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1.  Noxious bombardment of the Trigeminal Sensory Nucleus will cause sensory sensitization, causing the Trigeminal Sensory Nucleus to produce pain signals well after the noxious input has terminated (2:30) 

2.  Muscle force is a function of the number of fibers being innervated (4:30) 

3.  Masticatory purposeful necessity dictates the degree of muscle fiber innervation. (6:35) 

4.  Incisor-only contact governs temporalis innervation to 30% of maximum force. (7:14) 

5.  Canine-only contact through the long axis allows ~75% of maximum force. (7:36) 

6.  The first rule (of only two) of Parafunctional Control is to minimize elevator contraction intensity by providing for incisor edge contact only in all excursions. (7:58) 

7.  Natural incisal biting does not adversely load the TM joint (8:11) 

8.  Elevating the mandible “through the air” does not register a reading on EMG.(8:40) 

9.  Maximum Clenching Voltage occurs with a splint with posterior coverage (9:40) 

10.  Occlusion stipulates an active contraction of the elevator muscles (11:30) 

11. Posterior contact does not cause elevator hyperactivity, it allows for it. (15:00) 

12. The occluding scheme governs the degree of muscle contraction intensity (15:10) 

13. There’s no pathologic condition as independent hyperactive lateral pterygoids. (18:45) 

14. Lateral pterygoids encounter resistance (and then fatigue) when attempting to move or open the mandible while the teeth are persistantly being occluded by the elevators. (21:30) 

14. A contact is not an object, it is the result of a persistance elevator activity. (23:40) 

15. The degree of elevator intensity that occludes the teeth dictates the degree of resistance encountered by the lateral pterygoid’s attempt at discluding the teeth. (23:55) 

16. The force vector generated by a lateral pterygoid when a contralateral distal occludiing contact is maintained by the elevator, aims medially at the point of resistance (the contact), which applies considerable strain/load to the ipsilateral joint. (25:25) 

17. A better term for “posterior support for the joint” is “posterior immobilization of the condyle” (26:50) 

18. The functional purpose of canine teeth is clenching (grasping and holding). (29:15) 

19. Temporalis’ outlast masseters during prolonged clenching. (29:47) 

20. “Diagnosis” is the Nature and Cause of a Disease or Injury. (31:13) 

21. “Disc displacement with Reduction” is only half of a diagnosis, as it describes only the Nature of the presentation. (31:20) 

22. The Cause of a diagnosis is how something got that way, or how it stays that way. (32:00) 

23. Purposeless parafunction results in signs and symptoms. (35:00) 

24. “Primary Clenching” is the most extreme of bruxism, but causes no tooth wear or joint strain. (37:00)  

25. Bruxism is:  Jaw clenching, with or without forcible excursive movement, where the intensity of the clenching dictates the severity of the signs and symptoms. (37:34) 

26. The Primary Clenching patient is highly symptomatic (headache/migraine) and frequently goes undiagnosed due to lack of objective signs. (39:00) 

27. Centric Relation is when the medial pole of the condyle is at its most superior position (40:00) 

28. The TMJ is really two joints: The superior surface of the disc opposing the slope of the eminence; and the inferior surface of the disc opposing the superior surface of the condyle (40:35) 

29: Translation occurs on the superior surface of the disc (40:55) 

30. Pure translation from CR (lateral pterygoid contraction with no elevator activity) will disclude all of the teeth. (41:00) 

31. “Coming down out of CR” is the first line of defense in tradition occlusal therapy to disclude molars during parafunction. (42:00) 

32. Translation accounts for the A/P position of the bolus, rotation is commensurate with the vertical dimension of the bolus. (43:55) 

33. Excessive condylar rotation (excessive vertical dimension of the bolus) produces joint pain when biting on a rigid object. (44:00)

34. A common reason for NTI failure is excessive vertical dimension (allowing for an overly rotated condyle during a clenching event). (45:10) 

