Trigeminal Neuralgia (TN) is the most common of the cranial neuralgias, and the most common cause of non-odontogenic facial pain.1 It affects 4-5 persons per 100,000 per year,2 and occurs with a characteristic trigger zone that elicits intense shooting pain, which is uncharacteristic for the intensity of the stimulus. Actions that can set off TN pain are brushing teeth, shaving, chewing, or a cold wind blowing across the face.3

The diagnosis of TN is based on a history of shooting pain along a branch of the Trigeminal Nerve, precipitated by touching a trigger zone.1 The exact cause of TN remains controversial, because only 10% of the cases present with a vascular malformation or tumor, while the other 90% are classified as idiopathic,1 resultant from vascular compression and demyelination of the Trigeminal Nerve.3 However, in one MRI study, 10 out of 18 subjects demonstrated vessel-to-nerve contact on the non-painful side of the face, while 6 others had no neurovascular contact.4 Similarly, other authors who used MRI to examine TN patients found a lack of vessel to nerve contact in many of the TN.5 This lack of physical neurovascular compression indicates that other factors must be etiologic for TN, despite that TN pain can sometimes respond positively to microvascular decompression surgery (MVD), and TN can occur and reoccur without any neurovascular compression.6

Most authors do not consider the occlusion as a potential etiology for Trigeminal Neuralgia episodes. However, a recently published TN treatment study7 and 1 TN case report3 that employed 2 biometric technologies in concert (T-Scan 10/BioEMG III) to diagnose and treat the subjects’ occlusions with computer-guided occlusal adjustments, successfully lessened Trigeminal Neuralgia symptom frequency and intensity, and improved emotional well-being after treatment resolved the subjects’ chronic pain. This computer-guided occlusal adjustment procedure (known as Disclusion Time Reduction (DTR) with the Immediate Complete Anterior Guidance Development coronoplasty (ICAGD),8–10 employs highly precise, measured occlusal adjustments,11–16 which shortens the durations that posterior teeth contact and engage during excursive movements, to markedly lessen the occlusion’s afferent neurologic inputs to the Central Nervous System (CNS).17 This in turn lessens the efferent muscle contraction levels of the muscles involved in chewing and swallowing.17,18

To date, as only 1 computer-guided occlusal adjustment treatment study has focused solely on Trigeminal Neuralgia symptoms,7 the Objective of this study was to corroborate or refute whether Trigeminal Neuralgia frequency and intensity changed after patients underwent computer-guided occlusal adjustments, potentially determining if TN has a dental occlusal etiology. The null hypothesis was: Reducing the Disclusion Times with computer-guided occlusal adjustments will not change Trigeminal Neuralgia symptom frequency or intensity.

Methods and Materials

Thirty-one TN patients diagnosed at a Neurology Clinic (The National Institute of Mental Health & Neurosciences, Bengaluru, Kamataka, India), were referred to a prosthodontic dental office with chief complaints of Trigeminal Neuralgia pain to undergo a digital occlusion and muscle physiology evaluation. In addition to TN problems, some of the referred patients demonstrated chewing fatigue, chewing pain, chewing weakness, ongoing head, neck and facial pain and ongoing tension, and headaches around the eyes, midface and temples. All of these patients had anterior teeth that coupled or nearly coupled, demonstrated relatively normal occlusal relations. (Figures 1a, 1b & 1c), and presented with minimal or no Temporomandibular Joint structural breakdown.

Figure 1a
Figure 1a.A Trigeminal Neuralgia patient in Maximum Intercuspation (MIP), with adequate anterior overlap, but poor posterior maxillary to mandibular tooth angulation and lightly worn canines, both of which predispose the patient to posterior lateral excursive contacts.
Figure 1b
Figure 1b.The same patient’s early right excursion showing working side posterior group function contacts exist despite the right canines being in contact.
Figure 1c
Figure 1c.The same patient’s left excursion showed that despite left canine lift, the 1st and 2nd molars make working side excursive contacts because of the poor interarch tooth angulation, and the elevated posterior mandibular Curve of Spee.

