Last year I came across a case study published by a psychiatrist titled, "Tiagabine May Reduce Bruxism and Associated Temporomandibular Joint Pain." It can be read or downloaded for free at this address:
I tried taking Gabitril for several months with several dosage increases, but it didn't slow down the bruxing, though it relieves anxiety. Then, a few weeks ago, it occurred to me that every patient in the study was also taking some other psychotropic drug. I did a bit of research and found that they all affect the trigeminal nucleus, which has both efferent and afferent(inputs/outputs) connections with facial muscles, etc. So, it occurred to me that Gabitril may only stop bruxing if taken in conjunction with one of these other drugs. By the way, the other drugs are Lamictal, Lexapro, and Welbutrin.
I am gradually building up to a 100mg dose of Lamictal, currently being at only 50mg and I'm already bruxing less. I am on 12 mg of Gabitril,
I've been on this combination for almost 3 weeks, with no noticeable side effects. I go whole nights without bruxing. Sometimes I still brux, but with less force. I stopped using a mouth guard, even though I'd used one for years. I can't wait to get to 100mg of Lamictal! I'll keep you posted on my results!
These drugs are very expensive, so you may want to contact the drug manufacturers if you can't afford them. I should also mention that I'm on Inderal LA, 60mg, which may also help, but I suspect it actually makes me struggle more while sleeping, because it tends to decrease delta wave sleep, which is what you want more of. The more delta wave sleep, generally the less bruxing,
I hope this helps someone. I'm very excited about this! Let me know if you have any questions/concerns!
How are you reacting to Lamictal? Any side effects?
This presumption that delta sleep solves all issues is ridiculous. Although, I think science should advance to show how chronic pain effects the sleep patterns.
I can tell you that I dream a lot, and don't have bruxism problem either - quite the opposite, since childhood I slept with my mouth open and have trouble keeping it closed due to the anatomical features of the jaw.
Lamictal is another anti-seizure drug, with high risk profile. I decided to stick with clonazapam for a while, as I had severe drowsiness even at a minor dose. Not to mention blood pressure fluctuations.
What is Inderal - what is the generic name? Anti-seizure medications?
I'm reacting very well to Lamictal so far, with no noticeable side effects.
Yes, I suspect that the increase in delta wave sleep is merely a function of the lack of micro-arousals associated with bruxing, as opposed to being the causal mechanism for bruxing attenuation or cessation.
Inderal is a beta blocker. It lowers blood pressure, relieves anxiety, and even helps prevent the negatively valenced encoding of traumatic memories. I response very well to it, except it breaks my sleep up at times. However, it gives me a very, very deep sense of well being.
I just finished my 4th night with no bruxing and I feel great!!! Forget what you're on, unless it's stopped the bruxing entirely. Why tolerate sub-optimal results?
You have to start on low doses of Lamictal, so a script for Klonopin can help bridge the gap. I take 1mg and get nice and relaxed before bed. It has a rather large effect on bruxing for some, but it wears off over time. A warning with Klonopin though. It lasts about 12 hours, so you still may be quite high for a while in the morning!
I have no reason to believe that any drug other than Gabitril will work for this purpose right now. It is selective in the types of GABA receptors it affects and happens to increase delta wave sleep.
Don't mess around with store bought supplements unless you know they prevent the reuptake of or are agonists of these same GABA receptors.
Also, don't let the black lable warning about seizures in non-epileptics scare you. If you read the FDA warning, only 58 cases have been reported and almost all of them had anxiety or other psychological problems they were being treated for, along with other drugs that lower the seizure threshold.
The dose of Lamotrigine I'm currently on is 50mg just before bed. Typically, you start at 25mg and work up to 100 mg. I'll be at 100mg, x1/day in a week and then 2x/day. The bruxing stopped when I got to 50mg, but I'll feel more comfortable taking it twice a day so I can take naps. I've fallen asleep a couple of times in the afternoon on 50mg at night without consequence, but I want to play it safe.
As far as the black label warning concerning severe rashes, the incidence rate is somewhere between 5-10% and is rarely fatal. Problems are very, very rare when properly stepping up the dosage as my psychiatrist has me doing. She prescribes these drugs regularly. Note: Some patients and doctors think that at least one of the generics for this drug are inferior.
Clonodine is an alpha blocker with a large effect size on bruxing inhibition, but does not halt bruxing entirely. It might be worth trying if the above combinations fail, but expect inferior results. Also, Clonodine has some negative long-term consequences for some, involving cardiac health. Frankly, I'd try it if not for the above option, after botox. I'm not familiar with the patch delivery system.
