Migraine Pathophysiology as it relates to the NTI's method of action

The Trigeminal Nerve gets its name from its three sensory divisions:
1: Opthalmic (transmits sensations from around eyes, forehead, scalp, surface arteries of the brain;
2: Maxillary (upper jaw and sinuses);
3. Mandibular (lower jaw) providing sensations from everything below the cheekbone, including teeth, lips, gums, and the jaw joint. 

The third division of the Trigeminal Nerve also transmits motor  instructions to the jaw muscles. Necessary jaw muscle contraction intensity is regulated by the resistance encountered (hardness of food)

 

In migraine, the main center for sensation reception (called the "sensory nucleus") has somehow become hyper-sensitized, responding unfavorably to normal outside stimuli (termed, "dysmodulation") 

An example of "sensory dysmodulation" is the response to certain stimuli (commonly known as "triggers") with illicit neuropeptide secretions that irritate and inflame arteries surrounding the brain (via the first division of the trigeminal, resulting in migraine pain) and within the sinuses (via the second division, resulting in pain, stuffiness and discharge, or "sinus headache"). 

Until recently, the third division had been ignored as a possible contributing factor in migraine. (now published: Adjunctive treatment of chronic migraine using an oral dental device: overview and results of a randomized placebo-controlled crossover study). In a large percentage of migraine sufferers, the motor root (which travels within the same conduit as the sensory third division) is hyperactive during certain stages of sleep, commanding tremendous amounts of potentially damaging activity from the jaw muscles, termed "parafunction".  This results in a bombardment of noxious (negative) information going back to the sensory nucleus, thereby sensitizing it, making the patient far more susceptible to migraine attacks.

During uncontrolled nocturnal parafunction (jaw-clenching, either in a centered or a sideways-shifted position), massive amounts of noxious input (nociception) bombards the trigeminal sensory nucleus. (the average migraine patient can clench with 2x the maximum force as asymptomatic controls, and clench 14x more intensely during sleep. 

CONTROLLING PARAFUNCTION

By keeping the molar and canine teeth from touching (thereby minimizing the intensity of muscle contraction intensity) while minimizing the degree of condylar rotation (jaw opening) during the parafunctional events, nociception to the Trigeminal is inhibited. (therefore, it is not the presence of incisor (front tooth) contact that is therapeutic, but the absence of posterior and/or canine contact)
The NTI device reduces trigeminal motor hyper-activity and the resulting noxious afferent bombardment to the trigeminal sensory nucleus, thereby reducing dysmodulation.
 
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