Since the 31 patients were also primary muscular TMD patients, they were diagnosed with the T-Scan 10/BioEMG III synchronized technologies (Tekscan, Inc. South Boston, MA, USA; Bioresearch Associates, Inc. Milwaukee, WI, USA), Figures 2a and 2b. The process follows a sequence of having each patient close firmly into their Maximum Intercuspal Position (MIP), hold their teeth together inter-cuspated for 1-3 seconds, and then to commence a right or left excursion until only anterior teeth were in contact. This specific recording method insured that only high quality Disclusion Time and EMG data were obtained from each TN patient.19 All pre-ICAGD coronoplasty Disclusion Times values and excursive electromyography levels were recorded for comparison to each individual TN patient’s post ICAGD.

Figure 2a
Figure 2a.A pre-operative right excursion T-Scan 10/BioEMG III recording, (Force vs Time Graph; bottom right pane), to the right of the C Line, there is a working group function controlling the early right excursion (Force vs. Time Graph; the blue posterior right quadrant line rises in force), along with a marked non-working blockage (red brown column on tooth #15), which never is reduced by the ineffective anterior guidance (right anterior quadrant line red line never reaches the top of the graph).

The upper right EMG pane (to the right of line C) illustrates extreme right temporalis excursive muscle hyperactivity with the potential of spasm, which fires all through the right excursion (up to line D). Less excursive hyperactivity is present in both masseter muscles and the non-working left temporalis. The pre-ICAGD right Disclusion Time is prolonged at 2.36 seconds (Timing Pane).

Figure 2b
Figure 2b.A pre-operative left excursion T-Scan 10/BioEMG III recording showing extreme left temporalis excursive hyperactivity to the right of line C, with spasms of varying amplitude (upper right EMG pane) and lower excursive muscle firing in in both masseter muscles.

There is a working side group function that shares control of the left excursion with the anterior left quadrant (Force vs. Time Graph; bottom right pane; orange posterior left quadrant line and green anterior left quadrant line travel horizontally together across the graph). A non-working blockage (light green-yellow column on tooth #2), accompanies the excessive 1st molar force rise on tooth #14. The pre-treatment left Disclusion Time is very long = 3.79 seconds (Timing pane).

Disclusion Time and EMG levels, detected in follow up recordings made on Day 1, at 1 week and 1 month post ICAGD.

Also, each TN patient filled out a self-assessment Trigeminal Neuralgia questionnaire (Table 1). They self-reported their emotional state with the Beck Depression Inventory-II, they answered questions related to Pain Intensity, Pain Frequency, Functional Restrictions, and Frequency of Symptoms to assess the physical limitations of their TN condition.

Table 1.Significant changes in Disclusion Times from pre-treatment to post treatment.
Changes in Disclusion Timing Left Disclusion time Pre-TX (seconds) Right Disclusion time Pre-TX (seconds) Left DT Post-Treatment (seconds) Right DT Post-Treatment (seconds) Left DT 1-month post-Treatment (seconds) Right DT 1-month post-Treatment (seconds)
Mean 2.33 2.58 0.305 0.325 0.274 0.279
Standard Deviation (+/-) 1.24 1.94 0.061 0.085 0.064 0.054
Pre-Tx to Post-Tx Post-Tx to 1 Month Post Pre-Tx to 1 Month Post
Wilcoxon Signed-Rank p < 0.00001 0.00001 0.0004 0.00025 0.00001 0.00001

Subjects also completed the Patient Health Questionnaire 15 (PHQ 15) to determine if they exhibited any Somatic Symptom Disorder (SSD) prior to treatment. The 31 TN patients were fully informed they were to receive ICAGD, and have their enamel adjusted and polished, guided by the T-Scan 10/BioEMG III synchronization.

Next the ICAGD definitive occlusal adjustments were accomplished as previously described8–15 and summarized here. The TN patient’s teeth were air dried. They were then asked to close into their Maximum Intercuspal Position (MIP) with articulating paper (Bausch, Arti-Fol® blue 8μ, Germany) interposed between their teeth, and then to commence a right mandibular excursion out to the edges of their canine teeth, then slide back into MIP, and then make a left mandibular excursion out to the edges of the left side canine teeth, and back into MIP (Figure 3a).

