and rationale for a targeted approached of prevention
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Educational insights developed by James P. Boyd, DDS
Arteries and Nerves travel together Excessive Noxious Stimulation Suppressing Noxious Input Long-term efficacy of preventive modalities
The adjacent animated image is depicting normal afferent neural conduction from meningeal vasculature. These neurons of the first division of the trigeminal nerve are "reporting" the status of the vessels to the trigeminal sensory nucleus. The status may be that there has been enlargement of the arteries due to the presence of nitric oxide (as described below), or of a degree of inflammation. This is not a state of pathology and is the normal responsibility of the first order sensory neurons. The pathophysiology of migraine is a condition of abnormal responses to normal sensory inputs. Current therapeutic modalities for migraine simply stipulate this fact, and embark on altering the nature of neurotransmitter activity, either preceding the event (preventive medications), or during the event (abortive or "rescue" drugs). What has been generally overlooked is the etiology* of the abnormality of the sensory modulation. *(how it got that way and/or how it stays that way) |
INTRODUCTION
As described by Goadsby, migraine involves a "dysfunction of
brain
stem pathways that normally modulate sensory input". More
precisely, migraine involves abnormal
sensory modulation. While the current medical models for migraine pathophysiology include afferent input from the meningeal arteries to the trigeminal sensory nucleus, the effect of any other acute or chronic noxious afferent input from the other divisions of the trigeminal, primarily the mandibular (third) division and how that noxious afferent input effects sensory modulation, has been essentially ignored. |
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General
background
Medical research has identified two consistent features present in chronic migraine patients: an elevated sympathetic tone, and, in those patients with "aura" preceding the attack, a wave of cortical depression (as pictured to the right). The susceptibility to this depres- sion is either a genetic property of the subject, or is an environ- mental adaptation/alteration of normal. The depression is actually a "switching off" and then switching back on of the brain cells as the area of the wave passes. This wave of depression typically initiates in the occipital area of vision. The visual aura (sometimes described as con- centric areas of blindness) that is sometimes reported occurs simultaneously with the depression in that area. |
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As the brain
cells "switch back on", nitric oxide (NO) is
produced and finds
its way to the surface of the brain. There, the NO
causes the
surface
arteries to swell [left], which is physically sensed by trigeminal
nerve fibers that wrap around these arteries. It is not uncommon for a person to experience this wave of cortical depression without a migraine being triggered. Sometimes, instead of an aura (a result of the depression having its greatest impact in the occipital region), some people experience other physical sensations, such as arm tingling/numbness, or feeling a bit "spacey" for short periods. |
As the swelling enlargement of the intracranial surface arteries stimulates sensory fibers of V1 (ophthalmic branch of the tri- geminal, V), "noxious" (meaning potentially harmful) information is relayed to (afferent) the sensory nucleus of the trigeminal. Then, either as a result of genetic properties of the host (as in a pre-existing elevated sympathetic tone), or as a result of a pre-sensitization of the sensory nucleus (addressed further below), or both, Calcitonin Gene-Related Peptide (CGRP) is secreted by the nerve endings of V1 (as are other noxious chem- icals), thereby producing a frank inflammation of the arteries, which is thought to be primarily responsible for the patient's pain, throbbing and aversion to movement. |
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Perhaps in an attempt to counter-act the elevated sympathetic tone that occurs in response to the rapidly inflamed arteries, acetylcholine (ACh) is secreted by the parasympathetic nerve endings from the sphenopalatine ganglion (SPG), thereby causing swelling, pressure and inflammation of the nasal mucosa and also causes a heightened tension of the intrafusal fibers of the spindles primarily within the temporalis muscle (the main muscle of jaw clenching, a result of chronic elevated sympathetic tone), creating the sensation of tension or squeezing. The intense pain from spasming of these intrafusal fibers ("migraineous pain") far exceeds that of the chronic spindle tension of tension-type headache. |
 Sensitized neurons from the trigeminal spinal track cause inflammation and swelling along the greater occipital nerve and artery, causing cervical tension and pain. |
| The "pre-sensitization" of the Trigeminal Sensory Nucleus |
The most effective FDA approved migraine prevention modality.