35. The more distal a bolus is, and the closer the opposing molars are to each other, the more intense crushing can be with the condyles seated in their most stable position, (45:35) 

36. Splint failure can be due to the vertical dimension in the excursive/protrusive extremes (46:05) 

37. A “protrusive movement” when the incisors persist in occluding does not happen during purposeful mastication, but is a parafunctional act, and is better thought of as “protrusive resistance”.  (47:00) 

38. The term “Constricted envelop of function” is misleading and is better termed “parafunctional protrusive resistance”.  (47:35) 

39. A flat plane splint can relieve resistance to protrusive, allowing the patient to clench in extreme protrusion when they could not previously without the splint.  (49:50) 

40. The introduction of a splint can allow for new parafunctional positions (50:45) 

41. For the extreme protruding patient, a mandibular incisal device that extends distally is indicated. (52.20) 

42. The nature of the parafunctional occluding scheme allows for varying degrees of elevator intensity and joint strain/load. (52:52) 

43. Dentistry congratulates itself if/when occlusal therapy prevents joint discomfort even though pathologic clenching can persist. (56:05) 

44. Dentistry has been assuming that a “perfected occlusion” eliminates clenching. (57:00) 

45. Splint therapy goals: Decrease joint strain; protect teeth; minimize muscle intensity (57:57) 

46. An anterior midpoint stop on the splint will result in minimal muscle contraction while the mandible remains in a centered position (58:20) 

47. A Pankey Deprogrammer minimizes muscle intensity, but provides for a canine contact in excursionstherefore is not designed or intended for parafunction therapy. (59:05) 

48. Canine or posterior contact in excursion allows for intense clenching and joint strain  (1:00:35) 

49. The clenching intensity reduction of the NTI is not short lived and continues on indefinitely (1:01:21) 

50. Extreme excursive movement can bring the lower canine to the maxillary midline, indicating use of a mandibular NTI device. (1:02:05) 

51. Range of motion can increase due to NTI use, thereby allowing for parafunctional occluding schemes that were not producible at initial delivery. (1:02:02) 

52. The “upside down” nature of an articular displays the maxillary guide pin sliding down and forward on the guide plate, giving the false impression of mandibular retrusion (ie, condyles “up and back”.) 1:03:45)  

53. The anterior/superior force direction of the elevator muscles prevents “distalization” of the condyles. (1:04:05) 

54. Occluding contacts cannot “deflect” the mandible distally during parafunction, but rather, the contacting teeth may be traumatized (1:05:15) 

55. A common error in parafunctional control with an NTI is allowing for excessive condylar rotation (ie, excessive vertical dimension) in protrusion creating joint pain (where there may not have been previously).(1:07:20) 

56. The Discluding Element of a lower NTI should be sloped down toward the floor of the mouth to minimize vertical dimension  / condylar rotation in extreme protrusive. (1:08:17) 

57. In the circumstance where the DE has been adjusted for minimal vertical dimension in all excursions, but a posterior contact can still occur, reduce the tips of the occluding cusps to maintain disclusion. (1:09:25) 

58. As a patient’s condition adapts to a new treatment or adjustment, their abilities change and they are not the same patient that you started with and so must be reevaluated as a “new patient” at each encounter. (1:20:00) 

59. By employing opposing NTI devices (ie, a traditional NTI device opposing an NTI “slider”), irregularities in the heights of the incisors is no longer an issue. (1:20:16)  

60. The two goals of parafunctional control with an NTI are to: Minimize muscle contraction intensity; Minimize joint strain/load. (1:21:40) 

61. Load testing with a jig can produce joint pain when it creates excessive condylar rotation. (1:22:42) 

62. Don’t ask a suspected headache sufferer if they wake up with headaches, because they’ll probably say no. Instead, ask how often they wake feeling fabulous. (1:29:29) 