The pre-treatment T-Scan/BioEMG recordings (See Figures 2a and 2b) guided the clinician to adjust specific ink patterns on the occlusal surfaces as the patient moved in and out of MIP excursively. Definitive corrections were made on one side of the mouth using pear-shaped finishing burs (Mani Dia-Burs, Japan ISO no-237/021), to all the excursive frictional contacts located on inclined planes and on the buccal and lingual aspects of the molar and premolar buccal cusps (Figure 3a), leaving the central fossa, cusp tip, and the marginal ridge contact points intact (Figure 3b). These same molar and premolar excursive contacts were then eliminated on all involved surfaces on the opposite side of the mouth.

Figure 3a
Figure 3a.These articulating paper markings represent lengthy Disclusion Time showing the excursive friction present despite canine guidance contacts present.

The actual long Disclusion Time is impossible to determine just from these many linear ink markings.

Figure 3b
Figure 3b.Post ICAGD articulating paper markings representative of short Disclusion Time.

Note there are mostly point contacts visible, with few remaining linear frictional contacts present. Again, there is no way to compute the actual ICAGD-created Disclusion Time without remeasuring the right and left excursions with the T-Scan 10.

ICAGD was considered completed when all Class I, II, and III lateral posterior excursive interferences were visually absent, disclusion of all posterior teeth in the right and left excursions was verified and with the patient producing easier and faster lateral movements than pre-ICAGD. The remaining habitual closure contacts were located on cusp tips, fossae, and marginal ridges only (Figure 3b).

When only solid areas of contact in MIP remained and the T-Scan Center of Force trajectory rested near the T-Scan arch-half midline (indicating near equal right side-left side occlusal force arch half percentages), and with the habitual closure adjustments were completed, new excursive recordings were obtained to verify the Disclusion Times had been reduced to < 0.5 seconds in each excursion. Any remaining prolonged excursive contacts were adjusted until each excursion’s Disclusion Time was less than 0.5 seconds (Figures 4a and b). At 1 month post ICAGD, new habitual closure into MIP and excursive T-Scan 10/BioEMG III recordings were each excursion’s Disclusion Time was less than 0.5 seconds (Figures 4a and b).At 1 month post ICAGD, new habitual closure into MIP and excursive T-Scan 10/BioEMG III recordings were made, which guided further but minor, closure and excursive adjustments. At each recall, the TN patients filled out new TN symptom, Functional Restriction, PHQ 15, and BDI-II questionnaires, reflective of changes/no changes to their TN condition and their emotional well-being from undergoing ICAGD.

Figure 4a
Figure 4a.The right excursion after ICAGD and one follow up refinement at one week, showing less excursive muscle activity to the right of line C than was present pre ICAGD (Figure 2a).

There is a short-duration, low force working side group function visible, evidenced by the rising blue quadrant line just after C (Force vs Time graph; bottom right pane), which rapidly falls towards 0% force on the vertical axis, to completely dissipate when the red anterior quadrant line rises to the top of the graph. The corrected Disclusion Time = 0.28 seconds (Timing pane).

Figure 4b
Figure 4b.The left excursion after ICAGD and one follow up refinement at one week, showing markedly less excursive muscle activity to the right of line C than was present pre-ICAGD (Figure 2b).

Note that all 4 muscles stop firing before Line D, shutting down in far less time than before ICAGD (upper right EMG pane). The corrected short Disclusion Time was slightly outside the ideal physiologic range = 0.59 seconds (Timing pane), with the D line sitting very close to the C line, compared to the very distant line placements seen in Figure 2a. In the T-Scan data (left pane), early in the excursion there is a very short-duration low force working side group function and a low force balancing side contact present. After ICAGD, the black Total Force line has no steps or prolonged excursive friction present, enhancing rapid and free-mandibular lateral movement.


The objective of reducing the subjects’ Disclusion Times was clearly met as shown in Table 1. The Disclusion Time reductions were substantial and statistically significant for every subject in the TN group immediately after treatment, which further significantly reduced at 1-month post ICAGD (p < 0.00001).

The analysis of the Patient Health Questionnaire 15 data (Table 2) revealed that a low level of Somatic Symptom Disorder (SSD) was indicated for the group’s mean scores prior to treatment.

