatment or a course of acupuncture. But whether either technique actually 'causes' remissions, is quite a different and less certain matter. The pain relief obtained after MVD or peripheral surgery like Rhizotomy isn't really a "remission" as much as a longer-term correction of nerve compression or introduction of a controlled nerve scar (lesion) that interrupts the pain.
My two Red cents for whatever they're worth.
Regards
Red, you mentioned the issue of anesthesia during dental procedure. Got a question --- just asking your opinion. When my TN started it started directly in the tooth I had had a root canal on. The extreme stabs of pain and lightning strikes eventually proceeded to a crawling like on the roof of the mouth. BUT....that root canal was done 4 or 5 years or so before the TN started. Back then I thought about the root canal but discounted it because of the 4 or 5 years that had passed. What's your 2 Red cents? :)
Richard A. "Red" Lawhern said:
I was asked to comment on remissions for TN. In all candor, I don't think anybody knows with confidence what causes remissions -- any more than we know what causes many cases of TN itself. Some cases appear to be associated with blunt force trauma to the face, whiplash injury in car accidents, or anesthesia mis-administered during dental work. But a lot of cases are called "ideopathic" because the pain emerges "of itself", for no apparent external cause.
Similarly, some people associate remissions with particular treatments they've undergone or conducted themselves. B12 shots or pills are often discussed, though there doesn't appear to be any consistent medical evidence for B12 in the literature. People report that stress sometimes caused them breakthrough pain, and reduction of stress seems to help with whatever else they are doing to manage pain. Some people get long remissions after chiropractic treatment or a course of acupuncture. But whether either technique actually 'causes' remissions, is quite a different and less certain matter. The pain relief obtained after MVD or peripheral surgery like Rhizotomy isn't really a "remission" as much as a longer-term correction of nerve compression or introduction of a controlled nerve scar (lesion) that interrupts the pain.
My two Red cents for whatever they're worth.
Regards
TN is unfortunately, progressive. It seems that it may start out with intermittent flare-ups with periods of remission. This has typically been labeled Type 1 TN. The flare-ups may increase in frequency. When they are accompanied by a 24/7 burning sensation, Type 1 has morphed into Type 2. At the 2013 National Pain Association Regional Conference in Richmond, a couple of the presenters said that it was no longer thought correct to refer to Types 1 and 2, that Type 2 seems to be a disease progression. I'll have to check back through recent issues of the Facial Pain Quarterly, in which Jeffrey Brown, M.D., proposed new nomenclature in sorting the different types of TN. In trigeminal neuropathy, for example, a portion of the trigeminal nerve is demyelinated, either through pressures exerted during a facial surgery, or as a result of a traumatic brain injury. It is a form of TN that progresses -- worsens -- rapidly. This is what I observed with my daughter following her corneal transplant, when her eye tried very hard to perforate. I believe it was in the Winter, January 14 issue of the Facial Pain Quarterly that the National Facial Pain Association Research Foundation announced a new initiative to investigate applications of nano pharmaceuticals to target the glial cells in generating new myelin sheathing. In Fall, 2011, National Geographic Magazine ran a special issue. It had a catchy title like, "The Dark Matter of the Brain: Glial Cells." Neuroscientists at that time were just learning that there are 5 different types of glial cells, and that each plays a different role in the development and maintenance of the nervous system and the brain. Until recently, the glial tissue was thought just to be the "glue" that held the rest of the brain together, a rather ironic thought, given that 75% of the brain's weight is taken up by white matter. I believe it's the starr cells that pull of the trick of repairing the myelin.
When I first heard of arterial compressions de-myelinating a portion of the TN, it was from my daughter Emily, who had just been selected as one of the founding members of the Young Patients Committee of the National Facial Pain Association. She was busily going through their data bank of hundreds of peer-reviewed journal articles to learn as much as she could. And those journal articles, as well as all the presenters at the 2013 Regional Conference, talked about compressions and demyelination. Both "Insights" and "Striking Back," publications of the National Facial Pain Association, mention compressions and demyelination of the TN in contributing to trigeminal neuralgia.