63. Any NTI device (especially those provided by a lab) must be checked for all extreme excursions. (1:32:10) 

64. NTI Therapeutic Protocol is not indicated for asymptomatic bruxism patients. (1:36:37) 

DIAGNOSIS AND PREVENTION OF CHRONIC MIGRAINE IN THE DENTAL PRACTICE

1. The #1 cause of disability in adults under 50  is migraine. (1:41:16)
2.  Migraine diagnosis is made by subjective report.  The are no objective tests that diagnose migraine.  (1:41:25)
3.  In 99.82% of the time in patients diagnosed with migraine, there is no other intracranial pathology. (1:42:45)
4. Migraine is a condition of Trigeminal Sensory Dysmodulation (1:44:00)
5. A premier example of Trigeminal Sensory Dysmodulation is the secretion of CGRP (1:44:40)
6. Secretion of CGRP into the Trigeminal 1st Division produces inflammation and pain at the cerebral arteries, presenting as "migraine pain" (1:44:59)
7. Secretion of CGRP into the Trigeminal 2nd Division produces inflammation and pain within the nasal sinuses, presenting as "sinus infection" (1:45:10)
8. Secretion of CGRP into the cervical spinal tract produces "back of the head headache" and stiff/sore neck (1:45:21)
9. Secretion of CGRP into the Trigeminal 3rd Division produces pain throughout the maxilla and mandible, ie, "TMD" (1:45:31)
10. A sympathetic disturbance to the SphenoPalatineGanglion can trigger CGRP secretion, producing any of the pain presentations(1:45:45)
11. The throbbing sensation is actually sensitized Division 1 neurons sensing normal pulsing of the Cerebral Spinal Fluid (1:45:55)
12. Nociception is the detecting and encoding of potentially damaging damaging stimuli by the Trigeminal Sensory Nucleus (1:45:00)
13. Excessive nociception can sensitize the Sensory Nucleus, causing dysmodulation (1:46:00)
14. "Bucket Theory" of excessive nociception producing dysmodulation (1:46:38)
15. Migraine preventive protocol: CGRP antibodies, Botox to disrupt neural transmission, anesthetic nerve blocks, identify/manage sympathetic input, manage chronic nociception. (1:47:14)
16. Preventive methods are rarely evaluated for reducing disability, but instead count the "reduced number of migraine days" per month compared to placebo to claim statistical superiority (1:47:40)
17. While Aimovig is statistically superior to placebo in reducing the number of migraine days per month, the subject remains severely disabled  (1:48:07)
18. The "Headache Impact Test, 6 question" (HIT-6) is the most reliable method of assessing disability due to headache/migraine. (1:48:55)
19. When comparing Botox to placebo with the HIT-6, Botox produces a reduction of disability while placebo does not (1:49:25)
20. The average migraine sufferer has developed the ability to clench their jaws with twice the force as asymptomatic controls (1:50:00)
21. During sleep, sufferers may clench with 14x the EMG as controls(1:50:50)
22. Intense nocturnal jaw clenching is a profound source of nociception (1:51:11)
23. Jaw clenching can go completely undetected by both patient and practitioner (1:51:30)
24. Intense jaw clenching occurs in the lighter transition stages of sleep, often just before waking (1:51:40)
25. Waking every day with a headache is not usual for a chronic sufferer (1:51:53)
26. Instead of asking, "Do you have a headache when you wake up?", ask, "When you wake up, do you feel fabulous?" because waking with a degree of headache for the chronic sufferer is normal. (1:52:10)
27. A full coverage dental splint allows clenching to persist or intensify and is unpredictable at reducing migraine (1:55:12)
28. Nocturnal EMG of pain patients when using a full coverage dental splint: 52% of subjects decrease intensity; 28% show no change; 20% increase intensity (1:55:49)
29. Incisal-only contact governs clenching intensity to ~30% of maximum (1:56:10)
30. When comparing NTI to placebo for the reduction of disability of chronic migraine, placebo showed insignificant to no reduction, while NTI produced significant to profound reduction (1:57:33)