| The animation [right] depicts normal
masticatory motor and sensory
activity (chewing). Of the three branches of the trigeminal
nerve, the
third division (the mandibular, or V3) is the largest and most active,
due mainly to the abundance of sensory input from the oral cavity and
temporomandibular joint. During a normal chewing stroke, the motor nucleus of V innervates the elevating (closing) musculature of the mandible. As forces escalate on the oral structures, proprioceptive and nocioceptive afferent input to the mesencepha- lic and sensory ganglia serve to govern the forces applied. |
 At a certain threshold, elevating innervation is discontinued while innervation of jaw depressor (opening) activity ensues. |
| An elevated
sympathetic tone increases the intrafusal tension of the spindles
(primarily within the temporalis) and
allows nocturnal jaw-elevator muscle activity to go
un-governed, resulting in multiple nightly episodes of jaw-clenching
activity that can exceed the
subject's voluntary maximum. [right]. While
casually referred to as "bruxism", the term has unfortunately become
synonymous with "teeth-grinding". Although teeth-grinding
can ensue as
a result of the persisting jaw elevation and occluding of the teeth,
the intensity of the elevator
muscle activity (primarily the temporalis), dictates whether or not the
jaw depressors/openers (mainly the lateral pterygoids) can success- fully advance their respective condyles, resulting in varying degrees of teeth-grinding. |
EXCESSIVE
NOXIOUS
AFFERENT ACTIVITY As the elevator muscle activity
(clenching)
intensifies, the grinding activity becomes more forceful while limiting the range of
movement. As clenching intensity escalates, the lateral
pterygoids become overwhelmed, thereby eliminating teeth-grinding
activity, resulting in "primary clenching".
This purposeless act is generally referred to as masticatory parafunction, where the persistence of elevation provides a resistance to condylar advancement/translation and disclusion of the teeth. The combination of four factors determine the extent of the potential adverse results of the act: Duration; Frequency; Intensity; Position. The position refers to the nature of the scheme of the occluding teeth and orientation of the mandibular condyle within its fossa during the act. The more translated (advanced forward or towards the center of the jaw) the condyle is during the clenching activity, the more strain and load it is exposed to. |
| Less-than-maximal clenching activity
in the presence of a "mal- occlusion" (an occluding scheme of the teeth that obligates protective activity of the lateral pterygoid in order to protect the jaw-joint and mal-positioned teeth during chewing) can elicit considerable noxious afferent stimulation of the sensory nucleus, thereby further adding to its sensitization. The sensitized nucleus becomes "triggerable", responding to otherwise harmless noxious stimulations (i.e., glare, odors, food additives), and anything that further naturally elevates sympathetic tone. |
 In the absence of moderate to intense nocturnal clenching, dental occlusal therapy, including simple "adjustments" of the teeth, orthodontics, mouth splints, and crowns can successfully eliminate the noxious masticatory and nocturnal parafunctional stimulation. |
| While the frequency and duration of
parafunctional episodes remain a
function of the host's sympathetic tone, the intensity of the acts and
position of the condyles can be influenced by a strategically designed
oral orthotic.* In order to achieve excessive contraction intensities of the elevating musculature, the posterior and/or canine teeth must first occlude with each other, thereby "completing the circuit" and providing the resistance necessary to allow intense contraction activity (as in the animation above). By limiting the dental occluding contacts to include incisor teeth only (excluding the canine teeth) in any lateral movement of the mandible by the lateral pterygoids, the elevator muscle contraction is inhibited to <30% of voluntary maximum. |
INHIBITION
OF NOXIOUS SENSORY ACTIVITY (resulting in reduction of migraine attacks)  By
limiting the degree of separation of the posterior and canine teeth
during the events (achieved by particular alterations of the orthotic),
the translation of the condyle(s) and resultant strain and/or load can
also be minimized or eliminated.
*The NTI device (Nociceptive Trigeminal Inhibition), approved by the FDA for the prevention of medically diagnosed migraine pain and Temporomandibular Disorders. (by prescription only) 82% of migraine patients reported a 77% average reduction of migraine events within the first eight weeks of use. Duration and intensity of migraine attacks were similarly reduced. |
| The charts to the right are recordings of
temporalis EMGs (clenching inten- sities) of a migraine sufferer between midnight and 3am for 13 consecu- tive nights. Each vertical spike is a clenching episode. The patient had been wearing an NTI device for over two years, with complete resolution of her daily headaches and frequent migraine attacks. Nights 1 through 5 show her still using her NTI. The circled purple number represents the level of headache pain upon waking (on a scale of 0-10 with 10 being worst pain imaginable). She was restless and disturbed by the EMG leads for the first three nights. By the fifth night, she had become accustomed to them. Nights 6 through 9 are without using her NTI. She had been offered $50 per night (for up to 10 consecutive nights), to go without her NTI. |
LONG
TERM EFFICACY ( 6-year use follow-up survey: click here )  On the ninth morning she elected to no
longer continue without her NTI, as her headaches were becoming
intolerable.
Nights 10 through 13 are recordings of her return to use of the NTI device. |