One neuralgian told me that his/her neurosurgeon pulled a medical text from the shelf during an office visit to make the point that there is not a lot of material regarding TN that would-be neurologists must know before taking their medical boards. The neurologist in question opened the book to the two lines about TN that sufficed for preparation for licensure. It is not surprising that neurologists vary in their knowledge of TN and treatments for it.
The peer-reviewed literature, publications from the National Facial Pain Foundation, and presenters at conferences all address the implications of damage to myelin sheathing in TN. For a more exhaustive list of references, I must ask for a bit more time, unless you feel that I've answered your question sufficiently. Because it is on the chair sitting next to me, I can tell you that "Striking Back" makes references to myelin in 34 separate entries. On Page 34 (a coincidence), Wiegel and Casey state, "Most also agree that loss of or damage to the nerve's protective coating -- the myelin -- is related to the problem. The disagreement starts when it comes to explaining why the myelin is abnormal and war's causing the nerve to misfire." It is such a dreadful disease and we have so far to go in understanding it.
What is paradoxical about the stripping away of the myelin sheathing, whether by vascular compression, pressure from a tumor, or an injury from facial surgery, assault or head trauma, is that one might think that the nerve would lose some of its ability to function. It may be that the nodes of Ranvier can explain, in part, the heightened transmission of impulses in TN. It is at these nodes that there is a space in the myelin sheathing that seems to function in speeding nerve impulses along. (Illustrations of nerves with the nodes of Ranvier look like sausage strings -- I'm not making this up.) What remains unclear to neurologists and neurosurgeons is why the TN seems so switch gears to reporting only pain messages, rather than sending along the more usual sensations that the TN transmits. (Neurologists refer to pain reception as "nociception," a term that might come in handy if you ever attend a regional or national conference.) There are some people who have compressions but no TN. Perhaps they will provide the key to understanding why it is that some people develop the painful condition known as TN, while others do not..
Yes, I did hit "reply" too soon. Imagine my surprise when the screen suddenly changed! Sorry to have written The Great American Novel. If you'd like more, I can do some digging. Or not. ;)
Woman with the electric teeth said:
Hi again, Janet. Just got this reply from you, but there's nothing in it! Has it eaten your answer or did you hit reply too soon? (Done that one myself!) Hoping to hear from you....
Janet McGee said:
"Two Red cents" is so cute! For all of the wealth of information that neurologists, neuropsychologists, cognitive scientists and other extreme specialists have been able to add to our body of knowledge about our little grey cells, and now our little white cells, so much remains a mystery. We have much new, exciting, and helpful information coming down multiple pipelines. It's an exciting time, if you happen to be interested in the cognitive sciences.
Richard A. "Red" Lawhern said:
I was asked to comment on remissions for TN. In all candor, I don't think anybody knows with confidence what causes remissions -- any more than we know what causes many cases of TN itself. Some cases appear to be associated with blunt force trauma to the face, whiplash injury in car accidents, or anesthesia mis-administered during dental work. But a lot of cases are called "ideopathic" because the pain emerges "of itself", for no apparent external cause.
Similarly, some people associate remissions with particular treatments they've undergone or conducted themselves. B12 shots or pills are often discussed, though there doesn't appear to be any consistent medical evidence for B12 in the literature. People report that stress sometimes caused them breakthrough pain, and reduction of stress seems to help with whatever else they are doing to manage pain. Some people get long remissions after chiropractic treatment or a course of acupuncture. But whether either technique actually 'causes' remissions, is quite a different and less certain matter. The pain relief obtained after MVD or peripheral surgery like Rhizotomy isn't really a "remission" as much as a longer-term correction of nerve compression or introduction of a controlled nerve scar (lesion) that interrupts the pain.
My two Red cents for whatever they're worth.
Regards
Four to Five years is a bit too long to make a confident association of cause and effect, Jimmy. A few weeks is probably the "medical statute of limitations" on this kind of thing. Over-filling of a tooth root or damage to a nerve generally present pain within a few days tops.
