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,[13] 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).[14]
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. ...
http://en.wikipedia.org/wiki/NMDA_receptor
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). ...
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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.