Table 2.PHQ-15 group total scores indicating which symptoms were most prevalent pre-treatment and the extent of the group’s significant reductions after occlusal adjustment. Analysis by Wilcoxon Signed-Rank test.
Patient Health Questionnaire 15 Group Symptom Totals
Responses: 0 = not bothered at all, 1 = bothered a little, 2 = bothered a lot Pre-Tx Post-Tx 1 Month Post
Stomach pain 11 1 1
Back pain 29 6 1
Pain in arms, legs or joints (jaw, neck, etc.) 17 5 1
Mentrual cramps or other problems with your periods (Women) 8 0 0
Headaches 54 6 1
Chest Pains 0 0 0
Dizziness or ringing in your ears (tinnitus) 31 4 1
Fainting Spells 0 0 0
Feeling your heart pound or race 5 2 1
Shortness of breath 0 0 0
Pain or problems during sexual intercourse 0 0 0
Constipation, loose bowels or diarrhea 0 0 0
Nausea, gas or indigestion 0 0 0
Feeling tired or having low energry 31 6 1
Trouble sleeping or grinding teeth at night 30 7 1
Group Means (all symptoms totaled) 6.97 1.19 0.47
Standard Deviation (all symptoms totaled) 0.95 0.40 0.52
Pre-treatment to Post-treatment ^- p < 0.00001 -^
Post-treatment to 1 Month Post-treatment ^- p < 0.00001 -^
Pre-treatment to 1 Month Post-treatment ^--------- p < 0.00001 ---------^

NOTE: Pre-Tx = Pre-Treatment, Post-Tx = Post Treatment, 1 month Post = 1 Month Post Treatment

However, the mean scores were significantly reduced to minimal levels immediately post treatment and were significantly lower 1-month post treatment. No subject’s score indicated a medium level of SSD disorder (> 10) at any point in this study, and no subject’s score remained above 4 (low level SSD) post treatment. As such, Somatic Symptom Disorder was not present at any time within this group of 31 TN subjects.

Although the mean value of the BDI-II scores indicated the TN group taken as a whole, exhibited severe depression prior to treatment, with a mean score of 23.7 (+/- 2.07) out of a maximum of 63, all of the post treatment BDI-II scores immediately reverted to normal emotional levels (Table 3). This supports the contention that depression is secondary to physically painful conditions.

Table 3.Means and standard deviations of the group scores as reported from the Beck Depression Inventory II, Pain, Frequency of Symptoms, Functional Restrictions and Frequency of Pain. The Wilcoxon Signed-Rank Test was used to analyze these scores.
Group Mean Beck Depression Inventory - II Scores and Symptom Levels
Trigeminal Neuralgia Subject Group n = 31 BDI-II Scale
(0 - 2)
Pain Scale
(0 - 4)
Symptom Frequency
(0 - 3)
Functional Restrictions
(0 - 3)
Frequency of Pain
(0 - 3)
Pre-Treatment Mean Score (Standard Deviation) 23.7
(+/- 2.07)
(+/- 5.35
(+/- 3.94)
(+/- 2.96)
(+/- 4.30)
Wilcoxon Signed-Rank Test p < 0.00001 0.00001 0.00001 0.00001 0.00001
Immediately Post-Treatment Mean (Standard Deviation) 3.8
(+/- 2.22)
(+/- 1.42)
(+/- 1.23)
(+/- 0.52)
(+/- 0.94)
Wilcoxon Signed-Rank Test p < 0.00001 0.00001 0.00001 0.00001 0.08035
1 Month Post-Treatment Mean (Standard Deviation) 1.97
(+/- 1.58)
(+/- 0.90)
(+/- 1.05)
(+/- 0.37)
(+/- 0.72)

The mean Pain Intensity score for the group was 21.2 (+/- 5.35) out of a possible maximum of 48, or the equivalent of 4.4 on a scale from 0 - 10. A significant reduction in the mean group pain score was found immediately after treatment, and a further significant reduction was measured at 1-month post treatment (Table 3).

The mean Symptom Frequency group score was 15.8 (+/- 3.94) out of a possible maximum of 33, or the equivalent of 4.8 on a scale from 0 - 10. The frequency mean score reduced significantly immediately post treatment, and further reduced significantly at 1-month post treatment (Table 3).