NMDA blockers, if that's what you're referring to, have interesting properties like decreasing craving for opiods, but too often come with rather severe side effects. Is it the antagonists you were referring to?
Bruxing is simply the grinding of teeth. In the case of TMJ, this usually is involuntary and occurs during sleep. Most people grind rather lightly, a maybe 10% or so of us grind so hard, that we ruin our teeth and sometimes even our jaw joints.
There is such a thing as involuntary daytime bruxing, but it's far less common and results from a different mechanism.
I was at my family doctor today for this reason and he said it wasn't available after looking it up. I also phoned two different pharmacists, and they said it isn't available, even under a different name. It is also not listed on the Health Canada Drug Database.
But Buspar worked good for me, but I built tolerance. How about switching to Gabapentin? Or is there another drug with a similar chemistry to Gabitril? Have you or anyone else had success with any other drugs?
kk43, I'd have to research it further, but Gabapentin does have some special anti-nocioceptive (pain relieving) effects in the trigeminal areas of the brainstem. It is used to treat trigeminal neuralgia.
The key is to find a drug that stimulates those same GABA-ergic synapses. I'll check into it.
Lamotrigine, I told by my doctor was "a big gun", when I asked how it works, basically implying that the mechanism is not fully known, but has broad range, non specific effect on various receptor systems. A miracle drug for rare kind of seizure disorders, and while helpful for TMD sufferers, I think (given my experience) and what was mentioned above - inducing sleep (way too much sleepiness for me), make me hope and wait for the pharmaceutic research to give us a gift of
more specific, more targeted and precise medications. Perhaps someone with TMD disorder who is young will be moved to go into the field of neuropharmacology and help those who have lost the hope. I would be careful using this medication as first option for bruxism for numerous reasons mentioned above, and yet unknown effect - it's ability to bind to melanin containing tissues, especially the iris of the eyes.
Lamotrigine, appears to have some binding capacity for the NMDA receptors, as per wikipedia:
Mechanism of action
One proposed mechanism of action for lamotrigine involves an effect on sodium channels, although this remains to be established in humans. In vitro pharmacological studies suggest that lamotrigine inhibits voltage-sensitive sodium channels, thereby stabilizing neuronal membranes and consequently modulating presynaptic transmitter release of excitatory amino acids (for example glutamate and aspartate).
Glutamate and aspartate - excitatory amino acids...
NMDA receptor - Wikipedia,
The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function. ...
NMDA receptor antagonist -
NMDA receptor antagonists are a class of anesthetics that work to antagonize, or inhibit the action of, the N-methyl d-aspartate receptor (NMDAR). ...
few, and upcoming type of class of medications known as NMDA receptor reuptake inhibitors and/or modulators I hope will come out and be of use not only for chronic pain but also for over-excitation of neurons that cause such debilitating conditions as trigeminal neuralgia.
Ketamine, while not suitable, is a good example that these kind of receptors, along with numerous others such as GABA, serotonin, and noradrenaline play a significant role in pain perception sensitization.
But particularly, NMDA receptors and agents that work by agonizing, antagonizing, or partially antagonizing and/or inhibiting the reuptake might be useful; and I am sure will be developed, used more often in the future.
I am very happy about this in depth discussion. Showing people different options - from anti seizure medications, that work via changing the way nerve cells (neurons) communicate by slowing down/preventing them from taking in Calcium/Sodium to help neurons to slow down from firing so fast... to clonidine (yes, it is available as a patch, for transdermal delivery system, which is I think essential with drugs are very potent (same with fentanyl) - so that putting in on the skin, versus ingesting it orally, it is delivered over few days in a controlled fashion.
Another option - someone mentioned Buspar, I think it might be useful, thank you for sharing this. I want to add baclofen, as yet another option for both pain and bruxism.
Also, wanted to correct one point mentioned above -
clonidine is not a blocker in regular way of looking at it.
"Clonidine works by stimulating Î±2 receptors in the brain, which decreases cardiac output and peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic Î±2 receptors in the vasomotor center in the brainstem. This binding decreases presynaptic calcium levels, and inhibits the release of norepinephrine (NE). The net effect is a decrease in sympathetic tone."
It is indeed confusing, so I don't blame for confusing it and naming it as a blocker - it is an agonist, and yet it inhibits release of norepinephrine because the brain thinks that there is plenty of nerepinephrine in the brain (because clonidine attaches to the receptors and fools the brain). If it was not for the chronic pain, I would enjoy a graduate study program in pharmacology, w/ specific focus on neurology, neuropharmacology. Knowing the impact of chronic pain and how it impacts human mind drives me to research this subject, and contribute...