Jimmy Works said:
Red, you mentioned the issue of anesthesia during dental procedure. Got a question --- just asking your opinion. When my TN started it started directly in the tooth I had had a root canal on. The extreme stabs of pain and lightning strikes eventually proceeded to a crawling like on the roof of the mouth. BUT....that root canal was done 4 or 5 years or so before the TN started. Back then I thought about the root canal but discounted it because of the 4 or 5 years that had passed. What's your 2 Red cents? :)
Right. Logic would tell us that. I just wanted to get your opinion
Richard A. "Red" Lawhern said:
Four to Five years is a bit too long to make a confident association of cause and effect, Jimmy. A few weeks is probably the "medical statute of limitations" on this kind of thing. Over-filling of a tooth root or damage to a nerve generally present pain within a few days tops.
Jimmy Works said:
Red, you mentioned the issue of anesthesia during dental procedure. Got a question --- just asking your opinion. When my TN started it started directly in the tooth I had had a root canal on. The extreme stabs of pain and lightning strikes eventually proceeded to a crawling like on the roof of the mouth. BUT....that root canal was done 4 or 5 years or so before the TN started. Back then I thought about the root canal but discounted it because of the 4 or 5 years that had passed. What's your 2 Red cents? :)
Thank you, Janet, for that exhaustive reply - great stuff. I have always been of the opinion that the myelin sheath must be damaged in TN. In fact I lost my temper with my doctor when he said 'We've no proof that your myelin sheath is damaged", because I felt it was the one thing that is almost a dead cert, but the literature doesn't really seem to back that up.
I knew that there are many post mortem ops on people who turn out to have nerve compressions who have had no TN, so for me that has always proven that the myelin sheath must be playing a role in it. I knew nothing about the Glial cells, so thanks for that. I shall now be all over them like a rash!
Unfortunately, I will probably never attend a conference because I am in the UK and, being a much smaller country, there is simply not enough bodies to whip up a conference.
It was also completely new to me that there is some thought that TN1 morphs into TN2. I confess that is not a welcome thought. I have TN1 currently, classical symptoms. The only comfort I can see from becoming a TN2 type further down the line is they don't seem to get the 'highs' of severe electrical shocks and instead have a more constant but duller pain. But that is very small comfort indeed.
I have always wondered why MS sufferers can present with TN, and they have a myelin sheath problem, yet research for MS doesn't seem to have thrown any light onto TN itself. The diseases seem so closely linked you'd think something could be extrapolated that would be useful.
On the subject of pain, I know why people do this, I really do, but I find the constant pursuit of pain control to be very depressing and could wish people were pushing for a cure more. By which I mean, finding out what causes the disease, not just new ops to control it! I am trying to do that, for myself personally, not on a grander scale, but my doctor disapproves of my investigations and feels I should just sit quietly and accept my fate. He doesn't seem to think this might be depressing.
I've never seen the point in me joining the Facial Pain Association as I am in the UK and can't make full use of it, but would it be worth joining to get the magazines? I see you refer to them a lot and it would interest me more if they have a lot of new research in them. So little gets done on this disease that new research feels rarer than hen's teeth.
Janet McGee said:
TN is unfortunately, progressive. It seems that it may start out with intermittent flare-ups with periods of remission. This has typically been labeled Type 1 TN. The flare-ups may increase in frequency. When they are accompanied by a 24/7 burning sensation, Type 1 has morphed into Type 2. At the 2013 National Pain Association Regional Conference in Richmond, a couple of the presenters said that it was no longer thought correct to refer to Types 1 and 2, that Type 2 seems to be a disease progression. I'll have to check back through recent issues of the Facial Pain Quarterly, in which Jeffrey Brown, M.D., proposed new nomenclature in sorting the different types of TN. In trigeminal neuropathy, for example, a portion of the trigeminal nerve is demyelinated, either through pressures exerted during a facial surgery, or as a result of a traumatic brain injury. It is a form of TN that progresses -- worsens -- rapidly. This is what I observed with my daughter following her corneal transplant, when her eye tried very hard to perforate. I believe it was in the Winter, January 14 issue of the Facial Pain Quarterly that the National Facial Pain Association Research Foundation announced a new initiative to investigate applications of nano pharmaceuticals to target the glial cells in generating new myelin sheathing. In Fall, 2011, National Geographic Magazine ran a special issue. It had a catchy title like, "The Dark Matter of the Brain: Glial Cells." Neuroscientists at that time were just learning that there are 5 different types of glial cells, and that each plays a different role in the development and maintenance of the nervous system and the brain. Until recently, the glial tissue was thought just to be the "glue" that held the rest of the brain together, a rather ironic thought, given that 75% of the brain's weight is taken up by white matter. I believe it's the starr cells that pull of the trick of repairing the myelin.