The mean Functional Restriction score was 8.2 (+/- 2.96) out of a maximum of 27, or the equivalent of a score of 3.04 on a scale from 0 - 10. Immediately post treatment the score dropped significantly, and dropped again significantly at 1-month post treatment (Table 3).

The group’s mean Frequency of Pain prior to treatment was 9.6 (+/- 4.30) out of a possible maximum of 30, or the equivalent of 3.2 on a scale from 0 - 10. A significant reduction in the frequency of pain was reported immediately post treatment, to the extent that no further significant reduction was reported (or apparently needed). See Table 3.

Due to the complexity of the EMG data in this study with four muscles active at three different points in the recording sequence, and at three different times of observation, the analysis was applied to the mean activity of all four muscles as one group, because no single muscle can function alone as all activities require group contractions. At point “C,” defined as the starting point of any lateral excursion from maximum intercuspation (MIP), no significant increase was found between the mean pre-treatment value and the immediate post-treatment mean (Table 4). However, an increase in the point C mean EMG activity was significant at one month post treatment (p < 0.00001). See Table 4.

Table 4.EMG changes at “C”, “D”, and in MIP.
Significant Changes in the EMG Activity Levels at C
Pre-Tx Levels at C Post-Tx Levels at C 1 Month Post at C
Mean 37.1 49.0 33.6 28.7 40.0 42.7 34.0 29.0 60.2 70.1 67.5 64.9
SD 29.9 38.2 32.6 17.4 33.8 29.7 26.5 20.7 39.6 47.3 47.9 54.2
Paired t - test p < <-------- 0.38050 --------> <------- 0.00001 -------->
<-------------------------- 0.00001 --------------------->
Significant Changes in the EMG Activity Levels at D
Pre-Tx Levels at D Post-Tx Levels at D 1 Month Post at D
11.3 9.0 11.6 9.9 11.1 17.2 13.2 11.6 9.3 13.1 13.6 12.6
14.3 9.8 13.0 10.3 9.4 19.2 13.5 12.7 8.9 11.4 12.8 12.2
Paired t - test p < <-------- 0.00512 --------> <-------- 0.16555 -------->
<------------------------ 0.04427 ------------------------>
Significant Changes in the EMG Activity Levels at MIP
Pre-Tx Levels at MIP Post-Tx Levels at MIP 1 Month Post at MIP
102 84.3 107 80.4 152 142 145 124 145 138 118 111
48.4 46.6 61.0 63.4 50.1 60.3 67.1 72.8 56.2 74.4 61.1 66.5
Paired t - test p < <-------- 0.00001 --------> <-------- 0.01327 -------->
<------------------------ 0.00001 ------------------------>

At point “D,” defined as the 1st time moment when all posterior teeth are completely discluded and only anterior teeth are in contact during a lateral excursion made from Maximum Intercuspation (beginning at “C”, then going either left or right), a significant increase in EMG activity was found between the mean pre-treatment value and the immediate post-treatment mean (p < 0.00512). Although the increase was maintained, no additional significant increase in the mean EMG activity at D was found at the one-month post-treatment follow-up (Table 4).

The mean EMG activity at MIP increased significantly and quite dramatically from the pretreatment levels in the immediate post-treatment recordings (p < 0.00001). At one-month post-treatment, the mean EMG activity level of the group retreated significantly (p < 0.01328), but the mean activity levels still maintained significant increases compared to the pre-treatment levels (p < 0.00001). These changes indicated the TN groups’ muscle strength while holding their teeth in MIP improved after the occlusal treatment (Table 4).