When I first heard of arterial compressions de-myelinating a portion of the TN, it was from my daughter Emily, who had just been selected as one of the founding members of the Young Patients Committee of the National Facial Pain Association. She was busily going through their data bank of hundreds of peer-reviewed journal articles to learn as much as she could. And those journal articles, as well as all the presenters at the 2013 Regional Conference, talked about compressions and demyelination. Both "Insights" and "Striking Back," publications of the National Facial Pain Association, mention compressions and demyelination of the TN in contributing to trigeminal neuralgia.
One neuralgian told me that his/her neurosurgeon pulled a medical text from the shelf during an office visit to make the point that there is not a lot of material regarding TN that would-be neurologists must know before taking their medical boards. The neurologist in question opened the book to the two lines about TN that sufficed for preparation for licensure. It is not surprising that neurologists vary in their knowledge of TN and treatments for it.
The peer-reviewed literature, publications from the National Facial Pain Foundation, and presenters at conferences all address the implications of damage to myelin sheathing in TN. For a more exhaustive list of references, I must ask for a bit more time, unless you feel that I've answered your question sufficiently. Because it is on the chair sitting next to me, I can tell you that "Striking Back" makes references to myelin in 34 separate entries. On Page 34 (a coincidence), Wiegel and Casey state, "Most also agree that loss of or damage to the nerve's protective coating -- the myelin -- is related to the problem. The disagreement starts when it comes to explaining why the myelin is abnormal and war's causing the nerve to misfire." It is such a dreadful disease and we have so far to go in understanding it.
What is paradoxical about the stripping away of the myelin sheathing, whether by vascular compression, pressure from a tumor, or an injury from facial surgery, assault or head trauma, is that one might think that the nerve would lose some of its ability to function. It may be that the nodes of Ranvier can explain, in part, the heightened transmission of impulses in TN. It is at these nodes that there is a space in the myelin sheathing that seems to function in speeding nerve impulses along. (Illustrations of nerves with the nodes of Ranvier look like sausage strings -- I'm not making this up.) What remains unclear to neurologists and neurosurgeons is why the TN seems so switch gears to reporting only pain messages, rather than sending along the more usual sensations that the TN transmits. (Neurologists refer to pain reception as "nociception," a term that might come in handy if you ever attend a regional or national conference.) There are some people who have compressions but no TN. Perhaps they will provide the key to understanding why it is that some people develop the painful condition known as TN, while others do not..
Ah, don't worry, I've done it myself - time without number! And I would love more info. You couldn't write too much for me, ever. I belong to other forums elsewhere for hypothyroidism, coeliac disease and B12 deficiency, and I get loads of info from them, but that's because they have a LOT more members, and there is far more info out there for people to discuss. This TN forum, great as it is, is limited by sheer numbers of sufferers and the fact that scientists do very little research on TN. Subsequently I've given up trying to find anything new. It always just seems to be new operations and forms of pain control. While those are obviously essential, I never feel enlightened or uplifted by them. They just seem to be a horrible trap waiting for me at the end!
So yes, Janet, ANY research, or sources of good research, you could share with me - I'd be hugely grateful. Many thanks, Chancery
Janet McGee said:
Yes, I did hit "reply" too soon. Imagine my surprise when the screen suddenly changed! Sorry to have written The Great American Novel. If you'd like more, I can do some digging. Or not. ;)
Woman with the electric teeth said:Hi again, Janet. Just got this reply from you, but there's nothing in it! Has it eaten your answer or did you hit reply too soon? (Done that one myself!) Hoping to hear from you....
Janet McGee said:
FYI all: there is a substantial branch of TNA in the UK, centered primarily in the area around London, I believe. The TN Association of the UK also has a website at http://www.tna.org.uk/. "Living With TN" has about 400+ members in the UK, some of whom also belong to their more local TN organization.