The Results of this Trigeminal Neuralgia study corroborate the findings of the earlier ICAGD/DTR Trigeminal Neuralgia study7 and the TN case report.3 Significant TN symptom improvements were reported following ICAGD, along with other TMD symptom improvements. This study tracked Trigeminal Neuralgia pain intensity and frequency, which began improving within one week after ICAGD was rendered and which continued to improve over the next month’s observation. An example of the overall TN subjects’ improvements was detected by the increased “C time-point” muscle activity levels. This physiologic response resulted post-ICAGD because the subjects’ teeth fit together far easier and made contact more simultaneously (post-ICAGD the Occlusion Time shortens), which allowd all opposing intercuspating teeth to compress each other more evenly and more simultaneously into their PDLs. This in turn makes for more muscle activation in MIP. These EMG results are consistent with what has been reported when Botox has been employed with TN patients.20 But importantly with ICAGD, no toxin-induced muscle paralysis was needed, no problematic injection side effects occurred (facial asymmetry, headaches, and hematoma),20 and both pain resolution and improved muscle contractile capability resulted physiologically. Further, Botox is metabolized away. Conversely, ICAGD resolved TN in these 31 subjects in 1 month and requires minimal future occlusal intervention to maintain symptom resolution.3,7

A unique finding in the study was a small, but significant increase in the mean microvolts produced at “D.” This increase suggests that the end point of the excursion when only the anterior teeth were in contact was either more stable or more comfortable to the patients. Comfortable contacts elicit more intense contractions than less comfortable contacts in MIP and it is likely that stable and comfortable end points may have the same effect.

Importantly, the results of this pilot study directly contradict previous claims that Trigeminal Neuralgia is not occlusally related. In this ICAGD-treated TN patient pool, Trigeminal Neuralgia intensity and frequency significantly reduced immediately, and further reduced one month after their long Disclusion Times were shortened to within high tolerance Disclusion Times (Table 3). This finding suggests that posterior excursive occlusal contacts of prolonged duration (Disclusion Time > 0.5 seconds), when patients rub or clench their posterior teeth together, neurologically stimulates excessive electrical dental neural activity that can induce the “shock-like symptoms” that appear as Trigeminal Neuralgia episodes.

Of note is the fact that none of the 31 subjects were diagnosed with Trigeminal nerve neurovascular compression via MRI, but the whole group markedly responded to ICAGD treatment. This suggests that dental occlusion is important in cases without any neuro-vascular compression. Further, the occlusion may be the most significant TN etiologic factor regardless of whether neurovascular compression is present, since no MRI exams were used to show neurovascular compression was present in any of these 31 TN subjects. ICAGD removed the occlusal surface friction from the subject’s mandibular excursions to very high-precision numerical tolerance (DT < 0.5 seconds). This occlusal change eliminated the posterior tooth engagement, which then interrupted the excessive amounts of tooth initiated electrical output that stimulated TN symptom episodes. These physiologic changes were neurologically mediated within the Central Nervous System17 because the time-duration and volume of posterior teeth pulpal nerve fiber flexures and PDL nerve fiber compressions were both drastically reduced by ICAGD. Therefore short posterior disclusion in ≤ 0.5 seconds8–16 greatly reduced the frequency and seriousness of the Trigeminal Neuralgia symptoms.


Although the subject group showed definitive Trigeminal Neuralgia improvements this study’s limitations were; 1) that there were a relatively small number of subjects (31 subjects), 2) there were no control subjects to compare the treated subjects’ outcomes against, and 3) the follow up was short at only one month. However, the use of a TN Habits questionnaire helped overcome these limitations, as did the highly significant p values (many of the assessed physical and emotional conditions had p values < 0.00001) after treatment indicating the marked degree of symptom improvements among these TN subjects.


In this 31-patient pool, long Disclusion Time and excursive occlusal contacts were the primary etiologic factors for Trigeminal Neuralgia symptom episodes. ICAGD and DTR treatment positively lessened Trigeminal Neuralgia symptom frequency and intensity, indicating that an interrelationship exists between occlusion and Trigeminal Neuralgia physiologically. Tooth-borne Trigeminal Nerve CNS inputs from excursively contacting teeth contributed to the electrical shock-like pains from Trigeminal Neuralgia. Once removed via ICAGD, Trigeminal Neuralgia symptoms markedly resolved. A Trigeminal Neuralgia/Randomized Clinical Trial ICAGD study, could further reveal occlusion’s primary role in Trigeminal Neuralgia

Potential Conflict of Interest Statement

The 3rd author (R.B.K) is a consultant to Tekscan, Inc., but receives no monetary or other gain from the sale of product.

The 4th author (J.R.) is the Chairman of the Board of Directors of BioResearch Associates, Inc. and receives no commission from the sales of any products.