In MS patients, when TN occurs it is sometimes called "symptomatic" because it is believed that the mechanisms for MS pain generation in the trigeminal nerve are somewhat different from those that operate in classic TN. Plaques on the nerve may introduce discrete penetrating lesions that aren't quite the same thing as the indentations of the nerve which result from compression and stimulation by a blood vessel.
Otherwise, I'd have to say that the current trend in thinking is that classical symptoms of TN (volleys of electric shock stabs) are less likely to progress into the less typical symptoms of trigeminal neuropathic pain (throbbing, burning 24-7 pain at somewhat lower intensity), if pain control is gained early. At one time, it was common to speak of atypical TN as "pre-Trigeminal Neuralgia" because a lot of patients reported that form of pain as the first pain presentation. These days, the trends are also away from the distinctions TN-1 and TN-2, because doctors have always found the causes of atypical TN to be obscure when there is no obvious or discrete source of physical injury to the nerve in the patient's history.
Regards, Red
Just to echo Red’s last point, I was intially diagnosed with idiopathic TN2; I never had the classic TN1 symptoms. They’re really not sure whether I have “true” TN2, or trigeminal neuropathic pain (some unknown injury via nerve infection, etc). So I am intrigued by the atypical info and findings regarding facial pain. I believe Dr Kim Burchiel in Oregon is the one looking at whether there is any genetic component, chiefly b/c they don’t understand why some people with nerve compression don’t get TN, and some others have TN without nerve compression. Red, thanks for all your very informed posts on the latest knowledge regarding TN. I always learn a bit more each time I read your posts. Janet, thanks for your very thorough info as well. Nice job. This is how we all help each other :).
Hi Chancery,
What a beautiful name! First of all, may I ask where you live?
Secondly, if you have not done so, I'll bet you'd like to visit www.tnnme.com. It's an organization headquartered in Boston and headed by a power-house of a woman named Toni Saunders. There's a petition on the website addressed to the World Health Organization, asking that TN be including on the UN's Health Topics list, in order to attract more funding for research. If you have not yet joined, you can get a membership in the National Facial Pain Association (TNA) for $35. When I renewed my membership, they sent me a free updated copy of Striking Back! A Layman's Guide to Understanding and Treating What is Often Called the Worlds's Worst Pain. There are a number of Facebook support groups; one now has over 6,000 members. It's a wonderful source of inspiration and information. I'll have to get back to you with the exact name of the group. The International Trigeminal Neuralgia Awareness Fighters group is an affiliate of tnnme.com, and they put up occasional YouTube videos and sponsor walks to raise money and awareness for TN. The National Facial Pain Research Foundation is a non-profit organization that sponsors TN research in hopes of finding a cure. They've got research going in both Florida and California. One of the big undertakings is research into the genetic foundations of TN. I had not thought that much would come out of this avenue, as it is currently thought that only 5% of TN cases have a genetic basis. But, they've already published findings that have made me eat my words. The other main avenue of research is the nano-pharmaceuticals project, which hopes to trick the appropriate glial cells into applying new myelin sheathing to damaged nerves. They've already found out some amazing stuff about how, when you're in pain, signals are sent to the glial cells, which decrease production of dopamine (one of the "feel-good" neurotransmitters). When dopamine levels drop in response to pain, the sufferer feels anxious and depressed. While looking for a cure, they've found out something critical about the nature of pain that anyone might experience, and they've explained why it is that we get so moody when we're in pain. It also explains why so many TN patients benefit from a course of amitriptyline (Effexor), or another anti-depressant medication. Effexor is one of a class of drugs that affects both serotonin re-uptake and dopamine re-uptake. If it's OK with you, I've got to tend to my daughter's cat, as he tried to get his bladder blocked today. I'll be back to address more questions, and also give you the names of a couple of Facebook support groups (especially the one that shocked me by turning from a few hundred to over 6,000).
Talk to you soon,
Janet
Hello again, Chancery,
Now I see that you're in the UK. I just wanted to make sure that you saw Red's post about the UK branch.
I hope that the researchers have let you know that you're not making up any of your depression or anxiety. They are not just figments of your imagination but genuine neurological results of pain. Maybe there's a sweet-talking way of getting a research article or two into your doctor's hands.
Red, I loved your line about the statute of limitations on medical procedures. I'm going to have to steal it sometime. ;)
Janet